Critical Care Obstetrics part 66 potx

Women with signifi cant uncorrected congenital heart lesions, signifi cantly dilated aortic root in Marfan ’ s disease, congestive heart failure NYHA class III and IV despite optimized m

Critical Care Obstetrics, 5th edition Edited by M Belfort, G Saade,

M Foley, J Phelan and G Dildy © 2010 Blackwell Publishing Ltd.

Parturient with Cardiac Disease

Shobana Chandrasekhar & Maya S Suresh

Department of Anesthesiology, Baylor College of Medicine, Houston, TX, USA

Introduction and e pidemiology

Cardiac disease, a leading cause of non - obstetric mortality in

pregnancy, occurs in 1 – 3% of pregnancies and accounts for 10 –

15% of maternal mortality [1,2] Even though the incidence of

rheumatic heart disease is declining in developing countries, it

still accounts for a majority of mortality in obstetric cases The

incidence of congenital heart disease in pregnant women is

increasing in developed countries because of advances in the

diagnosis and treatment of congenital heart defects in

childhood

Cardiovascular maternal morbidity and mortality during

preg-nancy correlate strongly with maternal functional status [1 – 3]

Women with NYHA class I and II (no or minor symptoms)

toler-ate pregnancy without major deterioration, whereas those with

NYHA class III and IV during pregnancy are at risk for major

morbidity resulting in mortality upwards of 50% [4] Because of

the physiologic changes in pregnancy, further deterioration in

functional status in the range of 15 – 55% of symptomatic patients

can be expected during pregnancy [2] When a pregnant woman

presents with onset of cardiorespiratory deterioration the main

differential diagnoses include thromboembolism,

cardiomyopa-thy, dysrhythmia, pre - eclampsia, hemorrhage, and sepsis A less

commonly considered differential is underlying heart disease,

and this is something that should be excluded in all of these cases

Therefore the diagnosis of cardiac disease by history, physical

exam, ECG, CXR, and echocardiogram is essential to obstetric

and anesthetic management

In the United Kingdom Report of the Confi dential Enquiries

into Maternal and Child Health (CEMACH; formerly Confi dential

Enquiries into Maternal Deaths (CEMD)), cardiac disease was the

second commonest cause of maternal mortality Signifi cant and

increasing numbers of deaths occur in women without previously

known disease, either in those with risk factors or in those who develop conditions in the absence of risk factors [5]

Labor analgesic techniques and anesthetic management in the critically ill parturient are determined largely by the nature of the presenting illness Issues dictating choice of anesthetic technique are the patient ’ s ability to maintain her airway, coagulation status, intravascular volume, and requirements for ventilatory support and intensive care Fetal well - being is an important issue in the antepartum period Uteroplacental blood fl ow should be main-tained and hypotension should be avoided Maternal survival clearly takes priority Anesthesia itself is associated with known hazards, and the risks of each technique must be balanced against the possible benefi ts to both mother and baby in the context of the presenting illness

Physiologic c hanges of p regnancy r elevant to the c ardiorespiratory s ystem

Pregnancy - induced alterations of the cardiovascular and respira-tory systems are the result of both anatomic and functional changes The cardiovascular changes that occur during pregnancy improve oxygenation and fl ow of nutrition to the fetus Cardiac output increases up to 50% in the fi rst half of pregnancy due to increased stroke volume, and later in the pregnancy due to increased heart rate Hypotension and decreased cardiac output can occur due to inferior vena cava compression by the enlarged uterus Peripheral vascular resistance is decreased due to smooth muscle relaxation caused by increased circulating progesterone levels Systolic murmurs are a normal occurrence due to increased blood fl ow However, a diastolic murmur is not a normal fi nding during pregnancy During labor, cardiac output increases an additional 45% above that found in late pregnancy Mean arterial pressure increases 10 mmHg during each contraction Immediately after delivery, cardiac output increases by as much as 80% due to autotransfusion The autotransfusion results from an increase in preload secondary to release of vena caval obstruction by the enlarged uterus, and from autotransfusion of the blood during

Congenital h eart d isease ( CHD )

Congenital heart diseases with small left to right intracardiac shunts account for 60 – 80% of cardiac disease in pregnant patients

in the United States [2] Women with signifi cant uncorrected congenital heart lesions, signifi cantly dilated aortic root in Marfan ’ s disease, congestive heart failure (NYHA class III and IV) despite optimized medical treatment and palliative surgery, and those with increased pulmonary vascular resistance, are at increased risk for major morbidity and mortality and should be advised against pregnancy (Table 45.2 ) [6] The risks to mother and fetus of congenital heart disease during pregnancy are shown

in Table 45.3 The two most important predictors of fetal

mor-contraction and involution of the uterus Simultaneously,

sys-temic vascular resistance increases dramatically in the immediate

postpartum period (Table 45.1 & Figure 45.1 )

