Chapter 1: Basic Hemodynamic Monitoring in Obstetric Patients

The care of obstetric patients requiring hemodynamic monitoring can be quite complex. It requires a basic understanding of pregnancy physiology, monitoring equipment, and applications of information gathered. In this chapter, we will review invasive and noninvasive hemodynamic principles that provide the reader with a functional understanding of circulatory monitoring and ways to practically apply this understanding to normal and pathologic conditions in the gravid patient.

The interpretation of data gathered with hemodynamic monitoring is most useful when applied according to disease state and used to identify ominous changes before they result in clinical deterioration (Table 1-1). Responses to therapy can be closely followed with the help of hemodynamic monitoring using invasive and noninvasive techniques.

Functional Hemodynamics

Invasive Monitoring

J.C. Swan and W. Ganz first introduced this technology in 1970.¹ The pulmonary artery catheter (PAC) is guided into the superior vena cava (SVC) by way of the internal jugular or subclavian vein, then into the right atrium (RA); with blood flow it “floats” into the right ventricle (RV), past the pulmonary valve into the pulmonary artery, and the inflated balloon tip will end up positioned or “wedged” into a branch of the pulmonary artery. See Fig. 1-1. Measurements should be taken at end expiration.

Once “wedged,” the PAC waveform has a specific configuration; each portion relates to an action in the left atrial chamber. The “a wave” correlates to atrial contraction; one will notice a rise in pressure on the waveform. Next is the “x wave” which signifies atrial diastole and relaxation of the chamber in preparation for filling; one will notice a drop in pressure on the waveform. The next rise in pressure corresponds to passive left atrial filling and this is the “v wave.” The “y wave” denotes atrial emptying. See Figs. 1-2 and 1-3.

Cardiac output (CO) is often measured with a PAC using thermodilution. A small volume of liquid with a lower temperature than the blood is injected into the PAC where a thermistor measures the change in temperature as the blood flows through the heart chambers. These temperature change measurements can be plotted on a graph and the area under the curve (AUC) is used to estimate the cardiac output.¹ See Fig. 1-4 and Table 1-2.

Over the past 2 decades, the utility of the PAC in guiding the management of critically ill patients has been under scrutiny. Keeping in mind, outside of pregnancy, several multicenter studies have been unable to demonstrate mortality benefit with the use of a PAC at 30 days, 6 months, and 1 year in intensive care unit (ICU) and high-risk perioperative patients.^{1,2, 3} Clinicians overall have become less adept at interpreting data from PAC measurements as these data have been used less frequently over time. Aside from that, PAC placement is not without risk. Arrhythmias, iatrogenic pneumothorax, vascular rupture and thrombosis, valve injury, and central line blood stream infection can occur. Although the prevalence of these risks in recent literature ranges from 0.1% to 1.3%,^4,5 the consequence of a complication can be dire.

Evidence for PAC use in pregnancy is scarce in modern literature. In obstetrics, the primary indication for invasive hemodynamic monitoring has been in women with severe preeclampsia complicated by acute kidney injury (AKI) and oliguria, as well as those with pulmonary edema where PAC has been shown to facilitate management.⁶ Other studies and reports have shown it to be helpful in the management of women with severe valve disease, pulmonary hypertension, cardiomyopathy, septic shock, and renal disease.⁷

The above-said information gathered from PAC measurements effectively provides a means to estimate the impact of the parameters that affect how well the heart pumps and the response to treatment. These parameters include venous return/preload, peripheral resistance/afterload, heart rate, and contractility. Functionally, if you want to determine the effect or adequacy of a volume load in patients who are fluid avid, you want to see an increase in blood pressure with a corresponding decrease in heart rate, as well as an increase in central venous pressure (CVP), pulmonary artery occlusion pressure (PAOP), stroke volume variation (SVV), and ideally CO.⁸ Patients who respond to volume can be safely given additional boluses with a low risk of developing pulmonary edema until adequate resuscitation is determined. Keep in mind that no one variable alone is an adequate measure of volume response when looked at independently, as noted in the FACCT study.⁹ It is the combination of measurements and trends that are most helpful in determining volume response.

