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Pharmacology II > Antiarrhythmics > Flashcards

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
Q

what are tx options for abnormal impulse conduction

A

prevent re entry by slowing conduction and or increasing the refractory period

26
Q

what is the aim of drug therapy for arrhythmias

A

modify impulse generation and conduction

27
Q

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

A

Class I drugs

28
Q

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

A

Class IA drugs

29
Q

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

A

Quinidine

30
Q

this Class IA drug shows alpha blocking activity ; increases steady state concentration of digoxin

A

quinidine

31
Q

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

A

procainamide

32
Q

This class IA drug has similar actions to Quinidine; metabolite is less active; side effects of dry mouth, urinary retention, blurred vision, and constipation

A

Disopyramide

33
Q

This class of drugs has a greater affinity for inactivated Na channels ; shortens repolarization

A

Class IB drugs

34
Q

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

A

Lidocaine

35
Q

These Class IB drugs are similar to lidocaine

A

Mexilitine and Tocainide

36
Q

this class IB drug is often used after MI

A

Mexilitine

37
Q

This Class IB drug has pulmonary toxicity

A

Tocainide

38
Q

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

A

Class IC drugs

39
Q

these two Class IC drugs have minimal biotransformation; long half life,; adverse effects of dizziness, blurred vision, HA, nausea, and arrhythmia

A

Flecainide and Propafenone

40
Q

this class of drugs are beta blockers ; diminish phase 4 depolarization ; useful in treating arrhythmias caused by increased sympathetic activity

A

Class II drugs

41
Q

this class II drug reduces incidence of sudden arrhythmic death after MI

A

propanolol

42
Q

this class II drug is the most widely used beta blocker to treat cardiac arrythmias; reduces the risk of bronchospasm

A

metoprolol

43
Q

this class II drug is short acting; used IV to treat arrhythmias that occur during sx or in emergency situations

A

esmolol

44
Q

This class of drugs diminishes the outward K current during repolarization of cardiac cells ; all have potential to induce arrhythmias

A

Class III K channel blockers

45
Q

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;

A

amiodarone

46
Q

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

A

amiodarone

47
Q

this class III drug is a amiodarone derivative ; shorter half life and side effects mainly GI

A

dronedarone

48
Q

This Class III drug has potent beta blocker activity ; lowest rate of acute or long term adverse effects

A

sotalol

49
Q

These Class III drugs have high risk of proarrhythmia; prolongs QT interval; 80% of drug eliminated unchanged

A

Dofetilide and Ibutilide

50
Q

this class of drugs are Ca channel blockers; they decrease inward current;

A

Class IV drugs

51
Q

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)

A

Verapamil and Diltiazem

52
Q

this Class IV drug is extensively metabolized by the liver

A

verapamil

53
Q

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

A

Adenosine

54
Q

This” other antiarrhythmic drug” Is less effective in presence of caffeine ( blocks adenosine receptors) ; adverse effects include flushing, shortness of breath, and chest burning

A

adenosine

55
Q

which drug shortens the refractory period in myocardial cells

A

digoxin

56
Q

this “other antiarryhtmic drug” can cause arryhtmia if too much ; supplementation aimed at balancing the gradients

A

potassium

Pharmacology II (31 decks)

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