Obstetric and Gynecologic Anesthesia: The Requisites

168 Pages·2006·1.92 MB·English

by  Ferne R. Braveman MD

THE REQUISITES TM
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First Edition 2006.
Library of Congress Cataloging-in-Publication Data
Obstetric and gynecologic anesthesia:the requisites in anesthesiology / [edited by]
Ferne R.Braveman.
p.;cm.– (Requisites in anesthesiology series)
ISBN 0-323-02420-3
1. Anesthesia in obstetrics.I.Braveman,Ferne R.II.Series.
[DNLM:1.Anesthesia,Obstetrical.WO 450 O14231 2006]
RG732.O275 2006
617.9'682–dc22 2005053001
Developmental Editor: Anne Snyder
Senior Project Manager:Mary Stermel
Marketing Manager:Emily Christie
Printed in the United States of America.
Last digit is the print number: 9 8 7 6 5 4 3 2 1
I would like to dedicate this book to my family,
whose support is unwavering.
v
Contributors
Ferne R. Braveman, MD Mirjana Lovrincevic, MD
Professor of Anesthesiology Clinical Assistant Professor of Anesthesiology
Adjunct Professor of Obstetrics and Gynecology School of Medicine and Biomedical Sciences
Director The State University of New York,University at Buffalo;
Section of Obstetric Anesthesiology Director
Yale University School of Medicine Regional Anesthesia/Postoperative Analgesia
New Haven,Connecticut Buffalo,New York
Pamela Flood, MD Julio E. Marenco, MD
Assistant Professor of Anesthesiology Assistant Professor of Clinical Anesthesiology
Columbia University; Columbia University College of Physicians and Surgeons;
Assistant Attending Attending Anesthesiologist
Columbia University Medical Center St.Luke’s Roosevelt Hospital
New York,New York New York,New York
Regina Y. Fragneto, MD Imre Redai, MD, FRCA
Associate Professor of Anesthesiology Assistant Professor of Anesthesiology
Director Columbia University School of Medicine
Section of Obstetric Anesthesia New York,New York
University of Kentucky College of Medicine
Lexington,Kentucky Alan C. Santos, MD, MPH
Chairman of Anesthesiology
Stephanie Goodman, MD Ochsner Clinic Foundation
Associate Clinical Professor of Anesthesiology New Orleans,Louisiana
Columbia University;
Associate Attending Jason Scott, FRCA
Columbia University Medical Center Consultant Anaesthetist
New York,New York Department of Anaesthesia
St.Thomas’Hospital
Ana M. Lobo, MD, MPH London,United Kingdom
Assistant Professor of Anesthesiology
Section of Obstetric Anesthesia Nalini Vadivelu, MD
Yale University School of Medicine Assistant Professor of Anesthesiology
New Haven,Connecticut Yale University School of Medicine;
Attending
Yale-New Haven Hospital
New Haven,Connecticut
vii
Preface
Obstetric and Gynecologic Anesthesia:The Requisites in throughout her pregnancy and into the postpartum
Anesthesiology provides a thorough and concise presen- period.The second section discusses care of the female
tation of the anesthetic considerations and management patient for gynecologic surgery,care of the female oncol-
of the female patient. The book includes a discussion of ogy patient,and care of the patient with chronic pelvic
the care of the pregnant patient,and it also provides infor- pain.The use of illustrations,tables,summaries,and case
mation for the care and management of the female patient studies should serve to make this a user-friendly text for
with unique pain management concerns as well as for her quick reference as well as a review of the subject.In total,
care related to gynecologic surgery. this volume should provide a concise reference for the
This book is intended for a wide audience,including care of our female patients.
the anesthesiologist needing a quick review,the resident I would like to acknowledge my many mentors,both
rotating in obstetrics and gynecology,and those prepar- past and present, without whom this book would not
ing for board examinations and recertification.Obstetric have been possible.Among them are Sanjay Datta,Gerry
and Gynecologic Anesthesia is presented in two major Ostheimer,Paul Barash,and Roberta Hines.The lessons I
sections. The first section reviews the physiology of learned from them will never be forgotten.
pregnancy and discusses care of the pregnant patient
ix
1
CHAPTER Maternal Physiology
and Pharmacology
STEPHANIE GOODMAN
PAMELA FLOOD
Physiology of the Obstetric Patient cause specific alterations that come together in the
Cardiovascular unique physiology of pregnancy.