There are specially made PACs that can measure oxygen saturation continuously and accurately estimate the mixed venous oxygen saturation (Svo₂) at the level of the distal pulmonary artery. The Svo₂ represents the amount of oxygen left in the circulation after passing through the tissues and measures the balance between oxygen consumption and delivery. The normal value for Svo₂ is 70% to 75%.¹⁰ It makes sense that Svo₂ is decreased in conditions that increase consumption, for example, exercise, shivering, severe anemia, hypoxemia, and decreased cardiac output. A very low Svo₂ (ie, 30%-40%) is seen with tissue ischemia.¹⁰

The CVP is an estimate of right ventricular preload. It can be elevated in cases of pulmonary edema, positive-pressure ventilation, right ventricular failure (more commonly as a sequelae of left ventricular failure), pulmonary hypertension, severe pulmonary stenosis, and tamponade. One CVP measurement alone is not helpful; the trend in measurement allows one to monitor response to therapy (ie, volume or diuresis) is most useful. One functional application of this is in patients who are receiving positive-pressure ventilation. If the patient is intravascularly depleted, as compared to those who are euvolemic, you will see a decrease in cardiac output with application of positive pressure (inspiration phase of mechanical ventilation) because the vena cava gets compressed in the thorax and this decreases venous return. The CVP in this circumstance may measure a little higher than expected because of increased intrathoracic pressure from positive-pressure ventilation, but the patient is still low in intravascular volume. In patients with normal hearts who are spontaneously breathing, the negative (decreased) intrathoracic pressure with inhalation “pulls blood into the heart” and increases venous return. The CVP typically decreases by 1 mm Hg during inhalation in spontaneously breathing patients.⁸ However, in spontaneous ventilation, it can decrease by more with intravascular depletion.

Measurements of the PAOP are used to indirectly estimate left atrial pressure or the pressure in the pulmonary veins. Following the trends in PAOP can be helpful in estimating pulmonary venous resistance and left atrial preload.¹ PAOP measurements are helpful in distinguishing cardiogenic (with both high PAOP and CVP) from noncardiogenic (low or normal PAOP and high CVP) pulmonary edema.¹

In pathologic conditions that involve pulmonary capillary wall damage or increased permeability (severe preeclampsia, sepsis, acute respiratory distress syndrome [ARDS], hemorrhagic shock in extremis), the CVP and PAOP can be anticipated not to correlate well.¹¹ Interestingly enough, disparate values between the CVP and PAOP have been demonstrated in gravid patients without left-sided heart failure and a structurally normal heart.¹² Because of this, CVP readings in pregnant patients cannot be used to make any assumptions about function of the left side of the heart and are most reliable at the extremes of values (really low or really high).¹² See Table 1-3.

Noninvasive Monitoring

Belfort et al¹³ was able to demonstrate a reasonable correlation between invasive and noninvasive monitoring by 2-dimensional (2D) echocardiogram in 11 critically ill gravidas.¹³ Stroke volume and cardiac output estimations correlated best, followed by pulmonary artery and ventricular filling pressures. This study provided some of the earliest evidence in support of noninvasive approaches to hemodynamic evaluation in pregnancy.¹ The practical application of noninvasive monitoring was demonstrated in a follow-up study by Belfort et al of 14 patients where all but 2 critically ill patients were able to be successfully managed without the use of a pulmonary artery catheter.¹⁴ Transesophageal Doppler can measure descending aortic flow used to estimate trends stroke volume and cardiac output which can be helpful during a code, particularly in the operating room.¹⁵

Stroke volume estimation by 2D echocardiogram techniques has been validated in pregnancy,¹⁶ and this value is then multiplied by the heart rate to obtain the cardiac output (remember CO = stroke volume [SV] × heart rate HR]). In the future, 3D echocardiogram techniques may replace 2D as they provide more accurate geometric assessment of the cardiac chambers and reduce inherent errors based on geometric assumptions made using 2D echocardiography.^{17,18, 19} Also, the accuracy between measurements of chamber volume and correlation to pressure depends on the compliance of the chamber measured. For example, if diastolic dysfunction is present (or conditions where the chamber does not relax well, ie, tachycardia, ischemia, sepsis, high intrathoracic pressure), the end-diastolic volume (EDV) measured by echocardiogram would be reduced but filling pressures measured by PAC would be elevated. The PAC measurement alone might cause one to think this patient has adequate volume, but these pressures are elevated in the context of poor wall compliance. Longitudinal studies have been performed to assess baseline 2D echocardiographic variables in pregnancy and postpartum (Table 1-4).

