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DYSPNEA ANDPULMONARY EDEMAHarrisons 17 th editionChapter 33
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Dyspnea
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DYSPNEA
American Thoracic Societydyspnea as a subjective experience of breathingdiscomfort that consists of qualitatively distinct
sensations that vary in intensity experience derivesfrom interactions among multiple physiological,psychological, social, and environmental factors, andmay induce secondary physiological and behavioral
responses.
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MECHANISMS OF DYSPNEA
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Motor Efferents
Disorders of the ventilatory pumpassociated with increased work of breathing or asense of an increased effort to breathe
The increased neural output from the motor cortex isthought to be sensed due to a corollary discharge that issent to the sensory cortex at the same time that signals
are sent to the ventilatory muscles.
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Sensory Efferents
Chemoreceptors in the carotid bodies and medullaactivated by hypoxemia, acute hypercapnia, andacidemia; leads to an increase in ventilation, produce
a sensation of air hungerMechanoreceptors in the lungs
stimulated by bronchospasm; lead to a sensation of chest tightness
J-receptors , sensitive to interstitial edema, andpulmonary vascular receptors
activated by acute changes in pulmonary arterypressure, appear to contribute to air hunger
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Sensory Efferents
Hyperinflationassociated with the sensation of an inability to get adeep breath or of an unsatisfying breath
Metaboreceptors, located in skeletal muscleactivated by changes in the local biochemical milieu of the tissue active during exercisewhen stimulated, contribute to the breathingdiscomfort
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Anxiety
Acute anxiety may increase the severity of dyspneaaltering the interpretation of sensory dataleading to patterns of breathing that heighten
physiologic abnormalities in the respiratory system
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ASSESSING DYSPNEA
Quality of Sensationdetermination of the quality of the discomfort
Sensory Intensity
modified Borg scale or visual analogue scale can be utilized to measuredyspnea at rest, immediately following exercise, or on recall of areproducible 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 asunpleasant and interpreted as abnormal.
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DIFFERENTIAL DIAGNOSIS
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Respiratory System Dyspnea
ControllerStimulated by acute hypoxemia and hypercapniaStimulation of pulmonary receptors: acute
bronchospasm, interstitial edema, and PEHigh altitude, high progesterone states (pregnancy),aspirin
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Respiratory System Dyspnea
Ventilatory PumpDisorders of the airways (asthma, emphysema, chronicbronchitis, bronchiectasis) lead to increased airway
resistance and work of breathingHyperinflation inability to get a deep breathConditions that stiffen the chest wall (kyphoscoliosis)and that weaken ventilatory muscles (MG and GBS)associated with increased effort to breathLarge pleural effusions increases the work of breathingand stimulates pulmonary receptors if there isassociated atelectasis.
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Respiratory System Dyspnea
Gas Exchangerinterfere with gas exchange: pneumonia, pulmonaryedema, and aspiration
direct stimulation of pulmonary receptors: pulmonaryvascular and interstitial lung disease and pulmonaryvascular congestion
relief of hypoxemia - small impact on dyspnea
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Cardiovascular System Dyspnea
High Cardiac OutputMild to moderate anemia: breathing discomfortduring exercise
Left-to-right intracardiac shunts: may be complicatedby the development of pulmonary hypertensionBreathlessness associated with obesity: due tomultiple mechanisms, including high cardiac outputand impaired ventilatory pump function
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Cardiovascular System Dyspnea
Normal Cardiac OutputCardiovascular deconditioning: early development of anaerobic metabolism and stimulation of chemo- and
metaboreceptorsDiastolic dysfunction: due to HPN, AS, or hypertrophiccardiomyopathyPericardial disease: constrictive pericarditis
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Cardiovascular System Dyspnea
Low Cardiac OutputCoronary artery disease and nonischemiccardiomyopathies: pulmonary receptors are
stimulated
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Approach to the Patient
Clinical Indicators in the historyOrthopnea: CHF, mechanical impairment of thediaphragm in obesity, or asthma triggered by
esophageal refluxNocturnal dyspnea: CHF or asthmaAcute, intermittent episodes: MI, bronchospasm, PEChronic persistent: COPD and interstitial lung diseasePlatypnea: left atrial myxoma or hepatopulmonarysyndrome
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Approach to the Patient
Physical ExaminationInability of the patient to speak in full sentences:problem with the controller ventilatory pump
Increased work of breathing (supraclavicularretractions, use of accessory muscles, and the tripodposition): ventilatory pump problem increased airwayresistance or stiff lungs and chest wall
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Approach to the Patient
Physical Examinationvital signs, respiratory rateexamination for a pulsus paradoxus >10 mmHg: COPD
signs of anemia (pale conjunctivae), cyanosis, andcirrhosis (spider angiomata, gynecomastia)
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Approach to the Patient
