Decrease—3rd trimester

Increase of 300 mL/contraction

Cardiac output Increase of 30%–50% Additional increase of 50%

Systemic vascular resistance Decrease Increase

3. D. Maternal intravascular fluid volume increases in the first trimester, and at

term, the plasma volume is increased by about 45%, while the erythrocyte volume

increases only 20%, accounting for the relative anemia of pregnancy despite the

higher hematocrit. This serves to decrease blood viscosity and improve flow. This

increase in maternal blood volume also allows women to better tolerate the blood

loss associated with delivery.

4. A. Cardiac output in the third trimester is increased by nearly 50% due to an

increase in both the stroke volume and heart rate to meet augmented maternal and

fetal metabolic demands.

5. C. The largest increase in cardiac output is seen immediately after delivery as

the increase in blood volume persists with an additional increase in intravascular

volume (300–500 mL) from the contracting uterus. This autotransfusion further

increases cardiac output. Patients with fixed stenotic valvular lesions therefore

should continue to be monitored closely after delivery.

6. D. Hyperventilation with oxygen consumption creates significant changes in

acid–base status that can be hazardous to the fetus. Extremely low PaCO2

levels

result in vasoconstriction and global reduction in placental perfusion and blood flow.

The alkalemia also shifts the oxygen–hemoglobin dissociation curve to the left,

impairing the release of oxygen from maternal blood to fetal blood. Both factors will

decrease the availability of oxygen delivery to the fetus (Fig 17-1).

Figure 17-1.

7. C. The anterior spinal cord achieves its blood supply from the anterior spinal

artery, which is single and unpaired. Due to this, injury or thrombosis can lead to a

unique constellation of symptoms consisting of loss of motor function, pain, and

temperature below the level of the injury, bilaterally. The posterior columns, carrying

fine touch and proprioception, are preserved as paired posterior spinal arteries

supply.

8. B. The presence of moderate–severe aortic stenosis makes it especially crucial

to minimize sympathetic output and hemodynamic deterioration. Though a regional

anesthetic is capable of attenuating the release of catecholamines during painful

labor, one must be vigilant to prevent hypotension. The abrupt hypotension following

spinal anesthesia with local anesthetics may result in cardiac hypoperfusion and

ischemia. Epidural anesthesia, with its slow onset to effect, is usually well tolerated,

especially with adequate volume loading. Inhaled nitrous oxide and oral analgesics

are unlikely able to provide adequate analgesia to maintain hemodynamic stability in

this patient with a fixed valve lesion.

9. A. Although there is an increase in cardiac output and plasma volume, the

systemic blood pressure in normal maternal physiology does not actually increase

due to decreases in systemic vascular resistance. In fact, the mean arterial pressures

generally decrease by approximately 10 to 15 mm Hg. Certainly, her fixed stenotic

lesion also contributes.

10. B. The mechanism of supine hypotension syndrome is decreased venous return as

a result of aortocaval compression by the gravid uterus when the pregnant woman

assumes the supine position. Removal of the compression with left-uterine

displacement can minimize this incidence, which is particularly important for patients

undergoing regional or general anesthesia because usual compensatory increases in

systemic vascular resistance will be blocked.

11. C. With increasing enlargement of the uterus, the diaphragm is forced cephalad,

which is responsible for decreasing the FRC. While supine, FRC can become less

than CC for many small airways resulting in atelectasis. Expiratory reserve volume

and residual volume are also decreased while both vital capacity and CC remain

unchanged.

12. B. Oxytocin remains a first-line agent in the prevention and management of uterine

atony. Oxytocin has important cardiovascular side effects, including hypotension and

tachycardia, setting the stage for myocardial ischemia. Slow continuous intravenous

administration of oxytocin minimizes maternal hemodynamic instability and also

encourages maintenance of uterine tone.

13. D. Decreased functional residual capacity (FRC) with increased minute ventilation

results in an escalation in rate at which changes of alveolar concentration of inhaled

anesthetics can be achieved, increasing speed of induction, emergence, and changes

in depth of anesthesia.

14. B. MAC progressively decreases during pregnancy—at term by as much as 40%—

for all volatile anesthetic agents.

15. C. Increased oxygen consumption and decreased reserve due to reduced functional

residual capacity can result in a rapid fall in arterial oxygen tension during apnea.