Arterial pressure waveform (APWF) monitoring uses the principle that stroke volume can be estimated from the morphology of the arterial pressure curve and has been validated for use in pregnant patients. Accuracy of APWF monitoring is limited by arrhythmias, use of intra-aortic balloon pump (IABP), septic shock, and liver failure.¹

Thoracic electrical bioimpedance technology has also been validated for use in pregnancy; however, estimations may be less reliable in obese patients and results are affected by maternal position.^21,22 One advantage of bioimpedance methods is the ability to follow beat-to-beat variations in CO.²³

Expected physiologic changes of pregnancy have been studied since the 1950s. Studies consistently demonstrate increased preload and volume over the course of gestation, starting as early as 7 to 8 weeks of pregnancy. Other changes include increased cardiac output, with stroke volume mainly driving this increase. The volume loading or “gestational hypervolemia” that occurs in pregnancy increases stroke volume and happens mainly over the first 2 trimesters of a normal pregnancy. Toward the end of the third trimester, cardiac output reaches a plateau and remains relatively constant until the time of labor.²³ See Table 1-5. There are dramatic hemodynamic changes that normally occur during labor which will be reviewed later in this chapter.

There tends to be little change overall in PAOP and CVP in pregnancy despite significant increases in volume.¹ This is due to progesterone-mediated decreases in systemic vascular resistance (SVR) and pulmonary vascular resistance (PVR). With less resistance, the circulatory system can accommodate more volume without a real appreciable change in pressure.

Cardiac remodeling occurs over time in pregnancy. This is evidenced by electrocardiogram (ECG) changes that reflect cellular hypertrophy, particularly of the left ventricle and slight change in cardiac axis toward left deviation,^1,23 which is partially an effect of the encroaching gravid uterus on the diaphragm. All chambers become enlarged, in particular the left atrium (LA).²⁰ This enlargement of the LA and stretching of myocytes can trigger supraventricular arrhythmias, particularly in predisposed patients (thyroid disease, congenital heart disease with and without repair). Annular diameters of the valves increase.²⁰ A flow murmur is normal in pregnancy. In over 90% of women, mild pulmonary and tricuspid regurgitation occurs; this is not considered pathologic.^24,25 Up to 33% of women will show evidence of clinically insignificant mitral regurgitation as well.²⁴

Effect of Position Change on Maternal Hemodynamics

A 20-week-sized uterus (at the level of the umbilicus) is large enough to compress the inferior vena cava (IVC), which reduces venous return leading to diminished stroke volume and cardiac output, ultimately resulting in decreased blood pressure. This phenomenon seen in pregnancy is called supine hypotension or supine hypotensive syndrome. Positional effects on cardiac output become more impressive as the pregnancy progresses. There can be up to a 30% decrease in cardiac output in the supine position as compared to the lateral recumbent position. A lateral tilt (or uterine displacement) of at least 15% is sufficient to relieve pressure from the gravid uterus on the IVC and restore normal cardiac output. This should be done anytime augmentation of cardiac output is necessary. During cardiac resuscitation, however, a 30% tilt is recommended for maximum augmentation of cardiac output.²⁶

Normal Intrapartum Changes

In the latter part of the third trimester, cardiac outputremains relatively stable but increases dramatically over the course of labor and immediately after the third stage.^23,26,27 These changes may be more pronounced in obese patients. With contractions, there is an “autotransfusion" of 300 to 500 mL of volume into the venous circulation, leading to a 30% to 50% increase over baseline in cardiac output intrapartum.^20,23,26,27 The increase in cardiac output is at its peak during the second stage of labor.^20,23 Pain response also contributes to the increase in cardiac output over the course of labor, and this effect is blunted by pain relief, in particular, regional anesthesia. One can anticipate a significant reduction in SVR with regional anesthesia. Data from patients having cesarean delivery and spinal anesthesia demonstrate a 26% to 31% decrease in SVR^{28,29, 30} and others have shown this to correlate with an average 20% decrease in mean arterial pressure (MAP) from baseline.³¹ Ways to decrease hypotension resulting from neuraxial anesthesia include left uterine displacement, intravenous pre- or cohydration with crystalloid (although there is some debate over success of this intervention alone to prevent hypotension), leg wrapping, low-dose intrathecal local anesthesia with supplemental opioid, use of phenylephrine as prophylaxis or treatment, and use of epidural block over spinal.²³ See Table 1-6.

