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Cardiac Arrest in the Operating Theatre - A Professor's Teaching Lecture for MD Final Viva
"Residents, pay close attention. Cardiac arrest in the OT is the ultimate test of the anesthesiologist. You are surrounded by every possible resource - monitoring, drugs, equipment, team. Yet the mortality remains above 50% in many series. Why? Because panic replaces protocol. Today, we remove the panic. By the end of this session, you will have a systematic, physiologically grounded response to this emergency."
Section 1: Epidemiology and Why the OT is Unique
Let's start with some numbers that should both reassure and humble you.
- Cardiac arrest occurs in approximately 1 in every 10,000 anesthetics when the cause is anesthesia-related
- Data from the ACS NSQIP database shows a broader incidence - 1 in every 203 surgical patients - with over 70% dying within one month
- When cardiac arrest is purely anesthesia-related, successful resuscitation occurs approximately 90% of the time
- Overall in-hospital survival to discharge is ~25% for perioperative cardiac arrest
Why is the OT the best place for cardiac arrest?
Three reasons:
- The patient is already fully monitored - you see it the moment it happens
- There is immediate expert personnel present
- All resuscitation equipment is at hand - defibrillator, drugs, airway
The causes are different from community cardiac arrest. In the OT, the cause is usually known or knowable within 60 seconds. This changes everything about your approach.
(Barash's Clinical Anesthesia 9e; 2023 ESAIC/ESTES Consensus Guideline - Hinkelbein et al., Eur J Anaesthesiol 2023)
Section 2: Classification of Causes - The "ANESTHESIA + H's & T's" Framework
I want you to think in two parallel streams:
- Anesthesia/surgery-specific causes (unique to OT)
- General ACLS causes (H's and T's - same as anywhere else)
Stream A: OT-Specific Causes (The Examiner's Favorites)
1. Airway Catastrophe - Hypoxia from Failed Intubation / Oesophageal Intubation
The #1 anesthesia-related cause of cardiac arrest. Unrecognized oesophageal intubation, failed airway in a can't intubate-can't oxygenate (CICO) situation, or airway obstruction.
Mechanism: Hypoxia → bradycardia → asystole. This follows a predictable downward spiral.
Prevention/Recognition: Capnography is MANDATORY. An absent or falling ETCO2 waveform after intubation = oesophageal intubation until proven otherwise. Never rely on chest rise, breath sounds, or stomach sounds alone.
Management: Immediately revert to basic airway - bag-mask ventilation, supraglottic airway (LMA). If all fail → emergency front-of-neck access (eFONA) - surgical cricothyroidotomy.
2. Drug-Related Causes
(a) Anaphylaxis
Severe IgE-mediated (or direct mast cell) reaction leading to massive vasodilation, bronchospasm, and cardiovascular collapse.
Common triggers in OT: Neuromuscular blocking agents (most common - rocuronium, succinylcholine), latex, antibiotics, chlorhexidine, contrast media, colloids.
Recognition: Cardiovascular collapse (hypotension, tachycardia) + bronchospasm + urticaria. But in the anesthetized patient, skin signs may be absent or masked by drapes.
Treatment:
- Epinephrine IV is the first-line drug - 0.1-0.5 mg (1:10,000) IV boluses, escalating as needed. NOT just IM.
- Stop the trigger
- Aggressive IV fluids (1-2 L rapid)
- Bronchodilators (salbutamol nebulized or IV)
- Antihistamines and corticosteroids are secondary
(b) Succinylcholine-Induced Hyperkalemia
In patients with burns, spinal cord injury, prolonged immobilization, rhabdomyolysis, or critical illness - upregulation of extra-junctional acetylcholine receptors causes massive K+ efflux.
Time course: Minimum 4 days post-injury before dangerous response occurs. Can be catastrophic months later.
Treatment: Stop succinylcholine. Calcium gluconate (membrane stabilization), insulin + dextrose, sodium bicarbonate.
(c) Local Anesthetic Systemic Toxicity (LAST)
Accidental intravascular injection or rapid absorption of local anesthetic causing CNS excitation followed by cardiovascular collapse.
Signs: Metallic taste, tinnitus, perioral numbness → seizures → cardiovascular collapse → cardiac arrest. Bupivacaine causes particularly refractory VF due to Na+ channel blockade.
Prevention: Test dose with epinephrine marker (1:200,000), incremental injection (3-5 mL every 90-120 seconds), aspirate before each injection.
