Antidysrhythmics Flashcards

(90 cards)

2
Q

What are the 2 major mechanisms that cause ectopic cardiac dysrhythmias?

A

Automaticity

Reentry

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3
Q

What is automaticity in the myocardium?

A

The ability of the cardiac muscles to depolarize spontaneously without electrical stimulation from the nervous system.

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4
Q

The discharge rate of normal or abnormal pacemaker activity may be accelerated by what: (4)

A
  • Drugs
  • Various forms of cardiac disease
  • Reduced potassium
  • Alterations of autonomic nervous system tone
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5
Q

What does enhanced normal automaticity result in?

What does abnormal automaticity result in?

A

Sinus tachycardia

Accelerated idioventricular rhythm

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6
Q

Reentry is responsible for most of the clinically important arrhythmias, including a-fib, a-flutter, AV nodal reentry, AV reentry involving a bypass tract, ventricular tachycardia after MI, and v-fib. True or false?

A

True.

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7
Q

What are other underlying mechanisms that can cause dysrhythmias? (7)

A

Myocardial Ischemia
Hypoxemia
Bradycardia–>ventricular dysrhythmias
Hypokalemia, hypomagnesemia–>ventricular dysrhy.
Volatile agents and other drugs
Acid-Base Changes–>**alkalosis **
ANS Changes

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8
Q

What are the following antidysrhythmic classes?

Class I
II
III
IV

A

I. Membrane stabilizers

II. Beta blockers

III. Prolong repolarization

IV: Ca channel blockers

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9
Q

How do Class I agents work? (3)

A

Decrease automaticity

Decrease conduction through bypass tracts by blocking “fast” Na channels

Decrease Phase 0 depolarization

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10
Q

What is Phase 0?

A

Rapid depolarization via Na channels

Gates close when 0 mV reached

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11
Q

What is Phase 1?

A

Partial repolarization (K moves out the cell)

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12
Q

What is Phase 2?

A

Plateau (slow Ca movement into cell to neutralize K out)

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13
Q

What is Phase 3?

A

Rapid repolarization

(Ca channel close and K continues to move out unopposed)

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14
Q

What is Phase 4?

A

Resting phase, repolarization

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15
Q

The Class I drugs are the membrane stabilizers that block _______ channels thereby inhibiting Phase ___ .

A

Sodium

0

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16
Q

What do Class IA drugs do? (3)

A

Depress Phase 0 depolarization

Prolong action potential duration

Slow conduction velocity

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17
Q

What are the Class IA drugs? (3)

A

Procainamide

Disopyramide

Quinidine

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18
Q

When is QUINIDINE indicated? (3)

What class drug is it?

A
  • A-fib
  • WPW
  • PVC’s

Class IA

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19
Q

What do Class IB drugs do? (2)

A

Shorten AP conduction

Have little effect on Phase 0

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20
Q

What are the Class IB drugs? (3)

A

Phenytoin

Lidocaine

Tocainide

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21
Q

What do Class IC drugs do? (3)

A

Greatly depress Phase 0 depolarization

Minimally affect AP duration

Slow conduction

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22
Q

What class of agents bind most rapidly to the receptors?

What class of agents have the slowest binding and dissociation from the receptor?

A

Class IB

Class IC

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23
Q

What % of patients with a-fib taking quinidine, procainamide, and disopyramide will convert to NSR?

A

25%

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24
Q

Class IA drugs can be given IM and are preferred to be given IV? True or false?

A

False

Not IM because of pain.

Limited via IV because of vasodilation and myocardial depression can result.

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25
Q

What drug is effective in the treatment of acute and chronic supraventricular dysrhythmias?

