FACULTY OF MEDICINE

Rehabilitation plan and

process of patient with

heart failure

Bachelor's thesis

Rana Mohammed Ismail

Supervisor: Mgr. Michal Úlehla

Department of physiotherapy and rehabilitation.

Field physiotherapy

Brno 2022

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Bibliographic record

Author: Rana Mohammed Ismail

Faculty of Medicine

Masaryk University

Hewlett-Packard Company

Title of Thesis: Rehabilitation plan and process of patient with heart failure

Nazev prace: Rehabilitační plán a postup u pacienta se srdečním selháním

Degree Programme: Bachelor programme

Field of Study: Physiotherapy

Supervisor: Mgr. Michal Úlehla

Year: 2022

Number of Pages: 140

Keywords: heart failure, cardiomyopathy, myocardial infarction, cardiovascular

rehabilitation, physiotherapy

Klicove slova: srdeční selhání, kardiomyopatie, infarct myokardu, kardiovaskulární

rehabilitace, fyzioterapie

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Abstract

This bachelor’s thesis deals with rehabilitation and physiotherapy of patients after heart failure.

It is divided into three parts. As first, the theoretical part focuses on the definition of the disease

and basics of anatomy, physiology of the heart and pathophysiology of heart failure. It includes

brief classification and stages, diagnostic criteria of the disease, as well as diagnostic methods

and treatment, prevention and complications of heart failure. The second part of thesis focuses

on different type and possibilities of rehabilitation, physiotherapy approaches after heart

failure. The third and the last part contains a practical case report of a patient who suffered

from heart failure including examination, short-term rehabilitation plan, individual exercise

session by the author which lasted for 5 days, and finally recommendations for follow-up care.

Anotace

Tato bakalářská práce se zabývá rehabilitací a fyzioterapií pacientů po srdečním selhání. Je

rozdělena do tří částí. Teoretická část se nejprve zaměřuje na definici onemocnění a základy

anatomie, fyziologii srdce a patofyziologii srdečního selhání. Zahrnuje stručnou klasifikaci a

stadia, diagnostická kritéria onemocnění, dále diagnostické metody a léčbu, prevenci a

komplikace srdečního selhání. Druhá část práce je zaměřena na různé typy a možnosti

rehabilitace, fyzioterapeutické přístupy po srdečním selhání. Třetí a poslední část obsahuje

praktickou kazuistiku pacienta se srdečním selháním včetně vyšetření, krátkodobého

rehabilitačního plánu, individuálního cvičení autora v délce 5 dnů a nakonec doporučení pro

následnou péči.

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Declaration

I hereby declare that this thesis with title Rehabilitation plan and process of patient with

heart failure I submit for assessment is entirely my own work and has not been taken from the

work of others save to the extent that such work has been cited and acknowledged within the

text of mine.

Brno March 22, 2022 .......................................

Rana Mohammed Ismail

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Acknowledgements

At this point I would like to express my gratitude to my supervisor Mgr. Michal Úlehla, for his

time and guidance, valuable advice, comments, and help in processing the work. I would like

to thank prof. MUDr. Jarmila Siegelová, DrSc. for her prudent organizing and teaching. Lastly,

I would like to express my sincere gratitude to Mr. L.P., for his willingness and cooperation

throughout the whole rehabilitation process.

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Table of Content

LIST OF FIGURES ................................................................................................... 14

LIST OF TABLES ..................................................................................................... 15

1 REVIEW OF THEORETICAL KNOWLEDGE ................................................ 21

1.1 GENERAL PART OF THESIS ...................................................................................................... 21

1.1.1 INTRODUCTION .................................................................................................................... 21

1.1.2 DEFINITION OF HEART FAILURE ..................................................................................... 23

1.1.3 INCIDENCE ............................................................................................................................. 23

1.1.4 CLASSIFICATION OF HEART FAILURE ............................................................................ 24

1.1.5 STAGES OF HEART FAILURE ............................................................................................. 27

1.1.6 ETIOLOGY AND RISK FACTORS OF HEART FAILURE .................................................. 28

1.1.7 PATHOPHYSIOLOGY OF HEART FAILURE ...................................................................... 31

1.1.7.1 SYSTOLIC DYSFUNCTION ........................................................................................... 34

1.1.7.2 DIASTOLIC DYSFUNCTION ......................................................................................... 35

1.1.8 ANATOMY OF THE HEART .............................................................................................. 36

1.1.8.1 THE HEART CHAMBERS ......................................................................................... 37

1.1.8.2 THE HEART VALVES .............................................................................................. 37

1.1.8.3 THE CONDUCTION SYSTEM .................................................................................. 38

1.1.8.4 THE CIRCULATORY SYSTEM................................................................................ 38

1.1.8.5 STRUCTURE AND FUNCTION ................................................................................ 39

1.1.8.6 EMBRYOLOGY .......................................................................................................... 40

1.1.8.7 BLOOD SUPPLY AND LYMPHATICS .................................................................... 40

1.1.8.8 INNERVATION OF THE HEART .............................................................................. 41

1.1.8.9 MUSCLES OF THE HEART ....................................................................................... 42

1.1.9 PHYSIOLOGY OF THE HEART ............................................................................................ 42

1.1.9.1 CARDIAC CYCLE ...................................................................................................... 42

1.1.9.1.1 PRESSURE AND FLOW ..................................................................................... 44

1.1.9.1.2 PHASES OF CARDIAC CYCLE ......................................................................... 45

1.1.9.1.2.1. ATRIAL SYSTOLE AND DIASTOLE ....................................................... 45

1.1.9.1.2.2. VENTRICULAR SYSTOLE ....................................................................... 45

1.1.9.1.2.3. VENTRICULAR DIASTOLE ..................................................................... 46

1.1.9.2 RESTING CARDIAC OUTPUT .................................................................................. 47

1.1.9.3 EXERCISE AND MAXIMUM CARDIAC OUTPUT ................................................. 48

1.1.9.4 HEART RATE ............................................................................................................. 48

1.1.10 DIAGNOSTIC CRITERIA OF HEART FAILURE .............................................................. 49

1.1.10.1 MEDICAL HISTORY AND PHYSICAL EXAMINATION .................................. 49

1.1.10.2 LABORATORY TESTS ........................................................................................... 49

1.1.10.3 CHEST RADIOGRAPHY ......................................................................................... 50

1.1.10.4 ELECTROCARDIOGRAPHY .................................................................................. 51

1.1.10.5 CLINICAL DECISION MAKING ........................................................................... 51

1.1.10.6 AN OVERVIEW OF HEART FAILURE EVALUATION AND DIAGNOSIS .... 52

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1.1.11 WARNING SIGNS AND SYMPTOMS OF HEART FAILURE ......................................... 54

1.1.12 HEART FAILURE DIAGNOSIS ......................................................................................... 55

1.1.13 HEART FAILURE TREATMENT ...................................................................................... 57

1.1.14. PREVENTION OF HEART FAILURE ............................................................................... 59

1.1.15 COMPLICATIONS OF HEART FAILURE ......................................................................... 62

1.2 SPECIAL PART OF THESIS ......................................................................................................... 64

1.2.1 GENERAL PRINCIPLES OF EXERCISE TESTING IN CARDIAC REHABILITATION 64

1.2.1.1 INTRODUCTION ......................................................................................................... 64

1.2.1.2 CARDIOPULMONARY EXERCISE TEST (SPIROERGOMETRY) .................. 64

1.2.1.3 CARDIAC STRESS TEST .......................................................................................... 66

1.2.1.4. DYNAMOMETRY .................................................................................................... 68

1.2.1.5. COMPREHENSIVE MEDICAL REHABILITATION ............................................ 68

1.2.1.5.1 PERIOPERATIVE CARDIAC REHABILITATION .......................................... 69

1.2.1.5.2 POST-OPERATIVE CARDIAC REHABILITATION ...................................... 70

1.2.1.5.2.1 PHASE 1: ACUTE, IN HOSPITAL PATIENT PERIOD ......................... 70

1.2.1.5.2.2 PHASE 2: SUBACUTE OUTPATIENT CARE (POST-DISCHARGE,

PRE-EXERCISE PERIOD), (2-6 WEEKS POST-SURGERY) .............................................. 71

1.2.1.5.2.3 PHASE 3: SUBACUTE OUTPATIENT CARE (POST-DISCHARGE,

PRE-EXERCISE PERIOD), (7-12 WEEKS POST-SURGERY) ............................................ 72

1.2.1.5.2.4 PHASE 4: MAINTENANCE (13 WEEKS AND BEYOND POST-

SURGERY) ................................................................................................................. 73

1.2.1.5.3 OUTPATIENT CONTROLLED PROGRAM ..................................................... 74

1.2.1.5.3.1 SPA TREATMENT ...................................................................................... 75

1.2.1.5.3.2 HOME EXERCISE PROGRAM ................................................................. 76

1.2.1.5.4 THERAPEUTIC PHYSICAL EDUCATION ...................................................... 76

1.2.1.5.4.1 RESPIRATORY PHYSIOTHERAPY .......................................................... 76

1.2.1.5.4.2 RESISTANCE TRAINING .......................................................................... 82

1.2.1.5.4.3 ENDURANCE AEROBIC TRAINING ....................................................... 86

1.2.1.5.5 PHYSICAL THERAPY METHODS .................................................................. 88

1.2.1.5.5.1 CARBONIC BATH ...................................................................................... 89

1.2.1.5.5.2 LOW-FREQUENCY ELECTRICAL STIMULATION ............................... 90

1.2.1.5.6 ERGOTHERAPY ................................................................................................. 90

1.2.1.5.7 PSYCHOLOGICAL AND SOCIAL PROBLEMS OF THE DISEASES ........... 91

1.2.1.5.8 INDICATIONS AND CONTRAINDICATIONS OF CARDIAC

REHABILITATION ............................................................................................................................... 93

2 CASUISTICS ............................................................................................................ 94

2.1 BASIC DATA ................................................................................................................................. 94

2.2 PLACE OF HOSPITALIZATION .................................................................................................. 94

2.3 DIAGNOSIS UPON ADMISSION.................................................................................................. 95

2.4 PRESCRIBED REHABILITATION ............................................................................................... 96

2.5 ENGAGEMENT OF AUTHOR IN THE REHABILITATION PROCESS ................................... 96

2.5.1 ANAMNESIS ........................................................................................................................... 96

2.5.2 PHYSICAL EXAMINATION ................................................................................................. 99

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2.5.3 INITIAL KINESIOLOGY EXAMINATION ....................................................................... 103

2.5.4 SHORT-TERM PLAN .......................................................................................................... 110

2.5.5 REHABILITATION PROCESS ............................................................................................ 112

2.5.6 KINESIOLOGICAL EXAMINATION AT DISCHARGE .................................................. 119

2.5.7 LONG-TERM PLAN ............................................................................................................ 120

3 CONCLUSION ..................................................................................................... 123

IBLIOGRAPHY ....................................................................................................... 125

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List of Figures

FIGURE 1 ANATOMICAL PARTS OF THE HEART

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FIGURE 2 THE FOUR VALVES OF THE HEART27 ............................................................................................................ 38

FIGURE 3 OVERVIEW OF CARDIAC CYCLE35 ................................................................................................................... 44

FIGURE 4 RELATIONSHIP BETWEEN THE CARDIAC CYCLE AND ECG35 ...................................... 47

FIGURE 5 MAJOR FACTORS INFLUENCING CARDIAC OUTPUT38 ........................................................................ 48

FIGURE 6 ALOGORITHM FOR EVALUATION AND DIAGNOSIS OF HEART FAILURE148 ........................... 53

FIGURE 7 BACK POSITION, POSTURAL DRAINAGE TECHNIQUE115 ................................................................... 78

FIGURE 8 SIDE LYING POSITION, POSTURAL DRAINAGE TECHNIQUE115 ..................................................... 79

FIGURE 9 STOMACH POSITION, POSTURAL DRAINAGE TECHNIQUE115 ......................................................... 79

FIGURE 10 DEPP BREATHING AND COUGHING TECHNIQUE117 ........................................................................... 81

FIGURE 11 OVERVIEW OF MAJOR CARDIOVASCULAR EFFECT OF EXERCISE131-132 .............................. 88

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List of Tables

TABLE 1 FRAMINGHAM DIAGNOSTIC CRITERIA FOR HEART FAILURE ................................................ 53

TABLE 2 WARNING SIGNS AND SYMPTOMS OF HEART FAILURE .......................................................... 54

TABLE 3 SUBJECTIVE PERCEPTION OF EFFORT ACCORDING BORG SCALE ........................................ 67

TABLE 4 SUBJECTIVE EVALUATION OF DYSPNEA ...................................................................................... 67

TABLE 5 RESISTANCE TRAINING PROGRAMMING FOR CARDIAC PATIENTS ...................................... 84

TABLE 6 RESISTANCE TRAINING BENEFITS FOR CARDIAC PATIENTS .................................................. 84

TABLE 7 ABSOLUTE AND RELATIVE CONTRAINDICATIONS FOR RT IN CARDIAC PATIENTS ....... 85

TABLE 8 ANTHROPOMETRY, LENGTH AND CIRCUMFERENCE IN OF THE UPPER EXTREMITY ... 106

TABLE 9 ANTHROPOMETRY, LENGTH AND CIRCUMFERENCE IN OF THE LOWER EXTREMITY... 107

TABLE 10 PERIMETER DIMENSIONS OF THE ABDOMEN AND CHEST IN ............................................. 107

TABLE 11 DEEP TENDON REFLEXES AND SUPERFICIAL REFLEXES .................................................... 108

TABLE 12 PATHOLOGICAL REFLEXES ........................................................................................................... 108

TABLE 13 MUSCLE SHORTENING TEST ........................................................................................................ 109

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Glossary

1-RM Repetition Maximum Approach

AACVPR Association for Cardiovascular and Pulmonary

Rehabilitation

ACC American College of Cardiology

ACD Arteria Coronaria Dextra

ACE Angiotensin Converting Enzyme

ADH Antidiuretic Hormone

ADHF Acute Decompensated Heart Failure

ADL Activity of Daily Living

AHA American Heart Association

AHF Acute Heart Failure

AKI Acute Kidney Insufficiency

ATP Adenosine Triphosphate

AV Atrioventricular

BNP B-Type Natriuretic Peptide

BP Blood Pressure

Bpm Beat Per Minute

CAD Coronary Artery Disease

CAGB Carbonic Acid Gas Bath

CHHF Chronic Heart Failure

CKTCH Cardio Surgery Clinic

CO Cardiac output

CO2 Carbon Dioxide

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COPD Chronic Obstructive Pulmonary Disease

CPAP Continuous Positive Airway Pressure

CPB Cardiopulmonary Bypass

CPR Cardiopulmonary Resuscitation

CPX Cardiopulmonary Exercise Test

CR Cardiac Rehabilitation

CRP Cardiac Rehabilitation Program

CRT – Ds Cardiac Resynchronization Therapy Device

CT Computerized Tomography

CVD Cardiovascular Disease

CVVHD Continuous Veno-venous Hemodialysis

DCM Delated Cardiomyopathy

DS Dorsal Septum

DVT Deep Vein Thrombosis

dx Dexter

E deceleration time Early left Ventricular Filling

e NOS Endothelial Nitric Oxide Synthase

E/A ratio Ratio of Early Left Ventricular to Atrial Filling

ECG Electrocardiography

Echo Echocardiogram

ECM Extracorporeal Membrane Oxygenation

EDV End Diastolic Volume

EF Ejection Fraction

EGF Epidermal Growth Factor

EPC Endothelial Progenitor Cell

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ESV End Systolic Volume

ET Exercise Test

HBP High Blood Pressure

HDL High Density Lipoprotein

HF Heart Failure

HFpEF Heart Failure with Preserved Ejection Fraction

HFrEF Heart Failure with Reduced Ejection Fraction

HR Heart Rate

HRSL Symptoms Limited Heart Rate

IADL Instrumental Activity of Daily Living

ICD Implantable Cardioverter Defibrillator

ICHD Ischemic Heart Disease

IEF Increased Expiratory Flow

IKAK First Internal Cardiology Clinic

IU International Unit

LA Left Atrium

LAD Left Anterior Descending Coronary Artery

LCA Left Coronary Artery

LCX Left Circumflex Coronary Artery

LDL Low Density Lipoprotein

LFES Low Frequency Electrical Stimulation

LK Left Kidney

LR- Negative Likelhood Ratio

LR+ Positive Likelhood Ratio

LV Left Ventricle

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LVEF Left Ventricular Ejection Fraction

M2 receptor Muscarinic Acetylcholine Receptor

MI Myocardial Infarction

mmHg Millimeter of Mercury

MRI Magnetic Resonance Imaging

MVR Mitrals Valve Replacement

NO Nitric Oxide

NSIAD’s Non-Steroidal Anti-inflammatory Drugs

NYHA New York Heart Association

OTS Orthotopic Transplantation of Heart

PDA Posterior Descending Artery

QOL Quality of Life

RC Ramus Circumflexus

RCA Right Coronary Artery

RER Respiratory Exchange Ratio

Res Resume

RIA Ramus Interventricularis Anterior

RMS Ramus Marginalis Sinister

ROM Range of Motion

RPP Rate Pressure Product

RT Resistance Training

RV Ramus Ventricularis

SA node Sinoatrial Node

SCD Sudden Cardiac Death

sin Sinister

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SKG Selective Coronarography

STEMI ST – Elevation Myocardial Infarction

SV Stroke Volume

TG Triglyceride

THR Training Hear Rate

VA ECMO Veno-Atrial ECMO (Extracorporeal Membrane

Oxygenation)

VCO2 Carbonic Dioxide Output

VE/VCO2 Minute Ventilation Per Unit Carbon Dioxide

Production

VLDL Very Low-Density Lipoprotein

VO2 Oxygen Consumption

VO2SL Volume of Oxygen Symptoms Limited

VSM Vascular Smooth Muscle

VT1 First Ventilatory Threshold

VT1 Second Ventilatory Threshold

WHO World Health Organization

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1 REVIEW OF THEORETICAL KNOWLEDGE

1.1 General Part of Thesis

1.1.1 Introduction

Heart failure has been described by some authors as the cardiovascular epidemic of the

21st century, characterized by its increasing incidence and prevalence, as evidenced by the

increased number of hospitalizations. This is mainly due to an aging population, as well as

better and more accessible medical care, which has progressively reduced mortality due to

ischemic heart disease (ICHD) or myocardial infarction (MI). In the 1950s when Eisenhower

had his heart attack, the treating physician did not have many options, accordingly the mortality

rate averaged 50 % for those reaching hospital. Heart attack survivors at that time were prone

to developing heart failure or sudden death. Today we are much more successful in treating

patients with acute myocardial infarction. The mortality rate today is 5 % for those getting to

hospital and receiving appropriate treatment in a hospital with capability to perform primary

percutaneous coronary intervention. Another reason for the increase in hospitalizations due to

heart failure is the prevention of sudden death in patients with impaired left ventricular function

by the use of devices and antiarrhythmic drugs. Finally, the introduction of drugs and

interventions for the treatment of high blood pressure has reduced the occurrence of myocardial

infarction but has led to an increase in heart failure with preserved and reduced ejection

fraction.1-2-3

Heart failure is the end stage of all diseases of the heart and is a major cause of

morbidity and mortality. Roughly 670,000 people are diagnosed with heart failure each year. It’s

the main reason people older than 65 go into the hospital.

Despite significant advances in diagnosis and treatment, both acute and chronic heart failure

represent a clinical syndrome with a serious prognosis. According to the Framingham Study,

the 5-year mortality rate for chronic heart failure (CHHF) is 25 % for men and 40 % for women.

In patients classified as New York Heart Association (NYHA) III and IV, mortality can be as

high as 20-50 % in one year.2 In most cases, patients with heart failure die from cardiovascular

causes, particularly from sudden cardiac death (SCD) and exacerbation of heart failure.4

Heart failure and its symptoms significantly affect a patient’s quality of life.

Physical training and rehabilitative care are an integral part of the treatment procedure for

patients with heart failure. They not only help improve the patient’s quality of life, but also

help prevent and treat other comorbidities. In the case of heart attack or another heart problem,

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cardiac rehabilitation is an important part of the recovery. Cardiac rehabilitation can help

prevent another heart attack, possibly a more serious one, and can help build heart-healthy

habits.

Generally, cardiac rehabilitation is an important program for anyone recovering from a

heart attack, heart failure, or other heart problem that required surgery or medical care.

Cardiac rehabilitation is a supervised program that includes physical activity. Education about

healthy living, including how to eat healthy, take medicine as prescribed, and quit smoking.

Counseling to find ways to relieve stress and improve mental health.

Anyone who has had a heart problem, such as a heart attack, heart failure, or heart

surgery, can benefit from cardiac rehabilitation. Studies have found that cardiac rehabilitation

helps men and women, people of all ages, and people with mild, moderate, and severe heart

problems.5

However, some people are less likely to start or finish a cardiac rehabilitation program,

including studies show that women, especially minority women, are less likely than men to

start or complete cardiac rehabilitation. This may be because doctors are less likely to suggest

cardiac rehabilitation to women. Older adults are also likely to join a cardiac rehabilitation

program following a heart problem. They may think they are unable to do the physical activity

because of their age, or they may have other conditions that can make exercising harder, such

as arthritis. The need to address other physical conditions makes cardiac rehabilitation

especially useful for older adults, since it can improve strength and mobility to make daily tasks

easier.

Cardiac rehabilitation can have many health benefits in both the short and long term,

including: strengthening the heart and body after heart complication, relieving symptoms of

heart problems such as chest pain, building healthier habits such as getting more physical

activity, quitting smoking, eating a heart-healthy diet, reducing stress, improving the mood,

lessen depression, increasing the energy and the strength to make daily activities like carrying

groceries and climbing stairs easier, preventing future illness and death from heart disease.

Studies have found that cardiac rehabilitation decreases the chance of death in the 5 years

following a heart attack or bypass surgery by about 35 %.6

The work itself is divided into a theoretical part, in which I focus on definition,

incidence, prevalence and etiology, pathophysiology, clinical manifestations, disease course,

diagnosis and, finally, treatment of heart failure, including comprehensive medical

rehabilitation. The second part is a case study, where I apply the theoretical knowledge

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presented in the first part to a specific patient and focus mainly on the possibilities of

rehabilitation.

1.1.2 Definition of heart failure

Heart failure also known as congestive heart failure and congestive cardiac failure, is a

pathophysiological condition in which the heart, as a pump, is unable to meet the metabolic

requirements of the tissue for oxygen and substrates despite normal or increased venous return

to the heart, is a long-term condition that gets worse over time. Although the name sounds like

your heart has stopped working, from a pathophysiological point of view heart failure doesn’t

mean the heart stopped working. Rather, it means that the heart works less efficiently than

normal for various possible reasons, blood moves through the heart and body at a slower rate

and the pressure in the heart increases. As a result, the heart cannot pump enough oxygen and

nutrients to meet the body’s needs. The chambers of the heart may respond by stretching to

carry more blood to pump through the body or by hardening and thickening.

This helps keep the blood moving, but the walls of the heart muscle may eventually

weaken and become unable to pump blood efficiently. The kidneys may respond by making

the body retain fluid (water) and salt. If fluid builds up in the arms, legs, ankles, feet, lungs, or

other organs, the body becomes congested. The term congestive heart failure is used to describe

the condition.

In other words, we can say that is when the heart is not able to pump blood as well as

it should. When heart’s pumping power drops, it can damage your organs and fluid can collect

in your lungs.7

1.1.3 Incidence

Over the last 30 years we have gone from famine to feast in terms of the epidemiological data

now published for heart failure (HF). The field started with the seminal publication on the

natural history of HF from the Framingham study in 1971 showing a prevalence of HF of

0.8 % in those aged between 50 and 59, rising to 9.1 % in those over 80 years with incidence

rates of 0.2 % at age 54 and 0.4 % at age 85. This was followed by a large European study the

men born in 1913, which gave similar figures of a prevalence of 2.1 % at age 50 and 13 % at

age 67 and incidence rates of 0.15 % and 1 % respectively at ages 50 and 67.

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These landmark studies relied on a clinical diagnosis of HF, based on symptoms, signs,

and scoring systems to identify cases. More modern epidemiological studies have used

definitions of HF which include objective measures of cardiac function in their definition, in

keeping with current European and United States guidelines for the diagnosis of HF. Initial

studies focused on systolic dysfunction because they reported at much the same time as the HF

treatment trials which also enrolled patients with systolic HF. More recently attention has

turned to describing the epidemiology of HF with preserved systolic function, in addition.

When describing the epidemiology of HF, it is worth bearing in mind that estimates of

incidence and prevalence will vary according to the definition of HF used and the type of cohort

being studied. This is especially important when assessing work which has objectively

measured left ventricular systolic function. Variables such as left ventricular ejection fraction

are normally distributed, so the cut point chosen is a critical determinant of the eventual results.

