Slide 1 Integrating The Cardiopulmonary System Into Physical ...

Integrating The

Cardiopulmonary System Into

Physical Therapy Practice

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Slide 2

Integrating The

Cardiopulmonary System Into

Physical Therapy Practice

Jamie Dyson

Kathy Swanick

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Slide 3

Objectives

At the conclusion of this continuing education course the participant

shall be able to:

• Describe cardiopulmonary anatomy

• Discuss cardiopulmonary pathophysiology

• Demonstrate chest physical therapy techniques

• Discuss results of pulmonary function tests

• Demonstrate appropriate manual and mechanical airway clearance

techniques

• Discuss modes of mechanical ventilation and invasive monitoring

• Perform Basic interpretation of EKG

• Discuss phases of cardiac rehab and energy conservation

• Discuss role in a medical emergency.

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Introduction-

Why

Cardiopulmonary

Physical Therapy?

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LIFE=

VENTILATION +

PERFUSION

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Vital Signs

• Heart Rate

• Pulse Oximetry

• NBP/ ABP

• MAP

• Temperature

• End Tidal CO2

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Vital Signs

Heart Rate

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Pulse Palpation

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Pulse Oximetry

An infrared light is used to measure

the percentage of hemoglobin

converted to oxyhemoglobin

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NBP/ ABP

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MAP

Mean Arterial Pressure

Its all about perfusion

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Slide 12

Temperature

Normal Oral

Temperature 98.6

degrees F or 37.0

degrees Celsius

Rectal or Core

temperatures will be

slightly higher.

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End Tidal CO2

The level of carbon dioxide in

the air exhaled from the body,

the normal values of which are

4% to 6%; that is equivalent to

35 to 45 mm Hg

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Slide 14

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Slide 15

The Human Movement System

Our Vision-

Transforming society by optimizing

movement to improve the human

experience

IDENTITY

FOUNDATION

The Core Of Physical Therapist Practice,

Education, And Research

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The human movement system comprises the

anatomic structures and physiologic functions that interact to move the body

or its component parts.

American Physical Therapy Association (2015).

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Slide 17

PRACTICE AND THE HUMAN MOVEMENT SYSTEM

Human movement is a complex behavior within a

specific context.

Provide a unique perspective on purposeful, precise, and efficient movement across

the lifespan based upon the synthesis of their distinctive knowledge of the movement

system and expertise in mobility and locomotion.

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Slide 18

PHYSICAL THERAPIST PRACTICE AND THE HUMAN MOVEMENT SYSTEM

Physical therapists examine and evaluate the movement system (including diagnosis and prognosis)to provide a customized and integrated plan of care to achieve the individual’s goal-directed

outcomes.

American Physical Therapy Association (2015).

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PRACTICE AND THE HUMAN MOVEMENT SYSTEM

Maximize an individual’s ability to engage with

and respond to his or her environment using movement-related

interventions to optimize functional capacity and

performance.American Physical Therapy Association (2015).

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Slide 21

http://www.wilkes.med.ucla.edu/inex.htm

Auscultation

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Auscultation

Breath Sounds

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Slide 23

AuscultationContinuous Breath Sounds

Wheezes- a high-pitched whistling sound

made on exhaling.

Rhonchi- a rattling or rumbling sound, kind

of like a garden hose when the water has

just been turned on

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Slide 24

Auscultation

Discontinuous Breath Sounds

Crackles- (Rales)– a crackling sound, like when paper is crinkled

Pleural Rubs- a soft brushing sound, like when sandpaper goes on wood.

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Review of

Pulmonary Anatomy

and Breathing

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Slide 27

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Surface Anatomy

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Slide 32

Oxygen entering an alveolus

dissolves in the film of water

on its wall

Oxygen is in higher

concentration inside the

alveolus than in the blood.

Oxygen moves from a higher

concentration to a lower

concentration by the process

of diffusion.

Carbon dioxide is higher in the

blood than in the alveoli.

Carbon dioxide also moves

from a high concentration to a

lower concentration by the

process of diffusion.

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Slide 33

The (VRG) and the (DRG) within the medullary rhythmicity

area cooperate to establish the pattern for spontaneous

ventilation and basal rate of ventilation which may be adjusted

by impulses from related respiratory control centers in the

pons

The (VRG) has both inspiratory and expiratory neurons;

• The autorythmic inspiratory neurons stimulate the

diaphragm and external intercostals (2 seconds) to cause

inspirations

• Antagonistic expiratory neurons fire ( 3 seconds) to permit

expiration

The (DRG) neurons are involved in altering the pattern for

ventilation in response to the physiological needs of the body

Control of Breathing

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Slide 35

Primary Muscles of Inhalation

Muscle Action Nerve Spine

DiaphragmElongates

the pleuraPhrenic C3,4,5

External

Intercostals

(11)

Elevates the

ribsIntercostal T1-11

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Slide 38

Accessory Muscles of Respiration

Muscle Action Nerve Spine

Sternocleidom

astoidElevates the sternum Accessory C2

Scalenes Elevate 1st 2 ribs Cervical Nerves C3-8

Serratus

AnteriorElevates 1st 8 ribs Long thoracic nerve C5-7

Pectoralis

Major

Increases thoracic

diameter

Lateral and medial

pectoral nervesC5-T1

Pectoralis

minorElevates ribs 3-5 Medial Pectoral nerve C8-T1

TrapeziusStabilizes the

scapula Accessory nerve C3-4

Erector Spinae Extends the trunkPosterior branch

spinal nervesAll

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Primary Muscles of Exhalation

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Slide 47

Forced ExhalationMuscle Action Nerve Spine

Rectus

Abdominis

Increase

intrathoracic

pressure

Thoraco-abdominal

nerveT7-12

Obliquus

Externus

Abdominis

Increase

intrathoracic

pressure

thoraco-abdominal

nervesT7-12

Obliquus

Internus

Abdominis

Increase

intrathoracic

pressure

thoracico-abdominal

nervesT6-L1

Transverse

Abdominis

Increase

intrathoracic

pressure

thoraco-abdominal

nerveT9-T12

Internal

Intercostals

Depresses

ribsIntercostal Nerve T1-T11

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Slide 48

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Pathophysiology Of

The Pulmonary System

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Slide 50

Atelectasis

Atelectasis is defined as a state in which the

lung, in whole or in part, is collapsed or without

air.

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Slide 51

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Atelectasis

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Slide 53

Atelectasis

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Slide 54

Obstructive Lung Disease

Decrease exhalatory airflow

Restrictive Lung Disease

Decreased inspiratory capacity

Pulmonary Disease

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Chronic Obstructive Pulmonary Disease (COPD)

Chronic Obstructive Lung Disease (COLD)

Chronic Obstructive Airway Disease (COAD)

Chronic Airway Obstruction (COA)

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Slide 56


Emphysema- permanent enlargement of air-spaces distal to the terminal bronchiole with destruction of their walls.

