Chapter 8, cont… (Page 4)

Pulmonary circulation

PAWP as a guide to left heart filling pressures. The relationship of PAWP to left heart hemodynamics is a complex one. This relationship can be simplified somewhat by examining the relationship between PAWP and left atrial pressure (LAP), left ventricular end­diastolic pressure (LVEDP), and left ventricular end­diastolic volume (LVEDV), which is a critical determinant of left ventricular function.

PAWP measurement would be most useful if the following were always true: (1) PAWP equals LAP equals LVEDP; and (2) LVEDP accurately reflects LVEDV so that an increase or a decrease in LVEDV proportionately changes LVEDP.

These ideal conditions are often assumed to be present during hemodynamic measurement, but in unhealthy patients they may not hold. Chronologic review of the Swan­Ganz literature reveals increasing sophistication in the understanding of this fact plus a better appreciation of the possible pitfalls in interpreting PAWP measurement.

Generally there is good correlation between PAWP and LAP, even in patients with heart disease, including those who have mitral stenosis. The difficulty arises in the correlation between PAWP and LVEDP. Before discussing this correlation, we will examine why it is important to know the LVEDP.

During diastole, blood from the left atrium flows past the mitral valve to fill the left ventricle. The more the myocardium is stretched, the more the blood volume that is ejected during systole increases. The degree of myocardial stretch at the end of diastole is often referred to as preload; with increasing preload, up to a point, the work produced by the myocardium (left ventricular stroke work) increases. This relationship is the essence of Starling's law of the heart (Fig. 8­12).

The degree of myocardial stretch is usually measured in vitro on isolated muscle preparations. In vivo, the degree of stretch correlates with the left ventricular end­diastolic volume (LVEDV). According to Starling's law, LVEDV is the left ventricular preload and bears the same relationship to left ventricular stroke work as does the degree of myocardial muscle stretch.

Stroke volume can also be substituted for left ventricular stroke work. Thus in vivo, Starling's law of the heart relates LVEDV to stroke volume ( Fig. 8­13)­­the higher the LVEDV (up to a point), the higher the stroke volume. Since cardiac output is the stroke volume times the heart rate, at a constant heart rate the same Starling relationship exists for LVEDV vs. cardiac output.

Shifts of the Starling curve can occur as a result of anything that alters myocardial contractility; the curve can be shifted to the left (increased contractility, as may occur from inotropic drugs) or to the right (decreased contractility, as may occur from myocardial infarction). A Starling curve shifted to the left will have an increased cardiac output for a given LVEDV; a curve shifted to the right will have a decreased cardiac output for a given LVEDV (Fig. 8­13).

Fig. 8­12. The Starling curve relates the degree of myocardial stretch (measured as end­diastolic fiber length) to the degree of muscle work (left ventricular stroke work). The former is the preload of the left ventricle and, in vivo, correlates with the left ventricular enddiastolic volume.

Starling's law is often reinterpreted to relate left ventricular end­diastolic pressure (LVEDP) to cardiac output (Fig. 8­13). LVEDP is the "filling pressure" of the left ventricle, i.e., the left ventricular pressure at the end of diastole. As the filling pressure increases (presumably reflecting filling volume), cardiac output increases, again up to a point. If this relationship is true and if PAWP accurately reflects LVEDP, PAWP can then be used as a measure of left ventricular preload. As a measure of preload, PAWP can serve as a valuable guide to therapy.

Fig. 8­13. The Starling curve in clinical practice. In clinical practice the stroke volume (or cardiac output) is used in place of left ventricular stroke work, and the left ventricular end­diastolic pressure (LVEDP) is used in place of left ventricular end­diastolic volume (LVEDV). This reinterpretation of the Starling curve allows pulmonary artery wedge pressure (PAWP) to serve as the basic measurement of left ventricular preload on the assumption that PAWP equals LVEDP and that LVEDP accurately reflects LVEDV. Changes in myocardial contractility affect the quantitative relationship between preload and stroke volume. The middle curve represents the normal relationship. Changes in contractility of the myocardium can displace the Starling curve to the left (increased contractility) or to the right (decreased contractility) .

