Catecholamine Effects on Cardiac Rhythm and Conduction
The effect of sympathetic stimulation on the human body is aptly described as “fight or flight.” It prepares the body to respond to emergencies by forcing the heart to increase blood supply to skeletal muscles and other vital organs necessary for self-preservation. The heart accomplishes this task through a combination of actions that work together to increase cardiac output, and the mechanism for such increased activity is catecholamine-mediated.
In contrast to parasympathetic stimulation, sympathetic stimulation of the heart increases the excitability of the cardiac muscle fibers. As a result, sympathetic stimulation can:
- Increase the rate of cardiac impulse generation in the sinoatrial (SA) node
- Increase the rate of cardiac impulse conduction along the conduction system
- Increase the force of atrial and ventricular contraction
Very strong sympathetic stimulation can increase the heart rate up to 3 times the normal rate and can increase the force of muscular contraction up to twice the normal force.
Stimulation of the sympathetic nerves releases the hormone norepinephrineat the sympathetic nerve endings. The precise mechanism by which this hormone acts on cardiac muscle fibers is somewhat unclear, but the belief is that it increases the permeability of the fiber membrane to sodium and calcium ions. In the sinus node, an increase of sodium-calcium permeability causes a more positive resting potential and also causes increased rate of upward drift of the diastolic membrane potential toward the threshold level for self-excitation, thus accelerating self-excitation and, therefore, increasing the heart rate.
In the atrioventricular (AV) node and AV bundles, increased sodium-calcium permeability makes it easier for the action potential to excite each succeeding portion of the conducting fiber bundles, thereby decreasing the conduction time from the atria to the ventricles. The increase in permeability to calcium ions is at least partially responsible for the increase in contractile strength of the cardiac muscle under the influence of sympathetic stimulation, because calcium ions play a powerful role in exciting the contractile process of the myofibrils.
At the level of the SA node, this increased permeability to sodium and calcium decreases the negativity of the resting membrane potential and increases the rate in which the threshold potential is reached. Therefore, the overall effect of norepinephrine in the SA node fibers is to increase the heart rate.
At the level of the AV node and His bundle, the increased permeability to sodium and calcium enhances the AV-nodal and His bundle fibers’ excitability and increases the conduction speed of cardiac impulses into the ventricles.
At the level of the atrial and ventricular muscles, the increased permeability to calcium in particular promotes stronger interaction between the actin and myosin filaments of the cardiac muscle fibers. This results in an increased force of cardiac muscular contraction after sympathetic stimulation.
Understanding catecholamine effects on heart rate, rhythm and contractility highlights the importance of this class of hormones in the body’s response to stress or danger. It also explains characteristic findings seen in disorders of the sympathetic nervous system. More detailed discussions can be found on ExpertCollege.com, along with other topics relevant to critical care.