Respiratory The adaptations that allow for the protection and
Central Nervous System nurturing of the growing fetus are generally well toler-
Head/Ears/Eyes/Nose and Throat ated by a healthy parturient.In this chapter,we will dis-
Gastrointestinal cuss the physiologic changes that occur in pregnancy in
Renal a review of systems for the parturient.We will then dis-
Hematologic cuss the pharmacologic changes of pregnancy with
Endocrine emphasis on the physiologic changes that underlie them.
Musculoskeletal These alterations should not be thought of as due to
Pharmacology in the Obstetric Patient disease, but rather as normal values during pregnancy.
Placental Transfer It is easy to imagine, however, that these physiologic
Local Anesthetics changes combined with the increased metabolic demand
Opioids of the growing fetus can worsen pre-existing maternal
General Anesthetics health problems and can even cause subclinical illness to
Inhalation Agents become manifest.
Benzodiazepines
Muscle Relaxants
PHYSIOLOGY OF THE OBSTETRIC
Vasopressors
PATIENT
Vagolytic drugs
Antihypertensive drugs
Cardiovascular
Antacids
Antiemetics From the moment of conception, the embryo pro-
duces substances that profoundly alter the mother’s
Physiologic changes occur during pregnancy that physiology. These substances prevent rejection of the
allow maternal adaptation to the demands of the growing embryo’s foreign proteins by the maternal immune sys-
fetus,supporting placental unit,and ultimately to facili- tem and favor transport to and implantation into the
tate labor and delivery.These modifications affect almost uterus. The effects of these embryonic-derived sub-
every organ system and influence the anesthetic and peri- stances are largely local until implantation when there is
operative management of the pregnant woman.The access to the maternal vasculature.At the time of implan-
physiologic changes of pregnancy,especially in the gas- tation (approximately 5 weeks after the last menstrual
trointestinal and cardiovascular systems,directly influ- period) changes in maternal osmoregulation begin with
ence the absorption,distribution,and elimination of increased maternal thirst and body water accumulation.
drugs.Profound changes in the hormonal milieu,the Embryonic human chorionic gonadotropin has been
mechanical effects of an enlarging uterus,the increased implicated in these early maternal physiologic changes.
metabolic demand of the fetal-placental unit,and the Osmotic thresholds for thirst and antidiuretic hormone
presence of the low-resistance placental circulation each secretion are reset to lower levels that allow for the
1
2 OBSTETRICAND GYNECOLOGICANESTHESIA:THE REQUISITES IN ANESTHESIOLOGY
volume expansion of pregnancy. At term, total body period,the cardiac output can be increased by as much
water is increased by 6.5 to 8.5 liters.This enormous vol- as 100%. The elevation in cardiac output is a result of
ume expansion results in the hemodilution of pregnancy both an increase in heart rate and stroke volume.Heart
and elevation of maternal cardiac output (Fig.1-1). rate begins to increase by 5 weeks gestation to a maxi-
The early volume changes of pregnancy lead to an mum of about 20% at term. Stroke volume reaches a
increased left ventricular end diastolic volume by the end maximum of a 25% increase by 20 weeks gestation.This
of the first trimester.Mild left ventricular hypertrophy is 2L/min increase in cardiac output mainly supplies the
similar to that achieved with athletic training.Both left and uterus, kidneys, and extremities. At term, the uterine
right atrial dimensions increase as aresult of the increased artery blood flow can be as high as 500 mL/min,which
preload to a maximum at30weeks gestation.There is no explains why an obstetric hemorrhage can so quickly
increase in central venous,right ventricular,pulmonary become life threatening.
arterial,or pulmonary capillary wedge pressures under It used to be thought that cardiac output declines
normal circumstances because of coincident dilation of around the 28th week of gestation,but it is now known
peripheral and pulmonary veins.Systemic vascular resist- that these findings were the result of positional aorto-
ance starts to decrease as early as 8 weeks of gestation. caval compression. Maternal cardiac output is depend-
Several factors,including elevated progesterone,nitric ent on position because after 24 weeks gestation, the
oxide,prostaglandins,and/or atrial natriuretic peptide, gravid uterus can completely obstruct venous return
may play a role. from the inferior vena cava in the supine position.