Treatment - LAST Protocol (ASRA Guidelines):
- Stop injection immediately
- Airway management, 100% O2, IV access
- Seizures: benzodiazepine (NOT propofol - cardiovascular depression)
- 20% Lipid Emulsion (Intralipid) - the specific antidote:
- Bolus: 1.5 mL/kg over 1 minute
- Infusion: 0.25 mL/kg/min
- Repeat bolus every 3-5 min if no response
- Maximum total dose: 10 mL/kg over first 30 minutes
- For cardiac arrest: standard ACLS + lipid emulsion
- Avoid propofol as lipid emulsion substitute (insufficient lipid load, adds cardiac depression)
(Miller's Anesthesia 10e, p. 1973; Barash's 9e, p. 2866)
3. Total Spinal / High Spinal Anesthesia
Excessive rostral spread of intrathecal local anesthetic, or accidental subarachnoid injection during epidural placement.
Mechanism: T1-T4 blockade → cardiac sympathetic denervation → bradycardia/asystole. Phrenic nerve (C3-5) blockade → respiratory arrest. Higher spread → brainstem → loss of consciousness.
Classic progression:
- Hand/arm tingling (cervical root involvement)
- Intercostal paralysis
- Diaphragm paralysis (C3-5)
- Apnea + LOC (brainstem)
- Cardiac arrest
Treatment: Supportive. Immediate:
- 100% O2, secure airway (intubate)
- Vasopressors (epinephrine/phenylephrine IV) for hypotension
- Atropine/epinephrine for bradycardia
- Psychological support and reassurance (patient may be conscious initially)
- Block resolves with time - generally recovers fully
(Miller's Anesthesia 10e, p. 6127)
4. Malignant Hyperthermia (MH)
Pharmacogenetic disorder (RYR1 gene mutation) causing uncontrolled Ca2+ release from sarcoplasmic reticulum after triggering agents.
Triggers: Volatile anesthetic agents (halothane, sevoflurane, desflurane, isoflurane) + succinylcholine.
Signs (early): Masseter spasm after succinylcholine, unexplained tachycardia, rising ETCO2 (despite adequate ventilation), hyperthermia (late sign), metabolic acidosis, hyperkalemia.
ETCO2 rise is often the FIRST sign.
Treatment (MH Crisis Protocol):
- Stop trigger agents immediately
- Call for help + MH hotline
- Dantrolene 2.5 mg/kg IV rapidly, repeat until ETCO2 falls (continue until crisis resolves, up to 10 mg/kg or more)
- 100% O2 at high flows to wash out volatile agents
- Active cooling (cold IV fluids, ice packs, cooled lavage)
- Treat hyperkalemia aggressively (cardiac arrest from K+ is a major risk)
- Bicarbonate for severe acidosis
- Continue surgery only if life-threatening
5. Venous Air Embolism (VAE)
Air entrainment into venous circulation causing an air-lock in the right heart/pulmonary circulation.
High-risk situations: Sitting craniotomy, neurosurgery with head elevated, total hip replacement (especially with pneumatic tourniquet deflation), laparoscopy (CO2 embolism), central line insertion.
Signs: Sudden unexplained hypotension, desaturation, "mill-wheel" murmur (churning sound in heart), sudden decrease in ETCO2 (air reduces pulmonary perfusion).
Treatment:
- Flood surgical field / stop air entry
- Aspirate via right heart/CVP catheter
- Place patient left lateral decubitus + Trendelenburg (Durant maneuver) - moves air bubble away from right ventricular outflow tract
- 100% O2 to dissolve air (NO nitrous oxide - it expands air bubble)
- CPR if arrest occurs - chest compressions may fragment large bolus
6. Tension Pneumothorax
Particularly relevant during positive-pressure ventilation, central line insertion, or thoracic/laparoscopic procedures.
Mechanism: Air accumulation in pleural space with mediastinal shift → obstructive shock → cardiac arrest. Positive pressure ventilation dramatically worsens tension.
Signs: Unilateral absent breath sounds, sudden hypotension, tracheal deviation (late), elevated airway pressures, desaturation, cardiovascular collapse.
Treatment: Do NOT wait for CXR in arrest. Immediate needle decompression (2nd intercostal space, mid-clavicular line) as emergency temporizing measure → definitive intercostal tube thoracostomy.
7. Cardiac Tamponade
Can occur post-cardiac surgery (acute pericardial hemorrhage), central line placement (cardiac perforation), or in trauma cases.
