Coronary Circulation

Guyton and Hall Textbook of Medical Physiology - Chapter 21

1. Introduction

2. Physiological Anatomy of the Coronary Blood Supply

Figure 21.3 - Coronary arteries (Guyton & Hall)

• The main coronary arteries lie on the surface of the heart (epicardial). Smaller arteries penetrate from the surface into the muscle mass.
• Only the inner 0.1 mm of the endocardial surface can obtain nutrition directly from blood inside the cardiac chambers - this source is miniscule.

Left Coronary Artery (LCA)

• Supplies the anterior and left lateral portions of the left ventricle
• Divides into:
  • Left anterior descending (LAD) branch
  • Left circumflex branch

Right Coronary Artery (RCA)

• Supplies most of the right ventricle
• Supplies the posterior part of the left ventricle in 80-90% of people (right dominance)

Coronary Venous Drainage

3. Normal Coronary Blood Flow

• Resting coronary blood flow: ~70 mL/min/100 g of heart weight = approximately 225 mL/min total
• This is about 4-5% of total cardiac output
• Coronary blood flow per gram heart weight is typically higher in women than in men

• Cardiac output increases 4- to 7-fold
• Work output of the heart may increase 6- to 9-fold
• Coronary blood flow must increase proportionately to supply the needed oxygen

4. Phasic Changes in Coronary Blood Flow (Systole vs Diastole)

Figure 21.4 - Phasic flow through left ventricular coronary capillaries

• During systole: LV coronary capillary flow falls to a low value - opposite to other vascular beds. This is because the intramuscular blood vessels are compressed by left ventricular contraction.
• During diastole: Muscle relaxes, no longer obstructs flow - blood flows rapidly throughout diastole.
• Right ventricle: Also shows phasic changes, but only partial because RV contraction force is much less than LV.

Key Exam Point: Unlike most other organs, the left ventricle is perfused primarily during diastole, not systole.

5. Epicardial vs Subendocardial Blood Flow

Figure 21.5 - Epicardial, intramuscular, and subendocardial coronary vasculature

• Epicardial coronary arteries - on the outer surface, supply most of the muscle
• Intramuscular arteries - penetrate the muscle from epicardial vessels
• Subendocardial arterial plexus - lies immediately beneath the endocardium

6. Control of Coronary Blood Flow

6a. Local Metabolic Control (PRIMARY Mechanism)

• Normally, about 70% of oxygen in coronary arterial blood is extracted as blood passes through the heart (very high extraction ratio compared to other organs)
• Because so little oxygen remains, the only way to supply more O2 is to increase blood flow
• Coronary blood flow increases almost directly proportional to oxygen consumption

Note: Adenosine, after causing vasodilation, is largely reabsorbed into cardiac cells to be reused for ATP production. In severe ischemia (lasting >30 minutes), about half of the adenine base can be lost from affected cells, and new synthesis is only ~2%/hour - this is a major cause of cellular death in myocardial infarction.

6b. Nervous Control of Coronary Blood Flow

• Sympathetic stimulation → increases heart rate and contractility → increases cardiac metabolism → causes local vasodilation → increases coronary flow proportional to metabolic needs
• Vagal stimulation → slows heart, depresses contractility → decreases O2 consumption → indirectly constricts coronary arteries

• Parasympathetic (vagal): Parasympathetic distribution to ventricular coronary system is sparse. Acetylcholine has a direct vasodilatory effect on coronary vessels.
• Sympathetic (alpha-adrenergic): Norepinephrine activates alpha-adrenergic receptors → slight coronary vasoconstriction
• Sympathetic (beta-adrenergic): Also activates beta-adrenergic receptors → coronary vasodilation
• Net result: In the normal heart, indirect metabolic effects dominate, so sympathetic stimulation overall increases coronary flow.

7. Ischemic Heart Disease

7a. Atherosclerosis

• Most common cause of diminished coronary flow
• Gradual cholesterol deposition beneath the endothelium, invaded by fibrous tissue, often calcified
• Forms atherosclerotic plaques that protrude into vessel lumens
• Common site: first few centimeters of major coronary arteries
• Women have lower prevalence of obstructive atherosclerosis than men, but sex differences are attenuated in older adults
• Coronary microvascular dysfunction and coronary vasospasm are also causes when no obstruction is detectable

7b. Acute Coronary Artery Occlusion

1. Thrombosis: Atherosclerotic plaque breaks through endothelium → platelets adhere → fibrin deposited → thrombus forms and occludes vessel. If the clot breaks away and travels distally = coronary embolus
2. Coronary artery spasm: Smooth muscle spasm due to:
   • Irritation by atherosclerotic plaque edges
   • Local nervous reflexes
   • Extreme emotional stress
   • Stimulant drugs (cocaine, amphetamines)
   • Tobacco use
   • Cold exposure
   • Spasm may lead to secondary thrombosis
   • Treated with calcium channel blockers or nitrate drugs

7c. Collateral Circulation - Lifesaving Value

• Normal hearts have almost no large communications between major coronary arteries
• Many anastomoses exist among smaller arteries (20-250 micrometers diameter)

8. Myocardial Infarction (MI)

8a. Immediate Effects

• Small ischemic area: Little or no muscle cell death; muscle becomes temporarily nonfunctional
• Large ischemic area:
  • Center: cells die within 1-3 hours (total cessation of blood supply)
  • Around dead area: nonfunctional zone (failure of contraction and impulse conduction)
  • Outer rim: weakly contracting zone (mild ischemia)

8b. Stages of Recovery

1. Dead muscle fibers at center → area enlarges over days as marginal fibers succumb
2. Developing collaterals supply the outer rim → some nonfunctional muscle recovers
3. After a few days to 3 weeks: nonfunctional muscle either recovers or dies
4. Fibroblasts grow into dead tissue → fibrous scar forms (ischemia stimulates fibroblast growth)
5. Fibrous scar undergoes progressive contraction over months to a year
6. Normal heart areas gradually hypertrophy to compensate

8c. Role of Rest in Recovery

• Excessive cardiac activity causes vessels of normal muscle to dilate greatly
• This diverts blood away from the ischemic area through small anastomotic channels - this is called the coronary steal syndrome
• Therefore, absolute body rest during the initial acute phase is critical
• However, progressive physical activity (cardiac rehabilitation) during recovery improves coronary blood flow and promotes formation of new collateral vessels

8d. Loss of Adenine in Ischemia (Cellular Mechanism)

• ATP → ADP → AMP → adenosine (leaks out of cells)
• Within 30 minutes, ~50% of adenine base can be lost from ischemic cells
• New adenine synthesis = only 2%/hour
• Once ischemia persists >30 minutes, relief may be too late to prevent cell death

9. Summary of Key Numbers to Remember