Normal Postpartum Changes

Within the first half-hour after the third stage with removal of the uteroplacental vascular shunt, the additional approximately 500 mL of volume is redirected to the maternal venous circulation.²⁷ The latter in combination with relief of aortocaval compression can result in upward of 60% to 80% increase in cardiac output over this period, which gradually decreases over time²⁷ but remains peaked for at least approximately 10 minutes after delivery.²⁸ Patients with cardiac risks should be closely monitored in the first 4 to 6 hours after delivery as this period is a vulnerable time for a cardiac event exacerbated by the hemodynamic changes of parturition. For women with disorders such as diastolic dysfunction, congenital heart disease, and valve disorders, prolonged noninvasive cardiac monitoring postpartum is indicated typically involving arterial-line monitoring and telemetry. In the 48 hours after delivery, cardiac output overall remains relatively elevated and gradually decreases over the subsequent 3 months.²⁷

As our maternal population ages and body mass indices (BMIs) increase, we are seeing more cardiovascular diseases and ICU admissions for heart failure of various causes.³² In addition, as heart surgery has advanced, there are more women of reproductive age with congenital heart disease who are becoming pregnant and can have cardiac complications as a result of normal physiologic changes of pregnancy. The CARPREG Investigators have developed a reliable prediction model of cardiac events based on maternal risk factors (Table 1-7). There are also data to suggest this model may be further modified in the setting of decreased subpulmonary ventricular systolic function and/or severe pulmonary regurgitation to predict cardiac events in women with congenital heart disease.³³ In this section, we will review the pathologic conditions one may encounter and provide a framework to understand their hemodynamic complexities.

Circulatory Shock States

“Shock” is defined by inadequate tissue perfusion. Poor tissue perfusion must be addressed by correcting the underlying disorder and supportive management with interventions to improve perfusion and tissue oxygenation. One should aim to maintain vasomotor tone with vasopressors if hypotension occurs. Maternal hypotension beyond 4 minutes has been shown to be deleterious to the fetus.³⁴ The converse is true with elevated maternal blood pressure in that increased maternal BPs have been shown to decrease placental perfusion. Increased placental resistive index (RI) has been noted with increasing MAPs. Mean arterial pressures between 100 and 129 mm Hg has been associated with normal RI. Mean arterial pressures greater than 140 mm Hg correlates consistently with abnormal resistive indices.³⁵ A MAP of greater than 65 mm Hg is typically adequate to maintain tissue perfusion in the nongravid state. In cardiac surgical cases on obstetric patients, one of the recommendations for cardiopulmonary bypass is to maintain a perfusion pressure of greater than 70 mm Hg.³⁶ Uteroplacental perfusion is much more complex and multiple factors need to be considered. Placental blood flow (PBF) approximates 80% to 90% of total uterine blood flow (UBF) at term and this relationship is linear. Three major characteristics of placental vascular control are important. These include (1) the relationship between perfusion pressure and flow, (2) the responses of the spiral arteries to vasoactive stimuli, and (3) the effects of contractions. Uterine venous pressure tends to be constant under most cases and systemic blood pressure may be used to approximate PBF changes. For example, a 25% decrease in MAP would be expected to cause a 25% decrease in PBF.³⁷

Volume resuscitation and vasopressor support are often needed simultaneously in states of hypovolemic and septic shock. In general, patients who are preload responsive require volume to increase blood flow, and administration of crystalloids is the typical first-line step (unless the shock is from pump failure). Volume responsiveness has been arbitrarily defined as a greater than or equal to 15% CO increase in response to a 500-mL bolus fluid challenge.³⁸ Other measures of volume responsiveness, such as systolic pulse pressure variation (sPPV) and stroke volume variation (SVV) using minimally invasive measures (ie, Vigileo, PiCCO, LiDCO), are based on changes in left ventricular output during positive-pressure ventilation. During the inspiratory phase of positive-pressure ventilation, intrathoracic pressure passively increases, with a corresponding increase in right atrial pressure; this causes decreased venous return which decreases right ventricular output, and ultimately left ventricular output after a few heartbeats.³⁹ In preload-dependent patients, the magnitude of the cyclic changes in left ventricular SVV and arterial sPPV is proportional to volume responsiveness.³⁸

