Brainscape's Knowledge GenomeTM

Browse over 1 million classes created by top students, professors, publishers, and experts.


See full index

CV Exam III > PHARMACOLOGYOFANTIARRHYTHMICS > Flashcards

PHARMACOLOGYOFANTIARRHYTHMICS Flashcards

1
Q

Class Ia: Na+Channel Blockers

A

Disopyramide(Norpace)

Quinidine

Procainamide*

double quarter pounder

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Class Ib: Na+Channel Blockers

A

Lidocaine(Xylocaine)*

Mexiletine

Tocainide

lettuce may tomato

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

Class Ic: Na+Channel Blockers

A

Moricizine

Flecainide(Tambocor)

Propafenone(Rythmol)

more fries please

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

Class II: β-Adrenergic Receptor Blockers

A

Esmolol(Brevibloc)*

Metoprolol (Lopressor, Toprol XL)*

Propranolol (Inderal)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

Class III: K+Channel Blockers

A

Amiodarone(Cordarone)*

Bretylium

Dofetilide(Tikosyn)

Ibutilide

Sotalol(Betapace)

a big dog is scary

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

Class IV: Ca2+Channel Blockers

A

Verapamil(Calan)*

Diltiazem (Cardizem)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Other ACLS Drugs

A

Adenosine

Atropine

Anticoagulants

Digoxin

MgSO4

Naloxone (Narcan)

Vasopressors

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

AV node slows done bc

A

calcium channels

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

TRANSMEMBRANE POTENTIAL

A

Resting membrane potential determined by concentrations of ions
Sodium (Na+), Potassium (K+), Calcium (Ca2+), Chloride (Cl-)

Ions unable to cross lipid membrane

Electrical gradient
-90 mV inside, 0 mV outside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

Na flow

A

chemical and electrical flow inside

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

K flow

A

electrical in and chemical out

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

CELL MEMBRANE

A

Depolarization opens the activation (m) gates

If inactivation (h) gates have not already closed, the channels are open and activated

Opening brief; open (m) gates very quickly followed by closure of (h) gates and channel inactivation

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

na channel blockers are state dependant and bind the

A

activated and inactivated states.

binds when activated or extending inactivated state so both are prolonging the ap duration and not alowing the na channel to open and fire again

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Cell depolarization

Phase - 0

A

rapid depolarization

abrupt increase in na permeability

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Cell depolarization

Phase - 1

A

brief repolarization

transient k efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

Cell depolarization

Phase - 2

A

plateau phase

ca influx balanced by k efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
17
Q

Cell depolarization

Phase - 3

A

repolarization

continued k efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
18
Q

Cell depolarization

Phase - 4

A

gradual depolarization

na leak balanced by k efflux

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
19
Q

ION MOVEMENTS DURING CONTRACTION

1

A

ca entry from outside the cell triggers the release of a much larger quanittiy of ca from the sr

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
20
Q

ION MOVEMENTS DURING CONTRACTION

2

A

increased ca conc initiates the contractile process

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
21
Q

ION MOVEMENTS DURING CONTRACTION

3

A

ca is removed by reuptake into the sr and by extrusion fro the cell by a ca/na exhanger

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

ION MOVEMENTS DURING CONTRACTION

4

A

sodium balance is restored by a na/k atapase

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
23
Q

Bundle of His and Purkinje fibers fast

A

Large Na+current

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
24
Q

P-wave

A

depolarization of atria

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Q

PR interval

A

AV nodal conduction time

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
26
Q

QRS

A

depolarization of ventricles, conduction time of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
27
Q

QT interval

A

ventricular action potential duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
28
Q

T-wave

A

repolarization of ventricles

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
29
Q

beta blockers cause heart block

A

increasing pr interval

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
30
Q

increasing qt interval causes

A

torsades

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
31
Q

Arrhythmias result from

A

Abnormal impulse generation

Triggered automaticity

Abnormal impulse conduction

Reentry

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
32
Q

Triggered automaticity

A

normal depolarization followed by an abnormal depolarization or beat

Early after depolarization –interrupts phase 3

Delayed after depolarization –interrupts phase 4 (from ca overload)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
33
Q