Leading cause is SMOKING

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Slide 57

Emphysema

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EmphysemaTwo Types

Centriloblular Emphysema

Panlobular Emphysema

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Slide 59

EmphysemaCentriloblular Emphysema

Inflammation, edema, thickened bronchiolar walls

Destruction of the bronchioles

Common in upper lobes and superior

segments of the lower lobes

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Slide 60

EmphysemaPanlobular Emphysema

Rare

Destructive enlargement of the alveoli

Alpha 1 antitripsen deficiency

Loss of recoil in the alveoli

Primarily lower lobes

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Develop Bullea- enlarged alveoli caused by decreased ability to exhale caused by increased lung compliance = decreased elastic recoil

Emphysema

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Slide 62

EmphysemaClinical Presentation

Dyspnea- with exertion

Accessory muscle

breathing

Pursed Lip breathing

Forward Posture

Barreled Chest

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Slide 63


Pink Puffers

Increased Respiratory Work

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Pink Puffer

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Slide 65


Reduced breath sounds in all lung fields

Wheezes

Increased Total Lung Capacity

Increased Residual Volumes

Increased dead Space

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Slide 66


Chest X-ray

Over inflated

Lungs

Flattened

Diaphragm

Elongated

Heart

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TreatmentNon PT

Iv Fluids

Antibiotics

Low Flow O2

Bronchodilators

Corticosteriods

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Slide 68

TreatmentNote

Hypercapnia commonly occurs in severe

Emphysema Oxygen given to patients with

emphysema may reduce their ability to breath,

resulting in hypercapnia. This is why exact

doses of oxygen are usually figured out for

those with emphysema so that they receive

neither too little nor too much oxygen. Note: if a

patient is actively short of breath, never

withhold oxygen from them.

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Slide 69

TreatmentPT

Energy Conservation

Exercise Program to decrease muscle wasting

Treatment of tight accessory muscles

Quit Smoking!!!!!!!!!!!

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Smoking Is The Leading

Cause Of Emphysema

All physical therapy practitioners will

have to discuss cessation of smoking

with their patients.

Lets get the facts

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Slide 71

Quit Now

20 minutes after quitting your heart rate and blood pressure drops

12 hours after quitting carbon monoxide levels in your blood drop to normal2 weeks to 3 months after quitting circulation improves and lung function increases

1 to 9 months after quitting coughing and shortness of breath decrease; cilia regain normal function, increasing the ability to handle mucus.

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Slide 72

1 year after quitting the excess risk of coronary heart disease is half that of a smoker5 years after quitting your stroke risk decreases to that of a nonsmoker 5 to 15 years after quitting.

10 years after quitting the lung cancer death rate is about half that of someone who continues to smoke. Quitting lowers the risk of cancers of the mouth, throat, esophagus, bladder, cervix and pancreas15 years after quitting the risk of coronary heart disease is lowered to that of a nonsmoker.

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Chronic Bronchitis

Chronic swelling and inflammation of the bronchi

and bronchioles

Diagnosis is based on a report of a productive

cough for 3 months during 2 consecutive years.


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Slide 74

Decreased number of cilia

Increased mucus

Bronchiolitis

Bronchiolar narrowing

Chronic Bronchitis

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Slide 75

• Caused by long term irritation of the

tracheobronchial tree

• Most common cause of irritation= smoking

• Cigarette smoke causes inflammation of the

epithelium = increased production of mucus from

goblet cells and mucus glands

• Smoking inhibits ciliary action and destroys cilia

• Can also be caused by allergens and air pollution

Chronic Bronchitis

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Hypersucretion of mucus + impairment of cilia =

chronic productive cough

Increased mucus = Increased risk of respiratory

infection

Chronic Bronchitis

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Slide 77

Chronic Bronchitis

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Slide 78

Blue Bloater

StockyAppear blue

due to

hypoxemia

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Chronic Bronchitis

Blue Bloater

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Slide 80

Chronic BronchitisTreatment

Non PTIv Fluids

Antibiotics

Low Flow O2

Bronchodilators

Corticosteriods

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Slide 81

Chronic Bronchitis

Treatment PT

Energy Conservation

Exercise Program to decrease muscle wasting

Treatment of tight accessory muscles

Quit Smoking!!!!!!!!!!!

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Asthma- chronic condition involving in which the

airways occasionally constrict, become inflamed, and

are lined with excessive amounts of mucus, often in

response to triggers

Triggered by exposure to an environmental stimulant

such as an allergen, environmental tobacco smoke,

cold or warm air, perfume, pet dander, moist air,

exercise or exertion, or emotional stress.


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Slide 83

Bronchial smooth muscle spasm

Inflammation of the mucosa

Overproduction of mucus

Asthma

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Slide 84

Asthma

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Asthma

Affects 5-10% of the US

Prevalent in people under 25- usually allergic

Appox 80% of children with asthma do not

have asthma after 10 years of age

Can have an adult onset- intrinsic asthma

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Slide 86

AsthmaClinical Signs

Tachypnea

Cough

Dyspnea

Wheezing

Chest Tightness

Diminished Breath Sounds

Prolonged Exhalation

Hyperinflated Lungs

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Slide 87

AsthmaTreatment- Non PT

Iv Fluids

Supplemental O2

Bronchodilators

Corticosteriods

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AsthmaTreatment- PT

Stop activities as symptoms arise

Take a good history prior to prescribing an

exercise program

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Slide 89

Bronchiectasis is a disease that causes localized

irreversible dilation of part of the bronchial tree.

Involved bronchi are dilated, inflamed and easily

collapsible resulting in airflow obstruction and

impaired clearance of secretions

Generally associated with a chronic necrotizing infection

within these airways


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Slide 90

Usually localized to a few segments or entire

lobe of one lung.

40-50% of cases are bilateral

Can cause varicese which can cause

hemoptysis

Bronchiectasis

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BronchiectasisCystic Fibrosis

Hereditary disease affecting the exocrine (mucus)

glands of the lungs, liver, pancreas, and intestines,

causing progressive disability due to multisystem

failure. Thick mucus production results in frequent

lung infections

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Slide 92

Cystic Fibrosis

Decreased pancreatic enzymes lead to poor

growth

Many die young in their 20s and 30s

Can be confirmed by high levels of salt found

during a sweat test.

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Slide 93

Cystic Fibrosis

Affects Multiple

Organs

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Bronchiectasis

Treatment

Non PT

Antibiotics

Oxygen

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Slide 95

BronchiectasisTreatment

PT

Chest Physical Therapy- percussion

Segmental breathing

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Slide 96


Environmental factors play a major role in

etiology

Characterized by stiffening of the parenchyma-

prevents lungs from expanding fully

Increased recoil of lung tissue

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Decreased Vital Capacity

Decreased Inspiratory Capacity

Decreased Total Lung Capacity

Decreased lung compliance

Decreased diffusing capacity

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Slide 98

Restrictive Lung DiseasePossible Causes

Pleural Effusion

Kyphoscoliosis

Obesity

Late Term Pregnancy

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Slide 99


Pulmonary Fibrosis

Sarcoidosis

Rheumatoid arthritis

Systemic Lupus Erythematosus

Scleroderma

Tuberculosis

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Restrictive Lung DiseasePulmonary Fibrosis

Causes

Inhaled environmental and occupational pollutants

Smoking!!!!!!!!!

