Hypertrophic Cardiomyopathy - Anaesthetic Considerations

Quick Answer

Hypertrophic cardiomyopathy (HCM) is the most common inherited cardiac disorder (1:500 population), characterised by asymmetric left ventricular hypertrophy with myocardial disarray, presenting significant anaesthetic challenges due to dynamic left ventricular outflow tract (LVOT) obstruction and diastolic dysfunction. The fundamental principle of perioperative management is maintaining afterload and avoiding tachycardia, hypovolemia, and increased contractility—all factors that exacerbate the dynamic LVOT gradient. Patients with resting gradients >50 mmHg or provocable gradients >80 mmHg are at highest risk for haemodynamic collapse. Preoperative assessment must include echocardiographic evaluation of LVOT gradient, degree of hypertrophy, mitral regurgitation severity, and identification of sudden cardiac death risk factors (massive LVH >30 mm, family history of SCD, unexplained syncope, non-sustained ventricular tachycardia). Anaesthetic technique should employ high-dose opioid-based technique with phenylephrine as first-line vasopressor (pure alpha-agonist avoiding beta-activity), generous fluid loading (10-20 mL/kg crystalloid), and maintenance of sinus rhythm. β-blockers and disopyramide should be continued perioperatively. Suxamethonium is relatively contraindicated due to fasciculation-related catecholamine surge; rocuronium is preferred with sugammadex reversal. Postoperatively, these patients require HDU/ICU monitoring with continuous arterial line and ECG monitoring for 24-48 hours. The 2024 AHA/ACC/HRS guidelines recommend ICD implantation for primary prevention in patients with ≥1 major risk factor or 5-year risk of SCD ≥6%. Perioperative mortality for non-cardiac surgery is 0.5-2% in specialised centres but rises to 5-10% in high-risk patients with poor baseline control. [1-8]

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Indigenous Health Considerations

Aboriginal and Torres Strait Islander Health

Aboriginal and Torres Strait Islander peoples in Australia experience a disproportionate burden of cardiovascular disease, with HCM often presenting late in the disease course due to barriers in accessing specialist cardiac care [9]. Indigenous Australians living in rural and remote communities face significant challenges in receiving genetic counselling and cascade screening for family members, which is essential for HCM management given its autosomal dominant inheritance pattern [10]. The life expectancy gap (8-10 years) contributes to under-recognition of inherited cardiomyopathies in First Nations communities, with many cases only identified after cardiac events [11]. Cultural safety considerations include the importance of family-centred decision-making—genetic testing discussions must involve extended kinship networks, not just the individual patient [12]. Many Indigenous communities have experienced historical trauma from medical research, necessitating transparent communication about genetic testing purposes and data sovereignty [13]. Language barriers and health literacy challenges require the involvement of Aboriginal Health Workers (AHWs) and Aboriginal Liaison Officers (ALOs) to ensure understanding of the lifelong nature of HCM monitoring and the importance of medication compliance [14]. For patients requiring complex surgery, cultural obligations around Sorry Business (bereavement practices) and the need for family presence at tertiary centres create additional logistical and financial burdens that must be proactively addressed through patient travel schemes and cultural support [15].

Māori Health

Māori populations in Aotearoa New Zealand face similar cardiovascular health disparities, with higher rates of sudden cardiac death in younger age groups compared to non-Māori [16]. The Te Whare Tapa Whā model of health (holistic wellbeing incorporating physical, mental, social, and spiritual dimensions) is particularly relevant for HCM management, which requires lifelong medical engagement [17]. Whānau (extended family) involvement in healthcare decisions is culturally expected, and discussions around genetic testing, ICD implantation, and surgical risk must include family members [18]. Data sovereignty is a critical concern—Māori communities have advocated for genetic data to remain under Māori control through established governance frameworks [19]. The principles of Te Tiriti o Waitangi (Treaty of Waitangi) require equitable access to specialist cardiac services, yet Māori patients with HCM often experience delayed diagnosis due to socioeconomic barriers and geographic isolation [20]. Culturally safe care includes acknowledging the spiritual dimension (wairua) of heart conditions—Māori may view heart disease through both biomedical and traditional lenses, requiring respectful integration of both perspectives [21]. Māori Health Workers and cultural navigators play essential roles in facilitating communication and ensuring care plans align with whānau obligations and cultural practices [22].

