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AS2.1-2 | Cardiopulmonary Resuscitation — Graded Quiz
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A 70-year-old man is found pulseless in the ICU. One nurse starts compressions while another prepares the defibrillator. The monitor shows VF. After one unsynchronised shock at 200 J (biphasic), compressions resume immediately without checking rhythm. Two minutes later, the rhythm is re-checked and shows organised sinus rhythm with a palpable pulse. At this point, which BEST describes the optimal immediate post-ROSC airway and ventilation strategy?
Correct. Post-ROSC airway management in a comatose patient requires definitive airway control (ETT). Ventilation targets are normocarbia (PaCO2 35–45 mmHg) and moderate oxygen saturation (94–98%), avoiding both hyperoxia and hypoxia, which independently worsen neurological outcome.
Post-arrest care is a bundle: TTM + normocarbia + normoxia + MAP >65 mmHg + early coronary angiography if STEMI. Each element independently reduces mortality.
After ROSC, a comatose patient needs a definitive airway. Ventilation targets are SaO2 94–98% (NOT 100% — hyperoxia increases reactive oxygen species injury) and PaCO2 35–45 mmHg (NOT hyperventilation — hypocarbia causes cerebral vasoconstriction and ischaemia). NRB masks are inadequate for definitive post-arrest management.
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An ALS team is managing a cardiac arrest. After the third defibrillation shock, the team prepares drugs. Amiodarone 300 mg IV is given. The arrest has been ongoing for 10 minutes. What is the NEXT dose of amiodarone if VF/pVT persists, and when is it given?
Correct. In refractory VF/pulseless VT, the ALS algorithm gives amiodarone 300 mg IV after the 3rd shock, followed by a supplemental dose of 150 mg IV after the 4th shock (i.e., after the next 2-minute CPR cycle and re-analysis).
Amiodarone is the antiarrhythmic of choice in shock-refractory VF/pVT. The two-dose regimen (300 mg then 150 mg) is sequential, each given after a CPR cycle, before re-analysis. Know the timing — it is a common exam discriminator.
Amiodarone dosing in cardiac arrest per ALS 2021 guidelines: 300 mg IV bolus after 3rd shock, then 150 mg IV after the 4th shock. Lidocaine (1 mg/kg) is an alternative when amiodarone is unavailable, not a planned sequential agent. A repeat 300 mg dose would exceed recommended dosing.
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A 6-year-old girl is found pulseless with a heart rate of 0 on the monitor. Two-rescuer paediatric BLS is in progress. The defibrillator arrives. The rhythm is confirmed as VF. What energy dose (J/kg) is used for the first and subsequent paediatric defibrillation shocks?
Correct. Paediatric defibrillation: 2 J/kg for the first shock, then 4 J/kg for all subsequent shocks (up to a maximum of 10 J/kg or the adult dose, whichever is lower). Weight-based dosing is essential to avoid myocardial injury from excess energy.
Always note the child's weight before resuscitation begins if known, or estimate (Broselow tape). The ceiling of 10 J/kg or adult dose prevents excessive energy delivery without sacrificing efficacy.
Paediatric defibrillation energy is weight-based: 2 J/kg (1st shock), 4 J/kg (subsequent; max 10 J/kg or adult dose). Adult doses (200 J biphasic) would be inappropriate without weight adjustment. The 1 J/kg doses cited are below current guideline recommendations.
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A 52-year-old man is brought to the ED after out-of-hospital cardiac arrest. ROSC was achieved after 18 minutes of CPR. He has no purposeful response to pain (GCS 5) and is intubated. His 12-lead ECG shows ST elevation in V1–V4. Which combination of post-resuscitation interventions is MOST appropriate?
Correct. When STEMI is identified post-ROSC, emergent coronary angiography (with PCI if indicated) should NOT be delayed by TTM or neurological status. Both TTM and emergent PCI are pursued simultaneously — current guidelines support this combined approach.
The post-cardiac arrest STEMI pathway: intubate → haemodynamic support → STEMI identified → emergent cath lab activation. TTM is initiated during transport/in the cath lab — do not use it as a reason to delay reperfusion.
STEMI post-ROSC is a time-sensitive emergency. Deferring angiography until neurological recovery is incorrect — the coronary culprit perpetuates myocardial dysfunction. Thrombolysis is a last resort (when PCI is unavailable), not contraindicated per se by CPR, but PCI is far superior. TTM and PCI are complementary, not competing.
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During CPR, end-tidal CO2 (EtCO2) monitoring is used. After 15 minutes of effective CPR, EtCO2 suddenly rises from 10 mmHg to 35 mmHg without a change in ventilation. What does this MOST likely indicate?
Correct. A sudden rise in EtCO2 to >35–40 mmHg during CPR is a reliable non-invasive indicator of ROSC. The restored cardiac output rapidly delivers metabolically produced CO2 to the lungs, raising the EtCO2 detectably. This should trigger a rhythm and pulse check.
EtCO2 is a continuous, hands-off ROSC detector. If EtCO2 jumps abruptly from low values to near-normal during CPR, pause compressions and check for pulse. This avoids missing ROSC and continuing unnecessary compressions.
EtCO2 in CPR: (1) confirms ETT placement (EtCO2 detected = tracheal), (2) indicates CPR quality (low EtCO2 <10 mmHg = inadequate compressions), (3) predicts ROSC (sudden rise >35 mmHg during ongoing CPR = ROSC until proven otherwise). Oesophageal intubation gives zero or near-zero EtCO2. Shallow compressions reduce EtCO2; they do not abruptly raise it.
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During a neonatal resuscitation, a term infant is born limp and apnoeic. After drying and stimulating for 30 seconds, the infant is still apnoeic. Five sustained inflation breaths are given. Reassessment shows heart rate 50/min and SpO2 70%. The airway appears clear. What is the CORRECT next step?