Abnormal impulse generation

A

Disturbance of impulse formation

Interval between depolarizations = duration of action potential + duration of diastolic interval (slope of phase 4)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
34
Q

Abnormal impulse conduction

A

Depressed conduction
Simple block
eg. AV nodal block, bundle branch block (beta blockers can cause this)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
35
Q

Reentry

A

Impulse reenters/excites areas of heart more than once

Must be an obstacle –establishes a circuit

Must be unidirectional block

Conduction time must be long enough that retrograde impulse does not encounter refractory tissues

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
36
Q

Anti-arrhythmic drugs can

A

Induce arrhythmias

Depress autonomic properties of abnormal pacemaker cell

Alter conduction characteristics of reentrant loop

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
37
Q

Anti-arrhythmic drugs

Induce arrhythmias

A

Must weigh benefits vs. risks

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
38
Q

Anti-arrhythmic drugs

Depress autonomic properties of abnormal pacemaker cell

A

Decrease slope of phase 4

Elevate threshold potential

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
39
Q

Anti-arrhythmic drugs

Alter conduction characteristics of reentrant loop

A

Facilitate conduction (shorten refractoriness)

Depress conduction (prolong refractoriness)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
40
Q

mechanisms that decrease spontaneous firing of pacemaker cell

A

Decreased phase 4 slope

increased threshold

increased maximum diastolic potential

increased action potential duration

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
41
Q

Decreased phase 4 slope

A

beta blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
42
Q

increased threshold

A

na and ca chanel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
43
Q

increased maximum diastolic potential

A

adenosine cause hyperpolarization

resting transmembrane is more negative so it takes more time to get to normal

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
44
Q

increased action potential duration

A

k chanel blockers

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
45
Q

k chanel blockers

A

increase refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
46
Q

CLASSIA NA+ CHANNEL BLOCKERS Overview

A

Disopyramide
Quinidine
Procainamide*

Proarrhythmic(TdP) (can increase QT)

Use-dependence
Open/inactivated channel binding
Block tissues more frequently depolarized (tachycardia)

Intermediate kinetics

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
47
Q

CLASSIA NA+ CHANNEL BLOCKERS General

A

slope of phase 0 is less and extend refractory period

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
48
Q

CLASSIA NA+ CHANNEL BLOCKERS Effects

A

Decrease Conduction Velocity

increase refractoriness

Decrease Autonomic Properties

49
Q

increase refractoriness is a

A

K channel blocking effect

50
Q

1a and 1c decrease

A

heart rate

51
Q

Procainamide effects

A

Slows upstroke of action potential, slows conduction, prolongs QRS, prolongs action potential duration
Extracardiac: ganglion-blocking

likley due to k blocking affect

52
Q

Procainamide PK

A

Metabolite N-acetylprocainamide(NAPA) with class III activity

hepaitcally metabolized and renally excreted, short half life

53
Q

Procainamide therapeutic Use

A

Atrial and ventricular arrhythmias

54
Q

Procainamide ADRs

A

Excessive APD prolongation, QT prolongation, reversible lupus erythematosus (~33%)

arthritis arthralagia
it is 2nd or third line

55
Q

CLASSIB NA+ CHANNEL BLOCKERS Overview

A

Lidocaine*
Tocainide
Mexiletine

Not for atrial arrhythmias, just ventricular rhythyms

Activated and inactivated channel binding

Rapid kinetics

56
Q

CLASSIB NA+ CHANNEL BLOCKERS effects

A

can decrease refractoriness

see effects at faster hr

57
Q

Lidocaine effects

A

Decreases action potential duration, shortens phase 3 repolarization

58
Q

Lidocaine pk

A

Extensive first-pass metabolism (3% bioavailable), given IV

Therapeutic levels: 2-6 mcg/mL (helps with infusion rates and side-effects)

decrease ap duration shortens phase 3 repolarization

59
Q

Lidocaine therapeutic use

A

DOC for termination of VT and prevention of VF after cardioversion in setting of acute ischemia or mi

