Cor Pulmonale
Cor Pulmonale is right ventricular enlargement secondary to a lung disorder that produces pulmonsry artery hypertension.
Right ventricular failure follows. Findings include peripheral edema, neck vein distention, hepatomegaly and a parasternal lift.
Diagnosis is clinical and by echocardiography. Treatment is directed at the cause
Cor pulmonale results from a lung disorder, it does not refer to right ventricular enlargement to left ventricular failure, a congenital heart disorder or an acquired valvular disorder.
Cor pulmonale is usually chronic but may be acute and reversible.
Pathophysiology and Etiology
Lung disorders cause pulmonary hypertension by several mechanisms. Loss of capillary beds (e.g. due to bullous changes in COPD or thrombosis in pulmonary embolism), vasoconstriction caused by hpoxia, hypercapnia or both, increased alveolar pressure (e.g in COPD during mechanical ventilation), and media hypertrophy in arterioles (often a response to pulmonary hypertension due to other mechanism)
Pulmonary hypertension increases after load on the Right Ventricle, resulting in the same cascade of events that occurs in HF, including elevated end-diastolic and central venous pressure and ventricular hypertrophy and dilation. Demands on the right ventricle may be intensified by increased blood viscosity due to hypoxia induced polycythemia. Rarely, right ventricle failure affects the left ventricle if a dysfunctional septum bulges into the left ventricles, interfering with filling and thus producing diastolic dysfunction.
Acute cor pulmonale usually results from massive pulmonary embolization or from injury due to mechanical ventilation for acute respiratory distress syndrome.
Chronic cor pulmonale is caused usually by COPD (Chronic bronchitis, emphysema) and less often by extensive loss of lung tissue due to surgery or trauma, chronic unresolved pulmonary emboli, pulmonary veno-occlusive disease, scleroderma, pulmonary interstitial fibrosis, kyphoscoliosis, obesity with alveolar hypoventilation. In patients with COPD, an acute exacerbation or pulmonary infection may trigger Right Ventricle overload. In chronic cor pulmonale, risk of venous thromboembolism is increased.
Symptoms, signs and Diagnosis.
Initially, cor pulmonale is asymptomatic, although patients usually have significant symptoms due to underlying lung disorder (e.g dyspnea, exertional fatigue). Later, as right ventricle pressure increases, physical signs commonly include a left parasternal systolic lift, a loud pulmonic component of the second heart sound(S2), and murmurs of functional tricuspid and pulmonic insufficiency . Later an RV gallop rhythm (3rd [s3] and 4th [s4] heart sounds) augmented during inspiration,distended jugular veins( with a dominant a wave unless tricuspid regurgitationis present), hepatomegaly and lowe-extremity edema may occur.
Cor pulmonale should be suspected in all patients with one of its causes. Chest X-rays show RV and proximal pulmonary artery enlargement with distal arterial attenuation.
ECG evidence of RV hypertrophy (e.g right axis deviation, QR wave in lead V1 ,and dominant R wave in lead V1 , and dominant R in leads V1 to V3 ) correlates well with degree of pulmonary hypertension .
However because pulmonary hyperinflation and bullae in COPD cause realignment of the heart, physical examination, X-rays, and ECG may be relatively insensitive
Echocardiography or radionuclide imaging is done to evaluate left ventricle and right ventricle function. Echocardiography can assess right ventricle systolic pressure but is often technically limited by the lung disorder.
Right heart catheterization may be required for confirmation.
Treatment
Treatment is difficult and focuses on the cause, particularly alleviation of or moderation of hypoxia.
If peripheral edema is present .diuretics may seem appropriate, but they are helpful only if Left ventricle failure and pulmonary fluid overload are also present, they may be harmful because small decrease in preload often worsen cor pulmonale.
Pulmonary vasodilators (e.g hydralazine, Ca chanel blockers, nitrous oxide, prostacyclin), although beneficial in primary pulmonary hypertension, are not effective. Digoxin is effective only if patients have concomitant Left ventricle dysfunction, caution is required because patients with COPD are sensitive to digoxins effects.
Phlebotomy during hypoxic cor pulmonale has been suggested, but the benefits of decreasing blood viscosity are not likely to offset the harm of reducing O2-carrying capacity unless significant polycythemia is present.
