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an increased risk to the mother and fetus. Women with preexisting
deaths. One report described the use of an ICD in a woman with
cardiac rhythm disorders are likely to have an exacerbation
ARVC at 21 weeks™ gestation. This life-preserving treatment
of dysrhythmia during pregnancy, which increases the risk
was associated with a normal remainder of the pregnancy and
of adverse fetal complications.35 Women with congenital heart
an uneventful forceps delivery.101 Another case described the
disease, especially those with subpulmonary ventricular systolic
successful use of an epidural anesthetic for labor and C/S in a
woman with ARVC and indwelling ICD.103 dysfunction and/or severe pulmonary regurgitation, may develop
sustained dysrhythmias during pregnancy (3% risk in one study).32
The treatment of the pregnant patient with cardiac dysrhyth-
Postural orthostatic tachycardia
mias may require important modifications of standard dysrhyth-
syndrome (POTS)
mia management. The goal is to protect the mother and her fetus
through delivery, after which chronic or definitive therapy can be
Postural orthostatic tachycardia syndrome encompasses a group
administered.106 New advances, such as ICD, allow immediate
of disorders characterized by orthostatic intolerance. In one case
treatment of dangerous heart rhythms, and fetal magnetocardio-
a parturient had worsening symptoms during pregnancy, which
graphy is a valuable new tool for rhythm diagnosis and for mon-
were managed by increasing the dose of beta-blockers. A labor
itoring maternal and fetal rhythms during therapy.107
epidural was used successfully and optimal postpartum analgesia
was ensured by using neuraxial opioids, NSAIDs, and bilateral
iliohypogastric and ilioinguinal nerve blocks. The aim was to REFERENCES
reduce the risk of triggering a tachycardic response to the stress
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¨
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53
1 Cardiovascular and respiratory disorders


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Chapter 2


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55
VASCULAR DISEASES
3
David R. Gambling




Introduction oxygen saturation (SaO2). When SaO2 is greater than 63%, three-
year survival is 55%. When SaO2 is less than 63%, three-year survi-
Maternal vascular lesions that become apparent during preg-
val is only 17%.7 Sudden death in primary pulmonary hypertension
nancy may be present before conception but only become symp-
may be caused by tachycardia and loss of effective atrial systole,
tomatic as a result of the physiologic changes of pregnancy. Blood
acute pulmonary embolism from deep venous thromboses, or
vessels are weakened by an increase in blood volume and cardiac
from RV ischemia or infarction.3 A rapid increase in venous return
output (CO); a decrease in systemic vascular resistance (SVR); and
to the right heart, and subsequently to the lungs, may produce a
hormonal changes. Hence, aneurysms can expand and rupture,
vagally-mediated bradycardia and fall in CO, which can be lethal.8
or arteriovenous (AV) malformations can grow and, if present in
In most cases, postmortem microscopic examination of the
the pulmonary circulation, can worsen a preexisting shunt. Some
lungs reveals that both lungs are affected by diffuse pulmonary
of the rare conditions described in this chapter affect blood ves-
vascular changes characterized by intimal proliferation, medial
sels in discrete areas of the body whereas others affect all blood
hypertrophy, and perivascular lymphocytic cuffing, described as
vessels. Often the disorders described are part of an autoimmune
plexogenic arteriopathy.9 Others have reported that thrombotic
disease process that impacts other organ systems. Many of the
pulmonary arteriopathy is a more likely cause of pulmonary hyper-
vascular disorders are associated with high maternal and neona-
tension.7 Primary pulmonary hypertension caused by pulmonary
tal mortality. For example, rupture of an enlarging aneurysm can
veno-occlusive disease with intimal proliferation and fibrosis of
cause abrupt, catastrophic blood loss and poor peripartum out-
intrapulmonary veins and venules occurs less frequently.3
comes. Likewise, pulmonary hypertension worsens during preg-
nancy and is often associated with maternal and/or neonatal
Signs and symptoms
death. This chapter discusses the clinical implications for the
obstetric anesthesiologist of most vascular lesions seen during
The signs and symptoms of primary pulmonary hypertension
pregnancy. Intracranial aneurysms during pregnancy are dis-
relate to RV compromise and failure. Dyspnea is caused by
cussed in Chapter 9.
decreased CO and ventilation/perfusion mismatch. Syncope is
due to a fixed CO with the inability of the heart to respond to a
demand for increased output. Angina is common, and probably
Primary pulmonary hypertension
results from RV ischemia and increased RV afterload. Other signs
Primary pulmonary hypertension is a progressive disease that and symptoms include fatigue, edema, and peripheral cyanosis.
produces a sustained rise of at least 25 mmHg in mean pulmonary Occasionally hoarseness may develop due to the pressure of an
artery pressure and an increase in pulmonary resistance, in the enlarging pulmonary artery on the recurrent laryngeal nerve,
absence of an identified pulmonary or cardiac lesion.1,2 This which is known as Ortner syndrome.3
inevitably leads to right ventricular (RV) dilatation and RV hyper- During physical examination of the parturient with pulmonary
trophy progressing to RV failure and death.1,3 The course of pri- hypertension, a RV heave may be present and an ejection click
mary pulmonary hypertension usually is slow, but unrelenting, may be heard over the pulmonic area. The second heart sound
with death occurring 4“6 years after the initial diagnosis. usually is split, with accentuation of the pulmonic component.
However, its course may be as short as six months from first There may be an ejection murmur and a regurgitant murmur over
symptoms to death. This condition is covered in other major the pulmonary valve. Jugular venous distension and prominent A
textbooks of obstetric anesthesia4,5 and the following represents waves usually are evident. Chest radiography (CXR) demonstrates
a brief outline of the importance of primary pulmonary hyperten- RV enlargement, hilar enlargement, and pruning of the peripheral
sion to the obstetric anesthesiologist. Discussion of the manage- vasculature. Electrocardiogram shows RV hypertrophy, and right-
ment of women with Eisenmenger syndrome (pulmonary axis deviation (see Figure 3.1). Pulmonary function tests may
hypertension secondary to a chronic, uncorrected left-to-right indicate restrictive disease due to decreased lung compliance
resulting from elevated pulmonary vascular pressure.3
cardiac shunt) is found in Chapter 1.
Primary pulmonary hypertension affects women four to five
times more often than men. It may arise at any age, but is most
Association with pregnancy
prevalent in the third and fourth decades6 with a mean age of
27 years at diagnosis.7 Among the prognostic indicators of survival, Among women of reproductive age, approximately 8% of primary
pulmonary hypertension is associated with pregnancy.9 It is
the most powerful and easily obtainable is the systemic arterial