Rural and Remote Considerations

For Indigenous patients in rural and remote Australia and New Zealand, HCM management presents unique challenges. The Royal Flying Doctor Service (RFDS) may be required for emergency transfer of unstable patients, with aeromedical retrieval considerations including altitude-related hypoxia effects on dynamic LVOT obstruction [23]. Telemedicine consultations with cardiogenetics specialists are essential for cascade screening in remote communities, though limited bandwidth and technology access can impede video consultations [24]. Many remote communities lack the infrastructure for ICD implantation and follow-up, requiring careful coordination with tertiary centres [25]. Community-based cardiac rehabilitation programs must be culturally adapted and accessible, recognising that standard urban models may not translate effectively to remote Indigenous contexts [26].

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Pathophysiology

Genetic Basis and Phenotypic Expression

Hypertrophic cardiomyopathy is caused by autosomal dominant mutations in sarcomeric protein genes, most commonly MYBPC3 and MYH7, encoding myosin-binding protein C and β-myosin heavy chain respectively [27]. Over 1,500 pathogenic variants have been identified, with variable penetrance and expressivity resulting in diverse phenotypes even within families [28]. The characteristic histopathological features include:

• Myocyte disarray: Chaotic arrangement of cardiac muscle cells [29]
• Interstitial fibrosis: Progressive replacement fibrosis contributing to diastolic dysfunction [30]
• Small vessel disease: Intramural coronary artery abnormalities causing microvascular ischaemia [31]
• Hypertrophy patterns: Asymmetric septal hypertrophy (most common), apical, concentric, or mid-ventricular variants [32]

Dynamic LVOT Obstruction

The pathophysiological hallmark is dynamic obstruction of the LVOT due to systolic anterior motion (SAM) of the mitral valve apparatus against the hypertrophied septum [33]. This creates a pressure gradient that varies with loading conditions:

[34-38]

Diastolic Dysfunction

Impaired ventricular relaxation and reduced compliance result in elevated filling pressures, particularly during tachycardia when diastolic filling time is shortened [39]. This creates a "preload-dependent" circulation where maintenance of sinus rhythm and adequate filling pressures are critical [40].

Myocardial Ischaemia

Despite epicardial coronary arteries being typically normal, patients experience supply-demand mismatch ischaemia due to:

• Wall stress from massive hypertrophy [41]
• Microvascular dysfunction from small vessel disease [42]
• Reduced coronary vasodilator reserve [43]
• Diastolic compression of intramural vessels [44]

Arrhythmogenesis

The substrate for ventricular arrhythmias includes:

• Myocardial disarray creating electrical heterogeneity [45]
• Fibrosis providing re-entry circuits [46]
• Myocardial scarring from microvascular ischaemia [47]
• Left atrial enlargement predisposing to atrial fibrillation [48]

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Clinical Presentation and Classification

Phenotypic Variants

1. Obstructive HCM (HOCM): Resting gradient ≥30 mmHg
2. Non-obstructive HCM (HNCM): No resting or provocable obstruction
3. Apical HCM: Hypertrophy confined to apex; associated with giant negative T-waves on ECG
4. Mid-ventricular obstruction: Cavity obliteration creating apical aneurysm
5. Massive concentric hypertrophy: Symmetric wall thickening >30 mm [49-53]

Sudden Cardiac Death Risk Stratification

The 2024 AHA/ACC guidelines use the HCM Risk-SCD calculator incorporating:

5-year SCD risk categories:

• Low risk: <4%—routine follow-up
• Intermediate risk: 4-6%—consider ICD after shared decision-making
• High risk: ≥6%—ICD generally indicated [54-56]

Symptoms

• Dyspnoea: Exertional, from diastolic dysfunction and elevated filling pressures
• Chest pain: Atypical, often post-prandial or nocturnal; microvascular angina
• Syncope: Exercise-related (exacerbated dynamic obstruction) or arrhythmic
• Palpitations: Atrial fibrillation (20-25% lifetime risk), ventricular arrhythmias [57-60]

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Preoperative Assessment

Essential Investigations

Echocardiography (Crucial)

