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addition to the increased SV. Plasma volume increases by 40“50%
logical agents commonly used in anesthetic and obstetric practice
from prepregnant levels. This raised plasma volume exceeds the
can have adverse hemodynamic effects (Table 1.1).
increase in red blood cells resulting in a relative anemia that may
Due to the nature and the rarity of the cardiac diseases discussed,
compromise oxygen delivery. Blood pressure (BP) usually falls
there is a lack of randomized controlled studies to guide our
during pregnancy due to progesterone-induced vasodilatation
practice. As a result, case reports and expert opinion will form the
and the low resistance placental bed. Pulse pressure widens due
basis of discussing the anesthetic techniques. However, management
to a greater reduction in diastolic BP compared to systolic BP.
options and anesthetic techniques must be individualized and
Hyperventilation associated with pregnancy results from the
based on the prevailing hemodynamic condition and obstetric needs.
respiratory stimulating effects of progesterone and leads to hypo-
carbia (PaCO2 27“34 mmHg) and a mild respiratory alkalosis (pH
of 7.40“7.45).
Scope of the problem
Labor pain, periodic changes in venous return due to uterine
An estimated 0.2“3.0% of pregnant patients have cardiac disease,1 contractions, and maternal expulsive efforts increase CO approxi-
an increasing cause of maternal mortality.2,3 The 2000“ 2 Confidential mately 45% above prelabor levels. These physiological stresses
Enquiries into Maternal Deaths in the United Kingdom reported that can be minimized by good analgesia and anesthesia, careful fluid
cardiac disease was the second most common nonobstetric cause and hemodynamic management, as well as careful positioning to
of maternal death after psychiatric disease.4 Cardiac disease is avoid aortocaval compression.10
also more common than the leading direct causes of maternal Further increases in preload occur after delivery due to auto-
death.4,5 The maternal mortality rate ranges from 0.4% in New transfusion from the contracting uterus and relief of aortocaval
York Heart Association (NYHA) class I“II women to 6.8% in class compression.11 These fluid shifts cause further stress on an
III“IV (Tables 1.2 and 1.3). Despite a dramatic decline over the last already potentially compromised cardiac lesion. Postpartum nor-
few decades in the incidence of rheumatic heart disease among malization of systemic vascular resistance (SVR) and loss of the
women of childbearing age in the developed world, more women low resistance placental bed increases afterload. Careful fluid and
with partially or fully corrected congenital heart disease (CHD) hemodynamic monitoring for days to weeks postpartum are
are surviving to reproductive age because of improved surgical essential to minimize potential problems in this crucial period.
techniques and advances in medical management.6,7
The principal danger for a pregnant woman with a heart lesion
Symptoms and signs of normal pregnancy
is cardiac decompensation because of the inability to meet the
and heart disease
additional demands imposed by the physiological changes of preg-
nancy and parturition. In addition, infection, hemorrhage, and Easy fatigability, dyspnea, and orthopnea of normal pregnancy
thromboembolism can compound the risk. Maternal and neonatal may simulate heart disease. Orthopnea is more common in obese
outcomes can both be improved by meticulous peripartum care. women and may be due to limitation of diaphragmatic motion.
However, some women with serious cardiac disease may still suffer Chest pain during pregnancy is most often due to hiatal hernia,
significant morbidity and mortality despite optimal medical care.4,8 esophageal reflux, or distension of the ribcage. Tachycardia is
normal in pregnancy, as are premature atrial and ventricular
depolarizations. Orthostatic syncope may occur with sudden
Physiology of pregnancy
assumption of the upright position. Syncope occurring in later
A comparison between normal cardiopulmonary parameters in pregnancy is usually due to supine hypotension secondary to
the pregnant and nonpregnant states is shown in Table 1.4. inferior vena caval compression.