Beck's Triad: Hypotension + raised JVP + muffled heart sounds. But in anesthetized patient, Beck's triad may be incomplete.
Signs in OT: Unexplained hypotension, equalization of filling pressures (CVP = PAWP), decreasing cardiac output, paradoxical pulse, tachycardia, pulsus paradoxus.
Treatment: Pericardiocentesis (subxiphoid approach) - Seldinger technique. Definitive: surgical drainage. TEE is invaluable for diagnosis.
8. Acute Coronary Syndrome / Massive MI
Plaque rupture triggered by surgical stress, tachycardia, hypotension, anemia, or hypercoagulable state.
Treatment: Standard ACLS. Post-ROSC: urgent 12-lead ECG, cardiology consultation, cath lab if STEMI.
Stream B: The H's and T's (AHA 2020 ACLS Guidelines)
These apply in OT just as in any other setting:
| H's | T's |
|---|
| Hypovolemia - massive hemorrhage | Tension pneumothorax |
| Hypoxia - airway failure, aspiration | Tamponade (cardiac) |
| Hydrogen ion (Acidosis) | Toxins - drugs, local anesthetics |
| Hypo/Hyperkalemia | Thrombosis, pulmonary (massive PE) |
| Hypothermia - cold irrigation, prolonged surgery | Thrombosis, coronary (MI) |
| Hypoglycemia | |
(Barash's Clinical Anesthesia 9e, p. 2243; AHA 2020 ACLS Guidelines)
Section 3: Recognition in the OT
In a monitored patient, recognition should be immediate. Do not spend >10 seconds confirming - if the patient is pulseless and unresponsive, start CPR.
Key monitors to watch:
- SpO2 waveform loss (first sign often)
- ETCO2 sudden drop to zero (no cardiac output = no CO2 delivery to lungs)
- Arterial line trace goes flat
- ECG: VF, pulseless VT, asystole, PEA
- Surgical field: sudden "empty" vessels, no bleeding
ETCO2 is your CPR quality monitor:
- During good CPR, ETCO2 should be >10 mmHg
- ETCO2 >40 mmHg during CPR = very likely ROSC
- Helps guide compression quality without interrupting CPR
Section 4: The OT Cardiac Arrest Algorithm - 2020 AHA / 2023 ESAIC-ESTES
Immediate Response (First 30 seconds)
- Call for help - designate team leader immediately
- Confirm cardiac arrest - pulse check <10 seconds
- Start high-quality CPR - 30:2 if not intubated; continuous compressions if intubated
- Apply defibrillator pads
- Assess rhythm
CPR Quality Standards (2020 AHA)
| Parameter | Target |
|---|
| Rate | 100-120 compressions/min |
| Depth | 5-6 cm sternum depression |
| Recoil | Full chest recoil (no leaning) |
| Interruptions | Minimize - <10 sec pause |
| Ventilation (intubated) | 1 breath every 6 seconds (10/min) |
| Ventilation rate | DO NOT over-ventilate - increases intrathoracic pressure, reduces venous return |
Shockable vs. Non-Shockable Rhythms
Shockable: VF / Pulseless VT
- Shock immediately: Biphasic 120-200J, monophasic 360J
- Resume CPR immediately after shock (do NOT check pulse first)
- Epinephrine 1 mg IV every 3-5 minutes (after 2nd shock)
- Amiodarone 300 mg IV bolus (after 3rd shock) - for refractory VF/VT
- Internal defibrillation (open chest): 10-50J if chest is open
Non-Shockable: Asystole / PEA
- CPR immediately
- Epinephrine 1 mg IV as soon as possible, then every 3-5 minutes
- Identify and treat H's and T's
- Atropine: NOT recommended for asystole/PEA (insufficient evidence, not harmful but not helpful)
Epinephrine mechanism in arrest:
- All benefit comes from alpha-adrenergic vasoconstriction
- Increases aortic diastolic pressure → increases coronary perfusion pressure → improves myocardial blood flow
- Beta effects are actually detrimental (increase post-ROSC arrhythmias and O2 demand)
(Barash's Clinical Anesthesia 9e, p. 1928-1932)
Section 5: OT-Specific Modifications to Standard ACLS
The 2023 ESAIC/ESTES Consensus Guideline (Hinkelbein et al.) emphasizes several OT-specific points:
-
Airway advantage: The anesthesiologist can maintain a definitive airway immediately - use it. Continuous capnography during CPR is essential.
