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Cor pulmonale
From WikEM
Contents
Background
- Remodeling of right ventricle in response to pulmonary pathology
- Often caused by COPD, pulmonary hypertension, PE, ARDS
Clinical Features
Pathophysiology
- Pulmonary vasoconstriction (hypoxia, acidemia)
- Destruction of pulmonary vasculature by emphysema, ILD
- Increased blood viscosity (sickle cell disease, polycythemia)
Chronic
Acute
- RV dilation
Signs and Symptoms
- Cough
- Dyspnea
- Tachypnea
- Hemoptysis
- Syncope
- Peripheral edema
- Cyanosis
Differential Diagnosis
- Cardiovascular
- Pulmonary
- Other
- Pure volume overload
- Renal Failure
- Post-Transfusion
- Sepsis
- Pure volume overload
Evaluation
Blood tests
- CBC (polycythemia)
- ABG (oxygenation, acid-base status)
- alpha-1-antitrypsin
- ANA
- Coagulation studies (protein C/S, factor V Leiden etc)
CXR
- Enlarged pulmonary arteries
- Cardiomegaly
- Decreased retrosternal air space
ECG
- RVH
- Right axis deviation
- Right bundle branch block
- R:S ratio > 1 in V1
- TWI in V1-3 in acute right heart strain
- S1 Q3 T3 in acute right heart strain
- Large P wave in II, III, aVF
- Arrhythmia (PAC, SVT, MFAT, A-fib, A-flutter)
Echo
- Increased RV thickness
- RV dilation
- Tricuspid insufficiency
- High estimated PA pressures
- Septal bowing into LV
CTPA for PE
V/Q scan for PE
Management
- Treat underlying disease
- Fluids, vasoconstrictors to support BP in acute setting
- Oxygen therapy: decreases pulmonary vasoconstriction
- Diuretics: decrease RV filling volume
- Calcium channel blockers: vasodilate the pulmonary arteries
- Beta agonists (epoprostenol, iloprost): bronchodilate
- Phlebotomy for severe hypoxia leading to polycythemia
- Lung transplant or heart-lung transplant as last resort