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58 Cards in this Set
- Front
- Back
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phase 0 in Purkinje cells is done by ___. phase 0 in SA node is done by ___.
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purk - Na
SA - Na and Ca |
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why is atrial fibrillation problematic?
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does not alter CO, but can increase platelet aggregation and formation of clots
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name 4 supraventricular arrhythmias and 3 ventricular arrhythmias
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atrial arrhythmias
atrial fib atrial flutter PAT PVT PVC V fib |
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draw the SA node's membrane potential during a normal cycle and label phases. what 3 factors could increase automaticity?
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making the depolarization potential of phase four more negative
increasing the rate of depolarization in phase 4 making the threshold more negative |
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what 2 kinds of things can lead to abnormal generation of impulses?
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1. increased rhythm of secondary pacemakers
2. triggered events |
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what effects do:
increaed CO2 decreased O2 decreased pH increased temperature have on autorhythmicity? |
they increase it. these would all occur during ischemia and increase autorhythmicity
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what effect does decreased stretch have on autorhytmicity?
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it decreases autorhythmicity
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what effect does digitalis have on autorhythmicity?
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increase
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what effect do antiarrhythmics and beta blockers have on autorhythmicity?
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decrease
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what effects do catecholamines have on autorhythmicity?
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increase
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what effect does sympathetic stimulation have on autorhythmicity?
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increase
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what effect does parasympathetic stimulation have on autorhythmicity?
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decrease
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what effect does increased extracellular Ca have on autorhymiticty
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it increases autorhythmicity
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what effect does decreased extracellular K have on autorhythmicity?
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it increases autorhythmicity
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what effect does increased extracellular K have on autorhythmicity?
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it decreases autorhythmicity
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which causes increased autorhythmicity? extracellular or intracellular Ca?
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intracellular calcium overload increases autorhythmicity, but increasing extracellular ca increases the amount that comes into the cell!
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what is a delayed afterdepolarization?
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this is a triggered event, in which a secondary depolarization occurs in DIASTOLE *after* repolarization has been achieved.
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what is an example of a triggered event?
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a DAD
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which extracellular ion disturbances can trigger a DAD
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hypokalemia
combo of hyponatremia and hypercalcemia why - I have no fucking clue |
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what drugs can trigger a DAD?
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cardiac glycosides
catecholamines |
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what are 2 determinants of conduction velocity?
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upstroke velocity of phase 0
amplitude of phase 0 |
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a non uniformity of ___ and ___ results in re-entry arrhythmias
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excitability (ERP) and conductivity (CV)
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how does a lower RMP result in a higher CV?
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higher amplitude!
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why do ischemic cells conduct slower?
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they have a less negative RMP
they have a lower amplitude they have a decreased CV THEY ARE FUCKING SLOW CONDUCTORS!!! |
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how does an ischemic injury cause re-entry arrhythmia?
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there is an ischemic slow path tissue that sets up a block.
impulse takes the fast path and then turns retrograde and hits the area downstream to the block. by the time the retrograde impulse gets through the block, other tissue is ready to depolarize again because the whole process took so damn long |
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ischemia in ___ tend to cause unidiretional blocks?
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LBB and RBB
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how does ischemia result in a PVC?
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unidirectional block + re-entry = another ventricular depolarization without an atrial depolarization first
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what are the 2 causes of unidirectional blocks?
how do you treat each? |
Class IA, IC, and III are due to decreased membrane responsiveness and conduction velocity
treat by converting to bidirectional block (increase the ERP even more) Class IB is due to increased membrane responsiveness and incresed conduction velocity treat by eliminating the block (lidocaine) |
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3 conditions for cardiac re-entry
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1. contiguous loop circuit
2. unidirectional block 3. zone of slow conduction |
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why is a hypertrophied heart more prone to re-entry arrhythmias?
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1. longer fibers
2. slow conduction 3. unidirectional blocks |
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3 sites of re-entry arrythmias
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SAN and superventricular arrhythmias - recylces through SAN
Purkinje fibers in v tach Wolfe-Parkinson-White Syndrome - recyles through ventricles to the atria |
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what are examples of secondary antiarrhythmatic agents?
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1. cardiac glycosides - for paroxysmal tachycardia, atrial flutter, and atrial fib
2. adensosine - for supraventricular arrhythmias 3. magnesium sulfate - for refractory ventricular tachycardia 4. atropine - for vagal-stimulated heart block 5. phenylephrine - induces bradycardia via vagal reflex(same as cold water splash to face) |
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What are the class I-IV antiarrhythmic drugs?