-
Open Chest Cardiac Massage (OCCM): In cardiac surgery cases or when chest is already open - internal cardiac massage is far more efficient than external compressions (generates higher cardiac output). Use internal paddles for defibrillation starting at 10J.
-
Position: External CPR in prone-positioned patients - place pads at T7 and right shoulder; compressions at same location as standard. Do NOT routinely reposition prone patients unless compressions are completely ineffective.
-
Drug delivery: Intraosseous (IO) access - humeral IO is rapid and allows 100 mL/min flow. If no IV access, use IO. Do NOT use endotracheal route as primary route.
-
TEE: Provides real-time diagnosis of cause (wall motion abnormality, pericardial effusion, RV failure, PE) without interrupting compressions. Gold standard for intraoperative diagnosis.
-
Surgical control of hemorrhage: If cardiac arrest is due to surgical hemorrhage, surgical hemostasis takes priority alongside CPR.
-
REBOA (Resuscitative Endovascular Balloon Occlusion of the Aorta): In select trauma cases, can temporize hemorrhagic cardiac arrest by occluding descending aorta - complex, requires specific training and infrastructure.
Section 6: Drugs in OT Cardiac Arrest - Quick Reference
| Drug | Dose | Indication |
|---|
| Epinephrine | 1 mg IV every 3-5 min | VF, PEA, Asystole - ALL rhythms |
| Amiodarone | 300 mg IV bolus, then 150 mg | Refractory VF/VT (after 3rd shock) |
| Lidocaine | 1-1.5 mg/kg IV | Alternate to amiodarone if not available |
| Atropine | NOT recommended in arrest | No benefit in asystole/PEA |
| Calcium gluconate | 10-20 mL of 10% IV | Hyperkalemia, hypocalcemia, Ca-channel blocker OD |
| Sodium bicarbonate | 1 mEq/kg IV | Hyperkalemia, tricyclic antidepressant OD, severe acidosis >10 min arrest |
| Dantrolene | 2.5 mg/kg IV bolus | Malignant hyperthermia |
| 20% Lipid emulsion | 1.5 mL/kg bolus then 0.25 mL/kg/min | LAST (local anesthetic toxicity) |
| Magnesium sulfate | 1-2 g IV | Torsades de pointes, hypomagnesemia |
| Vasopressin | 40 units IV (single dose) | Can replace 1st or 2nd dose of epinephrine |
Section 7: Post-Resuscitation Care (Post-ROSC)
The battle doesn't end with ROSC. "Post-resuscitation disease" is real.
Post-Cardiac Arrest Care Algorithm - AHA 2020 (Barash's Clinical Anesthesia 9e)
Initial Stabilization Phase:
Airway:
- Secure airway with ETT + confirm with waveform capnography
- Ventilate at 10 breaths/min (start)
Respiratory:
- Titrate FiO2: SpO2 92-98% (avoid hyperoxia - generates free radicals)
- Titrate ventilation: PaCO2 35-45 mmHg (avoid hypocapnia - causes cerebral vasoconstriction)
Hemodynamic:
- Systolic BP >90 mmHg, MAP >65 mmHg
- Vasopressors/inotropes as needed
Continued Management:
12-lead ECG immediately - if STEMI → urgent cath lab. Do not let a recent surgery deter you if STEMI is confirmed and the culprit vessel is likely the cause of arrest.
Targeted Temperature Management (TTM):
- If patient is comatose (not following commands) after ROSC → TTM at 32-36°C for 24 hours
- Prevents secondary neurological injury from reperfusion
- Use cooling device with feedback loop
- Monitor core temperature continuously (esophageal, rectal, bladder)
- TTM + EEG monitoring + brain CT are all part of the comatose post-arrest bundle
Other:
- Maintain normoglycemia (hyperglycemia worsens neurological outcome)
- Continuous or intermittent EEG (detect subclinical seizures)
- Lung-protective ventilation
- Avoid hyperthermia after TTM completion
(Barash's Clinical Anesthesia 9e, p. 2301-2344; AHA 2020)
Section 8: DNAR Orders in the OT
This is a medicolegal topic that will definitely appear in your viva.