• LV wall thickness (maximum and distribution)
• Resting and provocable LVOT gradient (Valsalva, amyl nitrite)
• Mitral valve anatomy and SAM severity
• Degree of mitral regurgitation
• Systolic and diastolic function
• Pulmonary artery pressures [61-63]

Cardiac MRI

• Late gadolinium enhancement (fibrosis burden—arrhythmic risk)
• Apical variant identification
• Quantification of myocardial mass [64,65]

24-hour Holter Monitoring

• Detection of non-sustained VT
• Atrial arrhythmia burden
• Heart rate variability [66]

Cardiopulmonary Exercise Testing

• Functional capacity assessment
• Exercise-induced gradient provocation
• Arrhythmia provocation [67]

Genetic Counselling/Testing

• Cascade screening of first-degree relatives
• Prognostic implications of specific mutations [68,69]

Risk Stratification for Surgery

Medication Optimisation

Continue:

• β-blockers (reduce contractility, heart rate)
• Non-dihydropyridine calcium channel blockers (verapamil, diltiazem)
• Disopyramide (negative inotrope, reduces SAM)
• Amiodarone (if indicated for arrhythmia control)

Consider withholding on morning of surgery:

• ACE inhibitors/ARBs (hypotension risk with anaesthesia induction) [74-77]

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Anaesthetic Management

Goals and Principles

Primary Objectives:

1. Maintain afterload (avoid vasodilation)
2. Maintain preload (avoid hypovolemia)
3. Avoid tachycardia (maintain heart rate 50-70 bpm)
4. Avoid increased contractility
5. Maintain sinus rhythm [78-81]

Monitoring

Standard:

• 5-lead ECG (lead II for rhythm, V5 for ischaemia)
• Arterial line (continuous BP, arterial blood gas)
• Central venous pressure (preload assessment—maintain 8-12 mmHg)
• Urinary catheter (fluid balance)
• Temperature monitoring [82]

Consider:

• Pulmonary artery catheter (complex cases, severe pulmonary hypertension)
• TOE (real-time LVOT gradient assessment, filling status)
• BIS monitoring (avoidance of light anaesthesia with catecholamine surge) [83,84]

Induction

Premedication:

• Continue β-blockers morning of surgery
• Anxiolysis with cautious benzodiazepine dosing (avoid respiratory depression)
• Adequate analgesia to prevent catecholamine surge [85]

Induction Agents:

• Etomidate: Preferred—minimal cardiovascular effects, maintains afterload [86]
• Propofol: Use cautiously—causes vasodilation; small incremental doses with phenylephrine ready
• Ketamine: Avoid—sympathomimetic effects increase contractility and heart rate
• Thiopentone: Historically used but now rarely available [87-89]

Muscle Relaxants:

• Rocuronium: Preferred—no histamine release, no fasciculations
• Suxamethonium: Relative contraindication—fasciculations increase oxygen demand and catecholamines
• Cisatracurium: Acceptable—Hofmann elimination, cardiovascularly stable [90,91]

Maintenance

Preferred Technique: High-dose opioid-based balanced anaesthesia with low-dose volatile agent or TIVA [92-94]

Rationale:

• Opioids (fentanyl, remifentanil) provide analgesia without cardiovascular depression
• Minimal volatile requirement reduces vasodilation risk
• Avoidance of sympathetic stimulation [95]

Volatile Agents:

• All modern agents acceptable at <0.5-0.8 MAC
• Sevoflurane and isoflurane provide some cardioprotection via preconditioning
• Desflurane: avoid—sympathomimetic effects with rapid increases in concentration [96,97]

TIVA Alternative:

• Propofol + remifentanil infusion
• Caution with propofol-induced vasodilation [98]

Haemodynamic Management

Vasopressors:

• Phenylephrine: First-line—pure α-agonist increases afterload without β-activity [99]
• Vasopressin: Alternative—no inotropic effect, maintains coronary perfusion [100]
• Metaraminol: Acceptable—similar profile to phenylephrine [101]
• Noradrenaline: Use cautiously—has β-activity; may increase contractility and heart rate [102]
• Avoid: Adrenaline (epinephrine), dopamine, dobutamine—all increase contractility and heart rate [103]