Correct. Before starting chest compressions in neonatal resuscitation, you must first confirm effective lung aeration — evidenced by chest rise with inflation breaths. If the initial 5 breaths did not produce adequate chest rise (which the HR >40/min and low SpO2 suggest here), the priority is airway correction (reposition, suction, consider laryngoscopy) and 5 further breaths. Compressions on an unaerated lung are ineffective.
The neonatal resuscitation mantra: ventilation before compressions, airway confirmation before compressions. Compression without lung aeration circulates unoxygenated blood — it buys no time and wastes it.
Neonatal CPR rule: NEVER start compressions before confirming lung aeration. The failure checkpoint: 5 inflation breaths → assess chest rise → if no chest rise, reposition/suction/laryngoscope → 5 more breaths → if HR <60 and chest rise confirmed, THEN 3:1 compressions. Adrenaline is given much later (HR <60 after effective CPR + epinephrine trial). The 30:2 ratio does not apply to neonates.
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A 40-year-old woman develops cardiac arrest in theatre post-induction. The anaesthetist recognises the cardiac monitor shows pulseless electrical activity (PEA). Which of the following reversible causes should be excluded FIRST in this intraoperative context?
Correct. In the intraoperative setting, PEA most commonly results from tension pneumothorax (especially with positive pressure ventilation) or acute hypovolaemia (haemorrhage, anaphylaxis). These are rapidly reversible if identified immediately. While all 4 Hs and 4 Ts must be considered, contextual probability guides the search sequence.
Context shapes the 4H4T search order. Perioperative PEA: first exclude tension pneumothorax (needle decompression if suspected) and haemorrhage/anaphylaxis-driven hypovolaemia. A structured mental checklist is essential — no time for systematic review during PEA arrest.
PEA reversible causes (4 Hs and 4 Ts): Hypoxia, Hypovolaemia, Hypo/hyperkalaemia, Hypothermia; Tension pneumothorax, Tamponade, Toxins, Thrombosis. In the intraoperative setting, tension pneumothorax (high airway pressures, asymmetric breath sounds, tracheal deviation) and hypovolaemia (haemorrhage) are the most immediately lethal and most easily corrected. Hyperkalaemia and hypothermia are less acute.
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A team of 5 is conducting ALS on a 65-year-old man. After 30 minutes of refractory VF despite 8 shocks, optimal drug therapy, and correction of electrolytes, the consultant considers termination of resuscitation efforts. Which factor, if present, is MOST strongly associated with a meaningful chance of survival and should prompt continuation?
Correct. Witnessed arrest + immediate bystander CPR + shockable initial rhythm (VF/pVT) represent the best prognostic triad in cardiac arrest and individually and collectively favour continuation of resuscitation. A persistently low EtCO2 (<10 mmHg) despite optimal CPR is a poor prognostic indicator.
Termination of resuscitation is a clinical decision integrating: rhythm history, EtCO2 trend, time elapsed, reversible cause search results, witness status, and patient advance directives. No single factor is absolute — the triad of witnessed + CPR + shockable is the strongest continuation signal.
Prognostically favourable factors: witnessed arrest, immediate CPR, shockable rhythm, short time-to-defibrillation, young age, reversible cause identified. Persistently low EtCO2 (<10 mmHg) despite 20+ minutes of quality CPR is one criterion supporting cessation. Age and sex alone are not independent criteria. Absence of a reversible cause is unfavourable.
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During ALS, the team leader asks for adrenaline. The dose and route are 1 mg IV. However, IV access cannot be secured after 90 seconds. What is the CORRECT alternative route and dose?
Correct. Intraosseous access is the recommended alternative when IV access fails in cardiac arrest. The dose of adrenaline via IO is identical to IV — 1 mg. IO drug delivery is pharmacodynamically equivalent to IV in cardiac arrest because IO bones drain directly into venous sinusoids.
IO access can be established in under 60 seconds and is the first-line alternative to IV in cardiac arrest. Modern IO devices (e.g., EZ-IO) are reliable. Do not delay resuscitation pursuing failed IV — drill and go.
If IV access fails after 90 seconds in cardiac arrest, IO is the immediate next step (tibia or humerus). The drug dose is the same as IV. Endotracheal adrenaline (2–3× IV dose) is a last resort — absorption is unpredictable in cardiac arrest, and endotracheal drug delivery was removed as a primary recommendation in current guidelines. Intracardiac injection is obsolete and dangerous. IM is ineffective in arrested circulation.
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An anaesthesiology student is teaching a group of interns about adult BLS. One intern asks: 'Can I do compression-only CPR if I am unable to give rescue breaths?' Which response is MOST accurate for adult out-of-hospital cardiac arrest?
Correct. Compression-only (hands-only) CPR is endorsed for untrained or reluctant lay rescuers for adult cardiac arrest. Evidence shows survival rates similar to conventional CPR for the first several minutes because the lungs contain residual oxygenated air and cardiac arrest in adults is predominantly cardiac. Healthcare providers should give conventional CPR (30:2) whenever possible.
The cardiac arrest origin determines the ventilation requirement: adult (cardiac) = compression-only acceptable as lay fallback; paediatric/drowning/respiratory (hypoxic) = ventilation is essential and must not be omitted.
Compression-only CPR is a guideline-endorsed strategy for adult out-of-hospital cardiac arrest, especially for lay rescuers. It improves bystander CPR rates (removes ventilation as a barrier). However, healthcare providers, and ALWAYS in paediatric/neonatal arrest and drowning (respiratory origin), conventional 30:2 (or 15:2 paediatric two-rescuer) CPR with ventilation should be given.
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