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.
TABLE 1-7.Carpreg: Risk Factor Estimations of Cardiac Events ||Download (.pdf) TABLE 1-7. Carpreg: Risk Factor Estimations of Cardiac Events
|Complications ||Predictor ||Odds ratio (95% CI) ||P |
|Cardic ||Prior cardiac event or arrhythmia ||6(3-14) ||<0.001 |
| ||NYHA functional class >II or cyanosis ||6(2-22) ||0.009 |
| ||Left-sided heart obstruction ||6(3-14) ||<0.001 |
| ||Systemic ventricular dysfunction ||11(4-34) ||<0.001 |
| || ||Rate of primary cardiac events ||Rate of primary or secondary cardiac events, revised index |
| || || ||Validation group || || |
|No. of predictors ||Estimated risk, % ||Derivation group, revised index ||Revised index ||Original index ||Derivation group ||Validation group |
|0 ||5 ||7/249 (3%) ||5/137 (4%) ||5/136 (4%) ||10/249 (4%) ||6/137 (4%) |
|1 ||27 ||27/111 (24%) ||17/64 (27%) ||16/61 (26%) ||35/111 (31%) ||20/64 (31%) |
|>1 ||75 ||16/25 (64%) ||8/13 (62%) ||9/17 (53%) ||17/25 (68%) ||9/13 (6%) |
|C statistic (95% Cl) || ||0.83 (0.77-0.89) ||0.80 (0.72-0.88) ||0.79 (0.71-0.87) ||0.82 (0.76-0.88) ||0.81 (0.74-0.88) |
“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.
TABLE 1-8.Hemodynamic Profile of Shock States ||Download (.pdf) TABLE 1-8. Hemodynamic Profile of Shock States
|Shock state ||Hemodynamic parameter |
| ||CO ||LV filling pressure ||SVR |
|Hypovolemic ||↓ ||↓ ||↑ |
|Cardiogenic ||↓ ||↑ ||↑ |
|Obstructive ||↓ ||↑ ||↑ |
|Distributive ||↑ early ||↓ ||↓ early |
| ||↓ late || ||↑ late |
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.
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).
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.
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.
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
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
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.
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.
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
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.
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