The Heart and Circulation

Venous Pressure Changes: The veins near the heart show similar pressure waves to those in the right atrium. Since the veins and atria are in communication at all times except during the brief atrial systole, the atrial pressure changes will be transmitted back to the veins.

There are three maxima in each cardiac cycle lettered a, c and v. The [a] wave is caused by atrial systole. The sphincter-like action of the atrial muscle round the entry of the veins prevents this being due simply to a transmission of atrial systole to the veins. The pressure builds up because the veins are unable to empty their blood into the atria.

The [c] wave is synchronous with the pulse wave in carotid artery hence the letter c. It corresponds to the atrial pressure peaks occurring at 0.15 and 0.95 seconds and is duo to the bulging of the A-V valves during the isometric contraction phase.

The [v] wave corresponds to the peak in the atrial pressure, which occurs just before 0.45 seconds and is due to the filling of the atria whilst the A-V valves are shut and the upward movement of the A-V ring at the end of ventricular systole. These pressure changes in the veins produce the venous pulse which is visible in the neck veins when the subject is lying down.

All veins above the sternal angle are usually collapsed because their pressure is sub-atmospheric. No pulsations are therefore visible in the neck veins in the upright posture unless venous congestion is present.

The venous pulsations are seen best in the right external jugular vein which is in direct continuity with the superior vena cava and the right atrium. The venous pressure changes are too small to be palpable.

Ventricular Volume Changes The ventricular volume is constant during both the isometric contraction phase and the isometric relaxation phase. Thus with the onset of systole, for the first 0.05 second there is reduction in volume.

As soon as the aortic valve has opened the ventricular volume decreases as blood is ejected into the aorta. The ejection is rapid at first. Late in systole the ejection rate is reduced. For the first 0.05 second of diastole there is again no ventricular volume change as the ventricular muscle fibers relax isometrically.

As soon as the mitral valve opens the blood rushes into the ventricle, the ventricular volume increases rapidly at first and later more slowly. By the time 0.4 of the 0.5 second of diastole has elapsed the filling has been such that the ventricular volume has increased by 50 m1= 70% of the next stroke volume. Atrial contraction in the last 0.1 second of ventricular diastole completes the filling by the addition of a further 20 ml.

Murmurs Murmurs are sounds heard during the cardiac cycle in addition to the normal heart sounds. Those occurring during systole are known as systolic murmurs. Those occurring during diastole are termed diastolic murmurs. They are caused by turbulence in the blood as it flows through the valve.

Valvular disease may prevent adequate closure of the valves, so that blood regurgitates back through the partially closed valves. This will occur during systole in a case of mitral or tricuspid incompetence, giving rise to a systolic murmur. It will occur during diastole if the aortic or pulmonary valve is faulty-giving a diastolic murmur.

Murmurs are also caused by a narrowing of the valve orifice which is known as a stenosis. The murmur will occur during the rapid passage of blood through the valve. Thus, mitral and tricuspid stenosis will give rise to a diastolic murmur which will reach a maximum during late diastole when atrial contraction forces blood through the valve into the ventricle. Aortic and pulmonary stenosis will give rise to a systolic murmur.

If the turbulence produces vibrations of the chest wall with low frequency components, the vibrations can be felt when the flat of the hand (or the ulnar border of the hand) is applied to the chest wall. Such a palpable murmur is termed a thrill. In general, low frequencies can be felt rather than heard, whilst high frequencies can be heard rather than felt.

Heart Block The duration of the P-Q, or as it is often called the P-R, interval is a measure of the conduction time in the bundle. It is normally (0.15- 0.2) seconds. Any longer time denotes delay in the transmission along the bundle and maybe the forerunner of complete failure of conduction along the bundle known as heart block.

Complete heart block occurs when the ventricles will be cut off from the pacemaker and will stop beating. However, they may restart at a slow independent rate due to the inherent rhythmicity of the ventricular muscle. The rate (about 30 beats/minute) is often too slow for an efficient circulation.

In all probability the S. A In all probability the S.A. node and atria will continue at their original rate of 70 beats/minute. Atrial contractions will cease to be effective in aiding the circulation as many will occur whilst the A-V valves are shut. The ECG will show numerous P waves but few abnormal QRS complexes and there will be no time correlation between them.

In such a case an electrical stimulator may be implanted in the axilla or abdominal wall and connected to electrodes in the ventricle. Such a device acts as an artificial pacemaker and the ventricular contractions follow at the rate set by the electronic circuits. About 20 x 10-6 joules of energy are needed for each pulse.

If a ventricular beat originates at some ectopic focus, an abnormal QRST complex will appear on the E.C.G.

This is a common occurrence in young adults and is known as an extra-systole or dropped beat. The term dropped beat is used because the ectopic beat may prevent the next pacemaker beat from contracting the ventricular muscle.

There is therefore a pause until the next successive beat arrives [Fig-34B].

Atrial Fibrillation Atrial fibrillation occurs when the increased excitability of the atrial muscle leads to abnormal beats arising from ectopic loci in the atria. As a result, different parts of the atria are contracting and relaxing out of phase with one another.

The general appearance of the atria during fibrillation has been described as resembling a bag of wriggling worms. The atria never empty and the atrial wall becomes a quivering sheet of muscle.

In atrial fibrillation the atria cease to pump blood into the ventricles. In addition, the beat originated by the pacemaker is not transmitted to the ventricles. Instead, impulses down the bundle of His in a haphazard fashion at a rate too fast for the ventricle to respond to each impulse.

The ventricular contractions which do occur are irregular both in rate and amplitude. A proportion of these beats fail to develop sufficient pressure to open the aortic valve. As a result the radial pulse is "irregularly irregular" and the heart rate measured at the heart may be higher than if it is measured by the pulse at the wrist. This is known as a pulse deficit.

Ventricular Fibrillation Should the ventricular muscle fibrillate, the circulation stops immediately. Unless immediate cardiac massage is carried out, life will cease. Under suitable conditions ventricular fibrillation may be stopped by passing an electric current through the heart. The apparatus is termed a cardiac defibrillator.