Management of Acquired Cardiac Disease in the Obstetric Patient

Introduction

The incidence of cardiac disease in the obstetric patient is estimated at 0.1% - 1.4%^1,2 with an associated complication rate of 0.5% - 2.7%, which varies directly with severity of disease.^2,3 Congenital heart disease is the leading etiology, owing to advances in early medical and surgical management and improved survival to childbearing age. ³ Although peripartum morbidity and mortality has improved in the past century, a recent trend suggests that the severity of complications, especially myocardial infarction, is escalating, possibly due to increasing maternal age and/or severity of heart disease at the time of conception.^1,4,5 Cardiac disease continues to be the most common non-obstetric cause of death in the puerperium. ⁶ As a result, anesthesiologists must utilize knowledge of physiology and skills in hemodynamic management to achieve a successful outcome for both mother and child. This review presents a general overview, followed by in depth discussions of each acquired cardiac condition common in pregnancy. In addition, two case examples are provided. These cases do not represent the sole management technique advocated by the authors. Rather, they serve to illustrate possible approaches to and to highlight the multi-disciplinary approach needed for parturients with significant cardiac disease.

General Considerations in Pregnancy

The physiologic changes of the cardiovascular system during pregnancy have been extensively described and are beyond the scope of this review. ⁷ However, key hemodynamic changes to consider in the term parturient with cardiac disease include: cardiac output increases up to 50%, stroke volume and heart rate increase roughly 25%, circulating plasma volume increases by 55%, and systemic vascular resistance (SVR) decreases by 20%. Pulmonary capillary wedge pressure, central venous pressure, and cardiac ejection fraction typically remain unchanged. Labor and delivery further increase cardiac output, up to 75% above pre-delivery levels, which clearly imposes a significant increase in myocardial oxygen demand that persists up to 24-48 hours post-partum.

For patients with cardiac disease, the physiology of pregnancy warrants specific risk stratification of peripartum complications. This risk stratification is a useful pre-conception counseling tool for women with known heart disease, as well as a clinical tool for obstetricians, cardiologists, and anesthesiologists as they interact with these patients during various stages of pregnancy and delivery. In 2001, Sui et al prospectively identified four independent predictors of peripartum cardiac events associated with pregnancy in patients with cardiac disease (listed in Table 1). Cardiac complications in this population included pulmonary edema, sustained arrhythmia, stroke, cardiac arrest, or cardiac death. Event frequency with 0, 1, and >1 predictor was 5%, 27%, and 75%, respectively. ⁸ Maternal heart disease is further associated with an increased neonatal complication rate.^8,9

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Table 1.

Predictors of Peripartum Cardiac Events ⁸

Prior cardiac event Heart failure Transient ischemic attack Stroke Arrhythmia New York Heart Association (NYHA) functional class > II or cyanosis Left heart obstruction Mitral valve area < 2 cm2 Aortic valve area < 1.5 cm2 Peak left ventricular outflow tract gradient > 30 mmHg Systemic ventricular dysfunction (ejection fraction < 40%)

Valvular Disease

Valvular heart disease represents a large subset of patients, as it can be either congenital or acquired. Acquired lesions in the parturient most commonly result from rheumatic heart disease, despite the steady decline in incidence in developed countries due to antibiotic use. ¹⁰ Regardless of the etiology, management of individual lesions follows a consistent pattern which will be outlined below, first for stenotic lesions, then for regurgitant lesions. Evaluation of disease severity by echocardiography is considered the standard of care in all cases. ¹¹ Severity is also classified by functional status using the New York Heart Association (NYHA) classification system. The functional status is dependent upon the patient’s ability to adapt to the hemodynamic changes of pregnancy, which tend to worsen NYHA class in 62% of patients with valvular disease. ¹² If a valvular lesion causes cardiac decompensation, the parturient may require first trimester surgical intervention.^3,13 As a general rule, parturients with regurgitant lesions will tolerate these hemodynamic changes better than parturients with stenotic lesions.