60
Q

Lidocaine adrs

A

Least cardiotoxic but associated with neurologic (paresthesias, tremor, nausea, lightheadedness

levels greater than mcg/ml of what was previously stated

61
Q

CLASSIC NA+ CHANNEL BLOCKERS overview

A

Moricizine
Flecainide (used in afib)
Propafenone

High incidence of drug induced arrhythmias

Cannot be used in structural heart disease (results in increase mortality)

Slow kinetics

62
Q

CLASSIC NA+ CHANNEL BLOCKERS effects

A

decrease conduction vleocity significantly bc slow on and off, they slow phase 0 depolarization

63
Q

Flecainide overview

A

Blocks both Na+and K+channels but does not prolong action potential or QT interval

Therapeutic use:
Supraventricular arrhythmia

ADRs:
Severe exacerbation of arrhythmia

64
Q

Propafenone

A

Similar to flecainide+ β-blocking activity

65
Q

CLASSII Β-BLOCKERS overview

A 
Propranolol*
Esmolol*
Metoprolol

Decrease automaticity

Prolong AV conduction

Decrease heart rate and contractility

Decrease O2demand

66
Q

CLASSII Β-BLOCKERS therapeutic use

A 
Tachyarrhythmias
Atrial flutter
Atrial fibrillation
AV nodal re-entrant tachycardia
Hypertension
Heart failure
Ischemic heart disease
67
Q

CLASSII Β-BLOCKERS adrs

A

bradycardia, heart block, potential worsening of reactive airway disease (nonselective), cold extremities, fatigue, cardiac decompensation if heart relying on sympathetic drive (heart failure)

68
Q

Metoprolol pk

A

b1 selective

Onset of action: 1-2 hours (oral), 20 minutes (IV); t1/2: 3-4 hours

Significant first pass effect: 50%, CYP2D6 metabolism

69
Q

metoprolol toxicity

A

Similar to other B-blockers but with reduced risk of bronchospasm and diabetes

70
Q

Esmolol

A

B1-selective, ultra-short-acting

PK:
Onset of action: 2-10 minutes; duration of effect: 10-30 minutes
Metabolized by red blood cell esterases

71
Q

CLASSIII K+ CHANNEL BLOCKERS overview

A

Amiodarone*
Dofetilide
Sotalol

Diminish outward K+ during repolarization

Increase duration of action potential

Prolong effective refractory period

72
Q

CLASSIII K+ CHANNEL BLOCKERS effects

A

repolarization no effect of phase 0

73
Q

Amiodarone effects

A

Prolongs action potential duration (& QT interval), significantly blocks Na+channels, weak adrenergic and calcium channel blockade; broad activity

Extracardiac effects: peripheral vasodilation

74
Q

Amiodarone pk

A

Bioavailability: 35-65%; hepatic metabolism, major active metabolite

t1/2: 3-10 days (rapid component 50%), several weeks (slower component) (significant for drug interaction, so monitor closely (warfarin metabolism is decreased so you get more bleeding, so decrease warfarin)

Effect maintained 1-3 months after drug discontinued

75
Q

Amiodarone adr

A

Symptomatic bradycardia, heart block (those with preexisting AV node disease), accumulates in tissues, pulmonary toxicity (& fatal pulmonary fibrosis), abnormal LFTs, skin deposits, gray-blue skin discoloration (bc idodine is depsoited in skin it is part of the structure)

76
Q

Amiodarone ddi

A

MANY! CYP3A4 blockers (cimetidine) ↑ amiodarone levels; inducers (rifampin) ↓ amiodarone levels; reduce warfarin, statins, digoxin…33-50%

77
Q

CLASSIV CA2+ CHANNEL BLOCKERS

A

Verapamil
Diltiazem

Decrease inward Ca2+current

Decrease rate of phase 4 spontaneous depolarization

Slows conduction in Ca2+ dependent tissues(AV node)

