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1. Automatically look up that question from your bank
2. Answer it at MD exam level using references from:
   • Miller's Anesthesia
   • Barash's Clinical Anesthesia
   • Morgan & Mikhail's Clinical Anesthesiology
   • Relevant international journals (where applicable)

Q175: Factors Controlling Coronary Blood Flow

Introduction

Coronary Perfusion Pressure (CPP)

CPP (LV) = Aortic Diastolic Pressure (AoDP) - LV End-Diastolic Pressure (LVEDP)

CPP (RV) = Aortic mean pressure - RV end-diastolic pressure

• Tachycardia shortens diastolic filling time and reduces LV perfusion time - this is the most important cause of perioperative ischemia
• Raised LVEDP (e.g., volume overload, poor compliance) reduces CPP
• Hypotension reduces AoDP and compromises perfusion

Autoregulation

• Autoregulation is effective between perfusion pressures of 50-120 mmHg
• Below 50 mmHg, flow becomes pressure-dependent (autoregulation is lost)
• Autoregulation of subendocardial flow is lost when perfusion pressure falls below 40 mmHg
• Beyond 120 mmHg, forced vasodilation occurs

Metabolic (Local) Regulation - The Primary Controller

Endothelin-1 (ET-1) is a potent vasoconstrictor produced by endothelium; under normal conditions its effect is counterbalanced by tonic NO release. Pathologic states (diabetes, hypertension, heart failure) tip the balance toward vasoconstriction.

Coronary Vascular Reserve

• Normal CVR = 3-5 times basal flow (500-600% of baseline for LV and RV)
• CVR is reduced by: epicardial stenosis, pressure-overload hypertrophy, microvascular dysfunction
• Stenosis of 50% luminal diameter = first impairment in reactive hyperemia
• Stenosis of ~90% = abolishes peak hyperemia = unstable angina threshold

Autonomic (Neural) Control

Sympathetic Nervous System

• Direct effects: Both α1 and β2 receptors present
  • α1 receptors: predominantly on larger epicardial vessels → vasoconstriction
  • β2 receptors: predominantly on smaller intramuscular/subendocardial vessels → vasodilation
• Indirect effects (dominant): Sympathetic stimulation ↑ HR and contractility → ↑ MVO2 → metabolic vasodilation overwhelms direct vasoconstriction
• Net effect: coronary blood flow increases with sympathetic stimulation due to dominant β2 + metabolic override
• Pathological exception: In some individuals, disproportionate α1 activation causes vasospastic ischemia (variant/Prinzmetal angina)

Parasympathetic Nervous System

• Vagal innervation of ventricular coronary vessels is sparse
• Acetylcholine has a direct, weak vasodilatory effect on coronary arteries
• Indirect effect: Vagal slowing of HR ↓ MVO2 → indirect vasoconstriction
• Net effect: minor and usually clinically insignificant

Humoral / Endocrine Factors

Physical / Mechanical Factors

Extravascular Compression

• LV flow is predominantly diastolic
• Tachycardia is particularly harmful - reduces diastolic time disproportionately

Heart Rate

• Increased HR = reduced diastolic perfusion time (supply ↓)
• Increased HR = increased MVO2 (demand ↑)
• This double jeopardy makes tachycardia the most dangerous factor in myocardial ischemia

Ventricular End-Diastolic Pressure

• Elevated LVEDP compresses subendocardial vessels and reduces CPP gradient
• Morgan & Mikhail specifically list LVEDP as both a supply factor (reducing perfusion) and a demand factor (increasing wall stress)

Myocardial Oxygen Supply-Demand Balance (Summary Table)

Oxygen Consumption Distribution

• Basal requirements: 20%
• Electrical activity: 1%
• Volume work: 15%
• Pressure work: 64%

