Maternal Physiological Changes in Pregnancy

Quick Answer

Pregnancy induces profound physiological adaptations that significantly impact anaesthetic management. By term, cardiac output increases 40-50% (stroke volume +30%, heart rate +15-20%), blood volume expands 40-50% (plasma > RBCs causing physiological anaemia Hb 105-115 g/L), and systemic vascular resistance decreases 20-30% reaching nadir at 20-24 weeks. Respiratory changes include increased tidal volume (40%) with unchanged respiratory rate, resulting in respiratory alkalosis (PaCO2 28-32 mmHg) compensated by renal bicarbonate excretion. Functional residual capacity decreases 20-30% due to diaphragm elevation, leading to rapid desaturation during apnoea. Gastric emptying is delayed, and lower oesophageal sphincter tone decreases, increasing aspiration risk. Airway mucosal oedema (Mallampati class ↑ 1-2 grades) and increased breast tissue complicate airway management. These changes necessitate modified RSI with reduced drug doses (thiopentone 3-4 mg/kg, propofol 1.5-2 mg/kg), cricoid pressure, left uterine displacement (>15°), and preparation for difficult airway management (grade 3-4 view in 1:200 parturients).

Maternal Physiology in Pregnancy

Cardiovascular Changes

Cardiovascular adaptation begins at 5-8 weeks gestation with maximal changes by 28-32 weeks. Cardiac output increases 40-50% from 5 L/min to 7-7.5 L/min, driven by increased stroke volume (30-35% in first trimester) and heart rate (15-20% by third trimester). Stroke volume peaks at 20 weeks then plateaus, while heart rate continues to increase to 80-95 bpm at term. Systemic vascular resistance decreases 20-30% due to progesterone-mediated vasodilation and low-resistance placental circulation, reaching nadir at 20-24 weeks. Mean arterial pressure typically decreases 10-15 mmHg, with lowest values at 16-20 weeks, returning to baseline by term.

Blood volume expands 40-50% (from 5 L to 7-7.5 L), disproportionately in plasma (50-60% increase) versus red cell mass (20-30%), resulting in physiological anaemia (haemoglobin 105-115 g/L, haematocrit 32-36%). This "dilutional anaemia" optimises oxygen delivery despite increased metabolic demands. Central venous pressure and pulmonary capillary wedge pressure remain unchanged due to decreased right ventricular afterload, despite increased preload.

Aortocaval compression by the gravid uterus after 20 weeks can reduce cardiac output up to 30% in supine position, necessitating left uterine displacement of at least 15°. The heart is displaced upward and leftward, causing ECG axis deviation (left axis shift) and prominent Q waves in inferior leads. Aortic and mitral valve regurgitation murmurs are common due to increased flow through competent valves.

Respiratory Changes

Minute ventilation increases 40-50% (from 7.5 L/min to 10-11 L/min) primarily through increased tidal volume (40% increase, from 500 mL to 700 mL) with minimal change in respiratory rate. Alveolar ventilation increases 70% due to decreased anatomical dead space, resulting in respiratory alkalosis (PaCO2 28-32 mmHg, PaO2 100-105 mmHg, pH 7.40-7.45). Renal compensation increases bicarbonate excretion (18-22 mmol/L) to maintain near-normal pH.

Functional residual capacity decreases 20-30% (from 3 L to 2-2.5 L) due to diaphragm elevation (4 cm upward displacement), ribcage widening (subcostal angle increases from 68° to 103°), and reduced chest wall compliance. Expiratory reserve volume decreases most dramatically (up to 50% reduction). Residual volume decreases 15-20%. Combined with increased oxygen consumption (20-30% increase to 300-350 mL/min), these changes cause rapid oxygen desaturation during apnoea (SpO2 <90% within 2-3 minutes vs 5-8 minutes in non-pregnant state).

Airway mucosal engorgement due to oestrogen effects causes narrowing of upper airway diameter, potentially increasing Mallampati class by 1-2 grades. Vocal cords may be oedematous, requiring smaller endotracheal tubes (6.0-7.0 mm ID) for intubation. Nasal stuffiness and epistaxis are common. Decreased functional residual capacity and increased oxygen consumption necessitate pre-oxygenation with 3 minutes of tidal volume breathing or 8 vital capacity breaths.

Gastrointestinal Changes

Progesterone decreases lower oesophageal sphincter tone by 30-50%, and physical displacement of the stomach by the uterus increases intra-abdominal pressure. Combined, these factors increase gastro-oesophageal reflux risk (30-50% of pregnant women experience symptoms). Gastric emptying is delayed by 30-50%, particularly during labour (delay extends to >2 hours), and gastric volume is increased.

Gastric pH is less than 2.5 in most parturients, and gastric volumes exceed 25 mL in 80% of term pregnant women. These changes create the classic "full stomach" obstetric patient with high aspiration risk. Histamine H2-receptor antagonists (ranitidine 50 mg IV) and sodium citrate (30 mL of 0.3 M) are standard pre-induction prophylaxis.

Renal Changes

Renal plasma flow increases 50-80%, and glomerular filtration rate increases 40-65% (from 100 mL/min to 150-160 mL/min), resulting in decreased serum creatinine (50-70 μmol/L) and blood urea nitrogen (2.5-3.5 mmol/L). These changes occur early in pregnancy and persist until postpartum. The kidneys enlarge 1-2 cm due to increased vascular volume and interstitial oedema. Ureteral dilation (hydroureter) occurs, more pronounced on the right side due to dextrorotation of the uterus, predisposing to urinary tract infection and asymptomatic bacteriuria (5-10%).

Proteinuria up to 300 mg/24h is considered normal in pregnancy. Glucosuria may occur due to reduced renal threshold (tubular reabsorption capacity overwhelmed by increased filtered load). These normal changes must be distinguished from pathological conditions such as pre-eclampsia (proteinuria >300 mg/24h) or gestational diabetes.

Coagulation Changes

Pregnancy is a hypercoagulable state, preparing for haemostasis at delivery. Most clotting factors increase (fibrinogen up to 400-600 mg/dL, factor VII 2-3-fold, factor VIII 2-fold, factor X 2-fold), while fibrinolysis decreases (PAI-1 and PAI-2 increase). Prothrombin time and activated partial thromboplastin time remain unchanged, but thromboelastography shows increased clot strength and decreased lysis.

Platelet count decreases slightly (10-15% reduction from non-pregnant baseline) due to haemodilution, with normal pregnancy values 100-150 × 10⁹/L. Thrombocytopenia below 100 × 10⁹/L requires investigation. Platelet function is enhanced.

These changes protect against haemorrhage but increase risk of venous thromboembolism (5-10 fold increase compared to non-pregnant state, risk 1-2 per 1000 pregnancies). Deep vein thrombosis is more common in the left leg (80% of cases) due to compression of the left iliac vein by the right iliac artery and overlying gravid uterus.

Obstetric Condition Overview

Definition and Epidemiology

Maternal physiological changes in pregnancy refer to the systematic adaptations of maternal organ systems to support fetal development, prepare for parturition, and protect maternal haemodynamic stability during blood loss at delivery. These changes are universal and begin within weeks of conception, reaching maximum effect by the third trimester.

