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Pharmacology > Part 26: Arrhythmia's > Flashcards

Part 26: Arrhythmia's Flashcards

1
Q

at a fundamental level arrhythmias occur when these is some disruption in the normal ______ system in the heart

A

electrical conduction

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2
Q

what are some noticeable symptoms of arrhythmias?

A

weakness, fatigue, dypsnea

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3
Q

give 4 possible causes of arrhythmias

A
  1. tissue damage due to an MI
  2. abnormal initiation of electrical stimuli
  3. anatomic abnormalities
  4. drug induced (inotropic drugs)
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4
Q

refractory periods of cardiac electrical activity prevents ____activity

A

abnormal

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5
Q

AP from the SA nodes propogate through the atria to cause ____

A

atrial myocyte depolarization and contraction that pump blood into the ventricles

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6
Q

the AV node acts as a___ and ____ point to allow propogation of electrical signal to the ventricles

A

regulator; distribution

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7
Q

the refractory period of the AV node prevents ____

A

the chance of extra action potentials being transmitted from the SA to the ventricles

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8
Q

the AV conduction system provides a delay between ____ and ____ to optimize cardiac output

A

atrial contraction and ventricle contraction

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9
Q

the P wave of an ECG represents ___

A

atrial depolaization prior to contraction

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10
Q

the QRS wave represents ____

A

depolarization of the ventricles

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11
Q

the T wave represents ___

A

ventricle repolarization (ventricles relax after systole)

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12
Q

the AV node receives signals from the SA node and propogates them to the ventricles the ____

A

purkinje fibers

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13
Q

the PR interval represents

A

conduction time from the atrium to the ventricle

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14
Q

what does the QT interval represent?

A

ventricular action potential duration

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15
Q

alterations in the ECG reflect ___ or ____ in the heart

A

changes or dysfunction

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16
Q

t/f in some cases, arrhythmias can be treated with electric shock therapy

A

t

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17
Q

_____ or _____ are used to interpret the abnormal electrical activity in the heart and promote the return of normal rhythm

A

electrical cardioversion or defibrillation

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18
Q

is the electric shock type therapy used long of short term for arrhythmias?

A

short term

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19
Q

the pharmacologic treatment of arrhythmias aims to reduce abnormal electrical conduction by modulating ____ and ____ pathways involved in these processes

A

ion channels; signalling

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20
Q

what are the 4 classes of anti-arrhythmic drugs?

A

Class 1: primarily block Na channels
Class 2: block Beta receptors
Class 3: prolong AP by blocking K channels
Class 4: block Ca channel to slow AP through the heart

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21
Q

voltage gated Na channels exist in what 3 forms?

A

resting, open, inactivated

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22
Q

what is the purpose of the “inactive” state of Na channels?

A

prevents premature re-opening of the channel before repolarization has occured

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23
Q

while the Na channel are inactive, this is called the ___ period

A

refractory

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24
Q

after an AP, the membrane repolarizes and allows the inactivation gate to relax the Na channel to the ____ state

A

resting

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25
Q

excitation “out of phase” with the global action potential propagation causes _____

A

abnormal conractility

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26
Q

if there is damage in a region of the heart that blocks or slows conduction of the electrical signal, the AP may become out of phase, causing ____

A

uncoordinated cardiac contraction

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27
Q

a reentry arrythmia can be initiated when ___

A

the AP slows down through a damaged region, allowing time for the AP to loop back around to the branch point and come back in the wrong direction

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28
Q

a reentry arrhythmia can occur because the cells around a branch point are not in the ___ state as they should be

A

inactive refractory

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29
Q

why is a reentry arrhythmia given that name?

A

bc the APs are going back to regions that have already been stimulated by AP b4 the next coordinated AP comes from teh AV node

30
Q

t/f it is good to block some Na channels to treat arrhythmias, but if you blocked all of them the patient would go into respiratory and cardiac arrest and would die and that would be bad

A

t

31
Q

___ is a “use dependent” Na channel blocker that is a local anesthetic that can be used in the treatment of arrhythmias

A

lidocaine

32
Q

why is lidocaine a “use dependent” Na channel blocker?

A

binds preferentially to the open, active Na channels, so it targets areas of the heart that are overactive (regions that cause arrhythmias)

33
Q

lidocaine’s binding kinetics cause the preferential binding to Na channels in cells with more ____ resting membrane potentials

A

depolarized

34
Q

why is it beneficial that lidocaine preferentially binds to cells with more depolarized membranes?

A

damaged tissues like those that are ischemic due to coronary artery blockage have more depolarized resting potentials, and they are more likely to cause arrythmias so blocking them is good

35
Q

t/f damaged cells have a more depolarized resting potential and this makes them more prone to excitation that can cause arrhythmias

A

t

36
Q

at what state of Na channel is lidocaine least likely to bind?

A

resting

37
Q

when the cell membrane is repolarized or hyperpolarized, lidocaine is ____ (more/less) likely to bind to its Na channels

A

less

38
Q

what is a benefit of lidocaine not binding to resting (repolarized/hyperpolarized) Na channels?