Certain medications

Therapeutic radiation

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Slide 101

Restrictive Lung DiseasePulmonary Fibrosis

The current thinking is that pulmonary

fibrosis begins with repeated injury to the

lining of the alveoli. The damage eventually

leads to scarring (fibrosis), which stiffens

your lungs and makes breathing difficult.

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Slide 102

Pulmonary Fibrosis

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Restrictive Lung DiseaseSarcoidosis

Disorder where one develops small inflammatory nodules and can affect multiple organs.

Affects African Americans> Caucasians.

Women > Men

Most cases can spontaneously regress.

Most common treatment is corticosteroids

Physical therapy interventions involve working on general conditioning and endurance.

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Slide 104

Restrictive Lung DiseaseRheumatoid Arthritis

Pleural disease can be a manifestation of RA

Causes fibrous tissue on outside of lung causing restriction.

In severe cases treated with decortication

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Slide 105

Restrictive Lung DiseaseSystemic Lupus Erthematosus

• Lupus can cause polyserositis around the lung tissue causing pleural effusion.

• Pneumonitis can also develop.• Patients will complain of dyspnea on

exertion pleural pain or discomfort and productive cough

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Restrictive Lung DiseaseScleroderma

• Scleroderma causes thickening and fibrosis of the connective tissue.

• Two thirds of patients can have pulmonary involvement.

• Chest x-ray will show fibrosis of middle and lower lung fields.

• Treatment is corticosteroids.

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Slide 107

Restrictive Lung DiseaseTuberculosis

Tuberculosis (TB) is a common and often

deadly infectious disease caused by

mycobacteria

The typical symptoms of tuberculosis are a

chronic cough with blood-tinged sputum, fever,

night sweats and weight loss.

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Slide 108

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Restrictive Lung DiseaseLung Cancer

Leading cause of death due to cancer

Smoking is leading cause

Can be primary or metastatic

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Slide 110

Other Pathologies

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Slide 111

Pneumonia• Inflammatory illness of the lung

• Alveoli fill with fluid

• Infection can be bacteria, viruses, fungi or parasites.

• Can be caused by chemical or physical injury to the lungs.

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Slide 113

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Slide 114

Ventilator Associated Pneumonia

Refers specifically to nosocomial bacterial

pneumonia that has developed in patients who

are receiving mechanical ventilation. Ventilator-

associated pneumonia that occurs within 48 to

72 hours after tracheal intubation is usually

termed early-onset pneumonia; it often results

from aspiration

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Ventilator Associated Pneumonia

Prevention

Good hand washing

Head of bed 30 degrees at all times.

Control of GERD

Change circuits frequently

Oral hygiene

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Slide 116

Aspiration Pneumonia

Foreign material enters

the bronchial tree

Usually in the right

lower lobe.

Early identification of

dysphagia

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Slide 117

Collapsed lung caused by

air in the pleural space.

Can be caused

spontaneously or by

disease or injury.

Air can come from within

the lung or from

atmosphere.

Pneumothorax

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Slide 119

Blood accumulating in the pleural cavity

Usually caused by trauma

Blood from the serous membrane lining the thorax and covering the lungs.

Hemothorax

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Slide 120

Empyema

A collection of pus in an existing cavity.

Can arise from pneumonia.

Drained with thoracentesis.

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Rib Fractures

Pain with breathing and/or movement.

Suppressed cough secondary to pain.

Grating sound with breathing or movement.

A portion of the chest wall moving separately from the rest of the chest- flail chest.

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Slide 122

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Slide 123

Chest Tube

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Chest Tube

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Slide 125

Obstructive Sleep Apnea

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Slide 126

Obstructive Sleep Apnea

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Pulmonary Function

Testing

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Slide 128

Tidal Volume (TV) The volume of air breathed in and out

without conscious effort

Inspiratory Reserve Volume (IRV) The additional volume of air that can be

inhaled with maximum effort after a

normal inspiration.

Expiratory Reserve Volume (ERV) The additional volume of air that can be

forcibly exhaled after normal exhalation.

Vital Capacity (VC) The total volume of air that can be

exhaled after a maximum inhalation:

VC=TV+IRV+ERV

Residual Volume (RV) The volume of air remaining in the lungs

after maximum exhalation. The lungs are

never completely emptied.

Total Lung Capacity (TLC) Vital Capacity+Residual Volume

Minute Ventilation The volume of air breathed in 1 minute

(TV) * breaths/minute

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Slide 129

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Pulmonary Function TestingHow much air volume can be moved into and out of the lungs?

How fast the air in the lungs can be moved in and out?

How is the compliance of the lungs?

How do the lungs respond to chest physical therapy and medications?

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Slide 131

Pulmonary Function TestingUses

Screening for presence of obstructive or restrictive diseases.

Evaluating a patient prior to surgery.

Evaluate the patient’s condition for weaning from a ventilator.

Documenting the progression of pulmonary disease

Documenting the effectiveness of interventions

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Slide 132

Pulmonary Function Testing

Age- As a person ages the natural elasticity of the lungs

decreases which means smaller and smaller lung volumes as one

age.

Gender- Lung volumes for males are larger than those of

females even if they are matched for height and weight.

Body height and size- A small man will have a smaller

PFT result than a man of the same age who is much larger

Race- Environmental Factors and Altitude may have an affect

on PFT results.

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Pulmonary Function TestingTerminology

• FVC- Forced Vital Capacity

• FEV1- Forced Expiratory Volume in 1 second

• FEV1/FVC- FEV1%- what percent of FVC is expelled in 1st second

• FEV3- Forced Expiratory Volume in 3 seconds

• FEV3/FVC- FEV3%- should be close to 100%

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Slide 134

Pulmonary Function TestingFVC

• Obstructive lung disease- FVC will be decreased due to obstruction and airway collapse during forced exhalation.

• Restrictive lung disease FVC will be smaller due to the lungs being smaller to start with because of the disease.

• Bronchodilators will improve FVC 10-15% with obstructive lung disease.

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Slide 135

Pulmonary Function TestingSVC

Slow vital capacity (SVC) test- Have the patient

slowly and completely blow out all of the air from

their lungs. Eliminates the strong

bronchoconstriction that come with a forced

exhalation. The VC may be larger with a SVC test

leading to an obstructive diagnosis.

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FEV1

• In healthy individuals it is common the exhale 75-80% of vital capacity in first second of FVC test.

• If FEV1 is low compared to predicted values the patient may have an obstructive or restrictive lung disease.

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Slide 137

Pulmonary Function TestingFEV1%

• Both FVC and FEV1 will be low in both obstructive

and resistive lung disease.

• If FEV1% is low (<70%) it is consistent with an

obstructive disease.

• If FEV1% is 85%-100% it is consistent with a

restrictive disease.

