COR PULMONALE

COR PULMONALE

Cor pulmonale is right ventricular enlargement (hypertrophy and/or dilation) that may progress to right heart failure. It is caused by diseases that induce pulmonary hypertension.

Cor pulmonale can be caused by several types of lung disease including COPD, restrictive lung disease, and respiratory insufficiency of central origin (obesity-hypoventilation syndrome).

It can also result from idiopathic pulmonary artery hypertension, that is, the pulmonary hypertension that occurs in the absence of left-sided heart disease, myocardial disease, congenital heart disease, or any other clinically significant respiratory, connective tissue, or chronic thromboembolic disease.

The most common cause of cor pulmonale is COPD.

Pathophysiology

The main pathophysiologic determinant of cor pulmonale is pulmonary hypertension. By various mechanisms, chronic lung disease induces an increase in pulmonary vascular resistance. Chronic alveolar hypoxia (PaO2 < 55 mm Hg) is the most important factor in this process. Acute hypoxia, such as seen in exacerbations of COPD or during sleep in patients with obesity-hypoventilation syndrome, causes pulmonary vasoconstriction.

Due to pulmonary hypertension, the right ventricle has an increased workload and right ventricular hypertrophy develops. Over time, right ventricular dysfunction occurs and eventually right ventricular failure is present.

Signs and Symptoms

Clinical manifestations of cor pulmonale may be obscured by co-existing lung disease. Clinical signs occur late in the course of the disease, and the most prominent of these is peripheral edema. As right ventricular function deteriorates, dyspnea increases and effort-related syncope can occur. Accentuation of the pulmonic component of the second heart sound, a diastolic murmur due to incompetence of the pulmonic valve, and a systolic murmur due to tricuspid regurgitation connote severe pulmonary hypertension. Evidence of overt right ventricular failure consists of increased jugular venous pressure and hepatosplenomegaly.

Diagnosis

The ECG may show signs of right atrial and right ventricular hypertrophy. Right atrial hypertrophy is suggested by peaked P waves in leads II, III, and aVF (“p” pulmonale). Right axis deviation and a partial or complete right bundle branch block are often seen with right ventricular hypertrophy. A normal ECG, however, does not exclude the presence of pulmonary hypertension.

Radiographic signs of cor pulmonale include an increase in width of the right pulmonary artery and a decrease in pulmonary vascular markings in the lung periphery. On the lateral projection of a chest radiograph, right ventricular enlargement is reflected by a decrease in the retrosternal space. However, this is a late sign.

Echocardiography can be a very useful diagnostic tool. It can provide numeric estimates of pulmonary artery pressure, assessment of the size and function of the right atrium and ventricle, and evaluation of the presence and severity of tricuspid or pulmonic regurgitation. Transthoracic echocardiography is often difficult to perform in patients with COPD because the hyperinflated lungs impair transmission of the ultrasound waves.

Treatment

Treatment of cor pulmonale is geared to reducing the workload of the right ventricle by decreasing pulmonary vascular resistance and pulmonary artery pressure.

Supplemental oxygen

Diuretics and digitalis

When cor pulmonale is progressive despite maximum medical therapy, transplantation of one or both lungs or a heart-lung transplant will provide dramatic relief of cardiorespiratory failure.

may be used to treat right heart failure that does not respond to correction of arterial blood gases. Diuretics must be administered very carefully because diuretic-induced metabolic alkalosis, which encourages CO2 retention, may aggravate ventilatory insufficiency by depressing the effectiveness of carbon dioxide as a stimulus to breathing. Diuresis can also increase blood viscosity and myocardial work. Digitalis can be used for treatment of atrial fibrillation, but it must be used very cautiously because the risk of digitalis toxicity is increased in the presence of hypoxemia, acidosis, and electrolyte imbalances to maintain the PaO2 above 60 mm Hg (SpO2 > 90%) is useful in both the acute and long-term treatment of right heart failure. Long-term oxygen therapy decreases the mortality of cor pulmonale and improves cognitive function and quality of life.Long-standing chronic hypoxia promotes pulmonary vasculature remodeling and an increase in pulmonary vascular resistance. Even mild hypoxemia may result in vascular remodeling, so it appears that other factors are also involved in the development of cor pulmonale.

MANAGEMENT OF ANESTHESIA

Preoperative Management

Preoperative preparation of patients with cor pulmonale due to chronic lung disease is directed toward (1) eliminating and controlling acute and chronic pulmonary infection, (2) reversing bronchospasm, (3) improving clearance of airway secretions, (4) expanding collapsed or poorly ventilated alveoli, (5) hydration, and (6) correcting any electrolyte imbalances.

Preoperative measurement of arterial blood gases will provide guidelines for perioperative management.

Antibiotic endocarditis prophylaxis should be considered for patients with valvular disease (tricuspid or pulmonic insufficiency).

Intraoperative Management

Induction of general anesthesia can be accomplished using any available method or drug. Adequate depth of anesthesia should be present before tracheal intubation because this stimulus can elicit reflex bronchospasm in lightly anesthetized patients.

Anesthesia is typically maintained with a volatile anesthetic combined with other drugs. Volatile anesthetics are effective bronchodilators.

N2O should be used cautiously as it increases pulmonary vascular resistance.

Large doses of opioids should be avoided because they can contribute to prolonged ventilatory depression in the postoperative period.

Positive-pressure ventilation improves oxygenation, presumably due to better ventilation-to-perfusion matching. Humidification of inhaled gases helps maintain hydration, liquefaction of secretions, and mucociliary function.

Intraoperative monitoring of patients with cor pulmonale is influenced by the invasiveness of the operation. An intra-arterial catheter permits frequent determination of arterial blood gases and subsequent adjustments in the inspired concentration of oxygen. Central venous catheters or pulmonary artery catheters may be useful depending on the complexity of the surgery. A trend value of right atrial pressure can provide some information about right ventricular function. Direct measurement of pulmonary artery pressure helps determine the time to treat pulmonary hypertension and the response to treatment. Transesophageal echocardiography is an alternative method for monitoring right ventricular function and fluid status. However, as noted previously, the need for trained personnel and expensive equipment prevents this monitoring modality from being universally available.

Regional anesthetic techniques can be used in appropriate situations in patients with cor pulmonale, but regional anesthesia is best avoided for operations that require high sensory and motor levels of anesthesia. Loss of function of the accessory muscles of respiration may be very deleterious in patients with pulmonary disease. In addition, any decrease in systemic vascular resistance in the presence of fixed pulmonary hypertension can produce a very significant degree of systemic hypotension.

Postoperative Management

The respiratory and cardiovascular status of a patient with cor pulmonale must be vigilantly monitored in the postoperative period and any factors that exacerbate pulmonary hypertension, such as hypoxia and hypercarbia, must be avoided. Oxygen therapy should be maintained as needed.

Muscle relaxants associated with histamine release should also be avoided because of the adverse effect of histamine on airway resistance and pulmonary vascular resistance.