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Cor pulmonale.pptx

  1. COR PULMONALE SUBMITTED BY Anmol Prashar Bsc.Nursing 4th year (Intern) Roll no 6
  2. CONTENTS  Definition  Subtypes of Cor Pulmonale  Mortality Associated with Cor Pulmonale  Etiology  Clinical Presentation  Pathophysiology  Diagnosis & Diagnostic Tests
  3. Medical Management Nursing Management Complications Health Education References
  4. DEFINITION  Cor pulmonale is a latin word means "pulmonary heart“  The world Health Organizaton in 1963 adopted this definition of cor pulmonale :" hypertrophy of the right ventricle resulting from diseases affecting the function and/or structure of the lungs, except when these pulmonary alterations are the result of diseases that primarily affect the left side of the heart , as congenital heart diseases.”
  5.  Cor pulmonale is a disease of the right ventricle characterized by hypertrophy and dilation that results from diseases directly affecting the lung parenchyma or lung vasculature. Of note ,right heart failure need not be present in cor pulmonale
  6. SUBTYPES OF COR PULMONALE  Cor pulmonale can be either acute or chronic in development.  Acute cor pulmonale is the result of a sudden increase in right ventricular pressure, as seen in massive pulmonary embolism or acute respiratory distress syndrome.  Chronic cor pulmonale can be further characterized by hypoxic or vascular obliterans pathophysiology.  The most common disease process associated with hypoxic subtype is chronic obstructive pulmonary disease (COPD).The most common process associated with obliterans subtype is pulmonary thromboembolic disease.
  7. The Mortality Associated with Cor Pulmonale  Patients with COPD have a 5-year survival rate, whereas patients with COPD and pulmonary artery pressure in excessof 25 mmHg have a survival of only 36%.  The 5-year survival rate for patients with COPD who develop preipheral edema is approximately 30%.  It is unclear whether pulmonary artery hypertension is the cause of death or whether it is a marker of increased motality.
  8. ETIOLOGY  Conditions that restrict or compromise ventilatory function, leading to hypoxemia or acidosis e.g. deformities of the thoracic cage, massive obesity.  Conditions that reduce the pulmonary vascular bed e.g. primary idiopathic pulmonary arterial hypertension, pulmonary embolus.  Disorders involving nervous system, respiratory muscles, chest wall , and pulmonary arterial tree may also be responsible for cor pulmonale.
  9. CLINICAL PRESENTATION  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 nocturnal dyspnea are rare symptoms of right HF, reflect the increased work of breathing in the supine position that results from compromised excursion of the diaphragm.  Tussive or effort-related syncopebecause of the inability of the RV to deliver blood adequately to the left side of the heart
  10.  Abdominal pain and ascites  Lower extremity edema  Shortness of breathwheezing  Tachypnea  Elevated jugular venous pressures  Hepatomegaly  Lower-extremity edema.  Cyanosis is a late finding
  11.  Chronic wet cough  Chest discomfort  Distention of neck veins
  13. PATHOPHYSIOLOGY  Hypoxic pulmonary vasoconstriction and arterial occlusion are the major causes of pulmonary hypertension.  Both produce reduced blood flow with increased vascular resistance.  Acute hypoxic pulmonary vaso —constriction optimizes ventilation — perfusion relationships when regional ventilation demands in the lung are not met.
  14.  However, chronic hypoxemia leading to chronic vasoconstriction produces smooth ms proliferation in small pulmonary arteries.  Decreased luminal cross sectional diameter leads to increased resistance and increased pulmonary artery pressure.  These architectural changes in pulmonary arteries may promote platelet aggregation and activation.  This leads to thrombi formation that further increases pulmonary vascular resistance and pulmonary hypertension.
  15.  Hypoxemia produces changes in vascular mediators such as Nitric Oxide, Endothelinl (ET 1) and platelet derived growth factors (PDGf A and B).  Nitric oxide is a vasodilator; hypoxemia reduces endothelial cell production of nitric oxide and results in impaired smooth ms relaxation.  Hypoxemia increases ETI production and PDGF A and B  ETI is apotent vasoconstrictor, and PDGF A and B results in pulmonary vascular remodeling.  All causes increased pulmonary artery resistance and causes pulmonary hypertension.