A

Quinidine

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26
What are the side effects of quinidine? (5)
* Prolonged QT * Syncope or sudden death * Hypotension * Allergic reaction (itch, hives) * Diarrhea
27
We use quinidine in the OR. True or false?
False.
28
What EKG changes will indicate that quinidine should be discontinued or the dose should be decreased?
50% increase in QRS duration or heart block will ensue
29
What pts should not be prescibed quinidine? (2)
prolonged QT interval AV heart block
30
What are the indications for procainamide? (3)
* PVT * PVC * Ventricular dysrhythmias Note: Not as effective in treating atrial tachydysrhythmias as quinidine.
31
What are the side effects of procainamide? (5)
* **Myocardial depression** * **Hypotension (by direct myocardial depression)** * **Asystole or v-fib (heart block or high conc. of drug)** * Lupus-like symptoms (SLE-like syndrome) * Rash Note: SLE is systemic lupus erythematasous Also, incidence of side effects are high!
32
What are the indications for disopyramide?
Atrial and ventricular tachydysrhythmias
33
What is the adminiatration for disopyramide?
Oral
34
What is the mechanism of disopyramide? When is the peak effect?
Simiar to quinidine, membrane stabilizing 2 hours
35
What are the side effects of disopyramide? (3)
**Direct myocardial depression--precipitating CHF, hypotension** Anticholinergic activity--dry mouth, urinary hesitancy Prolonged QT and paradoxical VT
36
What are the indications for lidocaine relating to dysrhythmias? (2)
PVC V-tach Note: **Minimal atrial effects!**
37
Lidocaine has significant 1st pass metabolism. True of false?
True.
38
What is the dose for lidocaine? IV IM IV infusion rate
2 mg/kg 4 - 5 mg/kg 1 - 4 mg/min
39
What is the mechanism of lidocaine? (2)
Delays the rate of Phase 4 depolarization Blocks Na channels in depolarized tissues Note: Not able to alter rate of atrial cells so not good for atrial tach.
40
What are the side effects of lidocaine? (3) \> 5 mcg/ml (in plasma) 5-10 mcg/ml \> 10 mcg/ml
Stimulation of CNS Seizures, hypotension CNS depression, apnea, cardiac arrest
41
What are the indications for phenytoin? (3)
Paradoxical VT Torsade de Pointes Digitalis toxicity
42
How can phenytoin be administered? What is the IV dose? What is the max dose?
PO, IV 1.5 mg/kg q5 min or 10-15 mg/kg 1 gram
43
What is the mechanism of phenytoin? (2)
Shortens QT interval Improved conduction through the AV node Note: Similar effects are lidocaine, but more profound.
44
What drug shortens the QT interval more than any other drug?
Phenytoin
45
What are the side effects of phenytoin? (4)
Bone marrow suppression Increased blood sugar CNS disturbances: cerebellar symptoms Hypotension
46
What is the indication for MEXILETINE and TOCAINIDE?
V-tach
47
What is the mechanism of MEXILETINE and TOCAINIDE?
Similar to lidocaine
48
What are the side effects of MEXILETINE and TOCAINIDE? (2)
Epigastric burning Neurologic effects
49
ON BOARDS What are rare effects of TOCAINIDE? (2)
Bone marrow depression Pulmonary fibrosis
50
When is FLECAINIDE indicated? (3)
Atrial tachdysrhythmias WPW Ventricular premature beats (sometimes)
51
What is the mechanism of FLECAINIDE? (2)
AV conduction block Decreased SA node function
52
What are the side effects of FLECAINIDE? (4)
Moderate negative inotropic effect Prodysrhythmic effect Vertigo Visual accomadation problems
53
What drug is most effective at suppressing premature ventricular beats and v-tach?
FLECAINIDE
54
What are the indications for beta blockers? (4)
A-fib A-flutter Paroxysmal AT Digitalis induced ventricular dysrhythmias
55
What are the common beta blockers? (3)
Propanolol Metoprolol Esmolol
56
What is the mechanism of Class II (beta blocking) drugs? (3)
Block sympathetic activity Decreased rate of Phase 4 depolarization Decreased rate of SA node discharge
57
What are the side effects of beta blockers? (5)
