Anesthesia Pearls

Pearl 20 of 25: Permissive Hypotension in Haemorrhagic Shock

1. Permissive hypotension (balanced resuscitation): accepting lower-than-normal BP during active uncontrolled haemorrhage to reduce bleeding while maintaining minimum organ perfusion.
2. Rationale: higher MAP achieved with aggressive fluid resuscitation → (1) Dilutes clotting factors, (2) Dislodges forming clots, (3) Worsens lethal triad (hypothermia from cold fluids, acidosis from crystalloids, dilutional coagulopathy), (4) Promotes ongoing haemorrhage.
3. Target: SBP 80-90 mmHg (MAP 50-65 mmHg) in uncontrolled haemorrhage BEFORE surgical source control. Maintain minimum brain and vital organ perfusion.
4. Duration: ONLY until surgical/interventional source control is achieved. Once haemostasis: RESTORE normal MAP (>65 mmHg) immediately.
5. Evidence: CRASH-1 (military trauma — penetrating). Bickell et al (NEJM 1994): delayed resuscitation improved survival in penetrating truncal trauma vs immediate resuscitation.
6. ABSOLUTE CONTRAINDICATIONS to permissive hypotension: (1) Traumatic brain injury (TBI) — need CPP >60 mmHg, MAP >80 mmHg. (2) Spinal cord injury — maintain MAP >85 mmHg (ASIA/AASCIS guidelines). (3) Pregnancy >20 weeks — uteroplacental perfusion requires adequate MAP. (4) Elderly patients — cerebral and coronary autoregulation impaired. (5) Severe coronary artery disease.
7. Penetrating trauma: clearest evidence for permissive hypotension. Blunt trauma: less evidence, particularly if TBI co-exists.
8. Damage control resuscitation (DCR): umbrella concept including — permissive hypotension + haemostatic resuscitation (1:1:1 blood products) + damage control surgery (rapid haemostasis, not definitive repair) + avoidance of lethal triad.
9. Vasopressors in haemorrhagic shock: noradrenaline to maintain minimum MAP. Does NOT treat hypovolaemia. Essential bridge to source control and volume replacement.
10. Anaesthetic implications: use low-dose agents for induction (ketamine 0.5-1 mg/kg). Etomidate for haemodynamically unstable. Avoid vasodilating agents. Have vasopressors running before induction.
11. Glasgow Coma Scale during permissive hypotension: monitor neurological status. Any deterioration in GCS → raise MAP immediately (TBI may have been missed).
12. Time-critical: permissive hypotension is a bridge strategy. Every minute of ongoing haemorrhage compounds lethal triad. Surgical team must be immediately available.
13. Haemostatic agents: TXA 1g within 3 hours (CRASH-2). Fibrinogen concentrate 4g if ROTEM FIBTEM A10 <10mm. Calcium gluconate 1g q4 units blood. All given while patient in active resuscitation phase.
14. Monitoring during permissive hypotension: lactate (rising = worsening tissue hypoxia), arterial line for continuous BP, urinary catheter (UO >0.5 mL/kg/hr despite low BP = adequate renal perfusion), clinical assessment.
15. Ethical considerations: in unconscious patients, next of kin consent may not be practical. This is an established emergency management strategy. Document rationale clearly.

Pearl 21 of 25: Septic Shock — Vasopressor Therapy (SSC 2024)

