Obstetric Anesthesia
Pregnancy physiology, neuraxial in labor, preeclampsia, PPH, placental disorders, fetal monitoring, neonatal resuscitation. ← All topics
Q1. Preeclampsia antihypertensive choice
A 28-year-old at 34 weeks with preeclampsia has BP 178/112. Magnesium sulfate is initiated. First-line antihypertensive therapy is:
A. Labetalol IV or hydralazine IV, or oral nifedipine if no IV access available
B. Methyldopa IV or oral, titrated slowly to avoid maternal sedation and hypotension
C. Esmolol infusion titrated to effect, with continuous maternal hemodynamic monitoring required
D. Sodium nitroprusside infusion with invasive monitoring reserved for refractory hypertension cases
E. Nicardipine infusion combined with enalapril for dual mechanism blood pressure control
Show answer
Answer: A. Labetalol IV, hydralazine IV, and oral nifedipine (when IV access is unavailable) are the three first-line antihypertensive agents for acute severe hypertension in preeclampsia. Methyldopa has a slow onset of action and causes sedation, making it unsuitable for acute management. Esmolol is a short-acting beta-blocker not routinely used as first-line therapy in preeclampsia. Sodium nitroprusside can generate cyanide metabolites with prolonged use and is reserved only for refractory cases with invasive hemodynamic monitoring. ACE inhibitors like enalapril are absolutely contraindicated in pregnancy due to fetal renal dysgenesis, oligohydramnios, and other teratogenic effects.
Q2. Postpartum hemorrhage sequence in preeclampsia
After oxytocin fails to control uterine atony in a patient with preeclampsia, the next-line agent is:
A. Methylergonovine 0.2 mg IM, which causes uterine contraction via smooth muscle stimulation
B. Carboprost 250 mcg IM, which causes uterine contraction via prostaglandin F2-alpha activity
C. Misoprostol 800 mcg PR, which causes uterine contraction via prostaglandin E1 receptor binding
D. Tranexamic acid 1 g IV, which reduces bleeding via inhibition of fibrinolysis pathways
E. Additional oxytocin bolus IV, which causes uterine contraction via oxytocin receptor activation
Show answer
Answer: B. In preeclampsia, methylergonovine is avoided as a second-line agent because it causes severe vasoconstriction and can dangerously elevate blood pressure in patients who are already hypertensive. The correct sequence for managing uterine atony in preeclamptic patients is: oxytocin first-line, then carboprost second-line, then misoprostol third-line, and finally methylergonovine only with extreme caution if other agents fail. Carboprost (prostaglandin F2-alpha) is the preferred second-line agent but should be avoided in patients with asthma due to bronchospasm risk. Tranexamic acid is an antifibrinolytic that may be used adjunctively but does not treat uterine atony directly. Additional oxytocin after initial failure is generally ineffective.
Q3. Aortocaval compression
A 38-week parturient lying supine becomes hypotensive, nauseated, and diaphoretic. The most appropriate first action is:
A. Administer intravenous phenylephrine bolus to restore maternal blood pressure
B. Manually displace the uterus to the left to relieve vascular compression
C. Place patient in Trendelenburg position to increase venous return
D. Administer rapid intravenous fluid bolus to expand intravascular volume
E. Manually displace the uterus to the right to improve cardiac output
Show answer
Answer: B. This patient is experiencing supine hypotensive syndrome, caused by compression of the inferior vena cava by the gravid uterus when lying supine. The most appropriate first action is left uterine displacement, either by tilting the patient 15 degrees to the left lateral position or by manually displacing the uterus to the left. This maneuver immediately relieves the compression and reverses the hypotension. Aortocaval compression in the third trimester can reduce cardiac output by 10 to 25 percent. While vasopressors or fluid boluses may be considered if initial positional changes are ineffective, they do not address the underlying mechanical cause. Right uterine displacement would be ineffective as the IVC lies on the right side of the spine and would worsen compression.
Q4. MAC in pregnancy
Compared to a non-pregnant patient, MAC for volatile anesthetics in a parturient is:
A. Increased by approximately 20%
B. Decreased by approximately 30–40%
C. Unchanged from baseline values
D. Increased by approximately 50%
E. Decreased by approximately 10%
Show answer
Answer: B. MAC is decreased by approximately 30–40% in parturients compared to non-pregnant patients. This reduction begins as early as the first trimester and persists throughout pregnancy. The mechanism is thought to involve increased progesterone levels and elevated endogenous endorphins. MAC returns to baseline values within hours after delivery. This clinically significant reduction means that pregnant patients require lower concentrations of volatile anesthetics to achieve the same anesthetic depth, which has important implications for dosing and monitoring during obstetric anesthesia.
