Coronary blood flow

Tamilselvi Ramanathan FRCA
Henry Skinner FRCA

The heart has the highest oxygen consumption heart muscle and blood flow to the left ventricle
per tissue mass of all human organs. The rest- is at its lowest. The force is greatest in the sub-
Key points
ing coronary blood flow is 250 ml min 1 (0.8 ml endocardial layers where it approximates to
min 1 g 1 of heart muscle); this repres-ents 5% intramyocardial pressure. In systole, Blood flow to the
of cardiac output.1 Ischaemia results when intramyocardial blood is propelled forwards heart occurs mainly
oxygen demand outstrips supply. during diastole.
towards the coronary sinus and retrogradely into
Arterial oxygen extraction is 70–80%, com- the epicardial vessels, which act as capa-citors. Coronary blood flow is
pared with 25% for the rest of the body. There- Flow resumes during diastole when the muscle mainly determined by
fore, increased oxygen consumption must relaxes. The coronary perfusion pres-sure is the local oxygen demand.
principally be met by an increase in coronary difference between the aortic dias-tolic pressure The vascular endothelium is
blood flow, which may increase fivefold during and left ventricular end-diastolic pressure the final common pathway
exercise. Supply usually closely matches any (LVEDP). Phasic changes in blood flow to the controlling vasomotor tone.
change in demand. However, an increase in right ventricle are less pronounced because of When anaesthetising patients
coronary blood flow can independently in- the lesser force of contraction. Central venous with coronary artery disease,
crease myocardial oxygen consumption (Gregg pressure may be a more appro-priate choice for maintain coronary perfusion
effect).2 This may be explained by full coronary downstream pressure to cal-culate the right- pressure and avoid
arteries splinting the heart and increasing the sided coronary perfusion pressure.2 tachycardia.
end-diastolic fibre length and contractility.

Anatomy Perfusion time

The two coronary ostia arise from the sinuses of Any increase in heart rate impinges on diastolic
Valsalva just above the aortic valve. The left time more than systolic time and reduces the
coronary artery divides into the left anterior perfusion time.
descending artery and circumflex artery. It sup-
plies the lateral and anterior walls of the left Vessel wall diameter
ventricle, and the anterior two thirds of the Vasomotor tone and deposits inside the vascu-
interventricular septum. The right coronary lar lumen determine the vessel wall diameter.
artery supplies the right ventricle, the posterior The interplay of various mechanisms that
wall of the left ventricle and posterior third of regulate the coronary vasomotor tone usually
the septum. The major coronary arteries divide favours vasodilatation (Fig. 1).
into epicardial arteries. Intramuscular arteries
penetrate the myocardium perpendicularly to
form subendocardial arterial plexuses. Factors influencing the
Most of the blood from left ventricular
vasomotor tone
muscle drains into the coronary sinus. The Myocardial metabolism
anterior cardiac vein receives blood from the
right ventricular muscle. They both open into Vasomotor tone is almost exclusively deter- Tamilselvi Ramanathan FRCA
the right atrium. Thebesian veins drain a small mined by local metabolic oxygen demand. Specialist Registrar in Anaesthesia
proportion of coronary blood directly into the Hypoxia causes coronary vasodilatation directly Queen’s Medical Centre
cardiac chambers and account for true shunt. but also releases adenosine and opens ATP- Nottingham
sensitive potassium channels. Pre-capillary NG7 2UH
Fax: 01159 700739
Determinants of coronary sphincters are relaxed and more capillaries E-mail: (for

blood flow recruited. correspondence)

Henry Skinner FRCA
Coronary perfusion pressure Autoregulation Consultant Anaesthetist
Nottingham City Hospital
During systole, intramuscular blood vessels are Under resting conditions, coronary blood flow Nottingham
compressed and twisted by the contracting remains constant between mean arterial NG5 1PB

