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Contents 1 The Conducting System of the Heart 1.1 Rate of Heartbeat 2 The Cardiac Cycle 2.1 Pressure Changes during the Cardiac Cycle 2.1.1 Left Atrium 2.1.2 Left Ventricle 2.1.3 Aorta 3 Cardiac Output 3.1 Regulation of Cardiac Output 3.1.1 Stroke volume 3.1.2 Heart rate 4 Further Reading 5 Comments

The Conducting System of the Heart

The autonomic nerves control the pace of the contractions of the heart muscle. These supply a group of special cells close to the opening of the superior vena cava. This is called the sinoatrial node (SAN).

Once stimulated waves of contraction pass from fibre to fibre in the arterial muscle across the atrial surface, but are stopped from going straight on to the ventricles by a membrane of connective tissue separating the atria from the ventricles, the atrioventricular septum. The impulse takes around 50ms to propagate across the whole atrial surface.

The stimulus then accumulates in the atrioventricular node (AVN), where there is a delay of around 100ms. This allows time for the atria to physically contract prior to the impulse being transmitted to the ventricles.

Impulses are then transmitted towards the ventricles via the atrioventricluar bundle, or Bundle of His. This travels into the interventricular septum, where it splits into two, the right and left bundle branches. These travel along the septum to the inferior (lower) pole of the heart, where they give rise to the Purkinje fibres. This takes around 25ms

The Purkinje fibres branch into the ventricular muscle, where the impulses directly stimulate contraction of the cardiac muscle cells (myocardium), propagation through the ventricular myocardium lasts around 50ms, and stimulates ventricular systole. The atriovantricular septum prevents 'backwash' of the impulses into the atria.

Rate of Heartbeat

The average rate of heartbeat is 72 beats per minute. Thus each complete cardiac cycle lasts 0.8 seconds, this is divided into systole and diastole as follows:

		Atria		Ventricles
Systole		0.1s		0.3s
Diastole		0.7s		0.5s

The combined period of atrial and ventricular systole is 0.4s, and the period of total diastole (i.e. neither atria nor ventricles are contracting) is 0.4s

When heart rate increases, the period of complete diastole is shortened. This occurs during activity, inspiration and response to some drugs e.g. caffeine. Heart rate decreases during sleep, expiration and some drugs e.g. alcohol.

The Cardiac Cycle

The heart muscle contracts rhythmically with a period of rest between each contraction. The contraction period is called the systole, and the relaxation period is called the diastole:

Atrial systole

The atria contract and force blood into the ventricles. The contraction occurs around the openings of the veins into the atria first so that these are closed up to prevent back flow into them.

Ventricular systole

The ventricles contract and force the blood under pressure, past the semi lunar valves into the arteries. The closing of the bicuspid and tricuspid valves prevents back flow. At the same time the atria and ventricles relax and blood begins to flow back into them from the veins.

Diastole

The muscles of both atria and ventricles relax. The heart fills with blood, which is prevented from flowing straight out again by closing the seminar valves in the arteries.

Pressure Changes during the Cardiac Cycle

Starting at the leftmost side:

Left Atrium

Pressure rises due to atrial contraction (atrial systole) thendrops as blood flows into the ventricle. Mitral valve then closes due to pressure in the ventricle rising above that in the atrium (first heart sound, A). Pressure in the atrium steadily rises as blood is returned to the atrium during systole, when the mitral valve is closed. The mitral valve then opens (D) and the pressure drops as blood flows under gravity straight through the atrium into the ventricle.

