Cardiac Conduction

ANATOMIC CONSIDERATION:

• SA node:
• Located in superolateral wall of right atrium, at SVC junction with right atrium.
• Internodal atrial pathways – 
• Three strips of connective tissues:
• Anterior (Bachman).
• Middle (Wenekebech).
• Posterior (Thorel).
• Connects SA node to AV node.
• Impulses from SA node travel to AV node along these interatrial pathways.

Atrioventricular/AV node:

• Located in right posterior portion of interatrial septum.
• Is continuous with bundle of His.
• Bundle of His originates from AV node.
• Continues downward into interventricular septum.
• Divides into right & left bundle branches.
• Left bundle branch further divides into anterior & posterior fascicles.
• Bundle branches & fascicles run sub-endocardially, on either side of interventricular septum.
• Contacts Purkinje system, spreading to entire ventricular myocardium.

• Cells of conductive system possess automaticity.
• I.e., Capability of spontaneous excitation.
• Yet, varied rate at impulse discharge at different parts of conductive system.
• SA node discharges impulses at fastest rate.
• Thus, rate at which SA node fires, determines heart rate.
• Hence, SA node is “Normal pacemaker of Heart”.
• I.e., Determines pace of heart.
• AV node has next highest automaticity after SA node.
• Thus, if SA node stops discharging, 
• AV node takes over cardiac pacemaker role.

• Cardiac impulse originates in SA node.
• SA node → Internodal atrial pathways → AV node → Bundle of His →  Purkinje system →  Ventricular myocardium.
• In ventricles, endocardial surface depolarizes before epicardial surface.

ORDER OF IMPULSE SPREAD:

1. Sequence of ventricular myocardial depolarization:

Depolarization starts at left side of interventricular septum.

↓

Moves to right across mid-portion of septum.

↓

Wave then spreads down septum to heart apex.

↓

Returns along ventricular walls to AV Groove.

↓

Proceeds from endocardial to epicardial surface.

↓

Last parts to be depolarized –

• Postero-basal portion of left ventricles.
• Pulmonary conus.
• Uppermost portion of septum.

2. Sequence of ventricular repolarization:

• Not same as that of depolarization.
• Epicardial surface repolarizes first.
• I.e., Repolarization spreads from epicardium to endocardium.
• Note: Comparatively, septum & endocardial surface depolarizes first.

AV NODAL DELAY:

• Cardiac impulse originates in SA node spreading to atria reaching AV node. 
• AV conduction speed nodal is only 0.05 min/sec.
• So that impulses take 0.1- 0.13 sec to travel across AV node.
• This 0.1 – 0.13 sec delay is”AV nodal delay”.

CAUSES: 

• Small size of AV nodal fibers.
• Fewer gap junctions → Leading to impaired conduction.
• Slow-response action potential at this site → Leads to decreased conduction velocity.

FUNCTIONS:

• Ensures complete atrial contraction & emptying, well before ventricular contraction.

Factors influencing:

Increases duration of nodal delay:

• Parasympathetic (vagal) stimulation – 
• Decreasing AV node excitability

Decreased nodal delay:

• With sympathetic stimulation

IONIC BASES OF ACTION POTENTIAL:

• Action potentials have different ionic mechanisms for their generation.
• In non-automatic fibers.
• Includes, caridac muscles in atria & ventricles.
• In automatic fibers:
• Includes, SA & AV node.

1. Action potential in non-automatic fiber:

• Normal RMP in myocardial fibers is about -90mV.
• AP in myocardial fibers has 5 phases – Phases (0-4).

Phase 0 – 

• Phase of rapid depolarization.
• Due to opening of fast sodium channels.

Phase 1 – 

• Initial phase of rapid repolarization.
• Due to closure of fast Na2+ channels.

Phase 2 – 

• Plateau phase.
• Due to opening of “Voltage-gated slow Ca2+channels.
• Also referred “Calcium-Sodium Channels”:
• Causing calcium influx.

Phase 3 – 

• Phase of final repolarization.
• Due to opening of K+channels.
• Membrane potential comes back to resting membrane potential.

Phase 4 – 

• Resting phase.
• I.e., Phase of resting membrane potential.

2. Action potential in automatic fibers:

• RMP of nodal fibers about -65 mV.

Differences between AP in automatic & non-automatic fibers:

• RMP of nodal fibers (-65 mV) less comparative to non-automatic fiber (-90mV).
• During resting phase (phase 4), 
• RMP moves steadily towards depolarization, without any neural/hormonal stimulus.
• Depolarization on reaching threshold level → Fires AP.

Functional significance of unsteady RMP:

• Nodal tissues generate rhythmic impulse “spontaneously”.

