BIOLOGY Volume 2 - A Guide to General Biology - 2004

14. TRANSPORT IN ANIMALS

14.7. The Heart

14.7.3. Myogenic Stimulation of the Heart

If an isolated mammalian Heart is placed in a well-oxygenated saline solution at 37 °C, it will continue to beat rhythmically for some time, despite the absence of signals from the nervous and endocrine systems. This demonstrates the myogenic (from the Greek myos — Muscle, genos — origin) nature of its heartbeat stimulation; in other words, it means that The Heart possesses a built-in mechanism that triggers its regular contraction and relaxation.

The stimulus for contraction originates in a specialized region of the right atrium wall near the entrance of the SUPERIOR VENA CAVA (Fig. 14.21). This is called the sinoatrial (sinuatrial) node, or the pacemaker, also known as the Keith–Flack node (referred to hereafter as the SA node). It consists of a small cluster of cardiomyocytes innervated by autonomic nerve terminals (Neurons of the Autonomic Nervous system — see the following section). The SA node is capable of independently stimulating heart contractions, though their rate is influenced by autonomic nervous activity, which thus modulates SA node function.

SA node Cells depolarize slowly during atrial diastole, meaning their transmembrane potential gradually decreases. At a certain point, an Action Potential is triggered within them (Section 17.1.1); impulses arise in exactly the same way in neurons. As the action potential spreads outward from the SA node, a wave of excitation sweeps through The cardiac muscle fibers, resembling a Nerve Impulse and causing them to contract. The SA node is called the pacemaker because it is the source of each excitation wave, which in turn acts as the stimulus for the next. Once initiated, the contraction spreads across the atrial walls via a network of cardiac muscle fibers at a speed of 1 m/s. Both atria contract more or less simultaneously. The muscle fibers of the atria and ventricles are separated by a Connective Tissue septum, and communication between them occurs through only one region in the right atrium — the atrioventricular (AV) node, or the Aschoff–Tawara node (Fig. 14.21).

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Fig. 14.21. Location OF THE sinoatrial node, atrioventricular node, and the bundle of His.

Structurally, the AV node resembles the SA node and is connected to a bundle of specialized muscle fibers known as the atrioventricular bundle, which serves as the sole pathway for conducting the excitation wave from the atria to the ventricles. Upon passing from the SA node into the AV node, the wave is delayed for approximately 0.15 s, allowing atrial systole to complete before ventricular systole begins.

The atrioventricular bundle connects to the bundle of His — a strand of modified cardiac muscle fibers that branches into finer fibers known as Purkinje fibers, which have almost entirely lost their contractile function. The bundle of His divides into right and left branches (corresponding to the ventricles). An excitation wave rapidly travels along these fibers at a speed of 5 m/s, engulfing the entire ventricular myocardium and causing the ventricles to contract simultaneously. Contraction begins at the apex of the heart (its lower part) and sweeps upward toward the base, pumping Blood into the Arteries that emerge vertically upward from the heart (Fig. 14.21). The electrical activity of different PARTS OF THE heart during the cardiac cycle can be recorded using electrodes placed at specific points on the body surface and a chart recorder. The resulting trace is called an Electrocardiogram (ECG). This Procedure is widely used in medicine because it helps detect and diagnose cardiac abnormalities (Fig. 14.22).

Fig. 14.22. Electrocardiogram (ECG) reflecting changes in myocardial electrical potential throughout the cardiac cycle. The deflection waves correspond to the following events: P — atrial depolarization and spread of excitation from the sinoatrial node during atrial systole; Q, R, and S — ventricular systole; T — onset of ventricular diastole.

Certain Properties of the myocardium ensure its rhythmic, continuous operation throughout a mammal's lifetime. Once any muscle begins to contract, it ceases to respond to subsequent stimuli until relaxation begins. This unresponsive state is termed absolute refractory period (Fig. 14.23). The refractory period of the myocardium lasts longer than that of other muscle types, allowing the heart to fully recover (“rest”) during diastole and work vigorously and rapidly without fatigue. As a result, the myocardium cannot enter a state of tetanus—that is, sustained contraction caused by frequent incoming excitation impulses—and thus avoids oxygen starvation. During muscle relaxation, the absolute refractory period is initially followed by a relative refractory period, characterized by reduced excitability, during which the muscle responds only to exceptionally strong stimuli (Fig. 14.23).

Fig. 14.23. The refractory period of the myocardium. The upper graph shows the Muscle contraction trace, and the lower graph shows changes in its stimulation sensitivity. (From Clegg & Clegg (2nd edition, 1963). Biology of the Mammal, Heinemann Medical Books.)