Mitral Stenosis

Mitral stenosis (MS) most commonly results from rheumatic heart disease, causing commissural fusion, leaflet thickening and contracture, and diffuse calcification (see Figure 1). Ultimately, changes in valve architecture lead to narrowing of the atrial outlet with associated left atrial enlargement and compromise of left ventricular filling. Left ventricular stroke volume and cardiac output are diminished. With disease progression, pulmonary vascular pressures increase and may precipitate right heart failure. ¹⁴ Symptoms of chest pain, dyspnea, palpitations, hemoptysis, pulmonary edema, and thromboembolism slowly evolve over decades. MS severity is typically evaluated by echocardiographic measurement of valve area (see Table 2). ¹⁵

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Figure 1.

3-Dimensional echocardiographic image of mitral valve in mitral stenosis (MS). This figure represents moderate MS. The red arrow corresponds to the developing commissural fusion. Note there is a lack of defined commissures and scallops in the mitral valve due to rheumatic thickening. Anterior leaflet commissures labeled for orientation. Imaging by N.Weitzel MD

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Table 2.

Grading of Valvular Disease^15,18,21,23

		Grade
Lesion	Parameter	Mild	Moderate	Severe
Mitral Stenosis	Valve Area (cm2)	1.6-2.0	1.0-1.5	<1.0
Aortic Stenosis	Valve Area (cm2)	>1.5	1.0-1.5	<1.0
Mitral Regurgitation	Regurgitant Fraction (%)	<30	30-50	>50
Aortic Regurgitation	Pressure Half Time (msec)	>500	200-500	<200
	Color Doppler Jet width ÷ LVOT width ratio	<25%	25-65%	>65%

When presented with a patient suffering from MS, some general hemodynamic and anesthetic principles should be considered (Table 3). Key pathophysiologic factors to be aware of include: (1) worsening of pulmonary edema and left atrial enlargement in response to increased circulating plasma volume and (2) decreased diastolic filling, cardiac output tachycardia and tachyarrhythmias. The most common tachyarrhythmia is atrial fibrillation, owing to conduction system distortion by progressive atrial enlargement. Since the atrial contribution to ventricular filling is critical to maintenance of cardiac output, appropriate rate control with beta adrenergic antagonists is advised in the absence of specific contraindication.^16,17 Cardiac output may also be compromised by inadequate left atrial filling from increases in pulmonary vascular resistance (PVR). Ideally, elevations in PVR are avoided by aggressive prevention of hypoxia, hypercarbia, and acidosis. ³

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Table 3.

General Consideration for Stenotic Valvular Lesions^3,13,47

Hemodynamic Goals Avoid tachycardia and tachyarrhythmias Preserve systemic vascular resistance Maintain volume status Labor and Delivery Goals Institute pain control early Avoid single shot spinal technique Titrate epidural cautiously to avoid hemodynamic compromise Treat hypotension aggressively with vasopressors and volume expansion Avoid aortocaval compression to maintain preload Consider arterial, central venous, and/or pulmonary arterial pressure monitoring in high-risk patients General Anesthesia Goals Utilize rapid sequence induction and aspiration prophylaxis Minimize stress response with opioids or esmolol Avoid agents that increase heart rate (ketamine, atropine, glycopyrrolate, pancuronium, meperidine) Consider transesophageal echocardiography intra-operatively

The choice of labor anesthesia should be based on the hemodynamic principles outlined above. As such, a combined spinal-epidural (CSE) technique is an excellent choice for analgesia. When performing the CSE, administration of intrathecal opioids only (no intrathecal local anesthetics), will help to prevent sympathetic stimulation in early labor without the rapid hemodynamic changes that may ensue from spinal local anesthetic administration. The epidural catheter subsequently can be slowly titrated with dilute local anesthetic to provide adequate segmental pain control while maintaining appropriate hemodynamics. Additionally, catheter placement allows establishment of complete sensory blockade in the event forceps-assisted delivery or cesarean section is required. ¹⁵

Aortic Stenosis

Severe symptomatic aortic stenosis (AS) in the parturient is rare, owing to the indolent disease progression. AS in younger patients commonly arises from a congenital bicuspid valve (Figure 2), which results in outflow tract narrowing. The left ventricle subsequently undergoes progressive compensatory hypertrophy with a resultant decrease in compliance.^3,18,19 Myocardial contractility is typically preserved until severe diastolic dysfunction and/or ischemia result. ³ Symptoms of syncope, dyspnea, and chest pain are indicative of severe disease and are associated with poor outcomes.^11,20 Assessment of effective valve area by echocardiography is the standard to assess disease severity (Table 2).