Pulmonary anatomic and physiologic changes during

preg-nancy place the pregnant patient at increased risk for hypoxemia

The anatomic changes occur to compensate for an enlarging

uterus The increased subcostal angle increases the chest

circum-ference There is increased diaphragmatic excursion and the

dia-phragm is elevated 4 cm in late pregnancy Pulmonary function

is also altered in pregnancy A 30% increase in tidal volume

occurs, with a corresponding 30 – 40% increase in minute

ventila-tion The expiratory reserve volume and functional residual

capacity decrease by 20% Respiratory rate, vital capacity, and

inspiratory reserve volume do not change P a O 2 is increased while

P a CO 2 and HCO 3 are decreased PaCO 2 decreases to 27 – 32 mmHg

in the second half of pregnancy as a result of the increased minute

ventilation Oxygen consumption increases progressively during

pregnancy and is maximum during the stress of labor

Figure 45.1 Cardiac output increases during labor

Table 45.1 Comparison of hemodynamic parameters in pregnant and

non - pregnant patients

Central venous pressure (mmHg) 1 – 10 Unchanged

Pulmonary artery pressure (mean) (mmHg) 9 – 16 Unchanged

Pulmonary capillary wedge pressure (mmHg) 3 – 10 Unchanged

Cardiac output (L/min) 4 – 7 ↑ 30 – 45%

Systemic vascular resistance (dyne - sec cm − 5 ) 770 – 1500 ↓ 25%

Pulmonary vascular resistance (dyne - sec cm − 5 ) 20 – 120 ↓ 25%

Heart rate 65 – 72/min ↑ 10 – 20%

Table 45.2 Absolute contraindications to pregnancy

Severe primary and secondary pulmonary hypertension Marfan ’ s syndrome with aortopathy and ascending aorta diameter > 40 mmHg Eisenmenger syndrome (cyanosis due to R to L intracardiac shunt)

Table 45.3 Risks of congenital heart disease to mother and fetus during

pregnancy

Risk to the mother Risk to the fetus

Pulmonary edema Intrauterine growth restriction Arrhythmias Prematurity

Heart failure Congenital heart disease (inherited) Hemorrhage from

anticoagulation

Teratogenic effect of drugs administered to the mother Death Intracranial hemorrhage

Fetal loss

bidity in these parturients are the presence of congestive heart

failure and persistent cyanosis in the mother

Left to r ight s hunts

Pathophysiology

The hemodynamic alterations depend on the size of the defect

Patients with atrial shunts, such as atrial septal defect (ASD) are

at low risk of hemodynamic deterioration or onset of

arrhythmias In the rare case of a marked clinical deterioration, catheter

based closing of the shunt is the fi rst - line treatment Ventricular

septal defect (VSD), and persistent patent ductus arteriosus

(PDA) are also usually well tolerated during pregnancy although

arrhythmias should be anticipated in these conditions The

hemodynamic alterations, complications and prognosis are

summarized in Table 45.4

Anesthetic m anagement c onsiderations in l eft to r ight

i ntracardiac s hunts

With small shunts right ventricular (RV) and pulmonary artery

(PA) pressures are unchanged and there is not much change in

pulmonary blood fl ow Risk of bacterial endocarditis is increased

With larger shunts, there is progressively increased pulmonary

Table 45.4 Left to right shunts

Size of defect Hemodynamic alterations Pregnancy complications Prognosis

Small RV and PA are unchanged Increased risk of endocarditis Usually uncomplicated course

Moderate RV and PA pressures are increased but remain below

systemic pressures Increased pulmonary blood fl ow Pulmonary vascular disease unlikely

LV volume overload and failure CHF and arrhythmias are likely

High chance of cardiac decompensation during pregnancy

Large RV and LV pressures equalize

Eisenmenger ’ s syndrome Pulmonary vascular disease likely

Heart failure, fetal hypoxemia Mortality can reach as high as 50%

Pregnancy is contraindicated

RV, right ventricle; PA, pulmonary artery; LV, left ventricle; CHF, congestive heart failure

Table 45.5 Antibiotic Prophylaxis for Genitourinary/Gastrointestinal Procedures

Standard Regimen Ampicillin, gentamicin, and amoxicillin Intravenous or intramuscular administration of ampicillin, 2 g plus gentamicin 1.5 mg/kg (not to exceed 80 mg), 30 min

before procedure; followed by amoxicillin, 1.5 g orally 6 h after initial dose; alternatively the parenteral regimen may

be repeated once 8 h after initial dose

Ampicillin/Amoxicillin/Penicillin Allergic Patient Region Vancomycin and gentamicin Intravenous administration of vancomycin, 1 g over 1 hr plus intravenous or intramuscular administration of gentamicin

1.5 mg/kg (not to exceed 80 mg), 1 hr before procedure; may be repeated once 8 hr after initial dose

Alternative Low - risk Patient Regimen Amoxicillin 3 g orally 1 hr before procedure; then 1.5 g 6 hr after initial dose

blood fl ow with resultant increase in RV and PA pressures Ultimately RV and left ventricular (LV) pressures equalize, leading to pulmonary vasoconstriction and irreversible vascular changes resulting in pulmonary hypertension and Eisenmenger ’ s syndrome

One of the primary goals in the anesthetic management of these women is to avoid pain thus mitigating the hemodynamic increases in pulmonary and systemic vascular resistance Avoidance of sudden decrease in systemic vascular resistance is also of paramount importance because it increases the L to R shunt thus increasing the incidence of hypoxemia