Q5. FRC and apnea time in pregnancy
A term parturient is more prone to rapid oxygen desaturation during apnea because:
A. Increased FRC (~20%) and decreased oxygen consumption (~20%)
B. Decreased FRC (~20%) and increased oxygen consumption (~20%)
C. Decreased FRC (~20%) with unchanged oxygen consumption
D. Increased FRC (~20%) with increased oxygen consumption (~20%)
E. Unchanged FRC with increased oxygen consumption (~20%)
Show answer
Answer: B. At term pregnancy, FRC decreases by approximately 20% due to equal decreases in both expiratory reserve volume (ERV) and residual volume (RV). Simultaneously, oxygen consumption increases by approximately 20% at baseline, and increases even more during labor (40% in stage 1, 75% in stage 2). This combination of reduced oxygen reservoir (lower FRC) and increased oxygen demand creates a dramatically shortened time to desaturation during apnea. This is why adequate preoxygenation is critical before any general anesthetic induction in the parturient, and rapid sequence induction with cricoid pressure should be strongly considered to minimize apnea time.
Q6. Magnesium sulfate toxicity
A preeclamptic patient receiving magnesium develops loss of deep tendon reflexes and respiratory effort begins to wane. The expected magnesium level is:
A. 5 mg/dL
B. 8 mg/dL
C. 12 mg/dL
D. 17 mg/dL
E. 25 mg/dL
Show answer
Answer: D. The therapeutic range for magnesium sulfate is 5–9 mg/dL. Loss of deep tendon reflexes occurs at levels of 10 mg/dL or greater. Respiratory paralysis typically occurs at levels between 15–20 mg/dL, which matches this patient's presentation of waning respiratory effort combined with absent reflexes. Cardiac asystole occurs at levels greater than 25 mg/dL. The antidote for magnesium toxicity is calcium gluconate 1 gram IV. Renal failure markedly increases the risk of toxicity because magnesium is renally excreted. Magnesium also potentiates nondepolarizing neuromuscular blocking drugs (NDNMBDs).
Q7. Category III fetal heart tracing
A category III fetal heart tracing includes:
A. Moderate baseline variability with early decelerations and normal heart rate
B. Absent baseline variability with recurrent late or variable decelerations or bradycardia
C. Mild variable decelerations with moderate variability and normal baseline rate
D. Tachycardia with moderate baseline variability and no recurrent decelerations present
E. Marked baseline variability alone without decelerations or rate abnormalities present
Show answer
Answer: B. Category III fetal heart rate tracings are abnormal and require prompt evaluation and intervention. They are defined by absent baseline variability in combination with any of the following: recurrent late decelerations, recurrent variable decelerations, or bradycardia. Alternatively, a sinusoidal pattern alone qualifies as Category III. These tracings are predictive of abnormal fetal acid-base status at the time of observation. Management includes intrauterine resuscitation measures such as maternal repositioning to left lateral position, intravenous fluid administration, supplemental oxygen, discontinuation of oxytocin if being administered, and consideration of tocolytic therapy. Preparation for expedited delivery should be initiated.
Q8. Late decelerations etiology
Late decelerations on fetal heart monitoring most likely indicate:
A. Umbilical cord compression during uterine contractions
B. Fetal head compression during uterine contractions
C. Uteroplacental insufficiency causing fetal hypoxemia
D. Maternal fever causing fetal tachycardia response
E. Normal fetal sleep cycles during labor
Show answer
Answer: C. Late decelerations are characterized by a nadir that occurs after the peak of the contraction with gradual onset (≥30 seconds from onset to nadir). The mechanism is uteroplacental insufficiency leading to fetal hypoxemia, which triggers reflex bradycardia via chemoreceptor stimulation or direct myocardial depression in severe cases. This is in contrast to early decelerations, which result from fetal head compression causing vagal stimulation, and variable decelerations, which result from umbilical cord compression. Maternal fever typically causes fetal tachycardia, not decelerations. Normal fetal sleep cycles do not produce decelerations.
Q9. Amnioinfusion
Amnioinfusion for recurrent variable decelerations is contraindicated in patients with:
A. Twin pregnancy (risk of overdistension)
B. History of uterine surgery (risk of rupture)
C. Polyhydramnios (risk of further fluid accumulation)
D. Maternal diabetes (risk of fetal macrosomia)
E. Anti-D antibody (risk of alloimmunization)
Show answer
Answer: B. Amnioinfusion involves saline infusion into the amniotic sac to relieve umbilical cord compression causing variable decelerations. It is contraindicated in patients with prior uterine surgery, including prior cesarean delivery or myomectomy, because the increased intrauterine pressure from fluid infusion increases the risk of uterine rupture at the scar site. Twin pregnancy, polyhydramnios, maternal diabetes, and anti-D antibody are not contraindications to amnioinfusion. The first-line intervention for recurrent variable decelerations is maternal repositioning to the left lateral position before considering amnioinfusion.
