Anesthesia Pearls

Pearl 1 of 25: Coronary Physiology and Myocardial Oxygen Supply-Demand Balance

1. Coronary perfusion pressure (CPP) = DBP - LVEDP. Coronary filling occurs ONLY during DIASTOLE in the left ventricle. Right ventricle perfused in both systole and diastole.
2. Normal coronary blood flow: 250 mL/min (5% of cardiac output). Can increase 4-5x with maximal vasodilation (coronary reserve).
3. Myocardial O2 extraction at rest is already 70-80% (highest of any organ) — cannot significantly increase during stress. Must increase blood flow.
4. Tachycardia simultaneously increases demand AND decreases supply (shortens diastolic filling time). Most dangerous haemodynamic event in IHD.
5. Rate-Pressure Product (RPP) = HR x SBP. RPP >12,000 = ischaemia threshold. Target RPP <10,000 in at-risk patients.
6. Autoregulation: CBF constant over MAP 50-120 mmHg. Below 50 mmHg: flow becomes pressure-dependent.
7. Subendocardium most vulnerable: farthest from epicardial supply, highest wall tension (Laplace), longest compression time.
8. Main determinants of O2 DEMAND: Heart rate (most important), contractility, wall stress. Laplace law: wall stress = (Pressure × Radius) / (2 × Thickness).
9. Main determinants of O2 SUPPLY: CPP (DBP - LVEDP), diastolic time, O2 content of blood (Hb × SaO2 × 1.34 + PaO2 × 0.003).
10. Target haemodynamics in IHD: HR 55-70 bpm, MAP 70-90 mmHg, DBP >60 mmHg, SpO2 >97%, Hb >8 g/dL.
11. Adenosine: most powerful endogenous coronary vasodilator. Released in ischaemia to increase flow. Also used in pharmacological stress testing to provoke steal.
12. Nitroglycerin (GTN): venodilator reduces preload and LVEDP → improves CPP. Also dilates epicardial arteries. Can paradoxically worsen ischaemia by reducing DBP in coronary steal anatomy.
13. Phenylephrine: pure alpha-1 agonist. Increases DBP and CPP without tachycardia. Preferred vasopressor in IHD.
14. ECG leads for ischaemia: II (inferior wall — RCA territory) + V5 (lateral wall — LAD/LCx territory) detect 96% of ischaemic events.
15. MINS (Myocardial Injury after Non-cardiac Surgery): troponin rise post-op without symptoms. Occurs in 8% of patients >45 years. Screen with hsTnT at 24 and 48 hours. 10x increased 30-day mortality.

Pearl 2 of 25: Anaesthesia for Ischaemic Heart Disease — Non-Cardiac Surgery

1. Revised Cardiac Risk Index (RCRI/Lee score): 6 risk factors scored 1 each. RCRI ≥3 = 5.4% major adverse cardiac events (MACE) risk. Risk factors: high-risk surgery, IHD history, CCF history, CVA/TIA history, insulin-dependent DM, creatinine >2 mg/dL.
2. Functional capacity assessment: >4 METs (climb one flight of stairs) = adequate. <4 METs = poor functional capacity → consider further cardiac evaluation. Cannot assess (obese, joint disease) → consider stress testing.
3. Beta-blockers: CONTINUE if already prescribed. DO NOT start new beta-blockers within 24 hours of surgery (POISE trial: increased stroke risk with acute perioperative initiation).
4. ACE inhibitors/ARBs: WITHHOLD morning of surgery (refractory hypotension with induction). Restart 24 hours post-op when euvolaemic.
5. Statins: CONTINUE perioperatively (pleiotropic cardioprotective benefits). Starting statins perioperatively is beneficial if not already prescribed.
6. Aspirin: CONTINUE for most non-cardiac surgery unless bleeding risk very high. DUAL antiplatelet therapy (DAPT): after DES minimum 6 months, after BMS minimum 1 month before elective surgery.
7. Timing after MI: elective surgery ideally >60 days after MI, optimally >6 months. Emergency surgery: proceed with intensive monitoring.
8. Induction: Etomidate preferred in severe LV dysfunction (minimal haemodynamic effect). Propofol: titrate slowly. Ketamine: AVOID (tachycardia, hypertension increase demand).
9. Laryngoscopy attenuation: Fentanyl 2-5 mcg/kg + Lidocaine 1.5 mg/kg IV + Esmolol 0.5 mg/kg before laryngoscopy.
10. Volatile agents: provide ischaemic preconditioning (cardioprotective). Isoflurane and sevoflurane both safe. Desflurane: avoid (tachycardia from sympathetic activation).
11. Vasopressors for hypotension: Phenylephrine first choice (increases DBP without tachycardia, improves CPP). Noradrenaline second. AVOID ephedrine (tachycardia dangerous in IHD).
12. Intraoperative ischaemia: ST depression >1mm or elevation >2mm in ≥2 leads. Treat: HR control (esmolol), increase MAP (phenylephrine), GTN for coronary vasospasm, senior help.
13. Post-operative MI: most occur Day 2-3 (catecholamine surge, hypercoagulable state). Monitor hsTnT at 24 and 48 hours in high-risk patients.
14. TOE/ECHO: wall motion abnormality is the EARLIEST sign of myocardial ischaemia — more sensitive than ECG or symptoms.
15. POISE trial: metoprolol started day of surgery reduced non-fatal MI but increased stroke and total mortality. Lesson: do not start beta-blockers acutely without titration period.