Because of hemodynamic responses secondary to increased stress hormones and catecholamines seen during labor and deliv-ery, parturients with NYHA class III and IV may require invasive monitoring to note the beat to beat changes In such cases con-tinuous arterial blood pressure monitoring with an arterial line, continuous ECG and central venous pressure (CVP) monitoring may be useful during both labor and cesarean section

Antibiotic prophylaxis for prevention of bacterial endocarditis, particularly in patients with ASD for uncomplicated delivery, is not advocated by the American Heart Association [4] (See Table 45.5 )

Anesthetic m anagement

Goals of anesthetic management include:

• avoiding decreases in systemic vascular resistance, thus mini-mizing the magnitude of the right to left shunt

• maintaining adequate intravascular volume and venous return Amongst the neuraxial anesthesia labor analgesic techniques the combined spinal/epidural (CSE) technique is most preferable Early establishment of CSE in labor with the use of intrathecal narcotics followed by epidural infusion of ultra low concentra-tions of local anesthetics can provide excellent analgesia without decreasing the systemic vascular resistance Phenylephrine is the drug of choice for managing hypotension in these patients The advantage of a CSE technique for labor analgesia is the ability to provide surgical anesthesia if a cesarean section is needed In the event that general anesthesia becomes necessary (due to lack of time to establish a regional block or if there are contraindications

to regional anesthesia), it is important to avoid decreases in SVR with intravenous induction and inhalational agents, and increases

in pulmonary vascular pressures Following acid aspiration pro-phylaxis, controlled induction with ketamine, or short - acting narcotics such as remifental is preferable in order to prevent large hemodynamic perturbations, and to minimize adverse effects on the fetus

Consultation with the neonatologist and plans for neonatal resuscitation are also important

Eisenmenger ’ s s yndrome

Pathophysiology

Eisenmenger ’ s complex is described as pulmonary hypertension with a reversible or bidirectional shunt through a large VSD The systemic and pulmonary circulations are in open communica-tion When the pulmonary vascular resistance rises or systemic vascular resistance falls, severe hypoxemia ensues due to blood bypassing the lungs

When fl ow through the pulmonary vascular bed is increased,

as in patients with congenital intracardiac (left to right) shunts, the vasculature is initially able to compensate for the increased volume However, over a prolonged period, there is thickening

of the vessel walls, resulting in an increase in pulmonary vascular resistance Eventually, as a result of the increased pulmonary vascular resistance, right - sided cardiac pressures become elevated leading to reversal in the intracardiac shunt The conversion or reversal to a right to left shunt with longstanding atrial or ven-tricular septal defect or a patent ductus arteriosus results in Eisenmenger ’ s syndrome A retrospective analysis (1978 – 1996) [9] , showed an increase in pulmonary artery pressure and pul-monary vascular resistance during gestation in some patients with moderate pulmonary hypertension at the beginning of the pregnancy The maternal death rate was 36% in a series of 73 patients with Eisenmenger syndrome Three women died during pregnancy and 23 died at the time of delivery or within 1 month postpartum Mortality was strongly associated with late diagnosis and late hospital admission, while severity of pulmonary hyper-tension was also found to be a contributing factor Neither the

In parturients with left to right shunts, the primary

consider-ations are alleviation of pain during labor and therefore the use

of a combined spinal/epidural (CSE) technique in early labor is

particularly advantageous Intrathecal lipophilic narcotics such as

fentanyl can be used to alleviate pain without causing any changes

in the hemodynamics (specifi cally the SVR) Furthermore, this

can be followed with ultra - low dose epidural infusion which

pro-vides continuous labor analgesia without any adverse effects on

the hemodynamics or progress of labor [7]

The technique of loss of resistance to saline should be used

during epidural placement in order to prevent air entry into an

epidural vein which can lead to paradoxical air embolism [8] In

addition, in those patients with potential intracardiac shunts air

fi lters should be used on all venous and arterial lines

Decompensation in the cardiac status is most likely

immedi-ately after delivery due to the autotransfusion that occurs from

the uteroplacental unit Close monitoring of the hemodynamics

are important Prevention of the Vasalva maneuver in the second

stage is important and decreasing the duration of the second stage

of labor by operative vaginal delivery and provision of adequate

analgesia is important Supplemental oxygen is helpful to increase

oxygen reserves and to enhance oxygen delivery to both mother

and fetus (Table 45.6 )

Cyanotic h eart d isease

Tetralogy of Fallot

Pathophysiology

Tetralogy of Fallot (TOF) is the commonest congenital heart

disease associated with the following conditions: right to left

shunt, VSD, right ventricular hypertrophy, pulmonary stenosis

with right ventricular outfl ow tract obstruction, and an

overrid-ing aorta Most women have correction in childhood but

some may present with residual defects The degree of

intracar-diac shunting, severity of right ventricular outfl ow obstruction,

and right ventricular function are primary determinants of

outcome

Table 45.6 Anesthetic management principles in left to right intracardiac

shunts

Management principles Rationale

Supplemental oxygen Increases oxygen reserves, especially in

second stage of labor Loss of resistance to saline technique

for epidural anesthesia

Decreases risk of venous air embolism and paradoxic air embolism Early combined spinal epidural

technique with intrathecal narcotics

and ultra - low concentration of

epidural infusion analgesia for

good pain control throughout labor

Avoid increases in maternal catecholamines

Cut short second stage of labor with

forceps/vacuum assist

Avoids Valsalva and hemodynamic changes associated with pushing

48 hours after delivery due to the increased risk of thromboem-bolism in these patients