During pregnancy, cardiac output rises gradually, This aortocaval compression is also called the supine
beginning by 8 to 10 weeks gestation.By the end of the hypotension syndrome.At this point in gestation,
second trimester, cardiac output is elevated by 50% of women are instructed to avoid the supine position for
nonpregnant values, and in the immediate postpartum this reason. If the parturient needs to be supine for
cesarean delivery, effective prevention of aortocaval
compression includes placing the patient in a modified
lateral decubitus position by elevating the right hip
142 (witha pillow or“wedge”),or by tilting the entire table
or bed to the left. Cardiac output is highest when
140 measured in the left lateral decubitus position and the
P knee-chest position.When fetal heart rate decelerations
Na
(mmol/l) 138 occur in labor, the parturient is placed in one of these
positions to maximize placental blood flow and thus
136 fetaloxygenation (Table 1-1).
During labor, cardiac output increases even more
134
from term values.In the absence of epidural anesthesia,
300 cardiac output can be increased from 7 to 10.5 L/m,
again because of increased heart rate and stroke vol-
296 ume. During a uterine contraction, autotransfusion
294
288
Table 1-1 Normal Hemodynamic Values in Pregnancy
P
osm
(mOsm/kg) 284
Normal Values Change at Term
280
Systolic blood pressure 115 No change
Diastolic blood pressure 55 20% decrease
276
Heart rate 90 bpm 20% increase
Cardiac output 7 L/min 40% to 50%
272 increase
Central venous pressure 4 No change
MP MP LMP 4 8 12 16 Pulmonary capillary 7 No change
wedge pressure
Weeks of pregnancy Systemic vascular 1200 dyne/cm/sec 20% decrease
Figure 1-1 Change in maternal osmotic threshold.One of the resistance
first physiologic changes in pregnancy is a change in maternal Pulmonary vascular 78 dyne/cm/sec 30% decrease
osmotic set point that occurs approximately 4 weeks after the resistance
LMP at the time of implantation.
Maternal Physiology and Pharmacology 3
occurs as the blood in the uterus is expelled into the
CASE REPORT
systemic circulation. This causes an acute increase in
maternal stroke volume and cardiac output. Epidural A 23-year-old G1P0 woman is at 24 weeks gestation with
analgesia prevents the baseline increase in cardiac out- a singleton pregnancy.She presents to the labor room
put,which is likely due to relief of pain and a resulting with acute shortness of breath and weakness.She is pre-
viously healthy except for a remote history of Rheumatic
decrease in heart rate, as well as vasodilatation caused
Fever at 6 years of age without known sequelae.Her
by sympathectomy.The acute increase in cardiac output
blood gas analysis shows a pH of 7.50,pCO is 28,and
that occurs with uterine contractions does persist even 2
pO is 76.Her cardiac exam is significant for normal S1
after epidural analgesia.Approximately 10 to 30 minutes 2
and S2 heart sounds with a S3 gallop,an opening snap,
after the delivery of the baby,the parturient experiences
and a II/IV low pitched rumbling diastolic murmur.An
a further 20% increase in cardiac output that is associated urgent transthoracic echocardiogram shows moderate
with sustained uterine contraction after placental expul- mitral stenosis and suggests elevated left atrial pressure.
sion. This transient phenomenon resolves within the
first hour,and is counterbalanced by the normal loss of QUESTIONS
approximately 500 mL blood at vaginal delivery and 1L at 1. Why would a previously asymptomatic woman with
cesarean delivery. All of the hemodynamic changes of mitral stenosis become acutely ill in pregnancy?
2. Is the patient’s cardiac rhythm potentially
pregnancy resolve within 2 to 4 weeks after delivery.
important?
Maternal blood pressure decreases in normal preg-
3. How would you stabilize this patient?
nancy. Blood pressure is the product of cardiac output
and systemic vascular resistance. Despite increases in
cardiac output just described,the decrease in maternal
blood pressure parallels the decrease in systemic vascu- diameter (Fig.1-2).This is likely due to ligamentous relax-
lar resistance. The diastolic blood pressure decreases ation.As the uterus expands and increases intra-abdomi-
more than the systolic blood pressure and nadirs at 15 to nal pressure,the diaphragm elevates.These mechanical
20 mm Hg lower than prepregnancy values by 20 weeks changes result in decreased static lung volumes.Total
gestation.This is primarily due to vasodilatation caused lung capacity decreases by 5%,which is mostly attributa-
by progesterone as well as the presence of the low-resist- ble to a 20% reduction in functional residual capacity
ance placental circuit. After 20 weeks gestation, blood (FRC) (Fig.1-3).Residual volume also decreases by about
pressure increases toward prepregnancy levels under the 20% in late pregnancy.Vital capacity does not change.At
influence of increasing cardiac output and consistently term,the FRC has decreased to 80% of the nonpregnant
reduced systemic vascular resistance.Under normal con- level,and when the pregnant patient assumes the supine
ditions, blood pressure should never exceed prepreg- position,the FRC falls even further.
