Cardiopulmonary Resuscitation of Pregnant Women

RlCHilRD V. LEE, M.D. Social trends and medical progress have expanded the number of
BRUCE D. RODGERS, M.D. pregnant women with pre-existing medical illness and the variety of
LAUREL M. WHITE, M.Di surgical, anesthetic, and medical procedures used in the care of pregnant
ROBERT C. HARVEY, M.D. women; conditions and procedures that predispose to events that may
Buffalo, New York require cardiopulmonary resuscitation. Primate pregnancy, especially
human pregnancy, produces important anatomic and physiologic effects
not found in quadripeds and which have important potential impact upon
the effectiveness of cardiopulmonary resuscitation. Many of the studies
of the physiology of cardiopulmonary resuscitation have been carried out
using nonpregnant quadripeds. The applicability of contemporary knowl-
edge and recommendations for cardiopulmonary resuscitation to preg-
nant women are, therefore, not clearly defined.

HISTORY
Resuscitation, especially for victims of drowning and sudden death, has
been practiced for time out of mind [I]. Artificial respiration by mouth-to-
mouth ventilation, by tracheal intubation, or by external thoracic com-
pression remained the mainstay of resuscitation until the close of the
19th century when open-chest cardiopulmonary resuscitation became
technically possible [2,3]. Open-chest heart massage and direct electri-
cal defibrillation were used as desperate measures until the 1950s when
external defibrillation became a proved technique.
During studies on closed-chest defibrillation, Kouwenhoven et al [4]
noted a rise in intraarterial pressure following application of defibrillator
electrodes to the chest wall of an experimental animal. The results of
their clinical and experimental studies on closed-chest cardiopulmonary
resuscitation were published in 1960 and have become the standard
cardiopulmonary resuscitation techniques. Sternal compression was
thought to empty the ventricle and produce forward flow of blood by
compression of the heart between the sternum and the vertebral column.
It is clear now that rhythmic increases in intrathoracic pressure, as well
as cardiac compression, are essential for the‘maintenance of circulating
From the Department of internal Medicine, the
Division of Maternal Fetal Medicine, Department
blood [5-71.
of Obstetrics and Gynecology, and the Depart- Postmortem cesarean section has a history as old as resuscitation [8-
ment of Anesthesia, Children’s Hospital of Buffa- 10]. Over the’ past century, life support technologies have altered the
lo and State University of New York at Buffalo definition of “postmortem” cesarean section. Long-term maintenance of
Requests for reprints should be addressed to Dr. “brain dead” mothers allowing delivery at times most propitious for the
Richard V. Lee, Department of Medicine, Chjl-
dren’s Hospital of Buffalo, 219 Bryant Street,
fetus has been accomplished [ 11,121. These events have added new
Buffalo, New York 14222. Manuscript accepted dimensions to contemporary ethical debates and to the information and
March 27, 1986. skills required of practicing obstetricians.

