Coronary Steal Phenomenon

Definition

• Katzung's Basic and Clinical Pharmacology, 16th Ed., p. 318

Pathophysiological Mechanism

1. Ischemic zone arterioles are already maximally dilated due to local autoregulatory metabolites (adenosine, CO2, H+, K+). They have no further dilatory reserve.
2. Normal zone arterioles retain the ability to dilate further in response to drugs or exercise.
3. When a potent non-selective coronary arteriolar dilator is administered:
   • Normal vessels dilate further - resistance drops, flow increases.
   • Ischemic vessels cannot dilate further - their resistance is fixed.
   • The pressure head driving flow into the ischemic territory falls (diverted into the low-resistance normal territory).
   • Net result: blood is redirected ("stolen") away from the ischemic zone into the normal zone.

"In the absence of drugs, arterioles in ischemic areas are usually maximally dilated as a result of local control factors, whereas resistance vessels in well-perfused regions are capable of further dilation. If a potent arteriolar dilator is administered, only vessels in the well-perfused regions dilate further, so more flow is diverted ('stolen') from the ischemic region into the normal region."

• Katzung's Basic and Clinical Pharmacology, p. 318

Collateral-Dependent Steal

Drugs That Cause Coronary Steal

Clinical Consequences

• In patients with stable coronary disease: steal can cause ST-segment depression and angina during pharmacological stress tests (this is the intentional basis for dipyridamole/adenosine stress imaging).
• In patients with unstable angina: transient coronary steal can precipitate myocardial infarction. Dipyridamole is therefore contraindicated in unstable angina.
  • Lippincott Illustrated Reviews Pharmacology, p. 986
• Sodium nitroprusside: significant intra-myocardial vasodilation → possible coronary steal → not recommended in active myocardial ischemia.
  • Braunwald's Heart Disease, p. 143

Structural/Anatomical Forms of Coronary Steal

• Goldman-Cecil Medicine, p. 1191

• Tintinalli's Emergency Medicine, p. 3456

Isoflurane and Coronary Steal - Historical Controversy

"There was a brief period of controversy concerning the use of isoflurane in patients with coronary disease because of the possibility for coronary 'steal' arising from the potent effects of isoflurane on coronary vasodilation. In clinical use, however, this has been, at most, a rare occurrence."

• Barash Clinical Anesthesia, 9e, p. 1403

Key Clinical Points Summary

• Coronary steal results from non-selective arteriolar dilation in the setting of fixed coronary obstruction.
• Arterioles distal to a significant stenosis are already maximally dilated and cannot respond to vasodilators - this is the key to understanding the mechanism.
• Dipyridamole and adenosine exploit this mechanism deliberately for pharmacological stress testing.
• In patients with active ischemia or unstable angina, avoid dipyridamole, adenosine-based agents, and nitroprusside due to steal risk.
• Structural steal (ALCAPA, coronary fistula) operates on the same hemodynamic principle but is anatomically driven rather than drug-induced.

Anaesthetic Management of Mitral Stenosis for Non-Cardiac Surgery

Understanding the Pathophysiology First

1. The pressure gradient across the valve (driven by left atrial pressure, LAP)
2. The duration of diastole (time for filling)

• Left atrium: Dilated, prone to SVTs and atrial fibrillation (AF)
• Pulmonary circulation: Elevated LAP → pulmonary venous hypertension → pulmonary edema; chronic cases develop irreversible pulmonary vascular disease
• Right ventricle: Pressure overload → RV failure; may develop tricuspid regurgitation
• Systemic emboli: Stasis in LA (especially with AF) → left atrial appendage thrombus → cerebral emboli

Pre-operative Assessment

• Dyspnea on exertion, orthopnoea, PND - grade per NYHA class
• Palpitations (AF is common in ~40%)
• Haemoptysis, hoarseness (from LA enlarging and compressing the left recurrent laryngeal nerve)
• History of systemic emboli or stroke
• Current medications: beta-blockers, digoxin, diuretics, anticoagulants

• ECG: Broad notched P wave (P mitrale) in sinus rhythm; AF is common; RVH if pulmonary hypertension present
• Echocardiography (TTE/TEE): Mitral valve area (MVA), mean gradient, pulmonary artery pressure, RV/LV function - this is the most important investigation
• CXR: LA enlargement, pulmonary congestion, Kerley B lines
• Exercise tolerance test: Useful if the severity on echo does not match symptoms

• Patients with severe MS, significant pulmonary hypertension, RV dysfunction, or recent decompensation are high-risk - consideration should be given to pre-operative balloon mitral valvuloplasty (BMV) before elective non-cardiac surgery, in line with ACC/AHA guidelines.
• Patients in AF with a dilated LA must be assessed for anticoagulation and rate control adequacy.

The Four Cardinal Haemodynamic Goals

• Tachycardia (any cause: pain, light anaesthesia, drugs)
• Sympathetic stimulation
• Rapid vasodilation (spinal anaesthesia, histamine-releasing drugs)
• Large, rapid fluid boluses
• Hypoxia and hypercarbia (both increase PVR, worsening pulmonary hypertension and RV strain)
• High airway pressures (increases PVR)

Pre-operative Optimisation

1. Rate control: Beta-blockers should be continued perioperatively. If rate is not controlled, titrate oral metoprolol or digoxin pre-operatively (target resting HR 60-70 bpm).
2. Anticoagulation management:
   • Patients with AF and MS are typically on warfarin (high thromboembolic risk).
   • For elective surgery: bridge with LMWH or UFH, or use DOAC as appropriate.
   • The INR target and bridging strategy must be individualised.
3. Diuretics: Continue diuretics to optimise volume status but avoid over-diuresis.
4. Atrial fibrillation: If new-onset AF with haemodynamic compromise, cardioversion may be required before elective surgery.
5. Antibiotic prophylaxis for infective endocarditis: Not routinely recommended for non-dental procedures per current guidelines (AHA), but institutional practice varies.

