Antiarrhythmics Flashcards

1
Q

FAST Cardiac AP

A

Cardiomyocyte (cardiac cells) action potential

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

FAST Cardiac AP

Phase 0

A

Rapid depolarization

Na+ channel opens → Na+ inward flow

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

FAST Cardiac AP

Phase 1

A

Begin repolarization

Na+ channel closes

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

FAST Cardiac AP

Phase 2

A

Plateau
Slow Ca2+ channels open → Ca2+ flows inward
Ø net ion movement

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

FAST Cardiac AP

Phase 3

A

Repolarization
Ca2+ channel close
K+ channel open → slow outward K+ efflux

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

FAST Cardiac AP

Phase 4

A

Pacemaker potential
Return to resting membrane potential
Diastole -90mV

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

SLOW Cardiac AP

A

Pacemaker action potential

SA/AV node

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

SLOW Cardiac AP

Phase 4

A

No resting membrane potential
Gradual depolarization
Slow inward Na+ & Ca2+ currents
Funny channels

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

SLOW Cardiac AP

Phase 0

A

Slower depolarization
Ca2+ mediated
Upstroke
Threshold -40mV

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

SLOW Cardiac AP

Phase 3

A

VGCa2+ channels close rapidly
↓Na+ permeability
↑K+ permeability → repolarization

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

Cardiac Pacemaker

A

SA node

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

NSR

A

Normal sinus rhythm

60-100bpm (70-80)

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

AV Node Conduction Rate

A

40-60bpm

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

Purkinje Fibers Intrinsic Rate

A

15-40bpm

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

Arrhythmia

A

Disturbance in the heart electrical activity

Atrial, junctional, or ventricular

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

When to intervene & treat arrhythmias?

A

Arrhythmias → cardiac dysfunction

↑demand ↓CO → hemodynamic compromise

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

Arrhythmia Types

Altered Automaticity

A

Latent pacemaker cells take over the SA node role → ectopic beats

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

Arrhythmia Types

Delayed After-Depolarization

A

Normal cardiac cell AP triggers abnormal depolarizations

Repetitive discharge or arrhythmias

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

Arrhythmia Types

Re-Entry

A

Refractory tissues reactivated repeatedly & rapidly d/t unidirectional block → causes abnormal continuous circuit

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

Arrhythmia Types

Conduction Block

A

Impulse fail to propagate in non-conducting tissues d/t ischemia, scarring, fibrosis (damaged tissue)

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

Non-Pharmacological Arrhythmia Treatments

A
Acute:
- Vagal maneuvers
- Cardioversion
Prophylactic:
- Radiofrequency catheter ablation
- Implantable defibrillator
Pacing - external, temporary, or permanent
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
22
Q

Class I Antiarrhythmics

A

Phase 0 Na+ channel blockers → decreases AP propagation (depolarization rate) & slows conduction velocity
Sub-classes IA/B/C

Used to treat SVT, Afib, & Wolfe-Parkinson White

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

Class IA

A

Disopyramide (Norpace), Procainamide (ACLS), & Quinidine

Slow conduction velocity & pacemaker rate
Intermediate Na+ channel blocker (dissociation) ↓depolarization rate
Direct depressant effect on SA/AV node
↑AP duration

