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commonplace in ARDS and must be aggressively treated with
damage. Microvascular damage leads to increased capillary
antimicrobial therapy.
permeability and subsequent interstitial and alveolar edema.
Alveolar damage results in loss of surfactant and subsequent
Respiratory support
alveolar collapse. Alveolar edema and collapse contribute to
Patients with ARDS require endotracheal intubation and positive
ventilation“perfusion (V/Q) mismatching and intrapulmonary
pressure ventilation in order to maintain adequate gas exchange
shunting with subsequent hypoxemia.
and facilitate O2 delivery. The decision to provide ventilatory
Pulmonary hypertension frequently develops leading to right
support should be made in a timely manner so as to optimize
ventricular (RV) dysfunction which reduces left ventricular (LV)
maternal condition and fetal O2 delivery.
preload and cardiac output (CO). Depressed CO further compro-
Optimal ventilator settings will provide adequate oxygenation
mises O2 delivery. Multisystem organ failure eventually ensues
without causing O2 toxicity, alveolar overdistention, baro-
and is a common cause of death (see Figure 4.1). Recent extensive
trauma, or hemodynamic compromise.9,10 The lowest inspired
reviews of pathophysiology are provided elsewhere.6,7
O2 concentration to maintain a PaO2 greater than 60 mmHg or a
SaO2 greater than 90% will reduce the risk of O2 toxicity. The use
Clinical course
of low tidal volumes in patients with ARDS is associated with
The pulmonary manifestations of ARDS develop within 24“48 lower mortality rates. In one report of more than 800 patients
hours of the initial insult. Initially, tachypnea may be the only with ARDS, mortality was significantly reduced with low tidal
volumes compared with traditional methods of ventilation.11
finding, followed by dyspnea and hypoxemia. Further progression
results in audible changes on lung auscultation, and radiological However, increased intrathoracic pressures and hypercapnia
evidence of diffuse pulmonary infiltrates. can result from this strategy. Positive end-expiratory pressure


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


Systemic or pulmonary insult
Table 4.1 Etiology of adult respiratory distress syndrome
in pregnancy

Sepsis
Activation of inflammatory mediators
chorioamnionitis
pyelonephritis
endometritis
Microvascular epithelial Alveolar epithelial
septic abortion
damage damage
Infectious pneumonia
Obstetric hemorrhage
shock
massive blood transfusion Increased capillary
Loss of surfactant
permeability
Severe preeclampsia
Aspiration
Embolism
thrombotic Interstitial and alveolar
Alveolar collapse
edema
amniotic fluid
venous air
trophoblastic
Connective tissue disease
Ventilation-perfusion mismatching
Substance abuse
Intrapulmonary shunting
Inhalation injury
Pheochromocytoma
Drug overdose
HYPOXEMIA
Modified from references 1, 2, 5, 36, and 37



PULMONARY
MULTISYSTEM ORGAN
is used to prevent alveolar collapse, recruit collapsed alveoli, HYPERTENSION
FAILURE
and improve oxygenation. However, excessive levels of PEEP
can decrease CO, reduce O2 delivery, and increase the risk of
barotrauma.
COR PULMONALE
Nitric oxide (NO) relaxes smooth muscle, and when inhaled
facilitates pulmonary vasodilation in ventilated areas of the lung.
Figure 4.1 Pathophysiology of ARDS.
In turn, this minimizes intrapulmonary shunting and improves
O2 delivery. Inhaled NO therapy for ARDS improves oxygenation
but does not change mortality.12,13 There are reports of the use of
level compatible with adequate CO. Fluid balance is maintained
inhaled NO in pregnancy, including one report of a pregnant
using crystalloid solutions to increase intravascular volume or
woman with fulminant respiratory failure.14 The potential benefit
diuretics to reduce intravascular volume when needed, using
of inhaled NO in carefully selected patients with intractable
data from pulmonary artery catheterization to guide therapy.
hypoxemia cannot be ruled out.15
Another pharmacological approach to the treatment of ARDS
Other therapies
has been the use of exogenous surfactant. Although preliminary
Since much of the lung damage from ARDS is caused by inflam-
studies seemed promising, no benefit in reducing mortality from
matory mediators, it has been hypothesized that pharmacological
ARDS has been demonstrated with the use of recombinant or
synthetic surfactant.16,17 agents capable of suppressing inflammation and promoting lung
repair could positively impact clinical outcomes. However, vari-
Fluid management ous novel anti-inflammatory and antioxidant therapies have not
yielded promising results.18,19,20,21,22,23 The value of corticoster-
Fluid balance can be difficult to achieve in ARDS. Widespread
oid therapy in ARDS is uncertain, although there is recent evi-
capillary leak with extravasation of fluids, plus intravascular
dence of a possible benefit in unresolving ARDS.24
hypovolemia, can depress CO and compromise tissue O2 delivery.
Prospective randomized trials have failed to show an advantage
However, intravenous (i.v.) fluid administration to correct hypo-
of extracorporeal membrane oxygenation (ECMO) over conven-
volemia may precipitate pulmonary edema and worsen tissue O2
tional treatment in patients with ARDS. However, case reports
delivery. Furthermore, the lower colloid oncotic pressure of preg-
have described recovery from ARDS in pregnancy following the
nancy may predispose a pregnant woman with ARDS to a greater
use of ECMO.25
risk of pulmonary edema. The PCWP should be kept at the lowest