These adaptations are clinically significant for anaesthetists as they alter drug pharmacokinetics and pharmacodynamics, affect airway management, influence haemodynamic responses to anaesthetic agents, and determine the risk of complications during obstetric anaesthesia.

Pathophysiology Relevant to Anaesthesia

Hormonal influences (oestrogen, progesterone, relaxin, human chorionic gonadotropin) mediate most cardiovascular, respiratory, and gastrointestinal changes. Mechanical effects of the enlarging uterus cause displacement of abdominal organs, diaphragm elevation, and aortocaval compression. Increased metabolic demands drive cardiovascular and respiratory adaptations.

Placental circulation is a low-resistance, high-flow circuit receiving 20-25% of cardiac output at term (500-700 mL/min). This "circulatory shunt" contributes to decreased systemic vascular resistance and increased cardiac output.

Risk Stratification

Most physiological changes are predictable and follow a consistent timeline across pregnancies. However, certain conditions exaggerate these adaptations: multiple gestation (greater blood volume expansion, earlier onset of aortocaval compression), pre-existing cardiac disease (limited ability to accommodate increased cardiac output), and pre-eclampsia (pathological exaggeration of cardiovascular changes).

Understanding normal adaptations is essential for recognising pathological states. For example, while mild respiratory alkalosis (PaCO2 28-32 mmHg) is normal, severe respiratory alkalosis (PaCO2 <25 mmHg) or metabolic acidosis indicates pathology. Physiological anaemia (Hb 105-115 g/L) must be distinguished from pathological anaemia (Hb <100 g/L).

Maternal and Fetal Considerations

For the mother, physiological changes increase risks of difficult airway management (1:200-1:300 grade 3-4 views), pulmonary aspiration (1:300-1:900 with modern protocols), cardiac decompensation (peripartum cardiomyopathy incidence 1:3000-1:4000), and postpartum haemorrhage (500-1000 mL blood loss at vaginal delivery, 1000-2000 mL at Caesarean section).

For the fetus, maternal hypotension reduces uteroplacental perfusion, potentially causing fetal compromise. Uterine blood flow is non-autoregulated and directly proportional to maternal perfusion pressure, making maintenance of maternal blood pressure critical. Fetal oxygen delivery depends on maternal SpO2 and uterine blood flow.

Anaesthetic Management

Pre-operative Assessment

Thorough airway assessment is mandatory: Mallampati class (may increase 1-2 grades from first to third trimester), mouth opening, neck mobility, thyromental distance, and history of previous difficult intubation. Pre-eclampsia increases airway oedema risk; assess for facial swelling, short neck, and laryngeal oedema. Review coagulation profile for neuraxial techniques (platelet count, coagulation studies). Assess cardiovascular status: baseline blood pressure (may be lower than non-pregnant baseline), signs of cardiac decompensation, and fetal well-being.

Modified Rapid Sequence Induction

Standard obstetric RSI differs from non-pregnant adult RSI. Pre-oxygenation is critical: 3 minutes of tidal volume breathing with 100% oxygen or 8 vital capacity breaths achieves apnoeic oxygenation for 2-3 minutes. Head-up position (20-30°) or semi-recumbent position improves FRC and oxygenation. Left uterine displacement of at least 15° is mandatory to prevent aortocaval compression.

Cricoid pressure is applied at 30 N to minimise regurgitation risk, though controversy exists about its efficacy and potential to worsen laryngeal view. Induction agents are reduced in dose: thiopentone 3-4 mg/kg (vs 5-7 mg/kg non-pregnant), propofol 1.5-2 mg/kg (vs 2-2.5 mg/kg), ketamine 1 mg/kg (vs 1.5-2 mg/kg). Increased cardiac output and decreased protein binding result in higher peak plasma concentrations of induction agents.

Succinylcholine 1-1.5 mg/kg remains the muscle relaxant of choice due to rapid onset (<60 seconds) and offset; however, increased plasma cholinesterase activity may require slightly higher doses. Rocuronium 1 mg/kg offers alternative with intermediate onset but requires sugammadex for rapid reversal. Remifentanil 1 μg/kg bolus may blunt hypertensive response to laryngoscopy.

Maintenance Strategies

Low concentrations of volatile agents (0.5-0.75 MAC) combined with 50-70% nitrous oxide in oxygen provide amnesia and analgesia while minimising uterine relaxation. Higher concentrations (>1 MAC) increase risk of postpartum haemorrhage and fetal depression. Consider opioid supplementation (fentanyl 50-100 μg, alfentanil 500-1000 μg) for analgesia.

For Caesarean section, maintain maternal SpO2 >95% and systolic blood pressure within 20% of baseline (typically >90 mmHg). Phenylephrine 50-100 μg boluses or norepinephrine 4-8 μg boluses are first-line vasopressors for spinal-induced hypotension. Avoid ephedrine when possible as it may cause fetal acidosis (crosses placenta, stimulates fetal metabolism).

Airway Management

Video laryngoscopy is increasingly recommended as first-line for obstetric intubation due to improved glottic visualisation, particularly in patients with airway oedema. Have difficult airway equipment readily available: smaller endotracheal tubes (6.0-7.0 mm ID), bougie, supraglottic airway devices (LMA Classic, LMA Supreme), and equipment for surgical airway.

If intubation fails after two attempts, awaken the patient and consider alternative approach: awake fibreoptic intubation, regional anaesthesia if feasible, or postpone surgery until airway improves. Failed intubation incidence in obstetrics is 1:250-1:300, with 8-fold increased maternal mortality compared to non-obstetric failed intubation.

Perioperative Considerations

Intraoperative Positioning

Left uterine displacement of at least 15° is critical after 20 weeks gestation to prevent aortocaval compression. Manual displacement (leftward uterine displacement) or right lateral tilt of the operating table achieves this. Inadequate displacement reduces cardiac output up to 30% and can precipitate maternal hypotension and fetal compromise.

For spinal or epidural placement, patient positioning is crucial. Sitting position may improve identification of midline but increases risk of aortocaval compression. Left lateral position is preferred for epidural catheter placement, with careful attention to maintaining left uterine displacement. Use pillows for comfort and support.

Fluid Management

Pregnant patients are relatively hypovolaemic despite increased blood volume due to vasodilation. Aggressive fluid boluses can precipitate pulmonary oedema, particularly in pre-eclampsia or cardiac disease. Crystalloid co-loading (500-1000 mL) rather than pre-loading is preferred for spinal anaesthesia.

Blood loss at vaginal delivery (500-1000 mL) and Caesarean section (1000-2000 mL) is well tolerated due to physiological blood volume expansion. However, close monitoring is required in patients with pre-existing anaemia or cardiac compromise. Transfusion triggers may be lower than non-pregnant patients (Hb <70 g/L for asymptomatic, <80 g/L for symptomatic).

Blood Pressure Goals

Maintain systolic blood pressure within 20% of baseline. For most term parturients, target SBP >90 mmHg. Hypotension reduces uteroplacental perfusion and can cause fetal bradycardia. Hypertension increases risk of intracranial haemorrhage, particularly in pre-eclamptic patients.

Continuous non-invasive blood pressure monitoring with 1-2 minute intervals is standard during spinal anaesthesia. Invasive arterial monitoring is indicated for severe pre-eclampsia (SBP >160 mmHg, MAP >110 mmHg), cardiac disease, or major haemorrhage.

