Antiarrhythmics Flashcards
(114 cards)
1
Q
What do antiarrhythmic agents focus on?
A
Cardiac ion channels (Na, Ca, K)
Adrenergic receptors
2
Q
What is the receptor target for class IA drugs and what EKG changes will you see?
A
Na and K channels
QRS and QT prolonged
3
Q
What is the receptor target for class IB drugs and what EKG changes will you see?
A
Na channels
QRS prolonged
4
Q
What is the receptor target for class II drugs and what EKG changes will you see?
A
Beta receptors
PR prolonged
5
Q
What is the receptor target for class III drugs and what EKG changes will you see?
A
K channels
QT prolonged
6
Q
What is the receptor target for class IV drugs and what EKG changes will you see?
A
Ca channels
PR prolonged
7
Q
Which antiarrhythmics are class IA?
A
Procainamide
Amiodarone
Moricizine
8
Q
Which antiarrhythmics are class IB?
A
Lidocaine
Phenytoin
9
Q
Which antiarrhythmics are class II?
A
Esmolol Amiodarone Propranolol Atenolol Labetalol
10
Q
Which antiarrhythmics are class III?
A
Bretylium Ibutilide Amiodarone Sotalol Dofetilide
11
Q
Which antiarrhythmics are class IV?
A
Verapamil
Diltiazem
Amiodarone
12
Q
What is the resting membrane potential?
A
Resting transmembrane concentration gradients for K and Na are maintained by active ion pumps and selective membrane conductance
-90 mV
13
Q
T/F: Sarcolemma is more permeable to K than to Na
A
True
14
Q
What are the phases of the cardiac action potential?
A
Phase 0: rapid depolarization Phase 1: Early rapid repolarization Phase 2: Plateau Phase 3: Rapid repolarization Phase 4: Spontaneous diastolic depolarization
15
Q
What happens during phase 0?
A
Action potential is initiated by an increase in Na conductance through ion-specific fast channels
vM becomes positive quickly
16
Q
What happens during phase 1?
A
Na permeability is rapidly inactivated over 1-2 ms
The cell starts to repolarize
17
Q
What happens during phase 2?
A
Repolarization is delayed by an increase in conductance of Ca through slow channels
18
Q
What happens during phase 3?
A
Complete repolarization due to inactivation of Ca conductance and an increase in K permeability
19
Q
What happens during phase 4?
A
Slow depolarization characteristic of all pacemaker cells
Results from a complex interaction between inward and outward currents of Ca and K during diastole
20
Q
These channels are responsible for phase 0 is SA and AV nodes, contribute to phase 2 in ventricular contractile cells, and affects phase 4
A
Slow channels, Ca mediated
21
Q
These channels are responsible for phase 0 (sharp upstroke in the His-purkinje system and atrial and ventricular muscle, rapid conduction velocity
A
Fast channels, Na mediated
22
Q
T/F: cells that do no undergo spontaneous phase 4 depolarization are automatic and capable of impulse generation
A
False: cells that undergo spontaneous phase 4…
23
Q
Factors that reduce ___ at the higher pacemaker sites will ___ favor the movement of the pacemaker to lower sites
A
Automaticity
passively
24
Q
What are the vagal influences that contribute to automaticity?
A
Digitalis drugs
Parasympathomimetic drugs
Halothane
25
What must happen for re-entry to occur?
Unidirectional block of impulse conduction (area of injury)
Slow conduction via an alternate pathway
Impulse finds the unidirectional block repolarized and able to conduct the impulse retrograde
Impulse reactivates the alternate pathway and repeats the process
26
Where can re-entry occur?
SA node
Atrium (aflutter, afib)
AV node
Ventricle (VT)
27
What does pharmacologic arrhythmia management rely on?
The different ion channels responsible for impulse generation in the atria and ventricles versus the SA and AV nodes
28
Which ion channels are responsible for impulse generation in the atria and ventricles?
Na channels
29
Which ion channels are responsible for impulse generation in the SA and AV nodes?
Ca channels
30
Which class of antiarrhythmic drugs are calcium channel blockers?
Class IV
31
Which class of antiarrhythmic drugs block fast Na channel with or without K channel blockade
Class I
32
Which class of antiarrhythmic drugs are beta blockers?
Class II
33
Which class of antiarrhythmic drugs are K channel blockers?
