Cor pulmonale: Difference between revisions
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==Background== | ==Background== | ||
*Remodeling of right ventricle in response to pulmonary pathology | *Remodeling of right ventricle in response to pulmonary pathology<ref>Aubry A, Paternot A, Vieillard-Baron A. [Cor pulmonale]. Rev Mal Respir. 2020 Mar;37(3):257-266. PMID 32088063</ref> | ||
*Often caused by [[COPD]], [[pulmonary hypertension]], [[PE]], [[ARDS]] | *Often caused by [[COPD]], [[pulmonary hypertension]], [[PE]], [[ARDS]] | ||
| Line 35: | Line 35: | ||
**[[pneumonia]] | **[[pneumonia]] | ||
*Other | *Other | ||
**Pure volume overload | **Pure [[fluid overload|volume overload]] | ||
***[[Renal Failure]] | ***[[Renal Failure]] | ||
***Post-[[Transfusion]] | ***Post-[[Transfusion]] | ||
| Line 42: | Line 42: | ||
==Evaluation== | ==Evaluation== | ||
===Blood tests=== | ===Blood tests=== | ||
*CBC (polycythemia) | *CBC ([[polycythemia]]) | ||
*[[ABG]] (oxygenation, acid-base status) | *[[ABG]] (oxygenation, acid-base status) | ||
*α-1-antitrypsin | *α-1-antitrypsin | ||
| Line 56: | Line 56: | ||
*[[Right bundle branch block]] | *[[Right bundle branch block]] | ||
*R:S ratio > 1 in V1 | *R:S ratio > 1 in V1 | ||
*TWI in V1-3 in acute right heart strain | *TWI in V1-3 in acute right heart strain (as opposed to upright t-waves in posterior MI) | ||
*S1 Q3 T3 in acute right heart strain | *S1 Q3 T3 in acute right heart strain | ||
*Large P wave in II, III, aVF | *Large P wave in II, III, aVF | ||
*[[Arrhythmia]] ([[PAC]], [[SVT]], MFAT, [[A-fib]], [[ | *[[Arrhythmia]] ([[PAC]], [[SVT]], MFAT, [[A-fib]], A-[[flutter]]) | ||
===[[Echocardiography]]=== | ===[[Echocardiography]]=== | ||
Latest revision as of 10:59, 22 March 2026
Background
- Remodeling of right ventricle in response to pulmonary pathology[1]
- Often caused by COPD, pulmonary hypertension, PE, ARDS
Clinical Features
Pathophysiology
- Pulmonary vasoconstriction (hypoxia, acidemia)
- Destruction of pulmonary vasculature by emphysema, interstitial lung disease
- 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)
- α-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 (as opposed to upright t-waves in posterior MI)
- S1 Q3 T3 in acute right heart strain
- Large P wave in II, III, aVF
- Arrhythmia (PAC, SVT, MFAT, A-fib, A-flutter)
Echocardiography
- 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
Disposition
See Also
External Links
References
- ↑ Aubry A, Paternot A, Vieillard-Baron A. [Cor pulmonale]. Rev Mal Respir. 2020 Mar;37(3):257-266. PMID 32088063