Chapter 8, cont… (Page 3)

Pulmonary circulation


Although the Swan­Ganz catheter is used for several measurements (see Table 8­3), the most useful measurement is the pulmonary artery wedge pressure (PAWP). Many factors can influence this measurement, and its proper interpretation in critically ill patients is not a simple matter. At the very least, correctly using PAWP requires knowledge of the full clinical situation, plus some familiarity with how respiration can affect pulmonary blood flow. Before discussing clinical use of the PAWP, its actual measurement is discussed in greater detail.

To measure PAWP, the catheter tip with the balloon inflated is ''wedged'' into a branch of the pulmonary artery (see Figs. 8­5 and 8­6). When the flow of the column of blood is interrupted by the inflated balloon, the tip of the catheter measures downstream pressure. Since it is the pulmonary artery branch that is occluded, downstream pressure is the pulmonary venous pressure. Pulmonary venous pressure reflects left atrial pressure and, under certain conditions, left ventricular end­diastolic pressure. Changes in these three pressures can profoundly affect gas exchange, and since leftsided pressures are not directly measurable at the bedside, PAWP is the ''window" through which these important pressures are viewed.

PAWP cannot accurately reflect left­side pressures unless it is measured accurately; an incorrectly recorded PAWP is worse than none at all. There are two principal ways to check that an accurate PAWP is being measured.

1. The pressure waveform obtained with the wedged catheter should be characteristic of left atrial pressure ( Fig. 8­6) and should represent a distinct change from the pulmonary artery pressure tracing. The PAWP pressure tracing should appear only with the balloon inflated; as soon as the balloon is deflated, the pulmonary artery waveform should reappear.

2. The mean wedge pressure should be lower than or equal to the diastolic pulmonary artery pressure. A mean wedge pressure higher than the diastolic pulmonary artery pressure suggests that something other than true wedge pressure is being measured; this incorrect measurement may occur when the balloon is inflated in a very small arterial branch ("overwedging" the catheter).

Another method used to check for true wedge position, but one not widely practiced, is to aspirate blood from the catheter when the balloon is inflated. If the catheter is occluding the pulmonary artery, the blood aspirated from the distal tip comes from the downstream pulmonary capillaries and should be fully oxygenated (i.e., close to 100% saturated). By contrast, mixed venous blood (obtained from a nonwedged pulmonary artery position) should be relatively desaturated. However, the pressure generated during aspiration may draw blood from a pulmonary shunt, or the catheter tip may reside in a low ventilation/perfusion region; for these reasons a partially oxygenated blood sample does not rule out a true wedged position.

For technical reasons it is often difficult to obtain repeated measurements of PAWP; among reasons for this difficulty are catheter migration within the pulmonary artery and balloon rupture. When PAWP is within a few mm Hg of diastolic pulmonary artery pressure, the latter can usually substitute for PAWP. When diastolic pulmonary artery pressure is much higher than PAWP, pulmonary hypertension is present, and diastolic pulmonary artery pressure cannot substitute for wedge pressure.

Clinical problem 5
How would you interpret the following pressures (in mm Hg) obtained from Swan­Ganz catheterization? In which patients could diastolic pulmonary artery pressure substitute for PAWP?

Patient A. PAP, 24/12; PAWP, 12

Patient B. PAP, 35/23; PAWP, 11

Patient C. PAP, 43/23; PAWP, 22

A major problem in hemodynamic monitoring is how to measure PAWP in a patient whose breathing is assisted by a ventilator, particularly if the patient is receiving positive end expiratory pressure (PEEP).* Do the increased airway pressures alter PAWP measurement'?

The answer to this question depends on three main factors: (1) fluid status of the patient; (2) level of airway pressure; and (3) position of the SwanGanz catheter tip within the patient's thorax.

The relationship of pulmonary vascular pressures to alveolar pressures can be used to divide the lung into three zones (Fig. 8­8). Since gravity has a profound effect on blood How within the lungs, in the upright lung there is relatively less blood How per unit long volume at the apices than at the bases (see also Fig. 5­7). As a result, pulmonary artery pressure and blood How are lowest at the top of the upright lung and highest at the bottom. By contrast, alveolar pressure is constant throughout the lung.

Figure 8-8

Fig. 8­8. Three zones of the lung in the upright position. See text for discussion. (From West, J.B., Dollery, C.T., and Naimark, A.: J. Appl. Physiol. 19:713, 1964.)

In Zone 1, near the top, the alveolar pressure (PA) is greater than both the pulmonary artery (Pa) pressure and the pulmonary venous (Pv) pressure. As a result, there is no blood flow in Zone 1. Zone I is not normally present in healthy lungs, but in respiratory patients (particularly those receiving artificial ventilation) there may be a Zone I of varying size .