nancy values.In addition,despite elevated angiotensin Maternal oxygen consumption increases approxi-
levels, pregnant women are resistant to angiotensin’s mately 20%,much of which is attributable to the oxygen
hypertensive effects in the absence of pre-eclampsia. consumption of the fetus, placenta, and uterus. The
Some pregnant women appear to have signs and combination of reduced FRC and increased oxygen con-
symptoms of cardiovascular pathology, but these can sumption puts the pregnant patient at risk for hypox-
be normal findings. Mild dyspnea on exertion, systolic emia during periods of apnea.Decreased oxygen supply
heart murmurs,a prominent third heart sound,periph- with increased demand results in a shorter period of
eral edema, and cardiomegaly can all be observed dur- apnea that can be tolerated before desaturation of the
ing normal pregnancy. Electrocardiographic changes mother’s blood occurs.One minute of apnea in the preg-
such as left axis deviation and nonspecific ST-segment nant patient can result in a 150 torr decrease in P O .
a 2
and T-wave changes can occur due to the heart’s shifted Adequate denitrogenation prior to the induction of
position in the chest.Characteristic pregnancy-induced general anesthesia is very important. This can be
echocardiographic alterations have also been described achieved by having the patient breathe 100% oxygen for
that reflect the changes discussed. In the third tri- a period of time before induction,to maximize the oxy-
mester of pregnancy, a mild left ventricular hypertro- gen tension within the FRC. This allows more time for
phy reflects increased myocardial contractility and left tracheal intubation prior to hemoglobin desaturation
atrial enlargement and is a result of elevated intravascu- during induction of general anesthesia or during emer-
lar volume. gency resuscitation.Speed in establishing control of the
airway and ventilation in a pregnant woman is critical.
There is no change in the strength or utilization of res-
Respiratory
piratory muscles,and thus maximum inspiratory and
Early in pregnancy the shape of the thoracic cage expiratory pressures do not change in pregnancy.By
becomes rounder and has a greater anterior-posterior about 8 weeks of pregnancy there is an increase in tidal
4 OBSTETRICAND GYNECOLOGICANESTHESIA:THE REQUISITES IN ANESTHESIOLOGY
Nonpregnant Pregnant
Figure 1-2 Maternal skeletal changes.The maternal rib cage is widened in anterior-posterior
diameter and fore shortened.
volume that is centrally driven and under the control of that the pain threshold is elevated in pregnancy. From
progesterone.No significant change occurs in respiratory ateleologic standpoint,an elevated pain threshold would
rate.Minute ventilation is thus increased in term preg- help the mother tolerate an impending,painful delivery.
nancy,to a level almost 50% higher than in nonpregnant In the third trimester of pregnancy,sensitivity to pain is
women.The increased minute ventilation results in reduced when tested with pressure or electricity. This
a decrease in P CO to approximately 30 mmHg and change in pain sensitivity is thought to be due to increases
a 2
asmall increase in P O to 105 mm Hg.Arterial blood pH in spinal dynorphin (an intrinsic κ-opioid) and upregula-
a 2
remains essentially normal (around 7.44) because of tion of descending inhibition from noradrenergic neu-
metabolic compensation.The kidneys increase excretion rons.However,sensitivity to traditional μ-opioid agonists
of bicarbonate ions resulting in reduced plasma bicarbon- is not changed.Changes in maternal pain sensitivity are
ate levels of approximately 20 mEq/L (Table 1-2). thought to be due to increases in progesterone and estro-
gen.More subtle changes may occur with the hormonal
changes of menstruation. These differences brought
Central Nervous System
about by pregnancy are currently being evaluated as tar-
Neurologic changes in pregnancy are more subtle gets for pain relief modalities specific to pregnancy and
than the cardiovascular and respiratory changes, but delivery. An example would be utilizing α -adrenergic
2
deserve consideration nonetheless.Many people believe agonists as adjuvants for epidural analgesia.
Nonpregnant Pregnant
Inspiratory reserve
Inspiratory reserve
volume
volume
Inspiratory Inspiratory
capacity capacity
Total
Tidal Tidal
lung
volume volume
capacity
Expiratory reserve Expiratory reserve
Functional volume volume Functional
residual
residual Residual
capacity
capacity Residual volume
volume
Figure 1-3 Static lung volumes.In pregnancy the tidal volume is increased.Functional residual
capacity is reduced largely as a result of decreased residual volume.A smaller functional residual
capacity leads to less oxygen reserve for the parturient in periods of apnea.
