Coronary Circulation and Anesthesia

1. Anatomical Overview

• Left coronary artery (LCA): Divides into the left anterior descending (LAD) and left circumflex (LCx). Supplies the anterior and left lateral left ventricle (LV).
• Right coronary artery (RCA): Supplies most of the right ventricle (RV) and the posterior LV in 80-90% of people (right dominance).
• Venous drainage: ~75% of LV coronary venous blood returns via the coronary sinus to the right atrium. RV venous blood drains via anterior cardiac veins. A small amount drains through Thebesian veins directly into cardiac chambers.
• Only the inner 0.1 mm of the endocardium can be nourished directly from intracavitary blood; the rest depends entirely on coronary flow.
• Guyton and Hall Textbook of Medical Physiology, p. 268

2. Normal Coronary Blood Flow

• Resting flow: ~70 mL/min/100 g of heart weight (~225 mL/min total), approximately 4-5% of cardiac output.
• During strenuous exercise, cardiac work increases 6- to 9-fold; coronary flow increases only 3- to 4-fold, necessitating increased metabolic efficiency.
• Guyton and Hall, p. 268

Phasic Flow (Systole vs. Diastole)

• Left ventricle: During systole, intramuscular blood vessels are compressed, causing a fall in coronary capillary blood flow - the opposite of other vascular beds. Blood flow is predominantly diastolic in the left coronary system.
• Right ventricle: Because RV contraction is weaker, phasic compression is only partial; flow occurs in both systole and diastole.
• Subendocardial vulnerability: During systole, the subendocardial plexus is most compressed (highest intramyocardial pressure). This is compensated by a rich subendocardial arterial plexus. In pathological states (e.g., LV hypertrophy, tachycardia, raised LVEDP), subendocardial ischemia is the first to occur.

3. Control of Coronary Blood Flow

Local Metabolic Control (Primary)

• Adenosine - released when ATP is hydrolyzed during hypoxia; most potent coronary vasodilator
• Hypoxia itself - directly dilates arterioles
• CO2 and H+ - vasodilators, though less important here than in cerebral circulation
• K+ ions, lactate, prostaglandins - also contribute

Autoregulation

Sympathetic and Neural Influences

• Costanzo Physiology 7th Edition; Guyton and Hall, p. 268-269

4. Myocardial Oxygen Supply-Demand Balance

Determinants of O₂ Supply

Determinants of O₂ Demand (MVO₂)

• Miller's Anesthesia, 10th ed.

5. Effects of Anesthetic Agents on Coronary Circulation

Volatile (Inhalational) Anesthetics

• All three produce dose-dependent reductions in systemic vascular resistance and blood pressure (vasodilation)
• Dose-dependent reduction in myocardial contractility (negative inotropy), though functional cardiac reserve is preserved
• Heart rate: sevoflurane has minimal HR effect at ~1 MAC; isoflurane and desflurane cause 5-10% HR increases

"Clinical outcome studies have been unable to find an association between the use of isoflurane in patients undergoing CABG operations with an increased incidence of myocardial infarction or perioperative death."

• Barash Clinical Anesthesia, 9th ed., p. 1427-1428

Anesthetic Preconditioning (Cardioprotection)

1. Volatile anesthetics diffuse into myocardial cell membranes and alter mitochondrial electron transport → generate reactive oxygen species (ROS)
2. ROS trigger protein kinase C (PKC) activation → opens K_ATP channels
3. ~30-40% of cardioprotection comes from reduced calcium loading into myocardial cells during ischemia
4. Improved mitochondrial membrane permeability to ATP precursors → better recovery of contractile function after reperfusion

• Barash Clinical Anesthesia, 9th ed., p. 1428-1429

Opioids

• Opioids have no significant effect on coronary vasomotion or myocardial metabolism at standard doses
• Do not produce coronary steal
• Do not diminish the ability of large coronary arterioles to respond to vasoactive agents
• Fentanyl at low concentrations (1-2 ng/mL) enhances baroreflex control of coronary conductance; at higher concentrations it depresses baroreflex control
• Opioids mimic ischemic preconditioning: Stimulation of cardiac κ- and δ-opioid receptors reduces infarct size in animal models; remifentanil also has protective effects partly via μ-agonism outside the heart
• Remote preconditioning (brief ischemia of limb, kidney, intestine) is mediated by myocardial κ-opioid receptors
• Clinically: high-dose opioid-based anesthesia maintains myocardial perfusion and O₂ supply/demand ratio as well or better than inhalation techniques for CABG
• Miller's Anesthesia, 10th ed., p. 2769-2770

Propofol (TIVA)

• Reduces systemic vascular resistance and blood pressure (vasodilatory), but does not cause coronary steal
• Provides cerebral and coronary protection through antioxidant properties at clinical concentrations
• Does not mimic ischemic preconditioning to the same degree as volatile anesthetics (controversial)
• Provides similar hemodynamic stability vs. volatile agents when carefully titrated

Nitrates and Vasodilators in Coronary Context

• Nitroglycerin: Beneficial in CAD - primarily a venodilator reducing preload; dilates large epicardial coronary arteries; does not cause steal
• Sodium nitroprusside: Can cause coronary steal phenomenon - its potent arteriolar vasodilation preferentially dilates non-stenotic vessels, diverting blood from collateral-dependent ischemic zones
• Morgan and Mikhail's Clinical Anesthesia, 7th ed.

6. Anesthetic Management in Patients with CAD

7. Summary Table: Anesthetic Agents and Coronary Effects

• Guyton and Hall Textbook of Medical Physiology (Ch. 21)
• Costanzo Physiology 7th Edition (Ch. on Special Circulations)
• Barash, Cullen & Stoelting's Clinical Anesthesia, 9th ed. (Ch. 18: Volatile Anesthetics)
• Miller's Anesthesia, 10th ed. (Ch. 22: Opioids; Ch. 49: Thoracic Anesthesia)
• Morgan and Mikhail's Clinical Anesthesiology, 7th ed.