This occurs despite careful preoxygenation, which importantly provides a time

buffer.

16. D. Minute ventilation is increased above prepregnant levels primarily by a

significant increase in tidal volume with smaller increases in respiratory rate. Resting

maternal PaCO2 decreases from 40 to about 32 mm Hg, though arterial pH

approaches normal levels with increased renal excretion of bicarbonate ions. At term,

PaO2 generally does not change significantly, though may be slightly decreased,

reflecting airway closure and atelectasis.

17. A. Elevated levels of 2,3-DPG decreases maternal hemoglobin affinity for oxygen,

shifting the P50 curve to the right (increasing it from 27 to 30 mm Hg) to enhance

oxygen delivery to tissues.

18. C. An increased metabolic rate in addition to the pregnancy-induced increase in

minute ventilation results in a markedly decrease in PaCO2

from 40 to 30 mm Hg.

Such that a PaCO2 of 40 to 45 on ABG would indicate CO2

retention. However,

respiratory alkalosis is minimized due to metabolic compensation with increased

renal excretion of bicarbonate and thus a lower HCO3 as compared to the

nonparturient. At 35 weeks’ gestation, a normal maternal pH is approximately 7.44.

Lastly, maternal position can affect PaO2

, even in healthy parturients. In the upright

position and breathing room air, PaO2 will be slightly greater than 100 mm Hg, as the

increase in cardiac output is greater than the increase in oxygen consumption.

However, as functional residual capacity decreases during pregnancy and is often

less than closing capacity in the supine position, PaO2 will frequently fall below 100

mm Hg, while supine likely reflecting atelectasis.

19. B. Engorgement of epidural veins occurs with progressive enlargement of the

uterus contribute to decrease in size of the epidural space and can predispose to

intravascular injection with attempted epidural anesthesia. Additionally, CSF volume

is decreased in the subarachnoid space, facilitating the spread of local anesthetics.

Therefore, in pregnancy, there is a decrease in dose requirements of local anesthetics

for neuraxial procedures.

20. A. Similar to physiologic anemia of pregnancy, dilution of serum albumin will

result in higher free blood levels of highly protein-bound drugs (e.g., fentanyl and

midazolam), resulting in a more robust clinical effect as compared to the nonpregnant

state. Though plasma cholinesterase activity is also decreased, this is unlikely to be

of clinical significance with regard to the duration of action of succinylcholine.

21. D. Cephalad displacement of the pylorus, decreased gastrointestinal motility, and

decreased pH of gastric contents all contribute to significant risk of aspiration and

resultant pneumonitis during labor and delivery. H2

-receptor antagonists, unlike

antacids, do not alter the pH of gastric contents already present in the stomach.

Avoidance or particulate antacids can minimize pulmonary damage should aspiration

occurs. Though metoclopramide can increase gastric motility to decrease the gastric

volume, opioid-induced hypomotility is resistant to this treatment.

22. C. Late decelerations are shallow, uniformly shaped decelerations that are

characterized by a gradual decrease from and return to baseline of the fetal heart

rate. The nadir of late decelerations usually is between 5 and 30 bpm below the

baseline. Late decelerations typically begin near the end of a contraction; with return

to baseline, FHR always occurring after the contractions have ended. Uteroplacental

insufficiency (e.g., umbilical cord compression, maternal supine hypotension

syndrome) contributes to late decelerations. Cephalopelvic disproportion and fetal

head compression are associated with early decelerations (Fig 17-2).

Figure 17-2.

23. C. The uterine vasculature is not autoregulated and remains essentially maximally

dilated under normal conditions during pregnancy. Epidural or spinal anesthesia does

not pathologically alter uterine blood flow as long as maternal hypotension is

avoided. Acceptable options include left-uterine displacement to minimize

aortocaval compression, increase IV fluids to improve volume status, Trendelenburg

position to encourage venous return, and α-adrenergic agents to increase maternal

arterial blood pressure. Prompt correction of maternal hypotension will lead to best

neonatal outcome.

24. B. The Apgar is a scoring system for evaluating an infant’s physical condition at

birth. The infant’s heart rate (1 pt), respiration (1 pt), muscle tone (0 pt), response to

stimuli (1 pt), and color (0 pt) are rated at 1 minute and again at 5 minutes after birth.