Obstetric Anesthesia and Uncommon Disorders, eds. David R. Gambling, M. Joanne Douglas and Robert S. F. McKay. Published by Cambridge University Press.
# Cambridge University Press 2008.
1 Cardiovascular and respiratory disorders

Table 1.1 Cardiovascular effects of commonly used anesthetic and obstetric drugs

Cardiac Myocardial
Heart rate Blood pressure SVR output contractility Venodilation

« « or # « or # « « «
" or « «
"" " " "
« to "
" ## # # "
" or « « to #
# ## # "
« to # with « to " « to " « « « to #
repeat doses
« or " « to # « « « « to "
« to " «
" " " "
« or " « « « « «
« « « « « «
« to # « « « «
« or " # # # # "
« or # # # # # "
« or " « or #
# # ## #
« or "
"" # ## # #
« or # ? «
" # # #
« or " « or " « or " « « or #
# or "
Nitrous oxide
« « « " " " if used for regional
# # " # # "
Lidocaine toxicity
« or " « or # « « or # «
" "" " " " #
« or " « to " « to # « « « to "
(<10 U)
# (>10 U
bolus dose)
« or # « «
# # "
Magnesium sulfate
« « to # «
## # ""
« to # « to # « to "
" " "

The response is represented by a five-point scale from a marked increase ("") to marked decrease (##), « is no effect, " is a slight increase, # is a slight
Secondary effect from endogenous catecholamine release
May decrease due to histamine release
There are various caveats in the interpretation of these data. Some values are derived from animal studies, some from human volunteers, and some
from patients. Values may vary depending on whether a patient is mechanically ventilated or breathing spontaneously. In addition, the hemodynamic
effects of these agents may change in the presence of other anesthetic agents. Finally, the hemodynamic response may be different in patients who are
hypovolemic, have sympathetic overactivity, or a sympathectomy. The values and ranges indicated in this table are the authors™ opinion of the most
likely clinical response for most patients and have been taken in part from the following texts:
Bowdle, T. A., Horita, A. & Kharasch, E. D. (eds). The Pharmacologic Basis of Anesthesiology: Basic Science and Practical Applications. New York:
Churchill Livingstone, 1994 and Norris, M. C. (ed). Obstetric Anesthesia. Philadelphia: J. B. Lippincott, 1993.

Some cardiovascular findings on physical examination may pressure is not elevated and the hepatojugular reflex is not posi-
be confusing. Peripheral edema occurs in 60“80% of pregnant tive. Pseudo-cardiomegaly is related to displacement of the apex
individuals, and is attributed to hemodilution, a fall in plasma by the gravid uterus. There is often a third heart sound due to
oncotic pressure, and an increase in capillary pressure secondary volume loading and right ventricular outflow tract murmurs
to raised venous pressure in the legs. However, this is not asso- are common.
ciated with hepatomegaly. Rales are likely the result of upward Certain symptoms and signs suggest the presence of heart
displacement of the diaphragm. Prominent peripheral and neck disease. A careful history and physical examination will allow
veins are related to the hypervolemia of pregnancy and the these to be differentiated beyond the symptoms and signs of
vasodilatory effects of progesterone. However, mean right atrial normal pregnancy. Symptoms suggestive of heart disease

Chapter 1

Table 1.2 New York Heart Association (NYHA) functional capacity and objective assessment a

Functional capacity Objective assessment

Class I. Patients with cardiac disease but without limitation of physical activity. No objective evidence of cardiovascular disease.
Ordinary physical activity does not cause fatigue, palpitations, dyspnea, or angina.
Class II. Patients with cardiac disease resulting in slight limitation of physical Objective evidence of minimal cardiovascular disease.
activity. They are comfortable at rest. Ordinary physical activity results in fatigue,
palpitation, dyspnea, or angina.
Class III. Patients with cardiac disease resulting in marked limitation of physical Objective evidence of moderately severe cardiovascular
activity. They are comfortable at rest. Less than ordinary activity causes fatigue, disease.
palpitation, dyspnea, or angina.
Class IV. Patients with cardiac disease resulting in inability to carry on any physical Objective evidence of severe cardiovascular disease.
activity without discomfort. Symptoms of heart failure or angina may be present
even at rest. If any physical activity is undertaken, discomfort is increased.

AHA medical/scientific statement: 1994 revisions to classifications of functional capacity and objective assessment of patients with diseases of the
heart. Circulation 1994; 90: 644.

