The pressure-volume curve during diastole is initially quite flat (compliant), which indicates that large increases in volume can be accommodated with only small increases in pressure. In contrast, the development of systolic pressure is considerable at the lower filling pressures. However, the ventricle becomes much less distensible with greater filling, as evidenced by the sharp rise in the diastolic pressure curve at large intraventricular volumes.
In a normal intact heart, peak force may be attained at a filling pressure of approximately 12 mm Hg. At this intraventricular diastolic pressure, which is near the upper limit observed in a normal heart, sarcomere length is near its resting length of 2.2 µm. However, the force causes filling pressures to peak as high as 30 mm Hg. At even higher diastolic pressures (>50 mm Hg), sarcomere length is no greater than 2.6 µm. This ability of the myocardium to resist stretch at high filling pressures probably resides in the noncontractile constituents of the heart tissue (connective tissue), and it may serve as a safety factor against overloading of the heart in diastole. Usually, ventricular diastolic pressure is approximately 0 to 7 mm Hg, and the average diastolic sarcomere length is approximately 2.2 µm. Thus a normal heart operates on the ascending portion of the Frank-Starling curve, as depicted in
Fig. 16.36 •Fig. 16.36 Relationshipofmyocardialrestingfiberlength(sarco-merelength)orend-diastolicvolumetotheforcedevelopedorpeaksystolicventricularpressureduringventricularcontractioninanintactheart.(RedrawnfromPattersonSW,etal.J Physiol. 1914;48:465.)
Cardiac muscle functions as a syncytium; that is, a stimulus applied to any part of the cardiac muscle results in contraction of the entire muscle. Gap junctions with high conductance are present in the intercalated disks between adjacent cells and facilitate conduction of the cardiac impulse from one cell to the next.
Cardiac muscle must contract repetitively for a lifetime, and hence it requires a continuous supply of O2. Cardiac muscle is therefore very rich in mitochondria. The large number of mitochondria (see
Fig. 13.1
B), which have the enzymes necessary for oxidative phosphorylation, allows rapid oxidation of substrates and synthesis of ATP and thus sustains the myocardial energy requirements.
CHAPTER 16 Elements of Cardiac Function
To provide adequate O2 and substrate for its metabolic machinery, the myocardium is also endowed with a rich capillary supply, approximately one capillary per fiber. Thus diffusion distances are short, and O2, CO2, substrates, and waste material can move rapidly between the myocardial cell and capillary. The transverse (T) tubular system within myocardial cells participates in this exchange of substances between capillary blood and myocardial cells (as described later, the T tubule system also plays a key role in excitation-contraction coupling). The T tubular system is absent or poorly developed in the atrial cells of many mammals.