Pearl 3 of 25: Coronary Steal Syndrome

1. Coronary steal: vasodilator drugs cause normal coronary arteries to dilate → blood diverts (steals) FROM collateral-dependent ischaemic zones → worsening ischaemia.
2. Anatomy required: stenosed vessel + collateral supply + normal vessels that can still dilate.
3. Steal anatomy present in ~23% of CAD patients (Warltier et al). Most common: multivessel disease with collateral-dependent myocardium.
4. Drugs causing coronary steal: Adenosine, Dipyridamole, Sodium nitroprusside, GTN/nitroglycerin, Hydralazine, Isoflurane (controversial).
5. Adenosine and Dipyridamole: used specifically IN pharmacological stress testing to PROVOKE steal and detect vulnerable zones (thallium/MIBI scan).
6. Isoflurane controversy: Priebe 1987 showed ischaemia. Most subsequent studies show no clinically significant difference vs other agents. Now considered clinically safe at standard doses.
7. AVOID coronary vasodilators in suspected steal anatomy: if intraoperative ischaemia detected, use phenylephrine (raises DBP, no vasodilation) not GTN.
8. GTN paradox: lowers DBP → reduces CPP → potentially worsens ischaemia in steal anatomy despite intended vasodilation.
9. Dipyridamole: withhold before surgery — potential trigger. Continue aspirin (anti-platelet effects beneficial).
10. Clinical diagnosis: ischaemia worse after vasodilator administration. Imaging: thallium scan with reversible defects in multiple territories.
11. CBF autoregulation: in severe CAD, coronary vessels are maximally dilated at rest (no reserve). Blood flow becomes entirely pressure-dependent. Any MAP drop = ischaemia.
12. Protection from steal: Adenosine receptor blockade (aminophylline 200 mg IV) can reverse adenosine-induced steal in stress testing emergencies.
13. Left main coronary artery (LMCA) disease: particularly dangerous — supplies 70% of LV. Any haemodynamic instability is catastrophic. These patients need very careful anaesthesia.
14. Coronary collaterals: develop over weeks-months of ischaemia. Well-developed collaterals provide protection but create steal substrate.
15. Key exam point: steal anatomy ≠ all CAD patients. Only those with specific anatomy (stenosis + collaterals + normal vessel) at risk. This is why most IHD patients tolerate isoflurane safely.