Much larger is Zone 2, where Pa is greater than PA and where PA is greater than Pv, at least during much of the respiratory cycle. Zone 2 blood vessels behave like collapsible tubes surrounded by a pressure chamber (so­called ''Starling resistors''), so that blood flow is determined by the difference between the arterial pressure and the alveolar pressure. This pressure difference is perhaps best appreciated during positive pressure ventilation; when alveolar pressure rises in Zone 2 units, pulmonary capillary blood flow may cease and resume only when alveolar pressure falls. In any situation.

as blood flow increases toward the bottom of the lung because of gravity, Pv approaches PA, and there is a decreasing tendency of blood vessels to collapse.

Finally, in Zone 3 Pv is always greater than PA (and still less than Pa), so pulmonary blood flow is uninterrupted, even during expiration.

The three­zone lung model's pressure relationships also hold true in the supine patient ( Fig. 8­9). The left atrium serves to demarcate the three zones. Zone 2 is at or close to the level of the atrium. Zone I lies above the atrium because the blood flow there is reduced by gravity; below the atrium, where blood flow is increased because of gravity, is Zone 3. These zones are not fixed in size, but instead are affected by both artificial ventilation and the patient's hemodynamic (fluid ) status.

Figure 8-9

Fig. 8­9. Three zones of the lung in the supine position. This model assumes that a PEEP of 15 cm H2O is transmitted to the alveoli and remains constant in all the alveoli. Vascular pressures vary depending on the vertical height of the blood column (and arc given in cm H2O for comparison with alveolar pressures). Pulmonary artery pressure is 13 cm H2O at the top of the lung, 20 cm H2O in the middle of the lung, and 27 cm H2O at the bottom of the lung. This difference in vascular pressure, in relation to the constant alveolar pressure, creates the three zones. At the top of the lung (Zone 1), there is no blood Row since alveolar pressure (PA) exceeds both pulmonary arterial pressure (Pa) and pulmonary venous pressure (Pv). A small Zone 2 exists in the middle where Pa is greater than PA, but where PA is greater than, or close to, Pv. Finally, in Zone 3, both Pa and Pv exceed PA, and there is continuous blood Row. (LUL, Ieft upper lung; LLL, lower left lung; LA, left atrium.) (From Tooker, J., Huseby, J., and Butler. J.: Am. Rev. Respir. Dis. 117:721725, 1978 .)


Artificial ventilation, by increasing alveolar pressures, can convert areas of Zone 2 into Zone I and areas of Zone 3 into Zone 2. For example, when a ventilator pushes air into the lungs, alveolar pressure may increase to the point of cutting off all blood flow; during exhalation, when alveolar pressure decreases, blood flow may then resume; such alternation of blood flow would define a Zone 2 region. Where alveolar pressures are such that no blood flows during the breathing cycle, a Zone I area exists; conversely, Zone 3 is the area where alveolar pressures never cut off blood flow.

During artificial ventilation airway pressures are much greater than they are during normal breathing, and PA can increase so that it exceeds either Pv (creating a Zone 2) or Pa (creating a Zone I ). The higher the airway pressure that is generated by the ventilator (peak inspiratory pressure or end expiratory pressure), the higher the alveolar pressure, and the greater the effect on pulmonary blood flow. Although an increase in the size of Zones I and 2 is a predictable result of artificial ventilation, neither the magnitude nor the clinical effect of the increases can be accurately predicted. Arterial blood gas measurements must be monitored to assess the effects of artificial ventilation on gas exchange.

Hypovolemia, by lowering pulmonary vascular pressure, can also convert areas of Zone 3 into Zone 2 or areas of Zone 2 into Zone 1. Generally, the more dehydrated the patient, the smaller is Zone 3 and the larger are Zones I and 2. A combination of artificial ventilation and dehydration can create relatively large Zones I and 2 and a correspondingly smaller Zone 3.

Many studies have attempted to clarify how artificial ventilation and intravascular fluid status affect pulmonary artery wedge pressure (PAWP). If the Swan­Ganz catheter tip is in Zone I or in Zone 2, the positive alveolar pressure can give a falsely high reading of PAWP; in fact, alveolar pressure may be measured and not PAWP. If the patient is not receiving PEEP, this problem can usually be circumvented by measuring PAWP only at the end of exhalation (Fig. 8­10). Without PEEP, end­exhalation alveolar pressure will be atmospheric (0), and a true wedge pressure measurement should be obtained .

PAWP measurement is more complex when the patient is receiving PEEP because end­exhalation pressure is always above atmospheric pressure. Some authors have recommended that patients be taken off PEEP when PAWP is measured, but this is not a good idea if for no other reason than the patient needs the PEEP and removing it could worsen oxygenation. Furthermore, the patient will remain on PEEP at all other times, so PAWP should be known while PEEP is being used. There is no easy solution to this dilemma, but several studies provide some reassurance. In general, PEEP of 1() cm H2O or less in a euvolemic patient does not influence PAWP to a significant degree. If there is concern that the patient is dehydrated, a fluid bolus (100 to 200 cc of intravenous saline) should be given before accepting a PAWP measurement as accurate.

More importantly, since the Swan­Ganz catheter is flow­directed, the catheter tip usually ends in Zone 3 where the influence of PEEP is minimal. (Since the vertical catheter position cannot be gauged with the routine anteroposterior chest x­ray film, some authors recommend obtaining a lateral film to check for catheter placement.) The important thing is to appreciate the potential influence of airway pressures and of PEEP on PAWP measurement and not to accept any measurement as valid without considering these influences.

