The regulation of acetylcholine on potassium channels, known as KACh, also has a depressing effect on the if and iCa currents. The effects of the autonomic nervous system on cardiac cells are discussed in more detail in the text.

When the SA node or other components of the atrial pacemaker complex are removed or damaged, pacemaker cells in the AV junction typically take over the role of pacemaker for the entire heart. After a certain period of time, which can vary, automatic cells in the atria usually regain dominance and resume their pacemaker function. The Purkinje fibers in the specialized conduction system of the ventricles also exhibit automaticity, firing at a very slow rate. In cases where the AV junction is unable to conduct cardiac impulses from the atria to the ventricles, these idioventricular pacemakers in the Purkinje fiber network initiate ventricular contractions, but at a frequency of only 30 to 40 beats per minute.

If an ectopic focus in one of the atria suddenly begins firing at a high rate (e.g., 150 impulses per minute) in an individual with a normal heart rate of 70 beats per minute, the ectopic site would become the pacemaker for the entire heart. If the rapid ectopic focus suddenly stops firing, the SA node would remain briefly inactive due to overdrive suppression. The interval from the end of the overdrive period until the SA node resumes firing is referred to as the sinus node recovery time. In patients with sick sinus syndrome, the sinus node recovery time is prolonged. The resulting period of asystole (absence of a heartbeat) may lead to loss of consciousness.

The automaticity of pacemaker cells decreases after being stimulated at a high frequency, a phenomenon known as overdrive suppression. Since the SA node has a higher intrinsic rhythmicity compared to other latent pacemaking sites in the heart, firing of the SA node tends to suppress automaticity in other locations.

Overdrive suppression is a result of the activity of membrane Na+,K+-ATPase. With each depolarization, a certain amount of Na+ enters the cardiac cell. The more frequently the cell is depolarized, the greater the amount of Na+ entering the cell per minute. At high excitation frequencies, the activity of Na+,K+-ATPase increases to remove this larger amount of Na+ from the cell. This action of Na+,K+-ATPase hyperpolarizes the cell since three Na+ ions are extruded in exchange for two K+ ions entering the cell. Consequently, slow diastolic depolarization requires more time to reach the firing threshold. Furthermore, when the overdrive suddenly stops, the activity of Na+,K+-ATPase does not immediately slow down but remains temporarily overactive. This continuous extrusion of Na+ counteracts the gradual depolarization of the pacemaker cell during phase 4, temporarily suppressing its intrinsic automaticity.

Starting from the SA node, the cardiac impulse spreads radially throughout the right atrium at a conduction velocity of approximately 1 m/second, following ordinary atrial myocardial fibers. A specific pathway called the anterior interatrial myocardial band, also known as Bachmann's bundle, directly conducts the SA node impulse to the left atrium. The wave of excitation then proceeds inferiorly through the right atrium and eventually reaches the AV node, which serves as the usual entry route for the cardiac impulse to the ventricles.
acetylcholine-regulated potassium channels (KACh). Acetylcholine also depresses the if and iCa currents. The autonomic neural effects on cardiac cells are described in greater detail in
When the SA node or other components of the atrial pacemaker complex are excised or destroyed, pacemaker cells in the AV junction generally take over the pacemaker function for the entire heart. After some time, which may vary from minutes to days, automatic cells in the atria usually become dominant again and resume their pacemaker function. Purkinje fibers in the specialized conduction system of the ventricles also display automaticity. These fibers characteristically fire at a very slow rate. When the AV junction cannot conduct cardiac impulses from the atria to the ventricles, these idioventricular pacemakers in the Purkinje fiber network initiate the ventricular contractions, but at a frequency of only 30 to 40 beats per minute.
Ifanectopicfocusinoneoftheatriasuddenlybegantofireatahighrate(e.g.,150impulsesperminute)inanindividualwithanormalheartrateof70beatsperminute,theectopicsitewouldbecomethepacemakerfortheentireheart.Ifthatrapidectopicfocussuddenlystoppedfiring,theSAnodewouldremainbrieflyquiescentbecauseofoverdrivesuppression.TheintervalfromtheendoftheperiodofoverdriveuntiltheSAnoderesumesfiringiscalledthesinus node recovery time. Inpatientswithsicksinussyndrome,thesinusnoderecoverytimeisprolonged.Theconsequentperiodofasystole(absenceofaheartbeat)maycauselossofconsciousness.
The automaticity of pacemaker cells diminishes after these cells have been excited at a high frequency. This phenomenon is known as overdrive suppression. Because the intrinsic rhythmicity of the SA node is greater than that of the other latent pacemaking sites in the heart, firing of the SA node tends to suppress the automaticity in other loci.
Overdrive suppression results from the activity of membrane Na+,K+-ATPase. A certain amount of Na+ enters the cardiac cell during each depolarization. The more frequently the cell is depolarized, the more Na+ enters the cell per minute. At high excitation frequencies, the activity of Na+,K+-ATPase increases to extrude this larger amount of Na+ from the cell. The activity of Na+,K+-ATPase hyperpolarizes the cell because three Na+ ions are extruded by the pump in exchange for two K+ ions that enter the cell (see ). Therefore, slow diastolic depolarization requires more time to reach the firing threshold. In addition, when the overdrive suddenly ceases, the activity of Na+,K+-ATPase does not slow instantaneously but temporarily remains overactive. This continued extrusion of Na+ opposes the gradual depolarization of the pacemaker cell during phase 4, and it temporarily suppresses the cell’s intrinsic automaticity.
From the SA node, the cardiac impulse spreads radially throughout the right atrium (see
Fig. 16.17 ) along ordinary atrial myocardial fibers at a conduction velocity of approximately 1 m/second. A special pathway, the anterior interatrial myocardial band (or Bachmann’s bundle), conducts the SA node impulse directly to the left atrium. The wave of excitation proceeds inferiorly through the right atrium and ultimately reaches the AV node (see
Fig. 16.17 ), which is normally the sole entry route of the cardiac impulse to the ventricles.