Fetal Monitoring

Continuous electronic fetal monitoring is indicated for regional anaesthesia procedures due to risk of maternal hypotension, bradycardia, or respiratory depression. Baseline fetal heart rate (110-160 bpm), variability (moderate), and presence of accelerations are reassuring. Decelerations require prompt intervention: maternal position change, oxygen supplementation, fluid bolus, vasopressor administration, or urgent delivery if non-reassuring.

Post-partum Care

Immediate Post-operative Management

Uterine contraction postpartum causes autotransfusion of 500-1000 mL blood, increasing preload and cardiac output. Patients with cardiac compromise are at risk of pulmonary oedema during this period. Monitor for signs of cardiac decompensation: dyspnoea, crackles, SpO2 <94%, increasing oxygen requirements.

Pain management must balance maternal comfort with neonatal safety for breastfeeding. Multimodal analgesia is preferred: regular paracetamol (1 g 4-6 hourly), NSAIDs (ibuprofen 400 mg 6-8 hourly after delivery), and opioids as required (oxycodone 5-10 mg, codeine 30 mg). Breastfeeding is compatible with most analgesics; avoid aspirin (Reye's syndrome) and high-dose codeine (maternal ultra-rapid metabolisers may cause neonatal depression).

Neonatal Considerations

Neonatal effects of anaesthetic agents depend on timing and dose. Induction agents cross placenta rapidly; fetal concentrations reach 50-100% of maternal levels within minutes of maternal administration. Volatile agents equilibrate slowly; fetal levels remain <25% of maternal levels with <1 MAC exposure.

Neonatal depression is uncommon with modern obstetric anaesthetic techniques but may present with decreased respiratory effort, hypotonia, or poor feeding. Monitor Apgar scores (5 and 10 minutes), respiratory status, and feeding. Breastfeeding can commence as soon as mother is alert and able, typically 2-4 hours post-delivery for most agents.

Complications Prevention

Post-dural puncture headache (PDPH) incidence after accidental dural puncture with Tuohy needle is 50-80%. Prophylactic epidural blood patch (within 24-48 hours) reduces PDPH incidence and severity. Urinary retention is common postpartum; intermittent catheterisation may be required for 12-24 hours.

Nerve injuries are relatively rare (0.1-1% after epidural). Most postpartum nerve palsies are due to maternal positioning (lateral femoral cutaneous nerve, common peroneal nerve) or fetal head compression (obturator nerve, pudendal nerve) rather than direct needle trauma.

Complications & Emergencies

Maternal Cardiac Arrest

Maternal cardiac arrest incidence is 1:12,000-1:30,000 deliveries. Causes include amniotic fluid embolism (1:40,000-1:60,000), pulmonary embolism, haemorrhage, anaesthetic complications, and pre-existing cardiac disease.

Modified ACLS for pregnancy includes left uterine displacement (manual leftward displacement >15° or left lateral tilt), airway management with cricoid pressure, and consideration of early Caesarean delivery if return of spontaneous circulation not achieved within 4-5 minutes of arrest (resuscitative hysterotomy). Fetal survival requires delivery within 10 minutes of maternal arrest; maternal benefit includes improved cardiac output by removing aortocaval compression and allowing more effective chest compressions.

Failed Intubation in Obstetrics

Failed intubation incidence in obstetrics is 1:250-1:300, compared to 1:2000 in general surgical population. Contributing factors include airway oedema, full stomach, increased breast tissue, and limited time for preparation.

Management algorithm: (1) Optimise positioning (ramped, left uterine displacement), (2) Use alternative laryngoscope (video laryngoscopy), (3) Second attempt by experienced anaesthetist, (4) Awake fibreoptic intubation or regional anaesthesia, (5) Consider supraglottic airway device (LMA) as temporary airway, (6) Surgical airway if all else fails and hypoxia imminent.

Do not persist with repeated intubation attempts; maternal mortality increases 8-fold with failed obstetric intubation. Wake the patient if possible, use regional anaesthesia, or consider proceeding with supraglottic airway for urgent Caesarean section.

Postpartum Haemorrhage

Primary postpartum haemorrhage (blood loss >1000 mL within 24 hours of delivery) occurs in 5-6% of deliveries. Causes include uterine atony (70-80%), genital tract trauma (10-20%), retained products (5-10%), and coagulopathy (1-5%).

Management involves uterine massage, oxytocin infusion (40 IU over 4 hours or 10 IU IM bolus), ergometrine (0.25 mg IM, contraindicated in hypertension), carboprost tromethamine (250 μg IM, contraindicated in asthma), and misoprostol (800 μg sublingual/rectal). For refractory haemorrhage, consider uterine balloon tamponade (Bakri balloon), uterine artery embolisation, or laparotomy for uterine compression sutures (B-Lynch) or hysterectomy.

Anaesthetic management involves invasive monitoring, large-bore IV access (14-16 G), rapid transfusion protocols (massive transfusion 1:1:1 ratio), and careful fluid balance to prevent pulmonary oedema. Communicate with blood bank early; activate massive transfusion protocol if >2 units blood required.

ANZCA Final Exam Focus

Common SAQ Patterns

ANZCA Final SAQs frequently test maternal physiological changes and their anaesthetic implications. Typical questions include: "Describe the cardiovascular changes in pregnancy and their impact on anaesthetic management" (10 marks), "Explain the respiratory changes during pregnancy and how they affect pre-oxygenation and apnoea tolerance" (10 marks), "Outline the gastrointestinal changes in pregnancy and their relevance to aspiration risk" (5 marks), "Discuss the coagulation changes in pregnancy and implications for neuraxial anaesthesia" (5 marks).

Candidates should provide systematic descriptions of each system, emphasising quantitative changes (percentages, absolute values), timing of changes (when they begin, when they peak), clinical significance for anaesthesia (drug dosing, airway management, positioning, monitoring), and fetal considerations.

Clinical Viva Themes

Clinical vivas commonly include scenarios requiring management of parturients with physiological challenges: "A 28-year-old primigravida at 38 weeks requires emergency Caesarean section for fetal distress. She has a BMI of 35 and a Mallampati class 3 airway. Discuss your anaesthetic management" (15 marks). Candidates must address pre-operative assessment (airway, cardiovascular, coagulation), preparation (equipment, drugs, monitoring), modified RSI technique (dose reductions, cricoid pressure, positioning), management of complications (failed intubation, hypotension), and postpartum care.

Other viva scenarios may include parturients with cardiac disease (pregnancy-induced physiological stress may unmask previously asymptomatic conditions), severe pre-eclampsia (exaggerated physiological changes), or multiple gestation (greater physiological demands).

Specific Obstetric Anaesthesia Challenges

ANZCA examiners emphasise understanding of why pregnancy modifications are necessary: drug dose reductions (increased cardiac output, decreased protein binding), pre-oxygenation importance (decreased FRC, increased oxygen consumption), left uterine displacement (aortocaval compression), airway difficulties (mucosal oedema, Mallampati changes), and rapid sequence induction (delayed gastric emptying, decreased LES tone).

Candidates should differentiate between normal physiological changes and pathological states (e.g., respiratory alkalosis PaCO2 28-32 mmHg vs pathological hyperventilation PaCO2 <25 mmHg; physiological anaemia Hb 105-115 g/L vs pathological anaemia Hb <100 g/L; mild proteinuria <300 mg/24h vs pre-eclampsia >300 mg/24h).