* Allergic rash * Bradycardia * Bronchospasm * CHF (worsen) * Mental depression, fatigue
58
What is a Class III drug?
Amiodarone
59
What is the indication for amiodarone? (2)
Refractory supraventricular / V tach WPW
60
Amiodarone is not very effective for atrial tach. True or false?
True.
61
What is the dose of amiodarone? initial IV dose IV infusion rate
150 mg/ 10 min 1 mg/min
62
What is the mechanism of amiodarone?
Prolongs refractory period in all cardiac tissue
63
What must you do when giving amiodarone?
Give slowly because it can cause hypotension.
64
What are the side effects of amiodarone? (3)
Pulmonary toxicity Ventricular tachydysrhythmias Hypotension
65
If the daily dose of amiodarone exceeds 400mg, what side effect is likely to occur? What is the course of treatment?
Pulmonary alveolitis Decrease FiO2 at lowest possible to maintain adequate oxygenation because of increased production of free oxygen radicals.
66
What are other side effects from chronic use of amiodarone? (10)
* Bradycardia **(resistance to atropine)** * Heart block * Neurologic abnormalities like muscle weakness, ataxia * Pulmonary fibrosis * Hypo/hyper thyroidism * Corneal deposits * Phytosensitivity * Cyanotic discoloarion of the face * Increased plasma transaminase * Displacement of digoxin from binding sites
67
What are the Class IV drugs? (2)
Verapamil Diltaizem
68
What are known as the supraventricular antidysrhythmics?
Class IV, Ca channel blockers
69
What are the indications for calcium channel blockers? (3)
Paroxysmal SVT Afib A-flutter
70
What drug may decrease the response to catecholamines and sympathetic stimulation which may manifest as sinus arrest, AV heart block, and result in low CO?
AMIODARONE
71
The use of what drug may indicate the potential need for a temporary pacemaker?
AMIODARONE
72
What is the dose of verapamil? PO IV
80 - 120 mg PO q 6-8 hours 5 - 10 mg IV
73
What is the dose of diltiazem? IV
20 mg IV Note: This is 2nd line drug to be used in beta blocker doesn't work.
74
What is the mechanism of action of Class IV drugs? (2)
Decrease phase 4 Depresses AV node
75
What is the metabolism and excretion of Class IV drugs?
Hepatic metabolism Renal excretion
76
What are the side effects of Class IV drugs? (3)
Hypotension AV block Direct myocardial depression (usually with chronic therapy)
77
What class of drug increases: effective refractory period action potential duration QT duration
Class IA Quinidine, Procainamide, Disopyramide
78
What class of drug decreases: depolarization rate conduction velocity
Class IA
79
What class of drug decrease: effective refractory period action potential duration
Class IB Lidocaine, Phenytoin, Mexiletine, Tocainide
80
What class of drug: decrease depolarization rate and conduction velocity increase PR, QRS, and QT duration
Class IC Flecainide
81
What class of drug decrease: conduction velocity automaticity QT duration
Class II Beta blockers
82
What class of drug: decrease conduction decrease automaticity increase refractory period increase PR duration **increase QT**
Class III Amiodarone
83
What class of drug decreases action potential duration?
Class IV Verapamil, Diltiazem
84
What are the indications for digitalis? (2)
**Atrial** tachydysrhythmias Heart failure
85
What is the oral dose of digitalis?
0.5 - 1 mg over 12-24 hours
86
What is the mechanism of digitalis?
Increase phase 4 slope Increased AV node refractoriness
87
What are the side effects of digitalis? (5)
* Digitalis toxicity * EKG changes--digitalis effect * Cardiac dysrhythmias * Nausea * Disturbance of cognitive function
88
When is adenosine indicated? (2)
PSVT (atrial tach) WPW
89
What is the dose of adenosine IV?
6 mg Repeat in 3 min with 6-12 mg
90
What is the mechanism of adenosine? (2)
Similar to Ca blocker Hyperpolarize the cell Note: Will see flat line on ECG!
91
What are the side effects of adenosine? (5)
* Headache * Facial flushing * Bronchospasm * Dyspnea * Transient AV block