Used to treat atrial & ventricular arrhythmias

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

Class IA Prototype

A

Quinidine

No longer manufactured

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
25
Disopyramide (Norpace)
Class IA Suppresses atrial & ventricular tachyarrhythmias PO route Significant myocardial depression & potential to precipitate CHF & HoTN
26
Procainamide
Class IA 1° used to treat ventricular tachyarrhythmias (less effective w/ atrial) ACLS
27
Procainamide PK
15% protein binding | Elimination 1/2 time 2hrs
28
Procainamide Dose
Load 100mg IV Q5min until rate controlled Max 15mg/kg Followed by 2-6mg/min infusion
29
Procainamide SE
Myocardial depression → HoTN Syndrome that resembles lupus erythematous Monitor blood levels*
30
Therapeutic Procainamide Levels
4-8mcg/mL
31
What drugs replaced IA drugs? Why?
Class IC | Toxicity potential to precipitate heart failure
32
Class IB
Lidocaine, Mexiletine, & Phenytoin ``` Fast Na+ channel blocker (dissociation) Inhibits Na+ ion influx Minimal effect on max velocity depolarization rate Shortens AP duration & refractory period ↓automaticity ```
33
Lidocaine
Class IB prototype | Used to treat ventricular arrhythmias; particularly effective to suppress re-entry rhythms (Vtach, fibrillation, PVCs)
34
Lidocaine PK
50% protein binding Extensive 1st pass effect Hepatic metabolism w/ active metabolite that prolong elimination 1/2 time 10% renal elimination
35
Lidocaine Dose
1-1.5mg/kg IV Infusion 1-4mg/min Max dose 3mg/kg
36
Lidocaine SE
Toxicity HoTN, bradycardia, seizures, CNS depression, drowsiness, dizziness, lightheaded, tinnitus, confusion, apnea, myocardial depression, sinus arrest, heart block, ventilatory depression, cardiac arrest, potential to augment pre-existing neuromuscular blockade
37
Mexiletine
Class IB PO agent Chronic ventricular tachyarrhythmias suppression - Consider cardiac clearance prior to surgery 150-200mg Q8H Amine group avoids hepatic 1st pass metabolism
38
Phenytoin (Dilantin)
Class IB Used to suppress ventricular arrhythmias associated w/ dig toxicity, other ventricular tachycardias, or torsades de pointes
39
Phenytoin PK
``` IV mix in NS (precipitates in D5W) Pain or thrombosis when admin in peripheral IV Rapid infusion → HoTN Hepatic metabolism; renal excretion Elimination 1/2 time 24hrs ```
40
Phenytoin Dose
1.5mg/kg IV Q5min up to 10-15mg/kg
41
Phenytoin SE
CNS disturbances, partially inhibits insulin secretion, bone marrow suppression, nausea Associated w/ Stevens-Johnson syndrome Toxicity - CNS symptoms, vertigo, ataxia, slurred speech
42
Therapeutic Phenytoin Levels
10-18mcg/mL
43
Class IC
Flecainide & Propafenone Slow Na+ channel blocker (dissociation) Potent ↓depolarization rate (phase 0) & conduction rate ↑AP & shortens AP duration Suppresses SA node w/ marked His-Purkinje conduction inhibition Used to treat PVCs or Vtach & atrial Wolfe-Parkinson White
44
Class IC Prototype
Flecainide PO agent Used to suppress PVCs, ventricular tachycardia, atrial tachyarrhythmias, Wolf-Parkinson White syndrome Pro-arrhythmic SEs
45
Propafenone
Class IC PO agent Suppresses ventricular & atrial tachyarrhythmias Pro-arrhythmic SEs
46
Class II Antiarrhythmics
β adrenergic blockers (phase 4) ↓SA node discharge → slows HR ↓myocardial oxygen requirements Slower conduction via atrial tissues & AV node → prolonged PRI interval ↑AP duration ↓automaticity Used to treat SVT, atrial (fib or flutter) & ventricular arrhythmias, suppress & treat ventricular dysrhythmias during MI & reperfusion, tachyarrhythmias 2° dig toxicity Propranolol, Esmolol, Metoprolol, & -olols
47
Class II Prototype
Propranolol Non-selective β adrenergic antagonist Used to prevent supra-/ventricular tachyarrhythmias reoccurrence precipitated by sympathetic stimulation ↑SA node conduction
48
Propranolol PK
Onset 2-5min Peak 10-15min DOA 3-4hrs Elimination 1/2 time 2-4hrs
49
Propranolol SE
``` ↓HR, contractility, CO ↑SVR & coronary vascular resistance Improved filling ↓MVO2 Bronchoconstriction ```
50
Metoprolol
Class II | Selective β1 antagonist
51
Metoprolol Dose
5mg IV over 5min | Max dose 15mg over 15min
52
Metoprolol PK
Onset 2.5min DOA 3-4hrs Hepatic metabolism Okay in mild CHF
53
Esmolol
Class II | Selective β1 antagonist
54
Esmolol Dose
0.5mg/kg IV bolus over 1min | Infusion 50-300mcg/kg/min
55
Esmolol DOA
< 10min | Hydrolysis via plasma esterases
56
Esmolol SE
Effects HR w/o significantly ↓BP (in small doses)
57