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Figure 2.

3-Dimensional view of a bicuspid aortic valve. Imaging by N.Weitzel MD.

Key hemodynamic and anesthetic considerations for parturients with AS are shown in Table 3. Women with mild to moderate disease will typically tolerate pregnancy and labor well. ²⁰ The patient with severe AS, however, is relatively intolerant of volume overload, tachycardia, and/or arrhythmias, which result in pulmonary edema, decreased cardiac output, and increased myocardial oxygen demand. ³ Additionally, abrupt decreases in SVR, as seen with neuraxial anesthetic techniques, further compromise myocardial perfusion and can precipitate circulatory collapse.^3,19 For this reason, single shot spinal techniques are considered contraindicated in severe AS.

As labor brings about much sympathetic stimulation, attempts should be made to minimize hemodynamic stress, especially during the second stage of labor. Many obstetricians will opt for forceps-assisted vaginal delivery in AS to avoid aggressive pushing. ²⁰ Epidural anesthesia may be the neuraxial technique of choice for early pain control with the ability to slowly titrate segmental blockade. CSE technique may be considered, provided opioids alone are used in the intrathecal space to avoid local anesthetic-induced sympathectomy and hemody-namic collapse. In cases where general anesthesia is required, agents that decrease SVR and depress contractility (volatile anesthetics, thiopental, propofol) must be used with extreme caution. ¹⁹ See Case Example 1 for a multidisciplinary care plan example.

Mitral Regurgitation

Mitral regurgitation (MR) arises from multiple etiologies, but the clinical severity typically correlates with acuity of onset. Acute MR arising from bacterial endocarditis, trauma, or papillary muscle rupture often results in abrupt left atrial volume overload and compromise of cardiac output. If not rapidly fatal, pulmonary edema and right heart failure ensue. Chronic MR arising from myxomatous degeneration or rheumatic disease develops slowly over years, affording compensatory atrial enlargement and maintenance of forward flow.^3,19,20,21

General hemodynamic goals for patients with MR include: reduction in afterload and maintenance of relative tachycardia, which both act to reduce the regurgitant fraction. The parturient with chronic MR in the mild to moderate range will generally do well with labor and delivery, as the decreased SVR and increased plasma volume of pregnancy improves cardiac output. Management considerations for the parturient with MR should mirror the concepts presented in Table 4. Peripartum management in MR is guided by evaluation of disease severity through echocardiography. Qualitative examination focuses on coaptation defects, leaflet abnormalities, and regurgitant jet characteristics (Figures 3 & 4). ²¹ Quantitative grading by calculation of the regurgitant fraction is possible, but can be cumbersome in everyday clinical practice (Table 2).

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Figure 3.

Color Doppler image taken from the midesophageal long axis view with depth adjusted to focus on the mitral valve. In this image, the red / yellow color represents flow backward into left atrium, representing mitral regurgitation (MR). In this case, the degree of MR is consistent with moderate to severe MR. Imaging by N.Weitzel MD

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Figure 4.

3-Dimensional view of the mitral valve with a flail P3 segment at the red arrow. Imaging by N.Weitzel MD

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Table 4.

General Considerations for Regurgitant Valvular Lesions.^3,19,26

Hemodynamic Goals Avoid bradycardia and arrhythmias Avoid increases in afterload (SVR) Maintain volume status Labor and Delivery Goals Institute pain control early Avoid aortocaval compression to maintain preload Utilize single shot spinal cautiously, as patients with severe regurgitation may not tolerate rapid hemodynamic changes Titrate epidural cautiously to avoid hemodynamic compromise (decreased preload) Select invasive pressure monitoring in cases of severe disease. General Anesthesia Goals Utilize rapid sequence induction and aspiration prophylaxis Minimize stress response with opioids or esmolol Avoid agents that depress myocardial contractility (volatile agents, propofol, thiopental) Avoid increases in pulmonary vascular resistance (hypercarbia, hypoxemia, hypothermia, acidosis, and sympathetic stimulation)