Fluid Management:

• Generous crystalloid loading (10-20 mL/kg pre-induction if NPO status allows)
• Maintain CVP 8-12 mmHg
• Blood products as indicated—avoidance of anaemia (Hb <80 g/L increases risk)
• Consider albumin for volume expansion [104-106]

Heart Rate Control:

• Target 50-70 bpm
• Bolus esmolol (100-500 mcg/kg) for acute tachycardia—ultra-short acting
• Metoprolol (1-5 mg IV) for sustained tachycardia
• Amiodarone (150-300 mg IV) for atrial fibrillation with rapid ventricular response [107,108]

Regional Anaesthesia Considerations

Neuraxial Blockade:

• High risk: Sympathetic blockade causes precipitous afterload reduction
• If essential for surgery (e.g., caesarean section), use gradual epidural titration with:
  • Aggressive preloading (20-30 mL/kg crystalloid)
  • Phenylephrine infusion prepared (50-100 mcg/min)
  • Low concentration local anaesthetic (0.0625-0.125% bupivacaine)
  • Avoid high spinal anaesthesia [109-111]

Peripheral Nerve Blocks:

• Generally acceptable—minimal systemic effects
• Caution with large volume blocks causing systemic local anaesthetic absorption [112]

Emergency Management

Acute LVOT Obstruction/Haemodynamic Collapse:

1. Call for help, notify surgeon
2. Stop surgical stimulation if possible
3. Trendelenburg position (increase preload)
4. Volume bolus 500-1000 mL crystalloid
5. Phenylephrine 50-100 mcg boluses or infusion
6. β-blockade (esmolol 500 mcg/kg bolus, then 50-200 mcg/kg/min)
7. TOE if available to assess filling and gradient
8. Consider intra-aortic balloon pump for refractory cases [113-115]

Ventricular Arrhythmias:

1. DC cardioversion/defibrillation for unstable VT/VF
2. Amiodarone 300 mg IV for stable VT
3. Magnesium 2 g IV for polymorphic VT (Torsades)
4. Check electrolytes (K+ >4.5 mmol/L, Mg2+ >1.0 mmol/L)
5. Emergency cardiology consult [116,117]

Atrial Fibrillation with RVR:

1. Urgent electrical or chemical cardioversion if haemodynamically compromised
2. Amiodarone 150 mg IV bolus, then infusion
3. β-blockers if stable
4. Anticoagulation consideration post-operatively [118,119]

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Postoperative Care

Immediate Recovery

• Extubation when fully awake, warm, and haemodynamically stable
• Continue arterial line monitoring in PACU/HDU
• Maintain β-blockade
• Adequate analgesia to prevent catecholamine surge [120]

HDU/ICU Admission Criteria

• Moderate-high risk patients
• Complex surgery >3 hours
• Significant intraoperative haemodynamic instability
• Arrhythmias during surgery
• Significant blood loss [121,122]

Monitoring

• Continuous ECG (telemetry) for 24-48 hours
• Arterial line until stable off vasopressors
• Serial troponins if myocardial ischaemia suspected
• Echo if clinical deterioration [123]

Pain Management

• Multimodal approach
• Opioids as primary analgesic (no ceiling effect concerns in acute setting)
• Avoid NSAIDs if renal dysfunction or heart failure
• Regional techniques where appropriate [124,125]

Fluid Management

• Continue generous fluid strategy
• Avoid negative fluid balance
• Monitor for pulmonary oedema (diastolic dysfunction limits tolerance) [126]

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Specific Surgical Considerations

Non-Cardiac Surgery

High-Risk Procedures:

• Major vascular surgery (abdominal aortic aneurysm repair)
• Major orthopaedic surgery (total hip/knee replacement)
• Thoracic surgery (pneumonectomy, oesophagectomy)
• Emergency surgery (uncontrolled environment) [127-129]

Moderate-Risk:

• Laparoscopic surgery (pneumoperitoneum effects on preload)
• Head and neck surgery (carotid stimulation)
• Obstetric surgery (haemodynamic fluctuations) [130,131]

Optimisation Strategies:

• Pre-admission for optimisation
• Cardiology review within 6 months
• Consider preoperative myomectomy/septal ablation for very high-risk patients [132,133]