Pearl 4 of 25: Anaesthesia for Mitral Stenosis — Five Goals

1. Normal mitral valve area (MVA): 4-6 cm². Symptoms at <2 cm². Severe MS: <1 cm². Pressure gradient across valve increases with tachycardia.
2. Five anaesthetic goals: (1) Slow HR 60-80 bpm, (2) Maintain sinus rhythm, (3) Avoid fluid overload, (4) Maintain SVR, (5) Avoid pulmonary vasoconstrictors.
3. Tachycardia is the MOST DANGEROUS haemodynamic event in MS. Reduces diastolic filling time → acute LA pressure rise → pulmonary oedema. Even HR 100 can precipitate flash pulmonary oedema.
4. New atrial fibrillation: treat IMMEDIATELY with amiodarone 300 mg IV or synchronised DC cardioversion if haemodynamically compromised. Loss of atrial kick = 20% reduction in cardiac output.
5. Drugs to AVOID: Ketamine (tachycardia), Pancuronium (vagolytic → tachycardia), Atropine (tachycardia), Ephedrine (beta effects → tachycardia).
6. Preferred vasopressor: Phenylephrine (pure alpha-1 → raises SVR without tachycardia). AVOID ephedrine (tachycardia worsens MS).
7. Preferred induction: Etomidate (no tachycardia, minimal haemodynamic effect) + high-dose Fentanyl (blunts laryngoscopy response).
8. Pulmonary hypertension: AVOID — hypoxia (worsens PVR), hypercapnia (worsens PVR), acidosis, N2O (increases PVR). Maintain normoxia, normocapnia.
9. Regional anaesthesia: spinal → sudden SVR drop → reflex tachycardia → decompensation. AVOID high spinal. Epidural preferred (gradual onset, controllable).
10. Fluid management: strict restriction. CVP monitoring useful. Avoid excess fluid (low oncotic pressure, high LA pressure → flash pulmonary oedema).
11. Echocardiography: PCWP reflects LA pressure. PCWP >20 mmHg = pulmonary congestion. TOE during surgery detects filling and function.
12. Severity: Mean gradient >10 mmHg = severe. PASP >50 mmHg = severe pulmonary hypertension. Plan for balloon mitral valvuloplasty (BMV) before major elective surgery if MVA <1 cm² and symptomatic.
13. Anticoagulation: therapeutic INR if AF present. Bridge with LMWH for surgery. High stroke risk in MS + AF (LA enlargement + stasis + hypercoagulable).
14. Temperature: maintain normothermia. Hypothermia causes vasoconstriction → increased afterload → worsens pulmonary hypertension.
15. Post-operative: HDU minimum 24 hours. Resume rate-control medications immediately. Restart anticoagulation as soon as haemostasis achieved.

Pearl 5 of 25: Perioperative Pacemaker and ICD Management

1. Pacemaker dependency: patient depends on pacemaker if underlying rhythm is absent or too slow to maintain circulation. MUST identify before surgery.
2. Assessment: identify device type, manufacturer, indication, underlying rhythm (is patient pacemaker-dependent?). Obtain device card or interrogation report.
3. Diathermy (electrosurgery) interference: monopolar diathermy most dangerous. Current can: inhibit pacing (treats as cardiac activity) → asystole in dependent patient. Also: cause inappropriate ICD shocks, programme changes, lead damage.
4. Bipolar diathermy: much safer — current stays between two closely-spaced electrodes. Use bipolar for pacemaker-dependent patients wherever possible.
5. Monopolar diathermy precautions: place return electrode (diathermy pad) as far from device as possible. Use short bursts (<1 second). Use lowest effective power. Keep diathermy path away from device-lead-heart axis.
6. ICD: deactivate before surgery (suspend shock therapy) to prevent inappropriate shocks from diathermy. Apply external defibrillator pads BEFORE deactivating. Use a magnet OR formal interrogation and reprogramming.
7. Magnet application to pacemaker: converts most pacemakers to asynchronous mode (DOO/VOO/AOO) — paces at fixed rate regardless of intrinsic rhythm. Prevents inhibition by diathermy. Rate varies by manufacturer (typically 65-100 bpm).
8. Magnet application to ICD: SUSPENDS shock therapy only. Does NOT convert to asynchronous pacing. If ICD also has pacing function, may still be inhibited by diathermy.
9. Temporary pacing: have transcutaneous pacing (defibrillator pads) available for ALL pacemaker-dependent patients. Particularly important when ICD is deactivated.
10. Electromagnetic interference (EMI) sources: monopolar diathermy, nerve stimulators, some surgical tools, MRI (special precautions needed — MRI-conditional devices only).
11. Monitoring: continuous ECG throughout case. Arterial line in pacemaker-dependent patients (pacing spikes without pulsatile trace = failure to capture).
12. Post-operative: reactivate ICD immediately after surgery. Request cardiology review and device interrogation within 24 hours of significant surgery.
13. Rate response: exercise-responsive pacemakers increase HR with movement. Shivering or fasciculations can trigger inappropriate rate increase.
14. CIED (Cardiac Implantable Electronic Device) categories: pacemaker, ICD, CRT (cardiac resynchronisation therapy — biventricular pacing for CCF + LBBB), CRT-D (CRT with defibrillator).
15. HRS/ASA consensus statement (2011): recommend liaison between anaesthesia team and device clinic before major surgery involving diathermy for all CIED patients.

