Anesthesia and Analgesia in the Pregnant Cardiac Patient


8


 


Anesthesia and Analgesia in the Pregnant Cardiac Patient


 


Katherine W. Arendt



Key Points


The majority of maternal deaths from cardiovascular disease are from acquired heart disease


The pregnancy heart team is a multidisciplinary team consisting of obstetrician, maternal-fetal medicine, anesthesiologist, and cardiologist working together to optimize outcome of pregnant cardiac patient


Women with high-risk maternal cardiovascular disease should deliver at a Level 4 Regional Perinatal Health Center


Neuraxial labor analgesia is an important component of labor management in patients with moderate to severe cardiovascular disease


In certain circumstances general anesthesia is a safer option than a neuraxial technique for surgical anesthesia


 


Introduction


Over the past 20 years, cardiovascular disease has gradually become the leading cause of maternal mortality in the United States [1]. Increased survival of congenital heart disease (CHD) patients has resulted in more women reaching childbearing age and presenting to labor and delivery units [24]. Factors such as increased maternal age and increased incidence of obesity, chronic hypertension, and diabetes has likely led to expansion of acquired heart disease seen among the childbearing population. Currently, acquired heart disease comprises the majority of maternal cardiac deaths [5,6].


Both the European Society of Cardiology and the American College of Obstetricians and Gynecologists (ACOG) guidelines for pregnancy and heart disease recommend that a pregnancy heart team care for pregnant patients with complex cardiovascular disease [7,8]. Such a team involves cardiologists, obstetricians, perinatologists, and anesthesiologists working together to achieve the best outcome for the pregnant patient with complex heart disease. The focus of this chapter is on the role of the anesthesiologist as a member of the pregnancy heart team. Specifically, this chapter will focus on anesthetic risk stratification, the physiologic changes of pregnancy, labor and delivery, hemodynamic goals for patients as they present for delivery, and appropriate anesthetic techniques to achieve those goals.


 


Anesthetic Risk Stratification


Stratification of the overall risk of pregnancy for women with cardiac disease is discussed elsewhere in this text (see Chapter 4). Tables 8.1 through 8.3 review tools used for risk-stratifying women with cardiac disease who are pregnant [911].




























































Table 8.1


CARPREG II Risk Score


Risk Factors


Points


Prior cardiac event or arrhythmia 


3


NYHA class >II or cyanosis


3


Mechanical valve


3


Ventricular dysfunction


2


High-risk left-sided valve disease/LVOT obstruction


2


Pulmonary hypertension


2


Coronary artery disease


2


High-risk aortopathy


2


No prior cardiac intervention


1


Late pregnancy assessment


1


Total Score


Risk of Cardiac Complications


0–1 points


5%


2 points


10%


3 points


15%


4 points


22%


>4 points


41%






















































Table 8.2


ZAHARA Risk Score


Risk Factors


Points


Mechanical valve prosthesis


4.25


Left heart obstruction


2.5


History of arrhythmia


1.5


Cardiac medication prior to pregnancy


1.5


Cyanotic heart disease (corrected or uncorrected)


1.0


NYHA class II


0.75


Systemic atrioventricular valve regurgitation > Mild


0.75


Pulmonic atrioventricular valve regurgitation > Mild


0.75


Total Score


Risk of Cardiac Complications


0–0.5 points


2.90%


0.51–1.5 points


7.50%


1.51–2.5 points


17.50%


2.51–3.5 points


43.10%


>3.51 points


70%




























Table 8.3


WHO Classification for Pregnancy


Risk Classification


Cardiac Lesions


Class I


No detectable increased risk of maternal mortality and no or minimal increase in maternal morbidity


Uncomplicated mild pulmonary stenosis


Ventricular septal defect


Patent ductus arteriosus


Mitral valve prolapse with no more than trivial mitral regurgitation


Successfully repaired simple lesions (atrial or ventricular septal defect, patent ductus arteriosus, anomalous pulmonary venous drainage)


Isolated ventricular extrasystoles and atrial ectopic beats


Class II


Small increased risk of maternal mortality or moderate increase in morbidity


Unoperated atrial or ventricular septal defect


Repaired tetralogy of Fallot


Most arrhythmias


Class II–III


Depends on patient


Hypertrophic cardiomyopathy


Native or tissue valvular heart disease not considered WHO I or IV


Repaired coarctation


Marfan syndrome without aortic dilatation


Bicuspid valve with aorta <45 mm


Mild ventricular impairment


Heart transplantation


Class III


Significantly increased risk of maternal mortality or severe morbidity, and expert cardiac and obstetric pre-pregnancy, antenatal, and postnatal care are required


Mechanical valve


Systemic RV


Fontan circulation


Unrepaired cyanotic heart disease


Other complex congenital heart disease


Marfan syndrome with aorta 40–45 mm


Bicuspid aortic valve with aorta 45–50 mm


Class IV


Pregnancy is contraindicated


Pulmonary hypertension


Eisenmenger syndrome


Systemic ventricular EF <30%


Systemic ventricular dysfunction with NYHA class III–IV


Severe mitral stenosis


Severe symptomatic aortic stenosis


Marfan syndrome with aorta >45 mm


Bicuspid aortic valve with aorta >50 mm


Native severe coarctation


Prior peripartum cardiomyopathy with any residual impairment of ventricular function