August 1986 The American Journal of Medicine Volume 91 311

CARDIOPULMONARY RESUSCITATION IN PREGNANCY-LEE ET AL

TABLE I Anatomic and Physiologic Effects of
Pregnancy Affecting Closed-Chest
Cardiopulmonary Resuscitation
Increased blood volume
Increased cardiac output
Decreased peripheral vascular resistance,
except in toxemic syndromes
Enlarging uterus and supine position
Decreased compliance for artificial
Decreased compliance for thoracic
Uterine compression of aorta and inferior vena
Decreased venous return
Aortoiliac occlusion with decreased
and uterine arterial flow
Increased oxygen consumption
Increased rate of acid metabolite production
PHYSIOLOGIC CHANGES OF PREGNANCY
IMPORTANT FOR CARDIOPULMONARY
RESUSCITATION
Pregnancy produces dramatic changes in cardiovascular
physiology [ 131 (Table I). Maternal blood volume and
cardiac output increase to about 150 percent of nonpreg-
nant values. Redistribution of blood volume follows
changes in peripheral vascular resistance and the growth
of the uteroplacental mass [ 141. In the nonpregnant state,
the uterus receives less than 2 percent of the cardiac
output. During pregnancy, the proportion of cardiac output
flowing to the uterus increases to 20 to 30 percent.
Maternal blood pressure usually decreases somewhat
during the second trimester, a time when the uteroplacen-
tal mass is growing most rapidly. Progesterone, atrial
natriuretic factors, and vasodilatory prostaglandins in-
crease during pregnancy and foster relaxation of tubular
structures and reduced peripheral vascular resistance.
Alpha- and beta-adrenergic receptors have been dem-
onstrated in the uterine vasculature [ 15,161. Adrenergic
stimulation at differing perfusion pressures revealed no
autoregulation of blood flow in pregnant sheep [ 151. By
the end of the first half and during the second half of
pregnancy, the uteroplacental vascular bed functions as a
maximally dilated, passive, low-resistance system so that
uterine blood flow is determined by perfusion pressure.
Therapeutic doses of vasopressors, especially alpha-ad-
renergic (norepinephrine) or combined alpha- and beta-
adrenergic agents (epinephrine), may produce uteropla-
cental vasoconstriction when the maternal cardiovascular
system has enhanced sensitivity to their action as occurs
with hypoxia or hypotension [ 14- 161.
During the second half of pregnancy, the enlarging
uterus can exert increasing pressure on the iliac veins and
arteries, the inferior vena cava, and the abdominal aorta
[ 17,181. Hypotension in the supine position may develop
in women late in pregnancy because compression of the
inferior vena cava and major pelvic veins by the heavy
gravid uterus may sequester as much as 30 percent of the
circulating blood volume. A 25 percent increase in cardi-
ac output occurred when pregnant patients close to term
were changed from the supine to the lateral recumbent
position [ 181.
Compression of the abdominal aorta by the gravid
ventilation
compression uterus can reduce uteroplacental blood flow and is more
cava likely to occur when intra-arterial pressures are dimin-
ished. Impaired uteroplacental blood flow because of
renal hypovolemia from blood loss or venous sequestration will
not improve with administration of oxygen or vasopres-
sors alone [14]. Vasopressors alone may further impair
uteroplacental blood flow; circulating blood volume must
be maintained or restored.
Pregnancy is a high-flow, low-resistance state of car-
diovascular homeostasis. Preexisting or acquired in-
creases in vascular resistance, such as valvular stenosis
or hypertension, and reductions in flow because of de
creased circulating volume or ineffective cardiac pumping
are poorly tolerated both by the mother and by the fetus
[ 131. Experience with cardiopulmonary bypass during
pregnancy indicates that the maintenance of high flow
rates is the best way to minimize fetal risk during open
heart surgery [ 191.
Pregnancy produces equally dramatic changes in res-
piratory physiology [20]. Increased ventilation, probably
due to central stimulation by progesterone, is apparent in
the first trimester, and by late pregnancy is about 50
percent greater than in the nonpregnant state. The arterial
carbon dioxide tension declines to about 30 to 35 torr, but
renal compensation for the respiratory alkalosis produced
by hyperventilation maintains a normal arterial blood pH.
Maternal hypocapnia and respiratory alkalosis may en-
hance removal of carbon dioxide and hydrogen ion pro-
duced by the fetus and may thus constitute an essential
component of feto-placental acid-base balance.
By the third month of gestation, the maternal basal
metabolic rate and oxygen consumption begin to rise
progressively until term, reflecting the metabolic activities
of the fetus and placenta and the hyperventilation of
pregnancy [ 141. The need for oxygen increases in order to
meet the metabolic demands of breast, uterine, placental,
and fetal growth. The pregnant patient is less tolerant of
hypoxia than the nonpregnant person. Hypoxia produces
a substantial reduction in uteroplacental perfusion: a re-
duction that can be minimized by alpha-adrenergic block-
ade [14-l 61. When pregnant ewes were subjected to
reduced inspired oxygen, there was a 17 percent diminu-
tion in uteroplacental blood flow at an arterial oxygen
tension of 55 torr and a 22 percent reduction at an arterial
oxygen tension of 30 torr [ 151. The incidence of terato-
genesis is increased in mothers undergoing cardiac sur-

