Cardiology: Electrical Activity of the Heart II
What are the two slowest structures responsible for electrical activation of the heart?
1. SA Node 2. AV Node
What are six mechanisms that contribute to the influence of parasympathetic activity on intrinsic heart rate?
Six mechanisms include: 1. increasing gK+ outflow. 2. decreasing the pacemaker currents (If) phase 4. 3. decreasing slow inward Ca+ currents. 4. vagal activity that also hyperpolarizes the pacemaker cell during Phase 4, which contributes to a longer time to reach threshold voltage. 5. decreasing conduction velocity at AV node as well. 6. inhibiting adenylate cyclase activity activates phosphodiesterase to oppose effects of NE on heart rate.
Dromotropy
conduction velocity
First degree heart block is common in _________.
athletes and younger individuals (not often pathological unless due to drug treatment like calcium channel blockers, cardiac glycosides, and cholinergics like cholinesterase inhbitors)
The largest decrease in impulse speed between the atria and ventricles occurs in the _____________.
atria-node region and the node region of the AV node
The parasympathetic nervous system releasing acetylcholine _________ heart rate, _____________ the pacemaker cell membrane, __________ the slope of pacemaker cells, has _________ of an effect on myocardial contractile force, and ____________ conduction speed at the AV node.
decreases; hyperpolarizes; reduces; less; decreases
Purkinje fibers are normally controlled by ______.
higher pacemakers This is because cells in the Purkinje fiber region have an intrinsic firing rate of 15 to 40 beats/minute.
Increasing Na+ and/or Ca+ permeability _________ automaticity of Purkinje fibers. Why?
increases; If Purkinje fibers are exposed to ACh, this allows K+ to flood out of the cell and lower the rate of PHase 4 for spontaneous depolarization. Similarly, sympathetic stimulation increases the rate of Phase 4 for spontaneous depolarization.
The sympathetic nervous system releasing epinephrine and norepinephrine _________ heart rate, __________ the slope of pacemaker cells, __________ myocardial contractile force, and ____________ conduction speed at the AV node.
increases; increases; increases; increases
The overall amplitude of an action potential is lower/higher in slow response cells.
lower
Defects in the HCN4 channel can provoke ________.
sick sinus syndrome
Third-degree heart blocks are associated with __________ caused by __________.
syncope (Stokes-Adams attacks); insufficient cerebral blood flow
The automaticity of Purkinje fibers differ from the SA node by _____.
the SA node being regulated by funny channel, K+ channel, and Ca+ while the Purkinje fibers being regulated by funny channels and diminishing K+ channel currents
Automaticity
the ability of the heart to initiate its own beat; "pacemaker"
The conduction of electrical impulses, especially in the cardiac conduction system, is influenced by ________.
the autonomic nervous system
Phase 3 repolarization at the AV node is mediated by _______.
the outward K+ current from voltage-gated K+ channels
Rhythmicity
the regularity of pacemaker activity of the heart
The automaticity in Purkinje fibers depends on _________.
the slow diastolic depolarization caused by funny channel and the gradually diminishing K+ channel currents
What are the three regions of the AV node?
1. Atria Node Region: contains pacemaker cells 2. Node Region: delay 3. Node-His Region: conducting nodal fibers interact with the bundle of His, which are also pacemaker cells
Three Types of AV Heart Block
1. First-Degree: partial degree 2. Second-Degree: partial degree 3. Third-Degree: complete block
Causes of AV Heart Block
1. Idiopathic Fibrosis and Sclerosis of the Conduction System (50%) 2. Ischemic Heart Disease (40%) 3. Drugs: i.e. β-blockers, calcium channel blockers, digoxin, and amiodarone 4. Increased Vagal Tone 5. Valvulopathy 6. Congenital Heart, Genetic, or Other Disorders
What are four factors that influence pacemaker cell discharge?
1. Rate of Depolarization in Phase 4 (Slope of Phase 4) 2. Threshold Potential 3. Resting Potential 4. Autonomic Effects
What is the effect of the parasympathetic nervous system on AV node conduction?
Acetylcholine released from the vagus nerve slows AV nodal conduction by binding muscarinic M2 receptors in the AV nodal membrane. Activation of these receptors increases K+ efflux through K+ channels, hyperpolarizing the cell.
Because the AV node is mostly Ca+ dependent, __________ are useful in slowing conduction through the AV node.
Ca+ channel blockers
True or False: The slow response AP cannot be produced in fast cardiac cells.