Class III
34
Which drugs are in class IC?
Flecainide
| Propafenone
35
How do class II antiarrhythmics work?
Decrease rate of depolarization
36
What are the effects on the action potential for type IA drugs?
Slows phase 0, prolongs 3
37
What are the effects on the action potential for type IB drugs?
Slows phase 0, shortens 3
38
What are the effects on the action potential for type IC drugs?
Very slow phase 0, no 3 effects
39
What are the effects on the action potential for type II drugs?
Reduces slope of 4
40
What are the effects on the action potential for type III drugs?
Prolongs phase 3
41
What are the effects on the action potential for type IV drugs?
Reduces slope of 4
42
What is the mechanism of action of Procainamide?
Na & K channel blocker
Depresses automaticity by decreasing the slope of phase 4 depolarization, increases refractoriness
Prevent re-entry by converting unidirectional to bidirectional block
43
What are the indications for Procainamide?
Ventricular tachydysrhythmias and atrial tachycardia in the presence of accessory pathways
SVT, afib, PVCs, and VT
44
What happens if you rapidly infuse Procainamide?
Severe hypotension from myocardial depression and vasodilation
45
T/F: There is a toxic metabolite with Procainamide
True
46
S/S of toxicity of Procainamide
```
Myocardial depression
Hypotension
QRS complex and QT prolongation
Heart block
Ventricular ectopy
Systemic lupus erythematosus-like syndrome possible with chronic administration
```
47
What is the mechanism of action of Lidocaine?
Na channel blocker
| Decrease the slope of phase 4 depolarization in purkinje fibers, reduce automaticity
48
What are the indications for Lidocaine?
First choice for ventricular arrhythmias particularly re-entry dysrthymias (PVCs and vtach)
Ineffective against supraventricular arrhythmias
49
What is the therapeutic concentration of Lidocaine?
1.5-5 mg/L
50
What are the s/s of toxicity of Lidocaine?
CNS: depression to stimulation (convulsions)
CV: may depress LV performance in pre-existing LV dysfunction, rarely cause further slowing in patients with SB
51
What is the mechanism of action of Dilantin?
Na channel blocker
Depresses phase 4 diastolic depolarization
Abolishes activity triggered by digitalis-induced after depolarizations (automaticity) in Purkinje fibers
52
What are the indications for Dilantin?
Useful in the suppression of ventricular dysrhythmias associated with dig toxicity
Paradoxical vtach or torsades de pointes that is associated with prolonged QTc interval
53
Why do you have to administer Dilantin via a central line?
Drug is highly alkaline and can cause phlebitis when administered through a peripheral IV
54
What are the s/s of toxicity of Dilantin?
```
Rapid administration assoc. with resp arrest, severe hypotension, vent ectopy and death
Drowsiness
Nystagmus
Nausea
Vertigo
Other cerebella signs
```
55
What is the mechanism of action of Flecainide?
Depresses action potential phase 0
Prolongs QRS and to a lesser extent PR interval
May suppress SA node like BBs and Ca channel blockers
Delays conduction in bypass tracts
56
What are the indications for Flecainide?
Effective in suppressing PVS and vtach
| Atrial tachydysrhythmias including WPW (delays conduction in bypass tracts)
57
What are the side effects for Flecainide?
Moderate negative inotropic effect
Vertigo
Difficulty in visual accommodation
58
What is the mechanism of action with Propranolol?
Beta blockade leads to slowing of the SA node (decreased slope of phase 4 depolarization)
Slow the rate depolarization of ectopic pacemakers
Prolonged AV nodal conduction
Increased refractoriness of AV node
59
What are the indications for Propranolol?
Control of SVT
Convert atrial tachyarrhythmias to SR
Slow ventricular response to afib and flutter
60
What are the toxicity effects of Propranolol?
Primarily due to beta blockade
Profound bradycardia or asystole
LV failure
Acute bronchospasm
61
How do Type III Antiarrhythmic drugs (K channel blockade) work?
Interrupts reentry by slowing conduction or increasing the refractory period
Prolongs the QT interval and induces triggered activity in the ventricle causing polymorphic VT (torsades)
62
What is the structural analog of thyroid hormone?
Amiodarone
63
What is the mechanism of action for Amiodarone?
