Coronary Blood Flow

Total coronary blood flow at rest is about 250 ml/min. The myocardium normally extracts about 70% of the oxygen content of coronary blood at rest; thus, increasing coronary perfusion is the only way to increase oxygen delivery. At rest the oxygen requirement of the myocardium is 10 ml/min/100 g at rest giving a total basal oxygen requirement of 30 ml/min for an adult. Cardiac muscle is versatile in its use of substrate, normally using 60% fatty acid and 40% carbohydrate as fuel. It may adapt to use different proportions and include ketone bodies as substrate.

Coronary blood flow and its distribution can be studied using:

• Coronary angiography—radiopaque dye is used to outline coronary vessels and radioactive xenon to quantify regional perfusion

• Thallium scan—radioactive thallium uptake is used as a marker of regional distribution of perfusion in the myocardium

• Technetium scan—selective uptake of radioactive technetium marks infarcted areas Factors Determining Coronary Blood Flow

Since the coronary arteries originate in the root of the aorta, aortic pressure provides the main driving force for coronary blood flow. Normally, this pressure is controlled by baroreceptor reflexes and, thus, regulation of coronary blood flow is achieved through coronary vasodilatation or vasoconstriction. Coronary vascular resistance is mainly controlled by local factors. Some of the factors affecting coronary blood flow are detailed below:

• Extravascular compression (extracoronary resistance)—this describes the external compression produced by myocardial contraction during the cardiac cycle. Coronary blood flow is reduced to zero in early systole and may even be transiently reversed (Figure CR.33). This 'squeezing' effect is greatest at endocardial levels and least towards the epicardium. However, in the normal heart endocardial and epicardial blood flows are about equal in the cardiac cycle. The bulk of coronary blood flow, thus, occurs during diastole. However, since diastole decreases as heart rate increases, coronary blood flow can become compromized by tachyarrhythmias. Counterpulsation or 'balloon pumping' assists coronary blood flow by inflating an aortic balloon cyclically during diastole

• Metabolic demands—the correlation between metabolic activity in the heart and coronary blood flow is fixed. Metabolites or an unidentified vasoactive agent, act to increase or decrease the oxygen supply if demand is varied. Alternatively, if the oxygen supply is limited cardiac activity adapts. Likely substances responsible for this effect include potassium ions and adenosine

• Autonomic system—activation of the sympathetic system tends to produce an increase in coronary blood flow. This occurs as a net result of increased metabolic demand in the face of the negative effects of increased contractility and heart rate on coronary blood flow. Under P blockade coronary vessels constrict in response to sympathetic stimulation. Stimulation of the vagus nerves produces slight coronary vasodilatation

Figure CR.33 Coronary blood flow and the cardiac cycle

• Coronary perfusion pressure (CPP)—this is the pressure across the coronary arteries and equals the difference between aortic pressure and intraventricular pressure. Autoregulation operates over a range of CPP between 60 and 180 mmHg. If CPP changes suddenly, coronary vessels respond by dilating or constricting to dampen dramatic surges or falls in coronary blood flow

Figure CR.34 Summarizes the factors affecting coronary vascular resistance

SUMMARY OF FACTORS AFFECTING CORONARY VASCULAR RESISTANCE

Factor

Effect on coronary vascular resistance

Sympathetic activity

alpha-receptors

beta-receptors

I

Vagal activity

I

Systolic compression

Coronary perfusion pressure

or I

Adenosine

1

Other metabolic factors

CO2, O2, H+, K+

X or

Figure CR.34 Cardiac Ischaemia

Figure CR.34 Cardiac Ischaemia

When the oxygen demands of the myocardium outstrip the oxygen supply, myocardial dysfunction and tissue damage follow. The oxygen requirements are related to the cardiac work rate, which in turn is dependent on systolic arterial pressure and cardiac output. Oxygen requirements are increased disproportionately by increases in systolic pressure, compared with cardiac output. Thus, if cardiac work is increased by increasing systolic pressure, oxygen requirements are much greater than if the increase in cardiac work were achieved by increasing cardiac output. 'Pressure' work is therefore more expensive than 'volume' work in terms of oxygen consumption. This is a major factor underlying the mortality associated with aortic stenosis. Clinically myocardial ischaemia results in the chest pain of angina pectoris and ultimately the tissue necrosis occurring in myocardial infarction.

Myocardial blood flow may be increased in ischaemic heart disease by:

• Coronary vasodilators (glyceryl trinitrate)

• Coronary thrombus dissolution (streptokinase)

• Coronary angioplasty (dilatation by catheter balloon)

• Coronary bypass graft

• Coronary laser endarterectomy Cerebral Circulation

The left and right carotid arteries join the basilar artery to form the circle of Willis from which the left and right anterior, middle and posterior cerebral arteries arise. The basilar artery is formed by the anastomosis of the two vertebral arteries. Each carotid artery supplies its own side of the brain, and there is no significant perfusion of the opposite side by a carotid. Cerebral venous drainage is via the internal jugular veins that are fed by the dural sinuses or directly by cerebral veins.

Brain cells are intolerant of hypoxia and require uninterrupted perfusion. Several seconds of total ischaemia can produce unconsciousness and several minutes may result in irreversible damage. Cerebral vessels are innervated by sympathetic fibres that enter the skull around the carotid arteries. These fibres originate in the superior cervical ganglia. There are also cholinergic fibres from the sphenopalantine ganglia and facial nerve. Cerebral vessels are supplied by sensory fibres originating in the trigeminal ganglia. The stimulation of sensory fibres on vessels by metabolites is thought to cause migraine.

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