The present chapter aims to outline the contemporary epidemiology of HF by describing its

prevalence, incidence, etiology and mortality as well as describing the trends which are

occurring in the area. It will discuss hospitalization rates, prognosis and economic burden in

both Europe and the United States.8

1.1.4 Classification of heart failure

• Classification based on the course of the disease:

We classify heart failure from several perspectives. Depending on the rate of onset of

symptoms, it is acute and chronic heart failure. AHF is when symptoms appear suddenly, or a

person experiences rapid worsening of existing symptoms of heart failure, with AHF, you

experience a sudden, rapid decline in heart functioning and the amount of blood your heart can

pump to the rest of your body. AHF occurs in people with or without previous heart issues.

Acute decompensated heart failure (ADHF) occurs in people with heart conditions, such as

coronary artery disease. De novo acute heart failure occurs in people with no history of heart

disease.9 They have ongoing health conditions, like diabetes, that damage their heart.

The first manifestation of heart failure is AHF in approximately 20 % of cases. One of

the most common symptoms of AHF is shortness of breath (dyspnea), you may experience:

heavy breathing, sensation like suffocating, struggling to breath while laying down, tight chest.

Other symptoms may include: arrythmia, cough, chest pain, fluid retention (edema) in the arms

or legs. Health issues that strain the heart increase your risk of heart failure: advanced kidney

25

disease, alcoholism, blood clot in the lungs (pulmonary embolism), diabetes, hypertension,

hyperthyroidism, stroke, sleep apnea. Existing heart problems that cause ADHF include:

arrythmia, coronary artery disease, heart valve disease. CHHF otherwise known as congestive

heart failure, is manifested by a gradual development of symptoms. It can occur as a result of

AHF, but it can also occur in patients without a previous acute episode. The symptoms of

CHHF is quite similar to the AHF such as: shortness of breath, tiredness, swelling of the legs

and ankles, chest pain and a cough. In the long run, it is usually progressive in nature, with the

rate of progression varying for each patient. With adequate therapy, progression may be

stopped until the disease subsides. A typical feature is the intermittent and fluctuating nature

of the disease – periods of relative stability are alternated by periods of worsening cardiac

compensation, which often lead to hospitalization.

An estimated 15 % of patients are in the advanced CHHF phase in the NYHA category

III – IV.1 It most commonly affects older people and people with other heart conditions and is

typically treated with a combination of lifestyle and diet changes, and medications. Chronic

heart failure is typically a long-term condition that gradually worsens over time. This is the

feature that differentiates it from AHF, which develops very suddenly. It cannot typically be

cured, but symptoms can be managed effectively.

• Another classification:

Heart failure often only affects the left or right side of the heart but can affect both. Doctors

differentiate between three types of heart failure, accordingly:

Left-sided heart failure: The left ventricle of the heart no longer pumps enough blood around

the body. As a result, blood builds up in the pulmonary veins (the blood vessels that carry blood

away from the lungs). This causes shortness of breath, trouble breathing or coughing –

especially during physical activity. Left-sided heart failure is the most common type.

Right-sided heart failure: Here the right ventricle of the heart is too weak to pump enough

blood to the lungs. This causes blood to build up in the veins (the blood vessels that carry blood

from the organs and tissue back to the heart). The increased pressure inside the veins can push

fluid out of the veins into surrounding tissue. This leads to a build-up of fluid in the legs, or

less commonly in the genital area, organs or the abdomen (belly).

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Biventricular heart failure: In biventricular heart failure, both sides of the heart are affected.

This can cause the same symptoms as both left-sided and right-sided heart failure, such as

shortness of breath and a build-up of fluid.

Left-sided heart failure is usually caused by coronary artery disease (CAD), a heart

attack or long-term high blood pressure. Right-sided heart failure generally develops as a result

of advanced left-sided heart failure and is then treated in the same way. It is sometimes caused

by high blood pressure in the lungs, an embolism in the lungs (pulmonary embolism), or certain

lung diseases such as chronic obstructive pulmonary disease (COPD).

• Classification based on pumping ability:10

Nowadays, heart failure is increasingly being classified based on the pumping ability of the

heart. This is because the pumping ability plays an important role when choosing the most

suitable medication. There are two different types of chronic heart failure:

Heart failure with reduced pumping ability: The medical term for this is “heart failure with

reduced ejection fraction (HfrEF), or systolic heart failure.” Systolic heart failure occurs when

the left ventricle loses its ability to contract, when the heart is too weak and doesn’t squeeze

normally. In people with systolic heart failure, blood fills the left ventricle at normal levels, but

it cannot be pumped in adequate amounts to support bodily functions. If the body’s tissues are

deprived of oxygen, organ failure may ensue. The most common causes of systolic heart failure

are coronary artery disease, hypertension, cardiomyopathy, myocarditis.10

Heart failure with preserved pumping ability: Doctors call this “heart failure with preserved

ejection fraction (HfpEF). Or diastolic heart failure.” Diastolic heart failure occurs when the

left ventricle loses its ability to expand due to stiffness. The heart chamber also is unable to fill

with enough blood normally during the resting periods of the cardiac cycle. As a result, there

is less blood available to pump out of the heart. Diastolic heart failure occurs when the left side

of the heart is too stiff to relax and fill normally with blood. The most common culprits of left-

sided heart failure are heart attack, coronary artery disease, hypertension. While the right side

of the heart is more commonly affected by: COPD, Rheumatic heart disease.10 As you get older,

the heart and blood vessels become less elastic, increasing the risk of developing diastolic heart

27

failure. Other causes of diastolic heart failure: diabetes, obesity, sedentary lifestyle, coronary

artery disease.10

It is also possible to be affected by a combination of these two types. Moreover, each

type of chronic heart failure can affect the left ventricle, right ventricle or both simultaneously.

The symptoms of chronic heart failure generally depend on the type of the condition being

experienced and its location, i.e. which ventricle is involved. The main symptom of left-sided

chronic heart failure is shortness of breath, which will generally become worse with activity or

when lying flat. A cough may also present. If the condition is affecting the right-side of the

heart, edema, a buildup of fluid causing swelling of the legs and ankles, is the most commonly

experienced symptom.10

1.1.5 Stages of heart failure

According to WebMD, in 2001, the American Heart Association (AHA) and American College

of Cardiology (ACC) described the “Stages of Heart Failure.” These stages, which were

updated in 2005, will help understand to that heart failure is often a progressive condition and

can worsen over time. They will also help to understand why a new medication was added to

the treatment plan and may also help understand why lifestyle changes and other treatments

are needed. The stages classified by the AHA and ACC are different than the New York Heart

Association (NYHA) clinical classifications of heart failure that rank patients as class I-II-III-IV,

according to the degree of symptoms or functional limits.11

• Stage A: Stage A is considered pre-heart failure. It means you’re at high risk of

developing heart failure because you have a family history of heart failure or you have

one or more of these medical conditions: hypertension, diabetes, coronary artery

disease, metabolic syndrome, history of alcohol abuse, metabolic syndrome, family

history of cardiomyopathy, history of taking drugs that can damage your heart muscle,

such as some cancer drugs. Simply, at high risk for heart failure but without structural

heart disease or symptoms of heart failure

• Stage B: Stage B is considered pre-heart failure. It means your healthcare provider has

given you a diagnosis of systolic left ventricular dysfunction, but you’ve never had

symptoms of heart failure. Most people with Stage B heart failure have an

28

echocardiogram (echo) that shows an ejection fraction (EF) of 40 % or less. This

category includes people who have heart failure and reduced EF (HF-rEF) due to any

cause. Simply structural heart disease but without signs or symptoms of heart failure.

• Stage C: People with Stage C heart failure have a heart failure diagnosis and currently

have or previously had signs and symptoms of the condition. Symptoms include

shortness of breath, fatigue, reduced ability to exercise, weak legs, waking up to urinate,

swollen feet, ankles, lower legs and abdomen.

• Stage D and reduced EF: People who have Stage D HF-rEF have advanced symptoms

that don’t get better with treatment. This is the final stage of heart failure.12

According to WebMD, The New York Heart Association (NYHA) clinical classifications

of heart failure rank people as class I-II-III-IV, according to the degree of symptoms or functional

limits.11

• Class I: Physical activity is not affected, and you have no unusual fatigue, shortness of

breath, palpitations, or pain during normal activities.

• Class II: Slight limitations on normal activities. You may have mild fatigue, shortness of

breath, palpitations, or pain during normal activities, no symptoms at rest.

• Class III: Marked limitation on normal activities. You have fatigue, shortness of breath,

palpitations, or pain during less than normal activities, no symptoms at rest.

• Class IV: You’re uncomfortable even at rest. Discomfort gets worse with any physical

activity.11

1.1.6 Etiology and risk factors of heart failure

Many other heart conditions can ultimately lead to heart failure. All of us lose some blood-

pumping ability in our hearts as we age, but heart failure results from the added stress of health

conditions that either damage the heart or make it work too hard. All of the lifestyle factors that

increase your risk of heart attack and stroke – smoking, being overweight, eating foods high in

fat and cholesterol and physical inactivity – can also contribute to heart failure.

Conditions that may lead to heart failure:13

1. Coronary artery disease. When cholesterol and fatty deposits build up in the heart’s

arteries, less blood can reach the heart muscle. This buildup is known as atherosclerosis.

29

The result may be chest pain (angina) or, if blood flow becomes totally obstructed, a

heart attack. Coronary artery disease can also contribute to having high blood pressure,

which may lead to heart failure over time.

2. Past heart attack (myocardial infarction). A heart attack occurs when an artery that

supplies blood to the heart muscle gets blocked. The denial of oxygen and nutrients

damages the heart’s muscle tissue – part of it essentially “dies.” The damaged heart

tissue does not contract as well, which weakens the heart’s ability to pump blood.

3. High blood pressure (hypertension or HBP). Uncontrolled HBP is a major risk factor

for developing heart failure. When pressure in the blood vessels is too high, the heart

must pump harder than normal to keep the blood circulating. This takes a toll on the

heart, and over time the chambers get larger and weaker. For those at risk of developing

heart failure, your doctor might prescribe medication to get your blood pressure below

130/80 mmHg.13

4. Abnormal heart valves. Heart valve problems can result from disease, infection

(endocarditis) or a defect present at birth. When the valves don’t open or close

completely during each heartbeat, the heart muscle has to pump harder to keep the blood

moving. If the workload becomes too great, heart failure results.

5. Heart muscle disease (dilated cardiomyopathy, hypertrophic cardiomyopathy) or

inflammation (myocarditis). Any damage to the heart muscle – whether because of drug

or alcohol use, viral infections or unknown reasons – increases the risk of heart failure.

6. Heart defects present at birth (congenital heart disease). If the heart and its chambers

don’t form correctly, the healthy parts have to work harder to compensate.

7. Severe lung disease. When the lungs don’t work properly, the heart has to work harder

to get available oxygen to the rest of the body.13

8. Diabetes. Diabetes increases the risk for developing heart failure. People with diabetes

tend to develop hypertension and atherosclerosis from elevated lipid level in the blood.

Both hypertension and atherosclerosis have been linked to heart failure.

9. Obesity. Obesity can cause the heart to work much harder than for a non-obese person.

Being obese is also a cause of sleep apnea and can cause cardiomyopathy.

10. Sleep apnea. Sleep apnea is a potentially life-threatening sleep disorder. Pauses in

breathing can contribute to severe fatigue during the day, increase your safety risks and

make it difficult to perform tasks that require alertness. Sleep apnea is also a risk factor

for medical problems like high blood pressure, heart failure, diabetes and stroke. In

30

some cases, people with heart failure may need to use a continuous positive airway

pressure machine (CPAP).13

Other conditions:

Less commonly, an otherwise healthy heart may become temporarily unable to keep up with

the body's needs. This can happen in people who have:

1. Low red blood cell count (severe anemia). When there aren't enough red blood cells to

carry oxygen, the heart tries to move the small number of cells at a faster heart rate. It

can become overtaxed from the effort.

2. An overactive thyroid gland (hyperthyroidism). This condition causes the body to work

at a faster pace, and the heart can be overworked trying to keep up.

3. Abnormal heart rhythm (arrhythmia or dysrhythmia). When the heart beats too fast, too

slow or irregularly, it may not be able to pump enough blood to meet all the body's

needs.

In these cases, the person may experience heart failure symptoms until the underlying problem

is identified and treated.13

According to WebMD, some drugs and natural supplements cause or worsen heart failure

because they: Are toxic to your heart, Affect the strength of heart muscle contractions, Make high

blood pressure worse, Prevent heart failure medications from working well.14

Prescription drugs: People with heart failure take an average of 6.8 prescription medicines

a day. The more drugs you take, the more likely you are to have a drug-drug interaction. This can

put your heart at risk.

These drugs can raise your risk of heart failure or related problems:

1. Nonsteroidal anti-inflammatory drugs (NSAIDs). Prescription NSIADs include

diclofenac, ibuprofen, indomethacin, and ketorolac. More than 70 million prescriptions

are written every year for this type of pain reliever. NSAIDs can boost heart failure odds

because they make you retain water and salt, make it harder for your blood to flow, and

make it tougher for diuretic drugs (often used to treat high blood pressure) to work

2. Diabetes medications. Your body gets rid of metformin through your kidneys, so it isn’t a

good choice if your kidneys don’t work like they should. Thiazolidinediones

(pioglitazone, rosiglitazone) cause fluid retention and weight gain in people with heart

31

failure and make people who don’t have it more likely to get it. Doctors aren’t sure why,

but dipeptidyl peptidase-4 inhibitors (alogliptin, linagliptin, saxagliptin, sitagliptin) seem

to send people with heart failure to the hospital.

3. Blood pressure medicine. Calcium channel blockers can worsen edema or fluid that stays

in your body’s tissues. Central agonists (clonidine, moxonidine) cause changes in the

way your body releases hormones that affect your heart.

4. Other types of drugs that can bring on heart failure include: Antifungal medications,

cancer medications, stimulants, antidepressants, tumor necrosis factor (TNF) inhibitor.

5. Natural supplements: There is no government regulation of natural supplements, so you

can't always be sure that a package contains what the label says. Some of them can

cause serious risks, especially if you have a health condition. That goes for vitamins, too.

They seem harmless because they occur naturally in food. But in pill form, it’s a different

story. More than 400 IU of vitamin E daily can increase your chances of developing heart

failure. Supplements can also interact with other drugs. One natural product may be fine

for your neighbor but put your health at risk.14

1.1.7 Pathophysiology of heart failure The primary pathophysiology of heart failure is decreased heart muscle efficiency as a result

of damage or overload. As a result, it can be caused by a variety of conditions, including

myocardial infarction (in which the heart muscle lacks oxygen and dies), hypertension (which

increases the force required to pump blood), and amyloidosis (in which it malfunctions).

During compression, proteins are deposited in the heart muscle, causing it to stiffen. Over time,

these increases in workload will cause changes in the heart.15

Because of the increased load on the ventricle, the heart of a person with heart failure

may have a lower force of contraction. An increase in ventricular filling causes an increase in

the force of contraction (according to Frank Starling's law of the heart) and thus an increase in

cardiac output in a healthy heart. This mechanism fails in heart failure because the ventricle

becomes so clogged with blood that contraction of the heart muscle becomes inefficient. This

is due to the dilated heart muscle's decreased ability to bind actin and myosin filaments.15

Reduced stroke volume can occur as a result of a failure of a systolic, diastolic, or both

failures. Reduced contractility is usually the cause of increased end systolic volume. End

diastolic volume is reduced as a result of impaired ventricular filling, which occurs when the

32

ventricle's compliance decreases (i.e., when the walls stiffen). As the heart works harder to

meet normal metabolic demands, the amount cardiac output can increase in times of increased

oxygen demand (e.g., exercise) is reduced. This contributes to the exercise intolerance

commonly seen in heart failure. This translates to the loss of one's cardiac nerve, or the ability

of the heart to work harder during strenuous physical activity. Since the heart has to work

harder to meet the normal metabolic demands, it is incapable of meeting the metabolic demands

of the body during exercise.

An increased heart rate, caused by increased sympathetic activity, is a common finding

in people with heart failure.16 In order to maintain adequate cardiac output. Initially, this helps

compensate for heart failure by maintaining blood pressure and perfusion, but it puts more

stress on the heart muscle, increasing coronary perfusion requirements, which can exacerbate

ischemic heart disease. Sympathetic activity may also cause an irregular heartbeat. An increase

in the physical size of the muscular layer of the heart may occur. This is caused by an increase

in the size of terminally differentiated myocardial fibers in an attempt to improve contractility.

This may contribute to an increase in rigidity and thus a reduced ability to relax during diastole.

Ventricular hypertrophy can also occur and contribute to an enlarged heart and the spherical

shape of a failing heart. An increase in ventricular volume also leads to a decrease in stroke

volume due to mechanical and ineffective contraction of the heart.17-18

The overall impact is a reduction in cardiac output and an increase in heart strain. This

raises the risk of cardiac arrest (due to irregular ventricular heart rhythms in particular) and

lowers blood flow to the rest of the body. Reduced cardiac output causes a variety of changes

in the rest of the body in chronic disease, some of which are physiological compensations and

others which are part of the disease process:23

1. Blood pressure in the arteries drops. Baroreceptors in the carotid sinus and aortic arch

that connect to the nucleus tractus solitarii are destimulated as a result. Catecholamines

are released into the bloodstream as a result of increased sympathetic activity in this

part of the brain. When alpha-1 receptors are binded, systemic arterial vasoconstriction

occurs. This helps to lower blood pressure, but it also raises total peripheral resistance,

which puts more strain on the heart. In an attempt to boost cardiac output, binding to

beta-1 receptors in the myocardium increases heart rate and makes contractions more

powerful. However, this increases the amount of work that the heart needs to do.

33

2. The posterior pituitary secretes vasopressin (also known as antidiuretic hormone or

ADH) in response to increased sympathetic activation, causing fluid retention in the

kidneys. Blood volume and blood pressure rise as a result of this.

3. Heart failure also limits the kidneys' ability to get rid of sodium and water, which

increases edema 19. Reduced blood flow to the kidneys stimulates the secretion of renin

- an enzyme that stimulates the production of powerful angiotensinogen that

compresses the vessels. Angiotensin and its metabolites cause further vasoconstriction

and stimulate increased secretion of the steroid aldosterone from the adrenal glands.

This promotes salt and fluid retention in the kidneys.

4. Chronically high levels of circulating neuroendocrine hormones including

catecholamines, renin, angiotensin, and aldosterone directly influence the myocardial,

producing long-term structural changes in the heart. Many of these remodeling effects

appear to be mediated by transforming growth factor beta (TGF-beta), which is a

common downstream target of the signal transduction cascade initiated by

catecholamines and angiotensin II,20-21and also by epidermal growth factor (EGF),

which is a target of the signaling pathway activated by aldosterone.22

5. Atrophy of muscle fibers occurs when skeletal muscle perfusion is reduced. This can

lead to weakness, fatiguability, and a loss of peak strength, all of which contribute to

exercise intolerance.23

Increased peripheral resistance and blood volume put additional load on the heart,

accelerating the deterioration of the myocardium. Vasoconstriction and fluid retention produce

an increased hydrostatic pressure in the capillaries. This shifts the balance of forces in favor of

interstitial fluid formation as the increased pressure forces additional fluid out of the blood,

into the tissue. Edema (fluid build-up) develops in the tissues as a result of this. Fluid

accumulation in right-sided heart failure often begins in the ankles, where venous pressure is

high due to gravity's effects (however if the patient is bed-ridden, fluid accumulation may begin

in the sacral area). It may also occur in the abdominal cavity, where the fluid buildup is called

ascites. In left-sided heart failure edema can occur in the lungs – this is called cardiogenic

pulmonary edema. This reduces spare capacity for ventilation, causes stiffening of the lungs

and reduces the efficiency of gas exchange by increasing the distance between the air and the

blood. The consequences of this are dyspnea (shortness of breath), orthopnea and paroxysmal

nocturnal dyspnea.

34

The symptoms of heart failure are largely determined by which side of the heart fails.

The left side pumps blood into the systemic circulation, whilst the right-side pumps blood into

the pulmonary circulation. Whilst left-sided heart failure will reduce cardiac output to the

systemic circulation, the initial symptoms often manifest due to effects on the pulmonary

circulation. In systolic dysfunction, the ejection fraction is decreased, leaving an abnormally

elevated volume of blood in the left ventricle. In diastolic dysfunction, the end-diastolic

ventricular pressure will be high. This increase in volume or pressure backs up to the left atrium

and then to the pulmonary veins. Increased volume or pressure in the pulmonary veins

interferes with normal alveolar drainage and encourages fluid flow from the capillaries to the

lung parenchyma, resulting in pulmonary edema. Gas exchange is hampered as a result of this.

As a result, shortness of breath, orthopnea, and paroxysmal nocturnal dyspnea are common

symptoms of left-sided heart failure. Patients with severe cardiomyopathy will experience cold

and clammy extremities, cyanosis, claudication, generalized weakness, dizziness, and fainting

as a result of decreased cardiac output and poor perfusion.

As a result of the low blood oxygen generated by pulmonary edema, the pulmonary

circulation becomes constricted, resulting in pulmonary hypertension. Since the right ventricle

generates lower pressures than the left ventricle (approximately 20 mmHg versus around 120

mmHg in a healthy individual) but produces cardiac output that is exactly the same as the left

ventricle, a small increase in pulmonary vascular resistance causes a large increase in the

amount of work the right ventricle must perform. However, the primary mechanism through

which left-sided heart failure leads to right-sided heart failure is unknown. Some theories

invoke mechanisms that are mediated by neurohormonal activation. 24

Mechanical effects may also play a significant role. As the left ventricle expands, the

intraventricular septum bends into the right ventricle, reducing the capacity of the right

ventricle.

1.1.7.1 Systolic dysfunction

Heart failure caused by systolic dysfunction is more easily identified. It can be described simply

as a failure of the heart's pump function. It is characterized by a lower ejection fraction (less

than 45 %). The strength of ventricular contraction is reduced, making it insufficient to generate

sufficient stroke volume, resulting in low cardiac output. In general, this is caused by

dysfunction or destruction of cardiac myocytes or their molecular components. Myocytes and

35

their components can be damaged by inflammation (such as in myocarditis) or by infiltration

(such as in amyloidosis). Toxins and pharmacological agents (such as ethanol, cocaine,

doxorubicin, and amphetamines) cause intracellular damage and oxidative stress.

The most common mechanism of damage is ischemia, which causes infarction and scar

formation. After a myocardial infarction, the dead muscle cells are replaced by scar tissue,

which detrimentally affects myocardial function. On an echocardiogram, this is manifested by

abnormal wall movement (hypokinesia) or absent wall movement (movement). The ventricular

diastolic end pressure and volumes rise as a result of insufficient ventricle emptying. This is

transmitted to the atrium. The increased pressure travels to the pulmonary blood vessels on the

left side of the heart, and the resulting hydrostatic pressure encourages fluid leakage into the

lung parenchyma, resulting in pulmonary edema. The increased pressure travels to the systemic

venous circulation and systemic capillary beds on the right side of the heart, causing fluid to

leak into the tissues of the target organs and extremities, resulting in associated peripheral

edema.25

1.1.7.2 Diastolic dysfunction

Heart failure caused by diastolic dysfunction is defined as the failure of the ventricle to

adequately relax in the backward direction and is characterized by a stiffer ventricular wall

during diastole. This leads in insufficient filling of the ventricle and, as a result, insufficient

stroke volume (SV). Final-diastolic pressures rise when ventricular relaxation fails, and the end

effect is the same as in the event of systolic dysfunction (pulmonary edema in left heart failure,

peripheral edema in right heart failure). Diastolic dysfunction can be generated by similar

processes as systolic dysfunction, especially those that impact heart remodeling.

Diastolic dysfunction may only appear in severe physiological states if systolic function

is maintained. The patient may be completely asymptomatic at rest. However, they are very

sensitive to increased heart rate, and may lead to sudden episodes of tachycardia (which can be

caused simply by physiological responses to stress, fever or dehydration, or by pathological

arrhythmias such as atrial fibrillation with ventricular response). Rapid flash of pulmonary

edema. Therefore, appropriate rate control (usually with a pharmacological agent that slows

AV conduction such as calcium channel blockers or beta-blockers) is critical to prevent acute

decompensation.

36

Echocardiography can determine left ventricular diastolic function by measuring

parameters such as the E/A ratio (ratio of early left ventricular to atrial filling), E deceleration

time (early left ventricular filling), and isovolumic relaxation time.25

1.1.8 Anatomy of the heart

According to Office of research administration at Texas Heart Institute.

The heart weighs between 7 and 15 ounces (200 to 425 grams) and is a little larger than the

size of your fist. By the end of a long life, a person’s heart may have beat (expanded and

contracted) more than 3.5 billion times. In fact, each day, the average heart beats 100,000

times, pumping about 2,000 gallons (7,571 liters) of blood.27-28-29

Fig 1: Anatomical Parts of the Heart26

Heart is located between your lungs in the middle of the chest, behind and slightly to

the left of your breastbone (sternum). A double-layered membrane called the pericardium

surrounds your heart like a sac. The outer layer of the pericardium surrounds the roots of your

heart's major blood vessels and is attached by ligaments to your spinal column, diaphragm, and

other parts of your body. The inner layer of the pericardium is attached to the heart muscle. A

coating of fluid separates the two layers of membrane, letting the heart move as it beats.