312 August 1986 The American Journal of Medicine Volume 81


gery with cardiopulmonary bypass during the first trimes-
ter, further emphasizing the importance of maintaining
adequate maternal oxygenation and uteroplacental blood
flow at any stage of pregnancy [ 191.
Respiratory mechanics and volumes are altered by the
cephalad displacement of the diaphragm by the enlarging
gravid uterus [20,21]. The diminution of functional residu-
al capacity thus produced is more dramatic in the supine
than in the sitting or upright postures. The combination of
diminished functional residual capacity and increased
oxygen consumption predisposes the pregnant patient to
precipitous drops in arterial and venous oxygen tension
during periods of reduced ventilation. Supine posture
causing reduced cardiac output magnifies the rate and
severity of the decline in oxygenation.
The gravid uterus and hypertrophied breasts may in-
crease the work of ventilation, especially when the patient
is supine [20,21]. The thorax may be rendered less
compressible to external pressure by the displacement of
abdominal contents by the gravid uterus. A progressive
increase in the oxygen cost of breathing during the last
four months of pregnancy has been attributed to an in-
crease in diaphragmatic work [2 11.
PHYSIOLOGY OF CARDIOPULMONARY
RESUSCITATION
The basic techniques of closed-chest cardiopulmonary
resuscitation have changed little in the 25 years since this
procedure was introduced [4,22]. Numerous studies have
documented that although contemporary cardiopulmo-
nary resuscitation is reasonably successful for rescuing
patients from responsive arrhythmias, it has been less
successful for resuscitation from asystole, refractory ar-
rhythmias, and electromechanical dissociation [7]. Pre-
existing and precipitating cardiopulmonary conditions of-
ten determine the outcome of cardiopulmonary arrest.
Recent experimental observations suggest that blood
flow and systemic perfusion during closed-chest cardio-
pulmonary resuscitation are produced by phasic fluctua-
tions in intrathoracic pressure, not by compression of the
heart between the spine and sternum [5-71. Changes in
intrathoracic pressure generated by external chest com-
pression are transmitted equally to the intrathoracic great
vessels and cardiac chambers. For forward flow to occur,
a pressure gradient from the arterial to the venous circula-
tion must be generated or maintained. The large peripher-
al arterial venous pressure gradients needed for systemic
perfusion are found only in vasculature protected by com-
petent venous valves. Such valves inhibit retrograde flow
from the great intrathoracic veins and allow a lower
pressure to be maintained in the venous system.
Increasing intrathoracic pressure augments arterial
pressure and flow produced by closed-chest massage.
Wilder et al [23] showed that simultaneous chest com-
Augusi
CARDIOPULMONARY RESUSCITATION IN PREGNANCY-LEE ET AL
pression and ventilation generated higher blood pressures
than alternating compression and ventilation in dogs.
Char&a et al [24] showed that simultaneous ventilation
and compression in human subjects produced higher
carotid artery blood flow and radial artery systolic pres-
sure than conventional chest compression. Systemic per-
fusion produced by pulses of increased intrathoracic pres-
sure explains the observations of Niemann et al [25] that
patients coughing during ventricular fibrillation could
maintain consciousness until definitive management
could be initiated. Attempts to improve closed-chest car-
diopulmonary resuscitation by increasing intrathoracic
pressure with abdominal binding have proved less suc-
cessful. Sanders et al [6] failed to resuscitate six dogs
with simultaneous chest compression-ventilation and ab-
dominal binding but were able to rescue five of six dogs
with standard closed-chest cardiopulmonary resuscita-
tion. Increased intrathoracic pressures obtained by ma-
nipulations of extrathoracic structures do not necessarily
improve the success of cardiopulmonary resuscitation.
Although no systematic studies on the hemodynamics
of cardiopulmonary resuscitation have been performed in
pregnant animals or humans, the physiology of human
pregnancy is likely to impede the success of cardiopulmo-
nary resuscitation. The mechanics of the gravid uterus in a
supine woman with cardiac arrest act like abdominal
binding, producing an increase in intrathoracic pressure,
diminished venous return, and obstruction to forward flow
of blood in the abdominal aorta.
The effect of the pregnant uterus on closed-chest
cardiopulmonary resuscitation was dramatized by the re-
port of DePace et al [26] of a young woman at 36 weeks’
gestation who had respiratory arrest during a massive
hemoptysis. Although the patient never had cardiac stand-
still or ventricular fibrillation, her physicians were unable
to generate a blood pressure despite endotracheal intuba-
tion, closed-chest cardiac massage, and vigorous fluid
and electrolyte therapy. The patient’s blood pressure rose
from 0 to 80 torr immediately upon evacuation of the
uterus by bedside cesarean section.
The circumstances of a patient such as the one de-