Stenotic l esions Pathophysiology

Congenital a ortic s tenosis

Congenital aortic stenosis is usually associated with a bicuspid aortic valve [11] Patients with aortic stenotic lesions, functional class NYHA > 2, cyanosis, severe left ventricular outfl ow obstruc-tion (aortic valve area < 1.5 cm 2 ) resulting in decreased cardiac output and uteroplacental blood fl ow, or impaired left ventricu-lar function are considered at high risk for morbidity and mortal-ity during pregnancy

Severe aortic stenosis (a peak transvalvular gradient greater than 50 mmHg) must be corrected before pregnancy Severe aortic stenosis carries a high risk of mortality during pregnancy Siu et al reported a maternal mortality rate of 11% and a peri-natal mortality rate of 4% [3] A Canadian study described 49 cases with a 10% risk of complications in patients with severe stenosis [12]

Conservative medical management is acceptable for mild to moderate aortic stenosis However, once surgical valve replace-ment for severe aortic stenosis is required during pregnancy, there is an increased (30%) fetal mortality [13] Intrapartum balloon valvuloplasty has been reported, but it is not widely available and needs to be done in centers with the necessary experience [14]

Pulmonary s tenosis

Pulmonic valve stenosis is rare as an isolated condition Untreated severe/symptomatic pulmonary stenosis causes arrhythmias and right heart failure leading to high maternal and fetal morbidity and mortality The right ventricular failure is a result of an inabil-ity to compensate for the increases in heart rate, right ventricular preload, and oxygen delivery and consumption associated with pregnancy

Management of isolated pulmonic stenosis by percutaneous balloon valvuloplasty has been shown to improve the outcome of pregnancy and has been used in some institutions with success [14;15] Beta - blockade and diuretics, as well as close hemody-namic monitoring, should be continued throughout the pregnancy

Pain control during labor is often inadequate with the systemic analgesics that have been recommended by some authors, and fetal cardiorespiratory depression is an unwanted side effect when high - dose narcotic analgesia is used

Anesthetic m anagement

Epidural/spinal local anesthetics should be avoided due to the risk

of hypotension and the risk of decreasing preload which may not

be well tolerated in patients with mild to moderate aortic and pulmonary stenosis However, epidural and intrathecal narcotics using fentanyl or sufentanil are very effective for pain control with minimal hemodynamic consequences The disadvantage of

mode and timing of delivery, nor the type of anesthesia and

monitoring correlated with maternal outcome Most fatalities

were described as sudden death or therapy - resistant heart failure

Because maternal and fetal mortality can be as high as 50% in

parturients with Eisenmenger ’ s syndrome, this condition is

con-sidered an absolute contraindication to pregnancy If the patient

decides to continue pregnancy despite counseling then the

fol-lowing modalities should be implemented: bed rest, hospital

admission by second trimester, continuous pulse oximetry,

sup-plemental oxygenation, and prophylactic antithrombotic

pro-phylaxis with heparin

Anesthetic m anagement

The important considerations in patients with large VSD and

severe symptoms are:

• avoidance of decrease in SVR and increase in PVR

• prevention of hypercarbia, hypoxemia, acidosis and high airway

pressures

Invasive monitoring should include continuous invasive blood

pressure measurement Assessment of central venous pressure

(CVP) is equally important to monitor the trends in right

ven-tricular fi lling pressures and the intravascular volume status

Continuous supplemental oxygen must be used throughout

labor

Perioperative risk in Eisenmenger ’ s syndrome is high for

patients undergoing non - cardiac surgery, and regional anesthesia

should be avoided because of the potential deleterious

hemody-namic effects Spinal or epidural anesthesia could decrease the

afterload, causing an increase in the magnitude of the right to left

shunt A review of 57 articles describing 103 anesthetic

proce-dures in patients with Eisenmenger ’ s syndrome showed the

overall perioperative mortality based on anesthetic management

to be 14% Patients receiving regional anesthesia had a mortality

of 5%, whereas those receiving general anesthesia had a mortality

of 18% This trend favored the use of regional anesthesia but was

not statistically signifi cant [10]

Since the primary objectives involve maintaining cardiac

output, preserving systemic vascular resistance and lowering

pul-monary vascular resistance, general anesthesia is the preferred

technique for parturients with Eisenmenger ’ s syndrome who are

undergoing cesarean section delivery However there are

anec-dotal case reports of the use of regional anesthesia for both

opera-tive and vaginal delivery

As mentioned earlier, combined/spinal epidural is the

pre-ferred technique for labor analgesia in these high - risk patients A

combination of 10 – 15 µg of fentanyl and bupivacaine 2.5 mg

intrathecally provides excellent analgesia with minimal

hemody-namic perturbation This is followed by a low - dose epidural

infu-sion of bupivacaine 0.0625 mg/mL and fentanyl 2 µ g/mL at

10 – 15 mL/hour

If cesarean section is needed the authors recommend general

anesthesia with ketamine as an induction agent and the use of

short - acting narcotics such as remifental Close monitoring in the

intensive care unit is recommended post operatively for at least

dose narcotic induction offers good hemodynamic stability and invasive monitors should be used to guide fl uid management The mild chronotropic effect of vasopressors like ephedrine and dopamine is helpful in managing decreases in blood pressure In general neuraxial blockade (particularly spinal anesthesia) for cesarean section is not recommended There have been some case reports showing success using titrated epidural analgesia for vaginal delivery [19]

