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Coronary Circulation - 8 Mark Notes

(Sources: Guyton & Hall Medical Physiology, Costanzo Physiology, Ganong's Review of Medical Physiology)

1. DEFINITION

Coronary circulation is the system of blood vessels that supplies oxygenated blood to the myocardium and drains deoxygenated blood back to the right atrium. It is the most important regional circulation because cardiac muscle has virtually no O2 reserve and depends entirely on continuous blood delivery.

2. ANATOMICAL CONSIDERATIONS

Arterial Supply

The two coronary arteries arise from sinuses (sinuses of Valsalva) behind the cusps of the aortic valve at the root of the aorta.

LEFT CORONARY ARTERY (LCA)

Supplies: anterior + left lateral walls of the left ventricle (LV), most of the interventricular septum
Divides into:
- Left Anterior Descending (LAD) - most important clinically; supplies anterior LV + septum
- Left Circumflex (LCx) - supplies posterior and lateral LV wall

RIGHT CORONARY ARTERY (RCA)

Supplies: right ventricle (RV), posterior LV (in 80-90% of people), SA node (~60%), AV node (~85%)
Main branches: marginal branch, posterior descending artery (PDA)

The myocardium is supplied through epicardial arteries on the surface → intramuscular arteries that penetrate inward → subendocardial arterial plexus (most vulnerable to ischemia).

Venous Drainage

Route	What it drains	Drains into
Coronary sinus	~75% of LV venous blood	Right atrium
Anterior cardiac veins	Most of RV	Right atrium (directly)
Thebesian veins	Small amount	All cardiac chambers directly
Arteriosinusoidal vessels	Connect arterioles → chambers	Cardiac chambers

3. CORONARY BLOOD FLOW - NORMAL VALUES

Parameter	Value
Resting flow	~70 mL/min/100 g OR ~225 mL/min total
% of cardiac output	4-5%
O2 extraction at rest	~70% (very high - almost maximal)
During exercise	Increases 3-4 fold

Because O2 extraction is already near maximal at rest, increased demand must be met by increased blood flow (not increased extraction).

4. PHASIC FLOW - SYSTOLE vs DIASTOLE

This is the unique feature of coronary circulation:

Left Ventricle:

During systole - intramyocardial pressure exceeds aortic pressure (LV pressure ~121 mmHg vs Aorta ~120 mmHg), compressing intramuscular vessels → blood flow falls to nearly zero
During diastole - muscle relaxes, vessels open → blood flow is maximal
Therefore, LV is perfused mainly during diastole
⚠ Tachycardia shortens diastole → reduces LV perfusion time → risk of ischemia

Right Ventricle:

RV contraction force is much lower; pressure differential (Aorta 120 vs RV 25 mmHg) remains positive during systole
Blood flow occurs throughout the cardiac cycle (not markedly reduced in systole)

Subendocardial region (innermost layer of LV wall) is most vulnerable because it faces the highest intramural compression during systole → most common site of myocardial infarction.

Region	Perfusion Timing
LV epicardium	Both systole + diastole
LV subendocardium	Diastole ONLY
RV myocardium	Both systole + diastole

5. REGULATION OF CORONARY BLOOD FLOW

A. Local Metabolic Control (PRIMARY - most important)

Blood flow is regulated mainly by local vasodilator metabolites matching O2 supply to demand:

Metabolite	Trigger	Effect
Adenosine (most important)	ATP → AMP → Adenosine when O2 falls	Coronary arteriolar dilation
Hypoxia / ↓ PO2	Increased cardiac work	Direct vasodilation
↑ CO2 / ↑ H+	Increased metabolism	Vasodilation
K+ ions	Action potentials, metabolic activity	Vasodilation
Nitric oxide (NO)	Shear stress, metabolites	Vasodilation
Prostaglandins	Metabolic demand	Vasodilation

Mechanism of adenosine: O2 demand↑ → ATP degraded → AMP → adenosine released → diffuses to coronary arterioles → vasodilation → ↑ blood flow → ↑ O2 delivery (active hyperemia)

B. Autoregulation

Coronary blood flow is autoregulated over a perfusion pressure range of 60-120 mmHg. If pressure drops below this, blood flow falls proportionally and ischemia results.