Physical ExaminationParadoxical movement of the abdomen (inwardmotion during inspiration): diaphragmatic weakness
Clubbing of the digits: interstitial pulmonary fibrosisJoint swelling or deformation, change consistent withRaynauds disease: collagen -vascular processassociated with pulmonary disease
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Approach to the Patient
Physical Examination of the ChestSymmetry of movementPercussion (dullness indicative of pleural effusion,
hyper-resonance a sign of emphysema)Auscultation(wheezes, rales, rhonchi, prolongedexpiratory phase, diminished breath sounds)
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Approach to the Patient
Physical Examination of the Heartsigns of elevated right heart pressures (jugular venousdistention, edema, accentuated pulmonic component
to the second heart sound)left ventricular dysfunction (S3 and S4 gallops)valvular disease (murmurs)
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Approach to the Patient
Diagnostic ExamsCXR
Lung volumes
hyperinflation: obstructive lung diseaselow lung volumes: interstitial edema or fibrosis,diaphragmatic dysfunction, or impaired chestwall motion
Pulmonary parenchyma - interstitial disease andemphysema
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Approach to the Patient
Diagnostic ExamsCXR
Prominent pulmonary vasculature
in the upper zones: pulmonary venoushypertensionenlarged central pulmonary arteries: pulmonaryartery hypertension
enlarged cardiac silhouette: dilatedcardiomyopathy or valvular disease
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Approach to the Patient
Diagnostic ExamsCXR
Bilateral pleural effusions: CHF and collagen vascular
diseaseUnilateral effusions: CA and PE
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Approach to the Patient
Diagnostic Exams
CT scan of the chestreserved for further evaluation of the lung
parenchyma (interstitial lung disease) and possible PE
ECG
Look for evidence of ventricular hypertrophy and priormyocardial infarction
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Approach to the Patient
Distinguishing Cardiovascular from RespiratorySystem Dyspnea
CARDIOPULMONARY EXERCISE TEST
determine which system is responsible for theexercise limitation
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Approach to the Patient
Distinguishing Cardiovascular from RespiratorySystem Dyspnea
CARDIOPULMONARY EXERCISE TEST
PULMONARY IF AT PEAK EXERCISE:achieves predicted maximal ventilationdemonstrates an increase in dead space orhypoxemia (oxygen saturation below 90%)develops bronchospasm
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Approach to the Patient
Distinguishing Cardiovascular from RespiratorySystem Dyspnea
CARDIOPULMONARY EXERCISE TEST
CARDIAC IF AT PEAK EXERCISE:heart rate is >85% of the predicted maximumif anaerobic threshold occurs earlyif the BP becomes excessively high or dropsif the O2 pulse (O2 consumption/heart rate, anindicator of stroke volume) fallsif there are ischemic changes on the ECG
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Treatment
First goal: correct the underlying problemresponsible for the symptomAdministration of supplemental O 2
COPD patients: pulmonary rehabilitation programshave demonstrated positive effects on dyspnea,
exercise capacity, and rates of hospitalization
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Pulmonary Edema
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MECHANISMS OF FLUIDACCUMULATION
balance of hydrostatic and oncotic forces withinthe pulmonary capillaries
Hydrostatic pressurefavors movement of fluid from the capillary into theinterstitium
Oncotic pressurefavors movement of fluid into the vessel
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MECHANISMS OF FLUIDACCUMULATION
Maintenancetight junctions of the capillary endothelium areimpermeable to proteins
lymphatics in the tissue carry away the small amountsof protein that may leak out
Pathologydisruption of the endothelial barrier: allows protein toescape the capillary bed and enhances the movementof fluid into the tissue of the lung
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Cardiogenic Pulmonary Edema
Hydrostatic pressure is increased and fluid exitsthe capillary at an increased rateEarly signs of pulmonary edema: exertional
dyspnea and orthopneaCXR: peribronchial thickening, prominent vascularmarkings in the upper lung zones, and Kerley Blines
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Noncardiogenic Pulmonary Edema
Hydrostatic pressures are normal
Leakage of proteins and other macromoleculesinto the tissue
Associated with dysfunction of the surfactant liningthe alveoli, increased surface forces, and apropensity for the alveoli to collapse at low lungvolumes
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Noncardiogenic Pulmonary Edema
Characterized by intrapulmonary shunt withhypoxemia and decreased pulmonary compliance
CausesDirect Injury to LungHematogenous Injury to Lung
Possible Lung Injury Plus Elevated HydrostaticPressures
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Cardiogenic vs Noncardiogenic
CARDIOGENIC PULMONARY EDEMAPhysical 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 infiltrates
pleural effusions
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Cardiogenic vs Noncardiogenic
NONCARDIOGENIC PULMONARY EDEMAPhysical Examination:
Findings may be relatively normal in the early stages
CXR:Heart size is normalUniform alveolar infiltratesPleural effusions are uncommon
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Hypoxemia
CARDIOGENICdue to ventilation-perfusion mismatchresponds to the administration of supplemental
oxygen
NONCARDIOGENICdue to intrapulmonary shuntingpersists despite high concentrations of inhaled O 2
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