12.2 Lecture - Heart's Rhythmicity and Action Potential

• The sinus node typically governs the heart's beat rate.
• The sinus node's resting membrane potential is -55 to -60 mV.
• Ventricular muscle fibers have a resting membrane potential of -85 to -90 mV.
• Leaky sodium and calcium ion channels in the S.A. node cause self-excitation and rhythmicity.
• A high extracellular sodium ion concentration and leaky sodium channels cause sodium to diffuse into the cell.
• The inward sodium diffusion gradually shifts the resting membrane potential in a positive direction.
• Calcium channels become activated, generating an action potential, once the potential reaches about -40 mV.
• After approximately 100 to 150 milliseconds open calcium channels close.
• Simultaneously, numerous potassium channels open, enabling potassium to diffuse out of the cell, repolarizing the fiber.
• Potassium channels stay open briefly, causing hyperpolarization to around -55 or -60 mV following repolarization
• Potassium channels then close, and leaky sodium channels initiate a positive drift in membrane potential.
• S.A. node fibers directly connect with surrounding atrial muscle fibers.
• When the S.A. node depolarizes, the impulse spreads through the atrial muscle to the AV node at 0.3 m/s.
• Faster conduction at about 1 m/s occurs through the anterior, middle, and posterior intermodal pathways.
• These pathways transmit impulses from the S.A. node to the A.V. node.
• There is an approximate 0.16-second delay for impulses traveling from the atria to the ventricles.
• The delay allows the atria to empty blood into the ventricles before ventricular contraction.
• The delay is primarily due to a reduced number of gap junctions between cells in the conducting pathways.
• A key feature of the AV bundle is its inability to conduct action potentials backward, except in certain abnormal conditions.

Insulation

• A continuous fibrous barrier separates atrial from ventricular muscle.
• The fibrous barrier insulates and prevents cardiac impulses from passing directly between the atria and ventricles.
• Due to insulation, atrial fibrillation can occur without affecting the ventricles.
• Purkinje fibers are large and conduct impulses at high velocity, roughly six times faster than ventricular muscle.
• This rapid conduction is attributed to a high permeability of gap junctions at the intercalated discs.
• The AV bundle descends within the interventricular septum.
• The AV bundle divides into the left and right bundle branches, which proceed toward the apex of the ventricles.
• Branches subdivide further before connecting with cardiac muscle fibers.
• Impulses spread through the entire ventricular muscle almost immediately, within approximately 0.03 seconds after entering the bundle branches.
• Rapid spread ensures coordinated ventricular muscle contraction for effective pumping.
• Once the impulse enters the ventricular muscle, its velocity slows to about one-sixth the speed of the Purkinje fibers.
• Impulses spiral and take approximately 0.03 seconds to traverse the ventricle, causing a spiral contraction.

Intrinsic Discharge Rates

• Without external stimulation, the S.A. node discharges at 60-100 beats per minute.
• Purkinje fibers discharge at a rate of 15 to 40 beats per minute.
• The S.A. node controls rhythmicity due to its faster discharge rate, a phenomenon called overdriving or over pacing.
• An ectopic pacemaker can develop elsewhere in the heart, leading to disorganized contraction.
• An AV block occurs when impulses from the S.A. node fail to transmit through the AV bundle.
• During an AV block, a new pacemaker may arise in the Purkinje system, driving the heart at 15 to 40 bpm.
• A delay occurs before the Purkinje system takes over, due to the over pacing effect of the S.A. node.

Autonomic Stimulation

• Parasympathetic stimulation releases acetylcholine at vagal nerve endings.
• Acetylcholine reduces the rate and rhythm of the S.A. node.
• Acetylcholine decreases excitability of the AV junctional fibers.
• Mild stimulation can slow the heart, while strong stimulation can halt the S.A. node or block impulse transmission for up to 20 seconds.
• Acetylcholine increases membrane permeability to potassium ions, causing rapid potassium efflux and hyperpolarization.
• Hyperpolarization reduces cell excitability.
• Sympathetic stimulation causes increased S.A. node discharge, enhancing conduction rate, excitability, and contraction force.
• Norepinephrine, released from sympathetic nerve endings, stimulates beta one adrenergic receptors.
• Beta one receptor activation increases membrane permeability to sodium and calcium ions.
• Increased sodium and calcium permeability results in a more positive resting potential, accelerating self-excitation.
• Action potentials conduct more easily through the bundles, reducing conduction time from atria to ventricles.