scribed by DePace et al encourage a reconsideration of a
role for thoracotomy and open-chest cardiac massage in
the resuscitation of pregnant women. Thoracotomy and
open-chest resuscitation are often the only effective mea-
sures for patients with chest trauma, tension pneumotho-
rax, massive pulmonary embolism, pericardial tampon-
ade, chest or spine deformities, and profound hypovole-
mia [27].
There are many reports of successful resuscitations
with open-chest massage following failure of external
cardiac massage. Human and animal studies have shown
that open-chest cardiac massage can produce superior
hemodynamic effects compared with closed-chest mas-
1988 The American Journal of Medicine Volume 81 313
CARDIOPULMONARY RESUSCITATION IN PREGNANCY-LEE
Grovid Uterus
J \u
Compression of Aorta Compression
t i
Hypotension
A 4 Cordio!Output
Uteroplocrntol
4
Blood Flow
Fetol
4
Acidosis
Fetol Compromise
Figure 1. Pathophysiology of cardiopulmonary arrest dur-
ing pregnancy. WC = inferior vena cava.
sage [6,7,27,26]. DelGuercio et al [29] reported that
internal cardiac massage doubled the cardiac index and
shortened the circulation time in 11 patients. Studies in
animals indicate that open-chest massage improves car-
diac output, arterial pressures, and carotid, coronary, and
aortic blood flow [7,26]. Not surprisingly, the benefits of
open-chest massage declined the longer unsuccessful
closed-chest massage was practiced; after 25 minutes of
closed-chest massage in dogs, there was no survival
advantage in performing thoracotomy and internal mas-
sage [26].
Fortunately, the uteroplacental circulation offers mini-
mal vascular resistance as long as adequate oxygenation
and acceptable acid-base balance are maintained. It is
possible that the pressure gradients generated by even
compromised standard cardiopulmonary resuscitation
may be adequate to sustain fetal life. However, maternal
hypoxia and acidemia produce vasoconstritiion and in-
creased resistance in the uteroplacehtal vasculature, and
because of increased oxygen consumption and carbon
dioxide and hydrogen ion production from the fetal placen-
tal metabolism, maternal apnea causes rapid rises in
arterial carbon dioxide tension and a precipitous decline in
314 August 1986 The American Journal
ET AL
pH and arterial oxygen tension. Delays or problems in
establishing effective ventilation magnify the circulatory
compromise of the uteroplacental unit and accelerate the
rate at which mother and fetus become unresuscitatable,
of IVC
despite adequate chest compression (Figure 1).
i
Venous Return CARDIOPULMONARY ARREST IN PREGNANT
PATlENTS
The causes of maternal cardiopulmonary arrest are legion
(Table II).
Before the onset of fetal viability, about the 24th gesta-
tional week, the objectives of cardiopulmonary resuscita-
tion can be directed almost exclusively to maternal con-
siderations. Successful recovery of maternal physiologic
Maternal function sufficient to maintain the pregnancy, eyen if such
Hypoxia recovery is incomplete in terms of independent and/or
conscious maternal existence, may be vital to the inter-
ests of the fetus and the family.
Prompt endotracheal intubation and frequent monitor-
Moternol ing of arterial blood gases and pH are essential [30].
Acidemio
Maintenance of the oxygen tension at 70 to 60 torr
(preferably greater) and the carb& dioxide tension at 30
to 35 torr is the goal of ventilation. If the pH is less than
7.3 when the partial pressures of oxygen and carbon
dioxide are acceptable, bicarbonate should be used.
Combined respiratory and metabolic alkalosis caused by
vigorous ventilation and bicarbonate administration may
be deleterious. Many centers have, therefore, discour-
aged the use of intravenous bicarbonate during cardiopul-
monary resuscitation. However, acidosis increases the
alpha-adrenergic reactivity of the uteropiacental vascula-
ture. We are therefore more inclined to give bicarbonate
during the resuscitation of a pregnant patient than during
the resuscitation of a nonpregnant patient.
The resuscitators are supposed to deliver 60 pounds of
force and to depress the sternum one and a half to two
inches [3 11. If adequate chest compression is not gener-
ating palpable pulses, simultaneous ventilation and com-
pression may be tried. Inadequate perfusion for 15 min-
utes should be a stimulus to consider thoracotomy and
open-chest cardiac massage [32].
The hemodynamic effects of the uterus mU.St be man-
aged by displacing the uterus from resting on the abdomi-
nal and pelvic great vessels. The use of a wedge, inflat-
able or solid, under the right flank and hip may help, as
can simply pushing the uterus to the left side. Placing the
patient fully in the left lateral decubitus position makes
external chest compression clumsy and ineffective. Oper-
ating room tables can be manipulated to produce favor-
able positioning and a strong surfabe for closed-chest
massage. Placing the patient on an operating room table
may facilitate the management of the resuscitation and
the patient.
If, after 10 to 15 minutes, external chest compression
of Medlcine Volume 81
 CARDIOPULMONARY RESUSCITATION IN PREGNANCY-LEE ET AL