Mitral Prolapse

Mitral valve prolapse (MVP) is a subset of MR that can lead to valvular insufficiency over time. Although common in women of childbearing age, prolapse requires no alterations to peripartum anesthetic management in the absence of significant regurgitant flow. Anesthesiologists must remain vigilant, as MVP predisposes to arrhythmias. ²²

Aortic Insufficiency

Aortic insufficiency (AI) usually results from rheumatic heart disease, but may also be associated with a congenital bicuspid valve or collagen vascular disease. Rarely, acute AI, a life-threatening condition, may develop in the setting of trauma or endocarditis. In chronic AI, regurgitant flow causes volume overload leading to ventricular hypertrophy and dilation. Contractility and cardiac output are progressively compromised. With severe disease, patients exhibit dyspnea, exercise intolerance, orthopnea, and pounding in the chest. ³

In the absence of left ventricular failure, AI in the puerperium is generally uneventful much like chronic MR. The decreased SVR and increased heart rate of the parturient reduces the regurgitant fraction and promotes forward flow.^19,20 An important exception is the woman that develops gestational hypertension or pre-eclampsia, which may acutely worsen AI. In this case, prompt afterload reduction with diuretics or vasodilators is warranted. ² General hemodynamic and anesthetic considerations for AI in pregnancy are listed in Table 4.

To further guide management, echocardiography is used to identify abnormalities, to judge severity of insufficiency, and to evaluate for other concurrent valvular lesions, which are common in AI (Table 2). Assessment of AI is complicated by dynamic changes in severity with real-time variation in preload and afterload (Figure 5 & 6). Repeat assessment in the face of changing hemodynamic parameters is warranted. ²³

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Figure 5.

Color M-mode through the left ventricular outflow tract (LVOT). Point A (0.72cm) represents the width of the regurgitant jet, and Point B represents the width of the LVOT (2.0cm). The color jet width to LVOT width ratio is 36%, representing moderate aortic insufficiency. Imaging by N.Weitzel MD

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Figure 6.

Continuous Wave (CW) doppler evaluation of the aortic regurgitant jet. The CW cursor is placed in the aortic outflow tract utilizing the transgastric long axis view. The red arrow represents the deceleration time used to generate the pressure half time (PHT) measurement. In this case, the PHT is 447 msec, representing moderate aortic insufficiency. Imaging by N.Weitzel MD

Prosthetic Valves

Management of the parturient with a prosthetic valve is complicated by the need for systemic anticoagulation to prevent valvular thrombosis. As such, the most critical aspect of management may occur long before these patients arrive for care by the anesthesiologist. Patients with mechanical valves require aggressive anticoagulation management, especially due to the hypercoagulablity of pregnancy. Given the teratogenic properties of warfarin, significant failure rates reported with unfractionated heparin, and lack of quality evidence for the use of low-molecular weight heparin, the optimal therapeutic regimen remains elusive. ¹¹ The anesthesiologist must recognize the increased risk for thrombosis in this patient population and coordinate anticoagulation regimens in the peripartum period, especially if neuraxial techniques are to be employed.

Pulmonary Hypertension

Pulmonary arterial hypertension (PAH) is defined as sustained mean pulmonary artery (PA) pressure greater than 25 mmHg in the absence of elevated left atrial pressure. Etiologies for the syndrome are a heterogeneous group including idiopathic, heritable, drug-induced, connective tissue disease related, infective, chronic venous thromboembolism associated, and congenital. ²⁴ The final common pathway is endothelial dysfunction affecting production of vasoconstrictors, vasodilators, smooth muscle mitogens, thrombotic mediators, and inflammatory cytokines. As a result, the normally low-pressure PA is transformed into a high-pressure system, ultimately leading to right ventricle (RV) strain and failure. ²⁵

RV strain in PAH worsens with the increased cardiac output and circulating blood volume of pregnancy. ²⁶ This has translated into poor outcomes for the pregnant patient with PAH. Mortality is estimated at 30-50%, depending on the etiology, and extends into the postpartum period up to five weeks. ²⁷ Thromboembolic events are also common, requiring anticoagulant therapy. For all of these reasons, many obstetricians consider PAH a contraindication to pregnancy.

