Williams Manual of Pregnancy Complications, 23 ed.

CHAPTER 46. Pulmonary Artery Catheterization

Use of the pulmonary artery catheter has contributed immensely to understanding of normal pregnancy hemodynamics as well as pathophysiology of common obstetrical conditions. These include severe preeclampsia–eclampsia, acute respiratory distress syndrome (ARDS), and amnionic fluid embolism. That said, in our experience, invasive hemodynamic monitoring is seldom necessary for critically ill obstetrical patients as it seldom changes management.

After years of use, randomized trials of medical and surgical patients have described no benefits with pulmonary artery catheterization and have not shown to improve survival or organ function. The indication for using invasive monitoring in obstetrical patients is limited and is based on the condition and individual needs of the patient.

Invasive monitoring is usually initiated through the internal or external jugular vein or the subclavian vein. The femoral and antecubital veins are used less frequently because of greater difficulty in positioning the catheter. However, the antecubital approach may be prudent in women with a coagulopathy.

HEMODYNAMIC INDICES

Hemodynamic information gained by pulmonary artery catheter monitoring includes continuous central venous pressures, pulmonary artery pressures, intermittent pulmonary capillary wedge pressures, and cardiac output via thermodilution. Heart rate and rhythm are monitored and may be continuously recorded. Systemic arterial blood pressure can be measured noninvasively (manual or automatic sphygmomanometers) or by arterial catheterization. However, hemodynamic information gained by pulmonary artery monitoring does not always reflect uteroplacental perfusion. Assessment of fetal heart rate pattern is more reliable for this purpose. Formulas for deriving various cardiopulmonary parameters are shown in Table 46-1.

TABLE 46-1. Formulas for Deriving Various Cardiopulmonary Parameters

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Cardiac output, stroke volume, and systemic and pulmonary vascular resistance can be corrected for body size by division of the results by the body surface area in order to obtain index values. Specific body surface area nomograms have not been developed for pregnant women; thus, nomograms for nonpregnant adults are used. Hemodynamic parameters for healthy nonpregnant and pregnant women at term are shown in Table 46-2. Increased blood volume and cardiac output are accommodated by decreased vascular resistance and increased pulse rate.

TABLE 46-2. Hemodynamic Changes in Normal Nonpregnant Women Compared with Those When Pregnant at Term

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INTERPRETATION

Cardiac function is assessed in four areas: preload, afterload, inotropic state, and heart rate. Preload is determined by intraventricular pressure and volume, thus setting the initial myocardial muscle fiber length. Clinically, the right and left ventricular end-diastolic filling pressures are assessed by central venous pressure and pulmonary capillary wedge pressure, respectively. Cardiac output plotted against central venous or pulmonary capillary wedge pressure constructs a cardiac function curve for the respective ventricle. The ventricular function curve demonstrates that a failing heart requires a higher preload or filling pressure to achieve the same cardiac output as a normally functioning heart (see Figure 46-1). Therapeutic manipulation of ventricular filling pressures and simultaneous measurement of cardiac output allows calculation of optimal preload at the bedside. Preload can be increased by the administration of crystalloid, colloid, or blood, and it may be decreased by the use of a diuretic, vasodilator, or phlebotomy.

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FIGURE 46-1 Ventricular function in ten healthy pregnant women at term. Individual values are plotted and all but one fall between the lines that define normal function. LSWI, left ventricular stroke work index; PCWP, pulmonary capillary wedge pressure. (Reproduced, with permission, from Cunningham FG, Leveno KJ, Bloom SL, et al (eds). Williams Obstetrics. 23rd ed. New York, NY: McGraw-Hill; 2010. Plotted data points from Clark SL, Cotton DB, Lee W, et al: Central hemodynamic assessment of normal term pregnancy. Am J Obstet Gynecol 161:1439, 1989.)

Afterload is defined as ventricular wall tension during systole and is dependent on end-diastolic ventricular radius, aortic diastolic pressure, and ventricular wall thickness. The extent to which right or left intraventricular pressures rise during systole depends primarily on the pulmonary or systemic vascular resistance. With heart failure, increases in afterload, such as with preeclampsia, worsen failure by decreasing both stroke volume and cardiac output. Afterload, like preload, can be increased or decreased therapeutically. Increases in afterload are mediated through α-adrenergic stimulation (e.g., phenylephrine). The intermittent intravenous administration of small incremental doses of hydralazine with intermittent arterial pressure monitoring has been proven safe for both mother and fetus in decreasing afterload or systemic vascular resistance. Sodium nitroprusside by continuous intravenous infusion is commonly used in medical intensive care units.

The inotropic state of the heart is defined as the force and velocity of ventricular contractions when preload and afterload are held constant. In low-output cardiac failure, both preload and afterload should be optimized. If this fails to restore cardiac output to an acceptable level, attention should be directed to improving myocardial contractility. β-Agonists such as dopamine, dobutamine, and isoproterenol are effective in improving cardiac output acutely. Digitalis may be used either short term or long term.

Heart rate is an important parameter, and either tachycardia or bradycardia may cause problems. If cardiac output is compromised because of bradycardia, treatment either with atropine or cardiac pacing is indicated. Sustained tachycardia can lead to congestive heart failure because of shortened systolic ejection and diastolic filling times or myocardial ischemia, especially with valvular heart disease. The pathophysiological basis of tachycardia should be determined and corrected; common causes include fever, hypovolemia, and pain.

COMPLICATIONS

The risk of invasive monitoring includes overinterpretation or misinterpretation of data. The most common complication is pneumothorax, which occurs in 5 percent of subclavian and 0.01 percent of internal jugular vein insertions. Intrathoracic bleeding has been reported during attempts at subclavian vein cannulation. The pulmonary artery catheter may incite a variety of ventricular and supraventricular arrhythmias as it passes through the right side of the heart, and disconnection of the catheter or introducer from the associated intravenous lines may cause massive hemorrhage. Rare complications include pulmonary artery rupture, pulmonary infarction, sepsis, knotting of the catheter, thromboembolism, and balloon rupture. Given a broad range of medical and surgical patients with conditions necessitating invasive monitoring, 3 percent will sustain a major complication, including death.


For further reading in Williams Obstetrics, 23rd ed.,

see Chapter 42, “Critical Care and Trauma.”