Key facts:
- Up to 60% of anesthesiologists mistakenly believe DNAR orders are automatically suspended in the OT
- This is legally and ethically wrong - advance directives are binding
- ASA, American College of Surgeons, AORN, and The Joint Commission all require reconsideration, not abandonment, of DNAR in the perioperative period
- The discussion must occur preoperatively, must be documented, and must be shared with the full OT team
- Families have successfully sued for damages when DNAR instructions were ignored
(Miller's Anesthesia 10e, p. 634)
Section 9: Prevention - The Anesthesiologist's Priority
"It is far better to prevent a cardiac arrest than to manage one."
| Prevention Strategy | Target |
|---|
| Capnography monitoring | Detect oesophageal intubation, monitor CPR quality |
| Difficult airway algorithm preparation | Avoid CICO situation |
| Test dose in regional anesthesia | Detect intravascular injection (LAST) |
| Incremental local anesthetic injection | Limit LAST risk |
| Avoid succinylcholine in at-risk patients | Prevent hyperkalemic arrest |
| MH triggering agent avoidance (susceptible patients) | Prevent MH crisis |
| Dantrolene stocked within OR | MH emergency readiness |
| Regular simulation and drill practice | Team performance in crisis |
| Crew Resource Management (CRM) | Communication errors reduced |
| Cognitive aids / checklists | Stanford Emergency Manuals in every OT |
VIVA QUESTIONS - Rapid Fire
Professor to Resident - typical MD Final Viva format
Q1. What is the incidence of cardiac arrest in the OT?
Approximately 1 in 10,000 anesthetics when purely anesthesia-related; 1 in 203 surgical patients in the broader NSQIP database.
Q2. Why does the OT have the highest CPR success rate within the hospital?
Because patients are already fully monitored, arrest is recognized immediately, expert personnel are present, and all resuscitation equipment is immediately available. When anesthesia-related, ROSC approaches 90%.
Q3. Name the H's and T's for reversible causes of cardiac arrest.
H's: Hypovolemia, Hypoxia, Hydrogen ion (acidosis), Hypo/Hyperkalemia, Hypothermia, Hypoglycemia. T's: Tension pneumothorax, Tamponade, Toxins, Thrombosis-pulmonary, Thrombosis-coronary.
Q4. What is the drug of choice for cardiac arrest? What is its mechanism?
Epinephrine 1 mg IV every 3-5 minutes. Its benefit is entirely through alpha-adrenergic vasoconstriction - increases aortic diastolic pressure → raises coronary perfusion pressure → improves myocardial blood flow. Beta effects are not beneficial during arrest.
Q5. A patient develops sudden hypotension, absent breath sounds on one side, and rising airway pressures during mechanical ventilation. What do you do?
Tension pneumothorax. Stop ventilation briefly to confirm, immediately perform needle decompression at 2nd intercostal space, midclavicular line, followed by intercostal tube thoracostomy. Do NOT wait for CXR in haemodynamic compromise.
Q6. You give succinylcholine to a patient who was in an ICU for 3 weeks with Guillain-Barré syndrome. She arrests 2 minutes later. What happened? How do you treat it?
Succinylcholine-induced hyperkalemia. Upregulation of extrajunctional acetylcholine receptors causes massive K+ efflux. Treatment: standard CPR, calcium gluconate 10 mL IV (membrane stabilization), insulin + dextrose, sodium bicarbonate. Avoid succinylcholine in any patient with >4 days of denervation, burns, prolonged immobilization, or critical illness.
Q7. A patient undergoing a femoral nerve block arrests. The preceding signs were tinnitus, then generalized convulsion. What is the diagnosis and treatment?
LAST - Local Anesthetic Systemic Toxicity. Specific treatment is 20% lipid emulsion: 1.5 mL/kg bolus over 1 minute → infusion at 0.25 mL/kg/min. Repeat bolus every 3-5 min. Maximum 10 mL/kg over 30 min. Standard ACLS simultaneously. Avoid propofol as a substitute - it adds cardiovascular depression and the lipid concentration is insufficient.
Q8. What are the signs of malignant hyperthermia and what is the specific drug?
Unexplained tachycardia + rising ETCO2 (most important early sign) + masseter spasm (after succinylcholine) + metabolic acidosis + hyperkalemia + hyperthermia (late). Specific treatment: Dantrolene 2.5 mg/kg IV bolus (repeat until ETCO2 falls), plus stop triggers, active cooling, treat hyperkalemia. Dantrolene prevents Ca2+ release from sarcoplasmic reticulum by blocking RYR1 channels.
Q9. What is the recommended defibrillation sequence and energy levels?
Single biphasic shock (120-200J; manufacturer-specific) → immediate CPR resumption (do NOT pulse check) → 2 minutes CPR → rhythm check. If VF persists: shock → CPR. Epinephrine 1 mg IV after 2nd shock. Amiodarone 300 mg IV after 3rd shock. Internal defibrillation (open chest): start at 10J, increase as needed.
