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).
|Table 81. Systemic and pulmonary circulations.|
|Systemic circulation||Pulmonary circulation|
|Path of blood||Left atrium|
|Function||Carries oxygenated blood from the left side of the heart through the systemic arteries to all the organs and tissues|
After delivering oxygen and receiving carbon dioxide in the systemic capillaries, returns deoxygenated blood through the systemic veins to the right atrium where the pulmonary circulation begins
|Carries deoxygenated blood from the right side of the heart through the pulmonary arteries to the lungs|
After receiving oxygen and delivering carbon dioxide in the pulmonary capillaries, returns oxygenated blood through the pulmonary veins to the left atrium where the systemic circulation begins
|Pressure||Relatively highpressure system; range of normal mean systemic arterial pressure is 70 to 105 mm Hg; easily measured with blood pressure cuff||Relatively lowpressure system; range of normal mean pulmonary artery pressure is 10 to 22 mm Hg; can only be measured with pulmonary artery catheter|
|Cause of elevated pressure||Unknown in majority of cases; renal disease in some patients; hypoxemia not a cause||Usually can be determined from full clinical picture; hypoxemia, leftsided heart failure, and destruction of pulmonary vascular bed among known causes|
|Treatment of elevated pressure||Lowsalt diet; weight reduction if overweight; if necessary, many different types of anti-hypertensive drugs are available, including diuretics||Depends on cause; for heart failure, digoxin and diuretics often effective; for hypoxemiainduced pulmonary hypertension, continuous oxygen therapy is treatment of choice; in some cases, e.g., primary pulmonary hypertension, there is no effective treatment|
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.
|Table 82. Causes of pulmonary hypertension|
|Disease or condition||Underlying mechanisms|
|Lung diseases, including all forms of restrictive and obstructive lung conditions||Hypoxemia; loss of pulmonary blood vessels; acidosis|
|Heart disease including left ventricular heart failure, mitral valve disease congenital heart disease||Increased pulmonary capillary hydrostatic pressure|
|Pulmonary thromboembolic disease||Pulmonary artery narrowing; loss of pulmonary blood vessels|
|Pulmonary arteritis||Pulmonary artery narrowing; loss of pulmonary blood vessels|
|Chest wall deformity||Hypoxemia acidosis; pulmonary artery narrowing|
|Idiopathic||Loss of pulmonary blood vessels; pulmonary artery narrowing|
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.
|SIGNS OF COR PULMONALE|
Physical examination increased intensity of second (pulmonic) heart sound; right ventricular heave when palpating anterior chest wall
Chest xray film enlargement of pulmonary arteries and right ventricular dilation
Electrocardiogram evidence of rightsided heart strain, such as tall R wave in precordial leads or tall, peaked P wave in lead II ( Fig. 83)
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
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.
|Clinical problem 1|
|A 64yearold man is admitted to the hospital because of dyspnea and leg edema. He has a long history of cigarette smoking. Previous pulmonary function studies showed severe, chronic airways obstruction.|
When examined, the patient has decreased breath sounds in both lung bases. The intensity of his second heart sound is increased; his pulse is 120/min, and his blood pressure is 135/72 mm Hg. The patient's abdomen is enlarged, suggesting ascites, and he has bilateral leg edema. A chest xray film shows an enlarged heart without lung infiltrates (see Fig. 81). While breathing room air, his PaO2 is 45 mm Hg, PaCO2 is 47 mm Hg, and pH is 7.35.
Based on this information, how would you assess this patient's hemodynamic status?
|Clinical problem 2|
|A 65yearold man is brought to the hospital after being found unresponsive on the floor of his apartment. On evaluation, he is alert but confused; his skin and mucous membranes are very dry. Vital signs are as follows: systolic blood pressure, 90 mm Hg in the supine position (by palpation over the brachial artery); pulse, 96 and regular; respiratory rate, 20/min; and body temperature, 97.4° F. In the sitting position the patient's blood pressure falls to 60 mm Hg systolic, and his pulse increases to 110/min. A chest xray film shows a normalsized heart with no pulmonary infiltrates, and an ECG shows only sinus tachycardia. Routine blood tests are ordered, including serum electrolytes.|
His hemodynamic status most likely reflects which of the following:
a. Cardiogenic shock
b. Pulmonary hypertension
c. Adult respiratory distress syndrome (ARDS)
d. Severe dehydration
e. Labile blood pressure
Is invasive hemodynamic monitoring indicated?
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
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