The heart has 4 chambers which shown in (Fig. 1). The upper chambers are called the

left and right atria, and the lower chambers are called the left and right ventricles. A wall of

muscle called the septum separates the left and right atria and the left and right ventricles. The

37

left ventricle is the largest and strongest chamber in your heart. The left ventricle’s chamber

walls are only about a half-inch thick, but they have enough force to push blood through the

aortic valve and into your body.

1.1.8.1 The Heart chambers

• The right atrium receives non-oxygenated blood from the body’s largest veins —

superior vena cava and inferior vena cava — and pumps it through the tricuspid valve

to the right ventricle.

• The right ventricle pumps the blood through the pulmonary valve to the lungs, where it

becomes oxygenated.

• The left atrium receives oxygenated blood from the lungs and pumps it through the

mitral valve to the left ventricle.

• The left ventricle pumps oxygen-rich blood through the aortic valve to the aorta and the

rest of the body.26

1.1.8.2 The Heart Valves

Four valves regulate blood flow through the heart, shown in (Fig. 2):

• The tricuspid valve regulates blood flow between the right atrium and right ventricle.

• The pulmonary valve controls blood flow from the right ventricle into the pulmonary

arteries, which carry blood to your lungs to pick up oxygen.

• The mitral valve lets oxygen-rich blood from your lungs pass from the left atrium into

the left ventricle.

• The aortic valve opens the way for oxygen-rich blood to pass from the left ventricle

into the aorta, your body’s largest artery.27

38

Fig 2: The Four Valves of the Heart27

Texas Heart Institute

1.1.8.3 The Conduction System

Electrical impulses from heart muscle (the myocardium) cause the heart to contract. This

electrical signal begins in the sinoatrial (SA) node, located at the top of the right atrium. The

SA node is sometimes called the heart’s “natural pacemaker.” An electrical impulse from this

natural pacemaker travels through the muscle fibers of the atria and ventricles, causing them to

contract. Although the SA node sends electrical impulses at a certain rate, your heart rate may

still change depending on physical demands, stress, or hormonal factors.28

1.1.8.4 The Circulatory System

The heart and circulatory system make up the cardiovascular system. The heart works as a

pump that pushes blood to the organs, tissues, and cells of the body. Blood delivers oxygen and

nutrients to every cell and removes the carbon dioxide and waste products made by those cells.

Blood is carried from your heart to the rest of your body through a complex network of

arteries, arterioles, and capillaries. Blood is returned to your heart through venules and veins.

If all the vessels of this network in your body were laid end-to-end, they would extend for about

60,000 miles (more than 96,500 kilometers), which is far enough to circle the earth more than

twice.29

39

1.1.8.5 Structure and Function

Three distinct layers comprise the heart walls, from inner to outer: endocardium, Myocardium,

Epicardium (inner layer of the pericardium).

The muscles of the heart, termed the myocardium, make up the middle and thickest

layer of the heart wall. This layer lies between the single-cell endocardium layer, which lines

the inner chambers, and the outer epicardium, which makes up part of the pericardium that

surrounds and protects the heart. Histologically, heart muscles are composed of cells called

cardiomyocytes that have unique structures and properties correlating to their contractile

function.30

Cardiomyocytes are striated, uninucleate muscle cells found exclusively in the heart

muscle. Unique cellular and physiological features of cardiomyocytes are intercalated discs,

which contain cell adhesions such as gap junctions, to facilitate cell-cell communication. These

discs reduce internal resistance and allow action potentials to spread quickly throughout the

entire heart muscle via the passage of charged ions. Thus, the heart muscle acts as a functional

syncytium with rapid synchronized contractions that are responsible for pumping blood

throughout the body. Functionally, the heart muscles rely on electrochemical gradients and the

potentials to generate contractile force for each heartbeat.

The sinus node, located within the right atrial myocardium, spontaneously depolarizes

and thus determines the heart rate. These depolarizations are currents of ion influx that are

carried from the sinus node to the heart muscle via conducting cells. When the depolarization

reaches the heart muscle, voltage-gated sodium channels open, allowing a rapid influx of

sodium ions into the cardiomyocytes, depolarizing the cells. The positive membrane potential

triggers voltage-gated potassium and then calcium channels to open, allowing potassium to

rush out and calcium to rush in. The initial influx of calcium is necessary for the second release

of calcium from the sarcoplasmic reticulum found within the heart muscle cells. The

accumulation of intracellular calcium ions binds to troponin C, moving tropomyosin aside to

allow actin-myosin binding and cross-bridge cycling responsible for muscle contraction.

The amount of calcium released is directly proportional to the amount of actin-myosin

interaction allowed and thus correlates with the contractile force of the heart muscle generated.

Physiologically, this corresponds with parameters such as stroke volume, ejection fraction, and

cardiac output used to assess heart function. At the end of each cycle, calcium gets restored to

the sarcoplasmic reticulum via SERCA (Sarco(endo)plasmic reticulum (SER) Ca2+ ATPase)

40

pumps while sodium-potassium and sodium-calcium ATPase pumps restore the cardiomyocyte

membrane potential so the cycle can repeat with the next incoming depolarization.30

1.1.8.6 Embryology

The heart muscle originates from the mesoderm layer and begins forming during the third week

of embryonic development. The mesoderm serves as the primary source for myocardial

precursor cells, which make up the cardiogenic or primary heart field during early

development. A primitive, horseshoe-shaped endothelial heart tube is formed and begins

contracting to facilitate the embryo’s early circulation system. Within the next several weeks,

the proliferation of cardiomyocytes is necessary for expanding the myocardial layer and

generating the multichambered system of the mature heart.

While existing cardiomyocytes contribute to the growth of the myocardium via

proliferation and organization, new heart muscle cells are also recruited from adjacent

mesenchymal layers that further expands the muscle layer.31

Following myocardial development, the heart walls undergo further maturation,

compaction, and trabeculation. Dilatations or swellings of the heart tube embryonic structures

along with neural crest cell migration facilitate the development of the chambers and

inflow/outflow tracts. These processes result in a mature and fully functional, contracting heart

by the eighth embryonic week and throughout adulthood.

1.1.8.7 Blood Supply and Lymphatics

The heart muscles’ blood supply comes directly from the system of coronary arteries that runs

within the epicardial layer. Two main coronary arteries, the left coronary artery (LCA) and the

right coronary artery (RCA), branch directly off the aorta via the coronary ostia. These arteries

and their branches supply tributary arteries that run perpendicular to the heart surface and

transverse from the epicardium, through the myocardium, and down to the endocardium.

The LCA quickly branches into the left anterior descending (LAD) coronary artery and

the left circumflex (LCX) coronary artery. The LAD runs vertically down the interventricular

groove towards the apex and supplies blood to the anterior left ventricular myocardium, the

anterior two-thirds of the interventricular septal myocardium, and the anterolateral papillary

muscle connecting the mitral valves. The LCX courses horizontally along the atrioventricular

groove and gives rise to the left obtuse marginal coronary artery, together supplying the lateral

41

and posterior left ventricular myocardium. The RCA runs horizontally along the right

atrioventricular groove and gives rise to the right acute marginal coronary artery, which

supplies the right ventricular myocardium. The RCA also gives rise to the posterior descending

artery (PDA) in about 90 % of the human population (the PDA comes from the LCX in the

other approximately 10 %), which supplies the posterior myocardium of both ventricles, the

posterior one-third of the interventricular septal myocardium, and the posteromedial papillary

muscle of the mitral valves.32

Blood flow via the coronary arteries to the myocardium occurs during diastole and

ventricular relaxation via the passive flow of blood into the aortic Ostia. During systole and

ventricular contraction, the coronary arteries become compressed, and thus impede myocardial

blood flow.

The venous system of the heart muscles runs parallel to the coronary arteries. Venous

drainage of the left ventricular myocardium is completed by the interventricular vein and the

great cardiac vein, which drains into the coronary sinus, found in the posterior right

atrioventricular groove, which then drains into the right atrium. The anterior cardiac veins are

responsible for draining blood from the right ventricular myocardium directly into the right

atrium.32

The cardiac lymphatic drainage system is comprised of lymphatic capillaries and pre-

collector vessels organized in plexuses within each of the heart wall layers. These lymphatic

vessels and plexuses flow from subendocardium, through the myocardium, up through the

subepicardium, into the mediastinal lymph nodes, and ultimately draining into both left and

right venous angles between the internal jugular veins and the subclavian veins. The source of

flow for lymphatic drainage comes from contractions of the myocardium, which generate force

to propel fluid movement through the system to the lymph nodes.33

1.1.8.8 Innervation of the heart

Heart muscles are innervated primarily by two nerves, the accelerans nerve and the vagus

nerve, which provide sympathetic and parasympathetic stimulation from the autonomic

nervous system, respectively. Intrinsic ganglia for the myocardium are present in the

epicardium, which receives signals from post-ganglionic sympathetic connections coming

from the accelerans nerve and pre-ganglionic parasympathetic connections from the vagus

nerve. Most post-ganglionic sympathetic connections synapse directly with the heart muscle

cells, releasing norepinephrine as the primary neurotransmitter.

42

Upon binding, norepinephrine stimulates beta-adrenergic receptors to increase

contractility of the myocardium via increasing calcium influx. Preganglionic parasympathetic

fibers synapse first with the epicardial intrinsic ganglia and then post-ganglionic neurons

directly synapse with the myocardium. Acetylcholine is the primary neurotransmitter for

myocardial parasympathetic signals, acting on muscarinic (M2) receptors on the

cardiomyocytes.34

1.1.8.9 Muscles of the heart

The muscle layer of the heart is termed the myocardium and is made up of cardiomyocytes.

The myocardium is found in the walls of all four chambers of the heart, though it is thicker in

the ventricles and thinner in the atria. This disparity is due to the difference in the generation

of the force of contraction needed for propelling blood between the atria and the ventricles,

with ventricles requiring much more power.32

1.1.9 Physiology of the heart Cardiac physiology, often known as heart function, is the study of healthy, unaffected function

of the heart, including blood flow, myocardial shape, the heart's electrical conduction system,

the cardiac cycle, and cardiac output, as well as how they interact and depend on one another.

1.1.9.1 Cardiac Cycle

The period of time that begins with contraction of the atria and ends with ventricular relaxation

is known as the cardiac cycle, in other words is the beginning of one heartbeat to the beginning

of the next. It consists of two periods:

• The period of contraction that the heart undergoes while it pumps blood into circulation

is called systole (Fig. 3).

• The period of relaxation that occurs as the chambers fill with blood is called diastole.

Both the atria and ventricles undergo systole and diastole.35

After emptying, the heart immediately relaxes and expands to receive another influx of

blood returning from the lungs and other systems of the body, before again contracting to pump

blood to the lungs and those systems.

Assuming a healthy heart and a typical rate of 70 to 75 beats per minute, each cardiac

cycle, or heartbeat, takes about 0.8 seconds to complete the cycle.36

43

The heart relaxes and expands at the beginning of the cycle, during ventricular diastole-

early, while receiving blood into both ventricles through both atria; then, near the end of

ventricular diastole–late, the two atria contract (atrial systole), and each atrium pumps blood

into the ventricle below it.37 During ventricular systole, the ventricles contract and pulsate (or

expel) two distinct blood supplies from the heart - one to the lungs and the other to all other

bodily organs and systems - while the atria relax (atrial diastole).38 During ventricular diastole,

the mitral and tricuspid valves, often known as the atrioventricular or AV valves, open to allow

filling. The atria begin to contract (atrial systole) late in the filling period, forcing a final crop

of blood into the ventricles under pressure. The ventricles then begin to contract (ventricular

systole) in response to electrical signals from the sinoatrial node, and as back - pressure against

them increases, the AV valves are forced to close, preventing blood volumes in the ventricles

from flowing in or out; this is known as the isovolumic contraction stage.37

Pressures in the ventricles rise quickly as a result of systole contractions, exceeding

pressures in the aorta and pulmonary artery trunks and driving the requisite valves (the aortic

and pulmonary valves) to open, resulting in distinct blood volumes being ejected from the two

ventricles. The ejection stage of the cardiac cycle is represented by the ventricular systole–first

phase, followed by the ventricular systole-second phase. The aortic and pulmonary valves close

once ventricular pressures fall below their peaks and below those in the trunks of the aorta and

pulmonary arteries.

The isovolumic relaxation phase begins next, during which pressure within the

ventricles begins to diminish significantly, and the atria begin to refill as blood returns to flow

into the right atrium (from the vena cava) and left atrium (from the pulmonary veins). The

mitral and tricuspid valves open again as the ventricles relax, and the completed cycle returns

to ventricular diastole and a new "Start" of the cardiac cycle.37-39

Blood pressure rises and falls throughout the cardiac cycle. A series of electrical

impulses produced by specialized pacemaker cells found within the sinoatrial node and the

atrioventricular node coordinate the movements of heart muscle.40

44

Fig. 3: Overview of the Cardiac Cycle35 The cardiac cycle begins with atrial systole and

progresses to ventricular systole, atrial diastole, and ventricular diastole, when the cycle begins again.

Correlations to the ECG are highlighted.

1.1.9.1.1 Pressure and flow

Fluids flow from areas of high pressure to areas of low pressure. As a result, blood will flow

into the atria from the higher pressure of the veins while the heart chambers are relaxed

(diastole). Because the pressure in the atria rises as blood comes in, blood moves passively

from the atria to the ventricles at first. The pressure within the atria rises even further when the

action potential causes the muscles in the atria to contract (atrial systole), pump blood into the

ventricles. During ventricular systole, the pressure in the ventricles rises, pumping blood from

the right ventricle into the pulmonary trunk and from the left ventricle into the aorta.38

45

1.1.9.1.2 Phases of cardiac cycle

At the beginning of the cardiac cycle, both the atria and ventricles are relaxed (diastole). Blood

is flowing into the right atrium from the superior and inferior venae cava and the coronary

sinus. Blood flows into the left atrium from the four pulmonary veins. The two atrioventricular

valves, the tricuspid and mitral valves, are both open, so blood flows unimpeded from the atria

and into the ventricles. Approximately 70–80 percent of ventricular filling occurs by this

method. The two semilunar valves, the pulmonary and aortic valves, are closed, preventing

backflow of blood into the right and left ventricles from the pulmonary trunk on the right and

the aorta on the left.38

1.1.9.1.2.1. Atrial systole and diastole

Contraction of the atria follows depolarization, represented by the P wave of the ECG. As the

atrial muscles contract from the superior portion of the atria toward the atrioventricular septum,

pressure rises within the atria and blood is pumped into the ventricles through the open

atrioventricular (tricuspid, and mitral or bicuspid) valves. At the start of atrial systole, the

ventricles are normally filled with approximately 70-80 % of their capacity due to inflow

during diastole. Atrial contraction, also referred to as the "atrial kick," contributes the

remaining 20–30 percent of filling. Atrial systole lasts approximately 100 ms and ends prior to

ventricular systole, as the atrial muscle returns to diastole.38

1.1.9.1.2.2. Ventricular systole

The QRS complex in the ECG represents ventricular systole, which occurs after the ventricles

have depolarized (Fig. 4). It can be separated into two periods, each lasting 270 milliseconds.

At the end of atrial systole and just prior to ventricular contraction, the ventricles

contain approximately 130 mL blood in a resting adult in a standing position. This volume is

known as the end diastolic volume (EDV) or preload.38

The pressure of the blood within the chamber rises initially when the muscles in the

ventricle contract, but it is not yet high enough to open the semilunar (pulmonary and aortic)

valves and be ejected from the heart. Blood pressure, on the other hand, rapidly climbs above

that of the atria, which are now relaxed and in diastole. Blood flows back into the atria when

the pressure rises, sealing the tricuspid and mitral valves. The volume of blood within the

46

chamber remains constant since blood is not evacuated from the ventricles at this early stage.

As a result, isovolumic contraction, also known as isovolumetric contraction, is the name given

to the first phase of ventricular systole.38

The contraction of the ventricular muscle has elevated the pressure within the ventricle

to a point where it is larger than the pressures in the pulmonary trunk and the aorta during the

second phase of ventricular systole, the ventricular ejection phase. The pulmonary and aortic

semilunar valves are opened as blood is pushed out of the heart. Because the existing pressure

in the aorta is so much higher, the left ventricle will generate far more pressure than the right

ventricle. Despite this, the amount of blood pumped by both ventricles is the same.

Stroke volume is the name given to this quantity. In most cases, the stroke volume will

be in the 70–80 mL range. Since ventricular systole began with an EDV of around 130 mL of

blood, this suggests that there is still 50–60 mL of blood remaining in the ventricle following

contraction. This blood volume is referred to as the end systolic volume (ESV).38

1.1.9.1.2.3. Ventricular diastole

Ventricular relaxation, or diastole, follows repolarization of the ventricles and is represented

by the T wave of the ECG. It too is divided into two distinct phases and lasts approximately

430 ms.

During the early phase of ventricular diastole, as the ventricular muscle relaxes,

pressure on the remaining blood within the ventricle begins to fall. When pressure within the

ventricles drops below pressure in both the pulmonary trunk and aorta, blood flows back toward

the heart, producing the dicrotic notch (small dip) seen in blood pressure tracings. The

semilunar valves close to prevent backflow into the heart. Since the atrioventricular valves

remain closed at this point, there is no change in the volume of blood in the ventricle, so the

early phase of ventricular diastole is called the isovolumic ventricular relaxation phase, also

called isovolumetric ventricular relaxation phase.38

In the second phase of ventricular diastole called late ventricular diastole, as the

ventricular muscle relaxes, pressure on the blood within the ventricles drops even further.

Eventually, it drops below the pressure in the atria. When this occurs, blood flows from the

atria into the ventricles, pushing open the tricuspid and mitral valves. As pressure drops within

the ventricles, blood flows from the major veins into the relaxed atria and from there into the

ventricles. Both chambers are in diastole, the atrioventricular valves are open, and the

semilunar valves remain closed. The cardiac cycle is complete.38

47

Fig. 4: Relationship between the Cardiac Cycle and ECG.35 Initially, both the atria and

ventricles are relaxed (diastole). The P wave represents depolarization of the atria and is followed by

atrial contraction (systole). Atrial systole extends until the QRS complex, at which point, the atria

relax. The QRS complex represents depolarization of the ventricles and is followed by ventricular

contraction. The T wave represents the repolarization of the ventricles and marks the beginning of

ventricular relaxation.

1.1.9.2 Resting cardiac output

Cardiac output (CO) is a measurement of the amount of blood pumped by each ventricle in one

minute. To calculate this value, multiply stroke volume (SV), the amount of blood pumped by

each ventricle, by heart rate (HR), in contractions per minute (or beats per minute, bpm). It can

be represented mathematically by the following equation: CO = HR × SV.

There are several important variables influences cardiac output (Fig. 5), including size

of the heart, physical and mental condition of the individual, sex, contractility, duration of

contraction, preload or EDV, and afterload or resistance. Normal range for SV would be 55–

100 mL. An average resting HR would be approximately 75 bpm but could range from 60–100

in some individuals.41

48

Figure 5. Major Factors Influencing Cardiac Output.38 Cardiac output is influenced by

heart rate and stroke volume, both of which are also variable.

1.1.9.3 Exercise and maximum cardiac output

In healthy young individuals, HR may increase to 150 bpm during exercise. SV can also

increase from 70 to approximately 130 mL due to increased strength of contraction. This would

increase CO to approximately 19.5 L/min, 4–5 times the resting rate. Top cardiovascular

athletes can achieve even higher levels. At their peak performance, they may increase resting

CO by 7–8 times. Since the heart is a muscle, exercising it increases its efficiency. The

difference between maximum and resting CO is known as the cardiac reserve. It measures the

residual capacity of the heart to pump blood.41

1.1.9.4 Heart Rate

Heart rate (HR) differ significantly depending on age, as well as exercise and fitness levels.

The resting heart rate of a newborn can be as high as 120 beats per minute. HR falls gradually

until young adulthood, and steadily increases with age.

Maximum heart rates are usually between 200 and 220 beats per minute, though they

can go higher in extreme cases. The ability to generate maximal rates decreases with aging.

This can be calculated by subtracting the individual's age from the maximum value of 220 bpm.

So, a 40-year-old person's maximum rate would be around 180, whereas a 60-year-old person's

maximum rate would be around 160.41

49

1.1.10 Diagnostic criteria of heart failure

1.1.10.1 Medical History and Physical Examination

Patients with heart failure can have decreased exercise tolerance with dyspnea, fatigue,

generalized weakness, and fluid retention, with peripheral or abdominal swelling and possibly

orthopnea.42Patient history and physical examination are useful to evaluate for alternative or

reversible causes including, coronary artery disease, hypertension, idiopathic cardiomyopathy,

valvular heart disease.43-44

Nearly all patients with heart failure have dyspnea on exertion. However, heart failure

accounts for only 30 percent of the causes of dyspnea in the primary care setting.45

The lack of dyspnea on exertion reduces the risk of systolic heart failure only slightly,

while the presence of orthopnea or paroxysmal nocturnal dyspnea increases the risk of heart

failure slightly, (positive likelihood ratio [LR+] = 2.2 and 2.6).46-47

The presence of a third heart sound (ventricular filling gallop) indicates a drop in LVEF

and an increase in left ventricular end-diastolic pressure. A third heart sound and a displaced

cardiac apex, despite being relatively uncommon observations, are good predictors of left

ventricular dysfunction and essentially rule in diagnosis of systolic heart failure (LR+ = 11 and

16).46-47

The presence of jugular venous distention, hepatojugular reflux, pulmonary rales, and

pitting peripheral edema is indicative of volume overload and enhances the probability of a

heart failure diagnosis. Jugular venous distention and hepatojugular reflex have a moderate

effect (LR+ = 5.1 and 6.4), whereas the others, along with cardiac murmurs, have only a small

effect on the diagnostic probability (LR+ = 2.3 to 2.8). The absence of any of these findings is

of little help in ruling out heart failure.46

1.1.10.2 Laboratory Tests

Alternative and potentially reversible causes of heart failure can be identified by laboratory

testing. lists laboratory tests appropriate for the initial evaluation of heart failure and other

potential causes, includes: Arterial blood gases (hypoxia, pulmonary disease), Blood cultures

(endocarditis, systemic infection), Human immunodeficiency virus (cardiomyopathy), Lyme

serology (bradycardia/heart block), Serum ferritin level, transferrin saturation (macrocytic

50

anemia, hemochromatosis), Thiamine level (deficiency, beriberi, alcoholism), Troponin and

creatine kinase-MB levels (myocardial infarction, myocardial injury).

Other laboratory tests should be performed based on physician discretion to evaluate

further causes or identify comorbid conditions that require enhanced control. Includes: A1C

level (diabetes mellitus), Lipid profile (hyperlipidemia).44-48-49

The levels of B-type natriuretic peptide (BNP) and N-terminal pro-BNP (the cleaved

inactive N-terminal segment of the BNP precursor) can be used to evaluate patients for heart

failure who have dyspnea. The atria and ventricles secrete BNP in response to stretching or

increased wall tension.50

BNP levels rise with age, are higher in women and African Americans, and can be

elevated in renal failure patients.46-51

Especially in elderly populations, BNP appears to be more reliable than N-terminal pro-

BNP. 50-51

Monitoring BNP levels in the acute and outpatient settings is supported by limited

evidence. BNP levels were reduced by 30 to 50 percent after hospital discharge, which resulted

in increased survival and lower rehospitalization rates. Outpatient care for BNP levels less than

100 pg. per mL (100 ng per L) and N-terminal pro-BNP levels less than 1,700 pg per mL (1,700

ng per L) resulted in fewer decompensations, hospitalizations, and death occurrences. 52

1.1.10.3 Chest Radiography

Because chest radiography can detect pulmonary causes of dyspnea, it should be done first to

rule out heart failure (e.g., pneumonia, pneumothorax, mass). When a patient with dyspnea has

pulmonary venous congestion and interstitial edema on chest radiography, the diagnosis of

heart failure is more likely (LR+ = 12). Other abnormalities, such as pleural effusion or

cardiomegaly, may slightly raise the risk of heart failure (LR+ = 3.2 and 3.3), while their

absence only helps to reduce the risk of heart failure (LR– = 0.33 to 0.48).46

51

1.1.10.4 Electrocardiography

In individuals with suspected heart failure, electrocardiography (ECG) can help detect other

reasons. Changes such as left bundle branch block, left ventricular hypertrophy, acute or prior

myocardial infarction, or atrial fibrillation can be detected and may require additional study

through echocardiography, stress testing, or consultation with a cardiologist. Systolic heart

failure is only marginally less likely (LR– = 0.27) when ECG results are normal (or modest

anomalies).47 Other abnormalities, such as atrial fibrillation, new T-wave changes, or any

abnormality, have a minor impact on the diagnosis of heart failure (LR+ = 2.2 to 3.8).46

1.1.10.5 Clinical Decision Making

Although the concept of heart failure is still up for debate, it is nonetheless a clinical diagnostic.

