Why does the sinus node normally control the heart's rhythmicity over the A-V node or Purkinje fibers?
Explanation
This question explores the fundamental principle of 'overdrive suppression,' which explains why the fastest pacemaker in the heart (the S-A node) sets the overall heart rate.
Other questions
What is the approximate resting membrane potential of a sinus nodal fiber between discharges?
What is the primary cause of the less negative resting membrane potential in sinus nodal fibers compared to ventricular muscle fibers?
At approximately what threshold voltage do the L-type calcium channels in sinus nodal fibers become activated to cause an action potential?
Which ion channels are primarily responsible for the action potential upstroke observed in the sinus node?
What is the primary reason fast sodium channels do not significantly contribute to the sinus nodal action potential?
The temporary state of hyperpolarization in a sinus nodal fiber, which follows an action potential, is primarily caused by which ionic event?
What is the approximate conduction velocity of the cardiac impulse in the specialized internodal pathways of the atria?
What is the primary function of the atrioventricular (A-V) node in the heart's conduction system?
What is the approximate total time delay for the cardiac impulse to travel from the sinus node, through the A-V nodal system, to finally reach the contracting muscle of the ventricles?
What is the primary anatomical reason for the slow conduction of the cardiac impulse within the A-V node?
What is the typical transmission velocity of action potentials within the ventricular Purkinje fibers?
What structural feature of Purkinje fibers is believed to be the cause of their rapid transmission of action potentials?
What is the term for a pacemaker of the heart that is located somewhere other than the sinus node?
What is the intrinsic rhythmical discharge rate of the atrioventricular (A-V) nodal fibers when not stimulated from an outside source?
What is the intrinsic rhythmical discharge rate of the Purkinje fibers?
What is the name of the syndrome characterized by a delayed pickup of the heartbeat by the Purkinje system after a sudden A-V bundle block, leading to fainting?
What are the two major effects of parasympathetic (vagal) stimulation on the heart?
What neurotransmitter is released at the vagal nerve endings to produce parasympathetic effects on the heart?
What is the ionic mechanism by which acetylcholine, released from vagal nerves, exerts its effect on the heart's conductive fibers?
Which of the following is a primary effect of sympathetic stimulation on the heart?
Norepinephrine released by sympathetic nerves mediates its effects on heart rate by stimulating which type of receptors?
Sympathetic stimulation is thought to increase the rate of self-excitation in the sinus node by increasing the fiber membrane permeability to which ions?
What is the typical diameter of the specialized cardiac muscle fibers found in the sinus node?
After originating in the sinus node and traveling through the internodal pathways, how long does it take for the cardiac impulse to reach the A-V node?
What is the duration of the delay that the cardiac impulse experiences within the atrioventricular (A-V) node itself before it enters the penetrating portion of the A-V bundle?
A special characteristic of the A-V bundle, which prevents re-entry of cardiac impulses, is its inability in normal states to do what?
What is the approximate velocity of cardiac impulse transmission through the ventricular muscle mass itself, after it leaves the Purkinje fibers?
In a normal heart, what is the approximate total time required for the cardiac impulse to be transmitted from the initial bundle branches to the last of the ventricular muscle fibers?
What is the term for the phenomenon where, following a complete block by strong vagal stimulation, the ventricles begin to beat at their own intrinsic rhythm after a 5 to 20 second pause?
During the phenomenon of ventricular escape, what is the typical contraction rate of the ventricles?
Why is the action potential in the atrial node slower to develop compared to the action potential of the ventricular muscle?
What is the name of the specialized atrial band that passes through the anterior walls of the atria to the left atrium?
What is the normal intrinsic rhythmical discharge rate of the sinus (S-A) node?
In which region of the heart's conduction system is the cardiac impulse delayed for more than 0.1 second before appearing in the ventricular septal A-V bundle?
Where is the atrioventricular (A-V) node located within the heart?
What is the primary importance of the 'one-way conduction' property of the A-V bundle?
The velocity of impulse conduction in the Purkinje fibers is approximately how many times greater than the velocity in the usual ventricular muscle?
The velocity of impulse conduction in the Purkinje fibers is approximately how many times greater than the velocity in some of the slower A-V nodal fibers?
In addition to slowing the rate of the sinus node, parasympathetic (vagal) stimulation also decreases the excitability of which other specific part of the conduction system?
What is the approximate resting membrane potential of sinus nodal fibers during the state of hyperpolarization caused by strong vagal stimulation?
Sympathetic stimulation, by increasing permeability to sodium and calcium, causes what change to the resting potential in the sinus node?
In a sinus nodal fiber, approximately how long after opening do the L-type calcium channels become inactivated (close)?
The specialized excitatory and conductive system of the heart normally ensures that the atria contract approximately how long before the ventricles?
Based on the timings provided for impulse spread, what is the approximate total time from the initial impulse at the sinoatrial node to the excitation of the last ventricular muscle fibers?
What is the primary role of the continuous fibrous barrier that separates the atrial muscle from the ventricular muscle?
By how much can maximal sympathetic stimulation increase the strength of heart contraction?
Under normal conditions, the continuous slow discharge of sympathetic nerve fibers maintains cardiac pumping at what level above that with no sympathetic stimulation?
The effect of vagal stimulation is mainly to decrease heart rate rather than the strength of contraction. This is explained by the distribution of vagal fibers primarily to which areas?
What is the name given to the inward-leaking currents of sodium that cause the slow rise in the resting membrane potential of sinus nodal fibers between heartbeats?