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Slide 138


Lets Give It A Try

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Pulmonary Function TestingCase 1

Predicted Values Measured Values % Predicted

FVC 6.00 liters 4.00 liters 67%

FEV1 5.00 liters 2.00 liters 40%

FEV1/FVC 83% 50% 60%

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Slide 140





FEV1/FVC 83% 50% 60%

Obstructed Lung Disease

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Slide 141


Case 2




FEV1/FVC 84% 79% 94%

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Predicted Values Measured

Values

% Predicted



FEV1/FVC 84% 79% 94%

Restricted Lung Disease

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Slide 143





FEV1/FVC 82% 77% 94%

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Slide 144


Predicted

Values

Measured

Values

% Predicted



FEV1/FVC 82% 77% 94%

Normal

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Pulmonary Physical

Therapy Lab

Including Vitals And

Breath Sounds

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Slide 146

Vents and Invasive

Monitors

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Slide 147

Modes of Mechanical Ventilation

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Modes of Mechanical VentilationTerms

Trigger- variable that causes a breath to be delivered- pressure, volume, flow

Flowrate- The speed at which a breath is delivered- liters/min

Frequency- breaths /time- breaths/minute

Spontaneous Breaths- Breathing through vent circuit without assistance

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Slide 149


Controlled Mechanical Ventilation (CMV)

Requires patient to be sedated and chemically

paralyzed. The vent delivers all breaths at a preset

frequency, volume and flow rate.

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Slide 150


Assist Control (AC)

The patient receives a preset volume, flow rate

and frequency. The patient can trigger the

machine to deliver a breath at the preset

parameters. All breaths are machine delivered.

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Assisted Mechanical Ventilation (AMV)

Similar to AC without a set frequency. The

patient triggers the vent to deliver a preset

volume at a set flow rate.

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Slide 152


Intermittent Mandatory Ventilation (IMV)

The vent delivers a set frequency and volume. The patient is allowed to take spontaneous

breaths. The machine may cycle a breath before the patient can exhale a spontaneous breath

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Slide 153


Synchronized Intermittent Mandatory Ventilation (SIMV)

Synchronizes the machine delivered breaths with the patients spontaneous breaths. If no inspiratory effort the

machine delivers a mandatory breath.

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Continuous Positive Airway Pressure (CPAP)

The patient spontaneously breaths and a preset level of pressure is constantly maintained. Can be used with both an artificial airway or with a

tight fitting mask.

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Slide 155


Bilevel Positive Airway Pressure (BIPAP)

Noninvasive form of mechanical ventilation-uses a tight fitting nasal or face

mask. There are different pressures for inhalation and exhalation but both above

atmospheric pressure.

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Slide 156


Airway Pressure Release Ventilation (APRV)

The patient spontaneously breaths with a set amount of CPAP. If additional ventilation is

needed the CPAP can be dropped allowing the patient to exhale. CPAP is restored once

exhalation is complete. Allows more patient control then traditional CPAP.

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Pressure Support Ventilation (PSV)

Patient is allowed to breath spontaneously with a preset inspiratory support until the flow rate reaches a minimal level. Patient controls the rate, TV and inspiratory time.

Can be used in conjunction with SIMV

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Slide 158


Mandatory Minute Ventilation (MMV)

The patient breaths spontaneously but a minimal level of minute ventilation will be achieved with ventilator

support. Usually used with PSV.

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Slide 159


Volume Assured Pressure Support (VAPS)

The patient breaths spontaneously in the PSV mode. The ventilator monitors each tidal volume. If the

patient is not going to achieve the set volume the vent will keep a constant flow rate and increase

pressure until volume is reached

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High Frequency Oscillatory Ventilation (HFOV)

High respiratory rates delivered- up to 900 breaths per minute at a very small tidal volume. Gas is pushed into

the lung during inhalation and pulled out during exhalation. Used in severe cases of pulmonary disease that do not respond to normal mechanical ventilation.

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Slide 161

When Can You Pull This Thing?

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Slide 162

Why are folks intubated?

Airway

Breathing

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Airway Issues

• Mechanical

Obstruction-

surgical or non

surgical

• Edema

• Inability to mobilize

secretions

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Slide 164

Breathing Issues

Obstructive Pulmonary Disease

Restrictive Pulmonary Disease

Respiratory Failure

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Slide 165

CPAP Trial

Intubated patient placed on CPAP of

5mmHg

ABGs drawn

Patient closely monitored.

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Leak Test

• Endotrachial balloon is deflated

• Looking for at least a 50% leak from

tidal volume

• Decreased leak= increased edema

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Slide 167

Before It Can Be Pulled

Wean pressure Support

Wean PEEP

Trach Collar trials

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Slide 168

Arterial Line

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Arterial Line

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Slide 170

Central Venous Pressure2-6 mm Hg

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Slide 171

Pulmonary Artery Catheter-Swan-Ganz

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Pulmonary

Left VentricleRight Ventricle

Systemic

PAP PAOP

CVP ABP

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Slide 173

Intra Cranial Pressure Monitor

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Slide 174

ICP Monitor

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Intra Aortic Balloon Pump

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Slide 176

Dialysis

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Slide 177

Continuous Renal Replacement Therapy

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Pulmonary Case

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Slide 179

History of Present Illness

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Slide 180

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PT Exam

• Pt received supine in bed on vent (desaturated over

night- orally intubated

• Mode SIMV rate of 2, PSV 10, PEEP 5, FiO2 40%,

• HR 98, BP 126/51, and O2 SAT 97%.

• Patient alert, pleasant, able to communicate by head

nodding and writing, and able to follow commands.

• Hemoglobin 8.5

• Trending Down

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Slide 182

Bed Mobility/Transfers

• Roll to Left Mod Assist

• Roll to Right Mod Assist

• Supine to Sit Deferred due to Hb

• Sit to Supine Deferred due to Hb

• Sit to Stand Deferred due to Hb

• Stand to Sit Deferred due to Hb

• Bed to Chair Deferred due to Hb

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Slide 183

Day 2

• Pt was received supine in bed on vent mode SIMV, rate 2, PSV 12, PEEP 10, FiO2 55%

• Hb stable at 8.4

• HR 100, BP 148/63, and O2 SAT 92.

• Pt family was present in room for TherEx.

• Pt transferred from supine to sit EOB Min A-performed deep breathing, diaphragmatic breathing and segmental breathing exercises. bed to chair min assist.

• Pt with BP to 173/70 HR 120- gait deferred at this time

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Slide 185

Day 3

• Oxygen Device: Ventilator

• O2 (%): 75

• Mode: SIMV + PS

• Total breaths/minute: 14

• Set breaths/minute: 14

• Set VT (mL): 700

• PS (cmH2O): 16

• Mean Airway Pressure (cmH2O): 23

• PEEP (cmH20): 18

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Slide 186

Day 3


• O2 (%): 75

• Mode: SIMV + PS



• Set VT (mL): 700

• PS (cmH2O): 16


• PEEP (cmH20): 18

Pt on Propofol

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Slide 188

Day 5


• O2 (%): 100

• Mode: PC/SIMV + PS



• PS (cmH2O): 12


• PEEP (cmH20): 26.