is ineffective despite ventilation, positioning, fluid volume, TABLE II Some Causes of Cardiopulmonary Arrest
and acid-base management, the clinician is confronted during Pregnancy
with a difficult decision about the patient 24 or more
Pre-existing heart disease
weeks’ pregnant: an operation under less than ideal cir- Congenital heart disease
cumstances becomes a necessary consideration. Acquired valvular disease
When fetal viability has been reached, the decision to Arrhythmia
expedite delivery in the face of maternal cardiac arrest is Idiopathic
Drug-induced
dependent on fetal status as well as on maternal status
Myocardial infarction
(Table Ill). There are presently no clear guidelines for Pregnancy-associated cardiomyopathy
such monitoring. Because the cervix isusually closed and Pregnancy-induced hypertension; toxemia
fetal membranes are intact, intermittent monitoring with a Angioedema of larynx/anaphylaxis
Envenomation
combination of external monitor and real-time ultrasound
Lightning
provides the only reasonable indication of fetal status. Cerebrovascular accident
Considerable artifact and motion interference is invariably Asthma
present; however, periods exist during maternal cardio- Pulmonary embolus
pulmonary resuscitation when there is a pause to ascer- Aspiration pneumonia
Overwhelming infection/septicemia
tain the cardiac rhythm and efficacy of therapy. At this
latrogenic
point, real-time ultrasound is performed to confirm fetal Hypermagnesemia
cardiac motion and to examine biophysical parameters of
Reference list available on request.
fetal well-being such as motion, tone, and breathing ef-
forts.
Between the 24th and 32nd weeks of gestation, we
believe that thoracotomy and open-chest cardiac mas- residua until a more propitious time for delivery of her
sage should be considered if standard cardiopulmonary fetus. Antibiotic therapy and wound management directed
resuscitatfon is ineffective for more than 15 minutes. If at minimizing the potential infectious, hemostatic, and
they are not successful for five minutes, emergency ce- mechanical effects of emergency bedside surgery will be
sarean section is mandatory. If open-chest massage is necessary if the mother survives, regardless of whether
successful, the mother may be maintained despite severe the chest or the abdomen or both are opened.

TABLE Ill Recommended Approach to Cardiopulmonary Resuscltatlon (CPR) during Pregnancy According to
Gestational Age
Less Than 25 Weeks 25 lo 32 Weeks 32 Weeks or More

Continue CPR until Position patient to Position patient to

appropriate end point decrease aortocaval decrease aortocaval
compression by uterus compression by uterus
Consider open-chest Special attention to Special. attention to
cardiac massage after fetal status, especially fetal status, especially
15 minutes of continuous with: with:
CPR; sooner if maternal Defibrillation Defibrillation
hypoxia or inadequate Lidocaine, verapamil Lidocaine, verapamil,
circulation uncorrected Epinephrine beta-blockers
by closed-chest CPR Consider open-chest Epinephrine
massage when decision Emergency cesarean section after
to perform emergency 15 minutes continuous CPR;
cesarean section is made sooner if maternal hypoxia
Emergency cesarean section after or inadequate circulation
15 minutes continuous CPR; uncorrected by CPR or
sooner if maternal hypoxia fetal distress
or inadequate circulation Continue CPR during
uncorrected by CPR and after delivery
Continue CPR during and Consider open-chest massage
after delivery if maternal condition after
delivery warrants