doi 10.1093/bjaceaccp/mki012 Continuing Education in Anaesthesia, Critical Care & Pain | Volume 5 Number 2 2005
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flow within the myocardium by restricting metabolically mediated flow increase and exerting an anti-steal affect. Probable mechanisms include the myogenic product of the coronary perfusion pressure and diastolic time. oxygen demand can be represented by the tension time regulation (slow). Antidiuretic hormone in physiological con. Oxygen delivery is the product of arterial oxygen carrying capacity and myocardial blood flow. The coronary circulation functions in a state of active vasodilata- tion. a ¼ alpha receptor. A ratio <0.Coronary blood flow Sympathetic stimulation Parasympathetic stimulation vasoconstriction in stressed patients. Abnormal endothelial nitric oxide production may play a role Humoral control in diabetes. heart rate and contractility Blood pressure ¼ 180/95 mm Hg dominate the subsequent response. Vasoconstrictors include endothelin and throm-boxane A2. stimulation of which produces vaso. Vasorelaxants are endothelium- derived relaxing factor. endothelium derived relaxant factor Myocardial oxygen balance (EDRF). Note that systolic time is typically fixed at 200 ms. M ¼ muscarinic receptor. 2 beta receptor. It modulates the contractile activity of the Adenosine underlying smooth muscle through synthesis and secretion of vasoactive substances in response to blood flow. dysfunction reduce the luminal diameter. Vasoconstriction Vasodilatation Hypoxia Vascular endothelium + K ATP The vascular endothelium is the final common pathway regulat-ing Endothelin ET vasomotor tone. The epicardial blood vessels Heart rate ¼ 120 min 1 primarily have a receptors. represents the myocardial oxygen supply-demand balance. Critical Care & Pain | Volume 5 Number 2 2005 . atrial natriuretic peptide. The diastolic pressure time index pressures of 60–140 mm Hg. vasoactive intestinal peptide. the strongest vasoconstrictor peptide yet iden- EDRF tified in humans. AT ¼ angiotensin receptor. Beyond this range. It also enhances calcium influx and Angiotensin II M releases endothelin. a potent vasoconstrictor.2 s ¼ 36 s mm Hg EVR ¼ 0. circulat-ing Shear forces Intraluminal pressure hormones and chemical substances. Critical stenosis occurs centration has little effect on the coronary circulation but causes when coronary blood flow is unable to respond to an increase in 62 Continuing Education in Anaesthesia. smooth muscle proliferation and endothelial gene-related peptide. Most vasoactive hormones require an intact vascular endothe-lium. and calcitonin Deposits of lipids.2 s) ¼ 24 s mm Hg TTI predominantly have b2 receptors (vasodilatation). response to intraluminal pressure changes (fast) and metabolic Similarly. as the metabolic effects of any change in blood pressure. Intramuscular and subendocardial blood vessels DPTI ¼ 80 mm Hg (60 s/heart rate – 0. LVEDP ¼ 15 mm Hg constriction. 1 Factors affecting coronary vasomotor tone. ET ¼ endothelin receptor. Angiotensin II causes coronary vasoconstriction independent of sympathetic innervation. The myocardial oxygen tension and presence of index (TTI). flow becomes (DPTI) is a useful measure of coronary blood supply and is the pressure-dependent. vasoconstrictors or vasodilators influence the range of coronary The ratio DPTI/TTI is the endocardial viability ratio (EVR) and autoregulation.67 stimulation increases myocardial blood flow through an increased metabolic demand and a predominance of b receptor activation. The other peptides cause α β endothelium-mediated vasodilatation. The EVR is normally 1 or more. The vasodilatory Diseases affecting the coronary blood flow effect of acetylcholine depends on an intact endothelium. which secretes vasodilators. the product of systolic pressure and systolic time.7 is associated with Nervous control subendocardial ischaemia. Parasympathetic influences are minor and weakly vasodilatory. nitric oxide. The net Fig. Such a value may be reached in a patient with the following Autonomic influences are generally weak. b ¼ response depends on the balance between the two opposing groups. atherosclerosis and hypertension. Vasomotor tone is ultimately mediated by the vascular endothelium. Coronary artery disease The peptide hormones include antidiuretic hormone. a vasodilator. nitric oxide and endothelin. prostacyclin and bradykinin. with diastole Alpha stimulation may play a role in the distribution of blood occupying the remaining time. KþATP ¼ ATP-sensitive potassium channel. It is difficult to tease out physiological data: the role of neural control on coronary blood flow. Sympathetic ¼ 180 mm Hg 0. Angiotensin-converting enzyme inactivates AT nitric oxide bradykinin.