If the patient is not preload responsive and has normal or increased vasomotor tone but is hypotensive, then the heart must be investigated for pump failure (cardiogenic shock).⁸ Echocardiogram is the mainstay of noninvasive diagnosis. Some patients may require pulmonary artery catheterization. In the setting of cardiogenic shock, if inotropic therapy is inadequate to improve cardiac output, augmentation with devices such as an intra-aortic balloon pump (IABP), an Impella or ventricular assist device can be lifesaving. Table 1-8 outlines the typical hemodynamic profile of the different types of shock.

Hypovolemic

The hemodynamic profile of hypovolemic shock shows decreased CO, decreased right- and left-sided preload (low CVP and PAOP, low ventricular filling pressures), and a compensatory increase in afterload (SVR). This can be the result of massive blood loss, gastrointestinal (GI) volume losses, third spacing as seen in burns and pancreatitis. Women with severe preeclampsia tend to have large amounts of third-space fluid (because of high hydrostatic pressure, leaky capillaries, and low oncotic pressure) and can show signs of hypovolemic shock with blood loss from delivery.

Cardiogenic

This is seen when the myocardium is not functioning and fails as seen in myocardial infarction (MI), cardiomyopathy, and ischemia, or other conditions leading to failure. Cardiogenic shock is the manifestation of heart failure at its extreme with evidence of hypotension and hypoperfusion requiring intervention (medical, minimally invasive, or surgical). The heart is typically big and noncompliant so the hemodynamic profile seen here is low CO and high ventricular filling pressures. The body is rote in recognizing hypoperfusion, from whatever cause of low CO, and will increase SVR as a compensatory reflex (similar to what is seen in hypovolemic shock; however, it is counterproductive in the case of pump failure).

Obstructive

Cardiac output is low in this setting because of some sort of obstruction either on the left or right side of the heart. Again, increased SVR is seen because of hypoperfusion as a result of the obstructed flow and ventricular filling pressures are high. Flow can be obstructed as a result of tamponade, constrictive pericarditis (as can be seen in metastatic cancer, viruses, or inflammatory states), or tension pneumothorax. All of the conditions described dramatically decrease venous return to the right side of the heart. The clinician should recognize the pattern of cardiac tamponade characterized by equilibration of diastolic pressures (on PAC measurement, the diastolic pressures will be the same) on the left and right side of the heart, often associated with a decrease in systolic blood pressure (SBP) by greater than 10 mm Hg with inspiration (pulsus paradoxus). These patients need preload/volume and treatment of the obstructive cause is the mainstay of management (ie, pericardiocentesis, needle decompression of tension pneumothorax). Interventions that decrease preload (diuretics or venodilators) can be deleterious.

Distributive

This is the one shock state in which SVR will be decreased (in early stages of septic shock one can see a transient increase in SVR) because of vasodilation. The profile seen in this type of shock can be variable depending on the cause (sepsis, anaphylaxis, neurogenic causes, or adrenal crisis) but typically involves a normal or increased CO with low SVR, and normal or low ventricular filling pressures.

Interventions aimed at correcting these shock states are first to correct and maintain normal mean arterial pressure and cardiac output. When there is pump failure without significant hypotension, therapy is aimed at reducing preload (with diuretics and venodilators like nitroglycerine) and afterload (with arterial dilators like hydralazine in gravid patients—angiotensin-converting enzyme [ACE] inhibitors if postpartum—and nitroprusside). In the setting of pump failure and hypotension, one must improve pump performance (inotropes, IABP, Impella device, or ventricular assist device [VAD]) to improve blood pressure before reducing preload and afterload. The goal of resuscitation is evidence of adequate tissue perfusion as measured by normalization of lactate and base deficit.