August 1888 The American Journal of Medicine Volume 81 315

 CARDIOPULMONARY RESUSCITATION IN PREGNANCY-LEE ET AL

TABLE IV Complications from Cardiopulmonary Spontaneous intrahepatic bleeding can occur in toxemia
Resuscitation during Pregnancy [33], and hepatic injury, including laceration or rupture of
Maternal Fetal the liver, may result from closed-chest cardiac massage
[34] (Table IV). The effectiveness of closed-chest cardiac
Laceration of liver Cardiac arrhythmia/standstill massage may be jeopardized by both pregnancy and
Rupture of uterus from maternal defibrillation
Hemothorax/ and drugs
pregnancy-induced hypertension. Internal cardiac mas-
hemopericardium Central nervous system toxicity from sage can be combined with vasodilators to maintain or
antiarrhythmic drugs improve uteroplacental and visceral perfusion that may
Altered uterine activity not otherwise be possible.
Altered uteroplacental perfusion There is no contraindication to external defibrillation
during pregnancy [35]. If the patient has experienced
cardiac arrest from ventricular fibrillation, prompt electri-
cal countershock, at maximum recommended levels,
should be used.
After 32 weeks, proceeding directly to emergency Lidocaine crosses the placenta but has been safely
cesarean section seems appropriate if standard cardio- used in many pregnancies [36] (Table V). At therapeutic
pulmonary resuscitation is ineffective for more than 15 maternal blood levels, there is no evidence of adverse
minutes. Once the decision to perform cesarean section effects on the fetal heart rate or the uteroplacental unit.
is made, it should be carried out as expeditiously as Toxic maternal blood levels have been associated with
possible. A cesarean section tray and sterile gown and cardiac and central nervous system depression in the
gloves for the primary operator and an assistant should be neonate. Intravenous beta-adrenergic blocking agents
immediately available and at the bedside during a mater- and quinidine may precipitate uterine contractions. Rapid
nal arrest. intravenous administration of calcium channel blocking
Cardiopulmonary arrest in toxemic patients may be agents such as verapamil may exacerbate maternal hypo-
precipitated by arrhythmia, congestive heart failure, or tension and cause uterine atony.
myocardial infarct, by intracranial bleeding, or by iatro- The use of epinephrine intravenously via central cathe-
genie events like hypermagnesemia. The vascular ter or by intracardiac injection is common when cardiac
changes of toxemia can produce substantial interference standstill or electromechanical dissociation occurs. Be-
with uteroplacental blood flow even with otherwise nor- cause alpha-adrenergic drugs like epinephrine cause
mal cardiac function. The use of vasoconstricting vase- uteroplacental vasoconstriction in hypoxic, acidemic
pressor agents may exacerbate the condition and reduce women, we do not encourage their use in this setting
further the chances of rescuing mother and/or fetus. without extreme caution. Open-chest cardiac massage by

TABLE V Commonly Used Drugs for Cardiopulmonary Resuscitation

Drug Clinical Application Comments

Epinephrine (and other Asystole/electromechanical dissociation, Use with caution: hypoxia in-
alpha agonists) hypotension, asthma creases sensitivity of utero-
placental vasculature. Mild
oxytocics
Digoxin Paroxysmal supraventricular tachycardia, Follow serum levels especially
especially atrial fibrillation/flutter when quinidine, verapamil are
used concomitantly
Lidocaine First choice in ventricular tachy- Excessive doses may cause
arrhythmias maternal seizures, fetal acidosis,
and fetal central nervous system and
cardiovascular depression
Verapamil Paroxysmal supraventricular tachycardia May cause maternal hypotension,
uterine atony
Beta-blockers Atrial and ventricular tachyarrhythmias May cause fetal bradycardia
Bretylium Ventricular tachyarrhythmias Relatively safe second-line drug
if lidocaine ineffective
lsoproterenol Asthma, electromechanical dissociation, Tocolytic, may cause metabolic
Terbutaline tocolysis (glucose, potassium) disarray,
Ritodrine tachycardia