Fig. 8­14. Left ventricular compliance curve­­LVEDV vs. LVEDP. A, Idealized ventricular compliance curve a linear function. The same change in pressure at an part of the straight line reflects the same change in volume. B, Actual ventricular compliance curve, a curvilinear function. The same change in pressure at different parts of the curve reflects a different change in volume

In many cases PAWP accurately reflects left ventricular filling pressure (LVEDP) and can be used as a guide to patient management. However, the relation between LVEDP and LVEDV is not a straight line (Fig. 8­14, A) but instead is curvilinear (Fig. 8­14, B). Ventricular compliance is the change in volume (LVEDV) per the change in distending pressure (LVEDP). Because this relationship is not linear, a change in LVEDP (and hence PAWP) cannot be assumed to reflect accurately a change in ventricular preload; in Fig. 8­14, B, a small pressure change in the ascending limb of the curve reflects the same volume change as does a large pressure change near the top of the curve. Furthermore, ventricular compliance curves are greatly altered with heart disease so that relationships between pressure and volume can be even more distorted; in the low­compliant, stiff left ventricle, a high LVEDP may actually reflect a relatively small LVEDV.

Positive end expiratory pressure (PEEP) can also affect ventricular compliance by increasing the intrathoracic pressure so that the pressure surrounding the left ventricle is increased. This effect is similar to the one PEEP has on elevating PAWP. Normally, at end­exhalation, the thoracic pressure surrounding the left ventricle is at, or close to, atmospheric pressure (zero). With PEEP this surrounding pressure may be positive (above atmospheric). As a result, a higher than normal LVEDP will be required to achieve a given ventricular volume, and the ventricle's compliance will be reduced. Fig. 8­15 shows how changes in left ventricular preload may not be reflected in the LVEDP.

In summary, there are several situations where PAWP may not reflect the true preload (LVEDV) of the left ventricle. These situations are summarized in the box on p. 170. Obviously, the true relationship of PAWP (as measured with the Swan-Ganz catheter) and the left ventricular preload is a complex one, especially when the patient is receiving artificial ventilation or when there is altered left ventricular compliance. There is no easy way to account for the multitude of factors listed in the box except to follow the patient closely, gauging changes in cardiac output, oxygenation, and urine output with changes in wedge pressure. PAWP is another, albeit important, measurement, that should never substitute for intelligent clinical assessment of the patient.

Fig. 8­15. The pulmonary artery wedge pressure (PAWP) reflects left ventricular end­diastolic pressure (LVEDP), but LVEDP may not accurately reflect left ventricular preload. The relationship is shown of the PAWP to the left ventricular preload (left ventricular volume) in three situations. In each situation PAWP is elevated to 25 mm Hg and accurately reflects an LVEDP of 25 mm Hg. A, The cause of the PAWP elevation is increased pleural pressure ( + 10 mm Hg), which might occur from positive end­expiratory pressure (PEEP) therapy. The increased pleural pressure adds to the LVEDP and is therefore reflected in the PAWP. However, the true left ventricular preload (left ventricular volume) is normal. B, The cause of PAWP elevation is an elevated left ventricular volume; pleural pressure is normal at­­5 mm Hg. Thus PAWP accurately reflects an elevated left ventricular preload. C, The cause of PAWP elevation is a stiff left ventricle, which might occur from myocardial ischemia. PAWP and pleural pressure are the same as in B, and left ventricular preload (left ventricular volume) is normal. (Modified from O'Quin, R., and Marini, J.J.: Am. Rev. Respir. Dis. 128:320, 1983.)

PITFALLS AND COMPLICATIONS IN HEMODYNAMIC MONITORING

There are probably more pitfalls and complications from use of Swan­Ganz catheterization than from any other technique mentioned in this book. Some of the potential pitfalls were discussed in the previous section on pulmonary artery wedge pressure. Pitfalls are errors in judgment or management; complications refer to problems with the technique itself. The box on p. 171 lists the common pitfalls and complications of this technique.

This list is by no means complete, but it does represent most of the problems likely to be encountered. Despite the potential for problems, one should not hesitate to use hemodynamic monitoring in the right situation. Properly used, hemodynamic monitoring (including arterial cannulation and blood gas analysis) can provide an accurate physiologic picture of critically ill patients.

HEMODYNAMIC MONITORING IN CLINICAL PRACTICE

Table 8­5 shows typical hemodynamic changes in some common clinical conditions; these changes represent the ''pure" cases. Many patients have more than one problem, e.g., adult respiratory distress syndrome (discussed in Chapter 11) and leftsided heart failure. To make things even more complicated, pulmonary edema can be aggravated by low oncotic pressure.

[Table of Contents][Previous Chapter][Chapter 8, Page 1][Chapter 8, Page 2][Chapter 8, Page 3][Chapter 8, Page 5][Next Chapter]