Monitoring

• Invasive arterial line: Allows beat-to-beat BP monitoring and arterial blood gas sampling. Establishes before induction.
• Central venous access (CVP): Useful to guide fluid therapy; prominent a waves (if sinus rhythm) and decreased y descent on PCWP waveform are characteristic; a prominent cv wave on CVP indicates secondary tricuspid regurgitation.
• Pulmonary artery catheter (PAC): May be considered in severe MS with pulmonary hypertension. Caution: PCWP in MS reflects the LA-LV gradient, not LV end-diastolic pressure. PA catheter carries risk of PA rupture in the setting of long-standing pulmonary hypertension.
• TOE (intraoperative TEE): Highly valuable - assesses ventricular filling, guides fluid management, detects ischaemia, evaluates RV function in real time.
• ECG: Continuous ST monitoring; rate and rhythm monitoring.

Choice of Anaesthetic Technique

Regional Anaesthesia

• Can be used safely in selected patients with mild-to-moderate MS.
• Epidural is preferred over spinal for major surgery - the gradual onset of sympathetic blockade is better tolerated than the abrupt vasodilation of spinal. Spinal causes sudden preload reduction that the fixed-output MS heart cannot compensate for.
• Slow, incremental epidural top-up with careful volume preloading reduces the risk of haemodynamic collapse.
• Severe MS is a relative contraindication to single-shot spinal anaesthesia, though it is not absolute if carefully managed.

General Anaesthesia

• Opioid-based induction (fentanyl or sufentanil) attenuates the sympathetic response to laryngoscopy - tachycardia at intubation is a key concern.
• Etomidate is the preferred induction agent if haemodynamics are precarious - minimal cardiovascular depression, maintains SVR.
• Ketamine is relatively contraindicated - causes tachycardia and sympathetic stimulation.
• Propofol must be used cautiously in small, titrated doses - significant vasodilation and myocardial depression.
• Thiopentone - causes vasodilation and reflex tachycardia; caution.
• Vasopressors (phenylephrine first-line, or vasopressin/norepinephrine) should be immediately available and often needed after induction to maintain SVR.

• Volatile agents (isoflurane, sevoflurane, desflurane) can be used, but titered carefully to avoid tachycardia and vasodilation.
• TIVA with propofol/remifentanil or an opioid-based technique with low-dose volatile is reasonable.
• Avoid histamine-releasing drugs (morphine, atracurium, mivacurium) - can cause vasodilation.
• Muscle relaxation: vecuronium, rocuronium (minimal cardiovascular effects) are preferred; pancuronium causes tachycardia - avoid.

• Adequate depth of anaesthesia and analgesia before laryngoscopy is essential to blunt the tachycardic response.
• Consider IV lignocaine (1.5 mg/kg) before laryngoscopy to blunt the pressor response.

Intraoperative Management

1. Heart rate control is the top priority at every moment.
   • Intraoperative tachycardia: deepen anaesthesia with opioid (fentanyl), give esmolol (IV bolus 0.5 mg/kg then infusion), or metoprolol IV.
   • Do not use meperidine (pethidine) - causes tachycardia due to its atropine-like structure.
2. Rhythm control:
   • New-onset SVT or rapid AF intraoperatively: treat aggressively.
   • Cardioversion for haemodynamically compromising arrhythmias.
3. Vasopressor choice:
   • Phenylephrine (pure alpha agonist) is preferred - raises SVR without causing tachycardia.
   • Ephedrine is less preferred - its beta-adrenergic activity causes tachycardia.
   • Vasopressin or norepinephrine are alternatives.
4. Ventilation:
   • Avoid hypoxia and hypercarbia - both increase PVR, worsen RV afterload.
   • Minimise PEEP where possible; high airway pressures increase PVR.
   • Target normocarbia or mild hypocarbia.
5. Fluid management:
   • Use guided by CVP/PAC/TEE.
   • Slow, cautious fluid administration in moderate-severe MS - the window between preload inadequacy and pulmonary oedema is narrow.
   • Avoid fluid overload - will precipitate acute pulmonary oedema.
6. Temperature: Maintain normothermia - shivering causes tachycardia and increased oxygen demand.

RV Failure - A Special Problem

• Optimise acid-base balance
• Hypocapnia, hyperoxia - both decrease PVR
• Inhaled nitric oxide or IV prostacyclins to reduce PVR
• Inotropes for RV failure: Epinephrine and milrinone are good options
• Avoid factors that increase PVR: hypoxia, acidosis, hypercarbia, high airway pressures, nitrous oxide

Postoperative Care

• High-dependency or ICU setting for severe MS or major surgery.
• Continue rate control (beta-blockers, digoxin if appropriate).
• Pain control is critical - inadequate analgesia → tachycardia → haemodynamic deterioration. Regional techniques (epidural analgesia post-operatively) are valuable.
• Monitor for:
  • Pulmonary oedema (fluid shifts postoperatively)
  • New-onset AF
  • Systemic emboli
• Resume anticoagulation as soon as haemostasis permits.
• Continue monitoring for RV failure (especially if pulmonary hypertension was present).

Summary: The "Avoid" and "Maintain" Checklist