Several organizations have produced diagnostic criteria, but the Framingham criteria are

widely accepted and include elements of the initial evaluation, which improves their accuracy.

And a more recent study analyzed them for systolic and diastolic heart failure. Both studies

found that systolic heart failure had a high sensitivity (97% vs. 89% for diastolic heart failure),

effectively ruling out heart failure when the Framingham criteria are not satisfied (LR– = 0.04).

The Framingham criteria have a minor impact in confirming a diagnosis of heart failure (LR+

= 4.21 to 4.57), but a considerable impact on excluding heart failure in general and diastolic

heart failure (LR– = 0.1 and 0.13).55-56

52

Table 1: Framingham Diagnostic Criteria for Heart Failure.55-56

(Heart failure is diagnosed when two major criteria or one major and two minor criteria are met)

Major Criteria Minor Criteria

Acute pulmonary edema Ankle edema

Cardiomegaly Dyspnea on exertion

Hepatojugular reflex Hepatomegaly

Neck vein distension Nocturnal cough

Paroxysmal nocturnal

dyspnea or orthopnea

Pleural effusion

Third heart sound gallop Tachycardia (> 120 beats per minute)

1.1.10.6 An Overview of Heart Failure Evaluation and Diagnosis

The most widely accepted and available approach for diagnosing systolic dysfunction is

echocardiography, which should be used after the initial evaluation to confirm the existence of

heart failure.44

Left ventricle ejection fraction (LVEF), left ventricular size, wall thickness, valve

function, and the pericardium can all be assessed using two-dimensional echocardiography

with Doppler flow studies. If high left atrial pressure, poor left ventricular relaxation, and

decreased compliance are observed, echocardiography can help diagnose diastolic heart

failure.44-57

Diastolic heart failure is frequently diagnosed clinically without conclusive

echocardiographic evidence. Transesophageal echocardiography, radionuclide angiography, or

cineangiography with contrast medium (during catheterization) can be performed to measure

heart function if echocardiography results are unclear or inadequate.58

Unless there is a contraindication to possible revascularization, the American Heart

Association and the American College of Cardiology suggest that the patient undergo coronary

angiography if angina or chest is present with heart failure. 3 In individuals with angina and a

low ejection fraction, coronary angiography has been demonstrated to improve symptoms and

survival.44

53

Figure 6: Algorithm for Evaluation and Diagnosis of Heart Failure. (BNP = B-type

natriuretic peptide).148 American Family Physician.

The figure above (Fig. 6) shows an algorithm for evaluating and diagnosing heart failure. The

initial evaluation is performed when a patient appears with heart failure symptoms in order to

detect alternative or reversible causes of heart failure and to confirm its presence. Systolic heart

failure is almost ruled out if the Framingham criteria are not met or if the BNP level is normal.

Echocardiography should be performed to assess LVEF when heart failure is suspected or if

diastolic heart failure is still suspected when systolic heart failure is ruled out. Treatment

options are guided by the final diagnosis and echocardiography results, with a consideration to

evaluate for coronary artery disease (CAD).

54

1.1.11 Warning signs and symptoms of heart failure

Table 2: Warning Signs and Symptoms of Heart Failure 59

Sign or Symptom People with Heart Failure

May Experience

Why It Happens

Shortness of breath (dyspnea) Breathlessness can occur

during activity, at rest, or while

sleeping, and can occur

suddenly, waking up. Patient

may need to prop up upper

body and head on two pillows

if there is trouble breathing

while sleeping flat. Patient

might frequently complain about waking up exhausted,

worried, or restless

Because the heart can't keep up

with the demand, blood "backs

up" in the pulmonary veins (the

vessels that return blood from

the lungs to the heart). Fluid

leaks into the lungs as a result

of this.

Persistent coughing or

wheezing

Coughing that produces blood-

tinged mucus that is white or pink in color.

Fluid builds up in the lungs

Buildup of excess fluid in body

tissues (edema)

swelling in the feet, ankles,

legs or abdomen or weight

gain. Patient may find that the

shoes feel tight.

As blood flow out of the heart

slows, blood returning to the

heart through the veins backs

up, causing fluid to build up in

the tissues. The kidneys are

less able to dispose of sodium and water, also causing fluid

retention in the tissues.

Tiredness, fatigue, dizziness a constant sense of exhaustion

and trouble performing routine

tasks such as climbing stairs,

carrying groceries, or walking

The heart can't pump enough

blood to meet the needs of

body tissues. The body diverts

blood away from less vital

organs, particularly muscles in

the limbs, and sends it to the heart and brain.

Lack of appetite, nausea a feeling of being bloated or

nauseous in the stomach

The digestive system receives

less blood, resulting in

digestion problems.

Confusion, impaired thinking Memory loss and

disorientation are common

symptoms. This may be

noticed first by a caregiver or relative.

Changing levels of certain

substances in the blood, such

as sodium, can cause

confusion.

Increased heart rate heart palpitation that feels like

your heart is speeding or

beating.

The heart beats quicker to

"make up" for the decrease of

pumping capability.

55

Although the body's ability to compensate for the failing heart initially is beneficial, in the long

run these adaptations contribute to the most serious cases of heart failure. For example:

• An enlarged heart eventually doesn't function as well as a normal heart, the increased

muscle mass adds stress to the entire circulatory system.

• Because of a lack of oxygen, the organ systems from which blood has been diverted

may eventually deteriorate.

• Blood vessel narrowing reduces blood flow and can lead to conditions like stroke, heart

disease, and clogged or blocked blood vessels in the legs and other parts of the body.

• Pumping blood too quickly over an extended period of time can harm the heart muscle

and disrupt its regular electrical signals, resulting in a dangerous heart rhythm

disorder.59

1.1.12 Heart Failure Diagnosis

The physician will take a full medical history, assess symptoms, and conduct a physical

examination to diagnose heart failure. Physician will also look for heart failure risk factors such

as high blood pressure, coronary artery disease, or diabetes.

Additionally, physician can listen to the lungs for signs of fluid buildup (lung

congestion) and to the heart for murmurs (whooshing sounds) that could indicate heart failure.

Veins in the neck may be examined, and fluid buildup in the abdomen and legs may be checked.

Following the physical examination, your physician may order some of the following tests:60

• Blood tests. Blood tests are performed to search for signs of heart disease.

• Chest X-ray. X-ray images can show the condition of the lungs and heart.

• Electrocardiogram (ECG). The electrical signals in the heart are recorded during this

quick and painless test. It can show the frequency and duration of heartbeats.

• Echocardiogram. Sound waves are used to produce images of the heart in motion. This

test reveals the heart's size, structure, and valves, as well as blood flow through the

heart. An echocardiogram can be used to measure ejection fraction, which reveals how

well the heart is pumping and helps diagnose heart failure and guides treatment.

• Stress test. Stress tests measure the health of the heart during activity. The patient might

be asked to walk on a treadmill while attached to an ECG machine, or might be given

56

an IV drug that boosts the effect of exercise on the heart. A stress test may be performed

while wearing a mask that monitors how well the heart and lungs get oxygen and exhale

carbon dioxide.

• Cardiac computerized tomography (CT scan). is used to find calcium deposits in plaque

of people with heart disease. They’re an effective way to spot atherosclerosis before

symptoms develop. The more coronary calcium, the more coronary atherosclerosis. That

gives a higher chance of cardiovascular problems in the future.

• Magnetic resonance imaging (MRI). MRI of heart shows damage by a heart attack or

if there is a lack of blood flow to the heart muscle due to constricted or clogged arteries.

A cardiac MRI may be done with a dye (contrast). It's important to tell the physician

about any problems with your kidneys before you receive a cardiac MRI because

Contrast can cause an uncommon but serious complication in people who have kidney

disease.60

• Coronary angiogram. This test involves inserting a thin, flexible tube (catheter) into a

blood vessel, commonly in the groin, and guiding it to the heart arteries. A dye

(contrast) is administered into the catheter to help the doctor locate blockages by

making the arteries appear more clearly on an X-ray.

• Myocardial biopsy. During this test the physician inserts a thin, flexible cord into a vein

in the neck or groin and takes very small pieces of the heart muscle for examination.

This test may be used to diagnose certain types of heart muscle diseases that cause heart

failure.

The results of tests used to detect heart failure assist doctors in determining the origin

of any signs and symptoms as well as determining a treatment plan. Doctors can use one of two

classification systems to select the appropriate treatment for heart failure:

• New York Heart Association classification. Heart failure is divided into four categories

on this scale:

- Class I heart failure. There are no heart failure symptoms.

- Class II heart failure. Everyday activities can be done without difficulty, but

exertion causes shortness of breath or fatigue.

- Class III heart failure. It's difficult to complete everyday activities.

- Class IV heart failure. Shortness of breath occurs even at rest. This category

includes the most severe heart failure.60

57

• American College of Cardiology/American Heart Association classification. This

stage-based classification system uses letters A to D and includes a category for those

at risk of developing heart failure:

- Stage A. There are several risk factors for heart failure but no signs or symptoms.

- Stage B. There is heart disease but no signs or symptoms of heart failure.

- Stage C. There is heart disease and signs or symptoms of heart failure.

- Stage D. Advanced heart failure requires special treatments.

Both classification systems used together to help determine the most appropriate

treatment options.60

1.1.13 Heart Failure Treatment

Heart failure is a chronic condition that requires lifelong treatment. However, the signs and

symptoms of heart failure might improve with treatment. Physicians sometimes can correct

heart failure by treating the underlying cause. For instance, repairing a heart valve or

controlling a fast heart rhythm may reverse heart failure. But for most people, treatment of

heart failure involves a balance of the right medications and, sometimes, use of devices that

help the heartbeat and contract properly. The main treatments are:61-65

• Medications:

- Angiotensin-converting enzyme (ACE) inhibitors. These drugs relax blood

vessels to lower blood pressure, improve blood flow and decrease the strain on the

heart. Examples include enalapril (Vasotec, Epaned), lisinopril (Zestril, Qbrelis,

Prinivil) and captopril.

- Angiotensin II receptor blockers. Losartan (Cozaar), valsartan (Diovan), and

candesartan (Atacand) are three medicines that offer many of the same benefits as

ACE inhibitors. They might be a great option for those who can't take ACE

inhibitors.

- Beta blockers. These drugs lower blood pressure and slow heart rate. Beta blockers

may help you live longer by reducing the signs and symptoms of heart failure,

improving heart function, and extending your life. Carvedilol (Coreg), metoprolol

(Lopressor, Toprol-XL, Kapspargo Sprinkle), and bisoprolol are among examples.

- Diuretics. Diuretics, often known as water pills, cause you to urinate more often

and prevent fluid from building up in your body. Diuretics like furosemide (Lasix)

help you breathe easier by reducing fluid in the lungs.

58

- Aldosterone antagonists. These drugs include spironolactone (Aldactone,

Carospir) and eplerenone (Inspra).

- Positive inotropes. People in the hospital with certain types of severe heart failure

may get these drugs by IV. Positive inotropes can help the heart pump blood more

effectively and maintain blood pressure.

- Digoxin (Lanoxin). This drug, commonly known as digitalis, makes heart muscle

contractions stronger. It also tends to slow the heartbeat. Digoxin reduces heart

failure symptoms in systolic heart failure.

- Hydralazine and isosorbide dinitrate (BiDil). This drug combination aids in the

relaxation of blood vessels. In severe heart failure symptoms and ACE inhibitors or

beta blockers haven't helped, it may be added given.61-65

• Devices for heart failure, implanted in the chest to control heart rhythm:

- Pacemaker. A pacemaker continuously monitors heart rate and provides electrical

pulses to the heart to keep it pumping at the proper rate. A cardiologist places the

device under the skin, usually under local anesthesia.

- Cardiac resynchronisation therapy. Cardiac resynchronization therapy (CRT) is

a form of pacemaker that can help by causing the left ventricle's walls to all contract

at the same time. This improves the efficiency of the heart's pumping.

- Implantable cardioverter defibrillators (ICDs). An ICD constantly monitors the

heart rhythm.

- CRT-Ds. Devices that combine cardiac resynchronization and defibrillation are

implanted into patients who need both.61-65

• Surgery for heart failure may include:

- Heart valve surgery. There are 2 types of valve surgery: valve replacement and

valve repair.

- Angioplasty or bypass. If your heart failure is caused by coronary heart disease,

your doctor may recommend one of the following treatments:

Coronary angioplasty – where a tiny balloon is used to stretch open a narrowed or

blocked artery. Coronary artery bypass graft (CABG) – where a blood vessel from

59

another part of the body is used to divert blood around narrowed or clogged parts

of an artery.

- Left ventricular assist devices. Left ventricular assist devices (LVADs) are

mechanical pumps that can help if your left ventricle isn't working properly, and

medication alone isn't helping. They can be used as a permanent treatment if a heart

transplant is not possible, or as a temporary solution while waiting for a transplant

- Heart transplant. Some people have heart failure that is so severe that surgery or

drugs are ineffective. These people's hearts might need to be replaced with a healthy

donor heart.61-65

1.1.14. Prevention of heart failure

According to Heart Information Center (Texas Heart Institute).69 Generally, heart disease is the

leading cause of death. It is also a significant contributor to disability. There are a variety of

factors that can increase your risk of heart disease. They're known as risk factors. You can't

control some of them, but you can control a lot of them. You can reduce your risk of heart

disease by learning about them.

The risk factors for heart disease that can't be changed:

• Age. As you become older, your chances of developing heart disease increase. Men and

women over the age of 45 and 55 are at a higher risk.

• Sex. Some risk factors may affect women's risk of heart disease differently than men.

For example, estrogen protects women from heart disease, but diabetes increases the

risk of heart disease in women more than it does in males.

• Ethnicity or race. Some people are at a higher risk than others. Heart disease is more

common in African Americans than in whites, whereas it is less common in Hispanic

Americans. East Asians, for instance, have lower rates, whereas South Asians have

greater rates.

• Family history. You have a greater risk if you have a close family member who had

heart disease at an early age.

To lower the risk of heart disease:

• Control your blood pressure. High blood pressure is a major risk factor for heart

disease. It is important to get your blood pressure checked regularly - at least once a

60

year for most adults, and more often if you have high blood pressure. Take steps,

including lifestyle changes, to prevent or control high blood pressure.

• Keep your cholesterol and triglyceride levels under control. High levels

of cholesterol can clog your arteries and raise your risk of coronary artery disease and

heart attack. Lifestyle changes and medicines (if needed) can lower your cholesterol.

Triglycerides are another type of fat in the blood. High levels of triglycerides may also

raise the risk of coronary artery disease, especially in women.

• Stay at a healthy weight. Being overweight or having obesity can increase your risk for

heart disease. This is mostly because they are linked to other heart disease risk factors,

including high blood cholesterol and triglyceride levels, high blood pressure, and

diabetes. Controlling your weight can lower these risks. Extra pounds can interfere with

blood circulation and put excess pressure and stress on the heart. Studies have shown

that even a modest weight loss of 5% to 10% can lead to significant improvements in

blood pressure, cholesterol, and co-morbidities associated with increased weight. A

healthy weight is defined as a body mass index (BMI) between 18.5 and 24.9.

Individuals with a BMI of 30 are considered obese.66-67

• Get regular exercise. Exercise has many benefits, including strengthening your heart

and improving your circulation. It can also help you maintain a healthy weight and

lower cholesterol and blood pressure. All of these can lower your risk of heart disease.

Aerobic activity in particular, such as high-intensity interval training (HIIT), which

alternates short stints of intense exercise with less vigorous ones, have been shown to

help strengthen and condition the heart so that it can function better. At least 30 minutes

per day (150 minutes per week) of moderate-intensity exercise, such as gardening, brisk

walking, dancing, or doubles tennis. This can be broken down into three 10-minute

sessions or two 15-minute sessions if that is easier to fit into a busy schedule.69

• Limit alcohol. Too much alcohol might cause your blood pressure to rise. It also adds

more calories, potentially leading to weight gain. Both of these factors increase your

chances of developing heart disease. Men should limit themselves to two alcoholic

drinks each day, while women should limit themselves to one.

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• Quit Smoking. Cigarette smoking raises blood pressure. The chemicals in tobacco can

directly damage arteries and contribute to congestive heart failure. [John Hopkins

Medicine. Congestive heart failure: prevention, treatment and research.].

Secondhand smoke can be just as harmful, as carbon monoxide can take the place of

oxygen in the blood, forcing the heart to pump harder. Once you quit smoking, you'll

notice an almost instantaneous improvement in your health:

o Within 20 minutes, heart rate decreases.

o Within 12 hours, carbon monoxide levels in the blood decrease to normal.

o Within 3 months, the risk of a heart attack decreases and lung function

improves.

o After 1 year, the added risk of coronary artery disease is half that of someone

who smokes.68

• Eat a Heart Healthy Diet: Limit saturated fat, trans fats, sodium, fatty cuts of red meat

and other proteins, and soda, baked goods, and other foods and beverages with large

amounts of added refined sugar.69-70

• Reduce Salt Intake: High levels of sodium in the diet can cause accumulation of fluid

in the body that consequently puts excess stress on the cardiovascular system.71 If you

have hypertension (high blood pressure), a primary risk factor for heart failure, it may

be advisable to reduce your intake of table salt, processed foods, and high-sodium

foods, such as bacon, ham. The goal is to reduce sodium consumption to 2,300

milligrams (mg) per day or 1,500 mg for people at a high risk of hypertension.

• Manage stress. Stress is linked to heart disease in many ways. It can elevate blood

pressure. Extreme stress can be a "trigger" for a heart attack. Also, some common ways

of coping with stress, such as overeating, heavy drinking, and smoking, are bad for the

heart.

• Manage diabetes. Having diabetes doubles your risk of diabetic heart disease. That is

because over time, high blood sugar from diabetes can damage your blood vessels and

the nerves that control your heart and blood vessels. So, it is important to get tested for

diabetes, and if you have it, to keep it under control.

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• Get enough sleep. Not getting enough sleep, raise your risk of high blood pressure,

obesity, and diabetes. Those three things can raise your risk for heart disease.

1.1.15 Complications of heart failure According to WebMD, if you have heart failure, your heart may not be strong enough to pump

out as much blood as your body needs. As it tries to move more blood, your heart gets larger. It

also pumps faster, and your blood vessels narrow to get more blood out to your body.

As your heart works harder, it may become weaker. Your body gets less oxygen, and you

might notice symptoms like shortness of breath, swelling in your legs, and fluid buildup.

Your body tries to keep the blood it has to supply your heart and brain. This leaves less for organs

like your kidneys and liver. A lack of enough blood can damage these organs.72

Common complications of heart failure:72

• Atrial fibrillation: is an irregular heart rhythm (arrhythmia), it can make heart failure

worse, and greatly increases risk of stroke, can cause palpitations.

• Ventricular fibrillation or tachycardia: Irregular heart rhythms (arrythmias), it can

cause syncope (fainting), palpitations, sudden death.

• Kidney failure: Reduced functioning of the kidneys, leading to decreased urine

output, fatigue, poor appetite, lethargy, ultimately life-threatening.

• Anemia: Decreased oxygen-carrying hemoglobin in red blood cells, causing weakness

and fatigue, may raise risk or problems linked to heart failure.

• Stroke: your brain is deprived of oxygen because its blood supply has been

significantly decreased or cut off, leading to loss of cognitive or motor function.

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• Heart valve condition: A leaky or tight valve reduces the efficiency of the heart’s

pumping action, makes heart failure worse, can predispose to atrial fibrillation, may

need surgical intervention.

• Cardiac cachexia: is an unintentional weight loss, can require supplemental nutrition,

can be life-threatening.

• Leg venous stasis and ulcers: venous stasis: skin thickens and looks shiny or scaly,

your hair might also fall out, skin may also turn brown or reddish. Ulcers: Injuries to

your swollen legs cause fluid to constantly ooze out of cuts in your skin.

• Liver damage: breaks down toxins so your body can remove them. It also stores bile, a

fluid used to digest food. Heart failure might deprive your liver of the blood it requires to

function properly. The fluid buildup that comes with it puts extra pressure on the portal

vein, which brings blood to your liver. This can scar the organ to the point where it

doesn't work as well as it should.

• Lung problems: A damaged heart can't pump blood as effectively from your lungs out

to your body. Blood backs up, raising pressure in the veins inside your lungs. This

pushes fluid into your air sacs. As liquid builds up, it gets harder to breathe. This is

called pulmonary edema.

• Extreme weight loss and muscle loss: Muscle and fat metabolism can be affected by

heart failure. You may lose a lot of weight and muscular mass as the disease

progresses. Muscles can shrink and weaken over time.72

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1.2 Special Part of Thesis

1.2.1 General Principles of Exercise Testing in Cardiac Rehabilitation

1.2.1.1 Introduction

Every patient must undergo a clinical assessment before being admitted to a cardiac

rehabilitation program (CRP), which includes a medical consultation, an evaluation of left

ventricle (LV) function (usually by echocardiography), a maximal exercise test (ET) limited

by symptoms, and blood tests to determine the cardiovascular disease (CVD) risk factor profile.

In some situations, patients require additional diagnostic testing after the clinical evaluation,

such as 24-hour Holter monitoring, an imaging technique to evaluate perfusion or coronary

anatomy, or bypass grafting.73-74

The ET is a very important part of this clinical assessment performed before admission

and repeated at the end of the CRP phase, because it gives data regarding functional capacity

and information regarding the adaptation to maximal and submaximal levels of exercise (HR

and BP), residual myocardial ischemia, and cardiac arrhythmias induced or worsened by

exercise and permits the identification of the training heart rate (THR) for the aerobic training.75

Besides the objective parameters mentioned above, the ET is very important from the

psychological point of view for many patients and partners, because they realize that the patient

usually has a better functional capacity than they could pre- dict. In the follow-up period, the

ET is very useful to detect or confirm eventual clinical status changes which occurred during

the program, update exercise intensity, measure the gains obtained after the CRP, and perform

global prognostic assessment.

1.2.1.2 Cardiopulmonary Exercise Test (Spiroergometry)

Cardiopulmonary exercise test (CPX) is the ideal ET to be used in all kinds of patients in the

setting of a CRP.76 Although it is almost mandatory to use it in heart failure patients, it is

frequently replaced in many CR centers, primarily in CAD patients with normal or near-normal

LV function, by the standard ET, which is more widely available and familiar to most

cardiologists, due to its higher cost, more complicated delivery, and interpretation.77 During the

CPX, peak VO2, ventilatory thresholds, VE/VCO2 slope, and O2 kinetics are measured beyond

all the parameters recorded in the standard ET, like maximal load reached, HR and BP changes

65

from rest to maximal exercise, and, during recovery, the eventual arousal of symptoms like

angina pectoris or ECG abnormalities (ST changes or arrhythmias).78 Considering the

parameters obtained from the CPX, peak VO2 is the most important because it is the gold

standard for functional capacity and it was identified as the strongest prognostic parameter in

CVD.79-80 Because continuous moderate aerobic training, the classic modality, is performed at

a percentage of peak VO2 ranging from 50 to 70 %, peak VO2 is therefore very significant

when prescribing exercise intensity.81 The first and second ventilatory thresholds (VT1 and

VT2), which are expected to occur at submaximal level during the CPX, are independent of

motivation, contrary to peak VO2. Due to this fact, they are considered good indicators of the

training effect of the program, if they occur at a higher percentage of VO2 max.

The determination of the ventilatory thresholds is also useful to calculate the training

intensity for moderate continuous aerobic training, which must start at the HR attained at the

level of VT1 and increased to HR reached at the VT2 moment.82-83

Simply, Spiroergometric stress testing is one of the most common types of stress

testing, and it should be done on every patient undergoing post-hospital cardiovascular

rehabilitation. This examination allows for a thorough evaluation of the cardiopulmonary

system's functionality. It's a requirement for suggesting safe and successful physical activity

and calculating the proper training load intensity. Most of the time, we use a bicycle ergometer.

During the assessment, we gradually increase the load until we reach the symptoms of the

patient's limited maximum, according to the ramp protocol. The load, heart rate, blood

pressure, and ECG are all recorded. We are currently monitoring different ventilation

parameters, including oxygen uptake (VO2), carbon dioxide output (VCO2), and minute

ventilation (VE), as well as parameters derived from them, such as respiratory exchange ratio

(RER), ventilation equivalent for oxygen (VE / VO2), and ventilation equivalent for carbon

dioxide (VE / VCO2). We also evaluate the maximum achieved, so-called peak values of

oxygen intake (VO2peak) and power (W peak) in spiroergometry, which provide information

on the patient's maximum aerobic capacity and performance.84-85

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1.2.1.3 Cardiac stress test

Simply, a stress test involves walking on a treadmill while the heart works harder and harder.