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I: fast Na channel blockers
IIA: Beta blockers, nonselective IIB: Beta blockers, cardioselective III: K channel blockers IV: slow Ca channel blockers |
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what is torsade de points and what can cause it?
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torsade de points is polymorphic ventricular tachycardia or a v tach run
it can be caused by a problem with the fast Na channel or the Potassium channel (Ikr) therefore it can be caused by class IA and III antiarrythmic drugs it seems to be triggered by a prolonged QT (think class IA) |
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what are class I antiarrhythmics and what do they treat?
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fast na channel blockers that treat a broad spectrum of atrial and ventricular arrhythmias
Class II Beta-Blockers Class III Potassium Channel Modulators (Phase 3) - Primarily Reentry arrhythmias Class IV Slow Calcium Channel Blockers (Phase 2 and Diastolic Depolarization) - atrial and AMI arrhythmias |
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what are class II antiarrhythmics and what do they treat?
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beta blockers that treat surpaventricular arrhythmias and ventricular arrhythmias associated with catecholamine excess (duh)
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what are class III antiarrhythmics and what do they treat?
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potassium channel blockers
they increase action potential duration and increase ERP they increase QT and can cause torsade de pointes they are used to treat reentry arrhythmias because they increase ERP without affecting conduction |
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what are class IV antiarrhythmics and what do they treat?
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these are slow Ca channel blockers that can treat:
1. supraventricular arrhthymias 2. ventricular arrhythmias associated with AMI |
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why aren't class IA drugs given by IV?
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because they have a side effect of cardiac depression or arrest if you give too much. once you give you cant take back
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what kind of cholinergic side effects do quinidine and other class IA have?
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class IA: anticholinergic on body and heart. dry mouth, blurred vision. decrease vagal stim of heart and can lead to PARADOXICAL VENTRICULAR TACHYCARDIA. this is because of increased conduction through AV node due to loss of vagal stim
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what is cynchonism
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s/e of quinidine
1. tinnitus 2. vertigo 3. headache 4. visual disturbances |
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what side effects does quinidine have?
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anticholinergic s/e that all IA have
also cynchonism - tinnitus, vertigo, headache, visual disturbances |
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why are class IB better than IA?
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minimal cardiac depression
dont increase QT interval conduction velocity not changed much |
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why is lidocaine such a good drug for arrhythmias in the ER?
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it has a short therapeutic half life of 15 minutes. it absorbs into tissues and goes away. if you leave them on drip overnight, it will build up and then you are in trouble because it has a chemical half life of 2 hours
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how the fuck does lidocaine decrease conduction velocity?
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it has some effect on potassium channel too??? probably what the fuck
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why aren't class IC first line?
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they are very potent and cause severe decrease in conduction (CV).
THEY ARE PROARRHYTHMIC because they can easily create another block elsewhere only used for chronic stable ventricular arrhythmias (a special case) for people who dont respond to other drugs |
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what drug for chronic stable ventricular arrhthmias?
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class IC
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why is propanolol good for arrhythmias?
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it has membrane stabilizing properties (quiniline like actions - blocks Na channels)
it is especially good for decreasing sudden death following AMI |
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Class III effect on QT?
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increase!
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how do you treat reentry arrhythmias?
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with K channel blockers (class III)
these increase ERP without affecting conduction velocity |
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why is amiodarone a dirty drug?
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mixed mode of action
class III with I, II, and IV affinity for Ca, K, and Na channels |
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what are class IV used for?
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supraventricular - think phase 0
ventricular arrhythmias associated with AMI |
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class III effect on conduction and action potential duration (QT)?
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prolong the QT w/o affecting conduction
perfect for reentry arrhtyhmias |
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side effects of class IV?
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heart failure (neg inotropy)
heart block (decrease CV in AV node) hypotension (due to vasodilation effects on VSM) constipation in elderly especially with verapamil VERAPAMIL makes you VERY constipated |
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example of a triggered arrhythmic activity?
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DAD - delayed after depolarization. another depolarization in diastole after repolarization has been achieved.
can be triggered by: cardiac glycoside (calcium overload) membrane instability (those pesky sodium channels) excess catecholamines serum electrolyte imbalances 1. high calcium and low sodium 2. low potassium |
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non uniformity of ___ and ___ cause re-entry arrhythmias
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conduction velocity
excitability |
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what are some determinants of conduction velocity?
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upstroke velocity of phase 0 (dV/dt)
amplitude (lower RMP=bigger amplitude=bigger CV. higher RMP (think hypoxic)...) |
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why does hypoxic heart tissue have a slower conduction velocity?
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more pos RMP -> less amplitude -> slower CV
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