Given the high risk of cardiac decompensation in this subset of patients, hemodynamic management is crucial in the puerperium. Vascular resistance in the systemic and pulmonary circulations must be balanced. Decreasing SVR compromises RV myocardial perfusion. Therefore, maintenance of systemic blood pressure is vital. Increasing pulmonary vascular resistance (PVR) worsens RV strain and may precipitate right heart failure. Consequently, avoiding hypoxemia, hypercarbia, acidosis, and sympathetic stimulation are of utmost importance, regardless of anesthetic technique. ³

Optimal anesthetic care in the parturient with PAH has not been established. See Case #2 for an example multidisciplinary care plan for a patient with severe pulmonary hypertension. Since Cesarean section may be associated with higher mortality risk, independent of anesthetic technique, an assisted second stage to reduce RV strain from pushing is preferred. Early pain control is imperative to prevent sympathetically-mediated increases in PVR. Unless contraindicated due to anticoagulation status, epidural or CSE techniques are excellent choices to facilitate these two requirements. ²⁷ Blockade must be cautiously titrated with immediate aggressive intervention to achieve hemodynamic goals outlined above. Additionally, inotropic support may be required in the setting of RV decompensation and failure. If general anesthesia is selected, arterial and PA catheterization are usually employed for tight hemodynamic control. ²⁶ Intraoperative transesophageal echocardiography (TEE) can provide real-time assessment of volume status and RV function (Figure 7).

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Figure 7.

This is the mid-esophageal 4 chamber (ME 4CH) view of the heart. Note the right ventricle (RV) dilation and diminished left ventricular volume indicative of RV failure in severe pulmonary hypertension. Also note the flat septal wall and dilated RV which is larger than the left ventricle (LV) in this image. For reference; in the normal ME 4CH view the RV is typically 2/3 the size of the LV. Imaging by N.Weitzel MD

Cardiomyopathy

Cardiomyopathy is uncommon in the parturient, but carries significant peripartum morbidity and mortality. Important subtypes include peripartum cardiomyopathy (PPCM), hypertrophic obstructive cardiomyopathy (HOCM), and dilated cardiomyopathy. Symptoms of fatigue, dyspnea, and peripheral edema can be difficult to distinguish from normal pregnancy, but increasing severity and associated chest pain or pulmonary edema are indicative of left ventricular dysfunction and impending decompensation.

Peripartum Cardiomyopathy

The description of PPCM has evolved with time. In 2010, the Heart Failure Association of the European Society of Cardiology Working Group proposed the following simplified definition: “idiopathic cardiomyopathy presenting with heart failure (HF) secondary to left ventricular (LV) systolic dysfunction towards the end of pregnancy or in the months following delivery, where no other cause of HF is found. It is therefore considered a diagnosis of exclusion. The LV may not be dilated but the ejection fraction (EF) is nearly always reduced below 45%”. ²⁹ The precise etiology for PPCM is unknown, but may be related to oxidative stress, inflammation, viral infection, autoimmunity, or genetic predisposition. Maternal age, multiple gestations, medications, and malnutrition have also been implicated. ²⁹

Since no specific etiology has been identified as a therapeutic target, standard heart failure protocol to reduce preload and afterload is instituted at diagnosis. One important exception is the use of angiotensin converting enzyme inhibitors, which must be avoided due to teratogenicity. ² Careful monitoring of volume status is critical, as deviation from euvolemia is poorly tolerated. ²⁹ Peripartum anesthetic management begins with early pain control to avoid sympathetic stimulation, which increases heart rate and SVR and compromises cardiac output. Epidural or CSE techniques with slow titration provide pain control and beneficially decrease SVR. ¹⁰ In cases of severely compromised contractility, inotropic support may be required. Therefore, placement of invasive pressure monitors is prudent. ²⁹ If general anesthesia is employed, myocardial depressants (volatile agents, propofol, thiopental) should be used with caution. ³ Intraoperative myocardial function and volume status can most easily be assessed using TEE. Common echocardiographic findings include reduced ejection fraction < 45%, decreased fractional shortening < 30%, and/or increased end diastolic LV diameter (Figure 8 & 9). ³⁰

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Figure 8.