Use dependent

78
Q

CLASSIV CA2+ CHANNEL BLOCKERS effects

A

block specific ca channel conformations

slow phase 4 spontaneous depolarization

79
Q

Verapamil effects

A

Blocks activated and inactivated L-type Ca2+ channels, slows SA node by direct action, suppresses both early and delayed afterdepolarizations
Extracardiac effects: peripheral vasodilation

80
Q

Verapamil pk

A

Bioavailability: 20% after oral administration

Extensively metabolized in the liver; t1/2: 7 hours

81
Q

Verapamil therapeutic use

A

SVT, decrease ventricular rate in AFiband AF, angina, HTN

supraventricular tachycardia

psvt

82
Q

Verapamil adr

A

Hypotension & VF if given to a patient with VT misdiagnosed as SVT; can induce AV block; constipation, lassitude, nervousness, peripheral edema

if you have ventricualr tachycardia

83
Q

OTHER ACLS DRUGS

A

Adenosine

Atropine

Digoxin

84
Q

Adenosine effects

A

Nucleoside, activates inward rectifier K+ current and inhibits Ca2+ current resulting in marked hyperpolarization and increased refractory period

85
Q

Adenosine pk

A

Metabolized in blood and tissue; t1/2: inosine >adenosine monophosphate and hypoxanthine

86
Q

Adenosine therapeutic use

A

DOC for conversion of paroxysmal SVT

87
Q

Adenosine adrs

A

Flushing, shortness of breath, chest burning, high grade AV block, atrial fibrillation, headache, hypotension, nausea, paresthesias

make sure you let pt know it will feel like they are having a heart attack while giving

88
Q

Atropine effects

A

Blocks actions of acetylcholine at parasympathetic sites, increases CO

89
Q

Atropine pk

A

30-50% excreted unchanged in the urine; t1/2: 2-3 hours

90
Q

Atropine therapeutic use

A

Bradycardia, neuromuscular blockade reversal, cholinergic poisoning

91
Q

Atropine adrs

A

Arrhythmia, tachycardia, dizziness, constipation, urinary retention

92
Q

Digoxin effects

A

Inhibits Na+/K+ATPase, results in positive inotropy, increased intracellular Na+, decreased Ca2+ expulsion, increased free Ca2+. Decreased HR, increased refractory period, decreased conduction velocity

93
Q

Digoxin pk

A

65-80% absorbed after oral administration

Not extensively metabolized, ~66% excreted unchanged by the kidneys. Must be dose adjusted in renal impairment

t1/2: 36-40 hours

positive inotropic

94
Q

Digoxin therapeutic use

A

AFib, SVT, heart failure

95
Q

Digoxin adrs

A

Nausea, vomiting, diarrhea, disorientation, visual disturbances, aberration of color perception, delayed afterdepolarization

yellow green halos in vision

96
Q

Type IA na channel blocker overall effects

A

Decrease conduction veloxcity

increase refractoriness

decrease autonomic properties

97
Q

Type IB na channel blocker overall effects

A

No effect on velocity

may decrease refractoriness

dissociate so quickly only effect fast hr

na channel blocker

98
Q

Type IC na channel blocker overall effects

A

Decrease conduction velocity

no effect on refractoriness

profound decrease in conduction velocity

99
Q

Type II Bblocker overall effects

A

Decrease conduction velocity

increase refractoriness

decrease autonomic properties

100
Q

type III K channel blocker overall effect

A

increase refractoriness

increase action potential duration

amiodarone has na beta blocker and ca blocker effects too

keep inside of cell more positive

101
Q

type IV Ca channel blocker overall effects

A

Decrease conduction velocity

Increase refractoriness

decrease autonomic properties

102
Q

TYPES OF ARRHYTHMIA

A

Supraventricular arrhythmias: originate above the Bundle of His; characterized by normal QRS complexes

Ventricular arrhythmias: originate below the Bundle of His

Conduction blocks: based on their level or location

103
Q

Supraventricular arrhythmias: originate above the Bundle of His; characterized by normal QRS complexes

