Chapter 8

Pulmonary circulation

OUTLINE

• Pulmonary vs. systemic circulation
• Pulmonary hypertension and right heart failure
• Causes of pulmonary hypertension
• Assessment of hemodynamic status
• Swan­Ganz catheterization
• Insertion of Swan­Ganz catheter­-pressure tracings
• Hemodynamic measurements and calculations
• Pulmonary artery wedge pressure­-measurement
• Pulmonary artery wedge pressure­­what does it represent?
• Pitfalls and complications in hemodynamic monitoring
• Hemodynamic monitoring in clinical practice
  

PULMONARY VS. SYSTEMIC CIRCULATION

Historically, physiologic assessment of the pulmonary circulation has lagged behind the measurement of lung mechanics and gas exchange. Although the systemic circulation is easily accessible for evaluation (e.g., routine blood pressure measurement), the pulmonary circulation was, until recently, hidden from view. This situation changed significantly with the introduction of cardiac catheterization in the 1950's. Even so, catheterization was a highly specialized test for years and was not routinely used in pulmonary patients. With the introduction of bedside right­sided heart catheterization in 1970, the clinical study of pulmonary hemodynamics entered a new era. The bedside catheter has allowed the study of pulmonary circulation in critically ill patients and has permitted the continuous monitoring of a patient's disease and its response to therapy. The result has both enhanced the knowledge of cardiopulmonary disease and contributed directly to patient care.
A review of the normal pulmonary circulation is helpful before discussing bedside catheterization. Fig. 2­12 diagrams the systemic and pulmonary circulations; Table 8­1 outlines the paths of blood flow for each circulation and lists the major physiologic differences between the two.

PULMONARY HYPERTENSION AND RIGHT HEART FAILURE

Pulmonary hypertension is defined as a mean pulmonary artery pressure greater than 22 mm Hg. Pulmonary hypertension can occur from several physiologic causes and disease processes (Table 82); the hypertension may be transient, as in reversible conditions such as an asthma attack, or chronic, as in emphysema. In some patients, two or more causes may contribute to pulmonary hypertension (e.g., left ventricular heart failure and pulmonary emboli).

Right heart failure is a decompensated state of the right ventricle and can result from sustained or severe pulmonary hypertension of any origin. When the right ventricle is unable to pump its full cardiac output against the elevated pulmonary pressure, systemic venous pressure increases and fluid "backs up" in the systemic veins. Untreated, the patient will manifest leg edema, ascites, liver engorgement, and weight gain. In the absence of left ventricular failure, there is no excess fluid in the alveoli, and the lungs will remain clear on chest x­ray. A chest x­ray from a patient with right­side heart failure is shown in Fig. 8­1; note the cardiomegaly and the absence of pulmonary infiltrates. Treatment of right heart failure attempts to relieve the pulmonary hypertension and uses low sodium intake and diuretic therapy to help mobilize excess body fluid.

CAUSES OF PULMONARY HYPERTENSION

Lung disease, a common cause of pulmonary hypertension, usually operates through one of the mechanisms listed in Table 8­2. Hypoxemia, a frequent manifestation of lung disease, is one of the most common physiologic mechanisms causing pulmonary hypertension. Fig. 8­2 demonstrates the effect of hypoxemia on mean pulmonary artery pressure, as well as demonstrating the interrelationship with acidosis. At normal pH, the arterial percent saturation of hemoglobin with oxygen SaO2) must decline to approximately 75% to achieve a doubling of mean pulmonary artery pressure. When pH is 7.3, the same doubling of pulmonary artery pressure occurs when the SaO2 is approximately 82%.

Fig. 8­1. Chest x­ray of a patient with pulmonary hypertension and right­sided heart failure. Note the enlarged heart (caused by an enlarged right ventricle), the enlarged pulmonary arteries, and the absence of lung infiltrates .


Both hypoxemia and acidosis cause pulmonary hypertension by constricting the small, muscular pulmonary arteries (those less than 0.2 mm in diameter). The exact mechanism for the vasoconstriction is unknown. The vasoconstriction may be caused by hypoxia­ or acidosis­mediated release of vasoactive substances or by a direct effect on pulmonary artery smooth muscle.

Hypoxemia is a clinically important cause of pulmonary hypertension because it is potentially reversible. Continuous oxygen therapy does reduce mortality from hypoxemic chronic obstructive pulmonary disease (see Chapter 9).
Another cause of pulmonary hypertension is the loss of pulmonary vasculature. Patients with severe emphysema can actually have near normal PaO2 yet manifest severe pulmonary hypertension because the destruction of lung tissue in emphysema may remove both alveoli and pulmonary capillaries. The remaining lung has mostly high­ventilation per fusion ratios that lead to increased dead space but not to significant hypoxemia (see Chapter 5). However, since there is a less vascular bed through which the right ventricle can pump its cardiac output, the pulmonary artery pressure is increased.