316 August 1966 The American Journal of Medlclne Volume 61

 CARDIOPULMONARY RESUSCITATION IN PREGNANCY-LEE ET AL

TABLE VI Approach to Cardiopulmonary Resuscitation durlng Pregnancy

Time Resuscitative Action Diagnostic Action Pharmacologic Action

0 Chest thump
Ventilation (mouth-to-mouth) Electrocardiography for rhythm Intravenous fluids
External cardiac massage Check for pulses and perfusion
Defibrillate Ventricular fibrillation-
lidocaine
intravenous access: central line Determine gestational age Supraventricular tachy-
arrhythmia-digitalis/
beta-blocker as appropriate
1 to 2 minutes Endotracheal intubation Measure arterial blood gases
plus ventilation with oxygen Check for pulses and perfusion pH less than 7.3-sodium bicarbonate
Check fetal heart, sonography AsystoleIbradyarrhythmia-
atropine
Pulmonary edema-furosemide
2 to 5 minutes Electrocardiography for rhythm Ventricular fibrillation-
lidocaine
Defibrillate as needed
Electrocardiography for rhythm Ventricular fibrillation-
bretylium
Position to move uterus Quick measure of blood pressure, Electromechanical dissociation-
to left pulses, perfusion calcium chloride, epinephrine (one
Portable chest radiography time only), isoproterenol
Measure arterial blood gases pH less than 7.3-sodium bicarbonate

5 to 10 minutes Continue ventilation plus Check fetal heart, sonography

external massage
Begin preparation for
operative procedure as
appropriate Check for tension pneumothorax,
Arterial line cardiac tamponade, hypovolemia
Defibrillate as needed Measure arterial blood gases pH less than 7.3-sodium bicarbonate
15 minutes Open-chest cardiac massage Continue as above Continue as above
and/or emergency cesarean
section as appropriate

preserving uteroplacental blood flow while simultaneously
increasing cardiac output would seem to offer a more
rational choice than desperate polypharmacy.
Delivery of a fetus after 15 minutes of unsuccessful
maternal cardiopulmonary resuscitation poses special
risks and problems in addition to prematurity. Such infants
are likely to be hypoxic and acidotic. Use of substantial
amounts of adrenergic drugs and glucose-containing solu-
tions during cardiopulmonary resuscitation may set the
stage for profound neonatal hypoglycemia. Antiarrhyth-
mic agents may produce therapeutic and toxic effects in
neonates. A neonatologist is an essential member of the
cardiopulmonary resuscitation team for pregnant patients.
A time sequence of recommended steps in the cardio-
pulmonary resuscitation of pregnant patients is given in
Table VI. The recommendations are arbitrary, based on
current understanding of the physiology of pregnancy and
cardiopulmonary resuscitation, and without adequate doc-
umentation from studies in pregnant human beings. Some
are controversial, especially in the absence of experi-
mental evidence, but represent a starting point for future
investigation.

REFERENCES
1. Lee RV: Cardiopulmonary resuscitation in the eighteenth chest cardiac massage. JAMA 1960; 173: 1064-1067.
century. J Hist Med Allied Sci 1972; 27: 418-433. 5. Weiseldt ML, Chandra N: Physiology of cardiopulmonary
2. Sladen A, Kouwenhoven WB, Jude JR, Knickerbocker GG: resuscitation. Annu Rev Med 1981; 32: 435-442.
Closed chest massage. JAMA 1984; 251: 3137-3140. 6. Sanders AB, Meislin HW, Ewy GA: The physiology of cardio-
3. White CS: The role of heart massage in surgery. Surg Gyne- pulmonary resuscitation. JAMA 1984; 252: 3283-3286.
col Obstet 1909; 9: 388-400. 7. Niemann JT: Artificial perfusion techniques during cardiac
4. Kouwenhoven WB, Jude JR, Knickerbocker GG: Closed arrest: questions of experimental focus versus clinical

August 1986 The American Journal of Medicine Volume 81 317

CARDIOPULMONARY RESUSCITATION IN PREGNANCY-LEE ET AL

need. Ann Emerg Med 1985: 14: 761-768. 945-952.