76
Chapter 4


Selective decontamination of the digestive tract, to limit trans- asthma worsens, possibly due to maternal hypoxemia, increased
systemic and pulmonary vascular resistance, and decreased CO.41
location of gut pathogens, can reduce mortality in critically ill
patients.26 Maternal and perinatal mortality increases when asthma control
is poor,40 or in severe asthmatics when mechanical ventilation
is required. Cesarean section is more likely in asthmatics.34,35,44
Obstetric management Babies of mothers with severe asthma are more prone to hypo-
glycemia as a result of maternal treatment with steroids.34
The risks and benefits of early, elective delivery must be assessed,
but no study has demonstrated an improvement in maternal
outcome with delivery of the fetus.5,27,28 However, when the
Management of asthma
maternal condition is such that placental O2 transfer is compro-
The characteristics of asthma include reversible airway obstruc-
mised, immediate delivery may be required to minimize perinatal
tion from bronchial smooth muscle contraction, mucus hyperse-
morbidity and mortality. Vaginal delivery is possible in ventilated
patients with ARDS3,29,30,31 and cesarean section (C/S) is typically cretion, and mucosal edema. This chronic inflammatory airway
disorder is exacerbated by release of histamine, prostaglandin
reserved for obstetric indications.
D2, and leukotrienes from mast cells after exposure to stimulants
such as cigarette smoke, viral infections, aspirin, cold air, or
Anesthetic management exercise. There is evidence that heredity plays a major role in
the development of asthma.45,46
Increased O2 consumption during active labor is well known.
Labor analgesia for mechanically ventilated patients can be pro-
vided with i.v. opioids, which in turn can decrease O2 consump- Clinical course
tion. However, epidural analgesia has been shown to have
The clinical course of asthma depends on the degree of broncho-
a beneficial effect on O2 consumption in a parturient with
spasm and subsequent alterations in oxygenation due to V/Q
ARDS.32 If a regional anesthetic is considered, attention must be
mismatching. Affected women typically present with chest tight-
given to intravascular volume, coagulation status, and the pre-
ness, wheezing, or breathlessness. Mild asthmatics usually
sence of infection. Technical factors often will limit the ability to
develop respiratory alkalosis due to hyperventilation resulting in
induce regional anesthesia in these women. In mechanically
decreased pCO2, with normal arterial pO2. Ventilation perfusion
ventilated patients, general anesthesia (GA) is often the most
mismatch worsens as asthma becomes more severe leading to
convenient choice of anesthetic for C/S.
arterial hypoxemia, hypercapnia, acidemia, and, if untreated,
respiratory failure. Even mild asthma is a threat to the pregnant
Asthma in pregnancy woman and her fetus, as pregnant women have reduced respira-
tory reserves and are more susceptible to hypoxemia.
Introduction
Asthma has been reported to affect 3.7% to 8.4% of pregnant
Evaluation
women.33 The natural course of asthma in pregnancy appears
variable, with conflicting reports in the literature.34,35,36 However, Clinical examination, arterial blood gas analysis and pulmonary
a significant proportion of patients experience a worsening function tests are required to determine the severity of asthma.
of their symptoms, whereas others may remain unchanged Clinical signs of severe disease include labored breathing, tachy-
or improve during pregnancy. Baseline asthma severity corre- cardia, pulsus paradoxus, prolonged expiration, central cyanosis,
lates well with asthma exacerbation during pregnancy. With and altered consciousness. Arterial blood-gas analysis provides
mild disease, 13% suffer exacerbations, whereas with severe objective assessment of maternal oxygenation, ventilation, and
asthma, exacerbations may occur in up to 50% of affected acid-base status. Measurement of the forced expiratory volume
women.37 Further, the risk of exacerbation following C/S is in one second (FEV1), which correlates with the peak expiratory
much higher than with vaginal delivery.38 Approximately two- flow rate (PEFR), is now used routinely in the assessment of
thirds of women show the same pattern in their asthma from one severity and management of asthma. FEV1 < 1 L indicates severe
pregnancy to the next.39 Status asthmaticus is a relatively uncom- disease with hypoxia and poor response to therapy.47
mon occurrence in pregnancy and is seen in approximately 0.2%
pregnancies.38
Management of chronic asthma
Experts agree that undertreatment is the single most important
Maternal and fetal effects of asthma
error in the management of asthma during pregnancy.36,39
Mild forms of asthma have minor effects on pregnancy and neo- Pregnant women and their physicians should be reassured that
natal outcome.40 There is a slight increase in the incidence of most of the regularly used drugs (including albuterol, terbutaline,
preeclampsia, preterm labor, low-birthweight infants, and peri- epinephrine, methylxanthines, cromolyn, oral steroids, and
natal mortality in pregnant asthmatics.36,41,42,43 The rate inhaled beclomethasone) have been used widely for many years
without any evidence of teratogenicity in humans.46,47,48 One study
of intrauterine growth restriction increases as the severity of



