Cor pulmonale: Difference between revisions
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==Clinical Features== | ==Clinical Features== | ||
===Pathophysiology=== | ===Pathophysiology=== | ||
*Pulmonary vasoconstriction (hypoxia, acidemia) | *Pulmonary vasoconstriction ([[hypoxia]], [[acidosis|acidemia]]) | ||
*Destruction of pulmonary vasculature by emphysema, | *Destruction of pulmonary vasculature by emphysema, [[interstitial lung disease]] | ||
*Increased blood viscosity ([[sickle cell disease]], polycythemia) | *Increased blood viscosity ([[sickle cell disease]], [[polycythemia]]) | ||
===Chronic=== | ===Chronic=== | ||
*[[RVH]] | *[[RVH]] | ||
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**[[Acute Valve Dysfunction]] | **[[Acute Valve Dysfunction]] | ||
**[[Aortic Dissection]] | **[[Aortic Dissection]] | ||
**[[ | **[[Dysrhythmia]] | ||
**[[Endocarditis]] | **[[Endocarditis]] | ||
**[[Hypertensive Emergency]] | **[[Hypertensive Emergency]] | ||
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===Blood tests=== | ===Blood tests=== | ||
*CBC (polycythemia) | *CBC (polycythemia) | ||
*ABG (oxygenation, acid-base status) | *[[ABG]] (oxygenation, acid-base status) | ||
*α-1-antitrypsin | *α-1-antitrypsin | ||
*ANA | *ANA | ||
*Coagulation studies (protein C/S, factor V Leiden etc) | *Coagulation studies (protein C/S, factor V Leiden etc) | ||
===CXR=== | ===[[CXR]]=== | ||
*Enlarged pulmonary arteries | *Enlarged pulmonary arteries | ||
*Cardiomegaly | *Cardiomegaly | ||
*Decreased retrosternal air space | *Decreased retrosternal air space | ||
===ECG=== | ===[[ECG]]=== | ||
*[[RVH]] | *[[RVH]] | ||
*Right axis deviation | *Right axis deviation | ||
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*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, A-flutter) | *[[Arrhythmia]] ([[PAC]], [[SVT]], MFAT, [[A-fib]], [[A-flutter]]) | ||
=== | ===[[Echocardiography]]=== | ||
*Increased RV thickness | *Increased RV thickness | ||
*RV dilation | *RV dilation | ||
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==Management== | ==Management== | ||
*Treat underlying disease | *Treat underlying disease | ||
*Fluids, vasoconstrictors to support BP in acute setting | *Fluids, [[vasopressors|vasoconstrictors]] to support BP in acute setting | ||
*Oxygen therapy: decreases pulmonary vasoconstriction | *[[Oxygen therapy]]: decreases pulmonary vasoconstriction | ||
*Diuretics: decrease RV filling volume | *[[Diuretics]]: decrease RV filling volume | ||
*[[Calcium channel blockers]]: vasodilate the pulmonary arteries | *[[Calcium channel blockers]]: vasodilate the pulmonary arteries | ||
*Beta agonists (epoprostenol, iloprost): bronchodilate | *Beta agonists ([[epoprostenol]], iloprost): bronchodilate | ||
*Phlebotomy for severe hypoxia leading to polycythemia | *Phlebotomy for severe hypoxia leading to polycythemia | ||
*Lung transplant or heart-lung transplant as last resort | *Lung transplant or heart-lung transplant as last resort | ||
Revision as of 18:36, 24 September 2019
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, 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
- 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