Each factor is scored 0, 1, or 2; the maximum total score is 10 (Fig 17-3).

Figure 17-3.

25. C. A team that is skilled at reviving newborn infants should be at the delivery if

meconium staining is found in the amniotic fluid. Newborns should be placed under

radiant heat sources to support body temperature, as heat loss can be rapid. If the

baby is active and crying, no treatment is needed. If the baby is not active and crying

right after delivery, the trachea should be suctioned. Avoiding positive-pressure

ventilation before suctioning can minimize further aspiration into the lungs.

26. D. The invention of the forceps has had a profound influence on obstetrics,

providing an alternative modality to surgical delivery during cases of difficult,

nonprogressing, or obstructed labor. High-forceps delivery refers to attempted

delivery prior to head engagement, which carries high risk and is no longer an

accepted practice. Certainly, there is risk to both mother and child. Maternal risks

include increased postpartum recovery time and pain, while in the fetus, forceps

assistance can cause minor injuries such as cuts and bruises, or more serious

damages such as facial nerve injury, clavicle fracture, and intracranial hemorrhage.

27. D. The fetal circulation is markedly different from the adult circulation as gas

exchange does not occur in the lungs but instead occurs in the placenta. The placenta

provides oxygen-rich blood via the umbilical vein to the fetal circulation and

removes deoxygenated blood via umbilical arteries. In addition, the fetal

cardiovascular system is designed in such a way that the most highly oxygenated

blood is delivered preferentially to vital organs (brain and heart) while minimizing

flow to nonvital fetal organs (liver and lungs). The presence of intra- and extracardiac

shunts achieves these circulatory adaptations in the fetus; the ductus venosus shunts

oxygenated blood away from the liver, while the ductus arteriosus shunts blood away

from the fetal pulmonary bed. The foramen ovale effectively shunts blood from the

right to the left atrium, resulting in equalization of right and left sides of the heart (Fig

17-4).

Figure 17-4.

28. B. Successful transition from fetal to neonatal circulation starts when the umbilical

cord is clamped and cut such that the placenta no longer acts as the “lungs” to

provide oxygen. The ductus venosus closes physiologically as soon as the umbilical

vein is obstructed with the clamping of the cord. With the loss of the placenta, a large

low-resistance bed, systemic vascular resistance rapidly increases. With the first

breath, the lungs inflate with a fall in pulmonary vascular resistance and increase

pulmonary blood flow. The rise in pulmonary venous return results in left-atrial

pressure being slightly higher than right-atrial pressure to close the foramen ovale.

Decrease in circulating prostaglandins and the higher blood oxygen content of blood

result in vasoconstriction of the ductus arteriosus.

29. C. Placental exchange of substances occurs principally by diffusion from the

maternal circulation to the fetus and vice versa, which depends on maternal–fetal

concentration gradients, maternal protein-binding, molecular weight, lipid solubility,

and the degree of ionization of that substance.

30. D. Local anesthetics easily cross the placenta, which is affected by several

independent factors, including maternal–fetal hemodynamics, permeability of the

placenta, concentration of free drug in the maternal plasma, and physiochemical

properties of the drug itself. Lidocaine is less lipid soluble than bupivacaine, which

is reflected in their lipid–water partition coefficients. Protein-binding also plays a

role in the diffusion of drugs across the placenta. The unbound form of the drug is

freely transferred, whereas protein-binding limits diffusion. High protein-binding, as

in the case of bupivacaine, leads to much lower fetal-to-maternal plasma ratio. Local

anesthetics are weak bases and therefore have minimal ionization at physiologic pH.

The closer the pKa

is to the physiologic pH, the more it will be affected by the acid–

base status of the fetus.

31. D. Somatic and visceral afferents from the uterus and cervix travel with

sympathetic nerve fibers en route to the spinal cord. These fibers pass through the

inferior, middle, and superior hypogastric plexuses to arrive at the sympathetic chain.

The first stage of labor is largely visceral (T10–L1) due to uterine contractions. As

labor progresses, the parturient encounters the second stage of labor with additional

somatic pain complaints as the fetus descends into the pelvis causing distension of

the vagina, perineum, and pelvic floor muscles. This somatic pain is transmitted via

the pudendal nerve (S2–S4).

