33 - Chapter 33 CARDIAC STRUCTURE AND FUNCTION Myocardial cells exhibit autorhythmicity even in completely isolated cells that continue to"beat in cell

Chapter 33 CARDIAC STRUCTURE AND FUNCTION The following material summarizes the key aspects of the myocardium that were presented in Chapters 2 and 23, in the context of heart muscle as an excitable tissue. The emphasis is now placed on the function of this highly specialized tissue. Some of the details provided earlier are reviewed quickly before they are developed in relation to the regulation of cardiac function. A. Structure of the muscle Cardiac muscle grossly appears to be syncytial; however, the cells are mononucleate but provided with very tight electrocoupling via gap junctions, within their multiple intercalated disks. Each cell is in direct communication with about a dozen others. Distinct striations are evident. It can be assumed at this level of treatment that the ultimate intracellular mechanisms of contraction described for skeletal muscle are broadly applicable to cardiac muscle. That is, Ca 2+ is needed to couple excitation and contraction, and the role of regulatory proteins, the function of crossbridges, ratchet mechanism for filament sliding, and adenosine triphosphate (ATP) hydrolysis are all essentially as described for skeletal muscle in Chapter 22. B. Electrophysiology A major distinction between muscle types is evident in the form of excitation at the sarcolemmal level. The nature of depolarization in cells of the pacemaker and those of the bulk of the myocardium was described in detail in Chapter 23. The following review items will indicate if the reader needs to return to the description in that earlier chapter. • Myocardial cells exhibit autorhythmicity - even in completely isolated cells that continue to "beat" in cell culture. • The cells forming the sinoatrial (SA) node (pacemaker), are most obviously autorhythmic, simply because of the instability of the recovery potential and the drift of potential up to threshold. • Because the cells are so tightly electrocoupled, the activity of the cell population as a whole tends to be dictated by the pacemaker cells - those with the fastest intrinsic rate of firing. • The intrinsic activity of the SA node is subject to influences from the autonomic nervous system. Most importantly, parasympathetic, cholinergic innervation from the vagus provides a means of slowing down the firing rate of the SA node. • Depolarization in the bulk myocardium is of very long duration, as is the refractory period. This prevents temporal summation and provides for an obligatory relaxation phase, needed for heart filling. Without this protection, a steady cycle of relaxation and contraction could not occur and the heart would be unable to act as a pump. Although the SA node normally provides the pacemaker role, if for some reason any other myocardial area develops excessive excitability and begins firing more frequently than the SA node, this new area can take over the pacemaker function. This is a well-known aspect of caffeine intoxication. Some other aspects of abnormal pacemaker function are noted in Box 33-1.