Left Ventricle

Pressure rises as blood is forced from the atria into the ventricle. The ventricle then contracts (ventricular systole), causing the mitral valve to close (A). Pressure rises sharply in line with ventricular contraction until the intraventricular pressure is greater than the pressure in the aorta (afterload), at which point the aortic valve opens (B) and blood is forced into the aorta. The lack of blood in the ventricle causes pressure to drop, until it drops below aortic pressure and the aortic valve closes due to backflow pressure in the aorta (second heart sound, C). Both the valves are now closed, and the ventricular pressure continues to drop as the myocardium relaxes (diastole), when the pressure drops below the left atrial pressure the mitral valve opens (D), blood flows into the ventricles under gravity, causing gradual pressure rise

Aorta

Blood pressure gradually drops following the previous heartbeat, til diastolic pressure is reached (B), at which point the aortic valve opens and blood from the contracting left ventricle is forced into the aorta, rapidly reaching the diastolic BP. The BP then drops as the myocardium begins to relax and backflow pressure on the aortic valve causes it to close (C). When the aortic valve closes, the arterial walls recoil (elastic recoil), causing the brief pressure rise, the dicrotic notch.

Cardiac Output

This is the amount of blood flowing from the heart at a given time. It depends on:

• Stoke volume (total ventricular output per contraction)
• Heart rate (i.e. number of beats per minute)

Cardiac output = stroke volume X heart rate

e.g.

• At rest: 110ml X 60bpm = 6.6L/min
• After intense exercise: 2L X 200bpm = 40L/min

Regulation of Cardiac Output

This can occur via 2 mechanisms. Those which affect stroke volume, and those which affect the heart rate:

Stroke volume

This is dependant on 3 factors, the amount of blood in the ventricles at the start of systole (i.e. the End Diastolic Volume, EDV) and the force of contraction produced by the ventricular myocardium, and the pressure in the arteries (namely the aorta) which has to be overcome to eject blood from the heart (the afterload).

• End Diastolic Volume can be affected by the amount of blood returned to the heart via the vena cava, the more is returned, the greater the potential for larger EDV. Also the length of diastole will affect EDV. The longer the diastole, the longer the ventricular filling time - so the more blood can enter the ventricles per beat.

• Contractile force can be increased or decreased by a number of mechanisms. The most fundamental of these is the preload, i.e. the amount of stretching of the ventricular myocardium prior to contraction. The effect this has on the contractility is determined by the Frank-Starling principle - which basically postulates that the greater the EDV, the greater the preload and stretching of the myocardium, and thus the greater the contractile force.
  The contractile force can also be influenced by external factors, namely autonomic activity and drugs. These can either increase contractility (positive inopropes) or decrease it (negative inotropes)
  • Autonomic activity can be sympathetic via the secretion of noradrenaline (NA) from postganglionic fibres innervating the heart or via the adrenal glands secreting NA and adrenaline - which all have a positive inotropic effect by increasing the metabolic rate of cardiac muscle. Autonomic activity can also have a negative inotropic effect via the parasympathetic nervous system, which innervates the heart via the vagus nerve, and releases acetylcholine (ACh) - causing hyperpolarisation of the myocardium resulting in decreased contractility. Autonomic activity also has a significant effect on heart rate (see below).
  • Positive inotropic drugs include adrenaline and digoxin. Negative inotropic drugs include calcium channel blockers (amlodipine, verapamil) procainamide and propafenone

• Afterload is increased with increased arterial pressure, such as in systemic hypertension (high blood pressure) due to either constriction of blood vessels (vasodilation) or increased blood volume.

Heart rate

Heart rate is largely determined by autonomic innervation and circulating hormones in the blood (and drugs which affect these).

• Autonomic innervation, as described earlier can be either sympathetic (to increase heart rate) or parasympathetic (to slow heart rate). These act on the SAN to increase or decreate the rate of repolarisation respectively, allowing for greater or fewer contractions. Increasing heart rate is a positive chronotropic (from chronos the greek for time, and trophe, to feed) effect, whereas decreasing it is a negative chronotropic effect.
• Positive chronotropes include theophylline, beta-agonists (such as salbutamol, the active ingredient in the blue inhaler used in asthma), and adrenaline (epinephrine) - either intrinsically produced by the adrenals, or administered by a doctor. Negative chronotropes include digoxin and beta-blockers (propanolol, atenolol)

Further Reading

Martini, FH. "Fundamentals of Anatomy and Physiology". 5th edition. Prentice Hall, New Jersey (2001). ISBN 0130172928

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