Pacemaker Potential/Prepotential:

• Slow & gradual depolarization between two action potentials 
• Ie., between one AP termination & beginning of other..

Slow late rapid depolarization happens: 

• Phase 1 & 2 (rapid repolarization & plateau) are absent.

2a. AP Ionic basis in SA & AV node:

• Prepotential/pacemaker potential
• Starts due to opening of “Funny” (F) channels.
• This produces funny current.
• Referred “funny” because
• Activation by hyperpolarization causes influx of Na2+ & K+.
• Predominantly Na2+ influx.
• Later part of prepotential due to,
• Opening of ‘T’ type calcium channels.
• T – Transient with calcium influx.
• When prepotential depolarizes, 
• Produces AP spike.
• Due to,
• Opening of ‘L’ type of calcium channels opening.
• L – Long-lasting Ca2+ influx.

Repolarization – 

• Opening of K+ channels.
• Resulting in K+ efflux.
• Later, efflux declines steadily.
• This indirectly contributes to pacemaker potential.

Comparison of AP in cardiac Muscles & Nodes:

EFFECT OF AUTONOMIC NERVOUS SYSTEM ON CARDIAC CONDUCTION:

• Vagus – 
• Has both parasympathetic & sympathetic innervations.
• Parasympathetic innervation – 
• Right vagus:
• Distributed primarily to SA node.
• Left vagus:
• Mainly to AV node.
• Because of embryological difference in SA & AV node development.
• SA node develops from structures on right side of embryo.
• AV node from left-sided structures.
• Sympathetic innervation – 
• On right side primarily distributed to SA node
• On left side primarily to AV node.

ANS EFFECTS ON CVS:

1. Parasympathetic/vagal stimulation:

• Negative chronotropic effect – 
• Decreased heart rate.
• Decreased slope/flattening of prepotential (pacemaker potential).
• Hence, increasing time-taken to reach threshold level.
• Thus, decreasing heart rate.
• Negative dromotropic effect – 
• Decreased conduction.
• Increased refractory period of all cardiac cell types.

2. Sympathetic stimulation:

• Positive chronotropic effect – 
• Increased heart rate.
• Increased slope of phase 4 prepotential (pacemaker potential).
• Hence, decreasing time-taken to reach threshold.
• Thus, increasing heart rate.
• Positive inotropic effect – 
• Increased contractility.
• Positive dromotropic effect – 
• Increased conduction velocity in conductive tissue.
• Positive bathmotropic effect – 
• Increased automaticity.
• Decreased refractory period of all cardiac cell types.

CARDIAC CONDUCTION

• SA node – Located in superolateral wall of right atrium, at SVC junction with right atrium.
• Conduction system entirely made up of modified cardiac muscles.
• Fastest conduction – Purkinje system.
• Conduction velocity – 4 (Maximum).
• Slowest conduction – AV node & SA node.
• Conduction velocity in AV & SA node – 0.05 (Minimum).
• SA node discharges impulses at fastest rate.
• Thus, rate at which SA node fires, determines heart rate.
• Hence, SA node is “Normal pacemaker of Heart”.
• I.e., Determines pace of heart.
• AV node has next highest automaticity after SA node.
• Sequence of ventricular myocardial depolarization:
• In ventricles, endocardial surface depolarizes before epicardial surface.
• Depolarization starts at left side of interventricular septum.
• Proceeds from endocardial to epicardial surface.

Sequence of ventricular repolarization:

• Epicardial surface repolarizes first.
• I.e., Repolarization spreads from epicardium to endocardium.
• AV conduction speed nodal is only 0.05 min/sec so that impulses take 0.1- 0.13 sec to travel across AV node. 
• This 0.1 – 0.13 sec delay called “AV nodal delay”.
• Due to fewer gap junctions → Leading to impaired conduction.
• Action potential in non-automatic fiber (Cardiac muscles – Atria & Ventricles):
• Normal RMP in myocardial fibers is about -90mV.
• AP in myocardial fibers has 5 phases – Phases (0-4).

1. Parasympathetic (vagal) stimulation:

• Negative chronotropic effect – Decreased heart rate.
• Vagal stimulation cause decrease in slope (flattening) of prepotential (pacemaker potential).

2. Sympathetic stimulation:

• Positive chronotropic effect – Increased heart rate.
• Sympathetic stimulation increases slope of phase 4 prepotential (pacemaker potential).
• Positive inotropic effect – 
• Increased contractility.
• Positive dromotropic effect – 
• Increased conduction velocity in conductive tissue.
• Decreased in refractory period of all cardiac cell types.