  16. DIAGNOSIS  History Collection  Physical Examination-increase in chest diameter, distended neck veins and cyanosis may be seen.  On auscultation of the lungs, wheeæs ard crackes may be heard  On percussion, hyper-resonance of the lungs may a sign of underlying COPD.  Pulmonary function tests  ABG analysis- Reveals decreased Pa02 & pH and Increased  Hematocrit: It is done to rule out polycythemia.
  17. DIAGNOSTIC TESTS Electrocardiography criteria of right ventricular hypertrophy  Right axis deviation.  P Pulmonale (large P wave ) in the inferior and anterior leads " right atrial enlargement  Right bundle branch block.  Right precordial T-wave inversions.  Delayed interinsicoid deflection of right precordial leads.
  18.  QR pattern in lead VI or V3R.  An R wave in VI or V3R.  An R/S ratio > 1 in VI or <1 in or /6.
  19. Chest Radiograph:  Enlarged pulmonary artery.  Enlarged right ventricle.  Distended azygous or other central vein.  Westermark sign "oligemia of lung lobe or entire lung  Hampton's hump "wedge shaped opacity  COPD signs as anterior-posterior diameter , flattening of diaphragm , honeycombing and hyperlucency.
  20. sensitivity of 84 % and specificity of 75% for the diagnosis of pulmonary hypertension.  There are data to suggest that an enlarged main pulmonary artery diameter and ratio of segmental pulmonary artery diameter to corresponding bronchus diameter > 1 increases the specificity of a pulmonary hypertension diagnosis.
  21.  An adequate examination is reported in up to 65 — 80 % of patients with COPD because of the technical difficulty associated with hyperinflation.  A better examination can be obtained with transesophageal echocardiography.  Doppler echocardiography has aided in the assessment of pulmonary artery pressure by measuring the flow of regurgitant blood across the tricuspid valave or by measuring right vetricular ejection flow.
  22. Right heart catheterization:  This is the gold standard for thorough evaluation and diagnosis of pulmonary hypertension. Radionuclide angiography (gated blood pool scan):  This test is most useful for measuring right and left ventricular ejection fraction. Magnetic resonance imaging:  This non invasive technique yields highly accurate dimensions of the right ventricle.
  23. MEDICAL MANAGEMENT Non pharmacological treatment:  Oxygen therapy  Phlebotomy  Non invasive positive pressure ventilation (NIPPV) Pharmacological treatment:  Diuretics  Anticoagulation  Vasodilators
  24.  This is considered a mainstay of treatment for patients with COPD.  Large controlled trials demonstrate that long term administration of oxygen improves survival in hypoxemic patients with COPD.  Oxygen therapy decreases pulmonary vascular resistance by diminishing pulmonary vasoconstriction and improves right ventricular stroke volume and cardiac output
  25. Phlebotomy  In patient with pronounced polycythemia (hematocrit >60 %), phlebotomy may provide symptomatic relief  In resting patients , phlebotomy can affect a mild decrease in pulmonary artery pressure and pulmonary vascular resistance.  In general , blood viscosity has less effect than blood volume on pulmonary arterial pressure.  Phlebotomy , with a goal hematocrit of 50 %, may improve exercise tolerance in patients with polycythemic COPD.
  26. PHARMACOLOGIC Diuretics  Diuretic therapy with salt restricted diet may be needed in congestive heart failure to take care of the excessive water that the lungs share and to improve alveolar ventilation and gas exchange.  However, the use of diuretics may produce hemodynamic adverse effects, such as volume depletion, decrease venous return to the right ventricle, and decreased cardiac output.  Another complication is the production of hypokalemic metabolic alkalosis, which diminishes the c02 stimulus to the respiratory center, decreasing ventilatory drive.
  27. Anticoagulation  Chronic anticoagulation with Warfarin may provide benefit for those patients with Cor Pulmonale resulting from thromboocclusive pulmonary disease. Vasodilators  Vasodilators improve cardiac output in many patients with cor pulmonale.  However, treatment with vasodilators may be associated with adverse effects, including systemic hypotension that coronary perfusion pressure, blunting of hypoxic pulmonary vasoconstriction and circulatory collapse.
  28. Different classes of vasodilators used in Cor Pulmonale Nonspecific vasodilators:  Hydralazine increases cardiac output in patients with COPD; however, its ability to decrease pulmonary artery pressure is unpredictable.  Nitroprusside may provide benefit but also runs the risk of systemic hypotension and compromise of adequate coronary perfusion pressure.  Calcium channel blockers such as Nifedipine reduce pulmonary vascular resistance and increase cardiac output only for the short term.  Verapamil and Diltiazem have not proved effective in dilating pulmonary vasculature.
