Docslide us dyspnea-and-pulmonary-edema

DYSPNEA AND PULMONARY EDEMAHarrison’s 17th editionChapter 33

Dyspnea

DYSPNEA American Thoracic Society

dyspnea as a “subjective experience of breathing discomfort that consists of qualitatively distinct sensations that vary in intensity experience derives from interactions among multiple physiological, psychological, social, and environmental factors, and may induce secondary physiological and behavioral responses.”

MECHANISMS OF DYSPNEA

Motor Efferents Disorders of the ventilatory pump

associated with increased work of breathing or a sense of an increased effort to breathe

The increased neural output from the motor cortex is thought to be sensed due to a corollary discharge that is sent to the sensory cortex at the same time that signals are sent to the ventilatory muscles.

Sensory Efferents Chemoreceptors in the carotid bodies and medulla

activated by hypoxemia, acute hypercapnia, and acidemia; leads to an increase in ventilation, produce a sensation of air hunger

Mechanoreceptors in the lungs stimulated by bronchospasm; lead to a sensation of chest tightness

J-receptors, sensitive to interstitial edema, and pulmonary vascular receptors activated by acute changes in pulmonary artery pressure, appear to contribute to air hunger

Sensory Efferents Hyperinflation

associated with the sensation of an inability to get a deep breath or of an unsatisfying breath

Metaboreceptors, located in skeletal muscle activated by changes in the local biochemical milieu of the tissue active during exercise

when stimulated, contribute to the breathing discomfort

Anxiety Acute anxiety may increase the severity of dyspnea altering the interpretation of sensory data

leading to patterns of breathing that heighten physiologic abnormalities in the respiratory system

ASSESSING DYSPNEA Quality of Sensation

determination of the quality of the discomfort Sensory Intensity

modified Borg scale or visual analogue scale can be utilized to measure dyspnea at rest, immediately following exercise, or on recall of a reproducible physical task.

alternative approach is to inquire about the activities a patient can do. The Baseline Dyspnea Index and the Chronic Respiratory Disease Questionnaire are commonly used tools for this purpose.

Affective Dimension for a sensation to be reported as a symptom, it must be perceived as unpleasant and interpreted as abnormal.

DIFFERENTIAL DIAGNOSIS

Respiratory System Dyspnea Controller

Stimulated by acute hypoxemia and hypercapnia

Stimulation of pulmonary receptors: acute bronchospasm, interstitial edema, and PE

High altitude, high progesterone states (pregnancy), aspirin

Respiratory System Dyspnea Ventilatory Pump

Disorders of the airways (asthma, emphysema, chronic bronchitis, bronchiectasis) lead to increased airway resistance and work of breathing

Hyperinflation inability to get a deep breath Conditions that stiffen the chest wall (kyphoscoliosis) and that weaken ventilatory muscles (MG and GBS) associated with increased effort to breath

Large pleural effusions increases the work of breathing and stimulates pulmonary receptors if there is associated atelectasis.

Respiratory System Dyspnea Gas Exchanger

interfere with gas exchange: pneumonia, pulmonary edema, and aspiration

direct stimulation of pulmonary receptors: pulmonary vascular and interstitial lung disease and pulmonary vascular congestion

relief of hypoxemia - small impact on dyspnea

Cardiovascular System Dyspnea High Cardiac Output

Mild to moderate anemia: breathing discomfort during exercise

Left-to-right intracardiac shunts: may be complicated by the development of pulmonary hypertension

Breathlessness associated with obesity: due to multiple mechanisms, including high cardiac output and impaired ventilatory pump function

Cardiovascular System Dyspnea Normal Cardiac Output

Cardiovascular deconditioning: early development of anaerobic metabolism and stimulation of chemo- and metaboreceptors

Diastolic dysfunction: due to HPN, AS, or hypertrophic cardiomyopathy

Pericardial disease: constrictive pericarditis

Cardiovascular System Dyspnea Low Cardiac Output

Coronary artery disease and nonischemic cardiomyopathies: pulmonary receptors are stimulated

Approach to the Patient Clinical Indicators in the history

Orthopnea: CHF, mechanical impairment of the diaphragm in obesity, or asthma triggered by esophageal reflux

Nocturnal dyspnea: CHF or asthma Acute, intermittent episodes: MI, bronchospasm, PE

Chronic persistent: COPD and interstitial lung disease

Platypnea: left atrial myxoma or hepatopulmonary syndrome

Approach to the Patient Physical Examination

Inability of the patient to speak in full sentences: problem with the controller ventilatory pump

Increased work of breathing (supraclavicular retractions, use of accessory muscles, and the tripod position): ventilatory pump problem increased airway resistance or stiff lungs and chest wall


vital signs, respiratory rate examination for a pulsus paradoxus >10 mmHg: COPD

signs of anemia (pale conjunctivae), cyanosis, and cirrhosis (spider angiomata, gynecomastia)