Ischemia: Supply vs. Demand

Anaesthetic Implications

• Volatile agents: Most are coronary vasodilators; net effect on CBF is variable due to simultaneous reduction in MVO2 and blood pressure
• Spinal/epidural to T4: Decreases CBF in proportion to MAP reduction; can improve regional myocardial function in ischemic patients by reducing afterload and MVO2
• High thoracic epidural: Beneficial in ischemic heart disease - reduces sympathetic tone, wall stress, and MVO2
• Tachycardia prevention is the most important intraoperative goal - the single factor that simultaneously reduces supply and increases demand
• Vasopressors: Pure α-agonists (phenylephrine) increase AoDP (supply) but also increase afterload (demand); ephedrine increases HR (harmful); norepinephrine is generally preferred in hypotension with tachycardia

Key Points for MD Exam

1. Primary controller = metabolic regulation via adenosine, NO, KATP channels
2. Autoregulation range = 50-120 mmHg; subendocardial autoregulation lost at <40 mmHg
3. LV perfused in diastole only - tachycardia is the most dangerous hemodynamic change
4. CPP (LV) = AoDP - LVEDP; both ends of this equation must be optimized
5. Neural control is secondary and overridden by metabolic control within seconds
6. Coronary reserve = 3-5x basal flow; stenosis >50% begins to impair reactive hyperemia
7. Pressure work accounts for 64% of MVO2 - hypertension is the biggest demand driver
8. Endothelium is central - eNOS/NO, endothelin-1 balance; disrupted in atherosclerosis/diabetes

Q275: Management of Cardiac Arrest in Pregnancy

Introduction

Epidemiology

• Incidence: ~1 in 12,000 hospital deliveries
• Pregnant women are typically younger than the traditional cardiac arrest patient but outcomes are poor
• Maternal death from anesthesia has declined; leading anesthesia-related causes include failed intubation/induction problems (23%), respiratory failure (20%), and high spinal/epidural block (16%)

Causes of Cardiac Arrest in Pregnancy - The "ABCDEFGH" Mnemonic

Why Pregnancy Alters Resuscitation

Key Physiological Differences Relevant to CPR

Immediate Resuscitation Steps (AHA/ERC Algorithm for Pregnancy)

Step 1: Call for Help - Activate the Team

• Immediately call for: obstetric team, neonatal team, senior anaesthesiologist, surgical team capable of caesarean section
• Assign a team leader
• Do NOT delay CPR for team assembly
• Fetal monitoring should NOT be attempted during CPR - it distracts from maternal resuscitation

Step 2: Assess Gestational Age / Fundal Height

• If fundus at or below umbilicus (<20 weeks): Standard adult CPR, no modifications needed
• If fundus at or above umbilicus (≥20 weeks): Apply left uterine displacement (LUD) while performing CPR

Step 3: Left Uterine Displacement (LUD)

• A dedicated team member provides continuous manual LUD from the patient's right side, displacing the uterus to the patient's left
• One-handed or two-handed technique (one-handed preferred to keep team members free for other tasks)
• Tilting the patient 15-30° to the left on a wedge is an alternative but reduces CPR quality - manual LUD on a flat surface is preferred
• Chest compressions should still be in the standard supine position; compressions with patient tilted laterally are less effective

High-Quality CPR in Pregnancy

1. Aspiration risk (full stomach)
2. O2 consumption 30% above normal → rapid hypoxia
3. Reduced FRC → faster desaturation

Defibrillation and Medications

Defibrillation

• Indicated for shockable rhythms (VF/pulseless VT) at standard energy levels (biphasic: 120-200 J)
• Remove fetal electronic monitoring equipment before shock
• Defibrillation is safe - negligible energy reaches the fetus
• Automated external defibrillators (AEDs) are safe in pregnancy

Pharmacological Treatment - Considerations in Pregnancy

Special rule for eclampsia patients: If magnesium sulphate infusion is running at time of arrest - stop infusion immediately and administer calcium gluconate 10 mL of 10% solution IV as antidote to magnesium toxicity.

The Most Critical Intervention: Perimortem Caesarean Delivery (PMCD) / Resuscitative Hysterotomy

Rationale

• The gravid uterus causes significant aortocaval compression even with LUD
• Delivery of the fetus reduces oxygen demand of the uterus, relieves IVC compression, allows more effective chest compressions, and may be the only way to achieve ROSC
• Both maternal and fetal survival can be improved by timely delivery

The "5-Minute Rule"

If ROSC is not achieved within 4 minutes of initiation of resuscitation, perimortem caesarean delivery should be commenced immediately - targeting delivery within 5 minutes of cardiac arrest.

