The vascular system of the body consists of separate pulmonary and systemic circulations operating in series (Figure 6-1). Each circulation receives its blood from the other; each has its own reservoir, pump, and set of vessels. The right ventricle receives mixed venous blood through the tricuspid valve from its reservoir, the right atrium, and pumps it through the pulmonic valve, which marks the beginning of the pulmonary circulation.¹ This relatively deoxygenated blood flows through pulmonary arteries and arterioles to an immense alveolar capillary bed where it is reoxygenated. The capillary bed consists of extremely short, interconnected segments spreading 75 to 100 mL of blood over a 70-m² area, or about half the size of a tennis court.¹ Comroe² described the capillary bed as two sheets of endothelium held apart in places by posts, similar to an underground parking garage. Rather than flowing through numerous individual tubes (as in systemic capillaries), pulmonary blood flows more like a sheet over the alveoli, maximizing its exposure to alveolar gases. This structural arrangement shortens the distance for oxygen and carbon dioxide diffusion between air and blood to one tenth of the diffusion distance that exists between systemic capillaries and tissue cells.¹

Figure 6-1 Comparison of pulmonary and systemic blood flows and pressures. (Adapted from Thibodeau GA, Patton KT: *Anatomy & physiology,* ed 5, St Louis, 2003, Mosby.)

After leaving the alveoli, the capillaries converge to form venules and veins. The newly oxygenated blood flows through four major pulmonary veins (two from each lung) into the left atrium, the reservoir for the left ventricle. The pulmonary vein orifices in the left atrial wall mark the end of the pulmonary circulation.¹ Blood continues to flow out of the left atrium through the mitral valve into the left ventricle, which pumps the blood through the aortic valve into the aorta. The aortic valve marks the beginning of the systemic circulation. The aorta distributes the oxygenated blood through its many branches to systemic arteries, arterioles, and capillary beds throughout the body, supplying oxygen to tissue cells and removing the carbon dioxide they produce. Beyond the capillary beds, systemic venules and veins converge to return the oxygen-poor blood to the right atrium via the vena cavae, which mark the end of the systemic circulation.

The total cardiac output (Q˙t) is simultaneously pumped through both circulations each minute. Right and left ventricular outputs must be essentially equal over time; otherwise, blood would accumulate in one of the circulations. Small differences in outputs may occur briefly for a few heartbeats, but over time, individual ventricular outputs are equal in healthy hearts. Figure 6-1 illustrates pulmonary and systemic circulations with their associated pressures.

The pulmonary arteries and arterioles have much thinner walls and less smooth muscle than systemic arteries and arterioles. Therefore, pulmonary arterioles cannot constrict as effectively as systemic arterioles. Pulmonary veins and venules also have sparse smooth muscle, differing little in structure from pulmonary arteries and arterioles. Pulmonary arteries generally follow a course parallel with bronchi, whereas pulmonary veins leave the lung through different routes. Without this anatomical difference, distinguishing pulmonary arteries from veins on a chest x-ray image would be difficult because of their structural similarities.²

Pulmonary capillaries also differ significantly from systemic capillaries; as noted previously, pulmonary capillary blood flows in thin sheets, as opposed to the distinctly tubular flow in systemic capillaries. The thin walls of pulmonary vessels and vast area of the capillary bed make the pulmonary vasculature highly distensible compared with the systemic vasculature.

Bronchial Vasculature

The supporting tissues of the tracheobronchial tree, including airways down through the terminal bronchioles, are supplied with oxygenated blood through the systemic bronchial arteries. (See the section on blood supply to the lungs in Chapter 1.) Bronchial systemic venous blood drains directly into the pulmonary veins, mixing oxygen-poor blood with freshly oxygenated pulmonary venous blood on its way to the left ventricle.³ Bronchial blood flow is only 1% to 2% of the cardiac output, which means that the anatomical shunt from this source is usually less than 2%; this also means that left ventricular output is about 1% to 2% greater than right ventricular output.³

CONCEPT QUESTION 6-1

Explain the way anatomical shunt through the bronchial circulation causes an oxygen pressure (PO₂) difference between alveolar gas and arterial blood.