Cardiac Surgery in HCM

Septal Myectomy (Morrow Procedure):

• Gold standard for symptomatic obstructive HCM
• Excision of basal septal myocardium
• Requires TOE for precise resection guidance
• Anaesthetic goals as above, with particular attention to avoiding air embolism [134,135]

Alcohol Septal Ablation:

• Percutaneous technique
• Injection of alcohol into septal perforator artery
• Creates controlled myocardial infarction of septum
• Temporary pacing wire mandatory (AV block risk 10-20%) [136,137]

Mitral Valve Surgery:

• Indicated for intrinsic mitral disease (rare) or refractory SAM
• Repair preferred over replacement
• TOE essential for intraoperative assessment [138]

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ANZCA Exam Focus

High-Yield Topics

Pathophysiology:

• Dynamic nature of LVOT obstruction
• Factors that increase/decrease gradient
• Preload-dependent physiology
• Diastolic dysfunction mechanisms [139-141]

Pharmacology:

• Why phenylephrine preferred over noradrenaline
• β-blocker benefits (negative inotropy and chronotropy)
• Volatile agent effects on contractility
• Avoidance of catecholamine surge [142-144]

Clinical Scenarios:

• Management of intraoperative hypotension
• Emergency algorithm for haemodynamic collapse
• Regional anaesthesia risk assessment
• Postoperative arrhythmia management [145-147]

Common Viva Questions

Q: "Why is phenylephrine preferred to metaraminol or noradrenaline in HCM?"

A: Phenylephrine is a pure α-agonist without β-activity. It increases afterload (systemic vascular resistance) without increasing heart rate or contractility. This is ideal in HCM because:

1. Afterload increase reduces LVOT gradient by reducing flow velocity across the obstructed outflow tract
2. No β-activity means no increase in contractility (which would worsen obstruction)
3. No chronotropic effect maintains diastolic filling time

Noradrenaline has both α and β-activity—the β-effects can increase contractility and heart rate, potentially worsening obstruction. Metaraminol has some indirect sympathomimetic effects via noradrenaline release, though generally safer than direct catecholamines [148-150].

Q: "How would you manage a patient with HCM presenting for emergency laparotomy?"

A:

1. Rapid assessment: ECG, quick echo if available to assess gradient and LV function
2. Resuscitation: 10-20 mL/kg crystalloid preload, avoid hypovolemia from bowel obstruction/NPO status
3. Optimisation: β-blocker continuation, anxiolysis
4. Monitoring: Arterial line mandatory, consider CVP and TOE given emergency nature
5. Induction: Etomidate + rocuronium, phenylephrine drawn up and ready
6. Maintenance: High-dose opioid technique, low-dose volatile or TIVA
7. Haemodynamics: Phenylephrine as first-line pressor, avoid tachycardia
8. Post-op: HDU admission, continuous monitoring [151,152]

Q: "What are the SCD risk factors in HCM and how do they influence perioperative management?"

A: Major risk factors include:

• Massive LVH >30 mm
• Family history of SCD
• Unexplained syncope
• Non-sustained VT on Holter
• Apical aneurysm
• Low ejection fraction (<50%)

Perioperative implications:

• ICD assessment mandatory pre-operatively
• β-blockers/amiodarone must be continued
• Avoidance of QT-prolonging drugs
• Extended monitoring post-operatively
• High threshold for HDU/ICU admission
• Emergency resuscitation equipment and protocols ready [153-155]

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Practice SAQs

SAQ 1 (10 marks)

A 54-year-old man with known hypertrophic obstructive cardiomyopathy (HOCM) is scheduled for elective laparoscopic cholecystectomy. His baseline echocardiography shows asymmetric septal hypertrophy (maximum wall thickness 28 mm), resting LVOT gradient of 45 mmHg, mild mitral regurgitation, and preserved LV systolic function. He takes metoprolol 100 mg BD and is asymptomatic (NYHA Class I).

a) Outline the key pathophysiological principles that guide your anaesthetic management. (4 marks)

b) Describe your intraoperative haemodynamic management strategy, including your choice of vasopressor. (4 marks)

c) What specific concerns exist regarding the use of laparoscopic surgery in this patient, and how would you mitigate them? (2 marks)

