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Department of Medicine Manipal College of Medical Sciences

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

2 Right sided heart disease secondary to lung disease
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 decrease L.V. volume – decresed coronary
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


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 because of rupture of a dilated or atherosclerotic pulmonary artery
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 the left recurrent laryngeal nerve by a dilated pulmonary artery
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 2. Followed by ejection systolic murmur
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

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


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


29 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

30 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.

31 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



34 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

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

36 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


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

39 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)

40 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

41 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

42 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

Beneficial effect not as obvious as in LVF modest effect of digitalis on failing right ventricle 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

44 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

45 1. Reduction of blood viscosity
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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