False: under some circumstances
What is the most common site of complete heart block?
His bundle electrograms reveal that the most common sites of complete block are distal to the bundle of His. Because of the slow ventricular rhythm (32 beats per minute), circulation of blood is often inadequate, especially during muscular activity. It can lead to an inability to maintain normal activity, consciousness, and normal function
What is the effect of hyperkalemia on membrane potential and heart function?
Hyperkalemia increases resting membrane potential (Vm) and converts fast response cells to slow response cells. However, these cells revert back into their normal state once extracellular K+ is reduced. In cardiomyocytes, hyperkalemia shifts the resting membrane potential to a less negative value (−90 mV to −80 mV), which in turn moves the resting membrane potential closer to the normal threshold potential of −75 mV, resulting in increased myocyte excitability. The SA node is much less permeable to K+ (than muscle cells) so action potential is less affected by changes in [K+]. Still, hyperkalemia can induces bradycardia or can even stop SA nodal firing. Hyperkalemia causes membrane depolarization, which diminishes the degree of hyperpolarization that occurs at the end of phase 3.
What is the effect of hypokalemia on resting membrane potential and associated maximal diastolic pressure, funny channel current, and repolarization?
Hypokalemia (serum K+ < 4 mmol/L) decreases resting membrane potential. As a result, hypokalemia increases the maximal diastolic potential, increases the funny channel current, driving up the rate of phase 4 depolarization and leading to tachycardia in Purkinje fibers (not so much in SA node), and enhances phase 3 repolarization.
The bundle branches eventually divide into a complex network of conductive fibers called ______.
Purkinje fibers
How do Purkinje fibers differ from other pacemaker cells?
Purkinje fibers also have innate pacemaker tissues, but do not use calcium currents in their spontaneous depolarization, only funny and K+ channels.
What are the widest cells of the heart?
Purkinje fibers are the widest cells in the heart at about 70-80 um in diameter, giving them a very high conduction velocity of 1 to 4 m/sec.
What is the major function of Purkinje fibers?
Purkinje fibers conduct the cardiac impulse to the ventricular endocardium. They are large fibers, so they have a very rapid conduction velocity.
How does second-degree heart block present?
Second-degree AV block presents with some normal P waves that are followed by QRS complexes, but some are not.
Since Phase 0 and Phase 4 of a pacemaker potential is determined by Ca+, what happens if extracellular Ca+ is reduced?
Since Phase 0 and Phase 4 of a pacemaker potential is determined by Ca+, if extracellular Ca+ is reduced, then the rate, amplitude, and grade is reduced. Calcium channel blockers achieve this effect.
Slow Response Cells Resting Membrane Potential: Amplitude: Overshoot: Rate of Change: Velocity:
Slow Response Cells Resting Membrane Potential: + Amplitude: short Overshoot: low Rate of Change: small Velocity: slow
What is the importance of the AV node?
The AV node connects the atrial and ventricular conduction system.
What is the effect of the sympathetic nervous system on maximum diastolic potential?
The effect of the sympathetic nervous system on maximum diastolic potential is a decreased MDP.
What is the function of the delay of the cardiac impulse at the AV node?
The function of the delay at the AV node is to allow ventricular filling, triggering a slow response.
What is the function of the septum?
The septum blocks all electrical signals except those communicated by the ventricular conduction system.
True or False: Phase 0 of action potentials at the AV node is not dependent on fast Na+ channels as in non-nodal tissue, but instead is generated by the entry of Ca+ into the cell through slow-inward, L-type calcium channels.
True
Left Bundle Branch
a bundle branch wider than the right branch that arises almost perpendicularly from the bundle of His and punctures the interventicular septum
Sympathetics __________ automaticity, thereby _________ heart rate.
enhance; increase
Parasympathetics __________ automaticity, thereby _________ heart rate.
inhibit; reduce
At rest, the ____________ nervous system tone predominates.
parasympathetic
The epicardial muscle action potential is ________ and begins in the _______.
shorter; epicardium
Purkinje Fibers
ventricular fibers that spread over the subendocardial surfaces of both ventricles
What are the two most common causes of AV heart block?
1. Idiopathic Fibrosis and Sclerosis of the Conduction System (50%) 2. Ischemic Heart Disease (40%)
What are the two types of second-degree AV heart block?