Pulmonary and Systemic Pressures

Figure 6-1 shows that the pulmonary circulation is a low-pressure, low-resistance system compared with the systemic circulation. The lower resistance in the pulmonary circulation is manifested by the fact that its pressures are lower even though it receives the same cardiac output as the systemic circulation receives. The resistance to blood flow in the pulmonary circulation is about one tenth as great as it is in the systemic circulation.¹

Blood flow through the pulmonary circulation is highly pulsatile rather than continuous as in systemic capillaries. The total volume of blood in the pulmonary circulation is about 450 mL, which is only 9% of the total circulating blood volume. About 70 mL of this blood is in the capillaries at any given moment; the rest is distributed equally between pulmonary arterial and venous vessels.³ The capillary blood volume of 70 mL is about equal to the volume ejected by the right ventricle with each contraction (the right ventricular stroke volume). Pulmonary capillary blood is thus almost completely replaced with each heartbeat, which means a red blood cell travels through the capillaries in about 0.75 second. Pulmonary blood flow almost stops between each ventricular beat, which explains its pulsatile nature.^1,3

The highly expandable pulmonary vascular bed serves as a backup reservoir that shields the left atrium from sudden changes in right ventricular output. If venous return to the right ventricle increases suddenly, as would occur during sudden strenuous exercise, left ventricular filling pressure increases gradually over two or three cardiac cycles rather than increasing abruptly.

Clinical Measurement of Pulmonary Blood Pressures and Flows

Measurement of Pulmonary Blood Pressures

Systemic blood pressure is easily measured by simple noninvasive means. However, measurement of pressures in the pulmonary circulation requires an invasive procedure called pulmonary artery catheterization. The special catheter used for this purpose was the subject of a study published in 1970 by Swan, Ganz, and others. Since then, the catheter has been marketed under the brand name Swan-Ganz, and the term Swan-Ganz catheter has become synonymous with pulmonary artery catheter. This catheter is a very thin, multilumen flexible tube with a balloon located at its distal end. The balloon can be inflated through a separate channel inside the catheter. The catheter contains at least two additional internal channels: the distal channel, leading to an opening at the tip of the catheter, and the proximal channel, leading to an opening located several centimeters back from the tip. Pressures can be measured or blood can be withdrawn through these channels via the proximal and distal ports of the catheter (Figure 6-2).

Figure 6-2 Typical quadruple channel pulmonary artery catheter. After insertion, the distal lumen rests in the pulmonary artery, and the proximal lumen rests in the right atrium. Both communicate with their respective injection ports. (From Wilkins RL, Stoller JK, Kacmarek RM: *Egan’s fundamentals of respiratory care,* ed 9, St Louis, 2009, Mosby.)

A physician inserts the catheter under surgically sterile conditions, sometimes at the bedside of a critically ill patient in a hospital intensive care unit. Proximal and distal channels are first filled with sterile fluid to remove all air; the catheter is then inserted into a large systemic vein, usually the right internal jugular or subclavian vein, and advanced until the tip enters the right atrium. At this point the balloon is inflated, allowing the bloodstream to direct the catheter tip across the tricuspid valve into the right ventricle—hence, the term flow-directed, balloon-tipped catheter. The physician advances the catheter until the bloodstream carries it through the pulmonic valve and into the pulmonary artery (Figure 6-3). During insertion, pressures at the catheter tip are continuously recorded by an electronic pressure transducer connected to the distal port. The stationary fluid column inside the distal channel reflects these pressures precisely because it is in direct contact with the blood at the catheter’s tip. The pressure waveforms are continuously displayed on the bedside monitor as the catheter is advanced; this helps the physician identify the position of the catheter tip because each cardiovascular structure produces unique pressure waveforms (Figure 6-4, A and B).

Figure 6-3 Pulmonary artery catheter in place. The *dotted circle* represents the wedge position. The heart is in diastole in this schematic. (From Martin L: *Pulmonary physiology in clinical practice,* St Louis, 1987, Mosby.)

Figure 6-4 Correlation between pulmonary artery catheter positions (A) and pressure waveforms (B). *RA,* Right atrium; *RV,* right ventricle; *PA,* pulmonary artery; *PAWP,* pulmonary artery wedge pressure. (From Wilkins RL, Stoller JK, Kacmarek RM: *Egan’s fundamentals of respiratory care,* ed 9, St Louis, 2009, Mosby.)