Pearl 6 of 25: Phaeochromocytoma — Perioperative CVS Management

1. Catecholamine crisis: BP can reach 300/180 mmHg. Tumour manipulation (surgical handling) causes massive catecholamine surge — most dangerous moment.
2. Rule of 10s: 10% bilateral, 10% malignant, 10% extra-adrenal (paraganglioma), 10% familial, 10% in children. Associated with MEN2, VHL, NF1, SDH mutations.
3. Preoperative preparation: MANDATORY alpha blockade for 10-14 days minimum before surgery. Phenoxybenzamine (irreversible, non-selective alpha blocker): start 10mg BD, increase to 1 mg/kg/day target.
4. CRITICAL RULE: Alpha block FIRST, then beta block. Beta blockade before adequate alpha block → PARADOXICAL severe hypertension (blocks beta-2 vasodilation → unopposed alpha-1 vasoconstriction).
5. Criteria for adequate preoperative preparation: BP <130/80 for 24 hours, orthostatic hypotension present (confirms alpha blockade), nasal congestion (alpha blockade sign), no ST changes for 1 week.
6. Volume expansion: high salt diet + liberal fluids pre-op. Chronic vasoconstriction causes hypovolaemia. Volume replacement prevents catastrophic hypotension after tumour removal.
7. Intraoperative crisis management: Phentolamine (non-selective alpha blocker) 1-5 mg IV bolus — onset 1 minute. Sodium nitroprusside infusion 0.5-10 mcg/kg/min. Nicardipine infusion.
8. Magnesium sulphate infusion 40-60 mg/kg/hr: reduces catecholamine release AND vasodilator. Useful adjunct for intraoperative pressure control.
9. Post-ligation hypotension: after tumour devascularisation, catecholamines fall precipitously. Prepare: 2-4L IV fluids rapidly, noradrenaline infusion ready BEFORE ligation.
10. Avoid: Ketamine (catecholamine stimulation), Halothane (sensitises myocardium to catecholamines → VF), Succinylcholine (abdominal fasciculations compress tumour), Morphine (histamine release), Droperidol (may release catecholamines).
11. Glucose monitoring: catecholamine withdrawal after tumour removal → rebound hypoglycaemia (insulin was suppressed by catecholamines). Check glucose every 30 min post-ligation.
12. Monitoring: Arterial line BEFORE induction (beat-to-beat BP during manipulation critical). CVP. Consider PA catheter or TOE for cardiac output monitoring.
13. Induction preference: Propofol (no catecholamine stimulation) + Fentanyl (high dose, blunts laryngoscopy) + Rocuronium (no histamine). Lidocaine 1.5 mg/kg before laryngoscopy.
14. Laparoscopic adrenalectomy: less surgical trauma BUT pneumoperitoneum increases intraabdominal pressure → can compress tumour. Haemodynamic instability similar to open approach.
15. Post-operative: 24-48 hour HDU/ICU. Confirm complete resection: 24-hour urine catecholamines at 1 week. Screen first-degree relatives for familial forms (genetic testing for MEN2, VHL, SDH mutations).

