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NSG 531 Advanced Pharmacology Exam Study Guide Objectives $10.49   Add to cart

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NSG 531 Advanced Pharmacology Exam Study Guide Objectives

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  • August 12, 2024
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Exam 3 Study guide

Week 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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