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ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara , Nepal

Cor pulmonale. ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara , Nepal.

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ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara , Nepal

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  1. Cor pulmonale ALOK SINHA Department of Medicine Manipal College of Medical Sciences Pokhara, Nepal

  2. . Cor pulmonale is defined as an alteration in the structure and function of the right ventricle caused by a primary disorder of the respiratory system – lung parenchyma, lung vasculature or thoracic cage Right sided heart disease secondary to lung disease Pulmonary hypertension is the common link between lung dysfunction and the heart in cor pulmonale

  3. Pathophysiology 1.Pulmonary vasoconstriction due to a.Hypoxia b.Blood acidemia 2. Obliteration of the pulmonary vascular bed secondary to lung disorders – a. emphysema b. pulmonary thrombo embolism c. interstitial lung disease

  4. 3. increased blood viscosity secondary to blood disorders • polycythemia vera • sickle cell disease • macroglobulinemia 4. idiopathic primary pulmonary hypertension

  5. Pul art pressure – dilatation of R V – reduced C O & septal displacement-- decrease L.V. volume – decresed coronary blood to R V – further detoriation of R V function Septum pushed to left Reversed Bernmeim’s effect

  6. patient with acute pulmonary hypertension due to pulmonary embolism After clot lysis

  7. Acute cor pulmonale a. massive pulmonary embolism (more common) b. acute respiratory distress syndrome (ARDS). is associated with R V dilatation

  8. Chronic cor pulmonale • C O P D > 50% of cases

  9. Disorders with primary involvement of pulmonary vasculature and circulation • Repeated pulmonary emboli • Pulmonary vasculitis • Pulmonary veno-occlusive disease • Sickle cell disease • High altitude disease with pulmonary vasoconstriction • Primary pulmonary hypertension

  10. Disorders with secondary involvement of pulmonary vasculature and circulation • Parenchymal lung diseases • Chronic obstructive pulmonary diseases • interstitial lung diseases • Neuromuscular disorders • myasthenia gravis • Poliomyelitis • amyotrophic lateral sclerosis • Obstructive and central sleep apnea • Thoracic deformities • Kyphoscoliosis • Ankylosing spondylitis

  11. CLINICALFEATURES

  12. Clinical manifestations of cor pulmonale nonspecific symptoms subtle in early stages of the disease mistakenly attributed to underlying pulmonary pathology which are: • Easy fatigability • Tachypnea • Exertional dyspnea • Cough Followed by

  13. 1. Anginal chest pain • Right ventricular ischemia (does not respond to nitrates) • Rt. coronary artery stretching in dilated A-V groove following RVH 2. Hemoptysis because of rupture of a dilated or atherosclerotic pulmonary artery

  14. 3. A variety of neurologic symptoms may be seen due to decreased cardiac output and hypoxemia • impaired cognitive & higher mental functions

  15. 4. Rarely hoarseness due to compression of the left recurrent laryngeal nerve by a dilated pulmonary artery 5. In advanced stages, passive hepatic congestion secondary to severe right ventricular failure lead to • anorexia • right upper quadrant abdominal discomfort • jaundice

  16. 6. Syncope with exertion • seen in severe disease • reflects a relative inability to increase cardiac output during exercise with a subsequent drop in the systemic arterial pressure 7. Peripheral edema

  17. Physical findings

  18. may reflect a. The underlying lung disease b. pulmonary hypertension c. RVH d. RV failure

  19. On inspection 1.An increase in chest diameter 2.Laboured respiratory efforts with retractions of chest wall 3.distended neck veins with prominent “a” or giant “v” waves 4.cyanosis may be seen

  20. RVH - characterized by • Epigastric pulsation • left parasternal heave • Apex beat: in 5th ICS outside MCL diffuse, ill suatained • + Hepatojugular reflex and pulsatile liver are signs of RV failure with systemic venous congestion • On percussion, hyper resonance of the lungs may be a sign of underlying COPD • ascites seen in severe disease

  21. On auscultation of the chest wheezes & crackles: signs of underlying lung disease in early stages 1. Splitting of the S2 2. Loud P2

  22. in advanced disease 1. sharp ejection click (single or multiple) over the pulmonary artery 2. Followed by ejection systolic murmur 3. Latter on: diastolic pulmonary regurgitation murmur (Graham steel) 4. may be S3 &/or S4 5. systolic murmur of tricuspid regurgitation