Q10. Placenta accreta risk
Placenta accreta risk is highest with:
A. Previous cesarean section with placenta previa in the current pregnancy
B. Multiparity with four or more previous uncomplicated vaginal deliveries
C. Maternal diabetes mellitus with poor glycemic control throughout pregnancy
D. Twin gestation with dichorionic diamniotic placentation and anterior placentas
E. Polyhydramnios with amniotic fluid index greater than 25 cm
Show answer
Answer: A. The combination of prior cesarean section and placenta previa dramatically increases accreta risk. The risk rises with each prior cesarean: 3% with one prior cesarean, 11% with two, 40% with three, and over 60% with four or more. Multiparity alone, diabetes, twin gestation, and polyhydramnios do not significantly increase accreta risk. Management of suspected accreta includes planned cesarean hysterectomy at 34 to 36 weeks, large-bore intravenous access, arterial line placement, blood product availability, cell salvage capability, possible interventional radiology balloon catheter placement, and a multidisciplinary team approach. Postpartum hemorrhage and placenta accreta are the leading causes of peripartum hysterectomy.
Q11. Vasa previa diagnosis and timing
Vasa previa is best managed by:
A. Expectant management with weekly nonstress tests until spontaneous labor
B. Antenatal diagnosis via transvaginal Doppler ultrasound and scheduled cesarean delivery at 34–37 weeks
C. Vaginal delivery with continuous fetal heart rate monitoring throughout labor
D. Tocolysis to prolong pregnancy until 40 weeks gestation for fetal maturity
E. Routine cesarean delivery at 39 weeks gestation without antenatal imaging
Show answer
Answer: B. Vasa previa occurs when fetal vessels traverse the membranes over the cervical os, placing the fetus at risk of exsanguination if rupture of membranes occurs. The condition is best managed by antenatal diagnosis using transvaginal ultrasound with Doppler, followed by scheduled cesarean delivery at 34–37 weeks before rupture of membranes can occur. This timing balances the risk of prematurity against the risk of spontaneous membrane rupture. The classic presentation of undiagnosed vasa previa is painless vaginal bleeding at the time of rupture of membranes accompanied by sinusoidal fetal heart rate pattern or bradycardia, requiring emergent cesarean delivery. Expectant management, vaginal delivery, and delaying delivery beyond 37 weeks all carry unacceptable risk of fetal exsanguination.
Q12. Hypertension in pregnancy first-line agents
First-line antihypertensives in pregnancy for chronic hypertension include all EXCEPT:
A. Labetalol, a combined alpha- and beta-adrenergic blocker
B. Methyldopa, a centrally acting alpha-2 agonist agent
C. Nifedipine, a dihydropyridine calcium channel blocker
D. Hydralazine, a direct-acting arteriolar vasodilator agent
E. Enalapril, an angiotensin-converting enzyme inhibitor drug
Show answer
Answer: E. ACE inhibitors such as enalapril and angiotensin receptor blockers (ARBs) are contraindicated in pregnancy due to serious fetal toxicity including renal agenesis, hypocalvaria, oligohydramnios, intrauterine growth restriction, and fetal demise. First-line antihypertensives that are safe in pregnancy include labetalol (combined alpha- and beta-blocker), methyldopa (central alpha-2 agonist), nifedipine (calcium channel blocker), and hydralazine (direct vasodilator). The mnemonic "Never feed a lab baby hydra and meth" reminds us that ACE inhibitors and ARBs are never used, while labetalol, hydralazine, and methyldopa are safe options.
Q13. Amniotic fluid embolism
A laboring patient suddenly develops dyspnea, hypotension, hypoxemia, then cardiovascular collapse and DIC. The mechanism of cardiopulmonary collapse is:
A. Mechanical obstruction of pulmonary vasculature by amniotic fluid debris causing acute right heart failure
B. Massive immunologic and inflammatory response causing biphasic pulmonary hypertension, biventricular failure, and subsequent DIC
C. Anaphylactic reaction to fetal antigens causing systemic vasodilation, capillary leak, and distributive shock
D. Sudden thrombotic pulmonary embolism from pelvic veins causing acute right ventricular strain and failure
E. Reflex vasovagal response to uterine distension causing profound bradycardia and loss of vascular tone
Show answer
Answer: B. Amniotic fluid embolism (AFE) is characterized by a massive immunologic and inflammatory response rather than simple mechanical obstruction. The pathophysiology is biphasic: the first phase involves acute pulmonary hypertension leading to right ventricular failure, which progresses to biventricular failure. The second phase involves disseminated intravascular coagulation (DIC) with consumptive coagulopathy and hemorrhage. Treatment includes standard ACLS protocols, aggressive blood product replacement to manage DIC, and consideration of ECMO for refractory cardiopulmonary collapse. Some protocols propose the A-OK regimen (atropine, ondansetron, ketorolac), though evidence is limited. Mortality remains high at 20–60% despite aggressive management.
