dyspnea and pulmonary edema
DESCRIPTION
17th editionTRANSCRIPT
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
Approach to the Patient
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)
Approach to the Patient
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
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
Approach to the Patient
Diagnostic Exams 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
Approach to the Patient
Diagnostic Exams 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
Approach to the Patient
Distinguishing Cardiovascular from Respiratory System Dyspnea CARDIOPULMONARY EXERCISE TEST
PULMONARY IF AT PEAK EXERCISE: achieves predicted maximal ventilationdemonstrates an increase in dead space or
hypoxemia (oxygen saturation below 90%)develops bronchospasm
Approach to the Patient
Distinguishing Cardiovascular from Respiratory System Dyspnea CARDIOPULMONARY EXERCISE TEST
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