Vaginal delivery has been reported in uncomplicated coarcta-tion [17] When cesarean seccoarcta-tion is needed for obstetric indica-tions, or in patients with poorly controlled blood pressure, general anesthesia is administered with invasive hemodynamic monitoring, intravenous antihypertensive drugs, including β blockade, and postoperative intensive care management

Aortic d issection

Pathophysiology

Patients with Marfan syndrome or bicuspid aortic valve may proceed to aortic root dilatation and dissection, secondary to the hyperdynamic and hypervolemic condition associated with preg-nancy There is an increased chance of acute Type A dissection

in parturients with Marfan syndrome, particularly when aortic root dilatation is greater than 4 cm, or if an increase in aortic size

is detected during pregnancy [20] Numerous case series have been reported with favorable out-comes in the mother, but fetal outcome, in majority of the cases (especially when acute aortic dissection occurred necessitating emergency surgery), is relatively poor [21,22]

It is hard to draw conclusions from so few patients, but it seems logical that emergent delivery of a viable fetus is preferable before emergent repair of aortic dissection In situations where, based

on gestational age, fetal viability is not assured, the mother ’ s condition takes priority and emergent repair of the dissection should be performed with the knowledge that the fetus will be unlikely to tolerate cardiopulmonary bypass and deep hypother-mic circulatory arrest Fetal protection can be attempted with pulsatile perfusion and minimizing the circulatory arrest time

Anesthetic m anagement

The considerations are similar to those in non - pregnant patients who undergo emergent cardiac surgery and cardiopulmonary bypass

Acquired h eart d isease Rheumatic m itral s tenosis Pathophysiology (Figure 45.2 & Table 45.7 )

Rheumatic mitral valve stenosis is the most frequent rheumatic heart disease (RHD) encountered in the pregnant population worldwide Mitral stenosis is the lesion that most frequently requires therapeutic intervention during pregnancy

In severe mitral stenosis the valve area reduction decreases left ventricular fi lling and causes a fi xed cardiac output state, elevated

this technique is the short duration of action of the neuraxial

narcotics, necessitating repeated lumbar punctures with the

sin-gle - shot technique A successful case using continuous spinal

anesthesia with narcotics (sufentanil) has been reported and

other lipid - soluble narcotics like fentanyl may also be used [16]

Left v entricular o utfl ow t ract o bstruction

Aortic c oarctation

Pathophysiology

Aortic coarctation is a fi xed left ventricular outfl ow obstruction,

causing elevated blood pressure proximal to the lesion and

hypo-perfusion distally The decreased left ventricular outfl ow causes

decreased uteroplacental perfusion with a fetal mortality that can

approach 20% [12] Parturients with uncorrected coarctation are

usually unable to meet the increased hemodynamic demands of

pregnancy Complications include left ventricular failure, aortic

rupture, aortic dissection and endocarditis due to associated

bicuspid aortic valve [11] These patients are also prone to

cere-brovascular accidents due to an association with aneurysms in the

circle of Willis

Uncomplicated uncorrected coarctation carries a maternal

mortality risk of less than 3% Severe complications include aortic

dissection and rupture (particularly in the third trimester),

con-gestive heart failure secondary to the increased pressure load on

the left ventricle, and bacterial endocarditis The increased

demands of pregnancy predispose to aortic dissection Coarctation

of aorta is also associated with a high incidence of bicuspid aortic

valve, aneurysms of the circle of Willis, ventricular septal defects,

and Turner syndrome An MRI of the brain in such patients is

not unreasonable to exclude berry aneurysms

Recent data on the outcome of pregnancy in patients with this

rare condition is limited A Mayo clinic review included a

com-parison of 50 women who underwent repair of aortic coarctation

before pregnancy and parturients who had unrepaired lesions In

118 pregnancies the miscarriage rate was 9% and the preterm

delivery rate was 3% One third of the women who had

uncor-rected coarctation had signifi cant hypertension during

preg-nancy There was one maternal death and a very low incidence

of cardiovascular complications [17]

Anesthetic m anagement

Patients with corrected coarctation and no arm/leg blood

pres-sure discrepancy; and those with an arm to leg residual gradient

of less than 20 mmHg, usually can expect a good pregnancy

outcome In these patients, both vaginal delivery with neuraxial

labor analgesia, and cesarean section with neuraxial anesthesia,

have been conducted with minimal morbidity [18]

Pregnant patients with uncorrected coarctation are, however,

at much greater risk, and anesthetic goals should focus on

main-taining a normal or high cardiac preload, SVR and heart rate In

most situations, abdominal delivery by cesarean section under

general anesthesia is recommended This includes pre - and

post-ductal arterial catheters in the upper and lower extremities and

PA catheter monitoring with intravenous β blockade A high

-delivery due to the auto transfusion from uterine contraction, with resultant augmentation in cardiac output