32. B. Lumbar sympathetic blocks and paracervical blocks, though rarely performed

for labor analgesia, are appropriate targets during the first stage of labor. However,

paracervical blocks are rarely used in current practice because of an association with

fetal bradycardia. Epidural and combined spinal–epidural techniques are ideal, in

that they are able to block the visceral afferent fibers responsible for the first stage of

labor and the somatic nerve fibers through which the second stage is transmitted. The

obstetrician can also provide pudendal blocks during delivery to mitigate somatic

pain during the second stage, though cannot mitigate visceral first stage pain.

33. D. Preeclampsia is a syndrome manifested after the 20th week of gestation, which

is characterized by systemic hypertension (>140/90 mm Hg), proteinuria (>0.5

g/day), generalized edema, and complaints of a headache. HELLP syndrome

(hemolysis, elevated liver enzymes, low platelets) is a severe form of preeclampsia.

Eclampsia is present when seizures are superimposed on preeclampsia, and it is

potentially life-threatening. Causes for maternal mortality in women with

preeclampsia include congestive heart failure, myocardial infarction, coagulopathy,

and cerebral hemorrhage. Definitive treatment is the delivery of the fetus and

placenta, after which preeclampsia usually abates within 48 hours.

34. A. The presence of hypertension with associated edema requires further workup

including complete blood count with platelets and prothrombin time/international

normalized ratio to ensure adequate hemostasis can be achieved. Usually, platelets

>100 K/ μL carry little increased risk, and one may safely proceed with epidural

placement. Platelet count <50 K/ μL is generally considered a contraindication to

neuraxial interventions due to high risk of epidural hematoma. Epidural anesthesia is

often viewed as the technique of choice for labor pain as the parturient remains

awake and alert without sedative side effects. However, systemic opiates are

reasonable if epidural is contraindicated for whatever reason, including patient

refusal. A general or regional anesthetic should not be used in attempts to lower

maternal blood pressure.

35. A. Transfer of drugs from mother to fetus takes place at the level of the placenta

mainly by diffusion. Thus, keeping maternal blood levels of drugs as low as possible

is a major strategy for decreasing the amount of drug that reaches the fetus. In

addition, since most of the blood in the umbilical vein travels directly to the liver, a

large portion of the drug will be metabolized before reaching vital fetal organs.

Furthermore, drug in the umbilical vein that bypasses the liver via the ductus venosus

to access the inferior vena cava will be diluted with blood from the lower extremities,

and this further reduces concentration of drugs in the fetal blood. Two things work

against these “safety features”: (1) fetal acidosis during times of distress causes

increased perfusion of the heart and brain and thus increases delivery of drug to these

important organs. (2) Fetal pH is lower than maternal pH and results in basic drugs

(such as local anesthetics) becoming more ionized when they reach fetal circulation.

This effectively traps them on the fetal side of the circulation, since ionized

molecules cannot easily cross the placenta. This also maintains a gradient for

diffusion. This is known as “ion trapping” and can be quite a significant effect

especially during times of fetal distress (when pH gets even lower).

36. B. Late decelerations are worrisome as it is a sign of fetal hypoxemia, which

requires prompt treatment. Uteroplacental resuscitation measures should be

implemented immediately in an attempt to improve uteroplacental perfusion and

oxygen delivery to the fetus. Supplemental oxygen should be provided to the mother,

and she should be placed in a lateral position to avoid aortocaval compression.

Maternal hypotension should be treated promptly with an IV fluid bolus and/or

administration of a vasopressor. In this case, phenylephrine may also improve her

tachycardia. Emergent cesarean delivery is indicated only if these utero resuscitative

measures are not successful. Discontinuation of the epidural infusion is

recommended only if the patient has an excessively high sensory level.

37. C. Definitive treatment is delivery of the fetus and placenta. In the interim,

magnesium and antihypertensive drugs may be required. Magnesium is effective by

decreasing the irritability of the CNS to decrease the risk of seizures. Though it

mildly reduces blood pressure due to its vasodilatory effect, it is not an effective

agent for severe hypertension. Antihypertensives are usually required when the

diastolic pressure is >110 mm Hg. Hydralazine and labetalol are the most commonly

administered. Hydralazine has the advantage of being a vasodilator; thus, it can

improve uteroplacental and renal blood flow. Labetalol, with its adrenergic blockade

may improve tachycardia. Keep in mind that labetalol has a much faster onset of

action (5 minutes) vs. hydralazine (30 minutes) as such may be more appropriate for

acute management of severe hypertension.