Risk stratification is important to the anesthesiologist because anesthesiologists are an integral part of the multidisciplinary team who help identify pregnancies at high risk for maternal harm during childbirth and triage these women to deliver at appropriate hospitals. To do this, anesthesia teams should have the ability to see high-risk pregnant patients in advance of delivery in a clinical setting to obtain an anesthetic, obstetric, and cardiac history; perform a physical exam; and review cardiac testing. The most important aspects of this consultation are reviewed in Box 8.1.






























































Table 8.4


Normal Cardiovascular Changes during Pregnancy


Variable


Direction of Change


Average Change


Blood volume



+35%


Plasma volume



+45%


Red blood cell volume



+20%


Cardiac output



+40%


Stroke volume



+30%


Heart rate



+15%


Femoral venous pressure



+15 mmHg


Total peripheral resistance



15%


Mean arterial blood pressure



15 mmHg


Systolic blood pressure



0 to 15 mmHg


Diastolic blood pressure



10 to 20 mmHg


Central venous pressure



No change


Anesthesiologists often prefer to think in physiologic systems when risk-stratifying patients for surgery or delivery. Understanding the hemodynamic changes of pregnancy and combining these changes with the physiologic vulnerabilities of various cardiac lesions allows the anesthesiologist to understand which lesions will perform poorly during pregnancy, under anesthesia, or under the physiologic stressors of labor, emergency surgery, or obstetric hemorrhage. The physiologic changes of pregnancy are reviewed in Table 8.4. How these changes affect the hemodynamics of a woman with specific cardiac lesions are reviewed in Table 8.5.

















































Table 8.5


The Hemodynamic Effects of Pregnancy in Specific Cardiovascular Diseases


Lesion


Hemodynamic Effects of Pregnancy and Delivery


Coronary artery disease


() The decreased SVR of pregnancy can result in lesser coronary perfusion to the myocardium


() The increase in HR during pregnancy can result in decreased coronary filling time


() Cardiac work can increase significantly during labor, especially painful labor


Severe LV dysfunction (e.g., dilated or peripartum cardiomyopathy)


() The increase in cardiac output and blood volume during pregnancy can result in heart failure/pulmonary edema


() The decrease in oncotic pressure during pregnancy can result in greater risk for pulmonary edema


() Angiotensive converting enzyme inhibitors must be stopped during pregnancy secondary to teratogenicity


() Patients with a prior episode of peripartum cardiomyopathy are at risk for further deterioration in LV function with subsequent pregnancies


Pulmonary hypertension


() The increased cardiac output of pregnancy may not be accommodated by the fixed pulmonary vasculature resulting in right heart failure and death


() The decreased SVR of pregnancy can decrease coronary filling to a dilating and failing right ventricle


() The hypercoagulable state of pregnancy can result in pulmonary emboli which are especially lethal in patients with pulmonary hypertension


Unstable arrhythmia history


() Pregnancy, labor, and delivery can trigger tachyarrhythmias


Aortopathy (e.g., Marfan syndrome)


() Pregnancy, labor, and delivery may increase dilation of aortic root


() Pregnancy, labor, and delivery increase the risk of aortic rupture in women with Marfan syndrome


Valvular lesions


Mechanical prosthetic valve


() Hypercoagulable state of pregnancy increases risk of valve thrombosis


() Vitamin K antagonists (most effective way to prevent valvular clot formation) are teratogenic; often suboptimal anticoagulation regimens are used during pregnancy


Mitral stenosis


() Because of relatively fixed preload to the LV, the heart may not be able to generate increased cardiac output and pulmonary edema will develop


() Decreased oncotic pressure further increases risk of pulmonary edema


() The increase in blood volume and heart rate in pregnancy increases left atrial pressure and may lead to atrial fibrillation and pulmonary edema


Aortic stenosis


() The decreased SVR of pregnancy can result in lesser coronary perfusion pressure to the thickened LV myocardium


() Because of LV diastolic dysfunction, excess volume can lead to pulmonary edema


Mitral/aortic insufficiency


(+) The decreased SVR results in a lesser regurgitant volume


() Pregnancy can worsen ventricular dilation


Shunt lesions


R-to-L shunt (e.g., TOF, Eisenmenger’s)


() The decrease in SVR increases right-to-left shunting and possible cyanosis


(+) In unrepaired TOF and normal RV function, the increase in blood volume is beneficial because adequate RV preload is necessary to eject blood past the outflow obstruction and increase pulmonary blood flowa


L-to-R shunt (e.g., VSD or ASD)


(+) The decrease in SVR decreases the left-to-right shunting


() The increase in blood volume can precipitate failure because the patient is in a state of compensatory hypervolemia

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Jul 17, 2021 | Posted by in OBSTETRICS | Comments Off on Anesthesia and Analgesia in the Pregnant Cardiac Patient
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