Pt now on Rocuronium

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Slide 189

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• Required placement of bilateral chest tubes

yesterday

• Also started on NO for significant hypoxia

• Responded well and his sats have improved

significantly to mid-high 90s

• Cont PCV and wean peep and FiO2 as tolerated

• Neuro GCS 3, sedated paralyzed

• Resp on 26 PEEP, 70% FiO2

Nitrous Oxide- local vaso-dilation

Day 7

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Slide 191

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Slide 192

• The patient remains intubated .

• He continues to require high levels of PEEP and FiO2

and to have low saturations and continues to be

febrile.

• He was started on cooling blanket to help lower his

temperature.

• He remains sedated and paralyzed.

• Yesterday he developed acute renal failure, hydration

was attempted and nephrology was consulted for

possible HD or CRRT.

Day 10

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• O2 (%): 100

• Mode: PC/SIMV + PS



• PS (cmH2O): 10

• PEEP (cmH20): 32

ABGs:

• Ph 7.15 PCO2 68 mmHg (35-45) PO2 71(80-100) mmHg. HCO3 23.1 22-26 mmol/l

Day 10

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Slide 194

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Slide 195

Day 11

Emergent laparotomy,

application of negative

pressure wound

therapy dressing

(ABThera placement) >

50 cm2

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Day 14

• Pt off paralytics/NO

• Vent- SIMV with PS rate of 8, 12 PS, 10 PEEP

and 60% FiO2

• PT resumed pt OOB to chair with max assist

• Extremity strength grossly 2/5

• Pt to have tracheostomy in am.

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Slide 197

Day 15

• Trached this am- - vent SIMV rate of 2, 12

PS, 10 PEEP 50% FiO2.

• PT- Ther- ex- OOB- chair max assist

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Slide 198

Day 16

• Off propofol

• Vent- SIMV rate of 2, 8 PS, 6 PEEP, 40%

Fio2.

• Trach Collar begun when OOB

• Began deep breathing and segmental

breathing exercises

• Pt to OR in pm for abdominal closure.

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Day 17

• Pt with 3/5 strength

• Tolerating 2 hours on trach collar

• Vent SIMV rate of 2, 6 PS, 5 PEEP, 40%

FiO2

• Gait trained 20 feet with PT

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Slide 200

Day 17

• Pt with 3/5 strength

• Tolerating 2 hours on trach collar

• Vent SIMV rate of 2, 6 PS, 5 PEEP, 40%

FiO2

• Gait trained 20 feet with PT

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Slide 201

• Transfer to Step-Down Unit

• Chest tubes out

• Foley Out

• Increased trach collar times to 24 hours-

• Rehab referral

• Progressing Mobility

• Speaking valve/Eating

Day 18-Day 20

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Day 21

• Trach red capped

• Gait trained 150 feet with rolling walker on

room air with supervision

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Slide 203

Day 22

• Discharge Home with parents and siblings

• Home Health PT/Nursing/RT

• Day 25 Trach Out.

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Slide 204

Airway Clearance Lab

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Review of Cardiac

Anatomy

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Slide 206

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Slide 207

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Slide 209

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Slide 210

Innervation Of The Heart

Intrinsic

• SA node is the pacemaker of the heart-

impulse formation 100 bpm

• SA node under parasympathetic control

which decreases the normal rate to 60-

90 BPM

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Innervation Of The Heart

Extrinsic

• Autonomic Nervous System

• Parasympathetic- Vagus Nerve

• Sympathetic- Upper Thoracic Nerves

• Cardiac plexus located near the tracheal bifurcation

• Supply the SA and AV nodes

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Slide 212

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Slide 213

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Pathophysiology of

the Cardiac System

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Slide 215

Cardiac Pathophysiology

• Coronary Artery Disease

• Congestive Heart Failure

• Valvular Heart Disease

• Athletic Heart Syndrome

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Slide 216

Coronary Artery Disease (CAD)

• Arteries on the walls of the heart are vital to the heart muscle’s survival, providing oxygen and necessary nutrients

• The disease process begins when atherosclerotic plaque begins to build up in the arteries

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Slide 218

Coronary Artery Disease

• Atherosclerosis

• Begins with trauma to the intima of the arterial wall

• Trauma related to list of risk factors

• Media (consists of smooth muscle is exposed to circulation

• Thought to be the origin of lesion.

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Slide 219

Atherosclerosis

• Platelet agitation at lesion site induce smooth muscle and endothelial replication

• Fatty streaks –low density lipoproteins (LDL) develop in smooth muscle of media

• Fibrous Plaque then develop impinging lumen

• Plaque – consists of connective scar like tissue, smooth muscle, and fat.

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Slide 221

CADOvertime, build-up of plaque can lead to arterial

occlusion, which can cause a devastating blockage

which will decrease or cut off oxygen to the myocardium

Major risk factors for CAD:

• Smoking

• High blood pressure

• Diabetes

• > 45 years old (men) > 55 years old (women)

• Family history

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Slide 222

Angina Pectoris

• Chest pain related to myocardial ischemia

• May be referred to left shoulder, neck, jaw, or between scapula.

• Anywhere above umbilicus could be anginalpain

• Three types

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Slide 224

Stable Angina

• Brought on by physical effort or stress

• Usually substernal nonradiating pain

• Last 5 to 15 minutes after stopping stressor

• Subsides completely with treatment

• Sublingual nitrate (nitro)

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Slide 225

Unstable Angina• Brought on by same triggers as stable angina

• Occurs more frequently

• Duration greater than 15 mins

• Intensity of pain more severe

• Indication of progression of CAD

• Increased risk for MI

• Less responsive to treatment can require hospitalization with IV nitrates.

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Variant Angina

• Occurs at rest- during waking hours

• Not influenced by exertion

• Dysrhythmias occur

• Caused by stenosis and coronary artery spasm

• Treated with Ca Channel Blockers

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Slide 227

Myocardial Infarction (MI)

• Necrosis of a portion of the myocardium

• Characterized by location, size and degree of involvement

• Location-anterior, posterior, lateral, inferior

• Size- large, small

• Transmural (full wall), subepicardial, subendocardial.

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Slide 228

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Myocardial Infarction

• Uncomplicated- small infarction, inferior portion of heart partial wall thickness = full recovery

• Complicated MI- one or combination of dysrhythmia, heart failure, thrombosis, damage to heart structure.

