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Cor Pulmonale

Cor Pulmonale

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Cor Pulmonale

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  1. Cor Pulmonale Dr. GerrardUy

  2. Definition • Cor Pulmonale • pulmonary heart disease • dilation and hypertrophy of the right ventricle (RV) in response to diseases of the pulmonary vasculature and/or lung parenchyma. • excluded congenital heart disease and those diseases in which the right heart fails secondary to dysfunction of the left side of the heart

  3. Etiology and Epidemiology • develops in response to acute or chronic changes in the pulmonary vasculature • Changes that are sufficient to cause pulmonary hypertension • Once patients with chronic pulmonary or pulmonary vascular disease develop cor pulmonale, their prognosis worsens

  4. Pathophysiology • pulmonary hypertension that is sufficient to lead to RV dilation, with or without the development of concomitant RV hypertrophy • Right ventricle: thin walled, compliant • Better suited for high volumes than high pressure • Sustained pressure overload (pulm HPN) and increased vascular resistance causes RV to fail

  5. Pathophysiology • Acute Cor Pulmonale • occurs after a sudden and severe stimulus with RV dilatation and failure but no RV hypertrophy • e.g massive pulmonary embolus • Chronic Cor pulmonale • more slowly evolving and slowly progressive pulmonary hypertension that leads to RV dilation and hypertrophy

  6. Factors that determine severity • hypoxia secondary to alterations in gas exchange • Hypercapnia • Acidosis • alterations in RV volume overload that are affected by: • exercise, heart rate, polycythemia, or increased salt and retention because of a fall in cardiac output

  7. Clinical presentation • Symptoms: • Dyspnea, the most common symptom • usually the result of the increased work of breathing secondary to changes in elastic recoil of the lung (fibrosing lung diseases) or altered respiratory mechanics • Orthopnea and paroxysmal nocturnal dyspnea are rarely symptoms of isolated right HF • reflect the increased work of breathing in the supine position that results from compromised excursion of the diaphragm

  8. Clinical presentation • Symptoms: • Tussive or effort-related syncope • because of the inability of the RV to deliver blood adequately to the left side of the heart • Abdominal pain and ascites • Due to right heart failure • Lower extremity edema • secondary to neurohormonal activation, elevated RV filling pressures, or increased levels of carbon dioxide and hypoxia,

  9. Clinical presentation • Signs • tachypnea • elevated jugular venous pressures • hepatomegaly • lower-extremity edema • Cyanosis is a late finding

  10. Diagnosis • ECG • P pulmonale, right axis deviation, and RV hypertrophy • Chest X Ray • enlargement of the main pulmonary artery, hilar vessels, and the descending right pulmonary artery • Spiral CT • acute thromboembolic disease

  11. Diagnosis • 2D echo • measuring RV thickness and chamber dimensions • Doppler echocardiography • assess pulmonary artery pressures • MRI • assessing RV structure and function, particularly in patients who are difficult to image with 2-D echocardiography because of severe lung disease

  12. Treatment • Primary goal: target the underlying pulmonary disease • decrease in pulmonary vascular resistance and relieve the pressure overload on the RV • General principles: • decreasing the work of breathing using noninvasive mechanical ventilation, bronchodilation, and steroids • treating any underlying infection • Adequate oxygenation (oxygen saturation 90–92%) will also decrease pulmonary vascular resistance and reduce the demands on the RV • Diuretics