Q14. Placental drug transfer
Which of the following crosses the placenta most readily?
A. Heparin, due to its small molecular weight and high lipid solubility
B. Glycopyrrolate, due to its tertiary amine structure and neutral charge
C. Insulin, due to its peptide structure and moderate lipophilicity
D. Atropine, due to its tertiary amine structure and lipid solubility
E. Succinylcholine, due to its small size and rapid onset of action
Show answer
Answer: D. Atropine crosses the placenta readily because it is a tertiary amine with high lipid solubility, allowing easy passage across lipid membranes. A useful mnemonic for drugs that do NOT cross the placenta is 'He Is Going Nowhere Soon': Heparin (large molecular weight, highly charged), Insulin (large peptide), Glycopyrrolate (quaternary amine, highly ionized), and Neuromuscular blockers including Succinylcholine (quaternary amines, highly ionized). Most anesthesia drugs cross readily, remembered by 'LoV BABE PONS': Locals, Volatiles, Benzodiazepines, Atropine, Beta-blockers, Ephedrine, Propofol, Opioids, Neostigmine, and Scopolamine. Heparin is too large and charged, glycopyrrolate is a quaternary amine that is ionized at physiologic pH, insulin is a large peptide hormone, and succinylcholine is a quaternary amine that remains ionized.
Q15. Glycopyrrolate vs atropine in pregnancy
When reversing neuromuscular blockade in a parturient, which anticholinergic should be paired with neostigmine?
A. Glycopyrrolate, because it does not cross the placenta and avoids fetal exposure
B. Atropine, because it crosses the placenta and prevents neostigmine-induced fetal bradycardia
C. Either agent, because both provide equivalent maternal and fetal muscarinic blockade
D. Scopolamine, because it crosses the placenta and provides superior fetal protection
E. No anticholinergic, because neostigmine alone is safe in pregnancy without adjuncts
Show answer
Answer: B. Neostigmine crosses the placenta but glycopyrrolate does not, which can leave the fetus exposed to unopposed muscarinic effects including bradycardia. Atropine crosses the placenta and protects the fetus from neostigmine-induced bradycardia by providing fetal muscarinic blockade. This is why atropine, not glycopyrrolate, should be paired with neostigmine when reversing neuromuscular blockade in parturients. Scopolamine is not used for neuromuscular blockade reversal. An anticholinergic is always required when administering neostigmine to counteract its muscarinic side effects.
Q16. Bupivacaine cardiotoxicity in pregnancy
Why is bupivacaine considered safer than lidocaine in the parturient despite being more cardiotoxic in general?
A. Rapid metabolism by plasma cholinesterase reduces fetal exposure and systemic accumulation
B. High protein binding and elevated pKa limit transplacental transfer to the fetus
C. Lower lipid solubility decreases placental crossing and reduces fetal drug concentration
D. Competitive antagonism by naloxone reverses cardiotoxic effects in mother and fetus
E. Hydrophilic properties prevent placental passage and minimize fetal drug accumulation
Show answer
Answer: B. Bupivacaine has a pKa of 8.1, making it mostly ionized at physiologic pH, and very high protein binding (95%), both of which significantly limit transplacental transfer to the fetus. In contrast, lidocaine has lower protein binding (approximately 65%) and can become ion-trapped in the fetus during fetal acidosis, leading to accumulation and potential toxicity. This makes bupivacaine safer for the fetus despite its greater cardiotoxicity in the mother. Bupivacaine is not metabolized by plasma cholinesterase (that applies to ester local anesthetics), is highly lipid-soluble (not low), is not reversed by naloxone, and is lipophilic (not hydrophilic). Ropivacaine is a newer alternative that combines high protein binding with lower cardiotoxicity than bupivacaine.
Q17. Stages of labor pain pathways
Pain during the second stage of labor is mediated primarily by which nerve roots?