Class III Antiarrhythmics
K+ channel blockers (phase 2/3) Prolongs cardiac depolarization ↑AP duration & lengthens repolarization Used to treat supra- & ventricular arrhythmias, prophylaxis in cardiac surgery patients w/ Afib, control rhythm in Afib, preventative therapy in patients not candidates to receive internal cardiac defibrillator Amiodarone, Sotalol. Dofetilide, & Ibutilide
58
Class III Prototype
Amiodarone Class I, II, & IV antiarrhythmic properties K+/Na+/Ca2+ channel blocker α & β adrenergic antagonist Used in prophylaxis or treatment atrial & ventricular arrhythmias (refractory SVT/Vtach/Vfib or atrial fibrillation)
59
Amiodarone PK
``` Extensive protein binding 96% Lipophilic w/ large Vd Prolonged elimination 1/2 life 29 days Hepatic metabolism w/ active metabolite Biliary & intestinal excretion ```
60
Amiodarone Dose
Bolus 150-300mg IV over 2-5min up to 5mg/kg | Followed by 1mg/hr infusion x6hrs then 0.5mg/hr x18hrs
61
Amiodarone SE
``` Pulmonary toxicity/edema ARDS Photosensitivity rashes Grey/blue skin discoloration Thyroid abnormalities Corneal deposits CNS/GI disturbances Pro-arrhythmic effects (Torsades de pointes) Heart block HoTN Sleep disturbances Abnormal LFTs Inhibits hepatic P450 ```
62
Therapeutic Amiodarone Level
1-3.5mcg/mL
63
What's the 1st line Vtach or Vfib treatment when resistant to electrical defibrillation?
Amiodarone
64
Sotalol
Class II/III Non-selective β adrenergic antagonist & K+ channel blocker *Caution in patients w/ asthma Used to treat severe sustained ventricular tachycardia & Vfib, prevent tachyarrhythmias reoccurrence, especially atrial fib & flutter Renal excretion
65
Sotalol SE
``` Prolonged QT interval Bradycardia Myocardial depression Fatigue Dyspnea AV block ```
66
Dofetilide & Ibutilide
Class III Used to convert atrial fib or flutter to NSR & maintenance NSR after conversion Pro-arrhythmic prolongs QT interval
67
Class IV Antiarrhythmics
Calcium channel blockers (phase 2) block slow Ca2+ channels Used to treat vascular (angina, HTN, pulm HTN, cerebral artery spasm, Raynaud, migraine) & non-vascular conditions (asthma, esophageal spasm, dysmenorrhea, premature labor) Verapamil, Diltiazem, & Nifidipine
68
Ca2+ Ion Channels | Locations
- Skeletal muscle cell membranes - Vascular smooth muscle - Cardiac muscle - Mesenteric muscle - Neurons - Glandular cells
69
Ca2+ Channel Blockers | MOA
Bind to the receptor on VGCa2+ ions to maintain the channels in an inactive or closed state Block slow Ca2+ channels → decreases conduction through the AV node and shortens phase 2 (ventricular myocytes AP plateau) Interfere with inward Ca2+ ion movement across myocardial & vascular smooth muscle cells - Primary site at AV node ↓heart contractility
70
Ca2+ Channel Blockers | Subtypes
L, T, N, & P channels
71
L-type Ca2+ channel determines ______
Vascular tone & cardiac contractility | ↓Ca2+ keeps intracellular Ca2+ levels low
72
Ca2+ Channel Blockers | CV Effects
↓contractility/inotropy ↓HR ↓SA node activity ↓conduction rate & impulses via AV node → vascular smooth muscle relaxation ↓SVR & BP (arterial > venous)
73
Ca2+ channel blockers are used to treat:
- SVT & ventricular rate control in A fib & A flutter - Used to prevent SVT reoccurrence NOT used to treat ventricular arrhythmias
74
Class IV Prototype
Verapamil - Synthetic papaverine derivative - Less vasodilation
75
Verapamil 1° Action Site
AV node - Depresses the AV node - Negative chronotropic effect on SA node - Negative inotropic effect on myocardial muscle - Moderate vasodilation on coronary as well as systemic arteries
76
Verapamil Clinical Usages
SVT, vasospastic angina pectoris, HTN, hypertrophic cardiomyopathy, maternal & fetal dysrhythmias, premature labor onset
77
Verapamil PK
Highly protein bound PO absorption w/ extensive hepatic 1st pass Active metabolite - Norverapamil Renal & bile excretion (urine almost unchanged) Oral peak 30-45min IV peak 15min Elim 1/2 time 6-12 hours
78
Verapamil SE
Myocardial depression, HoTN (treatment = 1G Ca2+ gluconate), bradycardia, constipation, nausea, potentiates NMB effects LA activity or toxicity w/ regional
79
Verapamil Dose
2.5-10mg IV over 1-3min (max dose 20mg) | Continuous infusion 5mcg/kg/min
80
Do NOT administer Verapamil IV w/ ______
β blocker
81
Verapamil Drug Interactions
Verapamil & β-blockers → heart block Verapamil ↑LA toxicity risk Verapamil & Dantrolene → hypokalemia d/t slowing inward K+ ions movement → CV collapse
82
Diltiazem