A

Sinus bradycardia

Sinus tachycardia

Paroxysmal supraventricular tachycardia

Atrial flutter

Atrial fibrillation

Wolff-Parkinson-White

Premature atrial contractions

104
Q

Ventricular arrhythmias: originate below the Bundle of His

A

Premature ventricular contractions

Ventricular tachycardia

Ventricular fibrillation

105
Q

Conduction blocks: based on their level or location

A

Supraventricular: 1st, 2nd, or 3rddegree AV block

Ventricular: right or left bundle branch block

106
Q

ATRIAL FIBRILLATION overview

A

Depolarization from ectopic focus or re-entrant circuit impact atria. No single pacemaker in control. “Irregularly irregular

pass through av node randomly

107
Q

ATRIALFIBRILLATION acute treatment

A

IV CCB, BB, or digoxin

B-blockers (propranolol, metoprolol, esmolol) 1stchoice in high catecholamine states. Should not be used acutely in systolic heart failure.

Non-DHP CCB’s (verapamil, diltiazem) IV produce rapid effects 4-5 min.

Digoxin has much slower onset (max effect 6-8 hours), less effective than BB/CCB in increased sympathetic tone.

108
Q

ATRIAL FIBRILLATION chronic treatment

A

oral BB, CCB

Digoxin if intolerable side effects to others

109
Q

ATRIAL FIBRILLATION long term strategy

A

Rate control > rhythm control +/-anticoagulation (CHADS2score)

Rhythm control indications –continued symptoms with adequate rate control, rate not adequately controlled, or intolerable side effects

if converting to normal sinus rhythm you can get ppoing and thrombis int he heart and you get score locck for chads score

110
Q

ATRIAL FIBRILLATION chemical vs electrical cardioversion

A

Direct current cardioversion most effective

Chemical options: ibutilideIV, propafenonePO, flecainide PO, amiodarone PO/IV, dofetilidePO

111
Q

ATRIAL FIBRILLATION maintenance of nsr

A

FDA indication –flecainide, dofetilide*, dronedarone

Others –propafenone, amiodarone*

*safe to use in patients with HF

112
Q

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA(PSVT) overview

A

AV nodal re-entry

Valsalva maneuver

113
Q

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA(PSVT) acute treatment

A

IV adenosine (DOC), verapamil, or diltiazem

Alternative –BB or digoxin if others fail

114
Q

PAROXYSMAL SUPRAVENTRICULAR TACHYCARDIA(PSVT) chronic treatment

A

radiofrequency catheter ablation potentially curative

Drugs –verapamil, diltiazem, BB, or digoxin

115
Q

Verapamil not given in vtac

A

so adenosine is drug of choice bc it has short half life and does not lead to hemodynamic compromise like verapamil does

116
Q

PREMATURE VENTRICULAR CONTRACTIONS(PVCS)

A

Ventricular arrhythmias arise from irritable foci within ventricular myocardium

Asymptomatic: do not use class Icagents
CAST trial associated with ↑ mortality

B-blockers within first 24 hours after MI if no contraindications (improves survival)

normally dont treat unless they had mi

117
Q

SUSTAINED VENTRICULAR TACHYCARDIA

A

Hemodynamic instability: synchronous cardioversion

Stable VT patients: procainamide, sotalol, amiodarone

Implantable cardioverter/defibrillator for

118
Q

Implantable cardioverter/defibrillator for

A

Survivors of cardiac arrest caused by VF or hemodynamically unstable sustained VT

LVEF ≤ 35%, prior MI at least 40 days after event and NYHA Class II or III

LVEF ≤ 30%, prior MI at least 40 days after event and NYHA Class I

After ICD, prophylactic ablation or adjunctive anti-arrhythmic drugs may be necessary depending on number of discharges

119
Q

TORSADES DE POINTES

A

Hemodynamic compromise: electrical cardioversion

Hemodynamically stable: MgSO4
Alternative: class Ibagents

CV Exam III (17 decks)

Brainscape helps you reach your goals faster, through stronger study habits.
© 2024 Bold Learning Solutions. Terms and Conditions