  29.  Prostaglandins decrease pulmonary artery pressure and increase right ventricular ejection fraction and cardiac output.  Aerosolized prostacyclin causes pulmonary artery vasodilatation and improves cardiac output and arterial oxyhemoglobin saturation in patients with chronic pulmonary hypertension.  3. Nitric oxide provides a real clinical scenario. It reliably decreases pulmonary vascular resistance without causing systemic hypotension and preserves or improves optimal ventilation-perfusion match. Its drawbacks are difficult administration, high cost, and a welldocumented tachyphylactic effect. Multiple studies have shown that its benefits are most significant for only 1-3 days, especially in patients with acute respiratory distress syndrome.
  30. Inotropes with vasodilatory properties:  Dobutamine is an inotropic agent with vasodilatory effect which improves right ventricular function and cardiac output, but its effect on systemic blood pressure is unpredictable.  Amrinone lowers pulmonary artery pressure and rises cardiac output and systemic blood pressure. Endothelin receptor antagonist:  Bosentan is an endothelin receptor antagonist that produces pulmonary vasodilation and attenuates ventricular remodeling and improve survival on chronic use.
  31. Role of digoxin in treatment  Cardiac output improves in about 10% of patients with primary pulmonary hypertension who receive digoxin.  This rate is similar to that in patient with left ventricular dyfunction.  Patients who receive digoxin also show a modest increase in pulmonary pressure, perhaps due to increase in cardiac output.  Clinical studies show improvement in right ventricular function only in those patients who have reduced left ventricular ejection fraction.  Recently, digoxin has fallen out of favor in the setting of left ventricular dysfunction; the trend in clinical medicine has been its continued use in rate control.
  33. Assessment  Determineif the patient has experienced orthopnea, cough, Eytigue, epigastric distress, anorexia, or weight gain Or has a history of previously diagnosed lung disorders.  Ask if the patient smokes cigarettes, noting the daily consumption and duration.Ask about the Color and quantity of the mucus the patient expectorates.  Determine the type Of dyspnea if it is related only to exertion oris continuous.  Observe if the patient has difficulty in maintaining breath while the history is taken.  Evaluate the rate, type, and quality of respirations.  Observe the patientfor dependent edema fromthe abdomen (ascites) and buttocksanddown both legs.  Inspect the patient's chest and thorax forthe general appearance and arteroposterior diameter.Look for theuse of accessory musdes in breathing.
  34. NURSING MANAGEMENT Nursing Diagnosis  Impaired tissue perfusion related to decreased cardiac contractility and expiratory airflow obstruction as evidenced by increased capillary refilling time >3 seconds  Activity intolerance related to decreased cardiac activity and laboured respirations as evidenced by difficulty in performing activities of daily living.
  35. respirations as evidenced by difficulty in performing activities of daily living  Anxiety related to breathlessness as evidenced by patient's verbalization and facial expressions  Imbalanced nutrition less than body requirement related to breathlessness as evidenced by weight loss.  Disturbed sleep pattern related to shortness of breath as evidenced by presence of dark circles around the eyes.
  36. COMPLICATIONS  Exertional syncope.  Hypoxia and significantly limited exercise tolerance.  Peripheral edema.  Peripheral venous insufficiency.  Tricuspid regurgitat ion.  Hepatic congestion and cardiac cirrhosis.  Death.
  37. HEALTH EDUCATION  Advice patient to take protein rich diet.  Educate patient regarding his disease condition.  Educate patient regarding modification in lifestyle like cessation of smoking & alcohol consunWion.Advice patient to reduce spicy & fatty foods.  Instruct patient to avoid caffeine intake which can increase pulse rate & produce angina.  Educate patient to minimize level of activities to prevent strain.  Advice patient for regular followup & care.
  38. REFERENCES  Page 26-30, 92 -154 Oxford handbook of clinical medicine 10th Edition  Fishman AP. Chronic cor pulmonale. American Review of Respiratory Disease. 1976 Oct;114(4):775-94.  Jardin F, Dubourg O, Bourdarias JP. Echocardiographic pattern of acute cor pulmonale. Chest. 1997 Jan 1;111(1):209-17.  Weitzenblum E. Chronic cor pulmonale. Heart. 2003 Feb 1;89(2):225-30.