A. T10–L1 via hypogastric plexus and sympathetic chain
B. T12–L1 plus S2–S4 via pudendal nerve and perineum
C. T6–T9 via splanchnic nerves and celiac plexus
D. L2–L4 via lumbar plexus and genitofemoral nerve
E. S1–S3 via pudendal nerve and inferior rectal branches
Show answer
Answer: B. Stage 1 labor pain (cervical dilation and uterine contractions) is mediated by T10–L1 visceral afferents via the hypogastric plexus. Stage 2 labor pain (perineal stretch and distention) is mediated by both T12–L1 and S2–S4 via the pudendal nerve. This dual innervation is clinically important because epidural anesthesia adequate for stage 1 may not fully cover the sacral roots, potentially requiring a saddle block or epidural top-up for adequate stage 2 analgesia. The pudendal nerve carries somatic sensory fibers from the perineum, vagina, and vulva during the second stage.
Q18. Test dose
The classic test dose for an epidural catheter is 3 mL of lidocaine 1.5% with epinephrine 5 mcg/mL. Why epinephrine?
A. Prolongs the duration of the test dose by causing local vasoconstriction
B. Reduces systemic absorption by causing local vasoconstriction at the injection site
C. Intravascular injection produces heart rate increase greater than 20 bpm within 30–45 seconds
D. Identifies subdural placement by producing a delayed onset of patchy sensory block
E. Identifies subarachnoid placement by producing rapid onset of dense bilateral motor block
Show answer
Answer: C. Epinephrine in the epidural test dose detects intravascular injection by producing a heart rate rise greater than 20 bpm within 30–45 seconds when the catheter tip is in a blood vessel. Lidocaine (not epinephrine) identifies subarachnoid placement by producing rapid dense block of the legs. In laboring patients, especially those on beta-blockers or experiencing frequent contractions, the heart rate response to epinephrine is less reliable. While epinephrine does cause vasoconstriction, this is not the primary purpose of its inclusion in the test dose.
Q19. Hemodynamic changes peak
Maternal cardiac output reaches its highest level:
A. End of 1st trimester, when cardiac output rises approximately 35% above baseline
B. End of 2nd trimester, when cardiac output rises approximately 45% above baseline
C. End of 3rd trimester, when cardiac output rises approximately 50% above baseline
D. Immediately after delivery, when cardiac output rises approximately 80% above prelabor baseline
E. Six weeks postpartum, when cardiac output returns approximately to prepregnancy baseline
Show answer
Answer: D. Maternal cardiac output rises progressively during pregnancy: 35% by end of first trimester and 50% by end of third trimester. During labor, cardiac output increases an additional 40% in stage 2. However, the absolute peak occurs immediately post-delivery, when cardiac output reaches approximately 80% above prelabor values. This dramatic increase results from autotransfusion of blood from the contracting uterus and relief of inferior vena cava compression. This physiologic peak is clinically critical in patients with fixed cardiac lesions such as severe mitral stenosis, aortic stenosis, or pulmonary hypertension, as the period immediately after delivery represents the time of greatest hemodynamic stress and highest risk for decompensation, not during delivery itself. By six weeks postpartum, cardiac output returns to prepregnancy levels.
Q20. Difficult airway in pregnancy
Compared to non-pregnant, difficult intubation in the parturient is more common because of:
A. Decreased functional residual capacity reducing time available for laryngoscopy and intubation attempts
B. Airway mucosal edema, capillary engorgement, enlarged tongue, and breast tissue limiting positioning
C. Decreased gastric emptying increasing urgency and stress during rapid sequence intubation procedures
D. Decreased lower esophageal sphincter tone requiring faster intubation and limiting visualization time
E. Increased aspiration risk necessitating cricoid pressure which can worsen glottic visualization
Show answer
Answer: B. All listed factors are true physiologic changes in pregnancy, but only choice B directly addresses anatomic factors that make laryngoscopy and intubation mechanically more difficult. Airway mucosal edema and capillary engorgement narrow the upper airway and increase friability. Tongue enlargement reduces oral cavity space. Breast enlargement and weight gain interfere with laryngoscope handle positioning. These changes necessitate using a smaller endotracheal tube (6.0 to 6.5 mm), ramping the patient, having video laryngoscopy and supraglottic airways immediately available, and aggressive preoxygenation. Mallampati scores typically worsen during labor and pushing. Decreased FRC (choice A) reduces safe apnea time but does not make intubation itself more difficult. Choices C, D, and E relate to aspiration risk, which increases urgency but does not directly impair visualization or tube passage.