  23. DIFFERENTIAL DIAGNOSIS • Congestive (biventricular) heart failure • Primary pulmonic stenosis • Primary pulmonary hypertension • Right-sided heart failure due to congenital heart diseases • Right heart failure due to right ventricular infarction

  24. INVESTIGATIONS

  25. Routine investigation: • Hematocrit • > 50 polycythemia • > 60 – indication for phlebotomy

  26. To confirm diagnosis • E C G • X ray chest • Echocardiography • Right heart catheterization

  27. E C G in Cor pulomale

  28. Electrocardiography (ECG) RVH or RV strain a. right axis deviation b. R/S amplitude ratio in V1 greater than 1 R/S amplitude ratio in V6 less than 1 c. P-pulmonale -increase in P wave amplitude in leads 2, 3, and aVF

  29. d. incomplete or complete right bundle branch block (RBB), especially if pulmonary embolism is the underlying etiology e. low-voltage QRS because of underlying COPD with hyperinflation and increased AP diameter of the chest.

  30. Chest roentgenography • enlargement of the central pulmonary arteries with oligemic peripheral lung fields- per. pruning • right descending pulmonary artery > 16 mm • left pulmonary artery >18 mm in diameter • R V H

  31. Elevated brain natriuretic peptide (BNP) level • Earliest evidence of CCF a natural mechanism to compensate for elevated pulmonary hypertension and right heart failure by a. promoting diuresis and natriuresis, b. vasodilating systemic and pulmonary vessels

  32. Arterial blood gas tests provide important information about the level of oxygenation and type of acid-base disorder

  33. To know the etiology • P F T to confirm underlying lung disease • To exclude pulmonary thromboembolism • Ventilation/perfusion (V/Q) scan or CT chest • Hypercoagulability states evaluated by levels of • proteins C and S • antithrombin III • factor V Leiden • antinuclear antibody (ANA) level for collagen vascular disease such as scleroderma • serum alpha1-antitrypsin

  34. MANAGEMENT

  35. Oxygen therapy • Diuretics • Vasodilators • Digitalis • Anticoagulation therapy are all different modalities used in the long-term management of Chronic cor pulmonale

  36. long-term oxygen therapy can be considered even if • PaO2 is greater than 55 mm Hg or • O2 saturation is greater than 88%. • ( because of vasodilator effect on pulmonary arteries)

  37. DIURETICS • Right ventricular filling volume markedly elevated • Diuretics may result in improvement of function of both the right and left ventricles adverse effects. a. Excessive volume depletion can lead to a decline in cardiac output b. hypokalemic metabolic alkalosis lead to cardiac arrhythmia Diuretics needs to be used with caution

  38. Vasodilator drugs In long-term management of chronic cor pulmonale have modest results 1.Calcium channel blockers • oral sustained-release nifedipine • diltiazem 2.beta blockers 3.Nitrates 4.angiotensin-converting enzyme (ACE) inhibitors • not routinely used. A trial of vasodilator therapy considered in patients with COPD with disproportionately high pulmonary blood pressure – more than 40 mm Hg

  39. NEWER VASODILATORS • endothelin receptor antagonist • (Bosentan) • prostacyclin PGI 2 analogues • Epoprostenol -i.v. • iloprost - M D I THEY HAVE SHOWN A PROMISING EFFECT IN REDUCING THE PULMONARY HYPERTENSION

  40. CARDIAC GLYCOSIDES NOT ROUTINELY INDICATED • Beneficial effect not as obvious as in LVF • modest effect of digitalis on failing rightventricle in chronic cor pulmonale • Must be used cautiously • should not be used during the acute phases of respiratory insufficiency • Patients with hypoxemia or acidosis are at increased risk of developing arrhythmias

  41. Theophylline • bronchodilatory effect • reduce pulmonary vascular resistance and pulmonary arterial pressures • weak inotropic effect and thus may improve right and left ventricular ejection • Strenghtens diaphragm • Stimulates the respiratory centre

  42. Phlebotomy • Mean Pul art press and PVR decrease in polycythemic patients after phlebotomy (hematocrit of >60 or 65) • The reduction of markedly elevated hematocrit level to about 50% by phlebotomy leads to 1. Reduction of blood viscosity 2. Reduction in PVR and pulmonary art pr 3. Improve gas exchange & increases exercise tolerance

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