The coronary circulation

Myocardial blood supply is from the right and left coronary arteries, which run over the surface of the heart giving branches to the endocardium (the inner layer of the myocardium). Venous drainage is mostly via the coronary sinus into the right atrium, but a small proportion of blood flows directly into the ventricles through the Thebesian veins, delivering unoxygenated blood to the systemic circulation. Oxygen extraction by the tissues is dependent on consumption and delivery. Myocardial oxygen consumption is higher than in skeletal muscle (65% of arterial oxygen is extracted as compared to 25%). Therefore any increased myocardial metabolic demand must be matched by increased coronary blood flow. This is a local response, mediated by changes in coronary arterial tone, with only a small input from the autonomic nervous system.

Teaching Point

Coronary blood flow occurs mostly during diastole, because during systole the blood vessels within the myocardium are compressed. Increased heart rates, which reduce the time for diastole filling, can reduce the myocardial blood supply and cause ischaemia. In heart failure, the ventricle is less able to empty and therefore the intraventricular volume and pressure is higher than normal. During diastole, this pressure is transmitted to the ventricular wall and opposes and reduces coronary flow, especially in the endocardial vessels.

 
Cardiac Output

Cardiac output (CO) is the product of heart rate (HR) and stroke volume (SV):

For a 70kg man normal values are HR=70/min and SV=70ml, giving a cardiac output of about 5litre/min. The cardiac index is the cardiac output per square metre of body surface area - normal values range from 2.5-4.0 litre/min/m².
Heart rate is determined by the rate of spontaneous depolarisation at the sinoatrial node (see above), but can be modified by the autonomic nervous system. The vagus nerve acts on muscarinic receptors to slow the heart, whereas the cardiac sympathetic fibres stimulate beta-adrenergic receptors and increase heart rate.

Stroke volume is determined by three main factors: preload, afterload and contractility. These will be considered in turn:

Preload is the ventricular volume at the end of diastole. An increased preload leads to an increased stroke volume. Preload is mainly dependent on the return of venous blood from the body. Venous return is influenced by changes in position, intra-thoracic pressure, blood volume and the balance of constriction and dilatation (tone) in the venous system. The relationship between ventricular end-diastolic volume and stroke volume is known as Starling's law of the heart, which states that the energy of contraction of the muscle is related/proportional to the initial length of the muscle fibre. This is graphically illustrated in Figure 2 by a series of "Starling curves".

Curves A and B illustrate the rise in cardiac output with increases in ventricular end-diastolic volume (pre-load) in the normal heart. Note that with an increase in contractility there is a greater cardiac output for the same ventricular end- diastolic volume. In the diseased heart (C and D), cardiac output is leass and falls if ventricular end-diastolic volume rises to high levels, as in heart failure or overload.

As volume at the end of diastole (end-diastolic volume) increases and stretches the muscle fibre, so the energy of contraction and stroke volume increase, until a point of over-stretching when stroke volume may actually decrease, as in the failing heart. Cardiac output will also increase or decrease in parallel with stroke volume if there is no change in heart rate.

The curves show how the heart performs at different states of contractility, ranging from the normal heart to one in cardiogenic shock. This is a condition where the heart is so damaged by disease that cardiac output is unable to maintain tissue perfusion. Also shown are increasing levels of physical activity which require a corresponding increase in cardiac output.

Afterload is the resistance to ventricular ejection. This is caused by the resistance to flow in the systemic circulation and is the systemic vascular resistance. The resistance is determined by the diameter of the arterioles and pre-capillary sphincters; the narrower or more constricted, the higher the resistance. The level of systemic vascular resistance is controlled by the sympathetic system which, in turn, controls the tone of the muscle in the wall of the arteriole, and hence the diameter. The resistance is measured in units of dyne.sec/cm⁵. A series of Starling curves with differing afterloads is shown in Figure 3, demonstrating a fall in stroke volume as afterload increases.

The relationship between stroke volume and afterload. A series of curves illustrates the effects of increasing afterload on systemic vascular resistance. As afterload increases, the patient moves to a lower curve, with a lower stroke volume for the same ventricular end-diastolic volume (preload). The relationship between systemic vascular resistance and the control of arterial pressure is discussed below.

Contractility describes the ability of the myocardium to contract in the absence of any changes in preload or afterload. In other words, it is the "power" of the cardiac muscle. The most important influence on contractility is the sympathetic nervous system. Beta-adrenergic receptors are stimulated by noradrenaline released from nerve endings, and contractility increases. A similar effect is seen with circulating adrenaline and drugs such as ephedrine, digoxin and calcium. Contractility is reduced by acidosis, myocardial ischaemia, and the use of beta-blocking and anti-arrhythmic agents.

Cardiac output will change to match changing metabolic demands of the body. The outputs of both ventricles must be identical, and also equal the venous return of blood from the body. The balancing of cardiac output and venous return is illustrated during the response to exercise. Blood vessels dilate in exercising muscle groups because of increased metabolism, and blood flow increases. This increases venous return and right ventricular preload. Consequently more blood is delivered to the left ventricle and cardiac output increases. There will also be increased contractility and heart rate from the sympathetic activity associated with exercise, further increasing cardiac output to meet tissue requirements.

Teaching Point

A pulmonary artery catheter can measure pressures in the right heart as it is floated into position. The catheter includes a small balloon which is transiently inflated to wedge it into a small pulmonary artery, occluding pulmonary arterial flow. This will give a characteristic waveform, and it is assumed that the measured pressure equals that in the left atrium. The catheter can also be used to measure cardiac output. However, in the absence of such monitoring, clinical examination gives a good indication of cardiac function. Skin temperature, capillary refill*, pulse rate and volume, urine output and level of consciousness are reliable markers of cardiac output, and are easily assessed. *Capillary refill- when pressure is applied to skin or a finger nail, it goes white. When the pressure is released, the colour rapidly returns within 2-3 seconds. This is capillary refill, and is prolonged when the peripheral circulation is poor due to hypovolaemia or a poor cardiac output.

(Continued ...)

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