Diastolic Function

Diastole can be broken down into the following stages:

• Isovolumetric ventricular relaxation

• Rapid ventricular filling

• Slow ventricular filling (diastasis)

• Atrial contraction

Although diastole appears to be a passive part of the cardiac cycle it has some important functions.

• Myocardial relaxation—a metabolically active phase. One essential process is the re-uptake of calcium by the sarcoplasmic reticulum. Incomplete re-uptake leads to diastolic dysfunction due to decreased end diastolic compliance. The negative slope of the ventricular pressure-time curve during isovolumetric relaxation (termed [dp/dt max] indicates myocardial relaxation. Increased sympathetic tone or circulating catecholamine levels give rise to an increased [dp/dt max]. This is known as positive lusitropy

• Ventricular filling—provides the volume for the cardiac pump. Most of the ventricular filling occurs during early diastole. There is only a small increase in ventricular volume during diastasis. As the heart rate increases diastasis is shortened first. When the heart rate > about 140 bpm, rapid filling in early diastole becomes compromised and the volume of blood ejected during systole (stroke volume, SV) is significantly decreased

• Atrial contraction—contributes up to 25% of total ventricular filling in the normal heart. This atrial contribution can become of greater importance in the presence of myocardial ischaemia or ventricular hypertrophy

• Coronary artery perfusion—greater part of left coronary blood flow occurs during diastole Cardiac Valves

The cardiac valves open and close passively in response to the changes in pressure gradient across them. These valves control the sequence of flow between atria and ventricles and from ventricles to the pulmonary and systemic circulations. Valve timing in relation to the ventricular pressure curve is shown in Figure HE.15.

The AV valves are the mitral and tricuspid valves. These prevent backflow from the ventricles into the atria during systole. The papillary muscles are attached to the AV valves by chordae tendinae. They contract together with the ventricular muscle during systole, but do not help to close the valves. They prevent excessive bulging of the valves into the atria and pull the base of the heart toward the ventricular apex to shorten the longitudinal axis of the ventricle, thus, increasing systolic efficiency.

Figure HE.15 Heart sounds and timing

The semilunar (SL) valves are the aortic and pulmonary valves. These prevent backflow from the aorta and pulmonary arteries into the ventricles during diastole. The SL valves function quite differently from the AV valves because they are exposed to higher pressures in the arteries. They are smaller (normal aortic valve area is 2.6-3.5 cm2 while normal mitral valve area is 4-6 cm2), therefore, the blood velocity through them is greater. Disease in the cardiac valves may cause them to leak when they are meant to be closed, thus, allowing backflow or regurgitation. This situation leads to inefficiency in producing cardiac output (CO), since the work done by the heart has to increase to compensate for the backflow and yet maintain adequate CO. Mitral and aortic regurgitation are the most common regurgitant lesions.

Alternatively, the orifice of a valve may become narrowed or stenotic. This obstructs the flow of blood through it and requires increased pressure gradients to be generated across the valve to achieve adequate blood flows. In mitral stenosis the valve area can be reduced by > 50%. This causes the left atrium to contract more forcefully to maintain ventricular filling. In severe cases a valve area of 1 cm2 can require the left atrium to produce peak pressures of 25 mmHg to produce normal CO. Aortic stenosis obstructs left ventricular output and increases the workload of the left ventricle. The stenosis can multiply the normal pressure gradient across the aortic valve during systole by ten times or more. When the aortic valve area decreases by 70% (< 0.8 cm2), the stenosis becomes critical and systolic pressure gradients across the valve of > 50 mmHg may be required, to produce normal CO.

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