Cor Pulmonale

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Chapter 23 Cor Pulmonale

3 What is the pathophysiology of right ventricular failure?

Under normal conditions, the pulmonary circulation is a low-resistance circuit, and the right ventricle generates the same stroke volume as the left ventricle with end-systolic pressures that are just 20% to 25% of those in the left ventricle. The low pressure within the thin free wall of the right ventricle also allows myocardial perfusion to occur both in systole and in diastole. Because of its structure, similar to that of veins rather than arteries, the right ventricle accommodates well additional volume but not higher pressure. When pressure overload occurs acutely, the right ventricle can only dilate and, if the pressure is sufficiently elevated, fail. Chronically, in response to increased systolic workload the free wall of the right ventricle hypertrophies and becomes similar to the left ventricle. Laplace’s law helps explaining the evolution from hypertrophy to dilatation and failure (Fig. 23-1): In a thin-wall chamber, an increase in intraluminal pressure increases wall stress unless thickness increases or the internal radius decreases. As the right ventricle hypertrophies, myocardial perfusion becomes limited to diastole, making its myocardium more susceptible to ischemia, and thus leading to dilatation and failure.

image

Figure 23-1 Diagrammatic cross-section of the right (RV) and left ventricular (LV) cavities. Left, Normal state. The right ventricle has a thin free wall and a characteristic crescentlike shape. Right, Right ventricular hypertrophy from pressure overload. The right ventricle assumes a spherical shape, thickened free wall, and an overall greater area than the left ventricle, which is normally the larger of the two ventricles.

(From Voelkel NF, Quaife RA, Leinwand LA, et al. Right ventricular function and failure. Report of a National Heart, Lung, and Blood Institute working group on cellular and molecular mechanisms of right heart failure. Circulation 114:1883-1891, 2006. Copyright 2006 American Heart Association.)

4 What are the causes of cor pulmonale?

Any process that results in pulmonary hypertension can cause cor pulmonale. Pulmonary hypertension is defined as mean PA pressures > 20 mm Hg at rest or > 30 mm Hg with exercise. The most frequent cause of pulmonary hypertension and cor pulmonale is COPD, due to chronic hypoxemia. In COPD the degree of hypertension is generally moderate, and oxygen supplementation may be effective in relieving some of the pressure load to the right ventricle and delaying failure. Additional causes of cor pulmonale include chronic pulmonary thromboembolic disease, left-sided cardiac abnormalities, untreated obstructive sleep apnea (OSA), interstitial lung diseases, and primary pulmonary hypertension. A comprehensive classification of the diseases of the lung associated with PA hypertension and cor pulmonale is shown in Table 23-1.

Table 23-1 Classification of cor pulmonale according to causative factor

Category Example
Diseases affecting the air passages of the lung and alveoli COPD
Cystic fibrosis
Infiltrative or granulomatous defects
Idiopathic pulmonary fibrosis
Sarcoidosis
Pneumoconiosis
Scleroderma
Mixed connective tissue disease
Systemic lupus erythematosus
Rheumatoid arthritis
Polymyositis
Eosinophilic granulomatosis
Radiation
Malignant infiltration
Diseases affecting thoracic cage movement Kyphoscoliosis
Thoracoplasty
Neuromuscular weakness
Sleep apnea syndrome
Idiopathic hypoventilation
Diseases affecting the pulmonary vasculature Primary disease of the arterial wall
Primary pulmonary hypertension
Pulmonary arteritis
Toxin-induced pulmonary hypertension
Chronic liver disease
Peripheral pulmonary stenosis
Thrombotic disorders Sickle cell diseases
Pulmonary microthrombi
Embolic disorders Thromboembolism
Tumor embolism
Other embolic processes (amniotic fluid, air, fat)
Schistosomiasis and other parasitic infections
Pressure on PAs Mediastinal tumors
Aneurysms
Granulomata
Fibrosis

Modified from Rubin LJ, ed: Pulmonary Heart Disease. Boston, 1984, Martinus Nijhoff, p 4.