77
1 Cardiovascular and respiratory disorders



Table 4.2 Usual doses of medications for chronic asthma Table 4.3 Pharmacologic step therapy of chronic asthma
during pregnancy and lactation during pregnancy

Medication Adult dose Category Step therapy

Inhaled corticosteroids Mild intermittent Inhaled beta 2-agonists as needed (for all
Beclomethasone CFC 168“840 mg/day categories).
42 or 84 mg/puff Mild persistent Inhaled cromolyn.
Beclomethasone HFA 80“480 mg/day Continue inhaled nedocromil in patients
40 or 80 mg/puff who have shown a good response prior
Budesonide DPI 200“600 mg/day to pregnancy.
200 mg/inhalation Substitute inhaled corticosteroids (see
below) if above not adequate.
Systemic corticosteroids Applies to all three corticosteroids
Moderate persistent Inhaled corticosteroids.
Methylprednisolone 7.5“60 mg daily
Continue inhaled salmeterol in patients
Prednisolone Short-course ˜˜burst™™ to achieve control:
who have shown a very good response
Prednisone 40“60 mg per day as single dose or two
prior to pregnancy.
divided doses for 3“10 days
Add oral theophylline and/or inhaled
Long-acting inhaled beta 2-agonists (preferably with inhaled
salmeterol for patients inadequately
corticosteroids)
controlled by medium-dose inhaled
Salmeterol 2 puffs q 12 hours
corticosteroids.
MDI 21 mg/puff
Severe persistent Above plus oral corticosteroids (burst for
Formoterol 1 capsule q 12 hours
active symptoms, alternate-day or daily
DPI 12 mg/single-use
if necessary).
capsule
ACAAI/ACOG recommendations (Ref. 59)
Cromolyn
Cromolyn 2“4 puffs tid-qid
MDI 1 mg/puff
cyclase to increase intracellular 30 -50 -cyclic adenosine monophos-
Leukotriene receptor phate (cyclic AMP) and cause bronchial smooth muscle relaxa-
Antagonists tion. Women with asthma should measure and record PEFR
Montelukast 10 mg qhs twice daily. The baseline values range from 380 to 550 L/min in
10 mg tablet pregnant women. Treatment depends on the severity of disease
Zafirlukat 40 mg daily (20 mg tablet bid) (see Table 4.3).49 For mild asthma, inhaled beta-agonists are used
10 or 20 mg tablet every three to four hours as needed, but inhaled corticosteroids
are recommended for persistent asthma. The use of inhaled
Methylxanthines (serum concentration of 5“12 mg/ml at steady state)
corticosteroids along with a beta-agonist may reduce hospital
Theophylline Starting dose 10 mg/kg/day up to
readmission for a severe exacerbation. Theophylline is a methyl-
300 mg max: usual max 800 mg/day
xanthine and a bronchodilator with possible anti-inflammatory
MDI ¼ metered-dose inhaler; DPI ¼ dry powder inhaler;
effects. This agent is useful for oral maintenance therapy if patients
CFC ¼ chlorofluorocarbon; HFA ¼ hydrofluoroalkane
do not respond to inhaled corticosteroids and beta-agonists.