Table 1.3 Maternal mortality associated with heart disease in Table 1.4 Normal hemodynamic and ventilatory parameters
pregnancy in the nonpregnant and pregnant patient

Group 1: Mortality <1% Percentage
Atrial septal defect Nonpregnant Pregnant change
Ventricular septal defect
4.3 Æ 0.9 6.2 Æ 1.0 þ 45%
Cardiac output (l/min)
Patent ductus arteriosus
71 Æ 10 83 Æ 10 þ 17%
Heart rate (beats/min)
Pulmonary/tricuspid disease
1530 Æ 520 1210 Æ 226 À 21%
Systemic vascular
Tetralogy of Fallot, corrected
Bioprosthetic valve
Mitral stenosis, NYHA class I and II
119 Æ 47 78 Æ 22 À 34%
Pulmonary vascular
Group 2: Mortality 5“15% resistance
2A Mitral stenosis NYHA class III“IV (dyne.sec.cmÀ5)
Aortic stenosis 86 Æ 8 90 Æ 6
Mean arterial pressure NSC
Coarctation of aorta, without valvular involvement (mmHg)
Uncorrected Tetralogy of Fallot 6.3 Æ 2.1 7.5 Æ 1.8
Pulmonary capillary NSC
Previous myocardial infarction wedge pressure
Marfan syndrome with normal aorta (mmHg)
2B Mitral stenosis with atrial fibrillation 3.7 Æ 2.6 3.6 Æ 2.5
Central venous NSC
Artificial valve pressure (mmHg)
Group 3: Mortality 25“50%
NSC ¼ no significant change.
Primary pulmonary hypertension or Eisenmenger syndrome
Adapted from: Clark, S. L., Cotton, D. B., Lee, W. et al. Central
Coarctation of aorta, with valvular involvement
hemodynamic assessment of normal term pregnancy. Am. J. Obstet.
Marfan syndrome with aortic involvement
Gynecol. 1989; 161: 1439“4.
Adapted from: Foley, M. R.: Cardiac disease. In Dildy, G. A., Belfort,
M. A., Saade, G. R., Phelan, J. P., Hankins, G. D. & Clark, S. L. (eds.),
General management principles of pregnant
Critical Care Obstetrics, 4th edn. Malden: Blackwell Science, 2004,
women with heart disease
pp. 252“74.

1. Take a detailed history and follow up patients regularly during
include severe or progressive dyspnea, progressive orthopnea, pregnancy
paroxysmal nocturnal dyspnea, hemoptysis, syncope with Patients with significant heart disease are usually diagnosed
exertion, and chest pain related to effort or emotion. Physical prior to pregnancy and may develop worsening of symptoms
findings strongly suggesting the presence of heart disease during their pregnancy. However, some cardiac lesions asso-
include cyanosis, clubbing, persistent neck-vein distension, ciated with few symptoms in the nonpregnant state may
palpable murmurs, diastolic murmurs, dysrhythmias, and true become symptomatic for the first time in mid to late pregnancy.
cardiomegaly. The hemodynamic changes that occur in pregnancy represent a

