01 PHYSIOLOGY

17. Coronary
circulation
Describe the coronary circulation.
What is autoregulation?
How is coronary blood flow
autoregulated?
> The arterial blood supply to the heart comes from the right coronary
artery (RCA) and the left coronary artery (LCA), which arise from the
anterior and posterior aortic sinuses respectively.
> The RCA supplies the right atrium, right ventricle, sinoatrial node and, in
90% of people, also the atrioventricular node.
> The LCA divides into the left anterior descending (LAD) artery and the left
circumflex (LCx) artery and supplies the left atrium, left ventricle and most
of the interventricular septum.
> In 30% of the population the LCA and RCA supply equal proportions of
blood while in 50% the RCA is the dominant vessel.
> Venous drainage occurs predominantly via the coronary sinus. This
receives blood from the great cardiac vein (draining the anterior aspect
of the heart) and the middle cardiac vein (draining the posterior aspect of
the heart). In addition, there are other vessels that drain directly into the
heart chambers including the thebesian veins, which contribute towards
true shunt.
> Autoregulation refers to the intrinsic ability of an organ to maintain a
constant blood flow despite a varying perfusion pressure. The heart,
kidney and brain are all examples of organs that exhibit this ability.
> The heart can autoregulate its blood supply at coronary perfusion
pressures (CoPP) between 60 and 180 mmHg. Outside this range, the
coronary circulation becomes pressure dependent.
Autoregulation occurs via a combination of the following mechanisms:
Metabolic: During periods of increased myocardial activity, local tissue
hypoxia and increased metabolic waste products such as H+, K+, adenosine
and CO2 cause vasodilatation of the coronary vessels, thereby increasing
coronary blood flow.
Myogenic: When the pressure within a small artery or arteriole is increased, the
smooth muscle within these vessels automatically constricts, thereby reducing
blood flow. The reverse happens when the pressure within these vessels falls.
Endothelial: Vascular endothelium produces various vasoactive substances
including nitric oxide (NO), endothelium-derived relaxing factor (EDRF) and
prostacyclin (PGI2), all of which produce vasodilatation; conversely endothelin
and thromboxane A2 produce vasoconstriction. When endothelium is
damaged (e.g. atherosclerotic plaques or ischaemia) the production of
these vasoactive substances is reduced, making coronary vessels prone to
vasospasm and platelet aggregation.
Autonomic: ANS exerts a weak effect on the coronary circulation.
α-adrenergic receptor stimulation causes vasoconstriction while β-adrenergic
and vagal stimulation leads to vasodilatation of coronary vessels.
Hormonal: Vasoactive hormones require an intact endothelium in order to
produce their effect. Atrial natriuretic peptide causes vasodilatation while
vasopressin and angiotensin II cause vasoconstriction.

54

9781785230981_text.indb 54 24/02/16 9:36 pm


What factors affect myocardial
oxygen supply?
What are the major determinants
of myocardial oxygen
consumption?
9781785230981_text.indb 55
CORONARY CIRCULATION
Myocardial oxygen supply is determined by coronary blood flow and the
arterial oxygen content (CaO2).
Determinants of coronary blood flow:
Coronary perfusion pressure (CoPP = Aortic pressure – Intraventricular
pressure). During systole the CoPP of the left ventricle can equal zero
(or less) and therefore coronary blood flow only occurs during diastole.
In systole:
LVCoPP = [SBP – LVESP] = [120 mmHg – 120 mmHg] = 0 mmHg
In diastole:
LVCoPP = [DBP – LVEDP] = [70 mmHg – 10 mmHg] = 60 mmHg.
However, the coronary blood flow to both atria and the right ventricle occurs
throughout the cardiac cycle.
In systole:
RVCoPP = [SBP – RVESP] = [120 – 25] = 95 mmHg
In diastole:
RVCoPP = [DBP – RVEDP] = [70 – 5] = 65 mmHg.
Perfusion time: As the heart rate increases, the diastolic time and therefore
the coronary perfusion time, especially to the left ventricle, is reduced.
Coronary vessel patency: Atherosclerotic vessels are stenosed and have a
reduced blood flow (as indicated by the Hagen–Poiseuille formula).
Coronary vessel diameter: The wider the diameter, the greater the blood
flow (hence the administration of GTN in angina).
Blood viscosity: Haematocrit is a major determinant of blood viscosity and
from the Hagen–Poiseuille formula it can be seen that as viscosity increases,
flow decreases. However, as haematocrit decreases, so does the oxygen-
carrying capacity of blood.
Determinants of arterial oxygen content:
CaO2 = [Hb × Sats × 1.34] + [PaO2 × 0.023]
From this equation it can be seen that the only parameters we can
manipulate are the Hb and the PaO2 (see Chapter 4, ‘Oxygen transport’, for
full explanation of the above equation).
The heart has the highest oxygen consumption per tissue mass of any
organ in the body, requiring 10 mL O2/min/100 g at rest and 70 mL/min/100 g
during heavy exercise (the kidney uses 5 mL/min/100 g while the brain uses
3 mL/min/100 g). As a result, the heart receives 5% of the cardiac output,
giving it a coronary blood flow of 250 mL/min.
In order to support such high oxygen consumption, the heart at rest extracts
approximately 70% of its coronary blood oxygen content (remember that the
rest of the body only extracts, on average 25%, of its arterial O2 content).
Therefore, during periods of increased mechanical activity the only way
the heart can meet its increased oxygen consumption is by increasing its
coronary blood flow.
Factors that determine myocardial oxygen consumption include heart rate,
contractility, afterload, tissue mass and temperature (cold cardioplegic
solutions are used during cardiopulmonary bypass surgery to reduce
myocardial oxygen consumption and minimise risk of ischaemia).
55
24/02/16 9:36 pm