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NSG 531 Advanced Pharmacology Exam Study Guide Objectives
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- NSG 531 (NSG531)
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- Rush University
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Exam 3 Study guideWeek 7: CV
• Describe ion transport during each phase of cardiac conduction.
o Cardiac action potentials are much slower than neuron action potentials
B/c heart needs to be slower b/c need to allow time for filling
Still have to hit threshold for an action potential to fire
o 2 action potentials in heart:
Pacemaker & non-pacemaker
• 5 phases Non-pacemaker Action Potentials:
o Occur in the atria & ventricular myocytes-- which are the contractile cells
of the heart
o 0 = depolarization
Na channels open-- voltage gated fast Na channels
Depolarizing current coming from/generated by pacemaker cells
o 1 = partial repolarization - b/c start returning back to resting membrane
potential
K channels open (not as fast as Na channels)
K leaving cell and taking + charge with it, bring us slightly
toward RMP
Na channels close-- b/c they are fast
o 2 = plateau - not making any headway in reducing the voltage within the
cell back down to the membrane potential
K still open
Ca channels open-- L type → long acting
Slow
Stay open for long period of time
Responsible for plateau
Plateau b/c K leaving and Ca coming in -- off setting each other
K + charge moving out of cell
Ca moving into cell, + charge entering
Filling time b/c no AP occuring, no contractions occurring
o 3 = repolarization- start overtime making movement & going back to our
resting membrane potential
Ca channels closed (L-type)
K still open
Taking + charge with it, moving back down to RMP
o 4 = resting membrane potential
• Refractory Period
o During phase 0,1,2, & part of 3
o The initiation of new action potential
Have to hit threshold for action potential to fire
o No matter how strong the stimulus is, if in phase 0-3 the contractile
myocytes is not going to respond to stimulus
o Many antiarrhythmic drugs increase the RP which reduces myocyte
excitability decrease HR & dysrhythmias
o Significance of refractory period:
Limits frequency of cardiac contractions
Allows for adequate filling time
Prevents sustained contractions
• 3 Phases Pacemaker cells
, o Cells w/in the sinoatrial (SA) node comprise the primary pacemaker site
o Differ from non-pacemaker AP in 2 ways:
No true resting potential-- never a flat line, it cycles
Generate regular, spontaneous action potentials
Depolarizing current carried by Ca, not by Na
Depolarizing current is carried primarily by relatively slow,
inward Ca currents
Influx of Ca is what is going to depolarize
pacemaker cells, not by opening Na channels
Are some Na channels in pacemaker cells, but they
are not important in the depolarizing it
o 0 = Rapid depolarization
L-type voltage gated Ca channels open--giving rise to AP
Ca channels slower, why no peak
Opened longer
Depolarize the cell
o 3 = Repolarization
Ca channels close (L-type), voltage gated K channels open (K
leaves the cell & takes its + charge w/ it)
o 4 = Slow depolarization
K channels close
Funny Na channels open
Called funny b/c they open up at very low voltages
Only stay open for brief period of time
In pacemaker cells not myocytes
4.5 -
T-Type(transient) Ca channels open→ open around -70,
stay open for short period of time, until threshold for L-Ca
channels to open & drive the depolarizing current
Cause phase 0 = opening up of funny Na channels that get
partway to threshold, which in turn opens the t-type Ca
channels which take us the rest of the way to threshold,
which then opens up the L-type Ca channels & fires off
another AP
• Non-pacemaker cells can mimic pacemaker AP under certain conditions→
hypoxia→ causes membrane depolarization which closes fast Na channels
o CAD not getting enough O2 delivered to their myocytes or non-
pacemaker cells & alters their AP
o Raises RMP-- higher than in a healthy cell b/c Na-K ATPase pump
doesn’t work well-- b/c ATP generated in the present of O2 (aerobic
process)
Function of Na-K ATPase pump is to keep the interior of the cell
negative relative to the exterior
Interior becomes less negative when pumps start to fail
When hit threshold or above threshold
Fast Na channels open at -70-- fast → they open quickly & close
quickly-- the voltage is what makes them close.
Open at -70-- when get to -65 they close. If RMP is -65 or -
62, Na channels be in closed state
, If they close at -65 and your RMP is higher than -
65.. Na channels will be in a closed state, they are
not going to open
Cells depolarize by Ca rather than Na b/c Na
channels closed.. So they adapt by now triggering
AP by Ca currents instead of Na currents, b/c Na
cannot move b/c have a depolarized membrane
Start generating pacemaker like AP from those cells
How you start getting ectopic folkeye?
Occur in disease ischemic tissue b/c not
getting enough O2 & ATPase pump aren’t
working→ shut off Na channels so AP
through Ca channels
• Describe the pathophysiology of delayed afterdepolarization and re-entry.
o After depolarization
After-depolarization of non-pacemaker cells (contractile cells) during
either phase 3 (repolarization) or phase 4 (RMP)
Spontaneous depolarization of non-pacemaker cells during phase
3-4… slightly faster than we want it
Premature contractions that occur after the effective
refractory period but before the optimal time for the next
depolarizing current to come in to trigger another AP
Most often caused by elevated intracellular calcium that triggers abnormal
action potential-- brings us up to threshold & open up fast Na channels
Associated with hypercalcemia, digoxin toxicity, hypokalemia (b/c K will
stay in cell longer due to concentration gradient), & excessive
catecholamines (have depolarizing effects b/c decrease Ca in a cell)
Treatment w/ Ca channel blockers, adjustment of digoxin dose,
normalization of K, & beta-blockers
o Re-entry- single impulse re-enters an area of the heart & repeatedly excites it
Conditions for re-entry/in order to occur
Physiologic ring
Unidirectional block
Effects the movement of the impulse (depolarization) down
but doesn’t effect the movement of the impulse up b/c that
part of the fiber is healthy enough to conduct the impulse
Conduction time > RP (refractory period)
Time it takes to circle around the ring has to be greater
than the refractory period
If smaller ring in phase 0-3 it’s impulse going to get
blocked b/c cell is in refractory period & it cannot
keep conducting
If the ring is larger enough that by the time it gets to
any part of the ring is already out of effective
refractory period & responsive to it.
Manifest as tachycardia or atrial flutter
Give K channel blockers to fix (prolonging the AP & prolonging
RP) or ablation
K channels open through most of AP
Soo then RP is longer than conduction time
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