C. Reactive Hyperemia

During systolic compression (brief occlusion), an O2 debt accumulates. When occlusion ends at diastole, flow surges above baseline to repay the O2 debt. This is reactive hyperemia.

D. Nervous Control (secondary - indirect > direct)

Stimulus	Direct Effect	Indirect Effect (via heart rate/contractility)	Net Result
Sympathetic (norepinephrine)	α1: vasoconstriction	↑ HR + contractility → ↑ O2 demand → metabolic vasodilation	Net: vasodilation (metabolic overrides)
Sympathetic (epinephrine)	β2: vasodilation	↑ HR + contractility → ↑ O2 demand	Net: vasodilation
Parasympathetic (ACh/vagal)	Direct: mild vasodilation	↓ HR + contractility → ↓ O2 demand → vasoconstriction	Net: reduced flow

6. CLINICAL SIGNIFICANCE

Myocardial Infarction: most common in subendocardial region of LV (LAD territory most often)
Tachycardia: reduces diastolic filling time → reduces LV coronary flow → angina risk
Aortic stenosis: LV must generate far higher pressure than aorta → subendocardial ischemia
Coronary artery disease (CAD): ~1/3 of all deaths in industrialized nations (Guyton)
Angina pectoris: chest pain when O2 demand exceeds supply

7. FLOWCHART: REGULATION OF CORONARY BLOOD FLOW

INCREASED CARDIAC WORKLOAD
(e.g., exercise, tachycardia, increased contractility)
            │
            ▼
    ↑ O2 Consumption by Myocardium
            │
            ▼
    Local Hypoxia / ↓ PO2
    ATP → AMP → ADENOSINE (+ CO2, H+, K+, NO)
            │
            ▼
    Coronary Arteriolar VASODILATION
    (Active Hyperemia)
            │
            ▼
    ↑ Coronary Blood Flow (up to 3-4x at peak exercise)
            │
            ▼
    ↑ O2 Delivery to Myocardium
            │
            ▼
    O2 demand is met → Adenosine recycled back to ATP
    (Negative feedback loop restored)

PHASIC CORONARY FLOW (Cardiac Cycle)

SYSTOLE                          DIASTOLE
   │                                │
LV intramural pressure HIGH     LV muscle relaxes
(~121 mmHg) compresses vessels  Vessels open fully
   │                                │
   ▼                                ▼
LV flow ↓ (near zero)           LV flow ↑ (maximal)
RV flow not much reduced         (subendocardial repaid)
   │                                │
   └──────────────────┬─────────────┘
                      ▼
           If systole prolonged / diastole shortened
           (e.g., tachycardia, aortic stenosis)
                      │
                      ▼
           Subendocardial ISCHEMIA → MI risk

8. SUMMARY TABLE (Quick Revision)

Feature	Detail
Origin of coronary arteries	Aortic sinuses (sinuses of Valsalva)
LCA supplies	Anterior LV, septum (via LAD + LCx)
RCA supplies	RV, posterior LV (in 80-90%), SA + AV nodes
Resting coronary flow	225 mL/min (~5% of cardiac output)
O2 extraction	~70% at rest (near maximal)
LV perfusion timing	Mainly diastole
RV perfusion timing	Both systole and diastole
Primary regulator	Local metabolites (adenosine, hypoxia)
Key vasodilator substance	Adenosine
Most ischemia-prone region	Subendocardium of LV
Venous drainage	Coronary sinus (75%) + anterior cardiac veins + Thebesian veins

Sources:

Guyton & Hall Medical Physiology - Chapter 21 (Coronary Circulation)
Costanzo Physiology 7th Edition - Special Circulations
Ganong's Review of Medical Physiology 26th Edition - Chapter 33

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