Pearl 7 of 25: Spinal Hypotension in Obstetrics — Prevention and Treatment

1. Incidence: 50-80% of patients undergoing spinal for LSCS without prophylaxis. Definition: SBP <80% of baseline OR absolute SBP <90 mmHg.
2. Mechanism: sympathetic block (T4-T10) → vasodilation (SVR falls) → venous pooling → reduced preload → reduced CO → hypotension. Aortocaval compression from gravid uterus worsens this.
3. Left uterine displacement (15° wedge under right hip): mandatory from 20 weeks gestation. Reduces aortocaval compression by 20-30%. Maintain throughout surgery.
4. Phenylephrine infusion: 25-50 mcg/min starting simultaneously with spinal insertion — reduces hypotension by 70-80% (COMET trial, Carvalho et al). FIRST-LINE vasopressor.
5. Phenylephrine vs Ephedrine: Phenylephrine preferred — preserves uteroplacental blood flow, better fetal pH and base excess. Ephedrine crosses placenta → fetal tachycardia and lactic acidosis.
6. Ephedrine: use when maternal bradycardia accompanies hypotension (pure alpha vasopressor worsens bradycardia). Dose: 6-12 mg IV bolus.
7. Crystalloid co-load: 500-1000 mL Ringer's Lactate simultaneously with spinal (NOT pre-load — ineffective in obstetrics as redistributes rapidly).
8. Target SBP: maintain ≥90% of baseline. DO NOT over-treat (phenylephrine-induced hypertension → reflex bradycardia → reduced CO).
9. Bradycardia treatment: if HR <60 bpm with hypotension → Ephedrine 6-12 mg IV. If severe bradycardia with cardiovascular collapse → Adrenaline 50-100 mcg IV.
10. Block height: target T4 (nipple line) for LSCS. Test with ice or ethyl chloride spray. T6 = inadequate (visceral pain during uterine manipulation). T2 = too high (respiratory embarrassment).
11. Hyperbaric bupivacaine 0.5%: 2.2-2.5 mL standard dose. Add fentanyl 25 mcg (improves quality) + morphine 100 mcg (post-op analgesia 12-24 hours).
12. Obese patients: hypotension more severe (more sympathetic blockade, greater weight on vena cava). Increase phenylephrine dose, more aggressive co-load.
13. Failed spinal: if inadequate block height despite repositioning and waiting — re-site (not supplement without limit). Avoid excessive supplemental opioids IV.
14. High spinal: features — difficulty breathing, arm weakness, Horner's syndrome, loss of consciousness. Treatment: immediate intubation, vasopressors (noradrenaline/phenylephrine), CPR if arrest.
15. Shivering post-spinal: very common (cold local anaesthetic, temperature redistribution). Warm IV fluids, warm forced-air blanket, pethidine 25 mg IV or tramadol 50 mg IV.

Pearl 8 of 25: Vasopressors in Anaesthesia — Classification and Clinical Use

1. Vasopressors increase SVR (afterload) to restore MAP. Inotropes increase cardiac contractility. Many drugs have both effects.
2. Phenylephrine: pure alpha-1 agonist. Increases SVR and MAP by vasoconstriction. No beta effects. May cause reflex bradycardia. Preferred for: obstetric spinal hypotension, IHD hypotension (no tachycardia). Dose: 50-100 mcg IV bolus; infusion 25-100 mcg/min.
3. Noradrenaline (Norepinephrine): alpha-1 + alpha-2 + beta-1. Powerful vasoconstriction + mild inotrope. First-line vasopressor for septic shock (SSC 2024). Dose: 0.01-3 mcg/kg/min infusion. Central line preferred.
4. Ephedrine: alpha + beta agonist. Indirect (releases noradrenaline) + direct. Increases HR, BP, CO. Useful when bradycardia + hypotension. Dose: 3-12 mg IV bolus. Causes fetal acidosis in obstetrics.
5. Adrenaline (Epinephrine): alpha-1 + alpha-2 + beta-1 + beta-2. FIRST-LINE for anaphylaxis (reverses all features). Also used in CPR (1 mg q3-5min). Increases lactate (glycogenolysis) — confounds lactate monitoring.
6. Vasopressin (ADH): V1 receptor vasopressor. Catecholamine-independent mechanism — works when catecholamine receptors downregulated in prolonged shock. Add to noradrenaline at 0.03-0.04 units/min when dose >0.25 mcg/kg/min (SSC 2024 — spares noradrenaline dose).
7. Dopamine: D1 + beta + alpha effects dose-dependent. No longer recommended as first-line (more arrhythmias vs noradrenaline — SOAP-II trial). 'Renal dose' dopamine (1-3 mcg/kg/min) is INEFFECTIVE and ABANDONED.
8. Dobutamine: beta-1 dominant. Positive inotrope + mild vasodilator. For cardiogenic shock/low CO states. Use WITH noradrenaline (dobutamine alone drops BP). Dose: 2-20 mcg/kg/min.
9. Metaraminol: alpha-1 agonist (similar to phenylephrine). Widely used in UK for spinal hypotension. Dose: 0.5-2 mg IV bolus; 20-50 mg in 500 mL infusion.
10. Angiotensin II (Giapreza): new agent. ATHOS-3 trial: effective in vasoplegic shock refractory to catecholamines. SSC 2024: may consider in refractory distributive shock. Dose: 2.5-80 ng/kg/min.
11. Milrinone: phosphodiesterase inhibitor. Positive inotrope + vasodilator (inodilator). Used in cardiac surgery (low CO after bypass), heart failure. Dose: 0.375-0.75 mcg/kg/min. Causes hypotension.
12. Levosimendan: calcium sensitiser. Inodilator. Cardiac surgery, acute decompensated heart failure. Long-acting (metabolites active 7-9 days). Improves cardiac efficiency without increasing O2 consumption.
13. Vasopressor vs inotrope distinction: septic shock — high CO but low SVR → vasopressor (noradrenaline). Cardiogenic shock — low CO, high SVR → inotrope (dobutamine). Mixed shock → both.
14. Vasopressor weaning: wean when MAP stable with decreasing requirements. Wean noradrenaline LAST (most important for maintaining organ perfusion). Vasopressin can be weaned first.
15. Perioperative vasopressor choice: spinal hypotension → phenylephrine/metaraminol. Induction hypotension (normovolaemic) → ephedrine or phenylephrine. Septic shock → noradrenaline. Anaphylaxis → adrenaline IM.

