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58 Cards in this Set

  • Front
  • Back
phase 0 in Purkinje cells is done by ___. phase 0 in SA node is done by ___.
purk - Na
SA - Na and Ca
why is atrial fibrillation problematic?
does not alter CO, but can increase platelet aggregation and formation of clots
name 4 supraventricular arrhythmias and 3 ventricular arrhythmias
atrial arrhythmias
atrial fib
atrial flutter
PAT

PVT
PVC
V fib
draw the SA node's membrane potential during a normal cycle and label phases. what 3 factors could increase automaticity?
making the depolarization potential of phase four more negative

increasing the rate of depolarization in phase 4

making the threshold more negative
what 2 kinds of things can lead to abnormal generation of impulses?
1. increased rhythm of secondary pacemakers
2. triggered events
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
what effect does decreased stretch have on autorhytmicity?
it decreases autorhythmicity
what effect does digitalis have on autorhythmicity?
increase
what effect do antiarrhythmics and beta blockers have on autorhythmicity?
decrease
what effects do catecholamines have on autorhythmicity?
increase
what effect does sympathetic stimulation have on autorhythmicity?
increase
what effect does parasympathetic stimulation have on autorhythmicity?
decrease
what effect does increased extracellular Ca have on autorhymiticty
it increases autorhythmicity
what effect does decreased extracellular K have on autorhythmicity?
it increases autorhythmicity
what effect does increased extracellular K have on autorhythmicity?
it decreases autorhythmicity
which causes increased autorhythmicity? extracellular or intracellular Ca?
intracellular calcium overload increases autorhythmicity, but increasing extracellular ca increases the amount that comes into the cell!
what is a delayed afterdepolarization?
this is a triggered event, in which a secondary depolarization occurs in DIASTOLE *after* repolarization has been achieved.
what is an example of a triggered event?
a DAD
which extracellular ion disturbances can trigger a DAD
hypokalemia

combo of hyponatremia and hypercalcemia

why - I have no fucking clue
what drugs can trigger a DAD?
cardiac glycosides
catecholamines
what are 2 determinants of conduction velocity?
upstroke velocity of phase 0

amplitude of phase 0
a non uniformity of ___ and ___ results in re-entry arrhythmias
excitability (ERP) and conductivity (CV)
how does a lower RMP result in a higher CV?
higher amplitude!
why do ischemic cells conduct slower?
they have a less negative RMP

they have a lower amplitude

they have a decreased CV

THEY ARE FUCKING SLOW CONDUCTORS!!!
how does an ischemic injury cause re-entry arrhythmia?
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
ischemia in ___ tend to cause unidiretional blocks?
LBB and RBB
how does ischemia result in a PVC?
unidirectional block + re-entry = another ventricular depolarization without an atrial depolarization first
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)
3 conditions for cardiac re-entry
1. contiguous loop circuit
2. unidirectional block
3. zone of slow conduction
why is a hypertrophied heart more prone to re-entry arrhythmias?
1. longer fibers
2. slow conduction
3. unidirectional blocks
3 sites of re-entry arrythmias
SAN and superventricular arrhythmias - recylces through SAN

Purkinje fibers in v tach

Wolfe-Parkinson-White Syndrome - recyles through ventricles to the atria
what are examples of secondary antiarrhythmatic agents?
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)
What are the class I-IV antiarrhythmic drugs?
I: fast Na channel blockers
IIA: Beta blockers, nonselective
IIB: Beta blockers, cardioselective
III: K channel blockers
IV: slow Ca channel blockers
what is torsade de points and what can cause it?
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)
what are class I antiarrhythmics and what do they treat?
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
what are class II antiarrhythmics and what do they treat?
beta blockers that treat surpaventricular arrhythmias and ventricular arrhythmias associated with catecholamine excess (duh)
what are class III antiarrhythmics and what do they treat?
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
what are class IV antiarrhythmics and what do they treat?
these are slow Ca channel blockers that can treat:
1. supraventricular arrhthymias
2. ventricular arrhythmias associated with AMI
why aren't class IA drugs given by IV?
because they have a side effect of cardiac depression or arrest if you give too much. once you give you cant take back
what kind of cholinergic side effects do quinidine and other class IA have?
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
what is cynchonism
s/e of quinidine
1. tinnitus
2. vertigo
3. headache
4. visual disturbances
what side effects does quinidine have?
anticholinergic s/e that all IA have

also cynchonism - tinnitus, vertigo, headache, visual disturbances
why are class IB better than IA?
minimal cardiac depression
dont increase QT interval
conduction velocity not changed much
why is lidocaine such a good drug for arrhythmias in the ER?
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
how the fuck does lidocaine decrease conduction velocity?
it has some effect on potassium channel too??? probably what the fuck
why aren't class IC first line?
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
what drug for chronic stable ventricular arrhthmias?
class IC
why is propanolol good for arrhythmias?
it has membrane stabilizing properties (quiniline like actions - blocks Na channels)

it is especially good for decreasing sudden death following AMI
Class III effect on QT?
increase!
how do you treat reentry arrhythmias?
with K channel blockers (class III)

these increase ERP without affecting conduction velocity
why is amiodarone a dirty drug?
mixed mode of action
class III with I, II, and IV
affinity for Ca, K, and Na channels
what are class IV used for?
supraventricular - think phase 0

ventricular arrhythmias associated with AMI
class III effect on conduction and action potential duration (QT)?
prolong the QT w/o affecting conduction

perfect for reentry arrhtyhmias
side effects of class IV?
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
example of a triggered arrhythmic activity?
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
non uniformity of ___ and ___ cause re-entry arrhythmias
conduction velocity
excitability
what are some determinants of conduction velocity?
upstroke velocity of phase 0 (dV/dt)
amplitude (lower RMP=bigger amplitude=bigger CV. higher RMP (think hypoxic)...)
why does hypoxic heart tissue have a slower conduction velocity?
more pos RMP -> less amplitude -> slower CV