Preeclampsia

Complicated severe preeclampsia is the most common reason for ICU admission in the obstetric population.^{40,41, 42} Because of this, it is imperative to understand the various hemodynamic challenges this condition presents. Noncardiogenic pulmonary edema in severe preeclampsia occurs more commonly than cardiogenic pulmonary edema⁴³ with the combined increased pulmonary vascular permeability and hydrostatic pressure as well as decreased colloid oncotic pressure. This recipe for third spacing is the cornerstone of preeclamptic physiology where the patient can have total body fluid overload but intravascular depletion. Women with pulmonary edema associated with severe preeclampsia will show evidence of high left- and right-sided filling pressures as shown by Gilbert et al⁴⁴ and require diuretic therapy. Women with preeclampsia and pulmonary edema or pleural effusions should have an echocardiogram done to assess cardiac function as well.

Intravascular depletion seen in preeclampsia can result in hyperdynamic cardiac function in order to maintain cardiac output. However, one caveat to hemodynamic assessment in patients with severe preeclampsia is the potential for significant underestimation of the cardiac output with transesophageal echocardiogram (TEE) by up to 40% as demonstrated by Penny et al.⁴⁵

The vast majority of patients with severe preeclampsia can be managed without need for invasive hemodynamic monitoring. Although no outcome benefits have been proven, a reasonable indication for PAC use is in severe preeclampsia with acute kidney injury (AKI) and persistent oliguria unresponsive to volume.⁴⁶ Clark et al was able to describe 3 hemodynamic patterns in severe preeclampsia complicated by oliguria: (1) those with decreased CO and high PAOP and SVR; (2) normal or increased CO and PAOP with normal SVR; (3) high CO and SVR with low PAOP.⁴⁶

Multiple Gestation

Carrying twins has been shown to cause an increase in blood volume and cardiac output by 10% and 20%, respectively, over singleton pregnancies.^47,48

Cardiomyopathy

In women with peripartum cardiomyopathy, one study showed an increased likelihood of normalization of cardiac function in those with left ventricular ejection fraction (LVEF) greater than 30% at the time of diagnosis.⁴⁹ Patients with hypertrophic obstructive cardiomyopathy (HOCM) need slower heart rates in order to adequately fill their left ventricle. Outflow obstruction in gravid patients with HOCM is exacerbated by decreased left ventricular filling from tachycardia, decreased preload and/or afterload, and providers need to be mindful of this when considering or providing regional anesthesia for these patients.

Valve Disease

As a rule of thumb, patients with left-sided regurgitant conditions (ie, mitral or aortic regurgitation) tend to tolerate the hemodynamic changes of pregnancy better than those with severe stenotic disease.

In general, the decreased SVR in pregnancy promotes forward flow and lessens the severity of regurgitant conditions. In comparison, left-sided stenotic valves create a condition of relatively fixed cardiac output in a patient with physiologic volume loading that may result in higher left atrial pressures which can lead to arrhythmias and failure.⁵⁰ Tachycardia in patients with severe stenosis (especially in the aortic valve) can lead to decreased coronary artery perfusion (as the coronary arteries branch off right beyond the aortic valve) and result in myocardial ischemia, failure, or infarction.

Mitral Stenosis

This is the most common valve lesion seen in pregnancy as a result of rheumatic disease worldwide.²⁷ Higher blood volume and a resistant, stenotic valve in these obstetric patients can lead to increased left atrial (LA) pressures, LA distension and SVT, as well as pulmonary edema and right-sided heart failure. In cases of a severely stenotic valve (area <2 cm²),³³ the mild tachycardia in pregnancy combined with small valve area can lead to decreased left ventricular filling, hypotension, and syncope. Preventing tachycardia with β-blockade (β₁ selective blockers like metoprolol are superior to nonselective blockers like labetalol) allows for more ventricular filling time and volume. Early regional anesthesia is helpful in attenuating tachycardia from pain and anxiety in labor. A “slow-dose” epidural is more favorable in these patients as rapid decreases in SVR can be deleterious to these patients who cannot compensate (by increasing cardiac output) for the low blood pressure that occurs with regional anesthesia.⁵¹ Those with severe stenosis may benefit from invasive peripartum (includes the immediate postpartum period) hemodynamic monitoring with a PAC or less invasive arterial pressure waveform monitoring along with CVP measurements to asses for evidence of volume shifts that can lead to cardiogenic pulmonary edema.⁵²