Q10. When should amiodarone be given during cardiac arrest?
After the 3rd failed defibrillation attempt in refractory VF or pulseless VT. Dose: 300 mg IV rapid bolus during arrest, then 150 mg supplements as needed. Maximum 2g/day. It improves survival to hospital admission (3 randomized trials) but has not shown survival to discharge benefit. Lidocaine 1-1.5 mg/kg is the alternative if amiodarone is unavailable.
Q11. ETCO2 drops suddenly to zero during surgery. What is your differential?
The ABCDE approach: (A) Oesophageal intubation / tube displacement, (B) Circuit disconnection, (C) Cardiac arrest / massive pulmonary embolism (no blood reaching lungs), (D) Massive air embolism. First check patient (is pulse present?), check airway, check circuit. ETCO2 also correlates with CPR quality - a rising ETCO2 during CPR indicates improving cardiac output.
Q12. How does CPR differ in a prone-positioned patient?
Per 2023 ESAIC guidelines: place defibrillator pads at T7 (posterior) and right shoulder (anterior). Compressions are applied at the same position as standard (lower third of sternum against the table). Do not routinely turn the patient supine unless compressions are definitively ineffective - repositioning wastes critical time.
Q13. What is TTM and when is it indicated post-ROSC?
Targeted Temperature Management at 32-36°C for 24 hours in comatose patients (those not following commands) after ROSC. Reduces secondary neurological injury from reperfusion. Do NOT allow hyperthermia. Monitor temperature continuously. Accompany with EEG monitoring (detect subclinical seizures), brain CT, and normoglycemia. Neuroprognostication should not occur before 48-72 hours post-arrest.
Q14. Can DNAR orders be automatically overridden in the OT?
No. This is a common misconception - 60% of anesthesiologists erroneously believe this. DNAR must be reconsidered, not abandoned in the perioperative period. Anesthesiologist must discuss with patient, document the agreement, and communicate with the full OT team preoperatively. Advance directives are legally binding. Courts have awarded damages when DNAR was overridden without consent.
Q15. What is the role of TEE during cardiac arrest in the OT?
TEE is the gold standard intraoperative diagnostic tool during cardiac arrest. It can identify: new RWMA (myocardial infarction), pericardial effusion/tamponade, right heart failure (PE), hypovolemia (empty heart), massive air embolism, and the adequacy of compressions - all without interrupting CPR. The 2023 ESAIC guidelines support its use in the OT setting.
Summary Framework for Exam
Cardiac Arrest in OT
│
├── RECOGNIZE (< 10 sec): Monitor loss, no pulse
│
├── CALL FOR HELP + START CPR (100-120/min, 5-6 cm)
│
├── DEFIBRILLATOR ON → Shockable? → Shock + CPR
│ ↓ Non-shockable?
│ CPR + Epinephrine
│
├── FIX THE CAUSE (H's & T's + OT-specific)
│ ├── Airway failure → Reoxygenate, eFONA
│ ├── Anaphylaxis → Epinephrine IV + fluids
│ ├── LAST → Lipid emulsion 20%
│ ├── Total spinal → Airway + vasopressors
│ ├── MH → Dantrolene + cooling
│ ├── VAE → Durant maneuver + O2
│ ├── Tension PTx → Needle decompression
│ ├── Tamponade → Pericardiocentesis
│ └── Hyperkalemia → Ca2+, bicarb, insulin
│
└── POST-ROSC → TTM (if comatose), STEMI? → Cath lab
SpO2 92-98%, PaCO2 35-45, MAP >65
"Remember - in the OT, cardiac arrest is different from the street. You know the cause, you have the team, you have the drugs. What you need is a calm, systematic approach and a team that communicates. Practice the drills, know the algorithms, and never let panic override protocol. That is what separates a good anesthesiologist from a great one."
Key References:
- Barash's Clinical Anesthesia 9e, Chapter 58 (pp. 4896-4948)
- Miller's Anesthesia 10e (pp. 634, 6127, 1973)
- Hinkelbein J et al. "Cardiac arrest in the perioperative period: a consensus guideline." Eur J Anaesthesiol. 2023 Oct (PMID: 37218626) - ESAIC/ESTES Practice Guideline
- AHA 2020 Guidelines for CPR and ECC (Circulation. 2020;142:S366-S468)
- ASRA Local Anesthetic Systemic Toxicity Checklist (2020)
- Morgan & Mikhail's Clinical Anesthesiology 7e