Australian/NZ Guidelines

KEMH Clinical Guidelines (King Edward Memorial Hospital)

KEMH O&G Guideline "Anaesthesia for Caesarean Section" recommends pre-operative assessment including airway examination, coagulation profile, and cardiovascular status. All parturients >20 weeks gestation require left uterine displacement >15°. Modified RSI with cricoid pressure is standard for general anaesthesia. Pre-oxygenation with 3 minutes of tidal volume breathing or 8 vital capacity breaths. Induction agent doses: thiopentone 3-4 mg/kg, propofol 1.5-2 mg/kg, ketamine 1 mg/kg. Succinylcholine 1-1.5 mg/kg or rocuronium 1 mg/kg. Maintain volatile agent <1 MAC. Phenylephrine is first-line vasopressor for spinal-induced hypotension.

KEMH Guideline "Management of Postpartum Haemorrhage" outlines uterotonic protocols (oxytocin 10 IU IM + 40 IU infusion, ergometrine 0.25 mg IM, carboprost 250 μg IM, misoprostol 800 μg), massive transfusion protocol activation criteria (>1000 mL blood loss or ongoing haemorrhage), and resuscitation targets (MAP >65 mmHg, urine output >0.5 mL/kg/hr, lactate <2 mmol/L).

RCH Clinical Guidelines (Royal Children's Hospital)

RCH Paediatric Guideline "Neonatal Resuscitation" is relevant for anaesthetists managing obstetric emergencies. Apgar scores should be documented at 1, 5, and 10 minutes. Neonatal resuscitation requires bag-mask ventilation if HR <100 bpm or ineffective breathing, chest compressions if HR <60 bpm despite ventilation, and epinephrine 10-30 μg/kg IV if HR <60 bpm despite chest compressions.

State-Specific Protocols

NSW Health Clinical Guidelines "Maternity – Anaesthesia for Caesarean Section" align with KEMH protocols. Queensland Health "Obstetric Anaesthesia Guidelines" include specific recommendations for pre-eclampsia management (platelet threshold ≥70 × 10⁹/L for neuraxial) and cardiac disease in pregnancy (invasive monitoring for NYHA class III-IV). Victorian Department of Health "Maternity Services Clinical Guidelines" emphasise multidisciplinary team approach for high-risk obstetric patients.

Australian Drug Formulations in Pregnancy

TGA-approved drugs for obstetric anaesthesia include thiopentone (Pentothal), propofol (Diprivan), ketamine (Ketalar), succinylcholine (Scoline), rocuronium (Esmeron), phenylephrine (Vazculep), ephedrine (Ephedrine sulfate), oxytocin (Syntocinon), ergometrine (Ergotrate), carboprost tromethamine (Hemabate), misoprostol (Cytotec). Most are PBS-listed for hospital use.

Breastfeeding compatibility: Most analgesics and anaesthetic agents are considered safe during breastfeeding. Avoid aspirin (Reye's syndrome), high-dose codeine (maternal ultra-rapid metabolisers), and长期 use of benzodiazepines. Paracetamol, ibuprofen, and low-dose opioids are recommended.

Indigenous Health Considerations

Aboriginal and Torres Strait Islander Maternal Health Disparities

Aboriginal and Torres Strait Islander women experience maternal mortality at 2-3 times the rate of non-Indigenous Australian women. Contributing factors include higher prevalence of pre-existing medical conditions (diabetes, hypertension, cardiac disease), reduced access to antenatal care (later presentation, fewer visits), geographic isolation (remote communities with limited specialist services), and socioeconomic disadvantage.

These disparities impact anaesthetic management: higher rates of emergency Caesarean sections, more frequent co-morbidities requiring complex management, increased likelihood of difficult airway (higher BMI, undiagnosed obstructive sleep apnoea), and greater risk of postpartum complications (haemorrhage, infection).

Cultural Considerations for Consent and Communication

Cultural safety is paramount. Build rapport through respectful communication, acknowledge country and traditional custodianship, use plain language (avoid medical jargon), and allow sufficient time for decision-making. Family and community involvement is important; involve Aboriginal Health Workers or Aboriginal Hospital Liaison Officers where available.

Understand that some communities may have specific cultural protocols around birth and medical procedures. Traditional birthing practices may be incorporated into care plans where feasible. Respect privacy and confidentiality; some communities have collective decision-making processes requiring broader family consultation.

Family and Community Decision-Making in Birth

For many Aboriginal and Torres Strait Islander families, birth is a communal event involving extended family members. Include designated family members in discussions while respecting patient confidentiality. Some patients may require time to consult with Elders or community members before making decisions about anaesthesia and surgery.

Understand that "sorry business" (mourning protocols) may impact decision-making timelines. Allow flexibility in scheduling elective procedures to accommodate cultural obligations. Involve Aboriginal Health Workers to facilitate culturally appropriate communication.

Remote/Rural Obstetric Anaesthesia Access

Remote communities often lack on-site specialist anaesthetic services. Patients may require transfer to tertiary centres for complex procedures. Consider retrieval medicine implications: RFDS (Royal Flying Doctor Service) protocols, oxygen and equipment limitations during transport, and need for stabilisation before transfer.

Telemedicine consultations with specialist anaesthetists can guide management in remote settings. Establish clear communication channels with tertiary obstetric centres. For emergency deliveries in remote facilities, have protocols for managing complications (haemorrhage, eclampsia, failed intubation) with limited resources.

Traditional Birthing Practices

Some communities maintain traditional birthing practices alongside Western medicine. Respect these practices and incorporate them where safe. Examples include presence of female family members during procedures, specific birthing positions, traditional healing practices (e.g., smoking ceremonies, bush medicine), and burial of placenta (whenua in Māori culture).

Discuss cultural preferences with patients and families. Work within hospital protocols to accommodate safe traditional practices where possible. Seek guidance from Aboriginal Health Workers or Māori cultural liaisons.

Assessment Content

SAQ Practice Question 1

Question: A 32-year-old primigravida at 38 weeks gestation requires emergency Caesarean section for fetal distress. She has a BMI of 38 and a Mallampati class 3 airway. Her baseline blood pressure is 110/70 mmHg and heart rate 85 bpm. Describe the maternal physiological changes in pregnancy relevant to your anaesthetic management for this patient, including drug dosing considerations, positioning, and airway management strategies. (20 marks)

Model Answer:

1. Cardiovascular changes and haemodynamic management (6 marks)

   • Cardiac output increased 40-50% (stroke volume +30%, heart rate +15-20%)
   • Blood volume increased 40-50% with physiological anaemia (Hb 105-115 g/L)
   • SVR decreased 20-30%, nadir at 20-24 weeks
   • Aortocaval compression: requires left uterine displacement >15° to prevent 30% cardiac output reduction
   • Baseline BP lower; maintain SBP >90 mmHg (within 20% of baseline)
   • Induction agent doses reduced: propofol 1.5-2 mg/kg (vs 2-2.5 mg/kg non-pregnant), thiopentone 3-4 mg/kg (vs 5-7 mg/kg) due to increased cardiac output and decreased protein binding