Aortic Stenosis

Patients with severe aortic stenosis (valve area <1.5 cm²)³³ will also be limited with a fixed cardiac output which is problematic as the coronary arteries branch off immediately beyond the valve. Decreased coronary artery perfusion can occur, resulting in ischemia and infarction risk. The mortality rate in these patients is as high as 17%.⁵³ They are vulnerable to cardiogenic pulmonary edema from rapid intrapartum and postpartum volume shifts. These patients may benefit from invasive monitoring to facilitate maintenance of adequate preload while avoiding pulmonary edema. Maintaining this balance means giving the patient volume in small crystalloid boluses if the CVP and PAOP pressures are too low. If the CVP and PAOP become persistently elevated with a corresponding drop in oxygen saturation and rales on lung auscultation, diuretic therapy is necessary.

Regurgitant Valves

Left-sided valve regurgitation (mitral and aortic valves) is well tolerated in pregnancy as the decrease in SVR and increased blood volume promote forward flow across the valves.⁵¹

Although the incidence of structural cardiac disease is low in obstetric patients, women in their reproductive years with these conditions are increasingly seen as advances in cardiac surgery and intensive care have improved. It is important to understand the baseline risk for morbidity and mortality in these patients. Women with New York Heart Association (NYHA) class I and II tend to tolerate pregnancy well, approximately 90% of obstetric patients with cardiac disease fall into these categories.²⁷ Up to 85% of maternal deaths related to cardiac disease are in women with NYHA class III or IV status at the beginning of pregnancy.²⁷ Patients with Eisenmenger or cyanotic heart disease have an unacceptably high mortality rate and are advised against pregnancy.²⁷

Physiologically, those with cyanotic disease would suffer from the decreased SVR in pregnancy as this can increase right- (deoxygenated)-to-left (oxygenated) shunting (R→L), decrease pulmonary perfusion, and lead to hypoxemia. Patients with high pulmonary pressures and a clinically significant septal defect rely on higher systemic pressures to maintain a relative left- (oxygenated)-to-right (deoxygenated) shunt (L→R). A memory aid is you always want the L to come before R (L→R) in the alphabet; if it does not, something is wrong. These patients do not tolerate loss of blood volume or hypotension well and can have severe hypoxemia with shock states from hemorrhage or sepsis, and the decrease in SVR that can occur with anesthesia.⁵⁴ Over time, even L→R shunts can increase the volume load to the right side (pulmonary side) and lead to pulmonary hypertension and shunt reversal (to R→L).

Pulmonary Hypertension

The maternal mortality rate from pulmonary hypertension (from primary or secondary causes) is reported to be 30% to 50%.^55,56 These patients should avoid pregnancy. If a pregnancy occurs that proceeds to viability, these women may benefit from peripartum PAC use as early rising PA pressures may allow for titration of vasodilators like epoprostenol⁵⁷ during labor or postpartum.

Ischemic Heart Disease

Maternal mortality as a result of maternal heart disease is rapidly increasing.³² There has been a trend toward increasing maternal age as well as obesity in the United States over the past few decades; with this a slight rise in peripartum ischemia and infarction has occurred.^27,58 A recent US population-based study noted the rate of MI in pregnant patients to be 6.2 per 100,000 deliveries (95% CI 3.0-9.4) with a fatality rate of 5.1%.⁵⁸ Compared to nonpregnant age-matched women, postpartum women have a 6-fold higher rate of MI.⁵⁹

Summary Statement

In order to adequately assess the hemodynamics of a particular gravid patient, one must understand the complex nature of her physiology. A multidisciplinary approach is helpful in patients with complex structural or functional cardiac disease in regards to pathophysiology and medications that are safe to give in pregnancy. The trend in evaluating cardiac function is moving to noninvasive approaches and echocardiogram is one of the most useful tools in noninvasive hemodynamic assessment. The intent of this chapter is to provide a solid foundation to help the reader better understand the unique hemodynamic profile of pregnancy and the tools used in the assessment of the gravid patient in whom cardiac monitoring might be helpful.