Quiz 4: Antiarrhythmics Flashcards
1
Q
What occurs at phase 0 during cardiac action potential:
A
- RAPID DEPOLARIZATION
- Action potential is initiated by an increase in Na+ conductance through ion-specific fast channels
2
Q
What occurs at phase 1 during cardiac action potential:
A
- EARLY RAPID RE-POLARIZATION
- Na+ permeability is rapidly inactivated over 1-2 ms
- The cell starts to repolarize
3
Q
What occurs at phase 2 during cardiac action potential:
A
- PLATEAU
- Repolarization is delayed by an increase in conductance of Ca++ through slow channels
- Maintains Vm at +10 to -20 mV for over 100ms
4
Q
What occurs at phase 3 during cardiac action potential:
A
- RAPID REPOLARIZATION
- Complete repolarization due to inactivation of Ca++2 conductance and an increase in K+ permeability
5
Q
What occurs at phase 4 during cardiac action potential:
A
- SPONTANEOUS DEPOLARIZATION
- Slow depolarization characteristic of all pacemaker cells
- Results from a complex interaction between inward and outward currents of Ca +2 and K+ during diastole
6
Q
Ion specific channels that are SLOW channels mediated by _______.
A
-Ca+2
7
Q
Slow conduction velocity is a _____ mediated and is responsible for phase __ and affects the __ and __ nodes.
A
- Ca+2
- 0
- SA
- AV
8
Q
Prolongs refractory period is a ___ mediated and contributes to phase __ in the ______ contractile cells.
A
- Ca+2
- 2
- ventricle
9
Q
Slow channels in cardiac electrophysiology affects phase __ in spontaneous depolarization.
A
0
10
Q
T/F: Slow channels in cardiac electrophysiology is facilitated by catecholamines.
A
TRUE
11
Q
Ion specific channels that are fast channels are mediated by __.
A
Na+
12
Q
Fast channels that are Na+ mediate in phase 0 are responsible for the rapid (sharp) upstroke in the _________ system and _____ and ______muscles.
A
- His-Purkinje
- atrial
- ventricular
13
Q
Na+ mediated cardiac channel have a SLOW conduction velocity.
A
FALSE (Na+ mediate cardiac channel have a FAST conduction velocity.)
14
Q
What is the difference in a comparison of a ventricular cell and the sinoatrial cell when considering the slow channel mediated activity?
A
-In ventricular cells Ca2 accounts for the plateau phase 2, while in S-A cells it is the prime determinant of initial depolarization phase 0.
15
Q
T/F: Cells that undergo phase 0 depolarization are automatic and capable of impulse generation.
A
FALSE (Cells that undergo phase 4 depolarization…)
16
Q
Factors that reduce automaticity at the higher pacemaker sites will _______ favor the movement of the pacemaker to lower sites.
A
-passively
17
Q
What factors will reduce automaticity at the higher pacemaker sites to passively favor the movement of the pacemaker to the lower sites?
A
- Vagal influences
- digitalis drugs
- parasympathomimetic drugs
- Halothane
18
Q
Ectopic foci result from enhanced automaticity at a site outside the SA node and are called ____ ___.
A
-Ectopic pacemaker
19
Q
What factors influence the ectopic pacemaker?
A
- Sympathomimetic influence
- Hypercarbia
- Hypoxia
- Dig. Toxicity
20
Q
For a re-entry arrhythmia to occur what must happen?
A
- Unidirectional block of impulse conduction (area of injury)
- Slow conduction
- Impulse finds the unidirectional block repolarized and able to conduct the impulse retrograde
- Impulse reactivates the alternate pathway and repeats the process
21
Q
Pharmacologic arrhythmia management relies upon the different ion channels responsible for impulse generation in the __ and __ versus the __ and __ nodes
A
- atria
- ventricles
- SA
- AV
22
Q
The Na+ channel drugs effect the ion channel where in the heart?
A
- Atria
- Ventricle
23
Q
The Ca++ channel drugs effect the ion channel where in the heart?
A
- SA node
- AV node
24
Q
Class I antiarrhythmic drugs mechanism of action:
A
- inhibits fast Na+ channels
25
What drugs fit within the antiarrhytmic drug class of I:
- IA: Quinidine, Procainamide, Disopyramide, Moricizine
- IB: Lidocaine, Mexilitine
- IC: Flecainide, Propafenone
26
Class II antiarrhythmic drug's mechanism of action is:
-Decrease rate of depolarization
27
What type of drugs fit within the antiarrhythmic class of II:
-Beta Blockers
28
Class III antiarrhythmic drug's mechanism of action is:
-Inhibit potassium ion channels
29
What type of drugs fit within the antiarrhythmic class of III:
- Amiodarone
- Sotalol
- Ibutilide
- Dofetilide
- Bretylium
30
Class IV antiarrhytmic drug's mechanism of action is:
Inhibit slow calcium channels
31
What type of drugs fit within the antiarrhythmic class of IV:
- Diltiazem
| - Verapamil
32
A sodium channel blocker is what class and how does it exactly work?