2. Respiratory changes and pre-oxygenation (5 marks)

   • Tidal volume increased 40%, minute ventilation increased 40-50%
   • FRC decreased 20-30%, diaphragm elevated 4 cm, ribcage widened
   • Respiratory alkalosis: PaCO2 28-32 mmHg, compensated by renal bicarbonate excretion (18-22 mmol/L)
   • Oxygen consumption increased 20-30% (to 300-350 mL/min)
   • Rapid desaturation during apnoea (SpO2 <90% within 2-3 minutes)
   • Pre-oxygenation critical: 3 minutes tidal volume breathing or 8 vital capacity breaths with 100% O2

3. Airway considerations and management (5 marks)

   • Airway mucosal oedema: Mallampati class increases 1-2 grades (class 3 common in obese pregnant patients)
   • Laryngeal oedema requires smaller ETT (6.0-7.0 mm ID)
   • Increased breast tissue may impede laryngoscope blade placement
   • Video laryngoscopy recommended as first-line for grade 3-4 views
   • Cricoid pressure (30 N) with modified RSI (though controversial)
   • Prepare for difficult airway: have bougie, supraglottic airway, surgical airway equipment

4. Gastrointestinal and other considerations (4 marks)

   • Delayed gastric emptying (especially during labour), increased gastric volume
   • Decreased lower oesophageal sphincter tone (30-50% reduction)
   • High aspiration risk: >25 mL gastric volume with pH <2.5
   • Prophylaxis: ranitidine 50 mg IV, sodium citrate 30 mL 0.3 M
   • Succinylcholine 1-1.5 mg/kg (plasma cholinesterase activity increased)
   • Maintain volatile agent <1 MAC to avoid uterine relaxation and postpartum haemorrhage

Total: 20 marks

SAQ Practice Question 2

Question: A 26-year-old woman at 28 weeks gestation presents with severe pre-eclampsia (BP 175/110 mmHg, proteinuria 3+, facial and hand oedema). She requires urgent Caesarean section for worsening fetal status. Discuss the pathophysiological changes in this condition that differ from normal pregnancy, and describe your anaesthetic management including neuraxial considerations, blood pressure control, and magnesium sulfate interactions. (20 marks)

Model Answer:

1. Pre-eclampsia pathophysiology vs normal pregnancy (5 marks)

   • Normal: SVR decreased 20-30%, BP decreases 10-15 mmHg, nadir at 16-20 weeks
   • Pre-eclampsia: Vasospasm overrides normal vasodilation, SVR increased, hypertension (SBP >140 mmHg or DBP >90 mmHg)
   • Endothelial dysfunction causes increased capillary permeability (pulmonary oedema risk), proteinuria (>300 mg/24h distinguishes from normal mild proteinuria)
   • Platelet consumption: thrombocytopenia (<100 × 10⁹/L) vs normal mild decrease (100-150 × 10⁹/L)
   • HELLP syndrome variant: haemolysis, elevated liver enzymes, low platelets
   • Cerebral autoregulation impaired: risk of intracranial haemorrhage during hypertension

2. Neuraxial anaesthesia considerations (5 marks)

   • Preferred over GA (avoid difficult airway, hypertensive response to intubation)
   • Spinal safe in stable pre-eclamptics: hypotension less severe due to increased SVR
   • Epidural allows titratable block; CSE provides rapid onset + catheter flexibility
   • Platelet threshold: ≥70 × 10⁹/L considered safe if stable, no coagulopathy (SOAP/ACOG consensus)
   • Contraindications: thrombocytopenia <50 × 10⁹/L, coagulopathy, active bleeding, severe pulmonary oedema
   • Reduced local anaesthetic dose required due to exaggerated spinal/epidural spread

3. Blood pressure management (5 marks)

   • Target: SBP 140-150 mmHg, DBP 90-100 mmHg (avoid overshoot below 120/70 mmHg)
   • Pre-induction control: labetalol 20 mg IV bolus (repeat to 200 mg), hydralazine 5 mg IV (repeat to 20 mg), or nifedipine 10 mg SL
   • Intraoperative control: esmolol 25-50 mg bolus ± infusion blunts catecholamine response to intubation
   • Neuraxial hypotension: phenylephrine 50-100 μg IV boluses (maintain MAP >65 mmHg)
   • Avoid ephedrine (may cause fetal acidosis, crosses placenta more readily)
   • Invasive arterial monitoring recommended for severe pre-eclampsia (SBP >160 mmHg, MAP >110 mmHg)

4. Magnesium sulfate interactions and monitoring (5 marks)

   • MgSO4 for seizure prophylaxis: 4 g IV loading over 15-20 min, then 1-2 g/hour infusion
   • Potentiates NMBAs: reduces acetylcholine release at neuromuscular junction
   • Succinylcholine: prolonged block (reduced dose to 0.8-1 mg/kg)
   • Rocuronium/vecuronium: potentiated, reduce dose 30-50%, mandatory TOF monitoring
   • Neuromuscular monitoring required before extubation (TOF ratio >0.9)
   • MgSO4 toxicity monitoring: patellar reflexes (loss at 3-5 mmol/L), respiratory depression (>5 mmol/L), cardiac arrest (>7-8 mmol/L)
   • Calcium gluconate 10 mL 10% IV for severe MgSO4 toxicity (cardiac arrhythmias, respiratory arrest)

Total: 20 marks

Final Clinical Viva Scenario

Setting: ANZCA Final Clinical Viva (20 minutes)

Topic: Maternal Physiological Changes in Pregnancy

Examiner: Thank you. Today we're going to discuss maternal physiological changes in pregnancy and their relevance to obstetric anaesthesia. Let's begin with the cardiovascular system. Can you describe the cardiovascular adaptations that occur during pregnancy?

Candidate: Pregnancy induces profound cardiovascular changes beginning at 5-8 weeks gestation, with maximum effect by 28-32 weeks. Cardiac output increases 40-50% from a baseline of 5 L/min to approximately 7-7.5 L/min at term. This increase is driven by two components: stroke volume increases by 30-35% in the first trimester, plateauing thereafter, while heart rate increases by 15-20%, reaching 80-95 bpm by the third trimester.

Systemic vascular resistance decreases by 20-30% due to progesterone-mediated vasodilation and the low-resistance placental circulation. Mean arterial pressure typically decreases by 10-15 mmHg, reaching its lowest point at 16-20 weeks before returning to baseline by term. Blood volume expands by 40-50%, from approximately 5 L to 7-7.5 L, with a disproportionate increase in plasma volume (50-60%) compared to red cell mass (20-30%). This results in physiological anaemia with haemoglobin of 105-115 g/L.

Examiner: Excellent. How do these changes affect your anaesthetic management, particularly drug dosing and positioning?

Candidate: The increased cardiac output and decreased protein binding affect drug pharmacokinetics. Induction agents are administered in reduced doses: thiopentone 3-4 mg/kg compared to 5-7 mg/kg in non-pregnant patients, propofol 1.5-2 mg/kg versus 2-2.5 mg/kg, and ketamine 1 mg/kg versus 1.5-2 mg/kg. These dose reductions are necessary because increased cardiac output delivers a larger proportion of the administered dose to the brain rapidly, achieving higher peak plasma concentrations.

Positioning is critical, particularly left uterine displacement. After 20 weeks gestation, the gravid uterus can compress the inferior vena cava and aorta, reducing cardiac output by up to 30% in the supine position. We achieve displacement of at least 15° through manual leftward uterine displacement or right lateral tilt of the operating table. This is mandatory for all anaesthetic procedures after 20 weeks.

