Yusra Pintaningrum

SMF Kardiologi & Kedokteran Vaskular

Fakultas Kedokteran Universitas Mataram – RSUP NTB
 Corpulmonale is the alteration of right
ventricular structure or function that is
due to pulmonary hypertension caused
by diseases affecting the lung or its
vasculature
 Pulmonary vasoconstriction (secondary
to alveolar hypoxia or blood acidosis)
 Anatomic reduction of the pulmonary
vascular bed (emphysema, pulmonary
emboli, etc)
 Increased blood viscosity (polycythemia,
sickle-cell disease, etc)
 Increased pulmonary blood flow.
 The most frequent cause of cor
pulmonale is chronic obstructive
pulmonary disease (COPD) due to
chronic bronchitis or emphysema
 In patients with COPD, an increased
incidence of right ventricular
involvement may correlate with
increasing severity of lung dysfunction
1. Fatigue, lethargy, and exertional syncope 
an inability to increase cardiac output
during stress because of vascular
obstruction in the pulmonary arterioles.
2. Typical exertional angina  primary or
secondary pulmonary hypertension
3. cough and hemoptysis : Less common
symptoms
4. Hoarseness  compression of the left
recurrent laryngeal nerve by a dilated main
pulmonary artery.
1. increased intensity of the pulmonic component of the
second heart sound, which may even become
palpable.
2. The second heart sound may also be narrowly split
3.a systolic ejection murmur and, in more severe
disease, a diastolic pulmonary regurgitation murmur.
4. Right ventricular failure leads to systemic venous
hypertension.  elevated jugular venous pressure
with a prominent V wave, a right ventricular third
heart sound, and a highpitched tricuspid regurgitant
murmur.
5. Edema  right heart failure
 The pathogenesis of edema in such
patients is not well understood
 Edema seems to occur primarily in
patients with hypercapnia, suggesting
that the high PCO2 rather than cardiac
dysfunction may be responsible for the
sodium retention in cor pulmonale
 Chest radiography
 Electrocardiography
 Two dimensional and Doppler
echocardiography (which can provide an
indirect measurement of pulmonary artery
pressure when tricuspid regurgitation is
present)
 Pulmonary function tests
 Radionuclide ventriculography
 Magnetic resonance imagingRight heart
catheterization
 Lung biopsy
Right axis deviation and R/S ratio greater than 1 in lead V1.
(RVH)
Incomplete or complete right bundle branch block.
 Increased P wave amplitude in lead II (P pulmonale) due to right atrial
enlargement
 Improve oxygenation (with hypoxemic
patients) or right ventricular contractility,
as well as attempts to decrease
pulmonary vascular resistance and
vasoconstriction (primarily via
vasodilators).
1. Oxygen therapy — Long-term oxygen therapy improves the
survival of hypoxemic patients with COPD
 relieves pulmonary vasoconstriction, thereby decreasing
pulmonary vascular resistance the right ventricle increases
stroke volume and cardiac output.
Renal vasoconstriction also may be relieved,  an increase in
urinary sodium excretion .
 improves arterial oxygen content delivery to the heart, brain,
and other vital organs.

2. Diuretics — If right ventricular filling volume is markedly

elevated, diuretic therapy might improve the function of both
right and left ventricles
3. Digoxin — Except in cases of
coexistent left ventricular failure,
clinical studies do not support the use
of digitalis in patients with cor
pulmonale.
4. Vasodilators — Several vasodilator
agents (including hydralazine,
nitrates, nifedipine, verapamil, and
ACE inhibitors)
 to ameliorate pulmonary hypertension.
5. Theophylline and the
sympathomimetic amines —
(terbutaline, etc)
Improve myocardial contractility
 Provide some degree of pulmonary
vasodilation
 Enhance diaphragm endurance
6. Almitrine —to improve arterial PO2
in patients with COPD Phlebotomy —
In patients with severe polycythemia
(hematocrit above 55 percent),
7. phlebotomy (to achieve a
 hematocrit of about 50 percent) 
decrease in mean pulmonary artery
pressure and pulmonary vascular
 associated with pulmonary hypertension
 In COPD,  pulmonary hypertension and
peripheral edema  a poor prognosis.
 peripheral edema : five year survival of
only approximately 30 percent
 pulmonary vascular resistance > 550
dynes-sec/cm rarely survive for more
than 3 years