1 Cardiovascular and respiratory disorders

significant stress test. Most women with cardiac disease who
Table 1.5 Endocarditis prophylaxis risk stratification
remain asymptomatic throughout pregnancy usually tolerate
labor and delivery. Conversely, women who are breathless at High-risk category (endocarditis prophylaxis recommended)
rest (NYHA IV) and groups 2 and 3 listed in Table 1.3, usually Prosthetic cardiac valves, including bioprosthetic and homograft valves
tolerate pregnancy poorly. Functional class NYHA III“IV patients Previous bacterial endocarditis
with surgically correctable lesions should be assessed for correct- Complex cyanotic congenital heart disease (e.g. single ventricle states,
ive surgery before pregnancy. transposition of the great arteries, Tetralogy of Fallot)
2. Understand the physiological changes of pregnancy Surgically constructed systemic pulmonary shunts or conduits
It is essential to understand the impact of physiological
Moderate-risk category (endocarditis prophylaxis recommended)
changes of pregnancy on the specific heart lesion in order to
Most other congenital cardiac malformations (other than those above
properly manage these patients.12
and below)
3. Multidisciplinary team approach
Acquired valve dysfunction (e.g. rheumatic heart disease)
Pregnant women with significant or complex heart disease
Hypertrophic cardiomyopathy
should be managed by a team in a specialist center.13 This
Mitral valve prolapse with mitral regurgitation Æ thickened leaflets
team should include representatives from obstetrics and peri-
Negligible-risk category (no greater risk than the general population
natology, anesthesiology, neonatology, cardiology, intensive
and endocarditis prophylaxis not recommended)
care, nursing, and social work. Patients should be seen regu-
Isolated secundum atrial septal defect
larly throughout their pregnancy and a management plan
Surgical repair of atrial septal defect, ventricular septal defect, or
should be formulated early in pregnancy before the onset of
patent ductus arteriosus (without residua beyond 6 months)
labor. High-risk women should be managed by senior anesthe-
Previous coronary artery bypass graft surgery
siologists experienced in treating pregnant patients with cardiac
Mitral valve prolapse without mitral regurgitation
lesions. Pediatric involvement is important, as there is a 5“15%
Physiologic, functional, or innocent heart murmurs
chance that the fetus will be affected by the same cardiac
Previous Kawasaki disease without valve dysfunction
defect.14 In addition, the fetus may be compromised by the
Previous rheumatic fever without valve dysfunction
mother™s cardiopulmonary insufficiency.15 In-utero echocar-
Cardiac pacemakers (intravascular and epicardial) and implanted
diography at 18 weeks™ gestation can detect most fetal cardiac
defects.16,17 Avoidance of pregnancy, or consideration of an
early therapeutic termination, in women with very high-risk From: Dajani, A. S., Taubert, K. A., Wilson, W. et al. Prevention of
cardiac disease (e.g., pulmonary hypertension) is prudent. bacterial endocarditis. Recommendations by the American Heart
4. Infective endocarditis antibiotic prophylaxis Association. Circulation 1997; 96: 358“66.
Although the risk of bacteremia following normal delivery
is low (0“5%),13 appropriate antibiotic coverage should be
provided for high-risk patients (especially those with prosthe- placenta and appears safe in women who breast-feed. Heparin
tic valves or a history of endocarditis) prior to labor, delivery, or is used to prevent and treat thromboembolism. For UFH, the
other surgical procedures (Tables 1.5 and 1.6).18 activated partial thromboplastin time (aPTT) should be mon-
5. Anticoagulation during pregnancy and peripartum itored because heparin requirements increase as pregnancy
Pregnancy is a hypercoagulable state, which increases the risk of progresses. Platelet count should be measured before neuraxial
thromboembolic events, especially in the cardiac patient with a blocks in patients on UFH for more than 4 days because of the
prosthetic heart valve, valvular heart disease, or heart failure.1 risk of heparin-induced thrombocytopenia.24 For LMWH,
Anticoagulant therapy should be considered in these high-risk monitoring of aPTT or anti-Xa level is not predictive of the
patients to prevent thromboembolism or thrombus formation. risk of bleeding and is therefore not always necessary or recom-
mended.24 Low molecular weight heparin offers potential
Warfarin: The use of oral anticoagulants during pregnancy is advantages over UFH including lack of need for laboratory
relatively contraindicated. Warfarin therapy in the first trimester monitoring, greater bioavailability, once-a-day dosing because
is associated with an increased incidence of fetal death and birth of its long half-life, and less thrombocytopenia and osteoporo-
defects (˜˜warfarin embryopathy™™). Warfarin use later in preg- sis. Its efficacy in preventing and treating thromboembolism
nancy is associated with prematurity and low birthweight, as (as well as the above mentioned advantages) are leading to the
well as neonatal cerebral hemorrhage.19,20 Despite these risks, widespread use of LMWH in obstetrics.
warfarin is sometimes administered in combination with low Thrombolytics: Streptokinase and urokinase are relatively con-
dose aspirin (80“100 mg/day) to patients with mechanical valves traindicated in pregnancy because of reports of placental abrup-
tion and postpartum hemorrhage.25 Streptokinase has been used
because of concerns about the efficacy of heparin in preventing
systemic embolism.21,22 Warfarin can be used in the postpartum successfully to treat prosthetic mitral valve thrombosis during
period and appears safe in women who breast-feed.23 pregnancy.26 The thrombosis was confirmed by echocardio-
Heparin: Heparin, unfractionated (standard, UFH) or low graphy and fluoroscopy at 28 weeks™ gestation in a woman with
molecular weight (LMWH), is the drug of choice during preg- a history of progressive exertional dyspnea. Valve function
nancy because it is a large molecule that does not cross the returned to normal within 18 hours of commencing treatment.

