Cardiac Electricity Flashcards
Fastest pacemaker in the heart
SA Node ~1000 cells
Functional adaptations of pacemaker cells
lack of ion channels that stop spontaneous depolarization; lack of myofibrils
Sinoatrial AP curve
shallow upstroke, repolarization to only -65mV
Atrial AP curve
Fast upstroke; 100 ms duration
Escape mechanism (heart)
Secondary means of creating electrical impulse to start ventricular contraction
AV Node
only place for transmission of the SA AP to ventricles
Ventricular myocyte polarization waves
endocardial to epicardial depolarization
epicardial to endocardial repolarization
Purkinje plateau
at 0 mV for 100-150ms then down to -85
Cardiac electrical cycle
0) Depolarization wave (upstroke)
1) Early repolarization wave
2) Plateau
3) Major repolarization wave
4) time between repolarization and next depolarization
Conduction velocity of various cardiac cells
AV/SA nodes = 0.05 m/s
Atrial/ventricular muscle = 0.3 m/s
Inter-nodal tracts 1.0 m/s
His/Purkinje fibers 3.0-5.0 m/s
variations in Na channel density responsible for differences
Important intervals for ECG
PR interval for inter-nodal conduction and His/Purkinje system
QT interval
SA and AV node lack which channels
Nv channels and IRK channels
Myocytes repolarization channel (all)
Potassium
Myocyte depolarization response (all)
VGCC for Calcium influx
Tetrodotoxin
blocks Na channels; useful for study of slow rising (calcium dependent) AP’s
Reasons for cardiac myocyte plateau
Calcium influx and slow opening K channels (K channels found in lower concentration on plasmalemma than in other excitable cells)
Sodium cardiac myocyte electrical cycle
immediate opening, inactivation in 1-3 ms, inactive until complete repolarization
Delayed potassium channel electrical cycle (cardiac myocyte)
open slowly (100-300 ms) and close slowly after repolarization
cardiac myocyte ‘the’ IRK channels
raise the resting conductance of K; can be blocked by Mg2+ above -50mV
L-type Calcium channels (cardiac electrical cycle)
open around -50mV, open for long duration, usually only 30% recruitment
Other types of Calcium channels
T-type (transient-type): in cardiac myocytes, open briefly at the upstroke, then close. N-type (neuronal): in neurons and not found in cardiac myocytes. Neither of these can be affected by dihyrdopyridine or cAMP (catecholamine stimulated cAMP)
NCX arrhythmia
when metabolically stressed, cardiac myocytes import too much Ca, this activates NCX which exchanges one Ca for 3 Na. This influx of Na can cause ‘after-depolarization’ and can potentiate a new AP
the ‘Ito’
Kv channel “calcium-independent transient outward” these are the cause of the phase 1 early repolarization (cardiac electrical cycle) and are only open briefly
the ‘Iks’
delayed K current ‘slow’ version
the ‘Ikr’
delayed K current ‘rapid’ version; commonly called HERG; together with Iks are responsible for QT time, ergo malfunctions in these can cause long QT times and arrhthymias
K ATP channels
ATP level sensing K channel that opens when ADP levels are too high (ATP too low); shortens AP’s; play a major role in ischemic attacks
GIRK (ACh activated K Channel)
respond to parasympathetic ACh release to slow heart rate; only found in atria
Long QT pathophys
Ikr and Iks channels are degraded prior to their insertion into the membrane; alternatively prolonged opening of the Na channels can cause late repolarization as well
K-ATP channel pathophys
if activated due to a drop in metabolic rate (ischemia); or if Na channels do not deactivate - depolarization; if K-ATP stays open, intracellular K migrates out causing further depolarization
ST depression
apparent depression of the ST wave due to higher resting potential - created by too much extracellular K levels (K-ATP open due to ischemia): depression=ischemia
ST elevation
conduct of a current through damaged tissue may result in an elevated ST wave; present in MI (STEMI)
How do you block ‘the’ IRK (result?)
Barium - result is spontaneous AP generation by all cardiac cells
mechanism of nodal pacemaking AP generation
1) non-specific cation channels depolarize to -50 mV
2) Ca channels depolarize to E-Ca
3) delayed K channels open to repolarize
4) slight undershoot, then non-specific channels depolarize again
the nonspecific cation channel current
effectively the background positive (depolarizing) current that counters the IRK channels; called “F-type current”; activated by repolarization and by sympathetics to increase HR
True pacemakers
healthy pacemakers, SA node
latent pacemakers
any cells outside the SA node that can generate a spontaneous AP, most notably the AV node and Purkinje fibers; common during atrial fib.
ectopic pacemaking
when cells outside the SA node actually do fire spontaneous AP’s, usually due to NCX arrhythmia