Figure 8-10

Fig. 8­10. Measurement of pulmonary artery wedge pressure (PAWP) during artificial ventilation. PAWP should be measured at the end of exhalation (arrows), where the influence from positive airway pressure is minimal.


The previous discussion deals mainly with artifact of measurement. Assuming an accurate, artifact­free pulmonary artery wedge pressure (PAWP) is measured, just what does it represent?

PAWP measurement is used to obtain information about the status of the left side of the heart and the pulmonary circulation distal to the catheter tip. There are thus two fundamental reasons for measuring PAWP: (1) as a guide to pulmonary capillary hydrostatic pressure, and (2) as a guide to filling pressures of the left atrium and ventricle.

Before the advent of Swan­Ganz catheterization in 1970, this hemodynamic information could be obtained only (at the bedside) by measurement of the central venous pressure (CVP). For CVP measurement a long catheter (approximately one third the length of a Swan­Ganz catheter) was placed in a large vein and then was connected to a vertical column of water. If there were no obstruction between the venous end of the catheter and the water column, the CVP was accurately recorded by observing the water level. Using this method, CVP in a healthy person is under 12 cm H2O (under 10 mm Hg).

Before the ability to measure PAWP, the CVP was used to indicate the left atrial and pulmonary venous pressures on the assumption that these pressures were transmitted unchanged to the pulmonary arteries, the right side of the heart, and the central venous system. Experience with the Swan­Ganz catheter has shown this transmission of pressures does not occur in many situations (Fig. 8­11). There is often a lack of correlation between CVP and PAWP, and it is now accepted that CVP is no substitute for PAWP in critically ill patients or in a patient with an acute myocardial infarction.

Figure 8-11

Fig. 8­11. Poor correlation between central venous pressure and pulmonary artery wedge pressure measurement. (r, Correlation of coefficient; SEE, standard error of estimate; n, number of patients studied.) (From Forrester, J.S., Diamond, G., McHugh, T.L., et al.: Reprinted by permission of N. Engl. J. Med. 285:190­193, 1971.)

PAWP as a guide to pulmonary capillary hydrostatic pressure. Except when PAWP is elevated by artifact (as from artificial ventilation), PAWP is a measure of the capillary hydrostatic component that tends to force plasma fluid into the pulmonary interstitium. This force, usually between 6 and 12 mm Hg, is opposed by the capillary oncotic pressure (normal value, 20 to 25 mm Hg) so that fluid does not accumulate in the lungs. The higher the PAWP or the lower the capillary oncotic pressure, the greater is the leaking tendency.

Although oncotic pressure can be directly measured on a pulmonary artery blood sample with an oncometer, it can also be assessed by the serum total protein or albumin concentration (normal values, 6 to 8 gm% and 3.8 to 5.0 gm%, respectively). The serum protein concentration correlates with the measured oncotic pressure; if the proteins are low, oncotic pressure is also reduced. A low oncotic pressure per se should not lead to pulmonary edema, but it can definitely contribute to pulmonary edema arising from increased hydrostatic pressure.

In any event, when an imbalance in oncotic and hydrostatic forces results in pulmonary edema, measurement of PAWP can provide important therapeutic information. (The physiologic mechanisms in pulmonary edema are discussed further in Chapter 11.)

When the only contributor to pulmonary edema is increased hydrostatic pressure, there is a useful correlation between PAWP and the chest x­ray. If PAWP is less than 18 mm Hg the x­ray should not show any signs of pulmonary edema. The minimal to moderate changes caused by pulmonary edema (beginning with a slight vascular redistribution to the upper lobes) may be found when PAWP is between 18 to 25 mm Hg. Above 25 mm Hg, frank changes of pulmonary edema may be seen, and the higher the PAWP is the more severe the x­ray appearance. To make these correlations it is important that the chest x­ray be obtained close to the time that the PAWP is measured.

For example, if the chest x­ray shows definite pulmonary edema and if an accurate PAWP measurement is 10 mm Hg before the patient has received any treatment, the cause definitely is not left­sided heart failure. Conversely, if the PAWP measurement is 35 mm Hg and the chest x­ray film is perfectly clear, either the PAWP is in error or the chest x­ray belongs to someone else!

Clinical problem 6
Following is the initial wedge pressure in three different patients, along with their blood pressure readings and serum albumin levels (pressures are in mm Hg; serum albumin is in gm%). On the basis of physical examination and chest x­ray films, each patient is suffering from pulmonary edema.

Patient A. Blood pressure, 70/50; PAWP, 7; serum albumin, 4.1

Patient B. Blood pressure; 135/83; PAWP, 27; serum albumin, 3.4

Patient C. Blood pressure, 125/75; PAWP, 16; serum albumin, 2.6

In regard to capillary hydrostatic pressure as a cause of pulmonary edema, how do you interpret each wedge pressure measurement?

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