A

allows for the normal neurotransmission and cardiac contraction to not be impeded

39
Q

if the depolarization gets beyond a certain point, what will happen to the lidocaine block of Na channels at repolarization?

A

lidocaine wont be released bc the resting potential isnt negative enough to reduce lidocaine’s affinity for the channel

40
Q

t/f lidocaine sequentially blocks Na channels with each AP

A

t

41
Q

if the dose of lidocaine is too high, it can cause toxicity to the CNS, presenting as ___

A

seizures and possible cardiac arrest

42
Q

beta blockers act to slow ___ and ___ and ____ HR

A

SA node firing and AV conduction ; decrease

43
Q

the early phase of SA AP is called_____. Why?

A

Phase 4; bc it starts after the previos AP has been generated

44
Q

phase 4 of the SA AP is a slowly ____ phase

A

depolarizing

45
Q

when the sympathetic nervous system is activated, the increased Ca influx into the SA cells causes the Phase 4 depolarization to occur ____ (faster/slower) which causes the slope of the AP curve to be ____ (increased/decreased)

A

faster; increased

46
Q

sympathetic activation of the SA dose cells causes the waveform to become _____ (wider/narrower)

A

narrower

47
Q

why does sympathetic activation cause a shortening of the SA action potential duration (APD)?

A

it causes the increased K efflux from the cell to repolarize the membrane more quickly

48
Q

sympathetic activation of the SA node has what 2 effects on the SA APs?

A
  1. shortening the AP

2. faster depolarization; increased rate of AP

49
Q

if we block sympathetic activation to the SA node, what is the effect on SA AP and heart rate?

A

slower depolarization and longer AP duration, fewer AP, and reduced HR

50
Q

beta blockers slow the propagation of AP through the ___ to the ____

A

AV node; ventricles

51
Q

how can beta blockers improve cardiac output for patients with tachycardic arrhythmia?

A

reduce AP firing frequency which reduces HR, allowing the ventricles to fill more completely before contraction which will improve cardiac output

52
Q

what family of anti-arrhythmetic drugs does diltiazem belong to?

A

Ca channel blocker (non-DHP type)

53
Q

diltiazem acts where?

A

vascular smooth muscle cells and cardiac muscle and electrical conductive cells

54
Q

what is the effect of blocking voltage gated Ca channels in the heart on contractility, SA node AP generation and conduction of APs through the AV node?

A

reduces contractility, decreases SA nodes AP generation, and slows conduction of AP through the AV node

55
Q

the SA cells spontaneously generate APs based on slow depolarization caused by ____ influx

A

Ca

56
Q

with use of diltiazem, what happens to the slope of the Phase 4 SA AP?

A

decreased

57
Q

the use of Ca channel blockers like Diltiazem causes the PR interval to be ____ (longer/shorter)

A

longer

58
Q

why is the PR interval slowed with the use us Ca channel blockers and B blockers?

A

the condition velocity from the atria to the ventricles is slowed when Ca channels are blocked

59
Q

do DHP Ca channel blockers like nifedipine act in the heart? Do they have arrhythmic effects?

A

no and no, the only act as vasodilators by blocking Ca channels in the vascular smooth muscle cells

60
Q

K efflux allows for ____

A

rapid membrane repolarization

61
Q

t/f without the K efflux, Na channels would not return to the rest state, which would prevent AP and contraction

A

t

62
Q

the rate of efflux of K from cardiac myocytes determines ___ and ____

A

AP duration (APD) and the refractory period

63
Q

how can blocking some K channels help in the treatment of arrhythmias?

A

will prolong AP and the time between ventricular contractions

64
Q

class 3 anti-arrhythmetic drugs target the ____ channels to prolong AP, primarily in the ____ myocytes

A

K; ventricular

65
Q

class 3 anit-arrhythmia drugs cause the lengthening of teh ____ interval on an ECG

A

QT

66
Q

amiodarone belongs to which class of arrhythmia drugs?

A

class 3 (K channel blocker)

67
Q

what is a complication that presents with class 3 drugs?

A

most also have other anit-arrhythmia actions

68
Q

Amiodarone also has anti-arrhythmic effects on ____ and ___ channels and on ____ receptors in addition to blocking K channels

A

Na; Ca; B

69
Q

amiodarone prolongs teh ____ interval of the ECG

A

QT

70
Q

what are some of the serious side effects of amiodarone ?

A

hepatic and pulmonary toxicity , thyroid hormone dysfunction (pts need to be monitored closely)

71
Q

why does amiodarone cause thyroid hormone dysfunction?

A

amiodarone has 2 iodines in its structure and bc the thyroid is the only organ that messes with iodine, amiodarone can interfere with the conversion of T4 to T3 and can impact TH production (sometimes causes hyper, sometimes hypo, how crazy)

72
Q

what is the wackiest ADRs of amiodarone?

A

its depsition in the skin and turning the skin greyish blue when exposed to sunlight (rare and typically in chronic use)

Pharmacology (49 decks)

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