Cardiac Electrophysiology Flashcards
Fast-response cardiac muscle cells
. Atrial and ventricular contractile cells
. Purkinje fibers
. Have fast conduction velocity
Slow response cardiac muscle cells
. Nodal (pacemaker) cells
. Have slow conduction velocity
Initiation of contraction in cardiac cells
. Propagated AP initiates it
. External innervation not needed to initiate, only modulate
. Gap-junctions allow rapid cell-cell communication so muscle acts as 1 unit
RMP in cardiac muscle cells
-85
. Close to skeletal muscle
. Greater gK/gNa than neurons
AP overshoot in cardiac muscle cells is ___
25 mV
Cardiac muscle cell AP
. All or none
. Rapid upstroke in fast response cells
. Plateau phase contributing to longer AP duration (200 ms)
.
Ionic basis of cardiac AP in fast response cells
. AP of cell divided into 5 phases (0-4) based on time-dependent changes in ionic conductance
Phase 0 of cardiac AP
. Rapid depolarization
. Due to opening of VG Na channels
Phase 1 of cardiac AP
. Early repolarization
. Due to inactivation of Na channels and opening of specific K channel that opens rapidly and spontaneously inactivates
. Current called transient outward current (Ito)
. Some contribution from Cl channels
. Magnitude of repolarization here has regional variation (prominent in purkinje and epicardial ventricular cells, small in endocardial ventricular myocardium)
T/F transient outward current in cardiac AP only contributes in early repolarization, not ate repolarization
T
Phase 2 in cardiac AP
. Plateau phase
. Little change in membrane potential for 100-200 ms
. Reflects balance btw depolarizing and repolarizing currents
. Inward Ca current through L type VG channels
. Small contribution from VG Na channels that don’t close rapidly or reopen (Na window current)
. Decline in Ito contributed somewhat
. Delayed rectifier K current from slowly activating K channels that are similar to repolarizing K channels in neurons
L-ty[e Ca current
. Similar to VG Na channels but w/ more depolarized potentials and slower kinetics
. Predominant in heart
. Modulated by ANS, hormones, and drugs
. Exist in other muscle APs but do not contribute
Why is Na window current clinically important?
Bloacking of this current is responsible for AP shortening effects of certain anti-arrhythmic agents
Phase 3 of cardiac AP
. Primary and final phase of repolarization back to RMP
. Due to inactivation of L-type VG Ca channels and progressive inc. in delayed rectifier K current
. Significant contribution of inwardly rectifying K current as delayed rectifer slowly declines
Phase 4 of cardiac cells
. Resting membrane to entail
. Due to inwardly rectifying K current
. Spontaneous opening of these channels causes high background K conductance
. Na conductance very low during this phase
. Small contribution from Na/K-ATPase by maintaining concentration gradient
Absolute Refractory periods in cardiac fast response cells
. From phase 0 until halfway through phase 3 (-50 mV)
. During this period there are not enough Na channels recovered to cause a depolarization even if all available ones were opened during large stimulus
Relative refractory period in cardiac cells
. From halfway through phase 3 to the end of phase 3 when all Na channels are available for normal depolarization
. Period occurs as progressively more Na channels recover from inactivation to be activated again
.
Supernormal period
. Follows relative refractory period sometimes
. Ability of stimulus slightly below normal threshold to elicit AP
. Full recovery time occurs when excitability returns to normal after this period
Long Q-T syndrome
. Unusually long ventricular AP duration
. Longer than normal refractory period that disrupts normal electrophysiological timing of heart
. Prone to arrhythmias
. Genetic, result of stroke, starvation, or drug-induced
. Mutations in Gene encoding for delayed rectifer channels or fast Na channels
Torsades de Pointes
. Very dangerous ventricular arrhythmia
. More in women than men
Romano-ward syndrome
. Has one copy of disease-causing variant (long QT)
. Prone to torsades de Pointes
. Not deaf
Jervell and Lange-Nielsen (JLN) syndrome
. 2 copies of disease-causing variant (long QT) . Prone to torsades de Pointes . Deaf . More severe heart rhythm problems . Appear early in life
