CVPR 03-25-14 09-10am Cardiac Conduction System - Horwitz Flashcards
Spontaneous depolarization in SA and AV nodes
Phase 4 (repolarization) is not as static as in contracile myocytes; there is a slow depolarizing due to the “funny current” or “pacemaker current” until a critical voltage is reached where a more rapid Phase 0 occurs entirely due to Ca2+ current (there is no fast Na+ current).
SA vs AV nodes in pacemaking
The SA node is the usual cardiac pacemaker b/c it has the fastest spontaneous rate…….the AV node has a slower spontaneous rate but it delays conduction at the junction between the atria & ventricles.
Phases 4 & 0 in Contractile Myocytes
Contractile myocytes have a stable baseline during repolarization in stage 4, but exhibit rapid robust increase during phase 0 due to the fast Na+ current; they are fairly good at conducting from cell to cell, enabling fairly rapid electrical excitation of the atria & ventricles
Purkinje cell action potentials
Have similar shape to contractiel myocytes w/ a slightly higher voltage during phase 0 and a longer total duration; Conduct faster than contractile myocytes (probably due to more fast Na+ channels); Allow extremely fast conduction from AV node to the ventricles through the left and right bundle & their extension into the myocardium.
Spread of electrical impulse, after initiation by pacemaker
Spreads rapidly through gap junctions
Gap junctions
Cylindrical structures formed by connexins that allow ions to pass from cell to cell
SA node - path of AP
SA located high in right atrium –> depolarization wave goes through rt then lt atrium, generating the P wave –> arrives at AV node btwn tricuspid & mitral valves separating atriua & ventricles (“junction”) –> Delay (allowing contraction of atria to end before ventricular contraction starts) –> enters ventricles –> throug bundle of His into Lt & Rt Bundle branches –> Purkinje cell fibers –> through contractile cardiac myocytes
Purkinje fibers
radiate toward contractile cardiac myocytes that induce contraction
Right bundle branch
A single entity primarily supplying the right ventricle
Left bundle branch
Divides into anterior & posterior branches (or fascicles) that supply corresponding regions of the left ventricle.
Bundle of His, Lt & Rt Bundle branches, & Purkinje fibers all contain cells that…
conduct depolarization very rapidly
Contractile myocytes
The majority of ventricular cardiac myocytes are primarily specialized to contract and conduct depolarization waves much more slowly than the specialized cells in the bundle of His, bundle branches & Purkinje fibers
Electrocardiogram (ECG)
Invented by Einthoven ~100 years about; Electrical signals of the heart can be recorded onthe skin surface, using electrodes
P wave of ECG
1st hump, due to depolarization of the atria
QRS on ECG
after P wave and before T wave; due to depolarization in the ventricles; The Q is an initial downward deflection, the R is the upward deflction, and the S is a terminal negative deflection.
T wave of ECG
last hump; due to repolarization of the ventricles
Repolarization of the atria on the ECG
Not seen, b/c it normally occurs at then same time as ventricular depolarization, and is buried in the much larger signal from the ventricles
Direction of repolarization/depolarization on ECG
On ECG, the T wave of ventricular repolarization is in the same direction as the QRS depolarization signal, whereas in individual myocytes, depolarization & repolarization are in opposite directions
Discordance
In each cardiac myocytes, repolarization is in the same direction as depolarization but b/c of different polarity, the two waves are in opposite directions.
Concordance
The QRS of depolarization and the T wave of repolarization are in the same direction on ECG. The endocardium depolarizes earlier than the epicardium; however, there is a transmural repolarization gradient and epicardial cells repolarize earlier than endocardial cells b/c they have shorter action potential duration….i.e., endocardial cells have a longer AP than epicardial cells
If QRS is positive, T wave should be…? If QRS is negative, T wave should be…?
If QRS +, T+. If QRS -, T -.
Discordance between QRS & T waves
In any lead, this is pathological, reflecting abnormalities such as ischemia or ventricular hypertrophy.