Q21. Aspiration prophylaxis
For elective cesarean delivery, recommended aspiration prophylaxis includes:
A. Sodium citrate administered 30 minutes before induction to neutralize gastric acid
B. Metoclopramide combined with H₂ blocker and sodium citrate before induction
C. Omeprazole administered orally the night before surgery to reduce acid
D. NPO status for 12 hours before surgery without pharmacologic agents
E. Cricoid pressure applied continuously from induction through intubation only
Show answer
Answer: B. The recommended aspiration prophylaxis for elective cesarean delivery is multimodal pharmacologic therapy combining metoclopramide, an H₂ blocker (such as famotidine), and sodium citrate. The H₂ blocker reduces gastric acid secretion over several hours. Metoclopramide promotes gastric emptying and increases lower esophageal sphincter tone. Sodium citrate, a non-particulate antacid, raises gastric pH immediately before induction. This combination addresses multiple mechanisms of aspiration risk. Sodium citrate alone provides only immediate pH neutralization without reducing volume or preventing reflux. Omeprazole alone requires longer onset and does not address gastric emptying. Prolonged NPO status alone is insufficient. Cricoid pressure remains controversial and is not a substitute for pharmacologic prophylaxis.
Q22. Massive transfusion protocol in PPH
In massive obstetric hemorrhage, the recommended ratio of packed RBC : FFP : platelets is:
A. 4:1:1 ratio to maintain oxygen-carrying capacity while minimizing coagulopathy
B. 1:1:1 ratio to provide balanced resuscitation and prevent dilutional coagulopathy
C. 6:2:1 ratio to prioritize hemoglobin levels while providing some clotting factors
D. 2:1:0 ratio to restore intravascular volume without risking platelet-related complications
E. 1:0:1 ratio to maximize oxygen delivery while avoiding plasma-associated transfusion reactions
Show answer
Answer: B. The recommended ratio for massive transfusion in obstetric hemorrhage is 1:1:1 (packed RBCs : FFP : platelets), providing balanced resuscitation that prevents dilutional coagulopathy. This approach is extrapolated from the PROPPR trial conducted in non-obstetric trauma patients. In obstetric hemorrhage specifically, additional measures include early fibrinogen replacement with cryoprecipitate when fibrinogen falls below 200 mg/dL, and tranexamic acid (TXA) administration within 3 hours of bleeding onset. The WOMAN trial demonstrated that 1g TXA reduces death from bleeding in postpartum hemorrhage. Recombinant factor VIIa may be considered after multiple rounds of massive transfusion protocol if bleeding remains refractory to standard measures.
Q23. von Willebrand disease in pregnancy
A 28-year-old G2P1 with type 1 vWD is admitted in active labor. Factor VIII level returns at 60% (well-compensated). The most appropriate plan is:
A. Avoid neuraxial anesthesia; proceed with general anesthesia for any required cesarean delivery
B. Neuraxial anesthesia is acceptable; administer DDAVP if needed for active bleeding postpartum
C. Continuous epidural anesthesia with prophylactic von Willebrand factor concentrate before placement
D. Prophylactic platelet transfusion before neuraxial placement; avoid epidural catheter techniques
E. Cryoprecipitate administration before any procedure; defer neuraxial until factor levels rechecked
Show answer
Answer: B. Type 1 von Willebrand disease is often well-compensated by the third trimester due to physiologic increases in factor VIII and von Willebrand factor levels. Neuraxial anesthesia is acceptable when factor VIII levels are greater than 50%, making this patient with a level of 60% an appropriate candidate. DDAVP (desmopressin) releases von Willebrand factor from endothelial stores and can be used if needed for active bleeding, though it should be avoided in type IIB von Willebrand disease due to risk of thrombocytopenia. Type III von Willebrand disease requires von Willebrand factor concentrate replacement. Neuraxial anesthesia should be avoided in untreated severe disease with factor VIII levels below 50%. Prophylactic factor replacement is not indicated when levels are already adequate, and platelet transfusion is not the primary treatment for von Willebrand disease.
Q24. Neonatal resuscitation HR threshold
According to NRP, chest compressions in a newborn are initiated when:
A. HR <100 despite tactile stimulation and initial positive pressure ventilation
B. HR <60 despite 30 seconds of adequate positive pressure ventilation with oxygen
C. HR <80 after birth despite warming and drying with tactile stimulation
D. HR <120 with apnea despite initial steps of warming and airway positioning
E. HR <100 immediately at delivery for any infant born before 37 weeks
Show answer
Answer: B. According to the Neonatal Resuscitation Program (NRP), chest compressions are initiated when the heart rate remains below 60 beats per minute despite 30 seconds of effective positive pressure ventilation with supplemental oxygen. Compressions are delivered at a 3:1 ratio with ventilation, providing 90 compressions and 30 breaths per minute. If the heart rate remains below 60 after 30 seconds of coordinated chest compressions and ventilation, epinephrine 10–30 mcg/kg IV should be administered and repeated every 3–5 minutes as needed. A heart rate below 100 prompts initiation of positive pressure ventilation, not compressions. The critical threshold for compressions is HR <60 after adequate ventilation has been attempted.