(NB 100 mg beclomethasone CFC (budesonide) is equivalent to 50 mg
Reduced plasma protein binding of theophylline in pregnancy
beclomethasone CFC-free (fluticasone) because the CFC-free
increases the availability of free (active) drug. Recommended
product has superior lung deposition. HFA is a nonozone depleting
plasma therapeutic ranges in pregnancy are between 5“12 mg/ml
propellant. CFC is an ozone depleting propellant that is to be phased
or 8“15 mg/ml.51 A comparison of oral theophylline with inhaled
out of production by international agreement).
beclomethasone, for maintenance therapy in pregnant women
with asthma, showed no difference in exacerbation rates and
found that maternal exposure to orally inhaled budesonide during
no difference in pregnancy outcome.52 However, women tend to
pregnancy is not associated with an increased risk of congenital
malformations or other adverse fetal outcomes.49 Table 4.2 shows discontinue oral theophylline because of its side effects.
Cromolyn and nedocromil, which inhibit mast cell degranula-
some common drugs and the doses used for chronic asthma.
tion, are used to prevent asthma, but are ineffective for treat-
Corticosteroids are anti-inflammatory agents that have three
ment of acute asthma. They are administered as aerosols and
distinct actions on gene expression and second messenger cas-
cades.50 The risk associated with use of oral corticosteroids dur- clinical experience suggests that fetal effects are minimal.
Leukotriene modifiers (zileuton, zafirlukast, and montelukast)
ing pregnancy is probably still less than the potential risks to the
inhibit leukotriene synthesis. These agents provide slightly
mother and the fetus from severe asthma. The low plasma levels
improved asthma control when given either orally, or by inhala-
achieved by inhaled corticosteroid make it unlikely that fetal
tion, for prevention of asthma.53 There is minimal information
effects will occur. Beta-2 adrenergic agonists activate adenyl



78
Chapter 4



Table 4.4 Management options of status asthmaticus

Drug Route Dose Comments

Oxygen face mask 40“60% Humidification important
Heliox face mask 70“80% helium, 20“30%
oxygen
Beta-2 adrenergic agonists
Terbutaline neb. 10 mg
Terbutaline s.c. 0.25 mg Repeat after 15“30 min, beware of hypotension


Albuterol neb. 5 mg
Repeat after 20 min ‚ 2
Epinephrine s.c. 0.3 mg


Steroids
Steroids " gestational diabetes þ fetal hypoglycemia
Methylprednisolone i.v. 60“125 mg
Hydrocortisone i.v. 100“200 mg Cover stressful events (e.g. delivery)
Prednisone/prednisolone o 30“60 mg daily
Methylxanthine
# if previous doses or on theophylline
Theophylline i.v. (slowly) 5 mg/kg loading dose
infusion 0.2“0.9 mg/kg/hr Check plasma theophylline levels
Therapeutic range?
Anticholinergic
Ipratropium neb. 0.5 mg Works best in combination therapy