Pearl 9 of 25: Haemodynamic Monitoring — Invasive and Non-Invasive

1. Arterial line (A-line): continuous beat-to-beat BP, easy arterial blood sampling. Indications: major surgery, haemodynamic instability, vasopressor infusions, frequent ABG needed. Sites: radial (Allen's test), femoral, brachial, dorsalis pedis.
2. Allen's test: compress radial + ulnar arteries → release ulnar → palm should pink up in <7 seconds. Tests ulnar collateral circulation. Abnormal test = relative contraindication to radial A-line.
3. Arterial line waveform: upstroke = systole, dicrotic notch = aortic valve closure, downstroke = diastole. Over-damped (flatline-like): air bubble, clot, kinked line. Under-damped (falsely high): long tubing, resonance.
4. Pulse pressure variation (PPV): variation in pulse pressure with respiratory cycle. >13% = fluid responsive (preload dependent). Requires: sinus rhythm, controlled ventilation, no spontaneous breaths, no RV failure.
5. Central venous catheter (CVP line): central venous access for: vasopressors, TPN, frequent blood sampling, CVP monitoring, rapid fluid resuscitation. Waveform: a-wave (atrial contraction), c-wave (tricuspid closure), v-wave (ventricular filling).
6. CVP limitations: CVP poorly predicts fluid responsiveness (Marik meta-analysis). CANNOT use static CVP alone to guide fluid resuscitation. Use dynamic measures (PPV, SVV, PLR).
7. Pulmonary artery catheter (PAC/Swan-Ganz): measures CO (thermodilution), PCWP (≈ LAP ≈ LVEDP), mixed venous O2. PCWP >18 = cardiogenic pulmonary oedema. Falling out of favour due to complications without proven outcome benefit.
8. Passive Leg Raise (PLR): non-invasive fluid responsiveness test. Elevate legs 45° from supine. Autotransfusion of 250-300 mL from legs. If CO increases ≥10% → fluid responsive. Works in AF, spontaneous breathing. Reversible — no fluid given.
9. Oesophageal Doppler: measures descending aortic blood flow → estimated CO and stroke volume. Non-invasive, minimal complications. Gold standard for GDFT in elective major surgery. Corrected flow time (FTc) <350 ms = hypovolaemia.
10. FloTrac/Vigileo: arterial waveform analysis. Continuous CO and SVV without PA catheter. Requires adequate arterial waveform. Less accurate in arrhythmias, very low or high vascular resistance.
11. Transoesophageal Echocardiography (TOE/TEE): gold standard for intraoperative cardiac assessment. Visualises: LV/RV function, filling (IVC collapsibility), regional wall motion abnormalities (ischaemia), aortic pathology, valve function, air embolism.
12. ScvO2 (Central venous O2 saturation): normal >70%. <65% = inadequate O2 delivery vs consumption (poor CO, anaemia, high consumption). Surrogate for SvO2. Rivers EGDT protocol target: ScvO2 >70%.
13. PRAM (Pressure Recording Analytical Method), LiDCO, PiCCO: less invasive CO monitoring techniques. Each has specific calibration requirements and limitations.
14. Non-invasive cardiac output (NICOM/USCOM): based on bioreactance or Doppler. No invasive lines. Lower accuracy but useful where invasive access not feasible.
15. Near-infrared spectroscopy (NIRS/rSO2): cerebral oximetry. Trend monitoring — desaturation <20% from baseline or absolute <50% = intervention needed. Cardiac surgery, carotid, beach chair position.