Antiarrhythmics Flashcards

1
Q

spontaneous depolarization is caused by inward positive current carried by ___ and ____ flow

A

Sodium and Calcium Ion Flow

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2
Q

what can cause an abnormality in cardiac rhythm

A

dysfunction of impulse generation or conduction

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3
Q

what is a slow heart rhythm

A

bradycardia

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4
Q

what is a rapid heart rhythm

A

tachycardia

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5
Q

what is a random beat of the heart

A

asynchronous fibrillation

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6
Q

myocardium responds to stimulation by ______ of the membrane; leads to shortening of the contractile proteins and then relaxation ; respond to stimuli as a unit

A

depolarization

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7
Q

how are action potentials generated

A

by pacemaker cells located in the SA node and AV nodes ; there are five phases

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8
Q

What are the five phases of the action potential

A

phase o: fast upstroke, phase 1: partial repolarization, phase 2: plateau, phase 3: repolarization , phase 4: forward current

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9
Q

in this phase , theres a rapid Na influx, through open fast Na channels

A

Phase o: fast upstroke

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10
Q

in this phae, transient K channels open and K efflux returns TMP to 0 mV

A

Phase 1 : partial repolarization

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11
Q

in this phase, influx of Ca through L type Ca channels is electrically balanced by K efflux through delayed rectifier K channels

A

Phase 2: plateau

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12
Q

IN this phase, Ca channels close and the delayed K channels remain open and return the TMP to -90 mV

A

phase 3: repolarization

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13
Q

in this phase, Na and Ca channels are closed , open K channels keep the action potential stable at -90 mV

A

Phase 4: forward current

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14
Q

T or F: the force of contraction is directly related to the concentration of unbound cytosolic Ca

A

T

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15
Q

Agents that increase Ca levels or increase Ca sensitivity _______ the force of contraction ( inotropic effect)

A

increase

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16
Q

What are some source of ic Ca

A

voltage sensitive channels , exchange with Na, released from sarcoplasmic reticulum and mitochondria

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17
Q

what would happen to cardiac muscle if cytosolic Ca levels remained high

A

cardiac muscle would be in a constant state of contraction

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18
Q

How is Ca removed

A

NA exchange and uptake by Sarcoplasmic reticulum and mitochondria

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19
Q

what are the two basic mechanisms of arrhythmias

A

disturbances in impulse formation and disturbances impulse conduction

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20
Q

these conditions : ischemia, acidosis or alkalosis, electrolyte imbalance, autonomic influences, drug toxicity, and stretching of cardiac tissue can exacerbate__________

A

arrhythmias

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21
Q

the SA node=

A

the pacemaker

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22
Q

what can lead to abnormal automaticity

A
  1. if sites other than SA node show enhanced automaticity ( generate competing stimuli)
  2. If myocardial cells are damaged, they may remain partially depolarized ( reach fire threshold earlier)
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23
Q

what are tx options for abnormal automaticity

A

drugs block either Na or Ca channels to reduce the ration to K ; decreases the frequency of discharge

24
Q

what can lead to abnormal impulse conduction

A

block of nerve impulses can cause short circuit ( re entry defect, premature contraction)

25
what are tx options for abnormal impulse conduction
prevent re entry by slowing conduction and or increasing the refractory period
26
what is the aim of drug therapy for arrhythmias
modify impulse generation and conduction
27
These class of drugs bind to open or inactivated Na channels ; have a greater effect in frequently depolarizing ; don't interfere with normal heart beat; subdivided into IA, IB, and IC
Class I drugs
28
These Class I subgroup drugs has a greater affinity for Na channels ; dissociate from Na channels slowly and they slow the rate of rise of the action potential
Class IA drugs
29
this type of CLass IA drug is rapidly absorbed after oral administration; extensive metabolism by P450 enzymes; has adverse effects of arrhythmia , GI disturbances, and blurred vision
Quinidine
30
this Class IA drug shows alpha blocking activity ; increases steady state concentration of digoxin
quinidine
31
this Class IA drug is a derivative of procaine; short half life; lupus like syndrome can develop; Fewer GI side effects and has CNS side effects
procainamide
32
This class IA drug has similar actions to Quinidine; metabolite is less active; side effects of dry mouth, urinary retention, blurred vision, and constipation
Disopyramide
33
This class of drugs has a greater affinity for inactivated Na channels ; shortens repolarization
Class IB drugs
34
This Class IB drug is also a local anesthetic; has little effect on atrial or AV junctions arrhythmias; Given IV; Large therapeutic index ; Mild CNS effects
Lidocaine
35
These Class IB drugs are similar to lidocaine
Mexilitine and Tocainide
36
this class IB drug is often used after MI
Mexilitine
37
This Class IB drug has pulmonary toxicity
Tocainide
38
this class of drugs has greater affinity for open Na channels ; depresses the rate of rise of the action potential; slowly dissociates from resting Na channels
Class IC drugs
39
these two Class IC drugs have minimal biotransformation; long half life,; adverse effects of dizziness, blurred vision, HA, nausea, and arrhythmia
Flecainide and Propafenone
40
this class of drugs are beta blockers ; diminish phase 4 depolarization ; useful in treating arrhythmias caused by increased sympathetic activity
Class II drugs
41
this class II drug reduces incidence of sudden arrhythmic death after MI
propanolol
42
this class II drug is the most widely used beta blocker to treat cardiac arrythmias; reduces the risk of bronchospasm
metoprolol
43
this class II drug is short acting; used IV to treat arrhythmias that occur during sx or in emergency situations
esmolol
44
This class of drugs diminishes the outward K current during repolarization of cardiac cells ; all have potential to induce arrhythmias
Class III K channel blockers
45
This Class III drug is a complex drug; it shows Class I, II , III, and IV actions; has antianginal activity; therapy of choice for atrial fibrillation; most commonly Rx'ed;
amiodarone
46
this Class III drug is incompletely absorbed ; half life of several weeks; adverse effects include discontinuation of tx, interstitial pulmonary effects, GI intolerance, tremor, ataxia, and dizziness, BLUE SKIN DISCOLORATION ( can manifest in the retina) , NAION and WHORL KERATOPATHY
amiodarone
47
this class III drug is a amiodarone derivative ; shorter half life and side effects mainly GI
dronedarone
48
This Class III drug has potent beta blocker activity ; lowest rate of acute or long term adverse effects
sotalol
49
These Class III drugs have high risk of proarrhythmia; prolongs QT interval; 80% of drug eliminated unchanged
Dofetilide and Ibutilide
50
this class of drugs are Ca channel blockers; they decrease inward current;
Class IV drugs
51
These Class IV drugs are used to treat angina and HTN; absorbed well after oral admin; adverse effects include negative inotropic properties ( CI in pts with depressed cardiac function)
Verapamil and Diltiazem
52
this Class IV drug is extensively metabolized by the liver
verapamil
53
This "other antiarrhythmic drug" is a naturally occurring nucleoside; activates an inward rectifier K current and inhibits Ca current ; inhibits AV nodal conduction and increases the AV nodal refractory period
Adenosine
54
This" other antiarrhythmic drug" Is less effective in presence of caffeine ( blocks adenosine receptors) ; adverse effects include flushing, shortness of breath, and chest burning
adenosine
55
which drug shortens the refractory period in myocardial cells
digoxin
56
this "other antiarryhtmic drug" can cause arryhtmia if too much ; supplementation aimed at balancing the gradients
potassium