Chapter 1

Table 1.6 Adult antibiotic prophylaxis for genitourinary/gastrointestinal procedures

Situation a Regimen b

High-risk patients Ampicillin plus Ampicillin 2.0 g i.m. or i.v. plus gentamicin 1.5 mg/kg (not to exceed 120 mg) within
gentamicin 30 min of starting procedure; 6 h later, ampicillin 1 g i.m./i.v. or amoxicillin 1 g orally
High-risk patients allergic Vancomycin plus Vancomycin 1.0 g i.v. over 1“2 h plus gentamicin 1.5 mg/kg i.v./i.m. (not to exceed
to ampicillin/amoxicillin gentamicin 120 mg); complete injection/infusion within 30 min of starting procedure
Moderate-risk patients Amoxicillin or ampicillin Amoxicillin 2.0 g orally 1 h before procedure, or ampicillin 2.0 g i.m./i.v. within 30 min
of starting procedure
Moderate-risk patients Vancomycin Vancomycin 1.0 g i.v. over 1“2 h; complete infusion within 30 min of starting
allergic to ampicillin/ procedure

i.m. ¼ intramuscular; i.v. ¼ intravenous
Endocarditis prophylaxis not recommended for routine C/S and prophylaxis is optional for high-risk patients undergoing vaginal delivery.
No second dose of vancomycin or gentamicin is recommended.
From: Dajani, A. S., Taubert, K. A., Wilson, W. et al. Prevention of bacterial endocarditis. Recommendations by the American Heart Association.
Circulation 1997; 96: 358“66.

Table 1.7 ASRA guidelines for regional anesthesia in the anticoagulated patient a

Anticoagulant/thrombolytic Neuraxial placement considerations After placement / epidural catheter removal

Low dose LMWH2 (e.g. enoxaparin 10“12 hours after the last LMWH dose. After placement: first dose 6“8 hours; second dose no
0.5 mg/kg/day, dalteparin 120 U/kg sooner than 24 hours after the first dose.
q 12 h) After removal: minimum of 2 hours.
b, c
High dose LMWH (e.g. enoxaparin No sooner than 24 hours. After placement: no sooner than 24 hours. Indwelling
1 mg/kg q 12 h) catheters should be removed prior to starting
After removal: minimum of 2 hours.
d, f
Heparin IV 1 hour before any subsequent heparin 1 hour.
administration or 2“4 hours after the last
heparin dose.
d, e, f
Prophylactic heparin SC None. None.
Warfarin Discontinue 4“5 days prior; INR <1.5 before Neuraxial catheters should be removed when INR
considering regional anesthesia. <1.5.
Aspirin and NSAIDs No special dosing or timing considerations. No special dosing or timing considerations.
Platelet inhibitors (e.g. ticlopidine, 14 days for ticlopidine. 14 days for ticlopidine.
clopidogrel, GP IIb/IIIa) 7 days for clopidogrel. Platelet GP IIb/IIIa 7 days for clopidogrel. Platelet GP IIb/IIIa inhibitors:
inhibitors: eptifibatide and tirofiban (8 h) eptifibatide and tirofiban (8 h) to abciximab (48 h).
to abciximab (48 h).
Thrombolytics (e.g. streptokinase) Avoid except in highly unusual circumstances. Avoid except in highly unusual circumstances.

Adapted from the ASRA 2002 published guidelines: Horlocker, T. T., Wedel, D. J., Benzon, H. et al. Regional anesthesia in the anticoagulated patient:
defining the risks (the second ASRA Consensus Conference on Neuraxial Anesthesia and Anticoagulation). Reg. Anesth. Pain Med. 2003; 28: 172“97.
LMWH therapy should be delayed for 24 hours if the presence of blood during needle and catheter placement occurs.
Higher doses may require more caution.
It may be prudent to confirm that partial thromboplastin time (PTT) is within normal range prior to removal.
The risk of neuraxial bleeding may be reduced by delaying the heparin injection until after the block, and may be increased in debilitated patients or
after prolonged therapy.

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