1. Septic shock definition: sepsis + vasopressor requirement to maintain MAP ≥65 mmHg + lactate >2 mmol/L. Hospital mortality >40%.
2. Vasopressor initiation: start when MAP <65 despite initial fluid resuscitation (30 mL/kg). Do NOT delay vasopressors while giving fluids — start simultaneously if needed.
3. Noradrenaline: FIRST-LINE vasopressor in septic shock (SSC 2024). Alpha-1 dominant + mild beta-1. Increases SVR without excessive tachycardia. Central line preferred (extravasation risk with prolonged peripheral infusion — can start peripherally in emergency). Dose: 0.01-3 mcg/kg/min.
4. Vasopressin: ADD when noradrenaline dose reaches 0.25 mcg/kg/min. Dose: 0.03-0.04 units/min. V1 receptor vasopressor — catecholamine-independent mechanism (receptors not downregulated in prolonged shock). VANISH trial: vasopressin + hydrocortisone reduces RRT requirement.
5. Adrenaline: third-line if noradrenaline + vasopressin insufficient. Useful when cardiac dysfunction co-exists (beta-1 inotrope). Increases lactate (glycogenolysis) — confounds lactate monitoring if used. Dose: 0.01-1 mcg/kg/min.
6. Dopamine: NOT recommended as first-line (SOAP-II trial: more arrhythmias vs noradrenaline, no mortality benefit). Only use if: bradycardia + hypotension AND noradrenaline unavailable. No 'renal dose' dopamine — myth definitively abandoned.
7. Dobutamine: when septic shock + cardiac dysfunction (low CO despite adequate filling). Add to noradrenaline. Positive inotrope, mild vasodilator. AVOID alone (drops BP).
8. Angiotensin II (Giapreza): ATHOS-3 trial — effective in vasoplegic shock refractory to standard vasopressors. SSC 2024: consider in refractory distributive shock. Dose: 2.5-80 ng/kg/min.
9. MAP target: ≥65 mmHg standard. 60-65 mmHg for elderly (≥65 years) — OVATION trial. Higher MAP (70-80) for pre-existing hypertension. SEPSISPAM trial: MAP 65 vs 85 mmHg — no mortality difference but MAP 85 reduced RRT need in chronic hypertensive patients.
10. Capillary refill time (CRT): SSC 2024 adds CRT <3 seconds as resuscitation endpoint. ANDROMEDA-SHOCK trial: CRT-guided vs lactate-guided — same mortality, less fluid/vasopressors with CRT. Simple, bedside, free.
11. Vasopressor weaning: wean vasopressors when MAP stable and improving, source controlled, lactate normalising. Wean noradrenaline last. Can wean vasopressin first. Gradual reduction — sudden stop causes rebound hypotension.
12. Corticosteroids: Hydrocortisone 200 mg/day IV for septic shock requiring vasopressors. ADRENAL trial: faster vasopressor weaning. APROCCHSS trial: adds fludrocortisone 50 mcg oral daily — reduced mortality.
13. Peripheral vasopressor use: noradrenaline can safely be given peripherally for <24 hours in large antecubital or forearm vein for urgent resuscitation. DO NOT delay central access — but do not delay vasopressors either. Monitor infusion site closely.
14. Vasopressin in distributive shock: mechanism complementary to catecholamines. In prolonged shock: catecholamine receptors downregulate, ADH depleted. Vasopressin acts independently. Also: reduces catecholamine requirements (vasopressor-sparing).
15. Practical vasopressor algorithm (SSC 2024): Start noradrenaline → add vasopressin at 0.03-0.04 U/min when NE >0.25 mcg/kg/min → add adrenaline if CO low → add hydrocortisone → consider angiotensin II if refractory.