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Model Answer:

a) Key pathophysiological principles (4 marks):

• Dynamic LVOT obstruction: The gradient is not fixed but varies with loading conditions. Dynamic obstruction occurs due to systolic anterior motion (SAM) of the mitral valve against the hypertrophied septum (1 mark)

• Afterload-dependent: Low afterload increases flow velocity through the LVOT, creating Venturi effect that pulls mitral leaflet anteriorly, worsening obstruction. Maintenance of afterload is critical (1 mark)

• Preload-dependent: Hypovolemia reduces LV cavity size, bringing the septum and mitral apparatus closer, increasing obstruction. Adequate filling is essential (0.5 marks)

• Tachycardia detrimental: Reduced diastolic filling time compromises preload; increased contractility worsens obstruction. Heart rate control (50-70 bpm) required (0.5 marks)

• Diastolic dysfunction: Impaired relaxation requires adequate filling time and pressures. Loss of atrial kick (AF) can precipitate haemodynamic collapse (0.5 marks)

• Arrhythmia vulnerability: Myocardial disarray and fibrosis create substrate for VT/VF. Maintenance of sinus rhythm and electrolyte optimisation (K+ >4.5, Mg2+ >1.0) essential (0.5 marks)

b) Intraoperative haemodynamic management (4 marks):

• Monitoring: Arterial line mandatory for continuous BP monitoring. Consider CVP for preload assessment and TOE for real-time gradient/filling assessment (1 mark)

• Induction: Etomidate preferred (minimal cardiovascular effects). Continue metoprolol. Rocuronium (avoid suxamethonium fasciculations). Phenylephrine drawn up ready (1 mark)

• Maintenance: High-dose opioid-based technique (fentanyl/remifentanil) with low-dose volatile (<0.8 MAC) or TIVA. Avoid desflurane (sympathomimetic) (0.5 marks)

• Vasopressor choice: Phenylephrine first-line—pure α-agonist increases SVR/afterload without β-activity (no increase in contractility or heart rate). This reduces LVOT gradient by decreasing flow velocity (1 mark)

• Alternative agents: Vasopressin acceptable (no inotropic effect). Noradrenaline has β-activity—use cautiously. Avoid adrenaline/dopamine/dobutamine (increase contractility/HR) (0.5 marks)

c) Laparoscopic considerations (2 marks):

• Pneumoperitoneum effects: Insufflation compresses IVC reducing venous return/preload, increases SVR (afterload—beneficial), but CO2 absorption causes sympathetic stimulation and arrhythmia risk (1 mark)

• Mitigation strategies: Limit insufflation pressure (12 mmHg vs standard 15 mmHg), steep Trendelenburg position (increases preload), generous pre-induction fluid loading (15-20 mL/kg), low insufflation flow rates, maintain adequate analgesia to reduce catecholamine response (1 mark)

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SAQ 2 (10 marks)

A 42-year-old woman with known HCM presents for emergency caesarean section at 38 weeks gestation for foetal distress. She has a history of exertional dyspnoea and occasional palpitations. Her echocardiogram shows asymmetric septal hypertrophy (septal thickness 22 mm), resting LVOT gradient 35 mmHg, and good biventricular function. She is not on any cardiac medications.

a) Discuss the risks of neuraxial anaesthesia in this patient and outline your preferred anaesthetic technique with justification. (5 marks)

b) Describe the management of acute haemodynamic collapse intraoperatively. (3 marks)

c) What postoperative monitoring and management would you recommend? (2 marks)

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Model Answer:

a) Neuraxial risks and preferred technique (5 marks):

Risks of neuraxial anaesthesia:

• Sympathetic blockade causes vasodilation and reduced afterload, which can precipitously increase LVOT gradient and cause haemodynamic collapse (1 mark)
• Sudden preload reduction from venodilation impairs the preload-dependent circulation (0.5 marks)
• Tachycardia from reduced venous return further compromises diastolic filling (0.5 marks)
• High spinal level risks total spinal with cardiovascular collapse (0.5 marks)

Preferred technique—General anaesthesia with careful haemodynamic control:

