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.