• Prognosis is dependent on extent of damage to the ventricles

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Slide 230

Congestive Heart Failure

The inability of the heart to produce adequate cardiac output due to a structural

or functional problem-impairing the ability of the

heart to fill and pump blood adequately

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Slide 231

Risk FactorsCoronary artery disease

• It affects the heart by restricting or blocking the flow of blood

• Strongest risk factor in both men and womenSmoking Hypertension• Preexisting hypertension is present in 75% of heart

failure cases in the United StatesPrevious MIsDiabetes• More in women; associated with a 2-5 fold increase in

heart failureObesityValvular disease

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Other Risk Factors

• Anemia

• Thyroid

• Toxic agents: cocaine, alcohol, nonsteroidal agents

• Albuminuria

• Viruses/Infections

• Allergic reactions

• Blood clots in the lungs

• Dyslipidemia

• Chronic kidney disease

• Sleep-disordered breathing

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Slide 233

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Slide 234

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Valvular Heart Disease

• Congenital or Acquired

• Acquired- bacterial or viral infection of the heart valves

• Common over age of 65

• Some do not require treatment

• Mitral Valve prolapse – common in women vs men

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Slide 236

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Slide 237

Athletic Heart Syndrome

• Cardiovascular adaptation to intense exercise can mimic disease process

• Sudden cardiac death in athletes usually caused by hypertrophy, dysrhythmia or both.

• Can be manifestation of congenital abnormalities in electrical or mechanical function of the heart.

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Percutaneous Transluminal Coronary

Angioplasty (PTCA)

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Slide 239

• Checks for the presence of

heart disease (such as

coronary artery disease,

valve disease or disease of

the aorta)

• Evaluates the heart muscle

function

• Determines the need for

further treatment

(angioplasty, stent or

bypass surgery)

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Slide 240

Cardiac Stents

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Balloon Angioplasty

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Slide 242

Balloon Angioplasty

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Slide 243

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Slide 245

Sternotomy

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Slide 246

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Slide 248

Vein Harvest

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Slide 249

Bioprosthetic – These valves come from animals and in order to avoid rejection, they are specially treated with chemicals.

Mechanical – These are valves made of materials such as metal, carbon or synthetics. To prevent blood clots when these types of valves are used, anticoagulation is required.

Biologic – These are valves taken from the human heart of deceased donors. Once the valves are removed from the donor, they are frozen for use at a later date.

Valve

Replacement

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Heart Transplant

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Slide 251

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Slide 252

Ventricular Assistive Devices

• Bridge to Transplant

• Bridge to Recovery

• Destination Device

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Slide 254

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Slide 255

EKG

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Cardiac Action Potential

• Phase 0- depolarization- Na+ channels open

• Phase 1-prolonged action potential due to slow and extended opening of Ca channels -repolarization begins.

• Phase 2-outward flow of K+ and prolonged opening of Ca lead to a plateau phase

• Phase 3- closure of Ca channels and opening of K channels completes repolarization.

• Phase 4- resting phase Na and Ca are pumper out K is pumped in.

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Slide 257

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Slide 258

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Slide 260

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Slide 261

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EKG

• 12 Lead (view) of the heart

• Six Leads record frontal plane

• Six Leads record transverse plane

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Slide 263

Frontal Plane Leads

• 3 Bipolar limb leads I, II, III

– Single positive and single negative electrode

• 3 augmented unipolar limb leads

– aVR (right arm)

– aVL (left arm)

– aVF (left leg)

Have single positive lead derive negative from a

combination of other electrodes.

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Slide 264

Einthoven’s Triangle

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Bipolar Leads

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Slide 266

Augmented Leads

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Slide 267

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Axis Deviation

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Slide 269

Axis Deviation

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Slide 270

Precordial (transverse plane) Leads

• V 1-6

• V1 and V2 look at R

Ventricle

• V3 and V4 look at the

intraventricular septum

• V5 and V6 look at L

Ventricle

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Slide 272

EKG Evaluation

• What is the rate and pattern (regularity) is R-R

interval equal for each beat?

• Is the a P wave before each QRS? = atrial

• Is the a QRS after every P wave?= conduction

of atria to the ventricles

• P-R interval? Normal= 0.12-0.2 seconds > 0.2

seconds= conduction delay or block

• QRS normal duration (0.1 sec) and shape?

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Slide 273

Calculating Rate

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Calculating Rate

• Count the number of small boxes between

two R waves and divide into 1500.

• Count the number of R waves in a six

second strip and multiply by 10.

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Slide 275

Lets try it

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Slide 276

Sinus Rhythms

• Sinus Rhythm- 60-100 bpm

• Sinus Bradycardia- < 60 bpm

• Sinus Tachycardia- > 100 bpm

• These rhythms have normal P waves, PR

int and QRS int

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Supraventricular Dysrhythmias

• Atrial and junctional Mechanisms

– SVT

– Atrial tachycardia

– Atrial Flutter

– Atrial Fibulation

– Junctional Rhythm

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Slide 278

SVT

• Rate- 150-250- regular rhythm- no visible P waves-PR not measurable- QRS .12 or less

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Slide 279

Atrial Tachycardia

• Rate 150-250- regular- 1 P per QRS- PR

may be shorter, QRS .12 or less

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Atrial Flutter

• Atrial rate 250-450- ventricular varies- Atrial is

regular- ventricular can be irregular- P wave-

saw tooth- PR not measurable- QRS <.12.

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Slide 281

Atrial Fibrillation• Rate can vary- Irregularly Irregular- P waves chaotic- PR

not measured- QRS <.12.

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Slide 282

Junctional Rhythm• Rate- 40-60- regular- P waves inverted-before or after

QRS or absent- PR if present <.12- QRS .12 or less.

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Ventricular Dysrhythmias

• Premature Ventricular Contraction (PVC)

– Bigiminy

– Ventricular couplet

– Multifocal PVC (>1 etopic focus)

Ventricular Tachycardia

Ventricular Fibrillation

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Slide 284

PVC

• Rate varies- Can be regular or irregular- P wave

will be absent- unmeasurable PRI- QRS >.12.

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Slide 285

Bigiminy

• 1 PVC every other beat- regular-irregular rhythm

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Ventricular Couplet

• PVC occurs twice

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Slide 287

Multi-Focal PVC

• Can be both positive and negative since there

are different etopic origins

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Slide 288

Ventricular Tachycardia

• 3 or more PVC with rate >100 bpm- patient can be

asymptomatic- symptomatic or unconscious and

pulseless.

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Ventricular Fibrillation• No organized rhythm- needs immediate defibrillation

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Slide 290

Atrioventricular Blocks

First Degree AV Block

Second Degree AV Block• Mobitz Type 1- Wenckebach

• Mobitz Type 2

Third Degree AV Block

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Slide 291

First Degree Heart Block

• PR interval > .20

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Mobitz Type 1• PR interval progressively get longer than QRS drops

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Slide 293

Mobitz Type 2• Regular dropped QRS every 2nd third or 4th P wave- consistent

PR interval

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Slide 294

Third Degree Heart Block

• No conduction between A and V- both will have regular

rates- Ps can be hidden in QRS

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Story of the AV block Family

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Slide 296

Bundle Branch Blocks• Right Bundle Branch Block RBBB

• Left Bundle Branch Block LBBB

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Slide 297

Left Bundle Branch Block

• Increased QRS >.10s

• Once a widened QRS > 0.10s is identified, we look at leads closest to the LV to identify a LBBB.Leads V5,V6, I, and aVL are in close proximity to the left ventricle, and as such, are the best location to identify a LBBB.