Mitral stenosis with chronic left ventricular failure can result

in pulmonary hypertension by causing back - pressure distal to the pulmonary vasculature in either the left atrium or left ventricle This condition eventually causes structural changes in the vascu-lature and an increase in pulmonary vascular resistance Tolerance

of pregnancy when a woman has mitral disease depends upon the severity of the valve disease, the heart rate and rhythm, atrial compliance, circulating blood volume, and pulmonary vascular response

Patients with a mitral orifi ce area > 1.5 cm 2 can usually be treated medically, whereas parturients with more advanced mitral stenosis often require percutaneous mitral balloon valvotomy, a procedure with a very low complication rate in experienced hands Closed and open mitral commissurotomy has been per-formed with low maternal risk and a fetal survival of greater than 90% [23] Closed or open mitral commissurotomy, balloon val-vuloplasty, and valve replacement, are usually considered in patients with a valve area < 1.2 cm 2 , a poor response to medical therapy, and the absence of valve calcifi cation [25] Percutaneous balloon valvuloplasty of the mitral valve is the preferred method

left atrial and pulmonary arterial pressures, and eventually

pul-monary edema Compensatory RV hypertrophy leads to right

heart failure During gestation and labor, the increased cardiac

output and demands, plus the increased heart rate and decreased

left ventricular fi lling, increase the risk for pulmonary edema The

time of highest risk for pulmonary edema is immediately after

Pathophysiology

NlMVA 4–6 cm 2

Mild MS=1.6–2.0 cm 2

Mod MS=1.1–1.5 cm 2

Severe MS==1.0 cm 2

Increased LA pressures Pulmonary congestion

RV failure

Symptoms initially only noted during exercise or when during AF

Reduced stroke volume

Reduced LVEDV and LVEDP

Impaired filling of LV congestion

Chronic underfilling results in cardiomopathy

Impaired contractility

Mitral Stenosis

Mitral valve

CCF

Figure 45.2 Pathophysiology of mitral stenosis

MS, mitral stenosis; Nl MVA, normal mitral valve

area; LV, left ventricle; LVEDV, left ventricle

end - diastolic volume; LVEDP, left ventricle

end - diastolic pressure; RV, right ventricle; CCF,

congestive cardiac failure; AF, atrial fi brillation

Table 45.7 Interaction of Hemodynamic Changes on Pregnancy and Mitral

Stenosis

• Mitral stenosis limits ability to increase CO during pregnancy

• The increase in HR during pregnancy limits the time available for fi lling of the

LV & results in LAP & PAP pulmonary edema

• With the increase in HR, blood volume, and demands for increase in CO( late

trimester and L & D) causes the pressure gradient across the valve to quadruple

– thus increasing the functional cardiac status ( NYHAC)

• Approximately 80% off cases of systemic emboli occur in patients with atrial

fi brillation

CO, cardiac output; HR, heart rate; LV, left ventricle; LAP, left atrial pressure;

PAP, pulmonary artery pressure; L & D, labor and delivery; NYHAC, New York

Heart Association classifi cation

when intervention is needed during pregnancy [24] Kasb et al

[25] have shown that pregnant patients with symptomatic mitral

stenosis can be safely treated with β - blockade which signifi cantly

reduces the incidence of pulmonary edema It has also been

shown that patients with severe symptoms who undergo

valvu-loplasty or valve surgery before pregnancy have fewer

complica-tions than those treated medically Early preconceptional

counseling regarding management and risk of adverse cardiac

outcomes is important, especially in patients with severe mitral

stenosis (Tables 45.8 & 45.9 )

Anesthetic m anagement (Tables 45.10 & 45.11 )

Principles of anesthetic management include:

• prevention of pain and avoidance of increased sympathetic

stimulation which can result in tachycardia and augmentation of

cardiac output

• judicious preload with crystalloids

• invasive hemodynamic monitoring with a pulmonary artery

pressure catheter

In laboring parturients an early epidural can be placed and

boluses of medication can be given slowly Combined spinal/

epidural labor analgesia with a lipophilic narcotic and ultralow

concentration of bupivacaine as described above and in Tables

45.12 and 45.13 is the preferred technique Figure 45.3 shows a

technique of combining a lipophilic narcotic (fentanyl), given

intrathecally, with a hydrophilic narcotic like morphine, which

provides longer - lasting labor analgesia than a single narcotic

This technique also offers hemodynamic stability with reasonable

Table 45.8 Impact of Pregnancy - Induced Hemodynamic Changes and

Complications with Mitral Stenosis

An anatomically moderate stenosis become functionally severe

• NYHAC during pregnancy

• Pulmonary congestion

• Atrial fi brillation

䊊 Systemic emboli

• Paroxysmal tachycardia

NYHAC, New York Heart Association Classifi cation

Table 45.9 Preanesthetic evaluation

• Fatigue

• Dyspnea on exertion, paroxysmal nocturnal

dyspnea

• Orthopnea

• Dyspnea

• Hemoptysis

䊊 Rupture of bronchopulmonary varices

• Arrhythmias (atrial fi brillation)