neb. ¼ nebulized; s.c. ¼ subcutaneous; i.v. ¼ intravenous, o ¼ oral


currently available on the use of leukotriene modifiers during responding to 30“60 minutes of intensive therapy is termed status
human pregnancy (see www.nhlbi.nih.gov/health/prof/lung/ asthmaticus. Management of nonpregnant patients with status
asthma/astpreg/astpreg_qr.pdf ). asthmaticus in an intensive care setting results in a good outcome
in most cases.56 Fatigue, CO2 retention, and persistent hypoxemia
are indications for mechanical ventilation.
Management of acute asthma
Intravenous albuterol, terbutaline, and ritodrine have well-
The key to the successful treatment of acute asthma during preg- known tocolytic effects and are often used to treat preterm
nancy is a low threshold for hospital admission. Careful clinical labor. However, there is no evidence that these drugs interfere
assessment must be made upon admission and reviewed fre- with the course of labor when used by the inhaled or s. c. routes.
quently. Treatment goals include minimizing hypoxemia, hypercar-
bia, or alkalosis, all of which reduce fetal oxygenation. Intravenous
Intubation and ventilation
fluid administration helps to clear pulmonary secretions through
hydration, and supplemental O2 by mask should be administered If endotracheal intubation is required, aortocaval compression
after a blood-gas sample is obtained. It is recommended that pO2 be must be avoided and induction of anesthesia should include pre-
maintained at > 60 mmHg, and SaO2 > 95%. Monitoring includes oxygenation and precautions against aspiration of gastric contents.
continuous pulse oximetry and electronic fetal heart rate. Thiopental, etomidate, and ketamine have been used as induction
First-line therapy for acute asthma includes inhaled or subcu- agents, but the marked bronchodilator properties of ketamine
taneous (S/C) beta-adrenergic agonists (see Table 4.4), and corti- make it the preferred agent. However, seizure-like extensor spasms
costeroids should be given early when asthma is severe.54 have been reported following the administration of ketamine to
Intravenous methylprednisolone 40 to 60 mg, every six hours, or patients who had received aminophylline, so caution is neces-
sary.57 Alternatively, propofol, which provides better protection
equipotent doses of hydrocortisone by infusion, are given in
conjunction with beta-agonists. against bronchospasm than thiopental, can be used. The risk of
If initial therapy with beta-agonists fails to improve FEV1 or histamine release from succinylcholine is outweighed by the excel-
PEFR to >70% baseline values, or if respiratory distress persists, lent intubating conditions achieved. Intravenous lidocaine 1 mg/
kg has been advocated to minimize further bronchospasm.58 The
admission to an intensive care unit is recommended. An elevated
arterial pCO2 (>38 mmHg) is an ominous sign in pregnancy but alternative technique of using an inhalational induction with sevo-
would be considered normal in a nonpregnant woman. flurane is unlikely to be smooth or easy; moreover it may increase
Intensive therapy includes inhaled beta-agonists, i. v. cortico- the risk of pulmonary aspiration, and is not recommended. Once
steroids, and close observation for worsening respiratory distress the trachea is intubated, high concentrations of volatile anesthetic
or fatigue in breathing.55 Severe asthma of any type not agent can be used to break the bronchospasm.



79
1 Cardiovascular and respiratory disorders


Muscle relaxation should be provided by nondepolarizing
Table 4.5 Anesthetic and obstetric drugs to avoid
agents that do not release histamine (e.g. vecuronium). Peak air-
way pressures are likely to be high and careful manipulation of Prostaglandin F2a
ventilator settings is required to minimize the risk of barotrauma Ergonovine
(pneumothorax and pneumomediastinum). Normal physiologi- Aspirin and other NSAID
cal (pregnant) values for arterial pO2 and pCO2 are the desired Histamine-releasing drugs (e.g. atracurium, tubocurare )
endpoint. The use of PEEP is controversial in this setting.
NSAID ¼ nonsteroidal anti-inflammatory drugs

Labor and delivery
If the woman™s condition is too poor to tolerate a regional tech-
Asthma medications are continued throughout delivery. nique (i.e. restless, dyspnoeic, and unable to lie supine), GA is req-
Additional corticosteroids are administered if systemic steroid uired. The management of endotracheal intubation is described
therapy was used within four weeks. Hydrocortisone 100 mg i.v. above. Nitrous oxide may increase the degree of air trapping, reduce

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