Fig. 8­2. Effect of hypoxemia (reduced SaO2) and acidosis on mean pulmonary artery pressure. Percentages refer to SaO2. See text for discussion. (From Mathay, R.A., and Berger, H.J. : Cardiovascular performances in chronic obstructive pulmonary diseases, Med. Clin. North Am. 65(3):489­524, 1981; reprinted with permission from W.B. Saunders Co. Reproduced from J. Clin. Invest. 43:1146­1162, 1964, by copyright permission of the American Society for Clinical Investigation.)

Cor pulmonale refers to any right ventricular manifestation of pulmonary hypertension caused by lung disease. Cor pulmonale usually manifests as one or more signs of right­sided heart strain­-the effects of pulmonary hypertension on the right ventricle or right atrium (see the box on p. 152). Cor pulmonale is not synonymous with right heart failure. Of course, the basic cause of cor pulmonale, pulmonary hypertension, may also lead to right­sided heart failure.

Fig. 8­3. ECG readings. A, An example of P­pulmonale (large peaked P waves in lead 11 [arrows]), which represents right atrial dilation that results from increased pulmonary artery and right ventricular pressures. B, A normal ECG.

Perhaps the most common cause of pulmonary hypertension is left heart failure. (The most common causes of left heart failure are arteriosclerosis and systemic hypertension.) In left heart failure fluid backs up in the left atrium and in the pulmonary circulation, resulting in increased pulmonary artery pressures. Treatment is usually with digoxin and diuretics and is directed at the left ventricle. Unless the patient is hypoxemic, supplemental oxygen can be expected to have little benefit.
Mitral valve disease can cause profound heart failure and pulmonary hypertension by interfering with the flow of blood from the left atrium to the left ventricle; this interference can occur either through mitral stenosis (narrowing of the mitral orifice) or mitral regurgitation (ejection of blood back into the atrium during systole). Both conditions are easily diagnosed using noninvasive cardiac methods and are potentially correctable with mitral valve surgery. Years ago rheumatic fever was the principal cause of severe mitral valve disease. Rheumatic heart disease is now relatively uncommon in the United States, and as a consequence, the prevalence of severe mitral valve disease has decreased over the years. Nonetheless, mitral valve disease should always be considered when pulmonary hypertension is present without an obvious cause.
Pulmonary emboli are clots that usually arise in the deep veins of the thigh and pelvis, break off, and travel to lodge in one or more of the pulmonary arteries. If not fatal to the patient, these clots will usually dissolve with time; on occasion they organize and thrombose in situ. Both acute pulmonary emboli and pulmonary thrombi (emboli that organize and do not dissolve) are potential causes of pulmonary hypertension. Pulmonary embolism is a relatively common clinical condition and should always be considered as a cause of otherwise unexplained pulmonary hypertension.
Other, rarer causes of pulmonary hypertension are congenital heart disease, pulmonary arteritis (inflammation of the pulmonary arteries), and chest wall deformity. Within each category listed in Table 8­2 are many different disease entities, far too numerous to mention.
Pulmonary hypertension may also be of completely unknown origin (idiopathic). Idiopathic pulmonary hypertension has a predilection for young and middle­aged women and usually presents with the insidious onset of dyspnea. Diagnosis is made by catheterization of the right side of the heart, measurement of pulmonary artery pressures, and by ruling out all other possible causes (e.g., heart and lung disease). There is no effective treatment for this disorder, although several vasodilators have been tried on an experimental basis. Idiopathic pulmonary hypertension is usually fatal within 5 years from the time of diagnosis.

ASSESSMENT OF HEMODYNAMIC STATUS

Hemodynamic status refers to the status of the pressure and the flow within the pulmonary and systemic circulation. Patients manifesting shock. heart failure, pulmonary hypertension, fluid overload, and many other problems have altered hemodynamic status. In clinical practice, there arc two levels of hemodynamic assessment. The first level is noninvasive, meaning without cardiac catheterization or arterial pressure monitoring. Noninvasive hemodynamic assessment includes the history, physical examination, chest x­ray studies. pulmonary function tests, arterial blood gas measurement, observation of the patient's response to treatment and, occasionally, noninvasive heart studies such as the echocardiogram. In the vast majority of respiratory patients, hemodynamic status can be assessed noninvasively.

The second level of hemodynamic assessment is invasive and requires cardiac catheterization and arterial pressure monitoring. Until the early 1970's, catheterization was only possible in a special laboratory, and studies were usually limited to noncritically ill patients with valvular or coronary disease. The advent of the Swan­Ganz catheter, first introduced in 1970, made bedside catheterization feasible and revolutionized hemodynamic evaluation. In practice, most patients requiring bedside catheterization also have a small cannula inserted in a peripheral artery (usually radial) for continuous blood pressure monitoring. In addition, cardiac rate and rhythm are continuously monitored in all catheterized patients.

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