Pearl 22 of 25: Cardiac Output — Fick Principle and Measurement

1. Cardiac output (CO) = Heart Rate × Stroke Volume. Normal: 4-8 L/min. Cardiac index (CI) = CO/BSA. Normal CI: 2.2-4 L/min/m². BSA = body surface area.
2. Fick's principle: CO = O2 consumption (VO2) / [CaO2 - CvO2]. The amount of O2 consumed per minute = CO × (arterial O2 content - venous O2 content). This is the gold standard method.
3. Thermodilution (indicator dilution): cold saline injected via PA catheter proximal port. Temperature change detected distally. Stewart-Hamilton equation calculates CO. Three measurements averaged. Standard clinical method in ICU with PA catheter.
4. Transpulmonary thermodilution (PiCCO, TPID): cold saline via CVC, temperature detected in femoral/brachial artery. Allows: CO, EVLW, GEDV. No PA catheter needed.
5. LiDCO: lithium chloride bolus via peripheral IV → detected in arterial line. CO = amount Li / concentration-time curve. Then continuous waveform analysis.
6. Oesophageal Doppler: continuous CO based on descending aortic blood velocity (Doppler) × cross-sectional area. Corrected flow time (FTc) assesses preload.
7. Normal O2 delivery (DO2) = CO × CaO2 × 10. Normal: 550-1000 mL/min. O2 extraction ratio = VO2/DO2. Normal: 20-30%. In shock: extraction increases to maintain VO2.
8. SvO2 (mixed venous O2 saturation): normal 65-75%. <65% = O2 supply inadequate for demand (low CO, anaemia, high VO2, desaturation). ScvO2 (from CVC) is surrogate: target >70% in sepsis (Rivers EGDT).
9. Frank-Starling curve: increased preload → increased SV (to a limit). Beyond optimal preload: SV plateau or falls (ventricular failure). Fluid responsiveness assessment determines where on curve patient sits.
10. Determinants of stroke volume: Preload (LVEDV — Frank-Starling), Afterload (SVR — opposition to ejection), Contractility (inotropy — intrinsic myocardial function).
11. Ejection fraction (EF): normal >55%. EF 40-55% = mildly reduced. EF <40% = reduced systolic function. EF <30% = severe dysfunction. Note: EF measures systolic function only — diastolic dysfunction can occur with normal EF.
12. Diastolic dysfunction: impaired ventricular relaxation and filling. Common in hypertension, DM, elderly, hypertrophic cardiomyopathy. Normal EF but elevated filling pressures (LVEDP). Prone to pulmonary oedema with even moderate fluid loading. Treat with rate control, diuretics.
13. Oxygen delivery crisis: DO2 <330 mL/min = critical threshold. Below this: VO2 becomes supply-dependent (aerobic metabolism fails → anaerobic → lactate). Monitor: ScvO2, lactate, lactate clearance.
14. High CO states (hyperdynamic): sepsis (early), liver failure, thyrotoxicosis, pregnancy, AV fistula. Low SVR, high CO, warm peripheries, bounding pulses.
15. Low CO states (hypodynamic): cardiogenic shock, tamponade, severe AS. High SVR, low CO, cool clammy peripheries, low pulse pressure, elevated lactate. Treatment: inotropes, afterload reduction (if not in shock).

Pearl 23 of 25: Hypertrophic Cardiomyopathy (HCM) — Anaesthetic Management

1. HCM: genetic (sarcomere protein mutations) hypertrophy of LV, particularly asymmetric septal hypertrophy (ASH). Outflow tract obstruction (LVOTO) dynamic — worsens with: tachycardia, reduced preload, reduced afterload, increased contractility.
2. Dynamic obstruction: systolic anterior motion (SAM) of mitral valve → LVOT obstruction worsens → LV-aortic gradient increases. Gradient varies with loading conditions — NOT fixed like valvular AS.
3. Goal: AVOID conditions that WORSEN obstruction — tachycardia, hypovolaemia, vasodilation, positive inotropy.
4. Five anaesthetic goals: (1) Slow heart rate (60-70 bpm), (2) Maintain preload (avoid hypovolaemia), (3) Increase afterload (maintain SVR), (4) Reduce contractility, (5) Maintain sinus rhythm.
5. Drugs to AVOID: Vasodilators (GTN, SNP — reduce afterload → worsens gradient), Inotropes (adrenaline, dopamine, dobutamine — worsen LVOTO), Tachycardia-inducing drugs (ketamine, pancuronium), Diuretics in excess (reduce preload).
6. Drugs to USE: Beta-blockers (reduce HR, reduce contractility — key perioperative drugs), Phenylephrine (increases SVR without tachycardia — vasopressor of choice), IV fluids to maintain preload.
7. Preoperative: ensure patient on beta-blocker or verapamil (rate control and reduced contractility). Echo to assess LVOT gradient (resting and provocable) and mitral regurgitation.
8. Atrial fibrillation in HCM: very poorly tolerated — loss of atrial kick + ventricular filling dependent on atrial systole. Immediate DC cardioversion or amiodarone for rate control.
9. Induction: propofol titrated slowly (vasodilatory — use with caution), high-dose fentanyl to blunt laryngoscopy. Sevoflurane acceptable (reduces contractility and HR). AVOID ketamine.
10. Hypotension management: phenylephrine boluses (0.1-0.2 mg). IV fluid 500 mL bolus. Leg raising. Avoid adrenaline/ephedrine. If severe: noradrenaline infusion.
11. Spinal: very high risk — sudden sympathectomy → vasodilation → reduced preload AND afterload → dramatic worsening of LVOTO. Use with extreme caution. Epidural (gradual onset) preferable if regional needed.
12. Obstetrics and HCM: challenging. Labour pain → tachycardia → LVOTO. Early epidural (gradually titrated) preferred — reduces sympathetic surge from pain while carefully avoiding hypotension.
13. Sudden cardiac death risk: HCM leading cause of sudden cardiac death in young athletes (<35 years). ICD indicated: personal or family history of SCD, LV thickness >30 mm, non-sustained VT, hypotensive exercise response.
14. Obstructive vs non-obstructive: resting LVOT gradient >30 mmHg = haemodynamically significant obstruction. Some HCM patients have no obstruction at rest but provokable obstruction with dehydration, exercise, Valsalva.
15. Post-operative: adequate analgesia (pain → tachycardia → LVOTO). Beta-blockers continued post-op. Monitor ECG (arrhythmias). Fluid management critical — avoid both hypo- and hypervolaemia.

