CORONARY CIRCULATION
FACTORS AFFECTING
CORONARY CIRCULATION
ANATOMY
• The two coronary ostia arise from the sinuses of
Valsalva just above the aortic valve at the aortic root.
• The left coronary artery arises from left posterior aortic
sinus, divides into the left anterior descending artery
(giving diagonal branches) and circumflex artery.
• The right coronary artery arises from anterior coronary
sinus. Branches into right marginal, posterior
descending artery (determines dominance), Right
atrial, infundibular, nodal (60%) and terminal branches.
COLLATERAL
CIRCULATION
• The two coronary arteries anastomose in the myocardium.
• Extracardiac anastomosis also occurs with vasovasorum of
aorta, pulmonary arteries, bronchial arteries and phrenic
arteries.
• The major coronary arteries divide into subepicardial
arteries.
• Intramuscular arteries penetrate the myocardium
perpendicularly to form subendocardial arterial plexus.
• Small coronary arteries (subepicardial and subendocardial)
are the principle resistance vessel of the heart, change in
their diameter regulate the coronary blood flow.
VENOUS DRAINAGE
• Most of the blood from left ventricular muscle
drains into the coronary sinus .
• The anterior cardiac vein receives blood from the
right ventricular muscle.
• Thebesian veins drain a small proportion of
coronary blood directly into the cardiac chambers
and account for true shunt.
CORONARY BLOOD FLOW
• The heart has the highest oxygen consumption per
tissue mass of all human organs.
• The resting coronary blood flow is ∼250mlmin−1
(0.8mlmin−1 g−1 of heart muscle)
• Arterial oxygen extraction is 70–80%, compared
with 25% for the rest of the body.
• an increase in coronary blood flow can
independently increase myocardial oxygen
consumption (Gregg effect).
Factors affecting coronary
circulation
Physical
Coronary perfusion pressure
Perfusion time
Cardiac output
Vessel wall diameter
Chemical
Neural
Humoral
Reflex
Myocardial oxygen balance
• Coronary perfusion pressure
• During systole, the intramuscular blood vessels are
compressed and flow is the lowest.
• Flow occurs during diastole when the muscle relaxes.
• Perfusion time
• Increase in heart rate impinges on diastolic time
more than systolic time and reduces the perfusion
time.
• Cardiac output
• CBF directly proportional to cardiac output(CO)
• Vasomotor tone and deposits inside the vascular
lumen determine the vessel wall diameter.
Chemical
• Vasomotor tone is almost exclusively determined
by local metabolic oxygen demand.
Hypoxia (vasodilator)
Vasodilation
Adenosine & Opens the ATP sensitive k+ channels
• vascular endothelium is the final common pathway
regulating vasomotor tone.
• Neural
• Epicardial blood vessels (α receptors –
vasoconstriction)
• Intramuscular and subendocardial blood vessels (β2
receptors - vasodilatation).
• Sympathetic stimulation increases myocardial blood
flow through an increased metabolic demand ( β
receptor activation)
• Alpha stimulation - distribution of blood flow within
the myocardium.
Humoral
• vasoactive hormones require an intact vascular
endothelium.
• The peptide hormones include ADH, ANP, VIP, CGRP.
• Antidiuretic hormone in physiological concentration has
little effect on the coronary circulation but causes
vasoconstriction in stressed patients.
• The other peptides cause endothelium-mediated
vasodilatation.
• Angiotensin II causes coronary
vasoconstriction,enhances calcium influx and releases
endothelin, the strongest vasoconstrictor peptide.
• Angiotensin converting enzyme inactivates bradykinin, a
vasodilator.
Reflex
• Anreps reflex: Increased venous return
causes increased pressure in right atrium,
leading to reflex increase in myocardial
contractility and coronary blood flow.
• Gastro coronary reflex: Distention of the
stomach with heavy meal causes reflex
vasoconstriction of coronary blood vessels
decreasing coronary blood flow.
Myocardial oxygen balance
• Oxygen delivery is the product of arterial oxygen carrying
capacity and myocardial blood flow.
• The diastolic pressure time index (DPTI) is a useful
measure of coronary blood supply and is the product of
the coronary perfusion pressure and diastolic time.
• Similarly, oxygen demand can be represented by the
tension time index (TTI), the product of systolic pressure
and systolic time.
• The ratio DPTI/TTI is the endocardial viability ratio (EVR)
and represents the myocardial oxygen supply-demand
balance.
• The EVR is normally 1 or more. A ratio < 0.7 is associated
with subendocardial ischaemia.
Diseases affecting coronary circulation
• Coronary artery disease: Deposits of lipids, smooth
muscle proliferation and endothelial dysfunction reduce
the luminal diameter. Critical stenosis (diameter is
reduced by 50%.)
• Resting flow becomes affected (diameter is reduced by
80%.).
• Hypertension: The left ventricle undergoes hypertrophy
in response to raised afterload.
• There is an impaired vasomotor response to hypoxia in
hypertrophied tissue that makes it susceptible to
ischaemia.
• Heart failure: Impaired ejection results in larger
diastolic volumes, raised LVEDP and lower coronary
perfusion pressure.
Anaesthesia and myocardial oxygen balance
• Inhalation agents
• Halogenated anaesthetic agents activate
ATPsensitive potassium channels and lower
intracellular calcium.
• Results in negative inotropy
• Mimic the protective effect of discrete episodes of
myocardial ischaemia before a sustained ischaemic
insult, ‘ischaemic preconditioning’.
• Benzodiazepines
• Decreases SVR with minimum effect on cardiac
output, the baroreceptor reflex remains intact.
• Opioids
• Narcotics are adjuncts to help blunt sympathetic
response to noxious stimuli.
• A high dose of opioids causes inhibition of the
autonomic nervous system, direct myocardial
depression and may induce histamine release.
• Non-depolarizing agents are believed to elicit their
haemodynamic response by stimulating histamine
release and their action on muscarinic and
nicotinic receptors.
• Depolarizing muscle relaxant: Administration of
suxamethonium may lead to cardiac dysrhythmias
(junctional rhythm and sinus bradycardia) by its
muscarinic activity at SA node, and hyperkalemia
particularly to susceptible patients.