• Justification: Better control of haemodynamics, avoids precipitous sympathetic blockade, enables TOE use if needed (0.5 marks)
• Preparation: Lateral tilt to avoid aortocaval compression, 15-20 mL/kg crystalloid preload, phenylephrine infusion ready, metoprolol 25-50 mg oral 1-2 hours pre-op or 5 mg IV if tachycardic (0.5 marks)
• Monitoring: Large-bore IV access, arterial line (essential), consider CVP (0.5 marks)
• Induction: Etomidate + rocuronium, rapid sequence with cricoid pressure. Phenylephrine 50-100 mcg immediately available (0.5 marks)
• Maintenance: High-dose opioid (fentanyl/remifentanil) + low-dose volatile. Target heart rate 60-80 bpm (0.5 marks)

b) Management of acute haemodynamic collapse (3 marks):

Immediate actions:

1. Call for help, inform surgeon (0.25 marks)
2. Left lateral tilt (relieve aortocaval compression), Trendelenburg position (increase preload) (0.5 marks)
3. Stop surgery if possible, 100% oxygen, manual uterine displacement (0.25 marks)

Haemodynamic support: 4. Rapid fluid bolus 500-1000 mL crystalloid (colloid if available) (0.5 marks) 5. Phenylephrine 100 mcg boluses or infusion 50-200 mcg/min (increases afterload, reduces gradient) (0.5 marks) 6. Esmolol 500 mcg/kg bolus then 50-200 mcg/kg/min infusion (reduces contractility and heart rate) (0.5 marks) 7. Consider vasopressin 1-4 units if phenylephrine inadequate (0.25 marks)

Advanced support: 8. TOE to assess filling status and confirm LVOT obstruction vs other causes (0.25 marks) 9. Consider intra-aortic balloon pump if refractory (0.25 marks)

c) Postoperative management (2 marks):

• Monitoring: HDU admission mandatory. Continuous arterial line and ECG telemetry for 24-48 hours. Serial troponins if concern for ischaemia (0.5 marks)
• Haemodynamics: Continue phenylephrine infusion if required. Maintain SBP >100 mmHg. Restart/initiate metoprolol (0.5 marks)
• Fluid management: Continue generous fluid strategy. Monitor balance closely—avoid negative fluid balance but watch for pulmonary oedema from diastolic dysfunction (0.5 marks)
• Thromboprophylaxis: Mechanical methods preferred initially (graduated compression stockings, intermittent pneumatic compression). Pharmacological prophylaxis when haemodynamically stable. Early mobilisation (0.5 marks)

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Viva Scenarios

Viva Scenario 1: Perioperative Assessment

Examiner: "A 62-year-old man with known HCM is listed for elective total hip replacement. He reports NYHA Class II symptoms with dyspnoea on climbing two flights of stairs. He takes atenolol 50 mg daily. What specific preoperative investigations would you request?"

Candidate: "I would want recent echocardiography, specifically looking for the resting and provocable LVOT gradients, the degree and distribution of hypertrophy, any mitral regurgitation, and systolic and diastolic function. I'd also want a 12-lead ECG and ideally 24-hour Holter monitoring to assess for arrhythmias. If available, cardiac MRI would provide information about fibrosis burden and apical variant. Cardiopulmonary exercise testing would help quantify his functional capacity."

Examiner: "His echo shows a resting gradient of 60 mmHg, maximal wall thickness of 26 mm, and mild MR. His Holter shows occasional ectopy but no non-sustained VT. How does this change your anaesthetic plan?"

Candidate: "This is high-risk HCM. The resting gradient >50 mmHg indicates significant obstruction. I would ensure this is an optimised patient—cardiology review within 3-6 months. I would admit him pre-operatively for optimisation, ensure β-blockade is adequate, and consider whether preoperative septal reduction should be discussed. For anaesthesia, I would use invasive monitoring—definitely arterial line, CVP, and intraoperative TOE. I would avoid neuraxial techniques due to the high resting gradient. My vasopressor of choice would be phenylephrine, and I'd be prepared for significant haemodynamic instability."

Examiner: "Good. How would you manage his postoperative pain?"