Regarding blood pressure management, we target systolic blood pressure within 20% of the patient's baseline. Since baseline blood pressure is typically lower in pregnancy due to decreased systemic vascular resistance, for most term parturients we aim to maintain SBP above 90 mmHg. Hypotension reduces uteroplacental perfusion, which can cause fetal compromise.

Examiner: Good. Now let's move to the respiratory system. What are the key respiratory changes in pregnancy?

Candidate: Minute ventilation increases by 40-50%, from approximately 7.5 L/min to 10-11 L/min. This increase is achieved primarily through increased tidal volume, which rises by 40% from 500 mL to about 700 mL, with relatively minimal change in respiratory rate. The increased alveolar ventilation, coupled with decreased anatomical dead space, results in respiratory alkalosis with PaCO2 of 28-32 mmHg, PaO2 of 100-105 mmHg, and pH of 7.40-7.45. The kidneys compensate by excreting bicarbonate, typically to 18-22 mmol/L.

Functional residual capacity decreases by 20-30%, from approximately 3 L to 2-2.5 L. This reduction is caused by diaphragm elevation of approximately 4 cm due to the enlarging uterus, ribcage widening with the subcostal angle increasing from 68° to 103°, and reduced chest wall compliance. Expiratory reserve volume decreases most dramatically, by up to 50%, while residual volume decreases by 15-20%. These changes are clinically significant because they lead to rapid oxygen desaturation during apnoea, with SpO2 typically falling below 90% within 2-3 minutes compared to 5-8 minutes in non-pregnant patients.

Examiner: How do these respiratory changes affect your anaesthetic management, particularly regarding pre-oxygenation and airway management?

Candidate: Pre-oxygenation is absolutely critical given the decreased functional residual capacity and increased oxygen consumption (which increases by 20-30% to 300-350 mL/min). We achieve effective pre-oxygenation through either 3 minutes of tidal volume breathing with 100% oxygen or 8 vital capacity breaths. Positioning is important; we may use a head-up position of 20-30° or semi-recumbent position to improve functional residual capacity.

Airway management is affected by several factors. Oestrogen-mediated mucosal engorgement causes narrowing of the upper airway diameter. Mallampati class typically increases by 1-2 grades from the first to third trimester. Vocal cords may be oedematous, requiring smaller endotracheal tubes, typically 6.0-7.0 mm internal diameter. Nasal stuffiness and epistaxis are common due to mucosal oedema.

Video laryngoscopy is increasingly recommended as first-line for obstetric intubation due to improved glottic visualisation, particularly in patients with airway oedema. We must have difficult airway equipment readily available, including smaller endotracheal tubes, a bougie, supraglottic airway devices such as the LMA Classic or LMA Supreme, and equipment for surgical airway.

Examiner: Thank you. Let's discuss the gastrointestinal changes. What are the key alterations, and how do they affect aspiration risk?

Candidate: Progesterone causes decreased lower oesophageal sphincter tone by 30-50%. Additionally, physical displacement of the stomach by the enlarging uterus increases intra-abdominal pressure. Combined, these factors increase the risk of gastro-oesophageal reflux, with approximately 30-50% of pregnant women experiencing symptoms.

Gastric emptying is delayed by 30-50% during pregnancy, particularly during labour where the delay extends to more than 2 hours. Gastric volume is increased. Studies show that in most term pregnant women, gastric pH is less than 2.5 and gastric volumes exceed 25 mL. These changes create the classic "full stomach" obstetric patient with high aspiration risk.

For prophylaxis against aspiration, we administer a histamine H2-receptor antagonist such as ranitidine 50 mg intravenously and sodium citrate 30 mL of 0.3 molar solution before induction. Rapid sequence induction with cricoid pressure at 30 N is standard for general anaesthesia, though there is ongoing controversy about the efficacy and potential disadvantages of cricoid pressure.

Examiner: Excellent. You mentioned cricoid pressure is controversial. What are the arguments for and against its use in obstetric anaesthesia?

Candidate: Arguments for cricoid pressure include that it may reduce the risk of passive regurgitation by compressing the oesophagus between the cricoid cartilage and cervical vertebrae. In obstetric patients with delayed gastric emptying and lower oesophageal sphincter relaxation, the theoretical benefit is attractive.

However, several arguments against cricoid pressure have emerged in recent years. Studies have shown that cricoid pressure may worsen laryngeal view during laryngoscopy, particularly in obese patients or those with limited neck mobility, which are common in obstetric populations. It may also cause distortion of airway anatomy, making tube passage more difficult. There is debate about whether it actually prevents regurgitation, as the oesophagus may not be directly posterior to the cricoid cartilage in all patients, particularly in pregnancy where anatomical relationships may be altered.

Current practice varies among institutions. Many anaesthetists continue to use cricoid pressure for obstetric rapid sequence induction given the high aspiration risk, but they should be prepared to release it if it impedes intubation. The key is that cricoid pressure should not be prioritised over achieving successful airway management in a timely fashion.

Examiner: Good. Now let's discuss coagulation changes. What are the key alterations in the coagulation system during pregnancy?

Candidate: Pregnancy is a hypercoagulable state, representing an evolutionary adaptation to protect against haemorrhage at delivery. Most clotting factors increase: fibrinogen rises to 400-600 mg/dL, factor VII increases 2-3 fold, factor VIII increases 2 fold, and factor X increases 2 fold. Fibrinolysis is decreased through increased plasminogen activator inhibitors, particularly PAI-1 and PAI-2. Prothrombin time and activated partial thromboplastis time remain unchanged despite these changes, but thromboelastography shows increased clot strength and decreased lysis.

Platelet count decreases slightly by 10-15% from non-pregnant baseline due to haemodilution. Normal pregnancy values are 100-150 × 10⁹/L. Thrombocytopenia below 100 × 10⁹/L requires investigation for causes such as gestational thrombocytopenia, pre-eclampsia, HELLP syndrome, or immune thrombocytopenic purpura. Platelet function is actually enhanced during pregnancy.

Examiner: How do these coagulation changes affect your anaesthetic management, particularly regarding neuraxial techniques?

Candidate: The hypercoagulable state increases the risk of venous thromboembolism by 5-10 fold compared to non-pregnant patients, with an incidence of 1-2 per 1000 pregnancies. Deep vein thrombosis is more common in the left leg, occurring in approximately 80% of cases due to compression of the left iliac vein by the right iliac artery and overlying gravid uterus. This reinforces the importance of appropriate thromboprophylaxis and early mobilisation postpartum.

For neuraxial techniques, the concern is the rare but potentially catastrophic complication of spinal-epidural haematoma. We assess coagulation status before neuraxial placement. The current consensus from the Society for Obstetric Anesthesia and Perinatology and the American College of Obstetricians and Gynecologists suggests that neuraxial anaesthesia is generally safe with a platelet count of at least 70 × 10⁹/L, provided the count is stable, there is no concurrent coagulopathy, and the patient is not on antiplatelet therapy. For platelet counts between 50,000 and 70,000, the decision should be individualised based on airway difficulty and urgency of delivery.

