Coronary Circulation

The economy of the coronary circulation

The heart is the extreme case: it already extracts most of the oxygen delivered to it at rest, so it cannot meet extra demand by extracting more — only by increasing flow.

250 ml/min

coronary flow at rest

~5%

of cardiac output

70%

O₂ extraction by heart

25%

O₂ extraction, rest of body

Why that 70% matters

Coronary sinus blood is the most desaturated in the body (SvO₂ ≈ 30%).
Because extraction reserve is nearly exhausted, any rise in myocardial oxygen demand must be met by increased coronary flow — which can rise 4–5 fold to about 1000–1250 ml/min in exercise.
Myocardial O₂ consumption is about 10 ml/100 g/min at rest, rising to about 70 ml/100 g/min in heavy exercise. Compare kidney ~5 and brain ~3 ml/100 g/min.
Determinants of myocardial oxygen demand: heart rate, contractility, wall tension (preload and afterload). Heart rate is usually the one you can control.

Coronary perfusion pressure

The equation

CPP = aortic diastolic pressure − LVEDP, normally about 60–80 mmHg.
Left coronary flow occurs almost entirely in diastole — during systole, intramyocardial pressure exceeds the perfusion pressure and effectively occludes the vessels.
Right coronary flow occurs in both systole and diastole, because RV wall pressure is much lower.

Three things that reduce coronary perfusion

Falling aortic diastolic pressure — hypotension, aortic regurgitation, vasodilation.
Rising LVEDP — failure, fluid overload, ischaemia itself (a vicious cycle).
Tachycardia — diastole shortens disproportionately, so filling time and perfusion time both fall. This is why tachycardia is so dangerous in aortic stenosis and HCM.
The subendocardium is the most vulnerable layer: it is furthest from the epicardial vessels and exposed to the highest wall tension.

Arterial supply

Both coronaries arise from the ascending aorta: the right from the anterior aortic sinus, the left from the posterior (left) aortic sinus.

Artery	Branches	Territory
Right coronary (RCA)	Conus branch SA nodal branch Right marginal AV nodal branch Posterior descending (PDA) in a right-dominant heart	Right atrium · right ventricle · inferior wall of the LV · posterior third of the interventricular septum
Left main (LCA)	Divides into LAD and circumflex	Left atrium and left ventricle
Left anterior descending (LAD)	Septal perforators Diagonal branches	Anterior wall of the LV · apex · anterior two-thirds of the interventricular septum · most of the bundle branches
Circumflex (LCx)	Obtuse marginal branches	Left atrium · lateral and posterior LV. Supplies the SA and PDA in a minority of hearts

Conducting tissue — who supplies what

SA node: RCA in about 60%, circumflex in about 40%.
AV node: RCA in about 80–90%, circumflex in about 10–20%.
Bundle of His: dual supply — LAD and RCA (hence relatively protected).
Left and right bundle branches: LAD septal perforators.
This is why an inferior MI (RCA) classically causes bradycardia and heart block, while an anterior MI (LAD) causing block signifies a very large infarct and a far worse prognosis.

Dominance

Defined by which artery gives rise to the posterior descending artery. Right-dominant in about 70–80%, left-dominant in about 10%, co-dominant in the rest.

Venous drainage

Route	Drains	Into
Coronary sinus ~85% of venous return	Great cardiac vein (anterior) Middle cardiac vein (posterior) Small cardiac vein	Right atrium
Anterior cardiac veins	Anterior RV wall	Right atrium directly
Thebesian veins	Drain directly from myocardium into the chamber they lie beneath	Any chamber — including the left side

Why the Thebesian veins are examinable

Along with the bronchial circulation, they drain deoxygenated blood directly into the left heart — creating the normal anatomical (true) shunt of about 2–5% of cardiac output.
This is why a healthy person breathing 100% oxygen still has a PaO₂ below the theoretical alveolar value, and why the A–a gradient is never zero.

Control and measurement

Control of coronary flow

Metabolic factors dominate — adenosine (the most important), hypoxia, H⁺, K⁺, CO₂ and nitric oxide all vasodilate. Local metabolic control overrides autonomic tone.
Sympathetic outflow to the heart is T1–T5. Direct α₁ effects would constrict, but the increase in metabolic demand causes net dilation.
Coronary flow is autoregulated between a perfusion pressure of roughly 60 and 180 mmHg.

Measuring coronary and cardiac blood flow

Fick principle using nitrous oxide or argon, thermodilution, or radioactive thallium — all applications of the same indicator principle: flow = amount of indicator ÷ concentration difference.