• Characterized by an RSR segment or notched QRS

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Slide 299 Right Bundle Branch Block

• Look at Right chest Leads V1 and V2

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Slide 300


• ST segment elevation

• ST segment depression

• Inverted T wave

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ST segment elevation

• Transmural MI

• Use precordial leads to localize

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Slide 302 ST segment depression

• Myocardial ischemia- can be diagnostic

during exercise

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Slide 303 Inverted T wave

• Myocardial ischemia (can be old)

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EKG Lab

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Slide 305 1

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Slide 306 2

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Slide 308 4

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Slide 309 5

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Slide 311 7

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Slide 312 8

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9

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Slide 314 10

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Slide 315 11

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Slide 317

Answers• 1- Normal Sinus

Rhythm

• 2- Sinus Bradycardia

• 3-Sinus Tachycardia

• 4- SVT

• 5-A-fib

• 6-Junctional Rhythm

• 7-RBBB

• 8- Mobitz 1 HB

• 9- 3rd deg HB

• 10- STEMI

• 11- LBBB

• 12- V-fib

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Slide 318

Cardiac Rehab

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Cardiac Rehabilitation

Angina

Coronary Artery Disease


Heart Failure

Coronary Artery Bypass Grafting

Stent or Angioplasty

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Slide 320


Team Members

Cardiologist

Physical Therapist

Registered Nurse

Dietician

Exercise Physiologist

Psychologist

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Slide 321


Team Members

Patient

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Phases

Phase 1- inpatient

Phase 2- Outpatient- Monitored (3

months)

Phase 3 and 4- Outpatient- Unmonitored

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Slide 323


Phase 1Dietary Guidelines

Smoking Cessation

Activity Instructions

Self Monitoring and warning signs of MI

Medications

Get appointments for phase 2

Stress Management

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Slide 324


Phase 1

Do not lift pull or push greater than 10 pounds

Avoid overhead reaching

Do not reach behind your back

Avoid Valsalva

Use a rolling walker

Recommended for 6-8 weeks after sternotomy

Sternal Precautions

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Phase 1

Physical Therapy Evaluation

Early Mobility

Patient Education

Exercise Program

Walking Program

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Slide 326


Phase 1

Lifting- Limit to 10 pounds

Stair Climbing- Gradually resume- Limit trips at first.

Social Activities- Gradually return as you feel ready.

Walking or Stationary Bike- 7 days/wk- work up to

30 mins- Do not exceed 20 BPM over resting heart

rate.

Activity at Discharge

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Slide 327


Phase 1

Household Duties- Meal preparation, washing dishes,

light laundry and hobbies such as crafts or modeling

Sexual Activity- Wait 1-2 weeks and resume gradually

Return to Work- depends on type of work- MD must

release you to return to work.

Driving- MD must release the patient to drive.

Activity at Discharge

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Phase 1

Household/ Yard Duties- shoveling dirt or

snow, mowing the lawn- (even with rider),

vacuuming

Sports and Recreational Activities- No

bowling, golfing, fishing, jogging, swimming or

outdoor biking.

Activity at DischargeDo Not

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Slide 329


Phase 2

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Slide 330


Phase 2

Education

Risk Factor Modification

Exercise

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Phase 2

Meets 1-2 times per week for 1 hour

Heart rhythm, BP and pulse are monitored

Initial exercise prescription is 20-30 BPM above resting HR

progressing to 80% of Max HR.

Patients encouraged to do 30 mins of aerobic exercise on off days.

Resistance activity begins once MD clears sternotomy.

Supervised by Nurse, Exercise Physiologist or Physical Therapist.

Exercise

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Slide 332


Phase 3 and 4

Some hospitals offer in cardiac rehab

gym or wellness center

Programs at local fitness center

Progress monitored by MD

Patient responsibility

Education in phase 1 and 2 important

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Slide 333

Cardiac Stress Test

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Cardiac Stress Test

The stress test is used to evaluate the heart and

vascular system during exercise.

Is there underlying heart disease that only

becomes apparent when the heart is stressed by

exercise?

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Slide 335

Cardiac Stress Test

The patient is attached to a EKG machine and

BP cuff

Baseline EKG taken

Patient begins low level exercise either walking

on treadmill or stationary bike.

Graded increase every three minutes

At each stage vitals are recorded as well as

patient symptoms

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Slide 336

Cardiac Stress Test

• Maximal Stress Test- activity increased until

the patient cannot keep up any longer

because of fatigue, symptoms occur

(dyspnea, chest pain) or there are EKG

changes.

• Submaximal Stress Test- the patient

exercises only to a pre-determined level.

Usually used with patients with known CAD.

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Chemical Stress Test

Combines intravenous medication with an

echocardiogram to evaluate the left ventricle. the

medication takes the place of exercise and the echo

shows decreased movement of an affected wall

Adenosine most common drug

used.

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Slide 338

Echocardiogram

Sonography of the

heart- uses

standard ultrasound

to get a two

dimensional view of

the heart.

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Slide 339

Transesophageal Echocardiogram

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Ejection Fraction (EF)

Stroke volume = end diastolic

volume - end systolic volume

EF = stroke volume / end

diastolic volume

Normal Left Ventricle EF

values are 50-70%

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Slide 341


Echocardiogram

Cardiac catheterization

MRI

CT scan

Nuclear Medicine Scan

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Slide 342


What does this mean the Physical Therapists?

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Slide 345

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Cardiac Tamponade

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Slide 347

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Slide 348

Pericardial Effusion

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Cardiac Case

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Slide 350

History

• Patient is a 68 y/o male who presented to ED

complaining of severe shortness of breath and

dyspnea on exertion.

• In ED, patient found to be diaphoretic, in severe

respiratory distress, in atrial fibrillation with rapid

ventricular response, with ventricular rate 140s

bpm, oxygen saturation 78% on room air.

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Slide 351

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History Continued

• Left heart catheterization showed severe 3

vessel coronary artery disease

• Coronary Artery Bypass Grafting (CABG) x 5,

• Mitral Valve Repair

• CryoMaze Ablation

• Patient sent to CVICU for recovery, extubated

POD #1, reintubated and sedated soon after for

respiratory distress

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Slide 353

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Slide 354

Typical Open Heart Surgery

• Length of Stay in ICU/Cardiovascular Recovery

~1 day

• Extubated within 4 hours of surgery

• Total Hospital Length of Stay 4-6 days

• Ambulating 4-6 times a day once out of ICU

• Follow up with Surgeon 3-4 weeks as out-patient

• Begin Cardiac Rehab 2-3 weeks

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Open Heart Surgery

Medial Sternotomy

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Slide 356

Open Heart Surgery

CABG MVR

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Slide 357

PT Examination• Performed POD #2

• PLOF – Independent with all functional mobility and ADLs

• On 5 Liters O2, telemetry

• Bed Mobility – Max A for rolling and supine to sit transfer

• Transfers – Min A for sit to stand transfer and Mod A for bed to chair transfer with shuffling gait

