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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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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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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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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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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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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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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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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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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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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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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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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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Diagnostic ExamsCXR

Bilateral pleural effusions: CHF and collagen vascular

diseaseUnilateral effusions: CA and PE


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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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Distinguishing Cardiovascular from RespiratorySystem Dyspnea

CARDIOPULMONARY EXERCISE TEST

determine which system is responsible for theexercise limitation


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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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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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