Maternal Physiology and Pharmacology 5
circulating estrogen,nasal congestion frequently occurs
Table 1-2 Normal Arterial Blood Gas Values in during pregnancy and is associated with increased mucus
Pregnancy production (Table 1-3).
Trimester
CURRENT CONTROVERSIES:ENDOTRACHEAL
Nonpregnant First Second Third INTUBATION IN PREGNANCY
PaCO (mm Hg) 40 30 30 30 ● 90% of anesthesia-related maternal deaths occur
2
PaO (mm Hg) 100 107 105 103 under general anesthesia.
2
pH 7.40 7.44 7.44 7.44 ● Is general anesthesia more dangerous,or do sicker
HCO −(mEq/L) 24 21 20 20 women get general anesthesia for more emergent
3
situations?
CURRENT CONTROVERSIES:DOES PREGNANCY
CREATE RESISTANCE TO PAIN?
Gastrointestinal
● Is decreased pain sensitivity clinically relevant?
Under the influence of progesterone,gastrointestinal
● Does the parturient have different responses to
tone is reduced. The tone of the gastroesophageal
analgesic treatments than nonpregnant women?
sphincter is also reduced, increasing the incidence of
Than men?
gastroesophageal reflux, reflux esophagitis, and heart-
burn.This phenomenon affects between 50% and 80% of
all pregnant women.As a result,from the first trimester
Head, Ears, Eyes, Nose, and Throat of pregnancy, women have an increased risk of gastric
Pregnancy also causes anatomic changes in the airway, acid aspiration when their protective airway reflexes are
which can make endotracheal intubation more difficult. reduced with sedation or anesthesia. Classically, the
The maternal airway has received considerable attention pregnant patient has been considered to have delayed
due to the realization that approximately 90% of maternal gastric emptying and prolonged intestinal transit time.
deaths that are attributable to anesthetic causes occur This was thought to be caused by both endocrine and
under general anesthesia.The risk of failed intubation in mechanical factors: progesterone and the enlarging
apregnant patient is approximately 1:500,which is consid- uterus. More recent data suggest that pregnancy itself
erably higher than in the general population.The vocal does not delay gastric emptying. Studies of acetamino-
cords,arytenoids,and other glottic structures can be ede- phen absorption are used as an indirect measure of gas-
matous due to fluid accumulation,and visualization of tric emptying because it can only be absorbed when it
theairway and passage of the endotracheal tube may be passes into the more basic environment of the duode-
more difficult.Mask ventilation may be hindered by air- num.These studies show that there is actually no reduc-
wayobstruction due to weight gain and enlarged breast tion in gastric transit time during pregnancy. Residual
tissue of pregnancy.Difficult ventilation can substantially gastric volume and acidity are also unchanged in preg-
increase maternal morbidity and mortality in the event of nancy. However, gastric motility does decrease during
difficulty with tracheal intubation.The increased inci- active labor, which has been demonstrated by gastric
dence of difficult intubation in pregnancy is also correlated
with higher Mallampati scores in pregnancy.Mallampati
scores may actually worsen during the progress of labor,
Table 1-3 Mallampati Classification in Pregnancy*
perhaps as aresult of changes in fluid distribution and air-
way edema.For this reason,anesthesiologists must exam-
First Trimester (%) Third Trimester (%)
ine a patient’s airway immediately prior to urgent cesarean
delivery requiring general anesthesia,even if it has been
Class 4 42 56
assessed previously.Regional anesthesia is recommended Class 3 36 29
when possible for surgical delivery,particularly for an Class 2 14 10
obese parturient or one with an apparently difficult airway. Class 1 8 5
During pregnancy the oropharyngeal and nasal
*The Mallampati score was obtained in 242 women during the first and
mucosal capillaries are engorged,which predisposes to
third trimesters of pregnancy.The incidence of Class 4 airways was
bleeding with manipulation.Bleeding in this area can significantly increased in the third trimester (P< 0.001).Increased body
sometimes make a difficult intubation impossible.As a weight was positively associated with an increase in Mallampati score
(P< 0.005).Modified from Pilkington S,Carli F,Dakin MJ,etal:Increase
result,nasal intubation and nasal airways are not recom-
in Mallampati score during pregnancy.Br J Anaesthesia 74:638–642,
mended for use in the pregnant patient.Due to increased 1995.