• Decision to proceed should be made at 4 minutes so delivery is completed by 5 minutes
• Do NOT wait for ROSC before deciding
• Do NOT transfer to the operating theatre - perform at the site of arrest (wastes critical time)
• CPR must be continued throughout the procedure and after delivery
• No general anaesthesia or spinal required - the patient is in cardiac arrest

Indications

• Gestational age ≥20 weeks (uterus at or above umbilicus)
• Failure to achieve ROSC with standard + modified CPR within 4 minutes
• Non-survivable maternal trauma (proceed immediately regardless of ROSC status)

Surgical Technique

• Vertical midline incision (fastest, no need for sterile technique in arrest)
• Classical uterine incision
• Rapid delivery of fetus and placenta
• Hand the neonate to the paediatric/neonatal team immediately

Expected Outcomes Post-PMCD

• Maternal: venous return improves → may precipitate ROSC
• Neonatal: neurologically intact survival possible if delivered <5 minutes from arrest
• Best documented neonatal outcomes when delivery occurs within 5 minutes; meaningful survival possible up to 15-20 minutes

Reversible Causes - The 4H + 4T + Obstetric Causes

Post-Cardiac Arrest Care (Post-ROSC)

1. Transfer to ICU for continued monitoring
2. Targeted Temperature Management (TTM): Therapeutic hypothermia (32-36°C) - traditionally controversial in pregnancy but now recommended if patient remains comatose post-ROSC; fetal bradycardia expected but tolerated
3. Coronary angiography/PCI if MI suspected (ST elevation or high suspicion)
4. Neurological monitoring: EEG for subclinical seizures, CT head if SAH/stroke suspected
5. Fetal monitoring: Continuous CTG monitoring post-ROSC if pregnancy ongoing
6. Treat underlying cause aggressively
7. Multidisciplinary team involvement: obstetrics, cardiology, ICU, neonatology

Algorithm Summary

MATERNAL CARDIAC ARREST
        ↓
Call for help: OBG + Neonatology + Anaesthesia + Surgery
        ↓
Start CPR immediately (100-120/min, ≥5 cm depth)
        ↓
Assess fundal height
   < Umbilicus → Standard CPR
   ≥ Umbilicus → Manual Left Uterine Displacement (LUD) + CPR
        ↓
Secure airway: RSI (bag-mask initially) → ETT
Establish IV/IO access × 2
12-lead ECG/rhythm analysis → Defibrillate if VF/pVT
        ↓
Treat reversible causes (4H + 4T + obstetric)
Stop magnesium infusion → give calcium if Mg toxicity
        ↓
At 4 minutes: NO ROSC achieved?
        ↓
PERIMORTEM CAESAREAN DELIVERY (PMCD)
Target delivery within 5 minutes of arrest
Do NOT move to OT - deliver at bedside
Continue CPR throughout and after delivery
        ↓
POST-ROSC CARE:
ICU + TTM + Treat cause + Fetal monitoring

Key Points for MD Exam

1. Two patients - but maternal resuscitation always takes priority; do not attempt fetal monitoring during CPR
2. LUD is mandatory when fundus is at or above umbilicus (≥20 weeks) - it restores up to 30-40% of venous return
3. Airway is higher priority than in general adult - O2 consumption is 30% above normal, FRC reduced; hypoxia develops rapidly
4. Perimortem caesarean delivery within 5 minutes is the most important intervention when ROSC is not achieved - it improves both maternal and neonatal outcomes
5. Do not move to OT - deliver at the site of arrest
6. Stop magnesium immediately if infusing; give calcium gluconate if toxicity suspected
7. Defibrillation at standard energy is safe; fetal monitors must be removed before shock
8. Amniotic fluid embolism is a unique and highly lethal cause - consider in sudden intrapartum collapse with DIC
9. Post-ROSC - TTM is considered even in pregnancy; coronary intervention as indicated
10. AHA 2025 guidelines (PMID: 41122893) endorse this approach - "resuscitative hysterotomy" is now the preferred term over "perimortem caesarean"