• Pulmonary embolism

• Congestive heart failure

Murmur

• Presystolic accentuation or mid - diastolic murmur

䊊 Opening snap Signs of failure

䊊 Pulmonary edema

䊊 Jugular venous distension

䊊 Liver enlargement

䊊 Ascites

Table 45.10 Maternal Monitoring

• EKG

䊊 Maintain NSR

䊊 Detect arrhythmias

• Arterial catheterization

䊊 Beat - to - Beat monitoring( Labor & Delivery a dynamic state)

䊊 ABGs

䊊 Laboratory studies

• Swan Ganz catheter

䊊 Following trends

䊊 PAP & PCWP

䊊 Calculate parameters PVR, (R/O Pulmonary HTN), SVR, Assess CO, CI, EKG, electrocardiogram; ABGs, arterial blood gases; NSR, normal sinus rhythm; PAP, pulmonary artery pressure; PCWP, pulmonary capillary wedge pressure; PVR, pulmonary vascular resistance; HTN, hypertension; SVR, systemic vascular resistance; CO, cardiac output; CI, Cardiac Index

Table 45.11 Anesthetic Considerations and Challenges in Mitral Stenosis

• Prevent rapid ventricular rates

• Maintain sinus rhythm

• Minimize decreases in systemic vascular resistance

• Minimize or prevent increases in central blood volume

• Prevent increases in pulmonary artery pressure

䊊 Immediate postpartum

䊊 Avoid hypoxemia/hypoventilation

Table 45.12 Selection of Anesthetic Technique - Pros & Cons

• Combined Spinal – Epidural technique

䊊 Optimal technique

䊊 Intrathecal opioids during stage I ( excellent analgesia without sympathetic block)

䊏 15 – 25ugs fentanyl+0.25 – 0.5mgs morphine (preservative - free)

䊊 Dilute local anesthetics for late 1st stage and second stage of labor

䊏 0.625 – 0.125% bupivacaine + fentanyl 2 – 2.5ugs/ml

• Epidural with dilute local anesthetics

䊊 0.625 – 0.125% bupivacaine + fentanyl 2 – 2.5ugs/ml ugs/ml: micrograms per milliliter

Table 45.13 Advantages of anesthetic techniques

Intraspinal Narcotic Epidural Local Anesthetics

• Quick onset

• Selective analgesia

• No sympathetic block

• No motor block

Titratability of block

• Unlimited duration analgesia (catheter)

• Relative hemodynamic stability

• Ability to use different Local Anesthetics/ different situation

– 1st stage labor – 2nd stage labor – c/section – post op

been attempted in some centers as a temporizing procedure Aortic valve replacement performed antenatally has a maternal mortality of up to 11% [28]

Anesthetic m anagement

The goals of anesthetic management include maintenance of a slow heart rate, preservation of adequate preload and circulating blood volume, and control of systemic vascular resistance Oxygen supplementation, hemodynamic monitoring (continu-ous ECG, arterial catheter, central ven(continu-ous catheter/PA catheter), careful preloading and fl uid management strategies, left uterine displacement and cesarean delivery under general anesthesia, have all been recommended in patients with severe disease Phenylephrine is the vasopressor of choice to restore coronary perfusion pressure in patients with severe aortic stenosis when under general anesthesia [29]

In patients with milder aortic stenosis who are undergoing cesarean section single - shot spinal anesthesia is contraindicated However epidural anesthesia with incremental and careful titra-tion of local anesthetic has been administered with good maternal and fetal outcomes [30,31] In a case of mitral stenosis with pul-monary hypertension undergoing general anesthesia for urgent cesarean section, Batson and Longmire [32] demonstrated that alfentanil provided cardiovascular stability and allowed immedi-ate postoperative extubation, and that subsequent epidural mor-phine provided excellent postoperative analgesia Currently, ultra short - acting remifentanil is also used for induction of anesthesia

in pregnant patients with cardiac disease The combination of general anesthesia followed by postoperative epidural morphine allows early ambulation and helps with the prevention of throm-boembolism Any neonatal respiratory depression that occurs as

a result of this technique can usually be reversed with naloxone

Management of a trial fi brillation in p arturients with

m itral s tenosis

New - onset atrial fi brillation must be treated aggressively in preg-nant patients with mitral stenosis because of the increased reli-ance on the atrial component for cardiac output during pregnancy