1. In Mobitz type I second-degree AV block, the PR interval progressively lengthens with each beat until the atrial impulse is not conducted, and the QRS complex is dropped. This is known as Wenckebach phenomenon. AV nodal conduction resumes with the next beat, and the sequence is repeated. 2. In Mobitz type II second-degree AV block, the PR interval remains constant. Beats are intermittently non-conducted, and QRS complexes dropped, usually in a repeating cycle of every 3rd P wave (3:1 block) or 4th (4:1 block) P wave.
What are five major differences between the "fast response" action potential and the slow response action potential?
1. The upstroke slope (Phase 0) is less steep than the fast response action potential. 2. The early repolarization (Phase 1) of the fast response AP is absent. 3. There is not a conventional "plateau" in the slow response AP. This "plateau" is much shorter and is not "flat" as in fast response. 4. The transition from the plateau to the repolarization (phase 3) is continuous. 5. Phase 4 is not a resting phase in SA node in the slow response AP.
What are the five events of the "fast response" action potential?
1. Upstroke (Phase 0) 2. Early Partial Repolarization (Phase 1) 3. Plateau (Phase 2) 4. Repolarization (Phase 3) 5. Phase 4 is the resting membrane potential after the AP.
What is the effect of adenosine and AV node depolarization?
Adenosine is a nucleoside used to acutely treat certain forms of supraventricular tachycardia. Adenosine activates purinergic receptors on the AV nodal cell membrane, which activate ACh-sensitive K+ channels. This hyperpolarizes the cell membrane and inhibits depolarization. This slows (even blocking) conduction through the AV node, leading to negative dromotropy.
???
After administering a cardio-active drug, the following response was seen in pacemaker cells. The most likely test substance : A. Increased the maximum diastolic potential B. Increased the slope of phase 4 C. Allowed K+ to leave the cell D. a and d E. Increased the force of contraction
What is the effect of cellular hypoxia on heart rate? How?
Cellular hypoxia (i.e. ischemia) depolarizes the membrane potential, causing bradycardia. Without adequate O2, ATP-dependent ion pumps in the cell membrane cannot operate, and this can partially depolarize the cells. Because a hyperpolarized state at the end of Phase 3 is necessary for pacemaker channels to become reactivated, some pacemaker channels can remain inactive in depolarized cells. This relative depolarization can decrease pacemaker current and decreases slope of Phase 4, thereby decreasing heart rate. This is one basis for cellular hypoxia, leading to a reduction in pacemaker rate (bradycardia). Severe hypoxia can completely stop pacemaker activity.
Where does the cardiac impulse from the SA node go?
From the SA node, the cardiac impulse is carried radially outward through the right atrium along typical myocardial fibers which communicate via gap junctions, in the atria this occurs at a velocity of 1 m/sec. There is a specialized pathway, the anterior interatrial myocardial band called the Bachmann's bundle, which carries the impulse from the SA node to the left atrium.
How does first-degree heart block present?
In first-degree AV block, there are all normal P waves followed by QRS complexes, but the PR interval is longer than normal (> 0.20 second).
What is the relationship between K-ATP channels, hypoxia, and the SA node?
K-ATP channels are a very abundant K+ channel in heart tissue that are sensitive to intracellular nucleotides. K-ATP channels, normally inactive with high levels of ATP, are activated by declining ATP levels and/or increasing ADP levels. Decreased ATP allows K+ efflux out of the cell via the K-ATP channels and hyperpolarizes the cell. During repolarization, there is a greater K+ current, leading to a shorter AP. This moves the SA node away from threshold, increases maximum diastolic potential, lowers heart rate, and reduces energy needs. This is a mechanism by which the heart protects itself from conditions of diminished availability of nutrition.
How are non-pacemaker cells transformed into pacemaker cells?
Non-pacemaker cells can be transformed into pacemaker cells by stressing the cells. If cells becomes hypoxic, the membrane can become partly depolarized, which closes fast Na+ channels. At a membrane potential of about -50 mV, all the fast Na+ channels are inactivated in all fast response cells. When this occurs, action potentials can still be elicited; however, the inward current are carried by slow inward Ca+ channels exclusively. These action potentials resemble those found in pacemaker cells located in the SA node and can sometimes display spontaneous depolarization and automaticity. This mechanism may serve as the electrophysiological mechanism behind some types of ectopic beats and arrhythmias, particularly in ischemic heart disease and following myocardial infarction.
What is the effect of adrenergics on AV node conduction?