Pearl 24 of 25: Cardiac Tamponade — Recognition and Perioperative Management

1. Cardiac tamponade: accumulation of pericardial fluid (blood, effusion, gas) compresses all four cardiac chambers → reduces diastolic filling → falls in cardiac output → obstructive shock.
2. Pericardial effusion becomes tamponade when intrapericardial pressure exceeds intracardiac filling pressure. As little as 150-200 mL if acute (fibrous pericardium cannot stretch). 2 litres if chronic (pericardium stretches).
3. Causes: cardiac surgery (post-op), trauma, aortic dissection, malignancy (most common cause of chronic tamponade), viral/bacterial pericarditis, autoimmune, post-myocardial infarction (Dressler syndrome), uraemia.
4. Beck's triad: (1) Hypotension (reduced CO), (2) Raised JVP (obstructed venous return), (3) Muffled heart sounds (fluid dampens sounds). Classical but often incomplete — only 10-40% present with full triad.
5. ECG features: sinus tachycardia (compensatory), electrical alternans (alternating QRS amplitude from heart swinging in fluid — pathognomonic), low voltage, diffuse ST elevation (pericarditis if underlying).
6. Pulsus paradoxus: normal inspiration → negative intrathoracic pressure → blood pools in pulmonary vasculature → slightly reduces left heart filling. In tamponade: this normal effect is exaggerated. Fall in SBP >10 mmHg on inspiration = pulsus paradoxus. Assessed with arterial line or BP cuff.
7. Echo (TTE/TOE): most important diagnostic tool. Features: pericardial effusion circumferential, RA collapse (earliest sign), RV diastolic collapse (more specific), IVC plethora (dilated, non-collapsing on inspiration — high RAP), septal bounce.
8. Haemodynamic profile: equalisation of diastolic pressures (CVP = RVEDP = LVEDP = PCWP — all equal). Falling pulse pressure. Kussmaul's sign (JVP rises on inspiration — opposite to normal) — more classic for constrictive pericarditis.
9. Compensatory mechanisms: tachycardia (maintains CO), peripheral vasoconstriction (maintains BP). These break down suddenly → cardiovascular collapse. The patient may look 'well' then deteriorate suddenly.
10. Anaesthetic hazards: ANY of the following can cause catastrophic collapse — vasodilators (nitrous oxide, volatile agents, propofol — reduce SVR), IPPV (positive pressure reduces venous return → collapses right heart), induction agents (vasodilation → reduced SVR), tachycardia loss (beta-blockers, high opioid dose).
11. Definitive treatment: pericardiocentesis (needle drainage under echo guidance). Pericardial window (surgical) for recurrent or loculated effusions. In post-cardiac surgery: re-sternotomy.
12. Pre-induction: if patient haemodynamically unstable → pericardiocentesis BEFORE induction. Even 50-100 mL drainage dramatically improves haemodynamics.
13. If must induce before drainage: ketamine (maintains SVR, preserves sympathetic tone). Awake intubation if possible. Have phenylephrine ready. Maintain spontaneous ventilation as long as possible (IPPV can cause immediate arrest). External cardiac defibrillator pads in place.
14. Post-cardiac surgery tamponade: presents 1-3 days post-operatively. Chest drain cessation with suddenly worsening haemodynamics. Echo confirms. Emergency re-sternotomy is treatment.
15. Key physiology: in tamponade, the three compensatory mechanisms are: (1) Tachycardia, (2) Increased venous return (venodilation), (3) Peripheral vasoconstriction. Anaesthesia impairs all three → collapse.