Q25. Umbilical cord gas interpretation
Normal umbilical arterial cord gas (vs. venous):
A. pH 7.40, PaO₂ 80 mmHg, PaCO₂ 40 mmHg
B. pH 7.25, PaO₂ 16–20 mmHg, PaCO₂ 50 mmHg
C. pH 7.10, PaO₂ 10 mmHg, PaCO₂ 60 mmHg
D. pH 7.35, PaO₂ 40 mmHg, PaCO₂ 35 mmHg
E. pH 7.30, PaO₂ 30 mmHg, PaCO₂ 30 mmHg
Show answer
Answer: B. Normal umbilical arterial cord gas values are pH approximately 7.25, PO₂ 16–20 mmHg, PCO₂ approximately 50 mmHg, and base excess −4. In contrast, umbilical venous values are pH approximately 7.35, PO₂ approximately 30 mmHg, and PCO₂ approximately 40 mmHg. The umbilical artery reflects fetal status after placental gas exchange, showing lower pH, lower oxygen, and higher carbon dioxide than venous blood. Fetal scalp pH less than 7.20 suggests fetal acidosis. Fetal hemoglobin has a P50 of approximately 19 mmHg compared to adult hemoglobin at 27 mmHg, meaning the high-affinity fetal hemoglobin facilitates oxygen transfer across the placenta despite the relatively low fetal PO₂ values.
Q26. Tocolytic contraindications
Indomethacin should be avoided as a tocolytic after which gestational age?
A. 24 weeks gestational age due to risk of oligohydramnios and renal dysfunction
B. 28 weeks gestational age due to risk of necrotizing enterocolitis and bleeding
C. 32 weeks gestational age due to risk of premature ductus arteriosus closure
D. 34 weeks gestational age due to risk of intraventricular hemorrhage and seizures
E. 37 weeks gestational age due to risk of persistent pulmonary hypertension
Show answer
Answer: C. Indomethacin should be avoided as a tocolytic after 32 weeks gestational age because it risks premature closure of the ductus arteriosus through inhibition of prostaglandin synthesis. While indomethacin can cause oligohydramnios and renal dysfunction at any gestational age (particularly with prolonged use), the critical concern after 32 weeks is ductal constriction in the fetus. Other tocolytic considerations include magnesium sulfate, which should be avoided in myasthenia gravis and can cause neonatal hypocalcemia and osteopenia with prolonged use beyond 5-7 days. Nifedipine is contraindicated in AV block or pulmonary edema. Terbutaline can cause maternal hyperglycemia and tachycardia.
Q27. Cervical cerclage anesthesia
A 19-week parturient presents for prophylactic cervical cerclage. The preferred anesthetic is:
A. Spinal anesthesia with bupivacaine to T10 dermatome level
B. General anesthesia with sevoflurane and rapid sequence induction
C. Local infiltration anesthesia with lidocaine at cervical site
D. Lumbar epidural anesthesia with catheter to T6 level
E. Saddle block spinal anesthesia to S4 dermatome level
Show answer
Answer: A. Prophylactic cervical cerclage is best performed under spinal anesthesia with a sensory level from T10 to S4, which provides adequate surgical anesthesia for cervical manipulation while avoiding the risks of general anesthesia in pregnancy. The T10 level ensures coverage of uterine innervation. Emergent cerclage with bulging membranes is a different scenario where general anesthesia is preferred because it avoids increased intraabdominal and intrauterine pressure from neuraxial techniques and allows uterine relaxation with volatile agents. Rapid sequence induction is indicated for general anesthesia if the patient is beyond 18 to 20 weeks gestation due to aspiration risk. A saddle block to S4 alone would provide insufficient coverage as it would miss the T10-L1 uterine innervation. Epidural to T6 is unnecessarily high and risks hemodynamic instability. Local infiltration alone does not provide adequate anesthesia for cervical cerclage.
Q28. Plasma volume expansion
By term, maternal plasma volume has expanded by approximately:
A. 10%
B. 20%
C. 30%
D. 45–50%
E. 70%
Show answer
Answer: D. By term, maternal plasma volume increases by approximately 45–50%, while red blood cell volume increases by only 25–30%. This disproportionate expansion results in the physiologic anemia of pregnancy, with a dilutional decrease in hemoglobin concentration despite increased total red cell mass. Pregnancy is also a hypercoagulable state: fibrinogen and coagulation factors VII, VIII, IX, X, and XII all rise, while factors XI and XIII and antithrombin III fall. PT and PTT typically shorten by approximately 20%.