The electrical rhythms of the heart are monitored using an electrocardiogram (ECG). The

doctor will also check the blood pressure and see if there are any symptoms like chest pain or

exhaustion. Abnormalities in blood pressure, heart rate, or ECG, as well as worsening clinical

symptoms, may indicate coronary artery disease (CAD). When performing stress tests, it's

important to remember that the results are impacted not only by the patient's physical, mental,

and behavioral features, but also by environmental factors like temperature, room airflow, and

time of day, as well as the medication the patient is taking. Equipment’s of a stress measuring

are, ergometers (treadmills, bicycle ergometer, rowing ergometer), devices to measure

circulation parameters (ECG, pressure meters), devices to measure ventilation parameters

(spirometers, gas analyzers), dynamometers. Before a stress test is taken it is necessary to

choose the right stress protocol which will further specify the intensity of workload, its

duration: single-grade stress test, graded stress test, graded test with pauses, ramp, continual,

combined.86 During the stress test, the patient performs a subjective assessment of his feelings

most often using Borg scales. The scale 6-20 is used to evaluate the perception of the intensity

and stress of the load. The 0-10 scale is then used to assess dyspnea, chest pain, and lower limb

pain (HD). Individual results are recorded in the protocol and use the self-description of other

physical activity and the patient for self-control.87

Absolute contraindications for stress testing include acute and active chronic diseases,

unstable angina pectoris acute or unresponsive to therapy, clinical signs of cardiac, respiratory,

metabolic insufficiency, advanced aortic stenosis, cardiovascular aneurysm, malignant

hypertension, severe pulmonary hypertension, severe dysrhythmia. The relative

contraindications are then as follows: less severe heart rhythm and conduction disorders, some

congenital or acquired valve defects, conditions after complicated MI, some uncontrollable

metabolic diseases, serious systemic diseases, mental disorders and unwillingness to

cooperate.86-88

Borg rating of perceived exertion (RPE) is an outcome measure scale used in

knowing exercise intensity prescription. It is used in monitoring progress and mode of

exercise in cardiac patients as well as in other patient populations undergoing

rehabilitation and endurance training.

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Table 3: Subjective Perception of Effort According to Borg scale 6 – 20, Borg RPE Scale.85

Scoring Level of Exertion Scoring Level of Exertion

6 No Exertion 13 – 14 A little Hard

7 – 8 Extremely light 15 – 16 Hard

9 – 10 Very Light 17 – 18 Very Hard

11 – 12 Light 19 – 20 Extremely Hard

The original Borg scale ranges from 6 to 20, with a strong correlation to heart rate. Multiplying

each number by 10 gives the training heart rate at the moment of scoring. It was later

reconstructed into the Borg CR10 Scale or modified Borg Dyspnea Scale, which is primarily

used to diagnose breathlessness and dyspnea, chest pain, and musculoskeletal pain. The CR-

10 scale is best used when a sensation is felt in a specific location of the body, such as muscle

pain or pulmonary reactions.

Table 4: Subjective Evaluation of Dyspnea, Chest Pain and HD According to Borg Scale 0 – 10.86-87

Scoring Level of Exertion Scoring Level of Exertion

0 No Exertion 5 Severe

0.5 Extremely slight 6 Severe

1 Very Slight 7 Very Severe

2 Slight 8 Very Severe

3 Moderate 9 Extremely Severe

4 Somehow Severe 10 Maximal

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1.2.1.4. Dynamometry

Skeletal muscle strength measurement is becoming more significant as an outcome parameter

in patients with chronic heart failure.89 Muscle strength can be measured using dynamometers

during isometric (muscle length doesn’t change), isotonic, or isokinetic contractions. Isokinetic

dynamometers test muscles during a movement within a joint range. The so-called handgrip

test, which uses a hand dynamometer, is commonly used in internal medicine and cardiology.

It must be implemented before the inclusion of the strength training, as it allows you to

check the reaction of blood pressure and other cardiovascular function indicators to static load.

We speak of a normal reaction when blood pressure does not rise above 180/120 mm Hg)

during extended static exercise, and the intensity of strength training is further established by

the one repetition maximum approach (1-RM). The 1-RM test is not conducted in the case of

pressure hyperreaction, and training begins with light loads that gradually rise during the

rehabilitation program.84-86-87

1.2.1.5. Comprehensive Medical Rehabilitation

Cardiovascular disease (CVD) is one of the leading causes of death worldwide.90-91 Cardiac

rehabilitation is an integral part of the treatment of patients with heart failure.

According to PubMed, cardiac rehab, is a complex, interprofessional intervention

customized to individual patients with various cardiovascular diseases such as ischemic heart

disease, heart failure, and myocardial infarctions, or patients who have undergone

cardiovascular interventions such as coronary angioplasty or coronary artery bypass grafting,

that aims to help patients with cardiovascular diseases, such as acute and chronic heart failure,

regain and maintain their optimal physical, mental, social, occupational, and emotional health.

It also includes adhering to secondary prevention guidelines and leading a healthy

lifestyle.92 Cardiac rehabilitation programs are designed to assist patients cope with the

psychological and physiological effects of CVD, minimize the risk of CVD-related mortality,

and enhance cardiovascular function in order to help them achieve their highest quality of life

possible and to enable patients to return to an active social life, to work and recreational

activities 93. Improving total heart function and capacity, preventing or reversing the

progression of atherosclerotic disease, and gradually enhancing the patient's self-confidence

are all goals that must be accomplished.94 Patients may develop some cardiovascular problems

during cardiovascular rehabilitation as a result of increased physical and mental exertion. As a

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result, close collaboration with the attending physician is required, as is additional control by

a physiotherapist.84

Several organizations, including the American Heart Association (AHA), the American

Association for Cardiovascular and Pulmonary Rehabilitation (AACVPR), and the Agency for

Health Care Policy and Research, agree that a comprehensive cardiac rehabilitation program

should contain specific core components. These components should optimize cardiovascular

risk reduction, reduce disability, encourage active and healthy lifestyle changes, and help

maintain those healthy habits after rehabilitation is complete. Cardiac rehabilitation programs

should focus on95

• Weight management,

• Blood pressure management,

• Diabetes management,

• Lipid management,

• Patient assessment nutritional counseling,

• Tobacco cessation,

• Psychosocial management,

• Exercise training,

• Physical activity counseling.95

1.2.1.5.1 Perioperative Cardiac Rehabilitation

Pre-rehabilitation helps patients to overcome the stress of surgery by improving functional

capacity. Preoperative exercise decreases sympathetic over-reactivity, improves insulin

sensitivity, and increases the ratio of lean body mass to body fat. It also promotes physical and

psychological readiness for surgery, reduces postoperative complications and length of stay,

and improves the transition from the hospital to the community. Patient who were given

education regarding postoperative mobilization before surgery will respond more positively

and enthusiastically to the program.96

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1.2.1.5.2 Post-Operative Cardiac Rehabilitation

There is no place for "bedrest" in the management of patients with cardiovascular disease after

surgery. Early patient mobilization following cardiac surgery has been shown to improve

patient recovery. Physical activity, particularly walking exercise, should be started as soon as

possible following cardiac surgery to prevent complications.97

1.2.1.5.2.1 Phase 1: Acute, In Hospital Patient Period

While remaining in the hospital, patients with acute heart issues, such as those recovering from

heart surgery, may be referred to a cardiac rehab team. Depending on patient physical state,

this period will likely last between 1-14 days. This phase includes the following:

• Assessment: The patient will be visited by cardiac rehab specialists during this phase,

and the cardiac rehab team may perform the following tests: Heart rate, Blood pressure,

Oxygen saturation, Upper and lower extremity function, including strength and range

of motion (ROM), Functional mobility such as walking and self-care tasks. They will

also take a full medical history to rule out any potential risk factors or comorbidities.

• Education: Patient can begin receiving education and training in the following areas:

The cardiac event itself, Specific aspects of diagnosis and condition, managing

psychological reactions to the event, Managing cardiac pain and other symptoms,

Monitoring.

• Physical Therapy: Patient may be referred to an acute care physical therapist, who will

devise a carefully monitored, gradual, and very limited activity program to help you

patient get back on feet. This could start with simply sitting up in bed, progressing to

standing and checking range of motion, and then taking short walks around the hospital

wing. The rehabilitation team might also concentrate on activities of daily living

(ADLs) and educate the patient how to manage stress. Patients are advised to stay as

rested as possible until the treatment of comorbid disorders or post-operative

complications is completed.

• Discharging Plan: A plan for leaving the hospital will also be provided by the cardiac

rehab team. Before patient leave, they will examine walking skills, requirement for

home oxygen, and any other training or medical needs.

Throughout this phase, a mix of low-intensity physical activity, stress management

approaches, and risk factor education is recommended. The main goal of this phase is

preventing deconditioning, thromboembolic, pulmonary, inflammatory, and other

71

complications, as well as reducing muscle strength and joint stiffness. Our aim is to get the

patient ready for normal daily activities and assist with stress management. The content is

simple active non-strenuous exercises in the bed or at the bedside, to gradually begin with

walking, while evaluation patient physical activity by measuring the blood pressure and

heart rate as well as monitoring patient clinical condition and subjective feelings.98

1-2 days post-surgery: bed exercise to prevent deep vein thrombosis, the first day includes a

simple extremity movement with the least impact of gravity. The second day, the extremities

can be elevated above the surface. These simple exercises are also performed by patients

connected to mechanical lung ventilation, if their current medical condition allows it.

3-4 days post-surgery: sitting in bed or standing by the bed, the patient is usually transferred to

the cardiac surgery.

5-6 days post-surgery: ambulation in the room.

7-10 days post-surgery: ambulation in the hallways.

11-14 days post-surgery: ambulation around the ward at faster speeds, stair negotiation.119

1.2.1.5.2.2 Phase 2: Subacute Outpatient Care (Post-discharge, Pre-Exercise Period),

(2-6 weeks post-surgery)

Outpatient cardiac rehabilitation takes place once the patient is stable and cleared by

cardiology. Phase 2 usually lasts three to six weeks, but it can last up to twelve weeks in

some cases. It takes the form of an outpatient rehabilitation program, spa treatment or an

individual home rehabilitation program. The focus throughout this stage of therapy will

be on patient education. Patient will be given instructions on how to manage heart issue

and further information on heart-healthy living. During this time, health will be

continuously examined to ensure that the patient is progressing toward recovery. Once

patient is ready to begin exercising, he can move onto the next phase of rehab. A more

comprehensive patient-centered therapy plan is created, including three modalities:

information/advice, a customized training program, and a relaxation program. The goal of

the therapy phase is to encourage independence and lifestyle modifications in order to

prepare patients to return to their homes.

The main goal of this phase is to increase patient physical fitness and performance

to integrate him into a full active life and to be able to progress to phase 3. Posthospital

rehabilitation is appropriate for stabilized patients in NYHA functional classes I, II, and

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III. For patients in NYHA functional class IV, rehabilitation in the form of standard

endurance aerobic training is contraindicated.98-99-100

1.2.1.5.2.3 Phase 3: Subacute Outpatient Care (Post-discharge, Pre-Exercise Period),

(7-12 weeks post-surgery)

Those patients who have experienced a severe cardiac event or surgery will most likely need

to complete phases 1 and 2 before moving into phase 3, which is a full cardiac rehabilitation

program (CRP). Some patients with milder cardiac problems may proceed directly to phase 3.

Phase 2 is closely monitored and is intended for patients who are still significantly affected by

their heart problem, whereas phase 3 introduces more autonomous activities and self-

monitoring. The patient is usually ready to begin phase 3 cardiac rehab when the vital signs,

such as heart rate and blood pressure, remain stable while increasing activity and

workloads advised in the sub-acute phase of cardiac rehab.

A complete Phase 3 cardiac exercise and training rehab program typically consists

of 36 outpatient sessions, while some patients may need inpatient care or require less

sessions and/or monitoring.98

Phase 3 focuses on increasing flexibility, strengthening, and aerobic conditioning,

outpatient visits to specialist physicians are recommended to monitor cardiovascular

health and medication regimes, promote healthy lifestyle changes, and intervene as needed

to prevent relapse.99-101

Before patient begin, a physical therapist will assess range of motion, muscle strength,

resting heart rate, blood pressure, breathing, endurance levels, and any scar mobility difficulties

if you've had surgery. Warm-up, cardiovascular exercise (such as using a stationary bike or

treadmill), and cool-down are commonly included in the cardiac rehab exercise sessions.

Patient may also be encouraged to include some resistance training, depending on his physical

condition. Will be encouraged to keep track workout responses, such as heart rate, exertion

level, and blood pressure.

At this phase, the focus of training will most likely be on:

• Nutrition: For people with cardiovascular diseases, eating a heart-healthy diet is

critically important. To avoid putting excessive strain on the heart, a healthy weight

should be maintained as well. Heart-healthy diet includes fruits and vegetables, whole

grains, and lean proteins and is low in sodium, sugar, and trans fats.

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• Lifestyle: With a cardiac condition, patient may need to undertake lifestyle changes,

such as quitting smoking and exercising regularly, to improve long-term quality of life.

During Phase 3 of cardiac rehab program, the team of rehab specialists will provide

an assistance and advise on making the essential changes permanent.

• Stress management: In case of cardiac condition, it is critical to learn how to manage

stress effectively. Stress management training, such as breathing techniques and

meditation, may be included in the cardiac rehab program to help maintain stress levels

low once rehab is over.

The primary goal for Phase 3 of cardiac rehab is to educate patient with the knowledge

and skills necessary to manage heart problem on patient own and live a longer, happier, and

healthier life. When the patient finish his rehab program, he should know how to manage

his symptoms, cope with chest pain, monitor his blood pressure and exertion levels, and

manage his medications, oxygen, and other therapies on his own. The patient should also be

familiar with the elements of a heart-healthy lifestyle, such as how to exercise safely, eat well,

and handle stress. Ideally and by following these he should have fewer symptoms from

his heart problem and be less likely to have another episode or need to return to the hospital in

the future.98-99-101

1.2.1.5.2.4 Phase 4: Maintenance (13 weeks and beyond post-surgery)

If the patient has gone through the first three stages of cardiac rehabilitation, he should have a

good understanding of his heart disease and how to best manage it. Phase 4 essentially

continues for the rest of your life. During Phase 4, the patient should continue to follow

his rehab team's recommendations for exercise, nutrition, and lifestyle. He can either proceed

on his own or chose to self-fund further training with a physical therapist to assist him as he

progresses. He should see his doctor on a frequent basis to ensure that he is adequately

managing his cardiac condition and avoiding any flare-ups. The goal of Phase 4 is to keep up

with the lifestyle adjustments that started in Phase 3, stay on track with exercise routine, avoid

tobacco, eat well, and manage stress.98

The following activities are not recommended:

• Lifting and carrying heavy objects,

74

• Prolonged upper extremity activities above the head,

• Sports that involve jumping/rebounding,

• Strengthening in the form of resistance training (this should only performed under

the guidance of an experienced physical therapist).

The following activities are recommended:

• Alternating appropriate activities with a sufficient rest period,

• To prevent mucous formation, the patient should continue pulmonary physical

therapy learned in the hospital, including breathing exercises,

• Attempt to perform at least half an hour of endurance physical activity every day

(walking, stationary ergometer, swimming when the incision has healed) with

gradually increased duration of exertion,

• Rest in the case of heart palpitations, dyspnea or anxiety,

• Acclimatize during transitions from warmer to cooler areas.

1.2.1.5.3 Outpatient Controlled Program

The length of the outpatient rehabilitation program depends on patient health condition.

Generally, and in the majority of cases a typical program lasts for 10-12 weeks of structured

exercise sessions, for 2-3 times a week, each training unit lasts about 60-90 minutes and

takes place in the form of group exercises. A typical exercise unit consists of several parts

and begins with a warm-up that lasts for about 15 minutes, warm up has a goal to warming

up and prepare the heart for activity by boosting or increasing and making the patient

slightly breathless to prepare the body and muscles to minimize the risk of injury, The

training is low to medium intensity, and the phase is dynamic - which include dynamic warm-

up, dynamic stretching, and walking, for instance.

This followed by the main exercise component and can be called an endurance

aerobic phase, which lasts for 30-40 minutes it occurs in the form of continuous or interval

training, another modality is then circulating training in which the patient alternates

between different types of trainers such as a bicycle ergometer, rowing and elliptical

trainer, stepper, or treadmill, the staff will come over to check how patient doing and check

his pulse to determine whether if his achieving the target heart rate. Finally, this followed

by cool down (strengthening phase) that takes 10-15 minutes long. After exercise, the body

gradually transitions from exertion to rest, reducing the risk of hypotension, arrhythmia,

or myocardial ischemia. Finally cool down restores the heart rate and breathing to their

75

pre-workout levels. We include in this phase the Jacobson's progressive muscle relaxation

or Schultz's autogenous training The advantage of outpatient rehabilitation program is that

the patient is constantly monitored by medical personnel. The heart rate, blood pressure,

and, in high-risk patients, the ECG are all monitored during the training unit, the subjective

perception of exertion is assessed according to the Borg scales, and the occurrence of

symptoms indicating exercise intolerance is monitored. Another advantage of an

outpatient program is the opportunity to meet with other patients who are dealing with

similar issues, which can be beneficial to the patient's mental health.

Cardiac rehabilitation program requires a team approach, which includes a

multidisciplinary team that includes: Cardiologist, physiotherapist, occupational therapist,

psychologist, social worker, clinical nurse specialist.

Eventually, Exercise training has been proven to improve myocardial reserve flow,

improve endothelial function, and raise maximal oxygen uptake (VO2max). Additionally,

cardiac rehabilitation can help to quit smoking, lose weight, lower cholesterol, and lower

blood pressure.99 Milani et al. found that cardiac rehabilitation decreased depression in heart

disease patients who suffered a major coronary event.102 In heart failure patients with intact

ejection fraction, cardiac rehabilitation reduced hospital admissions and exhibited a long-term

reduction in all-cause mortality, according to a Cochrane analysis.

1.2.1.5.3.1 Spa Treatment

It can follow the hospitalization directly, or the patient undergoes it after an outpatient program.

Controlled physical activity, physiotherapy procedures, nutritional measures, psychotherapy,

and health education are all part of the spa treatment, which is monitored by doctors and

medical staff on a regular basis. Teplice nad Bečvou, Poděbrady, Konstantinovy Lázně,

Františkovy Lázně, and Libverda are spas that provide treatment for people with

cardiovascular disease.84 Patients are separated into groups during regulated physical exercise

based on the results of a stress test. Group therapeutic exercise for 30 minutes at least four

times a week, progressive ergometric training for 30 minutes at least four times a week, field

training and Nordic walking, and pool therapy, including swimming, are all part of this activity.

We emphasize weight loss in obese individuals; therefore, we incorporate a reduced-calorie

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diet as well as frequent physical activity. We include lectures on cardiovascular issues in the

cultural program as part of health education. Patients are educated on the basic anatomical,

physiological, and pathological understanding about the heart, blood arteries, and disorders that

affect them, as well as the major risk factors for these diseases and treatment options.85

1.2.1.5.3.2 Home Exercise Program

It is advised not only for patients who do not want or are unable to participate in an outpatient

program and spa treatment, but also for those who use it as a supplement to their therapy on

days when they do not participate in regulated training. The patient is instructed on the proper

workload type, intensity, and frequency. The basis is mainly endurance activity, patients are

recommended to walk, Nordic-walking, cycling on an ergometer or swimming. This activity

should be done 3-5 times a week for 45-60 minutes.

1.2.1.5.4 Therapeutic Physical Education

1.2.1.5.4.1 Respiratory Physiotherapy

Pulmonary complications after surgery prolong hospital stay and increase healthcare costs. We

performed a systemic review to determine to what extent respiratory physiotherapy prevents

such complications, and the best type of physiotherapy intervention. We chose the setting of

cardiac surgery for three reasons. Firstly, patients are prone to pulmonary complications after

surgery; up to 65 % of patients may have atelectasis, and 3 % may develop pneumonia.

Secondly, the prevalence of cardiac surgery is high; around 110 per 100 000 population

annually in the western world. Thirdly, the extra costs of pulmonary complications after cardiac

surgery exceed 28 000 € for each patient.103

Patients with heart diseases often develop changes in respiratory mechanisms and lead

to respiratory complications.104

Thus, physiotherapy in pre- and postoperative period have as main objectives the

pulmonary re-expansion, airway clearance, prevention of complications in the post-operative

period of cardiac surgery such as: atelectasis, pneumonia, pleural effusion, pneumothorax,

chylothorax, pulmonary hypertension, pulmonary hemorrhage, etc.105

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Atelectasis defined as collapse of certain region of lung parenchyma which is the most

common complication after cardiac surgery,106 by worsening oxygenation, decreasing

pulmonary compliance, leading to inhibition of cough and pulmonary clearance which may

lead to respiratory failure and increase pulmonary vascular resistance.107 Heart surgeries

associated with CPB have as adverse effect the increased capillary permeability that causes

edema, which results in decreased lung compliance and gas exchange,108 in addition to lead to

airway obstruction, atelectasis, decreased functional residual capacity and, therefore,

hypoxemia.109

• Physiotherapy in Pre – and Postoperative Period:

In the preoperative, respiratory physiotherapy uses techniques of clearance,

reexpansion, abdominal support. While vibration in the chest wall, percussion, compression,

manual hyperinflation, re-expansion maneuver, positioning, postural drainage, cough

stimulation, aspiration, breathing exercises, mobilization and AEF (acceleration of expiratory

flow), deep breathing, incentive spirometry and other modalities are used in postoperative

physiotherapy.110-111-112-113

Respiratory physiotherapy and exercise therapy are the core of medical rehabilitation

for patients suffering from acute and chronic cardiorespiratory disorders. Poor coordination

and muscle weakness of the inspiratory and expiratory muscles characterize these diseases, in

addition breathing exercise were shown that it improves the respiratory efficiency, increases

the diameter of airways, which helps to dislodge secretions, preventing alveolar collapse and

facilitating the expansion of the lung and peripheral airway clearance.114 As well as the effect

of increased expiratory flow (IEF) in heart rate, respiratory rate and oxygen saturation.113

The main techniques used in respiratory physiotherapy are:115

• Postural drainage technique: it’s a way using gravity to drain mucus out of the lungs by

changing positions, postural drainage is often done at the same time as percussion, which

involve clapping on back, chest or sides with a cupped hand in order to shake mucus

loose from the lungs. General guidelines on how to perform this technique are: each

position should be held for a minimum of 5 minutes. Positions can be done on a bed or

on the floor. In each position, patient chest should be lower than his hips to allow mucus

to drain. While in positions, patient should try to breath in through his nose and out

through his mouth for longer than he breath in for maximum effectiveness.

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It is recommended to perform these positions in the morning to clear mucus that built

up overnight or night before bed to prevent coughing during night.

- On back position (Fig. 7): the chest should be lower than the hips, which can achieve

by lying on a slanted surface or propping the hips up about 18 to 20 inches with

pillows.

- This position is the best draining the bottom front parts of the lungs.115

Fig 7: Back Position, Postural Drainage Technique.115

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- On sides position (Fig. 8): with pillows under the hips, lie on one side so that the

chest is lower than hips.

- To clear congestion from the bottom part of the right lung, lie on the left side.

- To clear congestion from the bottom part of the left lung, lie on the right side.115

Fig 8: Side Lying Position, Postural Drainage Technique. 115

- On stomach position (Fig. 9): Drape the body over a stack of pillows, and the rest of

the arms by the head, with patient chest lower than hips.

- This position is the best for clearing mucus in the lower back area of the lungs.115

Fig 9: Stomach Position, Postural Drainage Technique.115

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• Static and dynamic breathing exercise:116

Static breathing exercises:

- Diaphragmatic (abdominal) breathing - breathing is carried out mainly due to the work

of the anterior abdominal wall and diaphragm (for control, the patient's hands are

located on the anterior abdominal wall).

- chest breathing - breathing is carried out mainly due to work chest (for control, the

patient's hands are located on the chest).

- full breath - breathing is carried out due to the work of the chest and the anterior

abdominal wall (diaphragm), for control, one hand of the patient is located on the

anterior abdominal wall, the other on the chest.116

Dynamic breathing exercises:

- Are performed with the help of auxiliary respiratory muscles and consist of a

combination of breathing exercises and arm and leg movements. For instance,

spread arms to the sides and lean back while inhaling, then bring hands in front of

the chest and bend forward while exhaling. Exercise is utilized to expand the volume

of the lungs ventilated surface.

• Methodology:

- Start with 5-10 minutes of gymnastics. gradually increasing to 15-20 minutes,

eventually reaching 30-40 minutes.

- First, deep diaphragmatic breathing is taught (especially inhalation)

- The exhalation is carried out quickly, with the pronunciation of the sounds "he", "khe"

- Forced exhalation is combined with vibration massage in the drainage area.

- Cough movements are performed after several deep exhalations.

81

• Deep breathing and coughing technique:117

- Support the incision when coughing or sneezing by hugging your chest.

- Take 5 to 10 deep breaths followed by two double coughs four times a day for another

two weeks after you leave the hospital (Fig. 10).