For patients with chronic cor pulmonale, long –term anticoagulants reduce risk of venous thromboembolism
Cor Pulmonale is right ventricular enlargement secondary to a lung disorder that produces pulmonsry artery hypertension.
Right ventricular failure follows. Findings include peripheral edema, neck vein distention, hepatomegaly and a parasternal lift.
Diagnosis is clinical and by echocardiography. Treatment is directed at the cause
Cor pulmonale results from a lung disorder, it does not refer to right ventricular enlargement to left ventricular failure, a congenital heart disorder or an acquired valvular disorder.
Cor pulmonale is usually chronic but may be acute and reversible.
Pathophysiology and Etiology
Lung disorders cause pulmonary hypertension by several mechanisms. Loss of capillary beds (e.g. due to bullous changes in COPD or thrombosis in pulmonary embolism), vasoconstriction caused by hpoxia, hypercapnia or both, increased alveolar pressure (e.g in COPD during mechanical ventilation), and media hypertrophy in arterioles (often a response to pulmonary hypertension due to other mechanism)
Pulmonary hypertension increases after load on the Right Ventricle, resulting in the same cascade of events that occurs in HF, including elevated end-diastolic and central venous pressure and ventricular hypertrophy and dilation. Demands on the right ventricle may be intensified by increased blood viscosity due to hypoxia induced polycythemia. Rarely, right ventricle failure affects the left ventricle if a dysfunctional septum bulges into the left ventricles, interfering with filling and thus producing diastolic dysfunction.
Acute cor pulmonale usually results from massive pulmonary embolization or from injury due to mechanical ventilation for acute respiratory distress syndrome.
Chronic cor pulmonale is caused usually by COPD (Chronic bronchitis, emphysema) and less often by extensive loss of lung tissue due to surgery or trauma, chronic unresolved pulmonary emboli, pulmonary veno-occlusive disease, scleroderma, pulmonary interstitial fibrosis, kyphoscoliosis, obesity with alveolar hypoventilation. In patients with COPD, an acute exacerbation or pulmonary infection may trigger Right Ventricle overload. In chronic cor pulmonale, risk of venous thromboembolism is increased.
Symptoms, signs and Diagnosis.
Initially, cor pulmonale is asymptomatic, although patients usually have significant symptoms due to underlying lung disorder (e.g dyspnea, exertional fatigue). Later, as right ventricle pressure increases, physical signs commonly include a left parasternal systolic lift, a loud pulmonic component of the second heart sound(S2), and murmurs of functional tricuspid and pulmonic insufficiency . Later an RV gallop rhythm (3rd [s3] and 4th [s4] heart sounds) augmented during inspiration,distended jugular veins( with a dominant a wave unless tricuspid regurgitationis present), hepatomegaly and lowe-extremity edema may occur.
Cor pulmonale should be suspected in all patients with one of its causes. Chest X-rays show RV and proximal pulmonary artery enlargement with distal arterial attenuation.
ECG evidence of RV hypertrophy (e.g right axis deviation, QR wave in lead V1 ,and dominant R wave in lead V1 , and dominant R in leads V1 to V3 ) correlates well with degree of pulmonary hypertension .
However because pulmonary hyperinflation and bullae in COPD cause realignment of the heart, physical examination, X-rays, and ECG may be relatively insensitive
Echocardiography or radionuclide imaging is done to evaluate left ventricle and right ventricle function. Echocardiography can assess right ventricle systolic pressure but is often technically limited by the lung disorder.
Right heart catheterization may be required for confirmation.
Treatment
Treatment is difficult and focuses on the cause, particularly alleviation of or moderation of hypoxia.
If peripheral edema is present .diuretics may seem appropriate, but they are helpful only if Left ventricle failure and pulmonary fluid overload are also present, they may be harmful because small decrease in preload often worsen cor pulmonale.
Pulmonary vasodilators (e.g hydralazine, Ca chanel blockers, nitrous oxide, prostacyclin), although beneficial in primary pulmonary hypertension, are not effective. Digoxin is effective only if patients have concomitant Left ventricle dysfunction, caution is required because patients with COPD are sensitive to digoxins effects.
Phlebotomy during hypoxic cor pulmonale has been suggested, but the benefits of decreasing blood viscosity are not likely to offset the harm of reducing O2-carrying capacity unless significant polycythemia is present.
For patients with chronic cor pulmonale, long –term anticoagulants reduce risk of venous thromboembolism
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