An Overview

August, 1999

Jerry Allison
BCCM Year Level II

Dr. Violeta Abear and Dr. Reynaldo O. Joson

Legazpi City, Albay, Philippines

No one can discount, cor pulmonale is a health problem. It is a sensitive issue as well for it correlates well with COPD and that a root cause is smoking. A present and impending danger to the health of today's society. Before getting any further, let us first set its definition:

Cor Pulmonale refers to disease of the right ventricle that results from pulmonary hypertension secondary to a pulmonary disease. It is characterized by right ventricular dilatation, hypertrophy, and, eventually, failure.

For its Etiology:

Cor Pulmonale can occur in any condition that causes pulmonary hypertension. Acute cor pulmonale is most often due to extensive pulmonary embolization. Chronic cor pulmonale occurs most often in patients with COPD; stress in these patients may induce acute but reversible exacerbations of the cor pulmonale.

Indeed, in this occasion we are going to dwell more on the latter problem. It best suits the theme as both cardio and pulmo problems are correlated. It is also a pertinent and sensitive issue of today as COPD is characterized by chronic bronchitis and emphysema which are mostly blamed on the industrialized vice of smoking. A malady inherited since the era of Christopher Columbus. Smoking is no longer just an individualized problem for it has become a social issue as well, that, in reference to the proposition on passive smoking.

The pathophysiology of cor pulmonale is divided to two:

1. Mechanism of pulmonary hypertension , under this is

a. Hypoxia and acidosis - The vasoconstrictive effect of hypoxia is a potent stimulus for hypertension. This mechanism may be augmented by acidosis which has also an effect on the pulmonary vasculature.

b. Obliteration or obstruction of the pulmonary vascular bed - Substantial loss of the pulmonary vascular bed can result from emphysema.

2. Development of cor pulmonale - this is as follows:

a. Although acute hypoxia elicits approximately the same pressor response, each bout of pulmonary hypertension predisposes the patient to progressively higher levels of residual hypertension after recovery.

b. The resultant sustained pulmonary hypertension causes smooth muscle hypertrophy in the pulmonary arteries and then in the peripheral pulmonary vessels. The pulmonary vascular bed becomes more rigid and less reactive to changes in cardiac output.

c. This, in turn, affects the performance of the right ventricle, causing right ventricular hypertrophy and right-sided heart failure (i.e., cor pulmonale).

d. No reliable evidence supports the claim that cor pulmonale causes left ventricular failure.

The clinical features and diagnosis consist of:

1. Early in the course of the disease, patients may demonstrate pulmonary hypertension only in association with exercise.

2. The physical findings of peripheral edema, liver enlargement, and neck vein engorgement usually are associated with cor pulmonale but are nonspecific and do not contribute to the diagnosis except in advance disease.

3. An oxygen saturation of less than 85% usually causes pulmonary arterial pressure to increase above 25 mm Hg. Acidosis and exercise cause further elevations.

4. Roentgenographic findings, such as widening of the pulmonary arteries, are insensitive and unreliable indicators of pulmonary arterial pressure.

5. Electrocardiography shows the appearance of flat or inverted T waves in the right ventricular precordial leads, right axis deviation of greater than 30 in the mean electrical axis of the QRS, transient S-T depression of leads II, III, and aVF, and transient right bundle branch block.

6. Cardiac catheterization provides definitive diagnosis but rarely is necessary

For its therapy -- Prevention and treatment of cor pulmonale are focused on correction of hypoxia and acidosis, control of hypervolemia, and improvement of right ventricular failure. Among such is

1. Supplemental oxygen - The initial steps in the treatment of cor pulmonale are to administer supplemental oxygen and improve the patient's ventilatory status by treating the underlying lung disease. Because many patients are oxygen-sensitive, it is imperative not to give high-flow oxygen but to give just enough to keep the saturation at approximately 90%

2. Diuresis - Fluid retention is common and can compromise pulmonary gas exchange and heighten pulmonary vascular resistance. Improved oxygenation and salt restriction may control the cor pulmonale , but diuretics frequently are necessary

3. Phlebotomy - provides a short-term effect and may be useful when hematocrit is greater than 55%-60%

4. Digitalis - has no benefit unless there is left ventricular failure

5. Vasodilators - have been used, especially in cor pulmonale associated with obliterative vascular disease or fibrotic lung disease; however, the value of these agents is unknown.

By far that discusses the definition until the treatment of the disease. A person would really think twice before lighting that next cigarette as our case would later justify. The statistics show it all. Approximately 20% of hospital admissions for heart failure are caused by right ventricular failure associated with cor pulmonale. More than half of the patients with COPD have cor pulmonale, and this condition constitutes a good percentage of all adult heart diseases. Indeed, when we go out and preach our vocation, smoking negation must be a priority.

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