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




Figure 3.1 EKG from a patient with severe pulmonary hypertension. Note the deep S waves in leads I, II, V5, and V6 plus a prominent R wave in V1 (all circled). Provided
by Dr Renaldo Beyer, Cardiologist, Sharp Rees-Stealy Medical Group, San Diego, California.


pulmonary arterial hypertension.13 However, bosentan is not
possible that pregnancy initiates primary pulmonary hyperten-
sion in some women, but more likely symptoms of preexisting approved for use during pregnancy. Perioperative therapies
used during pregnancy have included nitroglycerin infusion,14
disease are unmasked by the increased hemodynamic stress of
pregnancy.9 When symptoms arise during pregnancy, the diag- inhaled nitric oxide (which is very expensive),15 or inhaled or
intravenous (i.v.) epoprostenol (prostacyclin).16,17,18
nosis is made only after excluding other causes of pulmonary
hypertension. These include amniotic fluid embolism, tropho-
blastic embolism, thromboembolism, obliterative hypertension,
Anesthetic management of women with primary
and Eisenmenger syndrome.9
pulmonary hypertension
Primary pulmonary hypertension and pregnancy is an omi-
nous combination. Maternal mortality ranges from 30“56%1,7,10 The principal goals of anesthetic management of primary pul-
with death often occurring during delivery, or from four days to monary hypertension include avoiding increases in pulmonary
five weeks following delivery despite intensive postoperative vascular resistance and pulmonary artery pressure, preventing
management.11 Death usually is sudden, precipitated by acute changes in RV preload, and maintaining left ventricular afterload
and RV contractility.19,20 Potent titratable drugs should be readily
RV failure. Absolute pulmonary artery pressure is a poor indicator
of the extent of the disease. However, a poor prognosis in available in the event of hemodynamic instability. The need for
pregnancy is associated with the presence of RV hypertrophy, inotropes (dopamine or dobutamine), pressors (phenylephrine or
low cardiac index (2“2.5 l/min/m2), increased right atrial ephedrine), or afterload reducers (nitroprusside or phentola-
pressure (>10 mmHg) and high pulmonary vascular resistance mine) during labor and delivery or cesarean section (C/S) should
(>1500 dynes.sec.cmÀ5).1 Other maternal risk factors include be anticipated. In one report, a vasopressin infusion was used to
late diagnosis and late hospital admission.11 Neonatal survival prevent systemic hypotension in a patient with primary pulmon-
was reported as 88% in one series.11 ary hypertension having surgery under spinal anesthesia.21
Prior to the onset of labor, the severity of pulmonary hyperten-
sion can be assessed by pulmonary artery catheterization, which
Treatment of primary pulmonary hypertension
also allows an assessment of the response of the pulmonary vascu-
lature to vasoactive drugs.19,22 Preoperative adenosine and nifedi-
A number of therapies have been tried to treat primary pulmon-
pine have been shown to reduce pulmonary vascular pressure23
ary hypertension. These include calcium channel blockers and
anticoagulation, prostacyclin, and, ultimately, lung transplanta- and may be useful adjuncts to oxygen therapy at the time of parturi-
tion.12 More recently, the successful use of the endothelin antago- tion. It is important to measure right- and left-sided pressures
nist, bosentan (Tracleer’), has been described in the treatment of continuously during labor and delivery. However, multiple