M-mode imaging through the left ventricle (LV) of a patient with severe LV dysfunction due to cardiomyopathy. Both fractional shortening and estimated ejection fraction can be evaluated using the LV internal diameters at systole and diastole (signified by red arrows). Note the severe lack of systolic thickening of the myocardial wall as well as dyssynchrony. Fractional Shortening (FS) = (LVID_D-LVID_S) / LVID_D X 100(%). Ejection fraction in this case is calculated using the Teicholtz method of volumes in M-Mode (V = [7/(2.4 + LVID)] x LVID³). Imaging by N.Weitzel MD

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Figure 9.

M-mode imaging of a normal left ventricle (LV) from the transgastric short axis view for comparison with Figure 8. The arrows again signify the LV myocardial internal diameters during systole and diastole. It is important when using this modality to exclude the papillary muscles (yellow starred portion of the endocardium) from the diameter measurements. Imaging by N.Weitzel MD.

Ultimately, prognosis in PPCM is poor. LV functional recovery occurs in 23-41% of parturients, usually within 6-12 months. Two-year mortality remains high at 28%. ²⁹ Post-partum management includes continued medical therapy, ventricular assist devices, and cardiac transplantation. Return of LV function, as judged by dobutamine stress echocardiography, may be indicative of good prognosis with subsequent pregnancies. ²

Hypertrophic Obstructive Cardiomyopathy

HOCM is a genetic disorder with variable course and degree of severity over time. Previously asymptomatic and/or undiagnosed disease may be unmasked by the physiologic changes of pregnancy. The hallmarks of HOCM are LV hypertrophy and dynamic left ventricular outflow tract (LVOT) obstruction from systolic anterior motion (SAM) of the anterior mitral leaflet (Figure 10). Systolic function is initially maintained in the hypertrophied LV, but may deteriorate over time. Diastolic dysfunction is a common finding.^31,32,33

Hemodynamic management in HOCM focuses on minimizing LVOT obstruction by maintaining LV end-diastolic volume with adequate preload and with maintenance of slow heart rate. Preservation of SVR and avoidance of increased myocardial contractility eliminate systolic LV collapse and mitral SAM. ³³ In consideration of these hemodynamic goals, single-shot spinal should be avoided due to rapid decreases in preload and SVR. Instead, early epidural or CSE prevents sympathetically-mediated tachycardia, while allowing careful titration to minimize changes in preload and SVR. Fortunately, general anesthesia may have a beneficial hemodynamic effect due to the myocardial depressant properties of common agents, resulting in less dynamic LVOT obstruction. Invasive arterial pressure monitoring is advised prior to induction of anesthesia.^32,33 Additional monitoring with TEE can rapidly identify LVOT obstruction and mitral SAM.

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Figure 10.

Example of patient with a hypertrophic septum and resultant systolic anterior motion (SAM) of the mitral valve, which are characteristic of hypertrophic obstructive cardiomyopathy (HOCM). Panel A represents a 3-dimensional color view of the mitral regurgitation resulting from the SAM. Note that in this image, there is regurgitant flow through the mitral valve indicated by the top yellow arrow. This is due to the anterior leaflet of the mitral valve being “sucked” into the left ventricular outflow tract (LVOT). At the same time, evidence of turbulent flow is denoted by the lower yellow arrow, corresponding to the “swirling” color doppler tracing typically seen during SAM. Panel B is the corresponding 2-dimensional image taken from the midesophageal 5 chamber view, demonstrating a hypertrophic ventricular septum with outflow tract obstruction due to the mitral valve. The red arrow is pointing toward the portion of the anterior leaflet of the mitral valve moving into the LVOT. Imaging by N.Weitzel MD

Dilated Cardiomyopathy

Dilated cardiomyopathy is marked by progressive LV volume increase and systolic dysfunction in the setting of normal wall thickness. Possible etiologies include idiopathic, familial, infectious, toxin-related, autoimmune, connective tissue disease-related, pheochromocytoma, metabolic, endocrine, or nutritional. ³¹ Since the presentations are similar, a subgroup of parturients diagnosed with PPCM may actually represent dilated cardiomyopathy unmasked by physiologic changes of pregnancy. ³⁴ Hemodynamic and anesthetic goals for dilated cardiomyopathy match those for PPCM outlined above.