unopposed systemic b2 Drugs and coronary blood flow stimulation reduces the afterload. it also regu- lates fibrous tissue formation after tissue injury. inotropy and mimic the protective effect of discrete episodes of myocardial ischaemia before a sustained ischaemic insult. Chronotropy and Impaired ejection results in larger diastolic volumes. distal arterioles dilate maximally to Drugs acting on angiotensin preserve flow up to the point where the vascular bed is maximally dilated. Statins inhibit HMG CoA reductase. This results in negative collaterals and a lower LVEDP. coronary vaso-dilation and Calcium channel blockers reduced afterload generally results in a favourable myocardial Compared to the non-dihydropyridines (verapamil and diltiazem) oxygen supply–demand ratio. Further stenosis leads to a drop in flow and flow becomes Angiotensin-converting enzyme inhibitors reduce conversion of pressure dependent. Over time. inotropes also reduce the LVEDP. Nitrates Nitrates produce vasodilatation in all vascular beds. Halogenated anaesthetic agents activate ATP-sensitive potassium cardia. raised LVEDP and lower coronary perfusion pressure. Coronary blood flow metabolic demand. lessened because of decreases in contractility and pressure load. Raised intra-myocardial pressure lowers the subendocardial blood flow. Flow in collaterals is also often pressure dependent. Theoretically. contractility and heart rate. In the failing heart. oxygen demand related to higher work-load. anticoagulants and lipid exerts a ‘positive inotropic effect’. The oxygen demand is Resting flow becomes affected if the diameter is reduced by 80%. and Antiplatelet drugs. less Isoflurane in particular causes coronary vasodilatation. inhibition of the sinus and atrioventricular nodes. The myocardial oxygen supply improves due to (conductance) vessels. Increased potassium efflux increases myocardial work and oxygen demand. In addition. Recent investigations in systemic vasoconstriction may help to improve the myocardial patients with coronary heart disease suggest that b-blockers do not perfusion but increases pressure load and oxygen demand. vasodilatation without reflex tachycardia. improves ejection fraction. The left ventricle undergoes hypertrophy in response to raised afterload. an enzyme These drugs restore coronary perfusion pressure in hypotensive involved in cholesterol synthesis. Any increase in occlusive thrombus. Antithrombin agents act at various sites in the aortic diastolic pressure may be offset by an increase in myocardial coagulation cascade to inhibit thrombin formation. depress the cardiac output as much as originally thought. Antiplatelet drugs pre-vent patients and may be especially beneficial in those patients heading platelet aggregation. Sympathetic-mediated inotropy depends on b1 stimulation. Critical Care & Pain | Volume 5 Number 2 2005 63 . They relieve coronary vasospasm but their balance main benefit is to reduce preload. coronary steal may occur Continuing Education in Anaesthesia. 3 Drugs such as losartan are angiotensin receptor antagonists and enhance Hypertension endothelial nitric oxide release. In patients on cardioselective b1-blockers. There is also an results in reduced intracellular calcium and muscle relaxa-tion. Potassium channel openers resulting in decreased capillary density. afterload and to increase max- imal coronary dilation. The myofibrillar growth outstrips the capillary net-work. It impaired vasomotor response to hypoxia in hypertrophied tissue dilates both normal and stenotic segments of the coronary arteries. and less negative Arterioles (resistance vessels) are dilated more than epicardial inotropy. Flow diverted into a dilated parallel bed angiotensin I to angiotensin II. so-called ‘ischaemic preconditioning’. With increasing stenosis. The pressure load Nicorandil is a novel anti-anginal agent. mediated by Anaesthesia and myocardial oxygen nitric oxide release. often the initial step in the formation of an towards the lower end of the autoregulation range. the dihydropyridines (nifedipine) produce more vasodilatation. Regional blood flow is improved due to dilatation of channels and lower intracellular calcium. Benefits may be offset by reflex tachy. coronary dilatation and lower LVEDP. The reduction in the heart rate prolongs the diastolic perfusion time and they inhibit stress-induced rises in myocardial contractility. b-Blockers Heart failure Coronary blood vessels contain b2 receptors. usually when the diameter is reduced by 50%.4 lowering drugs Vasopressors and inotropes These agents act inside the lumen to prevent further reduction in the vessel diameter. that makes it susceptible to ischaemia. These drugs reduce angiotensin- proximal to a stenosis is called coronary steal and can aggravate mediated vasoconstriction and enhance myocardial perfusion by ischemia.

Hall JE. 1996 and hypotension is permitted. Philadelphia: WB Saunders. eds. hypertension. 11: 517–20 healthy individuals but vasoconstriction in patients with coronary artery disease. Kaplan JA. production of angiotensin II and its pharmacologic inhibition: effects on cardia. 59: 60–8 pressure will lower the coronary perfusion pressure. 74: 503–13 myocardial oxygen demand. Volatile anaesthetic effects on ischemic myocardium. Norbert R. Cardiac Anaesthesia. Rumberger JA. Thor-acic 5. Reich DL. Sevoflurane and halothane do not 2. 1999 3. Critical Care & Pain | Volume 5 Number 2 2005 . 5 Edn. 9th Edn. Biccard BM. Guyton AC. Knight PR. Central neuroaxis blockade and coronary circulation. ischaemia in patients with coronary artery disease if tachycardia Philadelphia: WB Saunders. increase in shear forces and increased the coronary circulation. Lerman LO. 64 Continuing Education in Anaesthesia. 4th cause tachycardia or maldistribution of myocardial perfusion. Konstadt SN. Curr Opin Anaesthesiol 1998. Cardiac Perioperative stress results in sympathetically mediated tachy. Perioperative b blockade and haemodynamic potentially harmful response but any substantial fall in blood optimisation. Anaesthesia 2004. Mayo Clinic Proceedings 1999. Central neuraxial block obtunds this 4. Textbook of Medical Physiology. eds. Ritman EL. 11: 403–6 epidural analgesia also blocks sympathetic outflow to the heart. can provoke 1. Isoflurane however. Schmermund A.Coronary blood flow in a distinct anatomical pattern of coronary artery disease but this References has not been borne out in practice. Nader-Djalal N.6 See multiple choice questions 48–53. Curr Opin Anaesthesiol 1998. Sympathetic stimulation produces coronary vasodilatation in 6.