Q29. Spinal hypotension management
Spinal hypotension during cesarean is best managed with:
A. Rapid crystalloid bolus alone with patient positioning adjustments as needed
B. Co-loading with crystalloid plus phenylephrine infusion or boluses with left uterine displacement
C. Trendelenburg positioning only with careful monitoring of blood pressure throughout procedure
D. Ephedrine as first-line vasopressor with crystalloid bolus and patient repositioning
E. Vasopressin infusion or boluses with concurrent rapid crystalloid administration and positioning
Show answer
Answer: B. Phenylephrine is now the preferred vasopressor over ephedrine for spinal hypotension during cesarean delivery because it results in lower fetal acidemia, as demonstrated in CONSORT trials. Co-loading (administering rapid IV fluid at the time of spinal placement) is more effective than pre-loading. Left uterine displacement (LUD) must be maintained throughout to prevent aortocaval compression. Crystalloid alone is insufficient without vasopressor support. Trendelenburg positioning is not recommended as sole therapy. Ephedrine is no longer first-line due to increased fetal acidemia compared to phenylephrine. Vasopressin is not a standard agent for obstetric hypotension management.
Q30. PDPH risk factors
The risk of post-dural puncture headache is highest in which patient?
A. 65-year-old male undergoing spinal anesthesia with a 27-gauge pencil-point needle
B. 28-year-old female parturient with unintentional dural puncture using a 17-gauge Tuohy needle
C. 50-year-old obese female undergoing spinal anesthesia with a 25-gauge Quincke needle
D. 35-year-old male patient with a history of one prior uneventful spinal anesthetic
E. 12-year-old pediatric patient undergoing spinal anesthesia with a 22-gauge pencil-point needle
Show answer
Answer: B. The highest risk for post-dural puncture headache (PDPH) occurs with the combination of multiple risk factors: young age (less than 40 years), female sex, pregnancy, and large-bore cutting needles. The 28-year-old pregnant patient with unintentional dural puncture using a 17-gauge Tuohy needle has all of these high-risk features. The incidence of PDPH after accidental dural puncture with a Tuohy needle is 50 to 80 percent, compared to much lower rates with smaller gauge needles. Pencil-point needles such as Sprotte and Whitacre designs, as well as smaller gauge needles in the 25 to 27-gauge range, significantly reduce PDPH risk. Older age (over 60), male sex, and pediatric patients all have lower baseline risk. Treatment includes conservative measures such as hydration, caffeine, and abdominal binders, with epidural blood patch being the gold standard if conservative measures fail after 24 to 48 hours.
Q31. Anticoagulation and neuraxial in pregnancy
A parturient on prophylactic LMWH (enoxaparin 40 mg subq daily) needs an epidural. Per ASRA, the minimum interval from last dose to needle placement is:
A. 4 hours after the last prophylactic dose of enoxaparin
B. 8 hours after the last prophylactic dose of enoxaparin
C. 12 hours after the last prophylactic dose of enoxaparin
D. 24 hours after the last prophylactic dose of enoxaparin
E. 48 hours after the last prophylactic dose of enoxaparin
Show answer
Answer: C. Per ASRA guidelines, prophylactic-dose LMWH requires a 12-hour interval before neuraxial needle placement, while therapeutic-dose LMWH requires 24 hours. After needle placement, prophylactic LMWH should be restarted at least 12 hours later (therapeutic at least 24 hours later). For catheter removal, wait 12 hours after the last prophylactic dose, and delay the next LMWH dose until at least 4 hours after catheter removal. The 12-hour interval for prophylactic dosing balances the anticoagulant effect with the need for safe neuraxial anesthesia in obstetric patients.
Q32. Stage 1 hemorrhage definition
Per ACOG, postpartum hemorrhage is defined as cumulative blood loss of:
A. >500 mL cumulative blood loss after vaginal delivery only
B. >1000 mL cumulative blood loss or signs of hypovolemia within 24 hours
C. >2000 mL cumulative blood loss after cesarean delivery only
D. >300 mL cumulative blood loss with documented hypotension
E. Any cumulative blood loss in a patient with known coagulopathy
Show answer
Answer: B. ACOG (2017) revised the definition of postpartum hemorrhage to cumulative blood loss ≥1000 mL regardless of mode of delivery, or signs and symptoms of hypovolemia within 24 hours of delivery. This definition applies to both vaginal and cesarean deliveries. The previous threshold of 500 mL for vaginal delivery underestimated clinically significant hemorrhage. Etiology is remembered by the 4 T's: Tone (uterine atony, most common cause), Trauma (lacerations, uterine rupture), Tissue (retained placenta, placenta accreta spectrum), and Thrombin (coagulopathy, DIC).