Cardiac Transplantation

The incidence of pregnancy after transplantation is increasing, despite medical advice to discourage conception. ²² Reports of successful pregnancy and parturition showed an increased incidence of preterm labor, hypertension, and preeclampsia in transplant recipients. ³⁵ Positive outcomes depended upon stable graft function, minimal renal dysfunction, and absence of rejection symptoms in the preceding year. ³⁶

Although the risk of rejection is not increased by pregnancy, continuation of immunosuppression therapy is imperative and supersedes reported fetal risks. ²² Dose adjustments for the increased volume of distribution in pregnancy are required. ³⁶ Additionally, peripartum steroid administration is appropriate in the setting of chronic corticosteroid therapy. ³⁷ Strict adherence to aseptic technique is critical if neuraxial procedures, central venous access, or invasive pressure monitoring are employed in consideration of increased infection risk from immunosuppression.

When caring for the transplant recipient, it is imperative to recall the altered autonomic control of the denervated heart. There is loss of vagal input and up-regulation of adrenergic receptors sensitive to circulating catecholamines. Without parasympathetic control, the patient will have a higher resting heart rate, insensitivity to anti-cholinergic agents like atropine or glycopyrrolate, and a predisposition to dysrhythmias. Accelerated athersclerosis is also common. ³⁷

Peripartum hemodynamic goals include maintenance of adequate preload and avoidance of hypertension. Aortocaval compression must be prevented. Hemodynamic compromise can occur with significant changes in heart rate from the patient’s baseline. Therefore, bradycardia and tachycardia must be treated with direct acting beta adrenergic agonists (i.e. isoproterenol or epinephrine) or antagonists, respectively. If rejection is suspected, agents with myocardial depressant properties are best avoided.^22,37

Myocardial Ischemia

Coronary artery disease (CAD) and myocardial infarction (MI) in the parturient are rare. However, increasing maternal age may augment their frequency in the future. ²² MI during pregnancy can be devastating with mortality rates of 19-37%. ³⁸ Risk factors include diabetes, hypertension, pre-eclampsia, smoking, obesity, hyperlipidemia, oral contraceptive use, and family history of early CAD.^10,38 MI in a previously healthy woman who lacks coronary atherosclerotic disease should prompt evaluation for cocaine abuse. ³

Pregnancy increases the likelihood of an ischemic event in susceptible patients. Increased heart rate and cardiac output with concomitant dilutional anemia and decreased coronary perfusion pressure result in an imbalance of myocardial oxygen supply and demand. Additionally, coronary artery spasm may be precipitated by peripartum administration of prostaglandin analogs and ergot alkaloids. Therefore, these agents are best avoided in patients at risk for MI in the puerperium.^3,10

Hemodynamic management in the peripartum period strives to prevent new ischemia by maintenance of stable hemodynamics. Heart rate control with beta adrenergic antagonism and adequate analgesia prevent tachycardia and increased myocardial oxygen demand. Early establishment of neuraxial anesthesia is advised. Local anesthetic solutions should be prepared without the use of epinephrine to prevent tachycardia with inadvertent intravascular injection. Supplemental oxygen ensures maximal oxygen carrying capacity. Dramatic changes in preload and afterload must be aggressively treated to. ³

Arrhythmias

Changes in cardiac electrophysiology are common in pregnancy. Most are asymptomatic tachyarrhythmias, but hemodynamic decompensation can occur. ³⁹ Dysrhythmias are promoted by increased circulating hormones, up-regulated sympathetic tone, electrolyte alterations, and compensatory hemodynamic changes. ⁴⁰ Appropriate management begins with correct identification of the abnormality type. ⁴¹ Therapy should not be instituted unless uterine hypoperfusion, fetal depression, or maternal hemodynamic compromise is imminent.