8. Weber CE: Postmortem cesarean seotion: review of the 22. Songster GS, Clark SL: Cardiac arrest in pregnancy-what
literature and case reports. Am J Obstet Gynecol 1971; to do. Contemp Obstet Gynecol 1985; 27: 141-155.
110: 158-165. 23. Wilder RJ, Weir D, Rush BF, et al: Methods of coordinating
9. Arthur RK: Postmortem cesareari section. Am J Obstet Gyn- ventilation and closed chest cardiac massage in the dog.
ecol 1978; 132: i75-179. Surgery 1963; 53: 186-194.
10. Buchsbaum HJ, Cruikshank DP: Postmortem cesarean sec- 24. Chandra N, Snyder LD, Weisfeklt ML: Abdominal binding
tion. In: Buchsbaum HJ, ed. Trauma in pregnancy. Phila- during cardiopulmonary resuscitation in man. JAMA
delphia: WB Saunders, 1979; 236-249. 1981; 246: 351-353.
11. Hill LM, Parker D, O’Neill BP: Management of maternal 25. Niemann JR, Rosenborough JR, Hausknecht M: Cough-CFR.
vegetative state during pregnancy. Mayo Clin Proc 1985; Crit Care Med 1980; 8: 141-146.
,60: 469-472. 26. DePace NL, Betesh JS, Kotler MN: Postmortem cesarean
12. Dillon WP, Lee RV, Tronolone MJ, et al: Life support and section with recovery of both mother and offspring. JAMA
maternal brain death during pregnancy. JAMA 1982; 248: 1962; 248: 971-973.
1089-1091. 27. Stephenson HE Jr: Pathophysiological considerations that
13. Sullivan JM, Ramanathan KB: Management of medical prob- warrant bpen-chest cardiac resuscitation. Crit Care Mad
lems in pregnancy-severe cardiac disease. N Engl J 1980; 8: 185-187.
Med i 985; 3 13: 304-309. 28. Sanders AB, Kern KB, Ewy GA: Improved survival from
14. Brinkman CR Ill, Woods JR: Effects of hypovolemia and cardiac arrest with open chest massage (abstr). Ann
hypoxia upon the conceptus. In: Buchsbaum MI, ed. Trau- Emdrg Med 1983; 12: 138.
ma in pregnancy. Philadelphia: WB Saunders, 1979; 29. DelGuercio LRM, Feins NR, Cohn JD, et al: Comparison of
52-81. blood flow during external and internal cardiac massage
15. Dilts PV, Brinkman CR, Kirschbaum TH, Assali NS: Uterine in man. Circulation 1965; 32(suppl): 171-180.
and systemic hemodynamic interrelationships and their 30. Queenan JJ, ed: Managing OB/GYN emergencies (2nd ed).
response to hypoxia. Am J Obstet Gynecol 1969; 103: Oradell, New Jersey: Medlcal Economics Books, 1983.
138-157. 31. Standards for cardiopulmonary resuscitation (CPFt) and
16. Karlsson K: The influence of hypoxia on uterine and mater- emergency cardiac care. (ECC). JAMA 1980; 244:
nal placental blood flow, and the effect of alpha-adrener- 453-509.
gic blockade. J Perinat Med 1974; 2: 176-184. 32. Jacobson S: Current status of open chest procedures. Clin
17. Bieniarz J, Crottogini JJ, Curuchet E, et al: Aortocaval com- Emerg Med 1983; 2: 121-128.
pression by the uterus in late human pregnancy. Am J 33. Manas KJ, Welsh JD, Rankin RA, et al: Hepatic hemorrhage
Obstet Gynecol 1968; 100: 203-217. without rupture in preeclampsia. N Engl J Med 1985; 312:
18. Kerr MG: The mechanical effects of the gravid uterus in late 424-426.
pregnancy. J Obstet Gynecol Br Commonw 1965; 72: 34. Adler SN, Klein RA, Pellecchia C, Lyon DT: Massive hepatic
513-529. hemorrhage associated with cardiopulmonary resuscita-
19. Bernal JM, Miralles PJ: Cardiac surgery with cardiopulmo- tion. Arch Intern Med 1983; 143: 813-814.
nary bypass during pregnancy. Obstet Gynecol Sutv 35. Curry JJ, Quintana FJ: Myocardial infarction with ventricular
1986; 41: l-6. fibrillation during pregnancy treated by direct current defi-
20. Weinberger SE, Weiss ST, Cohen WR, et al: Pregnancy and brillation with fetal survival. Chest 1970; 58: 82-84.
the lung. Am Rev Respir Dis 1980; 121: 559-581. 36. Rotmensch HH, Elkayam U, Frishman W: Antiarrhythmic
21. Gee JBL, Packer BS, Millen JE, Robin ED: Pulmonary me- drug therapy during pregnancy. Ann Intern Med 1983; 98:
chanics during pregnancy. J Clin Invest 1967; 46: 487-497.

318 August 1988 The American Journal of Medicine Volume 81