NorEpi and Epi increase AV node conduction via β-adrenergic receptors, which activate adenylate cyclase and increase cAMP production. cAMP activates protein kinase A (PKA), which phosphorylates L-type calcium channels, ryanodine receptors (RyR), and phospholamban (PL). The result is more calcium entering cells via L-type Ca+ channels, more Ca+ being pumped into the SR by SERCA, and more Ca+ being released from the SR by ryanodine receptor. These changes in Ca+ handling increase AV nodal conduction speed and increase in the rate of AV nodal cell resetting following depolarization.
What is the effect of the sympathetic nervous system at the SA node?
Norepinephrine (NorEpi) released by the sympathetic nervous system binds to β1 adrenergic receptors, which are coupled to adenylate cyclase by the G-protein, Gs. The activation of adenylate cyclase by Gs increases the synthesis of cAMP, which activates protein kinase A (PKA). cAMP binds directly to HCN4 channels and increases the rate of Na+ influx through those channels. PKA also phosphorylates L-type Ca+ channels, which increases Ca+ influx to increase in both heart rate. These two action increases conduction speed at AV node.
What is the effect of sympathetic activation on the pacemaker?
Norepinephrine (or epinephrine, sympathomimetics, or catecholamines) released at SA node bind to β1 adrenergic receptors. This increases the rate of pacemaker firing primarily by increasing slope of phase 4, which decreases the time to reach threshold.
Where are pacemaker cells found?
Pacemaker cells are present in the SA node, AV node, and the His-Purkinje system. However, the AV node and Purkinje fibers are said to be "latent pacemakers, as they exhibit a natural self-excitatory discharge rate. However, since the discharge rate of the SA node is greater than the AV node and the Purkinje-His system, the impulses of the SA node discharge the AV node and Purkinje fibers before self-excitation occurs.
What is the effect of the parasympathetic nervous system on the control of conduction velocity by the AV node?
Parasympathetic (vagal) activation decreases conduction velocity, resulting in a negative dromotropy) at the AV node by decreasing the slope of phase 0 of the nodal action potentials. This leads to slower depolarization of adjacent cells, and reduced velocity of conduction. As a result, this matches the influence of the SA node and the AV node with ventricular function as well.
What is the effect of the autonomic nervous system on Phase 4 slope of the pacemaker potential?
Parasympathetic (vagal) activation releases acetylcholine onto the SA node that binds to M2 muscarinic receptors, thereby decreasing pacemaker rate (phase 4 slope) by increasing gK+ and decreasing the pacemaker currents (If) and slow inward Ca++ currents.
What is unique about the Purkinje fiber action potential compared to ventricular myocytes?
Purkinje fiber action potentials have a long plateau phase compared to ventricular myocytes. This prevents the heart from depolarizing too soon following depolarization or merged depolarizations, preventing tetany in the heart.
What is the effect of the sympathetic nervous system on the control of conduction velocity by the AV node?
Sympathetic activation of the AV node increases conduction velocity in the AV node by increasing the rate of depolarization via increasing the slope of phase 0. This allows for a more rapid depolarization of adjacent cells and more rapid conduction of action potentials. This conduction is termed dromotropy. As a result, sympathetics increase dromotropy.
What is the beginning of the specialized conduction system for the ventricles?
The Bundle of His is the beginning of the specialized conduction system for the ventricles.
What channel is responsible for the pacemaker potential? How?
The HCN4 (hyperpolarization-activated cyclic nucleotide gated ion channels) or If (funny) channels are responsible for the pacemaker potential. HCN4 is abundant in pacemaker cells of mammalian heart tissue and is also found in AV node and Purkinje fibers. HCN4 increases slow Na+ current inflow via direct binding to cAMP to the channel, demonstrating slow kinetics for the movement of ions. The current is activated in this channel most when the resting membrane potential is more negative (from −70 mV to −40 mV) (i.e. below -40 mV current flows in).
What is the effect of the extracellular K+ concentration on resting membrane potential?
The Nernst equilibrium of K+ is very similar to that of the resting membrane potential. As the extracellular concentration of K+ decreases, the membrane potential decreases and hyperpolarizes. However, it is more common to have an increase in extracellular K+ concentration. When extracellular K+ is increased, the resting membrane potential increases and depolarizes.
What is the only portion of the ventricle innervated by parasympathetics?
The Purkinje fibers are the only portion of the ventricle innervated by parasympathetics.
What is the blood supply of the SA node? What is the significance of this blood supply?
The SA node artery, a branch of the right coronary artery or circumflex artery, is the blood supply of the SA node. It can be damaged during cardiovascular procedures, having undesirable effects on the heart rate.
