Maximal stimulation of vagal fibres can actually lead to a complete cessation of ventricular contraction. This can result from either a block in impulse transmission through the AV junctional fibres or complete inhibition of rhythmic signal generation by the SA node. Even with continued parasympathetic stimulation, the ventricles will begin to beat (10 to 40 beats per minute) after a short interval (typically 5 to 10 seconds). This phenomenon is called ventricular escape and is the result of new rhythmic impulses being generated in an abnormal site, for example, the AV bundle.
The heart receives its sympathetic innervation from nerves originating in the medulla (cardiac accelerating centre) and upper thoracic spinal cord. These reach the myocardium via several nerves sometimes referred to as the accelerator nerves. Sympathetic fibres innervate SA and AV nodal tissue as well as cardiac muscle cells themselves. When stimulated, the sympathetic fibres release noradrenaline, which leads not only to an increase in heart rate, but to an increase in the strength of ventricular and atrial contraction as well. The heart rate may nearly triple, and the strength of contraction may nearly double, under the influence of maximal sympathetic stimulation.
Various parts of the circulatory system relay messages (e.g., regarding blood pressure) to the cardiac centres, which respond by sending messages to the heart via the vagus nerves. In this manner the cardiac centres are responsible for maintaining a balance between the inhibitory effects of the parasympathetic nerves and the stimulatory effects of the sympathetic nerves. When the parasympathetic messages decrease, the sympathetic nerves are able to function in an unopposed manner and thereby increase the heart rate. For example, severance of vagal nerve fibres results in an increased heart rate.
Hormonal influence
Under conditions of stress, adrenaline and noradrenaline are released from the tissues of the adrenal medulla into the general circulation. Each of these hormones produces an increase in heart rate.
Thyroid hormones, thyroxin (T4) and triiodothyronine (T3), also accelerate the heart rate and this is most likely due to a direct effect of these substances on the heart. The strength of heart contraction is also modulated by thyroid hormones. In slight excess they increase the strength of contraction, whereas in marked excess they actually reduce the strength of contraction.
Temperature
Elevation of the body temperature markedly increases the heart rate. This most probably results from an increased permeability of cardiac muscle-cell plasma membranes to the passage of various ions, thereby causing an accelerated generation of rhythmic action potentials. During fever, for example, it is not uncommon for the individual to experience a heart rate in excess of 100 beats per minute. Lowering of the body temperature, or hypothermia, is accompanied by a reduction in heart rate. This latter observation is taken advantage of clinically, for example, when the patient's temperature is deliberately lowered during heart surgery.
Electrolyte Balance
The effects of calcium, potassium, and sodium on action potentials and membrane potentials is discussed in the pages on . In addition the importance of calcium ions and their role in cardiac muscle contraction was indicated earlier in these pages. It should be apparent then that the concentrations of these particular ions within the extracellular environment may have a significant influence on cardiac function. Ordinarily the concentrations of these ions are kept within appropriate limits and thus do not affect the heart adversely. However, in instances where their concentration becomes excessive or deficient, cardiac function may be seriously affected.
An excess of potassium ions in the extracellular environment markedly reduces the heart rate as well as the strength of contraction. On the other hand, spastic contraction of the heart results from the presence of excess calcium ions. This typically results from the direct effects of calcium ions upon the contractile process of cardiac muscle. A marked reduction in the calcium ion concentration has effects similar to those observed with high potassium levels.
Excessive levels of sodium ions result in depression of cardiac function, which is thought to stem from their competition with calcium ions at some critical site during the contractile process. At the other extreme, a deficiency of sodium ions in the extracellular environment leads to the development of a potentially lethal condition called cardiac fibrillation. In this situation, the cardiac muscle contracts at an extremely high rate and in an uncoordinated fashion such that little or no blood is actually pumped by the heart.