58
Chapter 3


pulmonary capillary wedge pressure (PCWP) measurements should described the use of general anesthesia and extracorporeal mem-
be discouraged because of the risk of pulmonary artery rupture. brane oxygenation support for termination of pregnancy in a
woman with primary pulmonary hypertension.41
During delivery an increase in pulmonary vascular resistance
can occur as a result of hypercarbia, acidosis, hypoxia, stress, and Spinal anesthesia is contraindicated due to the risk of rapid-
pain.22 Epidural analgesia provides excellent pain control and onset deleterious hemodynamic changes. However, even when
attenuates many of these adverse effects. Investigators have general anesthesia is used in the presence of a pulmonary artery
reported successful management of labor and C/S using various catheter, and successful intraoperative control of pulmonary
doses of epidural local anesthetics, with and without fenta- artery pressure is achieved using iNO, nebulized iloprost, and a
nyl.1,8,22,24,25,26,27,28 The addition of fentanyl to labor epidural prostacyclin infusion, a patient can still die in the first few weeks
following surgery.42
infusions is a theoretical concern because of the potential to
cause myocardial depression in patients with compromised In summary, pregnancy should be discouraged in women with
hearts.29 However, it is unlikely that 2 mg/ml fentanyl at primary pulmonary hypertension and therapeutic abortion
10“15 ml/h would produce serum levels that would be clinically should be offered, especially with early clinical deterioration. A
important in this regard. Care should be taken to titrate the level multidisciplinary approach to the management of a parturient is
of analgesia to avoid hypotension and a reduction in RV preload. important, but mortality is high even with the most modern
treatment options.43
Excellent pain relief has also been obtained in patients with
pulmonary hypertension using intrathecal morphine.30,31
However, unless vaginal delivery is imminent, a neuraxial cathe-
Pulmonary arteriovenous malformations
ter technique is recommended. Forceps or vacuum extraction is
Introduction
often used to help prevent the untoward hemodynamic effects
caused by maternal pushing.
Pulmonary arteriovenous malformations (PAVM) are rare, thin-
Cesarean section can be performed after careful extension of an
walled vascular lesions that may complicate pregnancy because
epidural block to T4“5. The risk of severe hypotension is minimal
of rapid enlargement or rupture (see Figures 3.2 and 3.3). Most
as long as provisions to support blood pressure (BP) have been
PAVM are congenital but many patients are not diagnosed until
taken. Epidural anesthesia,32,33 combined spinal“epidural (CSE)
the second decade. They usually occur singly and grow slowly.
anesthesia,34 and general anesthesia all have been used success-
However, they can occur as discrete or multiple lesions, in one or
fully for C/S25,35 and tubal ligation36 in patients with primary
more lobes, and in one or both lungs,44,45 and many small AVM
pulmonary hypertension. Invasive monitoring was used during
may be scattered throughout the lungs.45,46 The mortality rate in
these procedures. If epidural anesthesia is used, it is uncertain if

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