38. B. All women in the peripartum period should be given a nonparticulate antacid

such as sodium citrate 30 mL to neutralize gastric contents. A rapid-sequence

induction should be performed following adequate preoxygenation. If a woman is in

shock, etomidate is preferable to thiopental or propofol as an induction agent.

Equipotent doses of all the volatile agents depress uterine contractility to an

equivalent, dose-dependent extent. Following retained placenta, there is an increased

incidence of endometritis; however, there is no consensus opinion on whether

antibiotic prophylaxis is routinely indicated.

39. D. Epidural abscesses are associated with headache, fevers/chills, nausea/vomiting,

low back pain, and bowel or bladder dysfunction that can range from retention to

incontinence. Hematologic evaluation would likely reveal an immune response with

elevated WBC.

40. C. Since the first reported case in 1898, PDPH has been a problem for patients

following dural puncture. Research over the last 30 years has shown that use of

larger-gauge needles, particularly of the pencil-point design, is associated with a

lower risk of PDPH than larger traditional cutting-point (Quincke) needle tips. Keep

in mind that gauge and bore diameter of a needle are inversely related such that a

22G is smaller compared to a 16G. A careful history should rule out other causes of

headache. A postdural component of headache is the sine qua non of PDPH. Highrisk patients include those <50 years, postpartum, and puncture with small gauge

(large bore diameter) needles.

41. B. Magnesium acts as a physiologic calcium blocker to provide uterine relaxation

in addition to electrical conduction disruption such that levels can be predicted

strength of deep-tendon reflexes. Similarly, postsuccinylcholine fasciculations are

blunted.

42. B. Nitroglycerin may be used as an alternative to terbutaline sulfate (β2 agonist) or

general endotracheal anesthesia with halogenated agents for uterine relaxation.

Inhaled anesthetics produce dose-dependent uterine vasodilatation with a decrease in

uterine contractility. Uterine relaxation produced by inhalation agents may be helpful

for removal of retained placenta. However, uterine vasodilatation might lead to

increased blood loss during obstetric surgery or delivery. Nitrous oxide does not

change uterine contractility in doses provided during delivery. Initiating treatment

with incremental doses of nitroglycerin may relax the uterus sufficiently while

minimizing potential complications (e.g., hypotension).

43. A. Maternal side effects due to β2

-agonist therapy (e.g., terbutaline, ritodrine) for

tocolysis include cardiopulmonary complications (e.g., arrhythmias, tachycardia,

hypotension, and pulmonary edema) and metabolic hyperglycemia.

44. D. Alkalization of the blood causes vasoconstriction, to provide a semblance of

hemostasis. Inhaled anesthetics, ritodrine, and nitroglycerine are all potent

vasodilators that can contribute to her ongoing blood loss.

45. C. Sodium thiopental is an ultra-short-acting barbiturate commonly used to induce

general anesthesia prior to intubation. Following a low dose, the drug rapidly reaches

the brain and causes unconsciousness within 30 to 45 seconds. At 1 minute, the drug

attains a peak concentration of about 60% of the total dose in the brain. Thereafter,

the drug distributes to the rest of the body, and in about 5 to 10 minutes, the

concentration is low enough in the brain such that consciousness returns. Thus, a onetime bolus displays first-order kinetics. Larger doses, or infusions, undergo slow

zero-order elimination kinetics such that thiopental is not used to maintain anesthesia

in surgical procedures (T½ 11.5– 26 hours) due to slow recovery. As such, larger or

repeated doses can depress the baby.

46. B. Umbilical cord blood gas analysis is recommended in all highrisk deliveries.

For most accurate interpretation, paired umbilical arterial and venous samples should

be taken soon after birth from a segment of cord that has been doubly clamped to

isolate it from the placenta. This cord blood will remain stable for up to 1 hour.

Infants with pH <7.0 at birth who are not vigorous are at high risk of adverse

outcome. Analysis of paired arterial and venous specimens can give insights into the

etiology of the acidosis. In combination with other clinical information, normal paire

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