Electrophysiology Flashcards
The action potential triggers
Contraction
How does the cardiac muscle AP differ from the skeletal muscle AP?
Duration of cardiac AP is longer
What generates the resting membrane potential of cardiac myocytes?
Relative permeability to charged ions and Ion pumps
Then, different ion concentrations create the
Electrical potential difference
A change in the electrochemical gradient for an ion that is permeable can alter the
Resting membrane potential
A change in ion conductance can alter the
Resting membrane potential
What is the effect on RMP for a cell if there is decreased Extracellular concentration of K+?
RMP becomes more negative
When we have loss of Na+/K+ ATPase due to ischemia, what happens to the RMP?
Becomes more negative
Characterized as rapid depolarization
Cardiac myocyte AP phase 0
In phase 0, action potential depolarizers cell to threshold (from -90 to -60), then we see rapid opening of
Voltage-gates Na+ channels
Voltage-mediated activation of fast Na+ channels allows
Rapid depolarization
Inactivate quickly during phase 0 so that conductance decreases
Voltage-gated Na+ channels
Inactivated channels cause the
Refractory period
What determines the rate of rise of the phase 0 upstroke?
Inward Na+ current
What is the effect of a pharmacological blockade of Na+ channels on the cardiac myocyte AP?
Peak would be lower and amplitude would be lower
How would a pharmacologic blockade of Na+ channels change the ECG?
QRS would be prolonged
How would phase 0 change if we had an increase in extracellular K+?
Cell slowly depolarizers and RMP becomes more positive
Slow depolarization from excess extracellular K+ causes Na+ channels to go from
Closed to inactive, without being activated
What is phase 1 of the cardiac myocyte AP?
Brief Repolarization
Characterized by a transient outward current (IKto) and rapid inactivation of FAST Na+ channels
Brief repolarization
Cells in the subepicardium are characterized as having a
Shorter AP
Phase 2 of the cardiac myocyte AP is?
Plateau phase
The major current leading to the plateau phase is the
Slow inward Ca2+ through L-type channels
Major Ca2+ channel in cardiac cells
-important pharmacologic targets
L-type channels
Counter-balance inward Ca2+ during the plateau phase
Outward K+ currents
Permits sufficient calcium entry into the cell to maintain the stores required for contraction
Plateau phase
Keeps the fast sodium channels inactivated for a substantial period of time to prevent too frequent APs
Plateau phase
Phase 3 of the cardiac myocyte AP is
Repolarization
Results in repolarization
IKr current
The action potential becomes narrower and we get faster repolarization if the
IKr current increases
What changes would we see in the cardiac myocyte action potential with a drug that blocks IKr?
Prolonged repolarization and longer AP
What changes would we see in the ECG of a patient taking a drug that blocks IKr?
Long QT interval
A long QT interval predisposes patients for
Arrhythmias
Phase 4 of the cardiac myocyte AP is the
Stable resting membrane potential
Characterized by a stable RMP, a sustained period of depolarization, and a LONG duration (150-250 msec)
Cardiac myocyte Non-pacemaker AP
Characterized by cells that lack the inward rectifying type of K+ channel (IK1) so RMP is less negative
Pacemaker potential
Characterized by an unstable RMP, automaticity, and no sustained plateau
Pacemaker APs
Phase 0 of the cardiac pacemaker potential is
Depolarization
During phase 0 of pacemaker potentials, we see increase Ca2+ conductance via
Voltage-gated L-type Ca2+ channels
One major characteristic of pacemaker potentials is that there is NO
Fast Na+ current
Phase 3 of the cardiac pacemaker potential is
Repolarization
In a pacemaker potential, depolarization leads to opening of
Delayed rectifier K+ channels
Phase 3 of the pacemaker potential ends when the cell reaches the
Maximum negative diastolic potential
Phase 4 of the cardiac pacemaker potential is the
Spontaneous depolarization cardiac pacemaker current
Which 3 currents contribute to the cardiac pacemaker current (phase 4)?
IF (funny current), outward K+ (IK+), and inward Ca2+ (ICa2+)
Activated by hyperpolarization (Anything greater than -50 mV)
-The more negative the membrane potential, the more intense this current is
Funny current (IF)
The “funny” current is regulated by
CAMP
The IF current moves through channels called
HCN channels
Is reverse-voltage dependent and has no inactivation state
Funny current
The HCN channels of the funny current are permeable to
Na+ AND K+
The K+ ion is more easily conducted across HCN channels, BUT under physiologic conditions, HCN channels carry
Inward Na+ current
Reverse-voltage dependence makes them unique among ion channels
HCN channels
Causes increased HCN activity
cAMP
The opening and closing of HCN channels determines the slope of
Phase 4
Activated towards the end of phase 4 of pacemaker potential
Inward Ca2+ (T-type) channels
Accelerates the rate of diastolic depolarization
T-type channels
Which three factors influence the intrinsic firing rate of the pacemaker cells?
- ) Slope of phase 4
- ) Maximum negative diastolic potential
- ) Threshold potential
The primary pacemaker is the
SA node
Has the fastest rate and suppresses the firing of other pacemakers
SA node
SA node activity is regulated by the
Autonomic Nervous System
The regulation of heart rate is called
Chronotropy
Increasing sympathetic ton causes an increase in
HR (positive chronotropic effect)
Increasing vagal tone causes a
Decrease in HR
In the heart, norepinephrine binds to
B1 adrenergic receptors
When norepinephrine binds to B1 adrenergic receptors, we see an increase in
cAMP
This increase in cAMP has what two main effects?
- ) Stabilized HCN in open position
2. ) Opens L(and likely T)-type Ca2+ channels
When acetylcholine is release, what does it bind to in the heart?
Muscarinic receptors (M2)
When acetylcholine binds muscarinic receptors (M2), it decreases
cAMP and If
Acetylcholine binding M2 activates a LIGAND-gated
K+ channel
Activation of the ACh-gated Ik will
Hyperpolarize the cell
