AS6.1-3 | Post-anaesthesia Recovery — Graded Quiz

In a post-laparotomy patient with haemodynamic instability and suboptimal oxygenation, continuous capnography is the most sensitive early warning of hypoventilation, apnoea, or circuit disconnection. It detects respiratory compromise before SpO2 drops, since pulse oximetry lags behind ventilatory failure especially on supplemental oxygen.

Capnography detects apnoea and hypoventilation earlier than pulse oximetry — SpO2 on supplemental O2 can remain normal for minutes after ventilation ceases. In PACU, capnography is essential monitoring for high-risk patients.

Active warming is important for hypothermia but does not directly detect ventilatory failure. Arterial lines and urinary catheters are valuable adjuncts but are not superior to capnography for early detection of respiratory deterioration in an unstable post-operative patient.

Aldrete ≥9 is a necessary but not sufficient criterion. Discharge requires also that pain is controlled (VAS ≤3–4), no active nausea/vomiting (PONV management), no shivering, and a formal sign-off by the anaesthetist or senior recovery nurse. Uncontrolled PONV and shivering are PACU complications requiring treatment before discharge.

PACU discharge criteria: Aldrete ≥9 + VAS pain score acceptable + no active PONV + no shivering + verbal communication adequate + surgical site reviewed. PACU nurses should not discharge patients who are vomiting or shivering even with adequate Aldrete scores.

Aldrete score alone does not override active clinical problems. A score of 10 is ideal but not routinely required. HDU escalation is needed for haemodynamic instability, not simply for PONV or shivering.

Current ALS algorithm for shockable rhythms (VF/pVT): shock → 2 min CPR 30:2 → rhythm check. If VF/pVT persists: 2nd shock → 2 min CPR → rhythm check. If VF/pVT persists: 3rd shock → 2 min CPR → adrenaline 1 mg IV + amiodarone 300 mg IV after the 3rd shock. Compressions at 100–120/min, depth 5–6 cm.

Shockable (VF/pVT): shock every 2 min with uninterrupted CPR (30:2); adrenaline 1 mg IV after 3rd shock, then every 3–5 min; amiodarone 300 mg IV after 3rd shock. Non-shockable (asystole/PEA): CPR + adrenaline 1 mg IV as soon as IV access — do NOT defibrillate.

Stacked shocks (without CPR) were abandoned in 2005 guidelines. Adrenaline is NOT given before the 3rd shock for shockable rhythms — this applies only to non-shockable rhythms (asystole/PEA). The 2-minute CPR periods are non-negotiable between each shock.

Bupivacaine is the most cardiotoxic LA and can cause refractory VF that does not respond to standard resuscitation. 20% Intralipid acts as a lipid sink, sequestering bupivacaine from cardiac tissue. Standard vasopressors do not reverse this mechanism. The missing intralipid represents a critical crash cart deficiency.

Bupivacaine = most cardiotoxic LA; avoid high-concentration IV regional. Max dose 2 mg/kg. LAST → 20% Intralipid 1.5 mL/kg bolus + 0.25 mL/kg/min infusion. Crash cart completeness is part of AS6.2 competency.

LAST from bupivacaine is NOT rare (femoral blocks use large volumes near vascular structures). Standard CPR may be inadequate without intralipid. Intralipid does not block sodium channels — it works via lipid partitioning (the 'lipid sink' hypothesis).

Acute severe bronchospasm in the PACU is a life-threatening AS6.3 complication. First-line is bronchodilator nebulisation (salbutamol + ipratropium). Ketamine (1–2 mg/kg IV) is a bronchodilator and is useful as an induction agent if intubation becomes necessary. IV magnesium is also used for refractory cases. Steroids help but are not fast enough for acute rescue.

PACU bronchospasm: salbutamol ± ipratropium nebulisation → IV hydrocortisone → IV ketamine (bronchodilator, useful as induction if intubation required) → IV magnesium 1.2–2 g over 20 min. Neostigmine is a bronchospasm TRIGGER — avoid in asthmatics or re-verify reversal indication.

Steroids alone are too slow for an acute severe episode. Neostigmine can actually worsen bronchospasm (cholinergic). Intubation without bronchodilators in active severe bronchospasm is dangerous — ventilation may be impossible. Bronchodilators are always first.