pain control in this high - risk group of parturients (personal

expe-rience of senior author) Clark et al have previously suggested

preloading with 5% albumin, but this is no longer routinely

advo-cated [26] Phenylephrine is the vasopressor of choice to manage

hypotension rather than ephedrine which causes tachycardia and

decreases the ventricular fi lling time, resulting in decreased

cardiac output Epinephrine - containing epidural solutions must

be avoided because of the potential for accidental epidural

intra-vascular injection and the associated adverse maternal

hemody-namic and uteroplacental blood fl ow effects Avoidance of the

Valsalva maneuver, and shortening the second stage of labor with

forceps or vacuum, are strategies that have been used successfully

in these patients Another advantage of an epidural analgesia for

delivery is the increased venous capacitance caused by the

sym-pathetic blockade This is analogous to the effect of

nitroglycer-ine, and helps to accommodate the autotranfused fl uid from

the uterus, mitigating the increased preload and preventing the

development of pulmonary edema

In our institution, when cesarean section is needed, gradual

titration of an epidural block with continuous monitoring of

blood pressure, pulmonary artery pressure and cardiac output is

performed A general anesthesia with a balanced anesthetic that

includes a high - dose narcotic and β - blocker has been used

suc-cessfully with intense invasive and/or transesophageal

echocar-diography hemodynamic monitoring

Aortic s tenosis

Pathophysiology

Amongst the acquired cardiac lesions, advanced aortic stenosis is

rare in patients of childbearing age If the aortic valve orifi ce area

is > 1.5 cm 2 , the hemodynamic changes of pregnancy are usually

well tolerated In those cases of more advanced aortic stenosis,

there is considerable risk of myocardial decompensation The

development of symptoms such as dyspnea, chest pain, syncope,

and arrhythmias are indicators of a complicated course Patients

with severe stenosis of < 0.5 cm 2 and a fl ow gradient greater than

60 mmHg are at high risk for left ventricular failure [27] Balloon

valvuloplasty, which carries the risk of severe regurgitation, has

Figure 45.3 Cardioversion in pregnancy

some of the indications for anticoagulation in a pregnant cardiac patient

Oral anticoagulation with warfarin has been associated with the lowest maternal mortality and rate of thromboembolism during pregnancy However, it is well known that warfarin use in the fi rst trimester can cause fetal growth restriction, spontaneous abortion, embryopathy and premature birth, and fetal and pla-cental hemorrhage in the third trimester [36]

Any decision to use warfarin or its derivatives in pregnancy should be accompanied by an in - depth informed consent discus-sion with the patient and her family, in which the relative fetal and maternal risks are outlined

Unfractionated heparin and low molecular weight heparin

do not cross the placenta, and are thought to have no fetal tera-togenic effects These drugs may not be as effective as warfarin in preventing thrombosis One accepted strategy is to use heparin

in the fi rst trimester of pregnancy, switch to warfarin or enoxa-parin until 35 – 36 weeks, and then restart heparin until delivery

A special concern in the anesthetic management of anticoagu-lated patients is the risk of epidural or spinal hematoma develop-ment during neuraxial anesthesia The American Society for Regional Anesthesia Consensus on anticoagulation and neuraxial anesthesia has stated that the decision to administer a neuraxial anesthetic in a patient receiving anticoagulants, particularly LMWH, should be based on an individual assessment of the risks and benefi ts for each patient Table 45.15 discusses some of these recommendations [37]

Ischemic h eart d isease Pathophysiology

Ischemic heart disease occurs in 1 in 10,000 pregnancies Risk factors in pregnancy include older age, smoking, hypercholester-olemia, hypertension, class H diabetes, intravenous administra-tion of ergometrine, pheochromocytoma, cocaine and other drug

Parturients with moderate mitral stenosis have an increased

inci-dence of atrial fi brillation and an associated increased maternal

mortality [33] (Table 45.14 ) Pharmacologic therapy includes β

blockers, calcium channel blockers and digoxin for heart rate

control Procainamide and quinidine are the preferred drugs for

suppressive antiarrhythmic therapy because of their safety profi le

in pregnancy [34] Although the safety of other antiarrhythmic

drugs such as sotalol and fl ecainide has not been established

in pregnancy they have been used in the management of fetal

tachycardia and no obvious maternal or fetal morbidity has

been recognized Amiodarone, on the other hand, has been

asso-ciated with neonatal hypothyroidism, congenital anomalies and

teratogenicity

Direct cardioversion should be considered if the patient is

hemodynamically unstable and this has been safely performed in

pregnancy [35] Cardioversion , if needed, should be undertaken

in the operating room with simultaneous preparation for

cesar-ean section Recommendations for cardioversion are described in

Table 45.14 and Figure 45.1

Anticoagulation t herapy in a p arturient

Mechanical heart valves, new - onset atrial fi brillation, dilated

cardiomyopathy, and cardiopulmonary bypass surgery are

Table 45.14 Cardioversion in Pregnancy

• Recommendations

䊊 Prepare for Emergency C - section

䊊 Monitoring – FHR monitoring

䊊 MAC Low energy levels biphasic

䊊 Anterior Posterior Gel Pad Placement

䊊 GETA for High energy levels

MAC, monitored anesthesia care; GETA, general endotracheal anesthesia; FHR,

fetal heart rate

Table 45.15 Recommendations based on American Society of Regional Anesthesia Guidelines for neuraxial block placement in parturients receiving anticoagulation

NSAIDs/aspirin No specifi c concerns No specifi c timing

Warfarin (Coumadin) Stop drug for at least 48 hours PT/INR checked subsequently should be

within normal limits before neuraxial attempts

PT/INR checked and confi rmed to be within normal limits before removal

Low molecular weight heparin Stop LMWH 12 hours before placing epidural catheter

If larger doses of LMWH have been used (e.g enoxaparin 1 mg/kg), a

24 - hour interval is needed before attempting neuraxial technique

At least 2 hours should elapse after removal of catheter before redosing LMWH to reinstitute anticoagulation

Monitoring anti - Xa levels is not recommended for LMWH activity

Thromboelastogram is used in some centers to determine coagulation status but cannot be recommended

NSAID, non - steroidal anti - infl ammatory drugs; PT, prothrombin time; INR, International Normalized Ratio (normal value is 1.2); LMWH, low molecular weight heparin