When the catheter is advanced far enough to wedge in a small branch of the pulmonary artery, the inflated balloon completely blocks blood flow to the downstream vessels supplied by that artery (see Figure 6-3, dotted circle). The pressure measured from the catheter tip in this wedged position is called the pulmonary capillary wedge pressure (PCWP). (When the balloon is deflated, flow resumes, and the catheter tip simply measures the pulmonary artery pressure [PAP].) The vessels extending beyond the artery blocked by the inflated balloon are in direct communication with the pulmonary capillaries and the pulmonary veins. Pulmonary venous pressure is nearly equal to left atrial pressure (LAP), which is essentially equal to left ventricular end-diastolic pressure (LVEDP), the pressure inside the filled ventricle just before it contracts (see Figure 6-3). This so-called filling pressure is also known as preload of the left ventricle. The PCWP is only slightly greater than the filling pressure of the left ventricle.³ The PCWP accurately reflects changes in LAP (or ventricular filling pressure) because the stationary fluid column inside the catheter is functionally extended from the catheter tip to the left atrium. For this reason, the PCWP is commonly used to assess the pumping function of the left ventricle. For example, if the left ventricle fails to contract with normal force, blood flowing into it dams up in the left atrium, pulmonary veins, and capillaries; consequently, the PCWP increases. In certain rare circumstances, the PCWP might not accurately reflect left atrial pressure: (1) if the pulmonary veins constrict and downstream resistance beyond the catheter tip increases or (2) if the catheter tip is in an area in the lung where alveolar pressure exceeds pulmonary venous pressure, as might occur in positive pressure mechanical ventilation. In the latter instance, high alveolar pressure compresses capillaries distal to the catheter tip, blocking its communication with the left atrium.

CONCEPT QUESTION 6-2

Why would a narrowed (stenotic) mitral valve affect the PCWP? (See Figure 6-3.)

CLINICAL FOCUS 6-1 Causes of Pulmonary Artery Catheter Pressure Waveform Shapes

Proper positioning of the pulmonary artery catheter is confirmed by waveform patterns produced as the catheter is advanced into the pulmonary artery (see Figure 6-4). The first waveform appears on the monitor when the tip of the catheter reaches the great vessels. This is known as the central venous pressure (CVP) and reflects pressure in the vena cava and right atrium. A normal value for CVP is about 2 mm Hg; this produces the low-amplitude waveform in Figure 6-4, B. In the right atrium, the balloon is inflated for two reasons: (1) to decrease the risk of cardiac arrhythmias induced by the catheter tip hitting the ventricular walls and (2) to allow blood flow to catch the balloon and carry the catheter forward.

The catheter passes through the tricuspid valve into the right ventricle. The pressure waveform increases in height as the ventricle contracts (systole) and decreases sharply to near 0 as the ventricle relaxes (diastole) (see Figure 6-4, B). During diastole, the pressure waveform slowly rises as blood flows into the right ventricle through the tricuspid valve. Normal right ventricular pressure is about 25/0 mm Hg (systolic/diastolic).

The striking difference between pulmonary artery pressure (PAP) tracings and tracings created by the right ventricle is the diastolic pressure in the pulmonary artery. Closure of the pulmonic valve prevents PAP from decreasing as much as it does in the right ventricle (see Figure 6-4). The ejection of blood from the right ventricle creates a steep rise in the systolic portion of the curve. After systole, PAP decreases sharply until the pulmonic valve closes. Closure of this valve abruptly stops blood backflow, creating a shock wave responsible for the dicrotic notch on the downslope of the waveform. Normal PAPs are about 25/10 mm Hg.

As the catheter floats into a small branch of the pulmonary artery, the inflated balloon blocks blood flow. The pressure tracing is similar to right atrial waveforms but is of even lower amplitude; this is known as pulmonary capillary wedge pressure (PCWP). Normal PCWP is 4 to 12 mm Hg and is about the same as pressure in the left atrium. If pulmonary vascular resistance (PVR) is normal, the pulmonary artery diastolic pressure is about equal to the PCWP.

The pulmonary artery catheter also can be used to assess right ventricular preload and pumping function because the proximal channel (see Figure 6-2) communicates with the right atrium. The pressure measured at the catheter’s proximal port reflects right atrial pressure (RAP), sometimes called central venous pressure (CVP).

