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


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.


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


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


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


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


Physical Examination vital signs, respiratory rate examination for a pulsus paradoxus >10 mmHg: COPD signs of anemia (pale conjunctivae), cyanosis, and

cirrhosis (spider angiomata, gynecomastia)


Physical Examination 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


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)


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)


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



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



Bilateral pleural effusions: CHF and collagen vascular disease

Unilateral effusions: CA and PE


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


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 ventilationdemonstrates 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 early if 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 redistribution interstitial 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

Dyspnea and Pulmonary Edema

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