Fig 10: Deep Breathing and Coughing Technique.117

The aim of each respiratory physiotherapy method is as following:118

• Deep breathing exercise: to encourage increased lung volume and prevent lung infection

and collapse.

• Hands-on technique and breathing facilitation exercises: to expand lung capacity.

• Percussions and vibrations: to help coughing and managing shortness of breath

• Breathing and circulation exercise: to prevent further respiratory and vascular

complications such as chest infection and deep venous thrombosis (DVTs).

• Uses of respiratory aids such as: flutter, acapella: reduce frequency of coughing.117

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The goals of respiratory physiotherapy are:118-119

• To influence symptomatology such as shortness of breath, cough, and bronchial

secretion hyperproduction.

• Regular exercise improves respiratory muscle strength, chest wall mobility, airway

patency, ventilation parameters, and physical fitness.

1.2.1.5.4.2 Resistance Training

Resistance training (RT) has increasingly become a critical component of cardiac

rehabilitation, because of its significant health advantages and positive effects on cardiac

comorbidities.120 Increased muscular strength and endurance are the most well-known benefits

of RT. Overall muscle strength improvements of 25 % to 30 % are typical seen. Furthermore,

feeble persons who exercise RT have shown a 46 % increase in muscle power.121-122-123

This is important for cardiac patients because many daily activities require greater

muscular strength and endurance. These activities include the following: Getting out of a chair,

carrying groceries, ascending stairs, and holding/carrying children and grandchildren.

Resistance training can provide them gain the muscle strength and confidence they need to live

a more active and independent life. Resistance training reduces cardiac demands at specific

workloads by lowering the rate-pressure product (RPP) (systolic blood pressure vs. heart rate),

making tasks like lifting heavy things safer. Aerobic fitness has been shown to improve with a

combination of cardiorespiratory exercise and RT.124-125

• RT programming for cardiac patients:

A personalized program should be designed once a patient has been medically cleared

to begin RT. Other health issues should be taken into account while designing an RT program.

There should be a balance among major muscle groups trained. This will prevent muscle group

strength imbalances, which could lead to musculoskeletal injury. To save time, both lower- and

upper-body muscular groups should be trained on the same day. Multi-joint exercises should

be emphasized for their efficiency and functional effects, while single-joint exercises should

be used to supplement the RT program.126

83

Despite the fact that there are recommended 1RM (repetition maximum) percentages

for lower- and upper-body exercises for cardiac patients, 1RM testing is frequently avoided

due to safety concerns and a lack of RT experience, which is typical among cardiac patients.

On the Borg Scale, an RPE (rating of perceived exertion) of 11 to 13 (very light to slightly

hard) is a good place to start for calculating initial loads for RT exercises.127-128 Once the patient

can easily complete 12 to 15 repetitions, a gradual increase in resistance (5 %) should be

implemented. The following are a few training recommendations:

- Perform a warm-up before starting any RT session; A general warm-up would consist

of 5–10 minutes of light aerobic exercise; Gentle stretching and/or active range of

motion exercises with minimal or no resistance would be included in a specific warm-

up.129

- Resist the desired movements/synergies while keeping resistances (weights, bands,

tubes, medicine balls, etc.) parallel to the plane of motion and opposite the intended

direction of their movements.

- Always maintain proper body and joint alignment (e.g., ankles, knees, and hips in line

during a leg press or squat).126

- Machines usually allow for shorter RT sessions, are easier to perform with proper

technique, and stabilize the body, minimizing the need for balance (more muscle

isolation).126

- Free weights typically use more muscles for balance and stabilization, offer a variety

of technique manipulations (e.g., various hand positions), and work the muscles in a

more functional manner.126

84

Table 5: Resistance Training Programming Guidelines for Cardiac Patients

ACSM's Guidelines for Exercise Testing and Prescription126

Modes: use a variety of modalities that include machines, free weights, band/tubing,

calisthenics, and exercise balls.

Sets: perform one set initially; if the patient is stable and time permits, greater strength gains

will occur by using multiple sets after the first 3 or 4 months.

Repetitions: select a weight/resistance that can be performed for 12 to 15 repetitions.

Exercises: perform 8 to 10 exercises for the major muscle groups (hips, thighs, chest, back,

shoulders, arms, abdominals, and lower back); emphasize multijoint exercises.

Exercise order: exercise large muscle groups before smaller muscle groups.

Intensity: us an RPE of 11 to 13 (Borg Scale) as a starting point; if appropriate, start with 30%

to 40% of 1RM for upper body exercises and 50% to 60% of 1RM for lower body exercises.

Frequency: perform 2 to 3 RT sessions/week on nonconsecutive days.

Cadence/tempo: use controlled movement; 2 counts during the concentric phase and 2 to 3

counts during the eccentric phase.

Breathing: exhale during exertion (lifting), and inhale when lowering the resistance.

Progression: Increase resistance by 5% when patients can comfortably complete 12 to 15

repetitions.

Range of motion: Exercise through a full pain-free range of motion while avoiding

hyperextension.

Table 6: Resistance Training Benefits for Cardiac Patients126

CSCS RESISTANCE TRAINING FOR CARDIAC PATIENTS, ACSM's Health & Fitness Journal

Increased muscular strength and endurance.

Prevention and management of chronic diseases and disabilities.

Modification of coronary risk factors.

Improved aerobic capacity when RT is combined with cardiovascular exercise.

Reduced cardiac demands with various physical activities.

Increased ability and confidence to perform tasks of daily living.

Enhancement of functional independence.

Prevention and reversal of muscle wasting (sarcopenia) and an increase in lean muscle mass.

Less fatigue

Decreased depression

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Fig 7: Absolute and Relative Contraindications for RT in Cardiac Patients

American Heart Association Council on Clinical Cardiology and Council on Nutrition, Physical

Activity, and Metabolism

Absolutive Contraindications

Unstable coronary artery disease.

Severe pulmonary hypertension (mean pulmonary arterial pressure of 55 mmHg).

Severe symptomatic aortic stenosis.

Uncompensated congestive heart failure.

Uncontrolled dysrhythmias.

Acute myocarditis, endocarditis, or pericarditis.

Uncontrolled hypertension (<180/110 mmHg).

Dissecting aortic aneurysm.

Marfan syndrome.

High intensity RT (80 % to 100 % 1RM) in patients with active proliferative retinopathy or

non-proliferative diabetic retinopathy.

Relative Contraindications (Should Consult a Physician Before Participation)

Major coronary artery disease risk factors.

Diabetes.

Uncontrolled hypertension (<160/100 mmHg).

Low functional capacity (< 4 METs).

Musculoskeletal limitations (including but not limited to arthritis, osteoporosis, tendonitis,

etc.)

Implanted pacemakers and defibrillators.

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1.2.1.5.4.3 Endurance Aerobic Training

Cardiovascular endurance training is the performed exercises involving the entire body at

moderate to high intensity for an extended period of time, which can effect on increasing the

heart and breathing rate. According to many experts, aerobic exercise is the most important

part of physical fitness. Cardiovascular endurance can be achieved by exercising aerobically

30 minutes per day, 3 to 7 days per week. Aerobic exercise is beneficial for cardiac patients

precisely in the following points:

- The heart pumps more efficiently.

- Lungs works better.

- Blood volume and delivery system are improved.

- Resting heart rate lower.

- Muscles, tendons, ligaments, bones get stronger.

- The body is more able to use fat as an energy source.

Based on the patient's fitness and condition, we can use three levels of training intensity:

low-intensity interval training, continuous training, and high-intensity interval training. Low-

intensity interval training is recommended for patients with significantly reduced EF LV (15-

20 %) in NYHA functional class III. The intensity of the exercise corresponds to 50-70 % of

the maximum power, as determined by a stress test performed to the patient's subjective

maximum. The load lasts 30 seconds, followed by a rest period. The intensity of the load is

gradually increased, and then exercises with a continuous form of load can be performed.

Continuous training is done in an aerobic zone of medium to high intensity. The first exercise

units last about 15 minutes and have a low intensity load of 40 - 50 % VO2peak. Depending

on the patient's medical condition and response to physical exercise, we gradually increase the

intensity of exercise to 70 % of the initial VO2peak, and the duration and frequency of exercise

can also be increased. Only patients in good clinical condition who are stable and very capable

can complete interval training at a high intensity of 85-95 % VO2peak. The load interval last

about 4 minutes, and the recovery time approximates 3 minutes.84-130

The overall effect and benefits of cardiovascular endurance training in post-cardiac

surgery patient are as following:

- Lower blood pressure.

- Higher insulin resistance.

- More favorable plasma lipoproteins profile.

- Increases cardiac output and blood pressure.

87

- Lower resting heart rate and cardiac hypertrophy.

- Improve overall stamina and the ability of the heart to pump oxygenated blood.

- Improving muscle strength and endurance.

In addition, these exercises include walking swimming, biking. Endurance exercise

keeps the heart, lung and circulatory system healthy. Increases in cardiac stroke volume and

heart rate during exercise raise cardiac output, which, combined with a transient increase in

systemic vascular resistance, raises mean arterial blood pressure.131

As it shown in (Fig. 11) long-term exercise, on the other hand, can promote a net

reduction in blood pressure at rest. A meta-analysis of randomized controlled interventional

studies discovered that 3-5 times per week of moderate to intense exercise lowers blood

pressure by an average of 3.4/2.4 mmHg.132

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Fig 11: Overview of Major Cardiovascular Effects of Exercise.131-132

(Matthew A. Nystoriak, Aruni Bhatnagar

Front Cardiovasc Med. 2018; 5: 135. Published online 2018 Sep

28. doi: 10.3389/fcvm.2018.00135)

Abbreviations: HR, heart rate; LV, left ventricle; eNOS, endothelial nitric oxide synthase;

NO, nitric oxide; VSM, vascular smooth muscle; BP, blood pressure; HDL, high density lipoprotein;

LDL, low density lipoprotein; VLDL, very low-density lipoprotein; TG, triglycerides; EPC,

endothelial progenitor cell.

1.2.1.5.5 Physical Therapy Methods

Physical therapy methods are only used as a supplement to complex therapy in the treatment

of people with cardiovascular disease or heart failure. The example of some methods we can

use in cardiac patient are: Balneological procedures, in particular using CO2 applications, are

usable, followed by low-frequency electrical stimulation (LFES) of skeletal muscles as part of

electrotherapy. If the patient has any of the contraindications for the procedure, we do not use

physical therapy.

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1.2.1.5.5.1 Carbonic Bath

The physiotherapy method of carbonic acid gas bath (CAGB) mediated through the effects of

carbon dioxide (CO2) is a minimally invasive treatment and prevention method of many human

disease. The carbonic bath has a reflective effect on the entire organism via the nervous system,

particularly on the cardiovascular system, and can therefore be used in the treatment of people

suffering from heart failure. We prepare it by saturating water under CO2 pressure in saturators,

with the bath containing at least 1000 mg of free CO2 per kilogram of water. The bath has the

greatest effect when the water temperature is low; in practice, a temperature of 34-28 °C is

often used. The rate of absorption is approximately 30 ml CO2/ min/m2 submerged skin

surface. Active hyperemia and skin erythema develop at the site of contact with the skin,

peripheral vasodilation and peripheral resistance decrease, and muscle blood flow improves.

There is a reduction in O2 consumption, overall metabolism, and as a result, the heart's

work is economized. In addition, the influence of a course of carbon dioxide baths,

hemodynamic parameters of cardiac output (cardiac and stroke volume) improved, rhythm

slowed, diastole become longer, and systolic and diastolic arterial pressures decreased. The

findings support the use of dry carbon dioxide baths during the recovery period for patients in

the I-III functional classes who have had a previous myocardial infarction or heart failure.

Additionally, diuresis is increased. The carbonic bath's result is determined by the

patient's reactivity, the time of application, the temperature of the bath, the size of the skin

surface that comes into contact with CO2, and the strength of the skin layer. The bath

duration should last between 8 and 25 minutes, with each positive step we gradually increase

the length by 2 minutes. The number of procedures should be in the range of 15. Furthermore,

it is best to start with partial baths and then progress to total baths after evaluating the effect on

the patient. We perform a dry wrap after the bath, and the patient rests on the bed for at least

30 minutes.133 Baths with carbonic dioxide are contraindicated in the following cases: cardiac

decompensation, epilepsy, tendency to hypertension, late-stage atherosclerosis, acute

inflammatory diseases, tachyarrhythmias, hypotension, coronary sclerosis, anemia.134

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1.2.1.5.5.2 Low-frequency electrical stimulation

Low-frequency electrical stimulation (LFES) is an acupuncture technique that stimulates

muscle contraction to mimic the benefits of resistance exercise. Furthermore, the effects of

low-frequency electrical stimulation (LFES) on muscle strength and blood flow in patients with

advanced chronic heart failure (CHHF). As well as (LFES) has the potential to reduce

breathlessness and increase exercise capacity in people with chronic heart failure. This method

is specially used in patients with NYHA III and IV functional clinical classifications.

These patients develop global hypoperfusion, which affects the skeletal muscles, as a

result of the significantly reduced function of the cardiovascular system. Moreover, muscle

atrophy may be present in up to 70 % of cases, with a predominance of type IIB muscle fibers

and a decrease in the absolute amount of type I and IIA aerobic fibers. Muscle atrophies are

associated with low exercise tolerance and dyspnea, which leads to further physical inactivity.

For LFES, we use biphasic pacing with a frequency of 10Hz and a mode of 20 seconds "on"

and 20 seconds "off." The pulse duration is 200 ms, and the maximum intensity is 60 mA.

We use LFES for 60 minutes per day, and then we can increase it to twice a day for 60

minutes. LFES can also be used in combination with traditional physical training. Due to the

fact that the method does not cause hemodynamic changes, it is well tolerated by patients and

can thus be used in patients who are unable to engage in physical activity, based on this the

benefit of LFES is that it acts locally without increasing the demands on cardiac work; there is

no increase in cardiac output. During stimulation, the heart rate and blood pressure do not

change. LFES has a positive effect on increase muscle strength; with LFES, we can achieve

stronger muscle contractions than with free training because there is maximum synchronization

of the activation of all motor units during electrical stimulation. It enables patients to perceive

shortness of breath and exertion during normal daily activities as less intense, thereby

improving their quality of life as a result of illness.84-135-136-137

1.2.1.5.6 Ergotherapy

According to the World Health Organization (WHO), there are known correlations between

cardiac dysfunction and the incidence of cognitive impairment, with some studies estimating

its presence in more than 17 % of cardiac patients, potentially increasing to around 75 % of

patients with heart failure. Although the severity of cognitive deficit varies, among cardiac

patient groups, impairment is frequently classified as mild, which means that there is a

91

cognitive deterioration greater than expected for the person's age and education level, which

may impair their ability to engage in more complex activities and behaviors.135

Patients with cardiac dysfunction are more likely to experience mild cognitive

impairment, which can impair their ability to successfully engage in daily activities crucial for

home and community safety, as well as maintaining health and well-being. Ergotherapy plays

a role in chronic disease management by assessing and improving functional abilities affected

by physical, emotional, and cognitive domains. While the ability to independently complete

basic activities of daily living remain intact, the capacity to engage in more complex activities

requiring a higher level of cognitive function may be compromised, resulting in increased

difficulty completing instrumental activities of daily living (IADL), completing work activities,

and engaging in self-management behaviors. IADLs are more cognitively demanding task

behaviors required for independent living, and they include activities such as shopping, meal

preparation, driving, and financial management.136-137 Therefore, Occupational therapy is an

important part of the rehabilitation of people with cardiovascular disease.

It helps patients to maintain, use and improve the skills necessary for the day-to-day,

work, leisure and recreational activities through meaningful employment, promotes the active

integration of patients into society and contributes to maintaining an optimal quality of life.

Specifically, occupational therapy deals with the training of motor functions, sensory functions,

cognitive, communication and social functions, activities of daily living (ADL), the use of

compensatory aids are included if the patient's condition requires it. In addition to therapy it

deals with diagnostic methods for instance. The occupational therapist assesses the patient's

ability to return to their original job or assists in the selection of a new suitable job based on

the patient's condition and abilities.119Therefore, ergotherapy intervention can decrease risk of

further potential decline and injury to prevent risk of readmission to the hospital. As a result it

is an absolute essential to helping patients regain their independence and ability to do what they

love and enjoy in life.

1.2.1.5.7 Psychological and Social Problems of the Diseases

Heart failure (CHHF) is the terminal stage of many heart diseases and a major cause of

morbidity and mortality. The incidence of congestive carditis increases steadily as treatment of

its coronary antecedents, such as myocardial infarction.138

It's easy to see the effects of heart failure on your body - such as shortness of breath,

fatigue, and edema. What isn't obvious is the toll a weakened heart can take on your emotions.

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Therefor psychosocial issues are important variables that need to be addressed in patients with

heart failure. Unfortunately, these issues are frequently overlooked. Depression and a lack of

social support have been shown to negatively impact HF patients. Patients with HF who are

depressed or lack social support have higher morbidity and hospital readmission rates are less

adherent to their medical regimen and have a higher overall cost of care.139 Living with this

condition can elicit a wide range of emotions, including fear and sadness, as well as anxiety,

depression, and even anger. By letting them simmer, they can wreak even more damage on

the heart, making it more difficult to treat. According to research, people who have a positive

outlook are more likely to take their medication. They also maintain heart-healthy habits such

as eating nutritious foods and exercising.

When a long-term disease, such as heart failure, is diagnosed, it is normal to experience

a wide range of emotions, including fear about the future, worry to lose control over the health,

anger, stress over the ability to manage the condition, loneliness.

By letting all these feelings to build up, could make matters worse. Stress and anger

can raise the BP (blood pressure) and make the heart work even harder. Both can be as bad for

the heart as high BP and cholesterol. Depression for at least two weeks affect up to 70 % of

people with heart failure, along with depression and sadness patient might have fatigue, lack

of energy, loss of appetite, feeling of emptiness, loss of interest in activities, trouble sleeping

or sleeping too much.140

As patients with heart failure experience various physical and emotional symptoms,

these symptoms limit patient’s daily physical and social activities and result in poor QOL

(quality of life), therefore maintaining QOL in these patients should be assessed appropriately

to determine its impact on patients daily life.141 One of the best ways to handle these

psychological issues is psychological support, rehabilitation helps to overcome the fear of

physical activity and thus manage the newly created stressful situation. The patient's closest

environment should be the one that helps him change his lifestyle. Relaxation training,

education to influence risk factors, including dietary recommendations, and breaking down

unhealthy habits should all be included.

Psychological rehabilitation aids in the suppression of the patient's psychosocial factors

and personality traits that may contribute to the development of heart failure. It aims to improve

patients' ability to respond optimally to crisis life situations, which is important for lowering

the cardiovascular system's reactivity. It also aids in the treatment of any depression, anxiety,

or emotional stress caused by the disease.

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On the matter of Social Services, social rehabilitation aims to achieve individuals

independence, self-sufficiency, by developing their specific abilities and skills, strengthening

habits, and practicing normal performance for independent living.

Cooperation with occupational therapists and social workers is used in the process of

social rehabilitation. Try to enable the patient to make the most of his remaining work potential

and reintegrate him into society.142

1.2.1.5.8 Indications and Contraindications of Cardiac Rehabilitation

Indications of cardiac rehabilitation are:143

• Recent myocardial infarction,

• Acute coronary artery syndrome,

• Chronic stable angina,

• Congestive heart failure,

• After coronary artery bypass surgery,

• After a percutaneous coronary intervention,

• Valvular surgery,

• Cardiac transplantation.

Contraindications of cardiac rehabilitation are:144

• Unstable angina,

• Acute decompensated congestive heart failure,

• Complex ventricular arrhythmias,

• Severe pulmonary hypertension (right ventricular systolic pressure greater than 60 mm

Hg),

• Intracavitary thrombus,

• Recent thrombophlebitis with or without pulmonary embolism,

• Severe obstructive cardiomyopathies,

• Severe or symptomatic aortic stenosis,

• Uncontrolled inflammatory or infectious pathology,

• Any musculoskeletal condition that prevents adequate participation in exercise.

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2 CASUISTICS:

2.1 Basic Data Name: L.P.

Age: 62.

Height: 171 cm.

Body weight: 78 kg.

Gender: Male

BMI: 26.67

Marriage status: Married.

Occupational status: Janitor.

Data provider: In Person

Admission date: 1st of October 2021.

Data record date: 26th of October 2021.

2.2 Place of Hospitalization

On the 1st of October 2021 Mr. L.P. was transferred unconscious to Saint Ann’s hospital

ambulance, to the Department of Internal Cardio-angiology, University Hospital at St. Anna in

Brno. In the morning of the 1st of October 2021, Mr. L.P. was found by his wife on the floor

conscious and he was experiencing pressure, tightness sensation in his chest, shortness of

breath and he had a feeling of fast beating (palpitations). After that his wife immediately called

the emergency medical help and the ambulance came and transferred him to the hospital.

He suffered from dilated cardiomyopathy and on this basis, he was transplanted by a

new heart on the 25th of March 2017, and more physiological findings occurred in 2017, diffuse

calcification of brachial artery. Unfortunately, about month ago he suffered from heart attack

(myocardial infarction) and he is waiting for the new heart transplantation for the second time.

Upon admission, diagnosis of Delated cardiomyopathy (DCM) was confirmed by

Echocardiogram and this examination allowed the doctor to see that there was left ventricle

and also right ventricle wall motion abnormalities, and severe depression of systolic function.

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2.3 Diagnosis upon admission

Upon admission the patient was diagnosed with Cardiorenal syndrome with oliguria on the

base of serious right ventricle dysfunction, tricuspid valve regurgitation, and signs of

hypervolemia, accumulation of fluid in the pleural cavity in an amount of 400 ml (Fluidothorax

bilateral) were confirmed.

Furthermore diagnosis were identified upon admission, they are as following:

– Acute kidney insufficiency AKI (acute on chronic)

– Continuous veno-venous hemodialysis (CVVHD) introduced from the 5th of November 2021,

anuria.

– from the 8th of November 2021 the patient is on the urgent waiting list for heart

transplantation.

– The State after Cardiopulmonary Resuscitation (CPR) for 5 minutes which took place on the

11th of November 2021, the patient was inserted with veno-arterial extracorporal membrane

oxygenation (VA ECMO).

– Subacute ST elevation myocardial infarction (STEMI) of the bottom wall and ramus

ventricularis selective coronarography (RV, SKG) on the 1st of October 2021 was diagnosed,

serious vasculopathy of graft with arteria coronaria dextra (ACD) obturation on the base of

massive thrombosis, additionally peripheral obturation of ramus interventricularis anterior

(RIA), ramus circumflexus (RC), ramus marginalis sinister (RMS), were identified.

– Furthermore, an ejection fraction of left ventricle (EFLV) of about 45 %- 35 % was diagnosed.

– The patient was implanted with implantable cardioverter defibrillator (1D-ICD) on the 21st

of October 2021.

– The patient underwent a heart transplantation surgery on the 25th of March 2017.

– Irregular, fast heart rate (Atrial fibrillation) was confirmed.

– Antireflux uretero-intestinal anastomosis procedure was introduced on the 15th of May 2019.

– Acneiform exanthema was identified.

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2.4 Prescribed Rehabilitation

It is recommended to customize a rehabilitation program of exercise and education, to help the

patient improve his health, recover and treat heart disease and decrease the risk of other heart

disease, the cardiac rehabilitation should involve exercise training such as resistance training,

endurance aerobic training with a minimal load which can be gradually increased over the time.

Emotional support and education about lifestyle changes such as eating a heart-healthy diet,

maintaining a healthy weight and quitting smoking, to reduce the symptoms and the

progression of the disease, help regaining strength. Thus, will improve and keep independence,

self-sufficiency and physical abilities of the patient.

2.5 Engagement of Author in the Rehabilitation Process

2.5.1 Anamnesis

I was introduced to my patient at the Department of Internal Cardio-angiology 4th floor,

University Hospital at St. Anna in Brno. The anamnesis was taken on the 26th of October 2021,

in a conversation form. The patient Mr. L.P had the full ability to respond to my questions

fluently, and he was fully responsive and cooperative, and in a very good mental status.

Current Complaint:

Unfortunately, Mr. L.P about month ago suffered from Acute transmural myocardial infarction

of the bottom wall, and now he’s hospitalized, and in the waiting list for a donor organ. In more

details, and according to the medical documents, the patient acceded the cardiac clinic, ward

32 on the 1st of October 2021, and this is because he suffered from a heart attack of the bottom

wall, which was confirmed by coronarography. The patient Kidney’s function has deteriorated

and there was a tendency to bradycardia. Exanthema also appeared at the patient chest.

The patient suffered from paroxysmal atrial fibrillation, and application of amiodarone

(sodium channel blockers) had no effect on him, after that he underwent electrical

cardioversion to restore a normal heart rhythm, and it didn’t show any effect too. After that his

renal function got worse, complex QRS spread and on this basis he was transferred to coronary

unit. After a period of time when the patient’s condition has stabilized, he was transferred back

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to ward 32. What happened day by day since he was admitted to the hospital according to the

medical documents:

On the 1st of October 2021, the patient was implanted with implantable cardioverter

defibrillator (ICD). Then on 2.11.202, his condition worsened with a signs of right-sided heart

failure, oliguria, and renal insufficiency progression. Then on the 4th of November 2021 the

patient returned back to the coronary unit, where he required dialysis and parenteral nutrition.