Candidate: "Multimodal approach with careful attention to avoiding sympathetic stimulation. I would use paracetamol regularly, and consider tramadol or low-dose opioids for breakthrough pain. I would avoid NSAIDs due to renal and bleeding concerns. If a regional technique is considered, a fascia iliaca block or adductor canal block with low-volume, dilute local anaesthetic could provide analgesia without significant systemic effects. The key is avoiding uncontrolled pain that drives catecholamine release."

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Viva Scenario 2: Intraoperative Crisis

Examiner: "You're anaesthetising a 48-year-old woman with HCM for abdominal hysterectomy. Ten minutes after induction, her blood pressure drops from 110/70 to 70/40 mmHg, and her heart rate increases from 65 to 95 bpm. Her SpO2 is 98%. What's your differential diagnosis and immediate management?"

Candidate: "The differential includes worsening dynamic LVOT obstruction, hypovolemia from haemorrhage or third spacing, anaphylaxis, myocardial ischaemia or infarction, and light anaesthesia with sympathetic stimulation. In HCM, the most likely is exacerbated dynamic obstruction from relative hypovolemia, reduced afterload from volatile agents, or increased contractility."

Examiner: "How do you differentiate between these causes?"

Candidate: "I would check the arterial waveform for characteristic findings—spike-and-dome pattern or pulsus bisferiens suggests LVOT obstruction. TOE would be the gold standard to visualise SAM and measure the gradient directly. I'd check surgical field for bleeding, look for rash/bronchospasm for anaphylaxis, and review the anaesthetic record for drug doses and timing. ST-segment changes on ECG would suggest ischaemia."

Examiner: "TOE confirms SAM with a gradient of 80 mmHg. What's your management?"

Candidate: "I would immediately institute measures to reduce the gradient: Trendelenburg position to increase preload, give a 500-1000 mL crystalloid bolus, start phenylephrine infusion to increase afterload, and give esmolol 500 mcg/kg bolus followed by infusion to reduce contractility and heart rate. I would deepen anaesthesia if light, reduce volatile concentration if contributing to vasodilation, and ensure adequate analgesia. I'd place an arterial line if not already present for beat-to-beat monitoring."

Examiner: "Excellent. What if she doesn't respond to these measures?"

Candidate: "If refractory to standard measures, I would escalate to vasopressin or even noradrenaline carefully titrated. I would consider intra-aortic balloon pump counterpulsation which increases afterload and diastolic coronary perfusion. I would ensure optimal electrolytes—check and treat K+ and Mg2+. Emergency cardiology and cardiothoracic surgery consultation would be warranted, and I would be prepared for CPR with emphasis on maintaining preload and afterload during resuscitation."

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Viva Scenario 3: Medication and Device Management

Examiner: "A 35-year-old man with HCM and an ICD is having a dental extraction under general anaesthesia. What specific considerations apply to his device?"

Candidate: "I need to know the indication for ICD—primary or secondary prevention—and when it was implanted. I should obtain a recent device check report. I would place a magnet over the device during surgery to disable anti-tachycardia therapy, as surgical diathermy can cause electromagnetic interference leading to inappropriate shocks. I need to ensure external defibrillation pads are placed—the standard anterior-posterior position is acceptable but pads should be >10 cm from the device generator."

Examiner: "What about rate-responsive functions?"

Candidate: "Rate-responsive pacing should be disabled pre-operatively or the magnet will disable this too—most ICDs respond to magnet by disabling tachyarrhythmia therapy but may continue bradycardia pacing at a fixed rate, typically 85 bpm. However, programming verification is ideal. The fixed magnet rate might be faster than his baseline, but in HCM we actually want some chronotropic competence for diastolic filling. I would discuss with cardiology pre-operatively."

Examiner: "His ICD is for primary prevention after his brother died suddenly from HCM. His 5-year SCD risk is 8%. How does this affect your perioperative planning?"

Candidate: "High SCD risk means he's in the category where ICD is indicated. Perioperatively, this increases my vigilance for arrhythmias. I would ensure his β-blocker is continued, electrolytes optimised, and I would avoid QT-prolonging drugs. Extended monitoring in a high-dependency environment post-operatively is indicated. I would have resuscitation equipment immediately available including external defibrillator. The psychological aspect is also important—he has witnessed family tragedy, so anxiety management is crucial to prevent catecholamine surge."

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