- Class I
| - Slow conduction and prolong the QRS complexes in the atria and ventricles
33
A calcium channel blocker is what class and how does it exactly work?
- Class IV
| - Slow the atrial rate (SA node effect) and slow conduction through the AV node (Prolonging the PR interval)
34
A potassium channel blocker is what class and how does it exactly work?
- Class III
- 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 de Pointes)
35
How does class Ia effect the action potential:
- slows phase 0 (Na channel blockade)
| - Prolongs phase 3 (K channel blockade)
36
How does class Ib effect the action potential:
- Slows phase 0 (Na channel blockade)
| - Shortens phase 3 (K channel promoter)
37
How does class Ic effect the action potential:
- Very slow phase 1
| - NO effect phase 3
38
How does class II effect the action potential:
-Reduces slope of 4
| Decreases heart rate
39
How does class III effect the action potential:
-Prolongs phase 3
| Blocks K+ ion Channel
40
How does class IV effect the action potential:
-Reduces slope of 4
| Calcium channel blocker
41
Which class has a less powerful sodium channel blocker? Class Ia or Class Ib
-Class Ib
42
What class of antiarrhythmic is associate with more of a prodysrhythmic effect?
-Class Ic
(Flecainide and Propafenone)
-Could consider Class III
43
What does Amiodarone and Sotalol block:
- Sodium channels (Class I )
- Beta Blockade (Class II)
- Calcium channel blockade (Class IV)
44
What are the two unclassified antiarrhythmic drugs?
- Adenosine
| - digoxin
45
What is prodysrhytmic effect?
-Brady/tachydysirhythmias that represent new cardiac dysrhytmias associated with chronic antidysrhytmic drug treatment.
46
What are the types of prodysrhytmic effects?
- Torsades de pointes
- Increased ventricualr tachycardias
- Wide Complex ventricular rhythm
47
What causes Torsades de Pointes?
-K channel blockade may prolong the QT interval and induce triggered activity in the ventricle causing polymorphic VT or ventricular fibrillation
48
What class block K+ and prolongs QTc interval?
- Class Ic
| - Class III
49
What are the predisposing factors for torsades:
DECREASE
- K+
- Mg++
- slow heart rate
- Pre-existing long QT interval
50
What is the treatment of Torsades??
- D/C the offending agent
- Correction of electrolyte
- Administer Mg++ 2 grams
- Increase HR with pacing or isoproterenol
- Cardiovert only if hemodynamically compromised
51
Incessant Ventricular Tachycardia is usually brought on by what class(es) of antiarrhythmics used:
- Ia
| - Ic
52
Wide complex ventricular rhythm are associated with what class?
-Ic
53
What are the goals of using antirrhytmic drugs:
- restore NSR
- Abolish ectopic beats
- control the heart rate
54
What would be some easily reversible conditions for the treatment of arrhythmias:
- Hypoxia
- Acidosis
- Hypercarbia
- Electrolyte imbalances
- Alkalosis
- Temperature
55
What does Halothane do to the heart?
-Makes it sensitive to catecholamine
56
What do inhalational agents do to the heart?
-affect conduction and cause junctional rhythms
57
What muscle relaxants are vagolytic:
- pancuronium
| - gallamine
58
What does succinylcholine do after repeated doses do to the heart:
- Cause SB
- Junctonal rhythms,
- ventricular arrhythmias
- asystole
59
What may be the first signs of ischemia with the heart?
- PVC
| - conduction changes
60
Yes/No: To increase the heart rate to an anesthetized patient you could give Pancuronium or gallamine.
YES
61
T/F: Intra-op bradycardia can be handled using a beta antagonist or a cholinergic agent.
FALSE (... Handled using a beta agonist or a anticholinergic agent.)
62
Intra-Op SVT cardioversion is needed if SBP < __ .
80
63
What type of drug would be avoided if patient has a AV reciprocating SVTs arise from reentrant circuits that involve accessory pathways (WPW or Pre-excitation).