Then an oncologist was consulted, and the patient was classified on the 8th of November in the

urgent waiting list for heart transplantation.

Furthermore, on the 11th of November 2021, the patient needed cardiopulmonary

resuscitation (CPR) that took about 5 minutes long, but intubation was not necessary. After that

he was transferred to the cardio-surgery-clinic (CKTCH) for veno-arterial extracorporeal

membrane oxygenation (VA ECMO) insertion as bridge to transplant, and as a temporary

solution to be stable and safe until getting new heart.

Family History:

Mr. L.P is married and lives with his family. Parents of the patient are not alive, his father

suffered from acute myocardial infarction and he died at the age of 49. Mother of the patient

suffered from diabetes mellitus type 2 and died because of diabetic complications at the age of

63. The patient has six siblings, one brother died from esophagus cancer at the age of 56, and

all the other siblings are healthy. The patient has one son and one daughter and they’re healthy

too.

Personal-History:

In 2004 the patient was diagnosed with an insufficiency of a valve in the heart, and that was

the beginning of the journey, on this basis after four years the patient was implanted with ICD

(implantable-cardioverter-defibrillator). The patient after that continued his life normally for a

ten years long without any disturbances or health problems, and unfortunately in 2014 the

patient was diagnosed with cancer of urinary bladder (Urothelial Carcinoma – high grade), and

he underwent chemotherapy as a treatment and it went unsuccessfully, on this basis the patient

had a surgery of urinary bladder removal (cystectomy) in January 2017 and now he is living

with a urostomy which is placed in a small, spout like a hole on he’s abdomen as a new passage

where urine will leave his body.

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In a meantime he also suffered from pulmonary embolism. Then in 2017 the patient

underwent the heart transplantation, because of cardiac decompensation, complicated by

hematuria and hemorrhagic shock, and an extracorporal membrane oxygenation (ECMO) was

inserted temporarily. And the patient got an injury of the right lung during surgery. And also

the patient was diagnosed by Muscle venous thrombosis of the right lower extremity which

was confirmed by sonography. The patient was diagnosed by a heart failure due to

arrhythmogenic left ventricular cardiomyopathy. Additionally, the patient suffered from

hypertension. The State after implantation of ICD in April 2014. The patient underwent

appendectomy surgery in 1969. And has an injury of ruptured tendon of the left hand.

Occupational History:

The patient used to work as a janitor, and now he is in pension. He has been working for 35

years long.

Social History:

The patient is married and lives with his wife, and he has two children, one girl and one boy.

He’s living in a flat and has about five stairs to climb.

Pharmacological-History:

The patient takes the following medications:

Envarsus 1.5 mg -0-0, Cetican 1mg -0-0.75 mg, Betaloc zok 200 mg tbl. 1-0-0,

Detralex 2-0-0, Magnosolv 1-0-1, Anopyrin 100 mg 0-1-0, Procoralan 7,5 mg tbl. 1-0-1, Furon

40 mg tbl. 1/2-0-0, Agen 5 mg tbl. 0-0-1, Alopurinol 100 mg tbl. 1-0-0 4x per week, Rocatrol

0.25 mg tbl. 1-0-0, Atoris 20 mg tbl. 0-0-1, Omnic 0.4 mg 0-0-1, Algifen gtt.d.p.d.p.

Medication at transfer:

Dobutrex 250mg ad FR 50 ml 10 ml/hod, Noradrenalin 5-amp ad FR 50 ml 0.10 ml/hod (stř.

TK > 65 mmHg), Smofkabiven 1970 ml + 1 amp. Cernevit + 1 amp. Tracutil 60 ml/hod, opak.,

FR 250 ml + Natriumglycerolphosphate 2amp=40 ml=40 mmol 80 ml/hod od 10h, s.c. Clexane

(enoxaparin) 0,4 ml 10 - 22, i.v. Torecan 1amp d.p. při nauzee, Certican (everolimus) snižuji

na 0,50mg tbl. 1 - 0 - 1, Advagraf (tacroimus) 0,5mg tbl. 1 - 0- 0, Rocatrol 0,25mgt bl. 1 - 0-

0, Trombex (clopidogrel) 75mg tbl ode dneška ex, Controloc (pantoprazol) 40 mg tbl dostal v

6,00, zítra v 6,00, Diazepam 5mg tbl 1/noc d.p.

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Abuses:

The patient drinks one small beer daily, and once a day the patient drinks coffee, other than

this the patient denies that he has any addictive habitudes, including alcohol, drugs and

smoking.

Allergic History:

Negate, the patient is not allergic to anything.

Sport History:

The patient doesn’t do any sports now; his job was the only activity he has ever done.

At home he is just resting, sometimes goes for walks and from time to time does some cycling

but irregularly. These are all his activities.

Rehabilitation History:

The patient had the rehabilitation only once in the hospital while he was waiting for the heart

transplantation in 2017 and then after he got transplanted, he went to Poděbrady spa and he

spent there about a month long.

Physiological Function:

The patient has got a urostomy after the removal of urinary bladder, and that’s why he doesn’t

need to urinate (urination by stomia) and has a regular formed defecation without admixture.

The patient negates sweating, he doesn’t sweat even at night, and he sleeps well without any

disturbances, and he’s weight is stable.

Operation History:

The patient also underwent an operation of appendectomy and the operations that were

mentioned before, heart transplant and urinary bladder removal.

2.5.2 Physical Examination The patient was lucid, cooperative and responsive, well oriented to person, place and time.

The patient weight is about 78 kg, and height 171 cm. The body structure corresponded to the

Ectomorphs somatotype which is characterized by long and lean, with little body fat and little

muscles.

The patient was able to actively change a position where the transition from lying down to

sitting and standing positions and he haven’t experienced any dizziness. The patient did not

have shortness of breath at rest. The heart rate measured by pulse oximetry was 85 beats per

minute, O2 saturation reached 97 %, Blood pressure was about 138/90 mmHg measured by a

blood pressure monitor (sphygmomanometer), and when he needed to visit the toilet or have

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some walk in the corridor he used to have the support from the walker. So, he can mobilize

with a walker independently and walk under assistant. The patient used to have a normal habit,

without shortness of breath and without cyanosis as well. There was no sign of surface injury,

and without neurological lateralization, no skin pathology, and normal coloring and turgor,

without swelling, unicteric.

Skin and mucosa:

Exposed skin and superficial mucosa are not completely normal with rashes and small raised

acne like bumps which can be observed in patients chest and upper back, due to an existence

of acneiform exanthema. Additionally, for the chest and neck, the skin was slightly red and dry

as a result of the insertion of the central venous catheter for medication administration; the skin

is otherwise normal in color, and with good elasticity, temperature, and moisture, and no

swelling. Surgical scars after the operations that the patient underwent can be observed clearly,

the scar along the chest bone (sternum) after the previous heart transplantation surgery, and the

scar that runs from just below the bellybutton to the pubic bone, can be clearly seen as well.

Lymph nodes:

Superficial lymph nodes were examined in the cervical region, axillary region, and abdominal

area. Lymph nodes were round in shape, medium in size, mobile, soft and palpable, and easy

to move, no abnormal magnification was found.

Head and face:

The head of the patient is slightly in a forward position. The pupils of both eyes are the same

size (isochoric pupils), no abnormal eyeballs protuberance. The eyes are symmetrical, no

conjunctival congestion, no edema, no icteric sclera, the cornea is transparent.

The patient could perfectly stick his tongue out in the middle line. No coating. The

shape of both ears is normal, the patient has got an oval shaped ear, bilateral asymmetry was

observed in the shape of the ear with no abnormal exudation. The sense of hearing is very good.

The nose is in center of the face with normal symmetry, length and width so the shape is normal

without edema on the nose mucosa. Functionally such as nasal breathing or ventilation function

is normal, without blockages, he can smell and taste very well, without inflammation. The

shape of the mouth is normal there wasn’t lip cyanosis or ulcer. Oral mucosa is normal. Uvula

located in the middle. Bilateral tonsils are normal.

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Neck:

The shape and length of the neck are normal and symmetrical. Lymphoid nodules and veins

are impalpable. The carotid pulse is normal, symmetrical and palpable, and there is no visible

bulging of the jugular vein. Bilateral thyroids are normal, soft, symmetrical, and non-tender

and it slides upwards slightly when swallowing, without visible enlargement.

Chest:

The shape of the chest cage is normal and symmetrical. The sternum located in the middle of

the chest, without pain upon percussion. Breathing rhythm is quite normal. There are a surgical

scars after the operations that the patient underwent which can be observed clearly, the scar

along the chest bone (sternum) after the previous heart transplantation surgery which is named

as (post sternotomy scar). The patient had a skin condition in which the hair follicles become

inflamed - follicular exanthema. There is alveolar breathing without special phenomena.

Tapping on the chest is clear and full without abnormalities.

Abdomen:

There was confirmed peristalsis (positive). There was no pain with percussion and resistance,

and no pain or tenderness on palpation in the hepatic and spleen region. Percussion is bilaterally

negative. As the patient underwent surgical removal of the bladder then, there is a stomia in

the right hypogastric area, stomia is where the urine collects and leave the body.

Spine and Extremities:

The spine is located in the middle of the body and extended from the base of the skull to the

tailbone. The patient has a slight thoracic kyphosis. No scoliosis observed. The spinal

movement is normal, within the normal range of physiological movement. The upper extremity

looked normal in length and in shape with no rash nor edema or any other abnormality, The

patient got an injury a ruptured tendon in the left hand. The range of motion was within the

normal range. In the lower extremity the patient is diagnosed with muscular vein thrombosis

and, edema on the left lower extremity above the ankle, with no sign of phlebitis. Peripheral

pulsation was palpable. The patient had a calm varicose vein. There are weak pulses felt in the

extremities.

Electrocardiogram (ECG) findings:

RS reg 85/min, PQ = 0,16, QRS = 0,08, STE 1,5mm III, aVF, 0,5mm I, STD 1mm al, aVL,

V3-5, rsrV1-2, T flat, PZ V5, osa – 30. Without ES. Elevation of DS.

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Additional Examination:

– On the 1st of October 2021:

1. FIRST INTERNAL CARDIOLOGY CLINIC – Coronarography findings:

Acute coronary syndrome: no stenosis of strain, inequalities in proximal ramus intermedius

artery, in ramus interventricularis anterior (v RIA-RD) there is 50 % bifurcated stenosis, in the

middle part of ramus interventricularis anterior (RIA) – there is multiple cascade stenosis to

90 %, and obturation of peripheral part of ramus interventricularis anterior (RIA), ramus

circumflexus (RC) and ramus marginalis sinister (RMS) can be observed.

Arteria Coronaria Dextra (ACD): massive thrombosis in the full length of the artery.

RLVG: hypokinesis DS, ejection fraction (EF) of the left ventricle 47 %.

Resume: serious vasculopathy of the graft with arteria coronaria dextera (ACD) obturation on

the basis of massive thrombosis, peripheral obturation of RIA, RC and RMS. EF of the left

ventricle LK 47 %.

The state after orthotopic transplantation of heart (OTS) on the 25th of March 2017 because of

decompensated cardiomyopathy (DCMP) and thrombotizatin of mitral valve replacement

(MVR).

– On the 4th of November 2021:

1. FIRST INTERNAL CARDIOLOGY CLINIC – findings of Sonography heart examination

by Vivid q, PACS 1443/17:

Left ventricle (LV): 45/37, interventricular septum (IVS) 10, dorsal septum (ZS) 10 – LV

without dilation or hypertrophy, dyskinesis of the large part of septum, akinesis of DS, ejection

fraction (EF) of 35 %.

Left atrium (LA): 39 Aorta: anulus 19 aorta ascendens 38.

Right ventricle (RV): 30 z PLAX, very serious dysfunction or akinesis found and, septal

dyskinesis, TAPSE 3 mm. there wasn’t pericardial effusion. Valve with physiological

morphology existed, and few congestions in hepatal vein existed too.

– Valves:

Mitral valve: asymmetric position, without pathological gradient, mitral valve regurgitation to

2nd degree, where the heart mitral valve doesn’t close tightly.

Aortic valve: without pathological gradient and regurgitation.

Tricuspid valve: there was a regurgitation of 2-3 degree.

Pulmonary valve: without regurgitation.

Resume: Serious dysfunction of the right ventricle, ejection fraction of left ventricle

(EFLV) of 35%. Fluidothorax I. sin. 300 ml, I. dx. 500-600 ml.

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– On the 4th of November 2021:

Clinical imaging method of X-ray examination of the heart and lungs findings:

Invisible line of pneumothorax, there is the central vein catheter on the left side in situ.

Congestive lung drawing. Wore bilateral transparency of the lung parenchyma – effusion.

Bilaterally unbounded diaphragm observed.

– On the 10th of November 2021:

1. FIRST INTERNAL CARDIOLOGY CLINIC: findings of Sonography heart examination

Vivid S7, Control:

Resume: Serious dysfunction of the right ventricle, ejection fraction of left ventricle (EFLV)

of 35%, Significant Tricuspid valve regurgitation. Ascites stationary. Accumulation of fluid in

the pleural cavity in an amount of 400 ml (Fluidothorax bilateral). Were diagnosed.

– Operation performance:

On the 21st of October 2021, primo-implantation of implantable cardioverter defibrillator

(ICD).

2.5.3 Initial Kinesiology Examination

I performed the following kinesiological examination on Mr. L.P with his consent, under the

assistance and supervision of my supervisor Mgr. Michal Úlehla:

1. Inspection.

2. Goniometry.

3. Anthropometry.

4. Neurological Examinations.

5. Muscle shortening test.

6. General movement stereotype.

7. Gait Examination.

8. Spinal Development Test.

Inspection:

Inspection is a visual examination, which was performed from 3 views, from the posterior view

(the behind), form the lateral view (from the side), and finally from the anterior view (from the

front). The aim of this examination is to check or look at or inspect specific areas in the patient

body, for normal colour, shape and consistency. Certain findings on inspection may alert the

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health care provider. For instance, the legs of the patient may be swollen. The health provider

will then pay attention to the common things that can cause leg swelling, such as extra fluid

caused by heart problems. Common areas which were inspected include the following:

1. The skin: to look for colour, bruising, cuts, moles or lumps.

2. Face and eyes: to see if they’re even and normal.

3. Neck and veins: to look for bulging or swollen.

4. Chest and abdomen: to see if there are any masses or bulges.

5. The legs: to see if there is any swelling.

6. The muscles: to check for good muscle tone.

7. The elbows and the other joints: check for swelling and inflammation, and if any

deformities are present.

I firstly asked the patient to take off his clothes and to stand in upright position with

both upper limbs aligned along the side of the body. Then I began my observation from the

posterior view. I tried to look for head, neck and shoulder position, if there is elevation or drop

of the shoulder, if there is head tilt or rotation, the spine if there is lateral deviation (scoliosis),

the scapula if there’s winging, pelvis and hip if there’s lateral pelvic tilt/shift, the knee if there’s

genu varum or genu valgum, ankle and foot to look for pes planus or pes cavus.

Posterior view findings as follow: shoulder elevation was observed on the patient as well as

scapula alata (winging). Non asymmetry of the chest found. Muscles of the neck in the right

side are more prominent. Varicose vein can be seen clearly in the back of both thighs. The hip

muscles are not asymmetry and shifting forward or anteversion of the pelvis was observed. The

patient has flat foot, and lower leg swelling (around the ankles). The patient knees are bowing

outward (genu varum) and the lower leg is angled inward (medially) in relation to the thigh

axis. The feet of the patient is pointing outward with tibia external rotation and knee facing

forward even when he walks can be seen clearly named as (Duck-footed or out-toeing).

I made an examination with the plumb line which was placed on the posterior of the

head and should pass through the occipital protuberance, spinous process of the vertebrae and

through gluteal cleft, between the legs. In the patient the plumb line wasn’t in a straight line

along the midline of the body, it was more to the lateral side. Hyper kyphosis the thoracic spine

was clearly observed as well.

And then I asked the patient kindly to turn, to make the next observation from the lateral

view, I tried to check for or to inspect for, head and neck, if there’s forward head position, and

if there’s flattened lordotic cervical curve or excessive lordotic curve (cervical lordosis). The

shoulder, if there’s forward shoulder, abducted/adducted shoulder. Thoracic spine, if there’s

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kyphosis. Lumbar spine, if there’s lordosis or flat back. To check for the chest, if there’s pectus

excavatum (funnel chest) is when there’s depression in the sternum, and to look also for pectus

carinatum (pigeon chest) is when part of chest bone is pointing outwards. Pelvis and hip, if

there is anterior pelvic tilt or posterior pelvic tilt. Knee to look for genu recurvatum (knee

extension greater than 5 degree).

Lateral view findings as follow: the head of the patient is in forward position. Thoracic

kyphosis was observed. The ribs cage of the patient is slightly uneven, or protruding might be

due to abdominal muscle weakness that causes the ribs to stick out. Prominence on the belly of

the patient. I made a plumb line examination as well, and the plumb line from the lateral view

should pass through the ear lobe to acromion process (shoulder) to the lateral malleolus. But in

my patient the plumb line didn’t follow the shoulder it was slightly in front of the shoulder as

the patient has a forward head position, and it followed the hip, and it was aligned before the

lateral malleolus as I mentioned because of forward head as well as hyper-kyphosis.

Finally, I asked the patient to turn to make the last observation from the anterior view.

I tried to look for head and neck, if there’s tilt of the head or rotation. The shoulder, if there’s

elevation or drop and also if the shoulder is abducted/adducted. The chest how it looks like,

especially the position of the clavicle, if it’s dropped, and if there’s any prominence in the ribs,

as well as the position of the sternum as the patient underwent an open-heart surgery. The hip,

if there’s rotation or lateral tilt/shift. The elbow if there’s cubitus valgus or cubitus varus. The

knee to look for genu varum or genu valgum, and if there’s external or internal tibial torsion.

To check for the ankle and the feet, if there’s hallux valgus (hammer toe).

Anterior view findings as follow: funnel chest was clearly observed, as well as post-sternotomy

scar was visible clearly as the patient underwent an open-heart surgery for heart transplantation

in 2017. ICD prominence. Elevation of the shoulder. Patient knees were marked by outward

bowing. It could be seen also that the lower legs (around the ankles) are swelled, bluish, black

coloured.

Goniometry:

As the patient is after a heart complication we tried to be in the safe side and didn’t went to

prone position (on the abdomen). And we tried to make it more general to not exhaust the

patient.

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Goniometry of the upper extremity:

The upper extremity overall was quite active in both right and left upper extremity. So, the

range of movement in the upper extremity is physiological, and no disturbance has been found

in the shoulder, elbow wrist joints all of them were in a very good status.

Goniometry of the lower extremity:

As a general examination of the lower extremity, the range of movement in both hip and knee

joint were active and around the physiological range and without any restriction or limitation.

While the ankle joint range of movement was limited and restricted in flexion, extension and

rotation, because of the swelling the patient has.

Anthropometry:

Then, we went for the third examination which is the (anthropometry) is to measure the length

and the circumference in (cm) of the upper extremity and the lower extremity. So

anthropometry is a systemic measurement of the physical properties of the human body, like:

the length of the arm and forearm, and the arm circumference, and the same for the lower

extremity. We performed anthropometry examination while the patient is in lying position to

make it convenient for him and to not to exhaust him as much as we can, and the patient was

fully cooperative so we went through it easily and without difficulties.

Table 8: Anthropometry, Length and Circumference in (cm) of the Upper Extremity.

Left Right

Arm and forearm 52 cm 54 cm

Arm 28 cm 29 cm

Forearm 25 cm 26 cm

Hand 18 cm 18 cm

Arm circumference (Relaxed) 26 cm 24 cm

Arm circumference

(Contracted)

28 cm 27 cm

Elbow joint circumference 24 cm 23 cm

Forearm circumference 23 cm 24 cm

Wrist circumference 17 cm 17 cm

Circuit over the metacarpus 21 cm 19 cm

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Table 9: Anthropometry, Length and Circumference in (cm) of the Lower Extremity.

Left Right

Functional length of the

lower extremity (spina iliaca

anterior superior to lateral

malleolus)

91 cm 85 cm

Anatomical length of the

lower extremity (umbilicus

to medial malleolus)

91 cm 91 cm

Thigh length 38 cm 37 cm

Lower leg length 38 cm 41 cm

Leg length 24 cm 25 cm

Thigh circumference 47 cm 44 cm

Circumference above the

knee

41 cm 40 cm

Knee circumference 40 cm 38 cm

Circuit through tuberositas

tibiae

35 cm 36 cm

Calf circumference 41 cm 40 cm

Circumference over the

ankles

31 cm 30 cm

Circumference over the

insteps

33 cm 33 cm

Circuit over the metatarsus 26 cm 26 cm

Table 10: Perimeter Dimensions of the Abdomen and Chest in (cm).

Abdominal circumference 93 cm

Chest circumference (Inhalation) 96 cm

Chest circumference (Exhalation) 92 cm

Findings of the anthropometry test for upper and lower extremities:

Luckily, we have succeeded to make the anthropometry test in both upper and lower extremities

by using the meter while the patient is in lying position, as well as the perimeter dimensions of

the abdomen and chest during inhalation and exhalation while the patient is in sitting position.

As indicated in the tables above, these are the patient measures that were taken. All of them

were within the physiological range. There was no difference in the length of the upper

extremities, as well as the lower extremities.

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Neurological examinations:

Table 11: Deep Tendon Reflexes and Superficial Reflexes

Left Right

Biceps tendon reflex Positive Positive

Triceps tendon reflex Positive Positive

Stylo-radial reflex Positive Brisk reflex

Patellar tendon reflex Positive Positive

Achilles tendon reflex Positive Brisk reflex Plantar reflex Positive Positive

Abdominal reflex Positive Positive

Table 12: Pathological Reflexes

Babinski sign Negative

Oppenheim sign Negative

Chaddock sign Negative

Cordon sign Negative

Deep tendon reflex examination findings:

Most of the deep tendon reflexes were examined and performed on the patient by the reflex

hammer, and all the answers were physiological and normal, without any abnormalities in the

central or peripheral nervous system.

Pathological reflex examination findings:

The Pathological reflex answers were all negative, so the patient negates any neurological

defect.

Muscle shortening test:

Muscle shortening can be defined as when the muscle at rest doesn’t reach its normal length.

And it’s usually characterised by pain, spasm, stiffness. It is classified as a functional disorder

of the motor system and it is reversible. The shortened muscle limit the range of movement

that lead to muscle overloading and imbalance and to some other deformities such as, tightness,

weakness, and it can be effected by the time the body static and the locomotive programs.

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It is divided into 3 degrees:

0 – No shortening.

1 – Small shortening.

2 – Large shortening.

X – Not measured.

Table 13: Muscle Shortening Test

Muscle/muscle group Left Right

Sternocleidomastoid X X

Levator scapulae X X

Trapezius (upper part) X X

Quadratus lumborum X X

Piriformis 0 0

Hip adductors 0 0

Hip flexors X X

Hamstring 1 1

Triceps surae 2 2

Findings of the shortening muscle test:

We didn’t succeed to do most of the shortening muscle tests, due to that the patient situation

didn’t allow us to be in some specific positions for performing the test, such as the muscles in

the neck area (sternocleidomastoid, levator scapulae, trapezius) the test of these muscles

require lateral flexion of the neck in a position that the patient cannot be in, because of the

central venous catheter that it inserted in the patient neck for medicaments administration. As

well as quadratus lumborum couldn’t be performed due to that the patient situation didn’t allow

him to be in a prone position nor in a lateral position (second testing method), would be

inconvenient for him.

Luckily, we’ve succeeded to perform some of the lower extremity muscles such as

piriformis, hip adductors, hamstrings, triceps surae, and I didn’t manage to perform the test for

hip flexors as it was difficult for the patient to be in a position that the test requires. And the

rating is on the table above, some shortening been found.

General movement stereotype:

The test was fully performed by the patient actively, by instructing the patient to do what I’m

doing. The patient did the test while he was in a sitting position. We were focused on the

sequencing and activation of all the synergists involved in the movement. And luckily no

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abnormal movement have been found or observed. All the movements were normal and around

the physiological range. As I mentioned above, we managed to do some of the movements

which can be done in a sitting position as the patient situation required.

Gait Examination:

Gait examination was carried out in the corridor by using the observation method. When

walking, the patient employed compensating aids. The patient was able to walk independently

with no dizziness, but not in a straight line, instead diverging to the right (for his safety I walked

next to him). Furthermore, findings were observed: the right and left lower extremities were

found to be in external rotation. His feet drag on the floor during walking phases, and he misses

the heel strike. The patient was able to walk on both his left and right legs' heels and toes. There

was no trunk rotation found, and the trunk was rigidly held during walking. After halfway down

the corridor, the patient had already experienced muscle weakness and pain in his lower leg, as

well as fatigue.