How do pacemaker cells control heart rate?
The SA node is the normal pacemaker of the heart. The pacemaker cells of the SA node exhibit progressive depolarization during phase 4 of the action potential, generating the "pacemaker potential." Cells in SA node are intrinsically leaky to Na+, generating the normal cardiac rhythm of 60-100 beats per minute.
Why is the SA node the primary pacemaker of the heart?
The SA node is the primary pacemaker of the heart because it has the highest rate of depolarization, with an intrinsic rate of 100 to 120.
What is overdrive suppression? What can it lead to?
The SA node is the primary pacemaker of the heart because it has the highest rate of depolarization, with an intrinsic rate of 100 to 120. The AV depolarization rate is 40 to 60 while the Purkinje fiber depolarization rate is 15-40. The latent pacemakers of the AV node, His bundle, and Purkinje fibers can become pacemakers when the SA node is depressed. By driving latent pacemakers to depolarize faster than their spontaneous rate, the SA node suppresses other pacemakers and lowers the maximum diastolic potential. Na+ influx from "rapid"/driven depolarization elevates Na+ in the cell and activates Na+/K+ ATPase. This hyperpolarizes cells away from their threshold, preventing their If channels from being able to reach threshold spontaneous depolarization. When the SA node pacemaker is depressed, the hyperpolarizing drive of the Na+/K+ pump decreases and lets "latent" pacemakers become active, as seen in sick sinus syndrome. However, there is usually a lag-phase until that happens.
What is the ionic basis of automaticity in pacemaker cells?
The atrial and ventricular cardiomyocytes require a stimulus to reach threshold. By comparison, the pacemaker cells of the SA and AV nodes reach threshold spontaneously. The current of Na+ influx through the HCN4 channel can determine the slope of phase 4. Following the establishment of a current through HCN4 channels, the rest of Phase 4 is determined by influx of Ca+ through T-type Ca+ channels, and Phase 0 is determined by Ca+ influx through L-type Ca+ channels. In Phase 3, K+ channels open, allowing K+ efflux and repolarization.
What is the fastest structure responsible for electrical activation of the heart?
The bundle branches and the Purkinje network are the fastest structures responsible for electrical activation of the heart.
What is the major difference between cardiac pacemaker cells and cardiomyocytes at the resting membrane potential?
The cardiomyocyte resting membrane potential is maintained by IK1 inward rectifying K+ channels while the cardiac pacemaker cell resting membrane potential is not maintained by this current.
What is the clinical significance of the AV node conduction delay?
The conduction times through the atria-node and node regions of the AV node account for the delay between the P-wave (the electrical spread of atrial excitation) and the QRS complex (the electrical ventricular excitation) in a electrocardiogram. This delay between atrial and ventricular excitation optimizes ventricular filling during atrial contraction. Without this delay, there would not be sufficient time for the ventricle to be filled. The delay also produces a unidirectional flow of depolarization.
What causes the delay in the AV node?
The delay in the AV node is caused by fewer gap junctions in the atria-node region and the node region of the AV node. It is also a small diameter conduit. The conduction velocity in the N-region (0.05 m/sec) is slower than in the atria-node region, but the path length in the atria-node region is longer.
What is the drug target of ivabradine?
The drug target of ivabradine is the HCN4 channel. Ivabradine is a HCN4 channel blocker, resulting in a reduced heart rate. As a result, ivabradine is used to treat chronic stable angina in patients intolerant of beta blockers.
What is the effect of the parasympathetic nervous system on maximum diastolic potential?
The effect of the parasympathetic nervous system on maximum diastolic potential is that K+ ACh channels that are present on the SA and AV nodes can cause membrane hyperpolarization in response to vagal stimulation, leading to an increase in MDP.
When does the funny current of the AV node activate?
The funny current of the AV node only activates when the SA node activity is depressed and does so at a slower rate of depolarization. Normally, the AV node funny current is suppressed by the upstream dominance of the SA node due to overdrive suppression.
What is the role of the parasympathetic nervous system on intrinsic heart rate?
The intrinsic heart rate is 100-120 bpm; however, a normal heart rate is around 72 bpm on average. This shows that the parasympathetic nervous system tonically slows the heart to 72 bpm, revealing that parasympathetic or tonic activation releases acetylcholine onto the SA node to slow the heart rate. WHen ACh binds to M2 receptors in the SA node, it decreases pacemaker rate (phase 4 slope), increasing the time required to reach threshold.