Paradoxical movement of the abdomen (inward motion during inspiration): diaphragmatic weakness

Clubbing of the digits: interstitial pulmonary fibrosis

Joint swelling or deformation, change consistent with Raynaud’s disease: collagen-vascular process associated with pulmonary disease

Approach to the Patient Physical Examination of the Chest

Symmetry of movement Percussion (dullness indicative of pleural effusion, hyper-resonance a sign of emphysema)

Auscultation(wheezes, rales, rhonchi, prolonged expiratory phase, diminished breath sounds)

Approach to the Patient Physical Examination of the Heart

signs of elevated right heart pressures (jugular venous distention, edema, accentuated pulmonic component to the second heart sound)

left ventricular dysfunction (S3 and S4 gallops)

valvular disease (murmurs)

Approach to the Patient Diagnostic Exams

CXR Lung volumes

hyperinflation: obstructive lung disease

low lung volumes: interstitial edema or fibrosis, diaphragmatic dysfunction, or impaired chest wall motion

Pulmonary parenchyma - interstitial disease and emphysema


CXR Prominent pulmonary vasculature

in the upper zones: pulmonary venous hypertension

enlarged central pulmonary arteries: pulmonary artery hypertension

enlarged cardiac silhouette: dilated cardiomyopathy or valvular disease


CXR Bilateral pleural effusions: CHF and collagen vascular disease

Unilateral effusions: CA and PE

Approach to the Patient Diagnostic Exams CT scan of the chest

reserved for further evaluation of the lung parenchyma (interstitial lung disease) and possible PE

ECG Look for evidence of ventricular hypertrophy and prior myocardial infarction

Approach to the Patient Distinguishing Cardiovascular from Respiratory System Dyspnea CARDIOPULMONARY EXERCISE TEST

determine which system is responsible for the exercise limitation


PULMONARY IF AT PEAK EXERCISE: achieves predicted maximal ventilation

demonstrates an increase in dead space or hypoxemia (oxygen saturation below 90%)

develops bronchospasm


CARDIAC IF AT PEAK EXERCISE: heart rate is >85% of the predicted maximum

if anaerobic threshold occurs earlyif the BP becomes excessively high or drops

if the O2 pulse (O2 consumption/heart rate, an indicator of stroke volume) falls

if there are ischemic changes on the ECG

Treatment First goal: correct the underlying problem responsible for the symptom

Administration of supplemental O2

COPD patients: pulmonary rehabilitation programs have demonstrated positive effects on dyspnea, exercise capacity, and rates of hospitalization

Pulmonary Edema

MECHANISMS OF FLUID ACCUMULATION balance of hydrostatic and oncotic forces within the pulmonary capillaries

Hydrostatic pressure favors movement of fluid from the capillary into the interstitium

Oncotic pressure favors movement of fluid into the vessel

MECHANISMS OF FLUID ACCUMULATION Maintenance

tight junctions of the capillary endothelium are impermeable to proteins

lymphatics in the tissue carry away the small amounts of protein that may leak out

Pathology disruption of the endothelial barrier: allows protein to escape the capillary bed and enhances the movement of fluid into the tissue of the lung

Cardiogenic Pulmonary Edema Hydrostatic pressure is increased and fluid exits the capillary at an increased rate

Early signs of pulmonary edema: exertional dyspnea and orthopnea

CXR: peribronchial thickening, prominent vascular markings in the upper lung zones, and Kerley B lines

Noncardiogenic Pulmonary Edema Hydrostatic pressures are normal Leakage of proteins and other macromolecules into the tissue

Associated with dysfunction of the surfactant lining the alveoli, increased surface forces, and a propensity for the alveoli to collapse at low lung volumes

Noncardiogenic Pulmonary Edema Characterized by intrapulmonary shunt with hypoxemia and decreased pulmonary compliance

Causes Direct Injury to Lung Hematogenous Injury to Lung Possible Lung Injury Plus Elevated Hydrostatic Pressures

Cardiogenic vs Noncardiogenic CARDIOGENIC PULMONARY EDEMA

Physical Examination: increased intracardiac pressures (S3 gallop, elevated jugular venous pulse, peripheral edema)

rales and/or wheezes on auscultation of the chest

CXR:enlarged cardiac silhouettevascular redistributioninterstitial thickeningperihilar alveolar infiltratespleural effusions

Cardiogenic vs Noncardiogenic NONCARDIOGENIC PULMONARY EDEMA

Physical Examination: Findings may be relatively normal in the early stages

CXR:Heart size is normalUniform alveolar infiltrates Pleural effusions are uncommon

Hypoxemia CARDIOGENIC

due to ventilation-perfusion mismatch responds to the administration of supplemental oxygen

NONCARDIOGENIC due to intrapulmonary shunting persists despite high concentrations of inhaled O2

Docslide us dyspnea-and-pulmonary-edema

Documents

Transcript of Docslide us dyspnea-and-pulmonary-edema