Cardio Flashcards
Sets frequency-dependent conduction
delay between the atria & ventricles
AV node
in pace-maker tissues
what channels are open in phase 4
Funny Na+ current
T-type Ca2+ current
L-type Ca2+ currents
in pace-maker tissues
what channels are open in phase 0
L-type Ca2+
what determines refractoriness?
Refractoriness is governed by the number of Na+ channels ready to be activated.
what is : important for the propagation of abnormal impulses
Effective refractory period/Action potential duration ratio
ERP/APD ratio
is a low or high ERP/APD ratio easiy to depolarize by abnormal impulses
lower
in what period is myocardial tissue more easily stimulated?
supranormal/supernormal period
cardiac Na+ channel:
what gates are open and close in resting state
m (activation gate) = closed
h (inactivation gate) = open
cardiac Na+ channel:
what gates are open and closed during depolarization
m (activation gate) = open
h (inactivation gate) = slowly closes
cardiac Na+ channel
what gates are open and closed during repolarization
m (activation gate) = open
h (inactivation gate) = closed
in what state of the Na+ channels are the myocardial muscles excitable?
rested state
what what Na+ channel stay and what phase are the channels closed and non-conducting
Inactivated state
phases 1-3
what determines ERP and RRP
The time course with which Na+ channel return from the inactivated to rested state determines the ERP and RRP.
what channel is active during a large duration of the AP - early component = major; late component = minor
Na+ channels
what class of antiarrhythmics target the fast, early Na+ currents
Ia
IIb
Ic
III
what drug affects the late Na+ current
Ranolazine
what happens if there is a enhanced late Na+ current
- increase intracellular Na+
- Inhibit Na-Ca exchanger
- Increase intracellular Ca2+
- Cellular Ca2+ overload
- -> mechanical dysfunction: abnormal contraction/relaxation
- -> electrical instability after-depolarizations, arrhythmias
what class of antiarrhythmics are “recovery” K+ channel blockers
Ia
Ic
III
K+ channel blockade prolongs what?
phase 3 repolarization
what voltage-dependent Ca2+ channel plays a key role in both pacemaker and non-pacemaker tissues
L-type Ca channel
in pacemaker cells in what phases is inward Ca2+ currents important
phase 4 and 0
how will blockade of Ca2+ channels affect pacemaker cell AP
affect on HR?
reduce slops of phase 4 (alpha angle) and phase 0 –> reduce HR
Cardiac Ca2+ channels exhibit slow kinetics –> recovery from inactivation occurs some time after full repolarization –> ____
“post repolarization refractoriness” (PRR)
what will decrease post repolarization refractioriness (PRR)
Sympathetic activation: increase # functional Ca2+ channels –> decrease PRR
what class of antiarrhythmics increases PRR
class III
inward Ca2+ currents Ca2+ channel blockers have little effect on the CONDUCTION OR REFRACTORINESS of what?
atrial, ventricular, His-Purkinje, or bypass tract
The major electrophysiological effect from block of cardiac Ca2+ channels are in the what?
slow-response tissues: SA & AV nodes
direct sympathetic activation of B1 receptros in pacemaker tissue cells has what effect on AP?
- Increased phase 4 slope
- Decreased threshold point
- -> Faster HR
what is the effect of sympathetic activation on non-pacemaker tissues
increase Ca2+ influx
increase SR Ca2+ release
increase SR Ca2+ uptake
Outcome of sympathetic activation on non-pacemaker tissues
Increased rate & force of contraction (inotropic)
Increased rate of relaxation (lusitropic)
Increased myocardial O2 demand
what occurs to pacemaker cell AP with PNS activation on the M2 receptor
- Decreased phase 4 slope
- More positive TP
- More negative MDP –> HR