In clinical practice, we review the coagulation profile, specifically platelet count and coagulation studies, prior to neuraxial procedures. We should avoid neuraxial techniques in patients with platelet counts below 50 × 10⁹/L, known coagulopathy, or current anticoagulation. For patients with borderline platelet counts, we weigh the risks and benefits, considering that general anaesthesia in the obstetric population carries a higher risk of failed intubation and aspiration.

Examiner: Thank you. This has been a comprehensive discussion. Let's finish with a clinical scenario. You're called to the labour ward for a 30-year-old primigravida at 38 weeks who requires urgent Caesarean section for fetal distress. She's obese with a BMI of 40, has a Mallampati class 3 airway, and is anxious. Her blood pressure is 125/75 mmHg and heart rate 88 bpm. Walk me through your anaesthetic management.

Candidate: My first priority would be a focused but thorough assessment. I would confirm the urgency of the situation, assess the fetal status, and evaluate the maternal airway given her obesity and Mallampati class 3. I would check her fasting status, any prior anaesthetic history, and current medications. I would review blood results if available, particularly coagulation status. I would establish rapport with the patient, explain the procedure, and obtain informed consent.

For preparation, I would ensure the operating room is ready with appropriate equipment. Given her airway and obesity, I would have video laryngoscope available, smaller endotracheal tubes (6.0-6.5 mm), a bougie, and supraglottic airway devices as backup. I would check that difficult airway cart is accessible. I would establish large-bore intravenous access, preferably 16-gauge or larger. I would ensure monitoring is connected: ECG, non-invasive blood pressure with 1-2 minute intervals, pulse oximetry, and capnography. I would have vasopressors prepared: phenylephrine 100 μg/mL for boluses, and have ephedrine and norepinephrine available.

I would pre-oxygenate the patient with 100% oxygen using a tight-fitting mask, ideally for 3 minutes of tidal volume breathing, or 8 vital capacity breaths if time is limited. I would position her in the ramped position using pillows or a ramp to align external auditory meatus with sternal notch, which improves laryngoscopic view. I would ensure left uterine displacement of at least 15°, either manually or through right lateral tilt.

Regarding anaesthetic technique, I would strongly consider neuraxial anaesthesia as the primary option. Spinal anaesthesia would provide rapid onset, which is advantageous given the urgency. Epidural, if already in situ for labour, could be topped up. Combined spinal-epidural offers both rapid onset and the flexibility of a catheter. If neuraxial anaesthesia is contraindicated or if the patient declines it, I would proceed with modified rapid sequence induction.

For general anaesthesia, I would administer premedication with ranitidine 50 mg IV and sodium citrate 30 mL if not already given. I would apply cricoid pressure at 30 N during induction. For induction agents, I would use propofol 1.5-2 mg/kg (accounting for her increased cardiac output) or thiopentone 3-4 mg/kg. I would administer succinylcholine 1-1.5 mg/kg for paralysis. After intubation, I would maintain anaesthesia with volatile agents at low concentration (0.5-0.75 MAC) combined with 50-70% nitrous oxide in oxygen. I would avoid high concentrations of volatile agents to prevent uterine relaxation and postpartum haemorrhage.

I would monitor blood pressure closely after spinal induction, treating hypotension with phenylephrine 50-100 μg IV boluses to maintain systolic blood pressure above 90 mmHg, which is within 20% of her baseline. I would monitor fetal heart rate throughout the procedure. After delivery, I would administer oxytocin 10 IU intramuscularly and consider an infusion. I would continue maintenance of anaesthesia, transitioning to lighter planes as appropriate. At emergence, I would ensure full reversal of neuromuscular blockade with TOF ratio greater than 0.9 before extubation.

Examiner: Excellent. Thank you for your comprehensive discussion.

Final Medical Viva Scenario

Setting: ANZCA Final Medical Viva (20 minutes)

Topic: Medical Problem-Solving in Maternal Physiology

Examiner: Good morning. Today we're going to discuss medical problem-solving related to maternal physiological changes in pregnancy. I have a series of short-answer questions for you. Let's begin.

Candidate: Good morning. I'm ready.

Examiner: Question 1: A 28-year-old woman at 34 weeks gestation presents for appendicectomy. Her pre-induction blood pressure is 95/60 mmHg. Is this concerning, and why or why not?

Candidate: This blood pressure is not concerning and is actually typical for pregnancy. During normal pregnancy, systemic vascular resistance decreases by 20-30%, reaching its nadir at 16-20 weeks gestation. This results in a decrease in mean arterial pressure of approximately 10-15 mmHg. A blood pressure of 95/60 mmHg at 34 weeks is within the expected range. What would be concerning would be a blood pressure significantly lower than this, which could indicate haemorrhage, sepsis from a perforated appendix, or other pathological processes. The key is to compare this blood pressure to her baseline if known, and to monitor for other signs of inadequate perfusion such as tachycardia, oliguria, or altered mental status.

Examiner: Good. Question 2: You perform a rapid sequence induction on this patient. Shortly after intubation, her oxygen saturation falls from 99% to 88% within 90 seconds. Why does this happen more rapidly in pregnancy than in non-pregnant patients?

Candidate: This rapid desaturation is due to several physiological changes in pregnancy. First, functional residual capacity decreases by 20-30% in pregnancy due to diaphragm elevation from the enlarging uterus and ribcage widening. This reduced oxygen reservoir means there's less oxygen stored in the lungs to draw upon during apnoea. Second, oxygen consumption increases by 20-30% to 300-350 mL/min due to the increased metabolic demands of the fetus and placenta. The combination of decreased oxygen stores and increased oxygen consumption leads to much more rapid desaturation during apnoea, typically within 2-3 minutes compared to 5-8 minutes in non-pregnant patients. This is why pre-oxygenation is absolutely critical in obstetric patients, using either 3 minutes of tidal volume breathing with 100% oxygen or 8 vital capacity breaths to maximise oxygen reserves.

Examiner: Excellent. Question 3: During the procedure, you notice the endotracheal tube is relatively large for her airway and there's some resistance on passage. What physiological change explains this?

Candidate: The endotracheal tube may appear relatively large because of airway mucosal oedema, a common physiological change in pregnancy. Oestrogen causes mucosal engorgement throughout the upper airway, including the pharynx, larynx, and trachea. This narrows the airway diameter and can increase Mallampati class by 1-2 grades from the first to third trimester. The vocal cords themselves may be oedematous. This is why we typically use smaller endotracheal tubes for obstetric intubation, usually 6.0-7.0 mm internal diameter, compared to 7.5-8.5 mm for non-pregnant adult females. Additionally, increased breast tissue in pregnancy can sometimes impede laryngoscope blade placement, contributing to difficulties. Video laryngoscopy is often helpful in these situations as it provides a better view of the glottis without requiring direct line-of-sight.

Examiner: Good. Question 4: After the procedure, the patient develops a severe headache that worsens with sitting and improves with lying flat. What is this, and how is it related to her pregnancy physiology?

Candidate: This is characteristic of a post-dural puncture headache, or PDPH. The headache is due to cerebrospinal fluid leak through a dural defect, causing traction on pain-sensitive intracranial structures when upright. While PDPH can occur in any patient undergoing neuraxial procedures, it's particularly relevant in obstetrics because epidural analgesia is commonly used for labour. The incidence of accidental dural puncture with a Tuohy needle is approximately 0.5-1.5%, and of those, 50-80% develop PDPH.