Potent inhibitor of abnormal automaticity
Prolongs the effective refractory period and action potential duration in all cardiac tissues including accessory bypass tracts (blocks inactivated Na channels and K movement, prolongs PR, QRS, and QT intervals)
May potentiate slowing of the SA node and AV conduction (may potentiate BBs and CCBs)
64
What are the indications for Amiodarone?
IV for the acute termination of ventricular and supraventricular arrhythmias
- Recurrent vfib or recurrent unstable vtach in pts unresponsive to or unable to tolerate other agents
- Effective in maintaining SR in patients with afib
- Suppression of tachydysrhythmias associated with WPW
65
What is the half life for Amio?
Prolonged t 1/2 of weeks to months in patients on the oral agent for several years
Omission of 1 or 2 doses unlikely to result in recurrence of arrhythmia
66
What are the toxicity effects of Amio?
```
-Resp: ARDS, pulmonary fibrosis
CV: bradycardia, hypotension, dysrhythmias, heart failure, heart block, sinus arrest
Heme: coagulation abnormalities
Hepatic: increased LFTs, liver failure
Endo: hypo or hyperthyroidism
```
67
What are you at risk for with Ibutilide (Corvert)?
Risk of prolonged QT
68
What are the indications for Corvert?
Conversion of afib/aflutter
Less hypotension than amio, but still prodysrhythmic
More rapid conversion that procainamide or sotalol
69
Are there renal and hepatic dosing adjustments of Corvert?
No
70
What is an alternative multichannel blocking antiarrhythmic?
Dronedarone (Multaq)
| Similar properties to amio but is structurally noniodinated
71
What is the indication for MULTAQ?
For a fib to maintain NSR
| Less efficacious but with less undesirable side effects or deaths
72
What are the contraindications for Dronedarone?
Increased risk of death stroke and heart failure in patients with decompensated heart failure or permanent afib
Second/third degree heart block, HR <50 bpm
Meds that inhibit CYP3A4, prolong QTc
Pregnancy
Significant liver disease
73
What is Sotalol?
Oral non-selective beta antagonist
Lengthens repolarization and effective refractory period in all cardiac tissues (prolongs action potential phase 3)
Lowers blood pressure
74
What are the uses for Sotalol?
PSVT
Vtach and vfib
Antihypertensive
75
How do calcium channel blockers work?
Inhibit inward slow Ca currents
| Slow the atrial rate (SA node effect) and slow conduction through the AV node (prolonging the PR interval)
76
What is the mechanism of action for Verapamil?
Selectively blocks slow channels by inhibiting the normal Ca influx into the cell
Slow channel activity is most important in SA and AV nodes (prolongs AV nodal conduction and refractoriness, depresses the rate of SA node discharge)
77
What are the indications for Verapamil?
Treat SVT
| Slow ventricular rate in afib and flutter
78
T/F: Verapamil has an effect on accessory tracts
False: No effect on accessory tracts
79
What are the toxicity side effects for Verapamil?
HYPOTENSION
Bradycardia, asystole, and AV block
Myocardial depression is uncommon in pts with reasonable LV function
80
What is the mechanism of action for Cardizem?
slow channel blocking prolongs AV nodal conduction and refractoriness
81
What are the indications for Cardizem?
Ventricular rate control in afib or aflutter
82
What is the mechanism of action for Digoxin?
Inhibits Na/K ATPase
Directly prolongs the effective refractory period in the AV node (slows the ventricular response rate in afib)
Indirectly increases vagal activity and reduces sympathetic activity
83
T/F: Digoxin enhances conduction through accessory pathways
True, can enhance ventricular response in WPW
84
What are the indications for Digoxin?
Ventricular rate control in afib, aflutter, and SVT
85
What are the toxicity side effects for Digoxin?
Alterations in cardiac rate and rhythm may stimulate almost every known rhythm disturbance but PVCs most common
86
What is the mechanism of action for Adenosine?
Activates K channels that hyperpolarize nodal tissue causing a transient 3rd degree AV block
- Less effect in the atrium
- Depression of the action potential in the AV node
- Methyxanthines inhibit the action of adenosine (bind to the adenosine receptor)
- Dipyridamole (adenosine uptake inhibitor) and cardiac transplantation (denervation hypersensitivity) potentiate adenosine's effects
87
What are the indications for adenosine?