Tachycardia + hypotension + anxiety in a conscious patient after spinal anaesthesia (with motor block resolved) is haemorrhagic shock until proven otherwise. Spinal sympathectomy causes bradycardia, not tachycardia. The surgeon must be called urgently and blood products made available while fluid resuscitation starts.

PACU tachycardia + hypotension = haemorrhage until excluded. Spinal sympathectomy = bradycardia with hypotension (compensatory reflexes fail). Always call surgeon, review wound, check surgical site, request CBC and cross-match in this scenario.

Residual sympathectomy does not persist after motor block resolution and classically causes bradycardia with hypotension. Anaphylaxis involves bronchospasm, urticaria, angioedema — not present here. Vasovagal is self-limiting with rapid recovery — not tachycardia with BP 70/40.

This is opioid-induced respiratory depression (OIRD) — recognised by somnolence, low RR, low SpO2, and large opioid dose. Naloxone is indicated but must be titrated (0.1–0.2 mg every 2–3 min) to avoid acute withdrawal, hypertension, and pulmonary oedema. Obese patients are at highest risk for OIRD post-operatively.

OIRD recognition: RR <10, somnolence, pinpoint pupils, large cumulative opioid dose. Treatment: airway support + TITRATED naloxone 0.1–0.2 mg IV q2–3 min. Bolus 0.4 mg = avoidable PACU error. Obese patients: higher risk due to OSA + blunted hypoxic drive.

0.4 mg naloxone bolus causes abrupt reversal with catecholamine surge, pulmonary oedema, and pain crisis. Nasopharyngeal airway alone does not address the opioid effect. Neostigmine reverses neuromuscular blockade, not opioid effect — here the problem is respiratory depression, not muscle weakness.

Post-operative shivering can increase oxygen consumption by up to 400%, threatening myocardial oxygen supply-demand balance in at-risk patients. Pethidine 12.5–25 mg IV remains the most evidence-based drug treatment (via kappa-opioid receptors); tramadol is an alternative. Active forced-air warming is the non-pharmacological cornerstone.

Post-operative shivering: O2 demand ↑ 400%, cardiac risk in IHD. Treatment: forced-air warming blanket + IV pethidine 12.5–25 mg or tramadol 1 mg/kg. Prevention: intraoperative warming, IV ondansetron, neostigmine avoidance.

Shivering increases, not decreases, metabolic rate. It does not cause vasodilation — it is usually associated with peripheral vasoconstriction. Neostigmine is not a treatment for shivering. Atropine addresses bradycardia, not shivering.

Spinal level T3 blocks the cardiac accelerator fibres (T1–T4), causing both bradycardia and vasodilation (loss of arterial and venous sympathetic tone). Treatment: IV atropine for HR, IV ephedrine (α+β) for BP, 15° Trendelenburg to increase venous return. Fluids alone are insufficient when the block is this high.

High spinal (≥T4): both HR and BP fall — dual pathology. Cardiac accelerators at T1–T4: blocked → bradycardia. Venous/arterial tone lost → hypotension. Treat: atropine 0.5–1 mg IV + ephedrine 6–9 mg IV + left lateral tilt (if pregnant) or leg elevation + fluids.

Fluids alone are insufficient — atropine and ephedrine are required when cardiac accelerator fibres are blocked. There is no intrathecal morphine mentioned. Anaphylaxis presents with urticaria, bronchospasm, and has different triggers. Nausea here is from hypotension + high sympathectomy, not vagal alone.

Progressive neck swelling after thyroid surgery = expanding haematoma compressing the trachea. This is a surgical emergency. The airway can occlude within minutes. Immediate actions: summon surgeon + senior anaesthetist, prepare for re-intubation, have surgical airway equipment ready. Waiting is fatal.

Post-thyroidectomy neck haematoma: surgical emergency. Signs: neck swelling + dysphagia + stridor. Action: immediate surgeon call, bedside preparation for surgical clip removal if airway critical, emergency re-intubation by senior anaesthetist. Dexamethasone is adjunctive only.

Waiting 1–2 hours for ENT review is unacceptable — airway compression can develop rapidly. Ice packs and supplemental oxygen do not address the haematoma. Dexamethasone alone is appropriate for mucosal oedema but not haematoma expansion. Surgical decompression may be needed immediately.