Blood drawn from the proximal channel is a mixture of superior and inferior vena cava venous blood. Because oxygen contents of these two sources may differ considerably, proximal channel blood is not a clinically acceptable mixed venous blood sample for purposes of measuring the average venous oxygen content of the body. A thoroughly mixed venous blood sample reflecting the true average venous oxygen content of the body must be obtained from the pulmonary artery, through the distal channel of the catheter (see Figure 6-2). By comparing the oxygen content of mixed venous blood with the oxygen content of systemic arterial blood, the oxygen consumption of the body can be assessed. (This is discussed in Chapters 8 and 12.)

By measuring and comparing pressures obtained from the pulmonary artery catheter (RAP, PAP, and PCWP), the

CLINICAL FOCUS 6-2 Differentiating Causes of High Pulmonary Artery Pressure

You have two patients with the following cardiac pressure values.

Patient A

Pulmonary artery (PA) systolic	38 mm Hg
PA diastolic	25 mm Hg
Pulmonary capillary wedge pressure (PCWP)	21 mm Hg

Patient B

PA systolic	40 mm Hg
PA diastolic	25 mm Hg
PCWP	10 mm Hg

Although both patients have elevated pulmonary artery pressures (PAPs), the reasons for this are quite different. The PCWP helps differentiate origins of high PAPs.

Discussion

In the following discussion, PCWP is used as a substitute for the left atrial pressure (LAP). PCWP (i.e., LAP) is elevated in Patient A and normal in Patient B. Pulmonary artery end-diastolic pressure (PAEDP) in Patient A is only 4 mm Hg higher than PCWP, whereas PAEDP in Patient B is 15 mm Hg higher than PCWP. In healthy people, the PAEDP is almost equal to the PCWP (PCWP = LAP) because pressures across the pulmonary capillary bed have enough time to equalize during diastole. High pulmonary vascular resistance (PVR) creates an increased PAEDP-PCWP difference because the resistance is located between the pulmonary artery and left atrium. In Patient B, PVR must be high, as shown by the high PAEDP-PCWP difference. The normal PCWP in Patient B suggests normal left ventricular pumping action. In Patient A, PVR must be normal because the difference between PAEDP and PCWP is small. The elevated PCWP (i.e., LAP) is transmitted back across the pulmonary capillaries, creating a proportionately high PAEDP, preserving the PAEDP-PCWP difference. Causes of increased PAP in Patient A may be left ventricular pumping failure or mitral valve narrowing. Causes of increased PVR in Patient B may be a pulmonary embolus or vasoconstriction induced by hypoxemia.

clinician can evaluate right and left ventricular function, differentiate the causes of increased PAP, and assess the risk of pulmonary edema. PAP might be increased because of excessive blood volume (hypervolemia) or because of left ventricular pumping failure in which blood dams up in the entire pulmonary circulation. The PAP might also be increased as a result of increased pulmonary vascular resistance (PVR). Increased pressures in either ventricle at the end of diastole, coupled with a low cardiac output, signal a loss of ventricular pumping ability, or a loss of contractility. Increased PCWP, regardless of the cause, means that the pulmonary capillaries are engorged with blood, increasing the likelihood that fluid will be forced into interstitial lung spaces and cause pulmonary edema. Understanding these relationships is essential for taking appropriate therapeutic actions.

Measurement of Pulmonary Blood Flow or Cardiac Output

The amount of blood the heart pumps each minute can be clinically measured with a pulmonary artery catheter via a thermodilution technique. In this method, a known volume of room temperature fluid (e.g., saline) is rapidly injected into the right atrium through the proximal injection port (see Figure 6-2). This volume of cool fluid rapidly flows into the right ventricle where it is pumped into the pulmonary artery. A temperature-sensing thermistor near the end of the catheter (see Figure 6-2) in the pulmonary artery records a sudden decrease in temperature as the bolus of cool saline passes by. If cardiac output is increased, blood temperature rapidly returns to its original value; if it is decreased, the temperature increases more slowly to the original value. A microprocessor receives information from the thermistor and computes the area under the temperature-time curve. The area under the curve is small for rapid blood flow and large for slow blood flow. The microprocessor uses the area under the curve and the volume of the injected fluid to compute the blood flow rate, or the cardiac output (Q˙t). Several determinations of cardiac output can be made within minutes in this fashion.