Class IV Benzothiazepine derivative Principle action site = AV node Intermediate potency b/w Verapamil & Nifedipine Minimal CV depressant effects Used to treat SVTs & HTN
83
Diltiazem Clinical Usages
SVT, vasospastic angina pectoris, HTN, hypertrophic cardiomyopathy, maternal & fetal tachydysrhythmias
84
1st line SVT treatment
DILTIAZEM
85
Diltiazem PK
``` PO onset 15min Peak in 30min 70-80% protein bound Excreted via bile & urine (inactive metabolite) Elim 1/2 time 4-6 hours ``` ↑dose w/ hepatic disease Mixed cardiac & vascular effects - myocardial depression, HoTN, bradycardia, & constipation
86
Nifedipine
Class IV Dihydropyridine derivative Used to treat angina pectoris 1° action site = peripheral arterioles
87
Nifedipine PK
``` IV, PO, or sublingual PO effects in 20min Peaks in 60-90min 90% protein bound Hepatic metabolism Renal excretion Elim 1/2 time 3-7 hours ```
88
Nifedipine SE
Coronary & peripheral vasodilation (properties > Verapamil) Little to no effect on the SA or AV node ↓SVR & BP Reflex tachycardia → myocardial depression in patients w/ LV dysfunction or on β-blockers
89
Ca2+ Channel Blockers SE
Cancer w/ prolonged administration Cardiac problems → hear block Bleeding d/t platelet dysfunction GI constipation Vertigo, HE, flushing, HoTN, paresthesias, & muscle weakness Induce renal dysfunction Coronary vasospasm w/ abrupt discontinuation (slow wean to discontinue)
90
Ca2+ Channel Blockers | Drug Interactions
Myocardial depression & vasodilation w/ inhalational agents Potentiate NMBs Interact w/ Ca2+ mediated platelet dysfunction ↑plasma Digoxin concentration via ↓plasma clearance H2 antagonists (Ranitidine & Cimetidine) alter hepatic enzyme activity → potential to ↑Ca2+ channel blockers plasma levels
91
Ca2+ Channel Blockers Toxicity
↑chronotropy | Reverse w/ IV Ca2+ or Dopamine administration
92
What Ca2+ channel blocker has the greatest impact on coronary artery dilation?
Nicardipine Table 18-2 Ca2+ channel blocker pharmacologic effects (Verapamil, Nifedipine, Nicardipine, & Diltiazem)
93
Clevidipine
Class IV Dihydropyridine Blocks 1° L-type channels POTENT vasodilator Metabolism via plasma esterases → reflex tachycardia & rebound HTN when d/c
94
Clevidipine Dose
Bolus 1mg 1-2mg/hr double every 90sec MAX 20mg/hr (up to 32mg/hr short duration)
95
Clevidipine Onset
< 30 seconds
96
Clevidipine DOA
< 1 min
97
Class V Antiarrhythmics
Other (unclassified drugs) Different MOA - not on ion channels or unknown Adenosine, Digoxin, Phenytoin (Dilantin), Atropine, & Magnesium
98
Adenosine
Class V Acute treatment ONLY Used to treat SVT or diagnose V tach
99
Adenosine MOA
Binds to A1 purine nucleotide receptors (activates adenosine receptors to open K+ channels & ↑K+ currents) shortens AP Slows AV node conduction ↓excitability (hyperpolarization)
100
Adenosine PK
Elim 1/2 time < 10 seconds | Metabolism via plasma & vascular endothelial cell enzymes
101
Adenosine Dose
6mg IV rapid bolus 1st dose 60% effective Repeat after 3min 6-12mg 2nd dose 90% 20mL rapid flush via large bore PIV or central line *Access closest to the heart*
102
Adenosine SE
Facial flushing, headache, dyspnea, chest discomfort, bronchospasm, excessive AV or SA nodal inhibition, & nausea Contraindicated in asthma or heart block (slows AV node conduction)
103
Digoxin
Class V Cardiac glycoside Used to treat A fib or A flutter (controls ventricular rate) especially w/ impaired heart function
104
Digoxin MOA
↑vagal activity ↓SA node activity & prolongs conduction impulses via AV node ↓HR, preload, & afterload Slows AV conduction via ↑AV node refractory period Positive inotropy used to treat CHF
105
Digoxin PK
``` Onset 30-60min Elim 1/2 time 36 hours Narrow therapeutic index Weak protein binding 90% renal excretion ``` Reduce dose in elderly or renal impaired patients
106
Digoxin Dose
0.5-1mg in doses divided over 12-24 hours
107
Therapeutic Digoxin Level
0.5-1.2ng/mL
108
Digoxin SE
Arrhythmias, heart block, agitation, anorexia, nausea, diarrhea, confusion - Potentiated by hypokalemia & hypomagnesemia
109
Digoxin Toxicity Treatment
Phenytoin (ventricular arrhythmias) Pacing Atropine Maintain normal electrolyte levels
110
Magnesium
Class V MOA at Na+, K+, & Ca2+ channels Used to treat Torsades de pointes
111
Magnesium Dose
1 gram IV over 20min
112
Antiarrhythmic Agents
Used to prevent, suppress, or treat a disturbance in cardiac rhythm - A fib, A flutter, SVT, V tach, V fib, brady arrhythmias, heart block