-Class II
(Beta blockers)
-Class IV
(Diltiazem and verapamil)
64
What drugs would work for a patient that has a AV reciprocating SVTs arise from reentrant circuits that involve accessory pathways?
- Adenosine
- Procainamide (Class Ia (WPW))
- Flecainide??
65
What are nonsustained VT:
- 3 or more PVC
- Rate exceeding 100 beats/min
- Last 30 seconds or less
- without hemodynamic compromise
- Preserved ventricular function, not predivitve of serious VT, no Tx. needed
- Evaluate and treat potential etiologies
- Poor LV function or severe LVH, prophylaxis with lidocaine
66
What drug would be given in Polymorphic VT:
- Class Ib (Lidocaine)
| - phenytoin
67
What drug would be give in sustained VT or VF:
- Class Ib (lidocaine)
- Class Ia (procainamide)
- Class III (Amiodarone)
68
What is the mechanism of action of procainamide:
- Class Ia
- Na+ and K+ channel blocker
- PREVENT reenty by converting unidirectional to bidirectional block
- Depresses automaticity by decresing the slope of phase 4 depolarization, increases refractoriness
69
What would be the indication for procainamide:
- ventricular tachydysrhythmias and atrial tachycardia in the presence of accessory pathways
- SVT
- A. Fib
- PVC
- VT
70
What drug toxicity results in the systemic lupus erythematosus like syndrome possible with chronic administration.
-Procainamide
71
Lidocaine is a __ channel blocker.
Na
72
T/F: Lidocaine is the first choice for supraventricular arrhythmias.
FALSE (..first choice for ventricular arrhythmias.)
73
Lidocaine is _____ against Supraventricular arrhythmias.
ineffective
74
What phase does lidocaine work in and where at can the effects be seen?
- Decrease phase 4
| - Purkinje fibers
75
What does lidocaine toxicity do to the CNS and CV system?
-CNS: depression to stimulation
-CV: depress LV function in preexisting LV dysfunction
CV:RARELY cause further slowing in patients with sinus bradycardia
76
Phenytoin is a __ channel blocker.
Na
77
Phenytoin _____activity triggered by digitalis induced after depolarization in purkinje fibers.
-abolishes
78
What drug would you use for ventricular dysrhythmias assoociated with digitalis toxicity.
Phenytoin
79
What is the problem with phenytoin when administered through a peripheral IV?
-Highly alkaline and can cause phlebitis
80
Phenytoin administered rapidly will cause:
- respiratory arrest
- severe hypotension
- Ventricular ectopy
- DEATH
81
What will phenytoin toxicity do to the CNS?
-Drowsiness, nystagmus, nausea, vertigo
82
T/F: Flecainide is used to treat WPW.
TRUE
83
What are the side effects of Flecainide?
- Moderate negative inotropic effect
- Vertigo
- Difficulty in visual accommdation
84
Propranolol toxicity includes:
- Profound bradycardia or asystole
- LV failure
- Acute bronchospasm
85
Amiodarone may ______ beta blockers and Ca++ channel blocker.
potentiate
86
T/F: Amiodarone would work in suppression of tachydysrhythmias associated with WPW.
TRUE
87
Where does amiodarone accumulate in the body?
Thyroid
88
Is Amiodarone lipid soluble or not?
Soluble
89
What is the half life of Amiodarone?
-Weeks to months
90
What are the toxicity of amiodarone?
- RESP: ARDS, pulmonary fibrosis
- CV : bradycardia, hypotension, dysrhythmias, heart failure, heart block, sinus arrest
- HEME: coagulation abnormalities
- Hepatic: increase in LFT and liver failure
- ENDO: hypo/hyperthyroidism
91
Dronedarone (MULTAQ) is just like ___ and is used for ____ and is ONLY administered __.
- amiodarone
- A. FIB
- PO
92
T/F: Verapamil has NO effeccct on accessory tracts.
TRUE
93
Digoxin slows the ventricular response rate in ____ but, enhances conduction through _______ pathways which can lead to increase ventricular response in __.
- A. Fib.
- accessory
- WPW
94
Digoxin inhibits what:
-Na+/K+ ATPase pump
95
Adenosine has what type of receptor?
-adenosine (A1 receptor)
96
What will methylxanthine do to adenosine?
-inhibits adenosine by binding to the A1 receptor
97
Dipyridamole will do what to adenosine?
-Potentiate adenosine effects by being an adenosine uptake inhibitor.
98
What will be seen with adenosine toxicity?
- Facial flushing
- dyspnea
- chest pressure most common but subsides in < 60 seconds
- May exacerbate bronchoconstriction in asthmatic.
