University of Minnesota
University of Minnesota
Make a Gift
Right Atrium
Right Ventricle
Pulmonary Trunk
Left Atrium
Left Ventricle
Coronary Arteries
Cardiac Veins
External Images
MRI Images
Comparative Imaging
3D Modeling
Anatomy Tutorial
Cardiovascular Magnetic Resonance Tutorial
Comparative Anatomy Tutorial
Conduction System Tutorial
Congenital Defects Tutorial
Coronary System Tutorial
Device Tutorial
Echocardiography Tutorial
Physiology Tutorial
Project Methodologies
Cardiovascular Devices and Techniques at U of Minnesota
References and Links
Atlas in the media
Surgery Department
Conduction System Tutorial
Overview of Cardiac Conduction Control of Ones Heart Rate Cardiac Action Potentials Gap Junctions Atrioventricular Node and Bundle of His Summary and References

Control of One's Heart Rate

Under normal physiologic conditions, the dominant pacemaker cells of the heart lie within the sinoatrial node; in adults, these pacemaker cells fire at rates between 60 to 100 beats per minute (i.e., faster than cells in any other cardiac region, See Figure 3). Even at rest, modulation by the autonomic nervous system dominates, with the primary drive from the parasympathetics; at rest or during sleep, the sinoatrial nodal rate decreases to about 75 beats per minute (bpm) or even slower.

In addition to pacemaker cells of the sinoatrial node, other cells within the conduction system are capable of developing autorhythmicity, specifically those within the atrioventricular node (junction region) and His-Purkinje system. Yet, rhythms generated within these cells are in a much lower range (25 to 55 bpm), hence not altering the intrinsic atrial rates (Figure 2). These lower rate rhythms are commonly referred to as ventricular escape rhythms and are important for patient survival, since they maintain some degree of cardiac output in situations when the sinoatrial and/or atrioventricular nodes are functioning inappropriately (e.g., in a patient with atrial fibrillation). Note that the various populations of pacemaker myocytes (i.e., in the sinoatrial and atrioventricular nodes) elicit so-called slow type action potentials (slow response action potential; see below).

Figure 3

Figure 3. A typical action potential of a ventricular myocyte and the underlying ion currents. The resting membrane potential is approximately ~90 mV (phase 4). The rapid depolarization is primarily due to the voltage gated Na+ current (phase 0), which results in a relatively sharp peak (phase 1) and transitions into the plateau (phase 2) until repolarization (phase 3). Also indicated are the refractory period and timing of the ventricular contraction. Modified from Tortora GJ, Grabowski SR. Principles of Anatomy and Physiology, ninth edition. New York: John Wiley & Sons, Inc., 2000.

In addition to the normal sources of cardiac rhythms, myocardial tissue can also exhibit abnormal self-excitability; such a site is also called an ectopic pacemaker or ectopic focus. This pacemaker may operate only occasionally, producing extra beats, or it may induce a new cardiac rhythm for some period of time. Potentiators of ectopic activity include caffeine, nicotine, electrolyte imbalances, hypoxia, and/or toxic reactions to drugs such as digitalis. It should also be noted that any cell(s) in the heart can take over pacemaker function if they are driven to do so, such as in electrical pacing via an implanted electrode/lead.

© 2021 Regents of the University of Minnesota. All rights reserved. The University of Minnesota is an equal opportunity educator and employer. Privacy Statement