Pearl 25 of 25: Perioperative Heart Failure — Recognition and Management

1. Heart failure (HF): inability of the heart to pump sufficient blood to meet metabolic demands, or only at elevated filling pressures. HFrEF (reduced EF <40%) vs HFpEF (preserved EF ≥50% but impaired filling) vs HFmrEF (mid-range 40-49%).
2. Preoperative risk: RCRI includes CCF as a risk factor (score 1). EF <35% = high perioperative cardiac risk. Decompensated HF (NYHA IV or acute) → postpone elective surgery until optimised.
3. BNP/NT-proBNP: best biomarker for HF. NT-proBNP >125 pg/mL = HF (age-dependent thresholds for acute: >450 if <50 years, >900 if 50-75 years, >1800 if >75 years). Predicts perioperative cardiac complications in non-cardiac surgery. Targets for optimisation: BNP <100 or NT-proBNP <400.
4. Preoperative optimisation: diuretics (target euvolaemia — no orthopnoea, no peripheral oedema), ACE inhibitor/ARB (afterload reduction — continue in HFrEF but hold day of surgery), beta-blocker (continue), SGLT2 inhibitor (DAPA-HF, EMPEROR-Reduced — stop 3 days before surgery — risk of DKA and euglycaemic ketoacidosis).
5. Key medications: ACE inhibitors reduce mortality in HFrEF (CONSENSUS, SOLVD). Beta-blockers (carvedilol, metoprolol, bisoprolol) reduce mortality in HFrEF. MRAs (spironolactone, eplerenone). SGLT2 inhibitors (empagliflozin, dapagliflozin) — newest class, stop 3 days before surgery.
6. Intraoperative anaesthetic principles: avoid tachycardia (already compromised CO), avoid excessive preload reduction (vasodilation from spinal/propofol → hypotension), avoid myocardial depression, maintain sinus rhythm.
7. Induction drugs: Etomidate safest induction in severe HF (minimal haemodynamic effect). Propofol: reduced dose, titrated slowly. Ketamine: generally avoid (increases SVR and HR — increased afterload in already failing heart — though useful in emergency when BP low).
8. Fluid management: HF patients have narrow therapeutic window. Hypovolaemia → hypotension (no reserve to compensate). Fluid overload → acute pulmonary oedema. TOE or oesophageal Doppler essential for GDFT.
9. Vasopressors for hypotension: noradrenaline first (maintains SVR). Dobutamine if CO also low (adds inotropic support). Milrinone if severe systolic dysfunction (PDE inhibitor — inotrope + vasodilator = inodilator).
10. Acute decompensated heart failure (ADHF) intraoperative: diuretics (furosemide 40-80 mg IV), vasodilators (GTN, SNP if systolic BP >90), morphine (vasodilation + anxiolysis), non-invasive ventilation (CPAP/BiPAP reduces preload and afterload).
11. Mechanical support: IABP (intra-aortic balloon pump) — reduces afterload, increases diastolic pressure, improves coronary perfusion. For high-risk patients or when medical treatment fails. Insertion before high-risk surgery in severe LV dysfunction.
12. Post-operative: continue HF medications. Fluid balance negative. HDU monitoring. BNP trend post-op. Restart ACE inhibitors when euvolaemic (24-48 hours post-op).
13. Regional vs general: regional anaesthesia generally preferred — reduced myocardial depression, less physiological stress, better post-op analgesia. BUT: sympathectomy from spinal/epidural can worsen hypotension in pre-load dependent HF.
14. TAVI (Transcatheter Aortic Valve Implantation): increasing numbers with HF + aortic stenosis presenting for non-cardiac surgery. Assess valve function, residual gradient, paravalvular regurgitation. Haemodynamic goals similar to post-surgical AS management.
15. Frailty and HF: many elderly HF patients are frail. Frailty index assessment preoperatively. Shared decision-making about surgery benefit vs risk. Prehabilitation (exercise programme) pre-operatively improves outcomes.