Spinal development test:

Finally, the last examination in my list. The spinal development test, schober test, thomayer’s

test, side bending test, OTTA’S test. Unluckily, due to the patient condition we didn’t succeed

to do any of them, as all of these tests required fully bending forward.

2.5.4 Short-term Plan

It was planned that the authors 10-12 sessions rehabilitation maximum and it was supposed to

be that we can make it maximally in 4 weeks, but unfortunately our plan didn’t went as we

planned it. Through all the examinations that I’ve went through with my patient Mr. L.P. I

realized that the patient had a few issues that we might need to focus and work on, in order to

see a little improvement after I finish with him the period of short-term plan rehabilitation.

And also to recommend the patient to focus on them when he begins with the long rehabilitation

plan.

The rehabilitation presented by the author was carried out in accordance with the

recommendations of my supervisor Michal Úlehla, as well as a personally created short

rehabilitation plan (exercise unit).

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Based on the examinations findings, I have set the following short-term goals:

1. To improve the overall motion and strength.

2. To improve the range of movement in the ankle joint and relieve the swelling.

3. As he’s using the walker, we needed to focus on some gait training to stabilize the patient

while he’s walking.

4. Improving the postural balance of the patient.

5. Increasing the lung capacity by doing some breathing exercises.

6. Improve the blood circulation by cardiovascular exercises.

7. Patient education as part of self-treatment with simple exercises.

And as I released from the first session my patient is active and didn’t need any assistance in

all activities but only in some of them, during walking for instance he needed some support.

The following exercises were used on my patient Mr. L.P.:

1. Cardiovascular exercises (circulatory) of the lower extremity, in lying, sitting and few in

standing position. Vascular gymnastics to prevent atherosclerotic plaques, thromboembolism

and Edema, to improve the cardiovascular system.

2. Cardiovascular exercises (circulatory) of the upper extremity.

3. Breathing gymnastics to improve ventilation.

4. Exercising using some adds like overball, theraband, balance disc.

5. Isometric and post-isometric exercises.

6. Exercising on bar in the corridor

7. Mobilization of the knee joint, balling for the swelling around the ankle joint, by using the

small spongy ball.

8. Gait training exercise. Training of mobility, and training walking by the walker. Exercises

to improve stability and reduce fear of unassisted walking (without the walker).

9. Passive and active exercise (with or without resistance).

10. Spinal stabilization training and posture improvement.

11. Flexibility exercises include stretching.

The main outcomes expected from my short motor plan were:

1. Better balance, range of motion and better movement in the joints.

2. Lower the blood pressure, lower the heart rate and better breathing. Improved circulation

and the way the body uses oxygen.

3. Better posture, better flexibility.

4. To be more active without getting tires or short of breath easily.

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5. More toned and stronger muscles.

6. Reduced stress, anxiety and depression.

7. Improved self-esteem of the patient.

8. Reduced the edema and the swelling around the ankle joint.

9. To be able to start walking without using the walker.

2.5.5 Rehabilitation Process

Mr. L.P used to have the stomia in the right hypogastric area, as well as the central venous

catheter which was placed on his neck, throughout the entire rehabilitation process. The first

visit took place in the afternoon, and after that we realized that it’s better to change our session

time to be before the noon around 11:00, as it was more convenient for the patient, due to that

he used to feel unwell somehow, after the lunch.

Session 1 – 26th of October:

In the afternoon of the 26th of October, the first session took place. In the Department of Internal

Cardio-angiology, University Hospital at St. Anna in Brno. Once I arrived there, me and my

supervisor discussed for about 15 minutes about my patient diagnosis in more details, and then

we moved together to the patient room. I introduced myself by the assistance of my supervisor,

and after the introduction, I explained to him why I have been assigned to him.

And what we are going to be doing in the upcoming days. Then I asked for his approval, to

make sure that I could go ahead and start taking the data. He gave us the oral consent that he

will be able to only share us he’s medical history and no more for that day.

We made it till the end and it took us almost 45 minutes. After I took the anamnesis/medical

history of the patient in the conversation/oral form under the supervision and the assistance of

my supervisor we made a deal with the patient that we will come the next day to start with the

kinesiological examinations.

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Session 2 – 27th of October:

Before the noon around 11:00 o’clock of the 27th of October, the second session took place.

The aim of this session was to conduct all the kinesiological examination, at the very beginning

before I start working with the patient, I asked him if he suffers from some troubles, if there

are any palpitations (quick beating of the heart), if he has any pain nor fatigue, these are the

subjective signs. And then we have also the objective signs such as the oxygenation of the

blood, heart rate and blood pressure. Also the exercise shouldn’t lead to extreme raise of the

blood pressure and heart rate too. The maximum of the heart rate during exercise shouldn’t go

over 120 bpm, also the blood pressure, the systolic BP shouldn’t raise more than 20 mmHg,

and the diastolic not more than 10 mmHg, and also the systolic blood pressure should not

decrease about 10-15 mmHg. The oxygenation of the blood should be at least 90 % that’s the

minimum. And also some limitations that depend on the patient physic.

Specially with the heart patients the deep bend over is contraindicated, and that’s the

reason why we weren’t able to perform the spinal development tests. The patient was

cooperative and continued actively until the end of the session, and while we’re conducting the

examination from time to time I kept asking the patient if everything is alright and if he became

exhausted or not. I conducted all the kinesiological examinations needed successfully without

any difficulties, in supine position such as anthropometry and some of the goniometry, in sitting

position we were able to conduct the neurological examination and the general movement

stereotype, in standing position we made the inspection by observing the patient in 3 views

(posterior, lateral, anterior).

The session has ended with a little walk in the corridor for about 5 minutes long with a

support of the walker, and that was for observing the way the patient walks (gait examination).

All the values and the measurements have been written down accurately.

This session was a bit exhausting for me and for the patient as well, but we ended having all

the remarks, values and the measurements that examinations required. The entire process took

us about one and half hour with a few breaks in between.

Session 3 – 28th of October:

The 3rd session took place around the noon of the 28th of October. As we’ve conducted the

medical history as well as the kinesiological examinations, we’ve started with the exercise unit.

At the very beginning I asked my patient how he’s feeling today, and if he’s willing physically

to exercise with me, after he gave me his consent. I continued with taking the oxygenation of

the blood by using pulse oximetry placed on the patient index it was around the physiological

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range 97 %, and then I placed the tonometer cuff on the patient arm in order to measure the

blood pressure as well as the heart rate before we start exercising, the patient had a low blood

pressure which was about 76/48 mmHg, and the heart rate was around the normal range 88

bpm. After we took all these values we started exercising. I planned to start with the patient

slowly and gradually increase the difficulty and the set of the exercises day by day more

exercises were added to the list. As the first day we began with the warm-up, cardiovascular

exercises for the lower extremity in lying (supine) position such as flex and extend the toes and

then I applied a small resistance, and flex and extend the ankle, rotation of the ankle, elevation

of the leg and return it back to the bed, flex the knee and extend it, move the leg to the side and

return it back, elevate the pelvis, bicycle, etc. The aim of the conditional training of vascular

gymnastics is to improve the blood flow. And then next we moved to the upper extremity, we

made cardiovascular exercises such as open and close the hand, rotate the wrist, flex and extend

the elbow. Hand to the shoulder and back to the bed, rotate or shrug the shoulder, bring the arm

to the side and return it back, internal and external rotation of the shoulder, put the right hand

on the left elbow and the left hand on the right elbow and bring it up above the head and down,

push by both hand (palms) into the bed hold and release, etc...

Then we moved to sitting position, we made some exercises of the lower extremity, like

extend and flex the leg while sitting, step on your toes and on your heel. Next, we tried some

breathing exercises, I instructed the patient to breath in deeply through the nose and count 1,2,3

and then breath out by the mouth and count 1,2,3,4,5,6. Abdominal breathing (breath in to the

abdomen from the nose while my hand are on patient belly and when he breaths out through

the mouth I put a little pressure on his belly), diaphragmatic breathing. Breathing exercises has

a positive impact on blood pressure, lung capacity and muscle tension, and as the patient breath

the cardiovascular system works to transport and circulate oxygen to every cell in his body.

Then, we tried to stand from the bed while I’m standing next to the patient and holding him as

a support and corrected his stand position, we exercised in standing position, like make a step

forward and a step backwards, etc.., then while the patient is standing, we made Romberg

examination, there was an imbalance. Next, I went to bring the walker, we walked in the

corridor for about 5 minutes, and we went back to the patient room. Lastly, I measured the

oxygenation of the blood, blood pressure and heart rate, with values of Blood O2: 100 %. Blood

pressure: 90/60 mmHg. Heart rate: 101bpm. That was all for this day, we tried to make it that

every day I prepare about 15-20 minutes exercise unit for the patient, and every new day some

new exercises were added. The whole process took us about 45 minutes.

Summary of the exercise unit (28th of October):

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Cardiovascular exercises for the lower extremity in supine position:

1. Flex and extend the toes (5x)

2. Flex and extend the ankles (5x)

3. Rotate the ankles (5x)

4. Elevate the leg and back (5x)

5. Flex the knee and back (5x)

6. Move the leg to the side (5x)

7. Elevate the pelvis (5x)

8. Bring the knee to the chest (3x)

9. Role the knee to the side (5x)

10. Bicycle (5x)

11. Hip rotation (5x)

Cardiovascular exercises for the upper extremity in supine position:

1. Close and open the hands (5x)

2. The hands to front and back (5x)

3. Rotate the wrist (5x)

4. Flex and extend the elbow (5x)

5. Elevate both arms up above the head breath in and bring it back breath out (5x)

6. Bring both hands to the shoulders and return it back to the bed (5x)

7. Put the right hand on the left elbow and the left hand on the right elbow and bring it up above

the head and down.

8. Rotate or shrug the shoulder (5x)

9. Boxing.

10. Stick both palms together and elevate up above the head then bring it back, do the same but

to the right and left side (5x)

11. Bring the arm to the side of the bed and back (5x)

12. Shoulder external rotation (5x)

13. Elevate both arms towards the sealing and elevate the shoulder away from the bed (5x)

Exercises in sitting position:

1. Exercises to strengthen the leg muscles.

2. Flexion and extension of the ankle (5x)

3. Step on the toes and then on the heels (5x)

4. Elevate one knee and then then the other towards the sealing (5x)

Breathing gymnastics in sitting position:

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1. Breath in deeply from the nose and count 1,2,3 and then breath out from the mouth and count

1,2,3,4,5,6. (5x)

2. Elevate your both arms up towards the sealing and breath in from the nose and then return

both arms back and breath out through the mouth. (5x)

3. Abdominal breathing (breath in into the abdomen from the nose while my hand are on patient

belly and when he breath out through the mouth I put a little pressure on his belly)

4. Diaphragmatic breathing. (5X)

Exercises in standing position:

1. Make a step forward and step backwards. (5x)

2. Elevate one knee and then the other towards the sealing as if you’re running bot slowly. (5x)

3. Bring one leg to the side and then the other. (5x)

Passive and active movements of the ankle joint for the swelling and the edema, as well as

balling technique.

Walking for 5 minutes in the corridor with the walker.

Session 4 – 29th of October:

The 2nd day of exercising took place in the afternoon, as my supervisor has told me that the

patient has been taken to some imaging method examination. I firstly measured the blood

oxygenation which was about 93 % before the exercise. The blood pressure was 78/65 mmHg

(low). The heart rate was 98 bpm. Every day we followed the same exercise unit which I have

in my plan and each day I added some new exercises as well as an exercise adds, and I increased

the set form 5x to 6x.

We started with the vascular gymnastics for the upper and lower extremities in supine position

and in sitting position.

As a second we moved to the isometric exercises, like squeeze the thigh (quadriceps

femoris), squeeze the glutes, push both knees against the bed, push both hands (palms) against

the bed, pushing both heels against the bed then relax, partially flex both knees and put both

hand on the abductors and push into abduction while putting resistance, do the same but into

adduction. As a third, isometric exercise for the upper extremity. Then, breathing gymnastics.

Next, we moved to an exercises with the overball in the lower extremity in supine position,

like, squeeze it and release between the knees, put it between the knees and extend one leg and

the other leg, squeeze it and release under the knees, put it under the heel and go forward and

117

backwards, hold the ball with both hands and pass it under the knee while the knee is flexed,

Then we moved with the overball to the upper extremity, hold the ball between the palms and

squeeze it and relieve, hold the ball and go to the front and back to the chest, and to the left and

right sides, hold the ball with both hands and put it above the head and raise up towards the

sealing and back down. Every exercise has 6 sets.

Passive and active movements of the ankle joint for the swelling and the edema, as well as

balling technique.

The session has ended with a small walk with a walker in the corridor for about 5 minutes. And

then after we returned back to the patient room I again measure the Blood O2: 96 %. Blood

pressure: 115/84. Heart rate: 109 bpm. The whole process took us about 45 minutes.

Session 5 – 1st of November:

The 5th session was the 3rd day of exercising, today Mr. L.P was more attentive and cooperative

throughout the entire session. The edema located around the ankles looked much better than

the previous days. The range of movement in the ankle joints increased and improved.

As always, it’s very important to start with taking the values of the blood oxygenation

which was about 92 %. The blood pressure: 98/73 mmHg. The heart rate: 86 bpm. After that,

we started training with the same exercise unit of the previous day, and I added more exercises

using an exercise adds at the end, so we started with the vascular gymnastics in supine, sitting

and standing position, then some isometric exercises for both upper and lower extremity were

performed, and after that we made some breathing exercises, then we moved to the exercising

unit using the overball. For today we added a new exercise adds which was the TheraBand, in

supine position patient secure the TheraBand around his hand and extend his elbow in a neutral

position and me as a therapist stood at the foot of the patient while holding the other side of the

TheraBand, and asked the patient to flex his shoulder with elbow extended for about (8x), next

the patient abduct his arm out to the side with forearm supinated (8x), then the patient placed

his arm extended and supinated on the bed and flex and extend his elbow (8x), then me as a

therapist I stood next to the patient head and the client and the patient flexes his shoulder to 90

degree, pulls down in extension (8x), the patient secure the TheraBand by both hands and

stretch it away from the body center and back (8x), etc..

Then, we practiced again active and passive movement in the ankle joint and I

performed balling technique. After that we went for gait training with an assistance using

walking aid (walker), before we began to walk I’ve adjusted the patient posture to be in an

upright position, with head and spine positioned correctly, we could walk today for about 8

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minutes long, without getting tired. Finally, the session has ended by measuring again the blood

O2: 109 %. The blood pressure: 117/79 mmHg. Hear rate: 120 bpm. The whole process took

about 45 minutes.

Session 6 – 2nd of November:

The 6th session was the 4rth day of exercising, the patient was fully cooperative and energetic,

but unluckily, my supervisor has got the information that they will take the patient for some

imaging method examination in 30 minutes, and for that reason the session lasted for

25 minutes only. As usual I firstly took the values of the blood oxygenation: 92 % measured

by oximetry. Blood pressure: 106/78 mmHg. Heart rate: 72 bpm measure by tonometer.

The exercise unit began with vascular gymnastic of the upper and lower extremity.

After that we made some breathing exercises in supine position, on that day we didn’t use any

exercising adds. Then the breathing exercises were followed by an active and passive exercises

for the ankles and then I performed balling technique for the edema around the ankles. Then I

asked Mr. L.P to move into sitting position and instructed him for some isometric exercises of

the upper extremity.

Then I asked the patient if he’s willing to have a small walk and he agreed, with the

walking aid we walked for about 9 minutes long and also we tried to climb the stairs, and the

patient was able to climb about 4 stairs up and down with assistance and support of me and my

supervisor as well, and while we’re on the way back to the patient room, we made some

exercises on the bar for about 4 minutes, I was instructing the patient, to face the bar and step

on your toes and back on your heel. Face the bar and elevate your leg to the side and with the

2nd leg as well. Keep the bar on your left or right side hold it and walk like a ballerina. Face the

bar and make a circle with your feet to the side.

We ended the session with taking the values of the blood O2: 102 %. Blood pressure:

118/82 mmHg. Heart rate: 127 bpm.

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Session 7 – 3rd of November:

The 7th session was the 5th day of exercising, the patient showed a great improvement

physically, and the edema around his ankles was getting better and better day by day. At the

beginning of the session, I took the measurements of blood oxygenation by oximetry placed on

patient index and it was about 94%. Blood pressure: 116/78 mmHg. Heart rate: 99 bpm, were

measured by tonometer.

Then we’ve started training in spine position, sitting and standing position vascular gymnastics

for the upper and lower extremities, for about 8 minutes long.

Next, we exercised using the overball for upper and lower extremities, for 6 minutes of time.

After that, for 3 minutes long we trained some isometric exercises. Then we worked on the

ankles we made some active and passive exercises for the edema and swelling around the

ankles and then I performed balling technique using the soft ball.

Next, we’ve added a new exercising adds, the (balance disc) for today’s exercise unit,

which has the aim of promoting the postural balance. I explained to the patient what is this

equipment for and how it will be used, and I asked him if he’s willing to move with us outside

in the corridor to exercise in front of the bar, he agreed. The exercise last for about 5 minutes

of time and then we went back to the room. As a final exercise unit for today we made some

breathing gymnastics as a form of relaxation. And as usual, the session has ended with taking

the measurements of the Blood O2: 107 %. Blood pressure: 123/83 mmHg. Heart rate:

135 bpm. The whole process took about 45 minutes long.

2.5.6 Kinesiological Examination at Discharge

The patient was transferred to cardio-surgery clinic for the heart transplantation. Before, we

conducted a brief kinesiological examination. The overall patient’s kinesiological examination

since the onset of our rehabilitation process haven’t improved, there were changes in patient’s

swelling (edema) around his ankles. There were not found any specific improvement in the

physical condition of the patient. Later the patient was transplanted with the heart of the donor.

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2.5.7 Long-term Plan

The patient condition hasn’t progressed much at that time, although his condition changed

continuously day by day during my therapy, these were rather slight deviations which are

minimal in comparison with his general health condition.

As he wasn’t fully independent when he left to the cardio-surgery clinic, there were still evident

symptoms remained, edema around his both ankles which aimed to achieve full recovery, or at

least a remarkable improvement, this includes an increase in the function and motion of the

legs.

Unfortunately, the time with the patient was short due to his deteriorating health

condition, we had to end the therapy, and urgently he went for the heart transplant.

So, medical rehabilitation now and specially after he will get transplanted plays a key role in

treating the patient. Its main goal is to maintain the functional state of the patient and thus lead

the patient to the maximum possible self-sufficiency.

A long-term rehabilitation plan should always adapt to his current physical and mental

condition.

Mr.L.P. after he got transplanted will continue his rehabilitation in outpatient care.

In a long-term rehabilitation plan, it is recommended that the patient continue regular training,

which may include exercises performed in hospital rehabilitation.

It is appropriate to gradually increase the intensity, density and length of this exercise according

to the current condition of the patient.

The exercise unit should be complex and consist of a warm-up phase, when it is appropriate to

include warming up in bed or walking, a relaxation phase, when we can use elements of

respiratory physiotherapy or stretching.

Gradually, it is appropriate to include the endurance phase, for example, with training walking

on stairs or riding a bicycle ergometer, and a strengthening phase, where we use dumbbells,

overballs or therabands. Interval training is also suitable, during which the phases of exercise

and relaxation alternate between exhalation.

To improve the patient's condition and health, I also recommend regular walking, including the

possibility of using Nordic walking sticks or swimming. Furthermore, we direct the patient to

inappropriate physical activities, such as excessive strength exercises with breath-holding, and

teach him to recognize symptoms resulting from excessive physical activity.

The patient should be actively involved in doing normal daily and leisure-time activities, such

121

as cooking or gardening. We constantly motivate the patient to adopt the right lifestyle, reduce

risk factors, and try to create a positive relationship with his regular physical activity.

A prerequisite for successful rehabilitation is the active participation of the patient.

Within one year after the heart transplant, the patient also has the opportunity to undergo

treatment at the spa. It combines not only physiotherapy procedures, group or individual

therapeutic physical education, advice on a healthy lifestyle, but also has an undeniably positive

effect on the mental state of patients. In the Czech Republic, for example, Teplice nad Bečvou,

Poděbrady, Konstantinovy Lázně, Františkovy Lázně, Libverda or Hodonín Spa focus on

treating patients with cardiovascular diseases. Possible collaboration with an occupational

therapist, social worker, or psychologist is also important.

The aim of the long-term hospital rehabilitation program up to heart transplantation is to

prevent deconditioning of the patient, maintain the highest possible muscle strength and overall

performance, range in the joints, prevention of inflammatory, thromboembolic, respiratory and

other complications and preparation of the patient for return to normal daily activities and

employment.

After transplantation, the patient should be acquainted with the possibilities of

posthospital rehabilitation, i.e. with an outpatient controlled program, spa treatment, individual

home training, risk factors and primary, secondary and tertiary prevention. The aim of this

post-hospital rehabilitation is to increase the patient's physical fitness and performance, adjust

the lifestyle, integrate the patient into a full active life and improve the overall quality of life.

In most patients, it is recommended to start outpatient rehabilitation immediately after

discharge from the hospital, no later than 3 weeks. In patients after extensive procedures, it is

recommended to wait with certain activities for 6 weeks, which is the time required for the

bone to heal and to prevent unstable sternum due to early overload. After a sternotomy, it is

important to wear a chest strap (most often an elastic rib) because it allows the sternum to be

immobilized and thus facilitates the healing process.

Aerobic muscle training is generally considered to be the most suitable method of muscle strain

for patients with cardiac disease, with medium-intensity physical activity (40-60 % of

maximum O2 consumption) being the most effective. The recommended safe intensity is below

the anaerobic threshold or 60 % VO2SL and 70 % SFSL.

Unsuitable activities in the first 2 months after surgery are lifting weights over 3 kg, sharp

changes in position, holding your breath, manual housework, long-term work with your hands

over your head, extreme endurance performance exceeding the anaerobic threshold, activities

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causing stress or with a possible risk of shocks on the chest and also some sports (tennis,

squash, strengthening, rebound and contact sports).

Therefore, it is important to find an appropriate aerobic physical activity to keep the patient

entertained and to run it at least three times a week for 30 minutes. This will make him take

care of himself regularly and not lose interest in the chosen activity.

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3 CONCLUSION

Throughout the entire process of writing this thesis, I have expanded my knowledge across

several aspects of cardiovascular system, including the anatomical and physiological concepts

of the heart as well as a brief pathophysiological overview of heart failure and implementation

of physiotherapy and rehabilitation for patient after the incidence of heart failure. At the end of

general part, the basic diagnostic criteria, methods and treatment procedures in the case of heart

failure were described. In the special part of the thesis, I provided information on the various

stages of cardiovascular rehabilitation, exercise testing in cardiac rehabilitation, as well as the

principles of aerobic endurance training, resistance training and physical therapy procedures.

Issues of social and psychological problems of patient with cardiovascular disease were also

briefly mentioned. The last part of the thesis is the case report of rehabilitation of Mr. L.P.

which took place in the Department of Internal Cardio-angiology, University Hospital at St.

Anna in Brno.

Comprehensive cardiovascular rehabilitation is an indispensable part of the therapy of

both acute and chronic heart failure. Preoperative rehabilitation was implemented on the patient

by me for 5 days long, and there was a minimal gradual improvement of the patient’s physical

condition. I would have liked to continue with my patient for a longer period of time to see a

significant improvement, but the patient’s condition was critical, and he was transferred to

cardio-surgery clinic for the heart transplantation. The patient had a significant deconditioning

and reduced functional capacity of cardiovascular system he was confined to bed for long

period of time and the doctor allowed only a minimal load during exercise.

During his stay complications arose that put the patient first on the waiting list for a

heart transplant. Therefore, after finding suitable donor, the transplant was performed without

delay. During my visits and day-to-day of exercising I can say that the patient himself was

satisfied and pleased with the rehabilitation procedure, he assessed cardiovascular

rehabilitation positively. It improved his physical and mental health performance, increase self-

sufficiency and independence, and thus makes it easier for him to return to a normal life. It is

crucial for the prevention of further disease progression or the prevention of other

comorbidities. Heart failure is a serious disease that not only significantly reduces a patient's

life expectancy but also greatly reduces his quality of life. For these reasons, I believe that more

programs to prevent this disease should be established, including improving and adhering to

the principles of a healthy lifestyle, which is closely related to the proper functioning of the

124

cardiovascular system. I also believe it is essential to improve education of patient, which will

allow for earlier recognition of disease symptoms and diagnosis.

I hope that the heart transplant operation went successfully and without any

complications, to continue with the postoperative comprehensive cardiovascular rehabilitation

which is absolutely an indispensable part of the therapy of both acute and chronic heart failure

and plays a crucial role in the improvement of patient’s physical and mental state.

Eventually, I am grateful to have completed the second half of my thesis. This entire

experience exposed me to a clinical environment and prepared me for my future practice, and

career.

125

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