PR interval on ECG
index of conduction time across the AV node
QT interval on ECG
total duration of depolarization & repolarization
Sinus node depolarization on ECG
This initiates the beat but is too small to see on ECG…so, the first signal is the P wave generated when the atria depolarize
ECG leads & shape of QRS
There are 12 different leads in the ECG and the shape of QRS depends on where the positive electrode is placed.
Why QRS voltage is much greater P voltage
b/c ventricular mass exceeds atrial mass
Why T wave is wider than QRS
b/c ventricular repolarization take considerable longer than depolarization
Direction of Activation wave relative to sensing electrode - effect on deflection direction recorded
If activation wave is toward a sensing electrode, a positive (upward) direction will be recorded
Muscle mass & voltage
The greater the muscle mass, the greater the voltage recorded
Direction of depolarization wave and placement of electrodes
SA node is high in right atrium, and depolarization wave sweeps downward & leftward. Thus, a lead with a positive electrode near the right arm normally has a predominantly negative QRS (i.e., a “QS” wave…not much of the R), while a lead w/positive electrode near the left leg has a positive QRS (pretty much just an R wave)
Movement of depolarization through ventricle
Upper portion of septum is depolarizated from Lt to Rt. Then, there is depolarization downward in septum to the apex. From the apex, depolarization moves upward in the free walls of both ventricles and finally into the base of the ventricles.
Direction of depolarization in layers of the cardiac wall
Depolarization goes from endocardium to epicardium
Sites at which Conduction can be Delayed/Blocked w/Clinical Consequences
SA node, AV block, Bundle branch blocks
SA node abnormalities
Commonly cause “sick sinus syndrome” resulting in slow sinus rates or takeover by other pacemakers which may be either too fast or too slow….Common in elderly & common reason to put in a pacemaker
AV block - 3 types
1st degree,
2nd degree,
3rd degree
1st degree AV block
Conduction delayed but all P waves conduct to ventricles…Fairly harmless…Often from drugs (beta or Ca2+ channel blockers)
2nd degree AV block
some P waves conduct but others do not…Can be problematic; typically slows HR significantly, associated w/MIs,etc; Sometimes requires pacemaker
3rd degree AV block
none of the P waves conduct & a ventricular pacemaker (purkinje cells, contractile myocytes) takes over…. very dire situation; Ectopic pacemakers = generally very & discharge the ventricles completely independently from SA/AV nodes; Usually requires pacemaker
Right bundle branch blocks
–> QRS widening w/delayed conduction to the right ventricle
Left bundle branch blocks
–> QRS widening w/delayed conduction to left ventricle
Blocking of left bundle fascicles
–> shifts in direction of depolarization but no QRS widening….e.g., frontal plane mean axis is altered (depolarization of septum in opposite direction)
3 common mechanisms leading to arrhythmia
Abnormal reentry pathways, Ectopic foci, Triggered activity
Abnormal reentry pathways
Can be present in atria, ventricles, or the junction tissue; Reentry occurs when there is a unidirectional block and slow conduction through the reentry pathway; After the slow reentry, the previously depolarized tissue has recovered and reentry into it will occur; Probably the most common mechanism of serious tachycardias
Ectopic foci
Occur when a focus of myocardium outside the conduction system acquires automaticity; if rate of depolarization exceeds that of the sinus node, an abnormal rhythm occurs….Can be isolated “ectopic beats” or sustain tachyarrhythmias.
Triggered activity
Abnormal “afterpolarizations” may be triggered by the preceding AP…… Both early afterpolarization (when AP has only partially repolarized) and delayed afterpolarization (after AP is complete) can trigger arrhythmias.
Arrhythmias due to triggered activity mechanism, on ECG
Usually associated with a delay in repolarization seen in the ECG as a “long QT interval”
Time period (on ECG) of absolute refractory period & meaning for shocks
Absolute refractory period occurs right before Q and lasts til middle of T (why you give shock during QRS…you know the shock won’t set off another beat at that time).
Time period (on ECG) of relative refractory period & meaning for shocks
Relative refractory period lasts during the later half of the T wave –> a shock could set off new irregular beats at this time…the longer the T wave (lengthier repolarization), the more chance of this there is