Treatment of PSVT including those that involve accessory pathways
88
Is Adenosine useful in the treatment of arrhythmias originating distal to the AV node or afib or flutter?
No
89
What is the half life of Adenosine?
1.5 seconds
90
How is Adenosine inactivated?
By cellular uptake
91
What are the toxicity effects of Adenosine?
Facial flushing, dyspnea, and chest pressure most common but subside in <60 seconds
May exacerbate bronchoconstriction in asthmatic patients
92
What are the Prodysrhythmic effects?
Brady or tachydysrhythmias that represent new cardiac dysrhythmias associated with chronic antidysrhythmic drug treatment
93
What are the types of prodysrhythmic effects?
Torsades de pointes
Increased ventricular tachycardias
Wide complex ventricular rhythm
94
What is the mechanism of action of Torsades?
K channel blockade may prolong the QT interval and induce triggered activity in the ventricle causing polymorphic VT or vfib
95
What is the treatment of Torsades?
Discontinue the offending agents
Correct electrolyte disturbances
Give 2 gm Mag
Increase HR if low with temp pacing or isoproterenol
Cardiovert only if hemodynamically compromised
96
What is incessant ventricular tachycardia precipitated by?
Class IA and IC drugs that slow conduction of cardiac impulses sufficiently to create a continuous ventricular tachycardia circuit (re-entry)
97
What is wide complex ventricular rhythm associated with?
Class 1C drugs in the setting of structural heart disease
98
What are the treatment goals of antiarrhythmic drugs?
Restore NSR
Abolish ectopic beats
Control HR
99
What inhalational agent sensitizes the myocardium to catecholamines that can lead to ventricular arrhythmias
Halothane
100
Affect conduction and cause junctional rhythms
Inhalational agents
101
A repeated dose of this muscle relaxant can lead to SB, junctional rhythms, ventricular arrhythmias and asystole
Succinylcholine
102
What might be a first sign of myocardial ischemia under anesthesia?
PVCs or changes in conduction
103
What are some therapeutic alternatives to treating arrhythmias?
```
Slowing the HR
-Treat underlying cause
-Overdrive pacing
-DC shock for severe hemodynamic impairment
Increasing the HR
-Stop manipulation
-Pancuronium
-Isoproterenol gtt
-Pacing
```
104
What is the treatment for intra-op bradycardia?
Lighten anesthesia
Anticholinergic agent
Beta agonist
Pacemaker
105
What is the treatment for intraop SVT?
Cardioversion if SBP <80 and ischemia to prevent irreversible complications (MI, stroke)
Focus on reversible causes
106
T/F: Most intraop supraventricular tachyrhythms are hemodynamically unstable and cardioversion is needed
False, most are hemodynamically stable and don't need cardioversion
107
What is the drug therapy for intraop SVT?
Adenosine (useful for PSVT)
108
What is the drug therapy for orthodromic conduction (QRS complex <120 ms)?
Vagal maneuvers or AV nodal blocking agents
IV adenosine
DC cardioversion for hemodynamically unstable pt
109
What is the drug therapy for AVRT and antidromic conduction (wide QRS complex)?
Procainamide, Amio or Ibutilide, slow conduction over pathways
AV nodal blocking agents could induce VT/VF because they could increase conduction in the accessory pathway
DC cardioversion with hemodynamic instability
110
T/F: You want to avoid Procainamid, Amio and Ibutilide in patients with antegrade accessory pathway conduction
True
111
What is the drug therapy for afib/aflutter?
Controlling ventricular rate is the mainstay of therapy
-AV nodal blockers Class II or IV (esmolol, metoprolol, propranolol, diltiazem or verapamil)
-Tensilon or Neostigmine
-Dig
-Vagal maneuvers, over-drive pacing, DC cardioversion
Class IA or III drugs more likely to terminate the arrhythmia
112
Giving this prior to DC countershocks may improve chances of sustained cardioversion
IV procainamide or amio
113
What is the treatment of sustained VT or VF?
DC countershocks
| Resistant VT or VF: IV lido or procainamide, IV amio
114
How do you treat polymorphic VT?
```
Asynchronous DC countershocks in patients with hemodynamic collapse
-IV mg, K repletion, increase HR, class IB antiarrhythmic drugs
```