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PT 2nd SessionPOD #2- during PT

treatment

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Slide 359

PT 2nd Session

• No specific complaints other than fatigue

• Sternal chest pain

• Increased HR 100 BPM

• No A-fib appreciated

• Diaphoretic

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Slide 360

PT 2nd Session

POD #2- during PT treatment

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As A Result

• Returned for Re-Do of angioplasty

• Extended Length of Stay

• Patient able to return home

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Slide 362

Medical Emergencies

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Slide 363

Medical Emergencies

A

B

C

D

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Medical Emergencies

Airway

Breathing

Circulation

Disability

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Slide 365

Airway Issues

D

O

P

E

Artificial Airway

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Slide 366

Dislodged

Obstruction

Pneumothorax/ Pulmonary Emboli

Equipment Failure

Artificial Airway

Airway Issues

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Less than 8 intubate

Laryngeal edema

Bronchospasm

Anaphylactic Shock

Airway Issues

Non Intubated Patient

Call for Help

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Slide 368

Airway Issues

Non Intubated Patient

Ambu-bag

100% non-rebreather

Nasal Cannula

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Slide 369

Breathing Issues

Tachypnea- pattern- rate

Auscultation

Pain

Chest x-ray

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Circulation Issues

EKG changes

Symptomatic versus Asymptomatic (BP)

Asystole, V-fib, 3rd degree heart block=

CPR

Arrythmias

Sinus Tachycardia/ Sinus Bradycardia

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Slide 371

Circulation Issues

Loss of Peripheral Pulses

PVD

Compartment Syndrome

EKG changes

Check Orthosis

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Slide 372

Circulation Issues

Tachycardia

Environmental

Tone

Autonomic Dysreflexia (hyperreflexia)

Anxiety

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Circulation Issues

Chest Pain

New Onset

Rib/ sternum fractures

Recent CPR

If any doubt get 12 lead

Stop activity!!!!!

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Slide 374

Circulation Issues

Bradycardia

Blood Pressure Stable

Supine to Trendelenburg Position

Level of Consciousness

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Slide 375

Medical Emergencies

Treat the Patient Not the

Monitor

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Physical Therapy Through the

Continuum

Intensive Care

Acute Care

In patient Care- rehab, SNF, ventilator unit.

Outpatient

Home Health

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Slide 377

End of Life Issues

DNR

Health Care Proxy

Living Will

Organ Donation

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Slide 378

Any Questions???

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References

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Slide 380

• Adler, J., & Malone, D. (2012, March). Early Mobilization in the Intensive Care Unit: A Systematic Review. Cardiopulmonary Physical Therapy Journal, 23(1), 5-13.

• Alfirevic, M. A., & Svensson, L. (2012). Transcatheter Aortic Valve Replacement. Anesthesiology Clinics, 355-381.

• American Physical Therapy Association. (2001). Guide to Physical Therapist Practice (2nd ed.). Alexandria: American Physical Therapy Association.

• Anderson, C. M., Overend, T. J., Godwin, J., Sealy, C., & Sunderji, A. (2009). Ambulation after deep vein thrombosis: A systematic review. Physiotherapy Canada, 133-140. doi:10.3138/physio.61.3.133

• Arabi, Y., Haddad, S., Shirawi, N., & Al Shimemeri, A. (2004). Early tracheostomy in intensive care trauma patients improves resource utilization: a cohort study and literature review. Critical Care, 8(5), 347-352.

• Brahmbhatt, N., Murugan, R., & Milbrandt, E. B. (2010). Early Mobilization Improves Functional Outcomes in Critically Ill Patients. Critical Care, 14, 321-323.

• Carrougher, G. J. (1998). Burn Care and Therapy. St. Louis: Mosby.

References

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Slide 381

• Carta, A., Parmigiani, F., Roversi, A., Rossato, R., Milini, C., Parrinello, G., . . .

Porru, S. (2010). Training in safer and healthier patient handling techniques.

British Journal of Nursing, 19(9), 576-582.

• Clark, D. E., Lowman, J. D., Griffin, R. L., Matthews, H. M., & Reiff, D. A. (2013).

Effectiveness of an Early Mobilization Protocol in a Trauma and Burns Intensive

Care Unit: A Retrospective Study. Physical Therapy, 93(2), 186-196.

• Coplin, W. M., Pierson, D. J., Cooley, K. D., Newell, D. W., & Rubenfeld, G. D.

(2000). Implications of extubation delay in brain-injured patients meeting

standard weaning criteria. American Journal of Respiratory and Critical Care

Medicine, 161, 1530-1536.

• Frownfelter, D., & Dean, E. (2012). Cardiovascular and Pulmonary Physical

Therapy Evidence to Practice (5th ed.). St. Louis: Elsevier Mosby.

• Husson, E. C., Ribbers, G. M., Willemse-van Son, A. H., Verhagan, A. P., &

Starn, H. J. (2010). Prognosis of six-month functioning after moderate to severe

traumatic brain injury: a systematic review of prospective cohort studies. Journal

of Rehabilitation Medicine, 42, 425-436. doi:10.2340/16501977-0566

References

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• Jewell, D. V. (2011). Guide to Evidence-Based Physical Therapy Practice

(2nd ed.). Sudbury, Massachusetts: Jones & Bartlett Learning.

• Lang, E. F. (2002). Acute Care Handbook for Physical Therapists. (J. C.

Paz, & M. P. West, Eds.) Boston: Butterworth-Heinemann Publishing

Company.

• Leonard , M. (2010). Patient safety and quality improvement: medical errors

and adverse events. Pediatrics in Review, 31(4), 151-158.

• Lippincott, Williams & Wilkins. (2013). Lippincott's Nursing Procedures (6

ed.). Philadelphia: Lippincott, Williams & Wilkins.

• Malone, D. J. (2006). Physical Therapy in Acute Care: A clinicians guide.

Thorofare, NJ.: SLACK Corporation.

• Manske, B. B. (2011). Clinical Orthopedic Rehabilitation: An Evidence

Based Approach. Philadelphia: Mosby.

• Norton, S. (2004). Complete Decongestive Therapy Course Manual. Norton

School of Lymphatic Therapy.

References

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Slide 383

• Paz, J. C., & West, M. P. (2002). Acute Care Handbook for Physical Therapists (2nd ed.). Boston: Butterworth-Heinemann.

• Ranchos Los Amigos National Rehabilitation Center. (2012). The rancho levels of cognitive functioning. Retrieved from rancho.org: http://www.rancho.org/research/bi_cognitive.pdf

• Rothstein, J. M., Roy, S. H., & Wolf, S. L. (1991). The Rehabilitation Clinical Specialists Handbook. Philadelphia: F.A. Davis Company.

• Stowers , R. (2008). A case study approach to professional development in physical therapy. Corpus Christi: Texas A&M University.

• U.S. Department of Health and Human Services. (2012). Guidelines summery-conditions requiring intracranial pressure monitoring/ extraventricular ventricular or lumbar drainage. Retrieved from National Guideline Clearing House: http://www.guideline.gov

• Watchie, J. (2010). Cardiovascular and Pulmonary Physical Therapy. Philadelphia: Saunders Elsevier.

References

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Slide 384

Thank You

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