What are the latent pacemakers? When can these pacemakers become the primary pacemaker?
The latent pacemakers of the AV node, His bundle, and Purkinje fibers can become pacemakers when the SA node is depressed.
Maximum Diastolic Potential
The maximum diastolic potential is the most negative voltage (usually -50 to -60 mV) reached by the cell membrane during the cardiac cycle in cells that do not have a constant resting potential. It is often reached at the end of phase 3 of the action potential. In pacemaker cells, this is a point of hyperpolarization. Depending how low this value is, pacemaker cells have to return from this point to reach threshold.
How does slow current Ca+ influx that determines conduction of the slow response?
The threshold potential of the slow response cells is -40 mV. Phase 0 is mediated by Ca+ influx, which is slow. This produces a slow conduction velocity in the SA and AV nodes (about 002 to 0.1 m/sec). By comparison, the conduction velocities for the fast cardiomyocytes are 0.3 to 1 m/sec and 1 to 4 m/sec in the Purkinje fibers.
What is the pacemaker threshold?
The pacemaker threshold is the membrane potential at which the cell will depolarize. A positive shift in threshold increases the time it takes for a cell to initiate an AP. A negative shift in threshold decreases the time it takes for a cell to initiate an AP.
What is the effect of the parasympathetic nervous system on the pacemaker threshold?
The parasympathetic nervous system inhibits cAMP formation, which decreases L-type Ca+ channel activity and raises threshold potential. As a result, it takes longer to reach threshold.
What are two effects of the parasympathetic nervous system on the SA node that oppose pacemaker automaticity and antagonize the effects of norepinephrine that are mediated by the production of cAMP?
The parasympathetic nervous system: 1. releases ACh that binds to M2 muscarinic receptors, stimulating the "inhibitory" G-protein, Gi 2. through the activation of Gi, inhibits adenylate cyclase by decreasing cAMP and activates K+ channels. This results in K+ efflux that hyperpolarizes cell. These two actions oppose pacemaker automaticity and antagonize the effects of norepinephrine that are mediated by the production of cAMP.
What are four mechanisms that contribute to the influence of sympathetic activity on intrinsic heart rate?
The sympathetic nervous system affects intrinsic heart rate by: 1. increasing "funny" pacemaker currents) via HCN4. 2. increasing slow inward Ca+ currents during the early phase and depolarization. 3. lowering the threshold for initiating phase 0 of the action potential. 4. enhancing conduction at AV node.
What is the effect of the sympathetic nervous system on the pacemaker threshold?
The sympathetic nervous system leads to the activation of PKA, which phosphorylates L-type Ca+ channels and lowers threshold. As a result, it takes a shorter amount of time to reach threshold.
Why is third degree heart block often referred to as complete heart block?
Third-degree AV block is often referred to as complete heart block because the impulse is unable to traverse the AV conduction pathway from atria to ventricles.
What is the one of the most common conditions requiring treatment by artificial pacemakers?
Third-degree heart block is one of the most common conditions requiring treatment by artificial pacemakers.
True or False: SA node depolarization is under the tonic influence of the autonomic nervous system.
True
What makes ventricular myocytes unique?
Unlike ventricular myocytes, several types of cells in the heart lack a true resting potential, allowing them to spontaneously depolarize and generate an AP through the heart. This conduction system is coordinated with pacemaker function and coordinates filling (diastolic) and contraction (systolic) functions.
Sinoatrial (SA) Node
a 2 mm deep and 5-8 mm thick structure located posteriorly within the epicardial groove of the sulcus terminalis at the junction of the superior vena cava and the right atrium that is composed of "pacemaker cells"
Right Bundle Branch
a direct continuation of the bundle of His which continues down the right side of the interventricular septum
Action potentials in the atrioventricular (AV) node are similar to those found in SA nodal cells. Therefore, APs in the AV node, like the SA node, are determined primarily by ________.
changes in slow inward Ca+ currents not fast Na+ currents
The ventricular action potential is a _______ action potential.
fast
The His/Purkinje network initiates a ___________ action potential.
fast response
The electrical events within the SA node pacemaker are the example of the __________ action potential.
slow response
The cardiac impulse triggered by the SA node is a __________ action potential that slows/hastens at the AV node.
slow response; slows
Pacemaker Cells
small, round cardiomyocytes of the SA node that induce signals to elongated cells that carry impulses to other regions of the node
