conduction vel. varies directly with the amp. of the A/P and the rate of change of potential during phase 0
the greater the amplitude of the A/P, the more effective are the local stimuli in depolarizing adjacent parts of the memb and the more rapidly is conduction velocity
slow rate of change of potential during phase 0 causes slowed conduction velocity
the less neg the memb potential, the less is the conduction velocity due to the inactivation (h) gates of Na+ channels
conduction in slow response
local circuits are also responsible for propagation of slow response
conduction is much slower than for fast responses
more likely to be blocked than are fast responses
Cardiac Excitability
fast response
effective refractory period: the interval from the beginning of the A/P until the fiber is able to conduct another A/P
cardiac fiber is not fully excitable until it has been completely repolarized
relative refractory period: before complete repolarization, an A/P may be evoked only when the stimulus is stronger than a stimulus that could elicit a response during phase 4
the later in the relative refractory period the fiber is stimulated, the greater is the increase in the amp. of the response and in the slope of the upstroke (due to decreased # of Na+ channels inactivated)
slow response
post-repolarization refractoriness: the relative refractory period extends well beyond phase 3, even after complete repolarization
Þ Ca+ channel repolarize slowly
recovery of full excitability is much slower than in fast response
these length refractory periods may also lead to conduction block
Effects of Cycle Length
changes in cycle length alter the duration of an A/P in cardiac cells and thus change their refractory periods
as cycle length diminishes, the A/P duration decreases due to changes in IK and Ito
the shorter the basic cycle length, the greater is the outward K+ current during phase 2, hence the shorter duration of the action potential
as cycle length decreases, the resultant increase in the outward K+ current shortens the plateau
Natural Excitation of the Heart
Introduction
the properties of automaticity (ability to initiate its own beat) and rhythmicity (regularity of such pacemaking activity) allow the heart to beat even when it is completely removed from the body
SA node generates impulses at greatest frequency; it’s the main pacemaker of the heart
2 or 3 sites located 1 or 2 cm from the SA node, serve along with the SA node as an atrial pacemaker complex
if the SA node is destroyed, the cells in the AV junction take over the pacemaker function
if the AV junction cannot conduct impulses, idioventricular pacemakers in the Purkinje fiber network initiate the ventricular contractions, but at a very slow frequency
Sinoatrial Node
Slow response: resting potent is less neg than a myocardial cell, the upstroke of the A/P (phase 0) is less steep, a plateau is not sustained, and repolarization (phase 3) is more gradual
This pacemaker fiber is characterized by a slow diastolic depolariz. throughout phase 4
Depolarization proceeds at a steady rate until a threshold is attained, triggering an A/P
3 ionic currents mediate the slow diastolic depolarization:
inward current, If
inward Ca current, ICa
outward K current, IK
overdrive suppression: the automaticity of pacemaker cells diminishes after a period of excitation at a high frequency
because the intrinsic rhythmicity of the SA node is greater than that of the other latent pacemaking sites in the heart, the firing of the SA node tends to suppress the automaticity in the other loci
excessive extrusion of Na opposes the gradual depolarization of the pacemaker cell during phase 4, and thereby suppresses the cell’s intrinsic automaticity transiently
Atrial Conduction
SA node Þ radially throughout right atrium Þ to left atrium via the anterior interatrial myocardial band (Bachmann’s bundle)
Reaches AV node
Compared to SA node, AV node has a briefer and less developed atrial plateau (phase 2), slower repolarization (phase 3)
Atrioventricular Conduction
The delay between atrial and ventricular excitation permits optimal ventricular filling during atrial contraction
The cells display postrepolarization refractoriness
As the time between successive atrial depolarizations is decreased, conduction thru the AV junction slows
1st degree AV block: an abnormal prolongation of the AV conduction time
2nd degree AV block: the conduction pattern in which only a fraction of the atrial impulses are conducted to the ventricles
may protect the ventricles from excessive contraction frequencies, wherein the filling time between contractions might be inadequate
3rd degree or complete AV block: the conduction pattern in which none of the atrial impulses reach the ventricles
Ventricular Conduction
Bundle of His divides into the right and left bundle branches
Right branch: direct cont. of the bundle of his
Left branch: thicker, arises almost perpendicularly from the bundle of his
Splits into a thin anterior division and a thick posterior division
right and left branches subdivide into Purkinje fibers
Because of the long refractory period of Purkinje fiber action potentials, many premature excitations of the atria are conducted thru the AV junction but are blocked by the Purkinje fibers
prevents premature contraction of the ventricles
when the atrium is excited at high repetition rates, it is the AV node that protects the ventricles from these excessively high frequencies
Electrocardiography
P wave = atrial depolarization
QRS complex = ventricle depolarization
T wave = ventricle repolarization
P-R interval = measure of time from the onset of atrial activation to the onset of ventricular activation
Pathological prolongations of the PR interval are associated with disturbances of AV conduction, which may be produced by inflammatory, circulatory, pharmacologic, or nervous mechanisms
Q-T interval = period of "electrical systole" of the ventricles; the QT interval is closely correlated with the mean A/P duration of the ventricular myocytes