Pregnancy physiology contributes to this presentation in several ways. First, the engorged epidural veins in pregnancy may increase the risk of inadvertent dural puncture. Second, there may be altered CSF dynamics during pregnancy that affect symptom presentation. Treatment ranges from conservative measures including bed rest, hydration, and caffeine, to epidural blood patch, which has a success rate of approximately 90% when performed 24-48 hours after the dural puncture.

Examiner: Excellent. Question 5: A different patient, a 35-year-old at 39 weeks, undergoes spinal anaesthesia for elective Caesarean section. Shortly after spinal placement, her blood pressure drops from 130/80 mmHg to 75/45 mmHg and her heart rate increases to 110 bpm. You administer phenylephrine rather than ephedrine. Why?

Candidate: I choose phenylephrine as the first-line vasopressor for spinal-induced hypotension in obstetrics for several reasons. Phenylephrine is a pure alpha-1 agonist that causes vasoconstriction without crossing the placenta significantly or stimulating fetal metabolism. Ephedrine, in contrast, crosses the placenta readily and can cause fetal acidosis by stimulating fetal metabolism and increasing oxygen consumption.

The physiological basis for this choice relates to the different haemodynamic profiles. While both drugs increase maternal blood pressure, phenylephrine tends to cause reflex bradycardia, whereas ephedrine increases heart rate. However, several randomised controlled trials have shown that phenylephrine results in better fetal acid-base status compared to ephedrine. Current consensus guidelines from the Society for Obstetric Anesthesia and Perinatology recommend phenylephrine as first-line for prophylaxis and treatment of spinal-induced hypotension in obstetric patients, typically in bolus doses of 50-100 μg.

Ephedrine is reserved for situations where spinal-induced hypotension is accompanied by significant bradycardia, where its mild beta-1 agonist activity may be beneficial. In my patient with a heart rate of 110 bpm, phenylephrine is appropriate as it will increase blood pressure while potentially bringing the heart rate down to a more normal range through reflex mechanisms.

Examiner: Very good. Question 6: Why is physiological anaemia in pregnancy not an indication for transfusion in the absence of symptoms or active bleeding?

Candidate: Physiological anaemia in pregnancy is not true anaemia but rather a haemodilution effect. Blood volume increases by 40-50% during pregnancy, with a disproportionate increase in plasma volume (50-60%) compared to red cell mass (20-30%). This results in haemoglobin of 105-115 g/L, which is lower than the non-pregnant normal range of 120-150 g/L but is physiologically appropriate for pregnancy. This "dilutional anaemia" is actually beneficial as it optimises oxygen delivery despite increased metabolic demands by reducing blood viscosity and improving placental perfusion.

The key point is that in physiological anaemia, oxygen-carrying capacity is maintained because the increased blood volume compensates for the decreased haemoglobin concentration. The body has also adapted to this lower haemoglobin level through increased cardiac output and right-shifted oxygen dissociation curve. Transfusion is only indicated if haemoglobin falls below 70 g/L in an asymptomatic patient, or below 80-90 g/L in a symptomatic patient or one with active bleeding, because below these thresholds the oxygen-carrying capacity becomes inadequate for the increased metabolic demands of pregnancy.

Examiner: Excellent. Question 7: A patient at 30 weeks gestation has arterial blood gas results showing pH 7.46, PaCO2 30 mmHg, PaO2 102 mmHg, and HCO3- 21 mmol/L. Are these results concerning?

Candidate: These results are normal for pregnancy and are not concerning. The pH of 7.46 and PaCO2 of 30 mmHg represent the expected respiratory alkalosis of pregnancy. Minute ventilation increases by 40-50%, primarily through increased tidal volume, causing increased CO2 elimination and respiratory alkalosis with PaCO2 typically 28-32 mmHg. The kidneys compensate by excreting bicarbonate, typically to 18-22 mmol/L, so the pH remains near-normal at 7.40-7.45.

The PaO2 of 102 mmHg reflects the improved oxygenation in pregnancy due to increased tidal volume and alveolar ventilation. If these results were concerning, I would expect either a more severe alkalosis (pH >7.50, PaCO2 <25 mmHg), which might indicate pathological hyperventilation from pain, anxiety, pulmonary embolism, or early sepsis, or metabolic acidosis, which could indicate pre-eclampsia with placental insufficiency, maternal hypoxia, or sepsis. But the values presented are within the normal range for pregnancy and represent successful renal compensation for respiratory alkalosis.

Examiner: Good. Question 8: During a postpartum haemorrhage, you notice the patient's blood pressure remains stable despite significant blood loss. Why might this happen, and what are the implications?

Candidate: This can occur due to the physiological adaptations of pregnancy that provide relative haemodynamic stability. Blood volume increases by 40-50% during pregnancy, creating a physiological reserve that buffers against hypotension in early blood loss. Additionally, the decreased systemic vascular resistance of pregnancy may initially maintain blood pressure even as cardiac output begins to fall.

The concerning implication is that blood pressure may be a late sign of haemodynamic compromise in obstetric patients. By the time hypotension develops, significant blood loss has already occurred, and the patient may be in compensated shock with tachycardia, oliguria, or other signs of inadequate perfusion. This is why monitoring for early signs of shock is critical in obstetrics, rather than relying solely on blood pressure.

Furthermore, in the immediate postpartum period, uterine contraction causes autotransfusion of 500-1000 mL blood from the uteroplacental circulation back into the systemic circulation. This autotransfusion can temporarily maintain blood pressure despite ongoing blood loss, creating a false sense of stability that can lead to under-resuscitation. It's therefore important to assess for other signs of adequate perfusion, such as urine output (>0.5 mL/kg/hr), lactate (<2 mmol/L), and mental status, and to have a low threshold for invasive monitoring and blood product administration in postpartum haemorrhage.

Examiner: Excellent. Thank you for your clear and thorough answers.

Key Learning Points:

• Blood pressure decreases 10-15 mmHg in pregnancy (95/60 mmHg at 34 weeks is normal) (PMID: 28445822)
• Rapid desaturation within 2-3 minutes due to decreased FRC (20-30%) and increased oxygen consumption (20-30%) (PMID: 29543469)
• Airway mucosal oedema requires smaller ETT (6.0-7.0 mm) due to oestrogen-mediated engorgement (PMID: 31124362)
• Post-dural puncture headache (PDPH) incidence 50-80% after accidental dural puncture; epidural blood patch 90% success rate (PMID: 29782215)
• Phenylephrine preferred over ephedrine for spinal hypotension (better fetal acid-base status, less placental transfer) (PMID: 30194848)
• Physiological anaemia Hb 105-115 g/L due to haemodilution; transfusion only if Hb <70 g/L asymptomatic (PMID: 27886186)
• Respiratory alkalosis PaCO2 28-32 mmHg, pH 7.40-7.45, HCO3- 18-22 mmol/L (PMID: 29543469)
• Blood pressure is a late sign of shock in obstetrics; 40-50% increased blood volume creates reserve (PMID: 28445822)

Marking Guide: 25 marks

• Knowledge: 10/25 (understanding of maternal physiological changes)
• Application: 10/25 (clinical reasoning and problem-solving)
• Communication: 5/25 (clear, concise responses)

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