Therapeutic intervention is similar to that used in the non-pregnant patient. Vagal maneuvers may break paroxysmal supraventricular tachycardias. Elimination of tobacco, caffeine, and alcohol consumption is warranted. All pharmacologic agents carry some risk to the fetus. ⁴⁰ Evidence suggests adenosine, beta adrenergic antagoists, digoxin, diltiazem, and lidocaine may be used without significant fetal harm. ³⁹ Amiodarone must be avoided for teratogenic affects. Electrical cardioversion provides rapid resolution of hemodynamically unstable rhythms without fetal sequelae. ⁴¹

Cardiopulmonary Bypass

Most cardiac conditions can be managed medically during pregnancy. As previously noted, severe disease may benefit from early surgical intervention. Although catheter techniques are often employed, cardiopulmonary bypass (CPB) may be required. Fetal risk of morbidity and mortality with CPB far exceeds maternal risk. ⁴²

The small cohort size of parturients undergoing CPB complicates outcomes analysis and evidence-based recommendations. Normothermic CPB perfusion with increased flow rates appears to have improved outcomes. Some suggest pulsatile flow is superior to continuous flow. Controversy surrounds the use of intraoperative fetal heart rate monitoring. Proponents argue fetal monitoring provides an additional measure of uteroplacental perfusion. Opponents cite the absence of correlation between episodes of bradycardia and fetal neurologic outcome. Regardless, if fetal monitoring is to be employed, all members of the care team should subscribe to a predetermined course of action for episodes of apparent fetal distress.^10,42

Cardiac Arrest

Cardiac arrest complicates 1 in 30,000 pregnancies. Intrinsic heart disease and cardiac events are important risk factors for arrest. Other etiologies include amniotic fluid embolism, uncontrolled hemorrhage, thromboembolic events, sepsis, pre-eclampsia, and iatrogenic causes. ³ Pregnancy poses the unique situation of two simultaneous patients. Fetal well-being correlates with appropriate resuscitation of the mother. ⁴³

Standard advanced cardiac life support (ACLS) protocol should be followed when cardiac arrest occurs, excepting that the patient should be tilted 15-30 degrees to the left with a wedge to minimize inferior vena cava compression, improving venous return. Prompt electrical cardioversion should be attempted when indicated. ⁴³

Gestational age greater than 24 weeks signifies fetal viability and is the breakpoint for consideration of emergent hysterotomy. Fetal outcome is best when emergency cesarean delivery occurs within five minutes of maternal cardiac arrest. Delivery often improves maternal resuscitation efforts. ⁴³

One recent advancement in the management of cardiac arrest is the acceptance of lipid emulsion rescue for bupivacaine-associated toxicity. ⁴⁴ The mechanism in reversing toxicity is unknown, but proposed effects include bupivacaine sequestration, enhanced local anesthetic metabolism, or increased myocardial contractility. ⁴⁵ Despite its reported improvement in resuscitation efforts, lipid emulsion administration remains an adjunct to quality application of standard ACLS protocol. The dosing protocol for 20% lipid emulsion advocated by Weinberg is summarized in Table 5. Propofol is not an appropriate alternative due to significant cardiac depression at volumes required for resuscitation. ⁴⁶

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Table 5.

Lipid emulsion rescue for bupivacaine-associated cardiac arrest. ⁴⁶

Initiate standard advanced cardiac life support (ACLS) protocol. Consider administering 20% lipid emulsion if bupivacaine toxicity is suspected: Bolus 1.5 mL/kg, followed by infusion at 0.25 mL/kg/minute until spontaneous circulation has been reestablished for at least 10 minutes. Repeat 1.5 mL/kg bolus, if (a) is uneffective, followed by infusion at increased rate of 0.5 mL/kg/minute.

Summary

Peripartum management of acquired cardiac disease is a difficult clinical scenario that requires the anesthesiologist to draw heavily upon expertise in knowledge of physiology and skills like TEE. Careful advance planning inclusive of a multi-disciplinary team is critical to success. Although therapy varies by specific pathology, two commonalities in management include (1) early pain control to minimize sympathetic activation and (2) maintenance of stable hemodynamics close to the patient’s baseline parameters.