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NUNA 680 - Pharm > Antidysrhythmics > Flashcards

Antidysrhythmics Flashcards

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1
Q

What is the incidence of arrhythmias during cardiac and non-cardiac surgery? Serious arrhythmias?

A

16.3-84%; less than 1%

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2
Q

What are the uses of antidysrhythmic drugs?

A

Control dysrhythmias perioperatively; maintenance therapy for a-fib and a-flutter refractory to ablation, and frequently shocked AICD patients

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3
Q

What are the two primary mechanisms of dysrhythmias?

A

Automaticity and re-entry

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4
Q

Explain the dysrhythmia mechanism of automaticity.

A

Condition where spontaneous depolarizations occur due to abnormal impulse generation in sinus or ectopic foci.

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5
Q

Explain the dysrhythmia mechanism of re-entry.

A

Impulses propagate more than one pathway (ex., WPW syndrome); seen more often with volatile agents because of suppression of SA node and conduction pathway

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6
Q

What factors promote dysrhythmias?

A 
Electrolyte imbalance
Hypoxemia
Acid base imbalance (alkalosis > acidosis)
Myocardial ischemia
Bradycardia
Increased mechanical stretch of myocardium
SNS stimulation
Drugs
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7
Q

Blocking ion channels manipulates various states of the action potential. Blocking Na+…

A

affects velocity of AP upstroke (ventricular tissue)

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8
Q

Blocking ion channels manipulates various states of the action potential. Blocking K+…

A

affects refractory

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9
Q

Blocking ion channels manipulates various states of the action potential. Blocking Ca+…

A

affects slope of phase 4 in nodal (pacemaker) tissue

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10
Q

What are prodysrhythmias?

A

Newly developed brady or tachydysrhythmias resulting from chronic antidysrhythmic therapy (ex., Torsades, VT, wide complex ventricular rhythm)

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11
Q

What is phase 0 of the ventricular action potential?

A

Rapid depolarization as a result of opening of Na+ channels and closing K+ channels. Sodium rushes into the cell.

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12
Q

What is phase 1 of the ventricular action potential?

A

The period of initial repolarization that results from the closure of Na+ and opening of K+ channels. K+ begins to leave the cell. Na+ can no longer enter the cell.

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13
Q

What is phase 2 of the ventricular action potential?

A

The plateau phase that results from the sustained Ca++ current that began with the initial depolarization. Ca++ continues to enter the cell.

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14
Q

What is phase 3 of the ventricular action potential?

A

Repolarization due to opening of K+ and closure of Ca++ channels. K+ continues to leave the cell, but Ca++ can no longer enter the cell.

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15
Q

What is phase 4 of the ventricular action potential?

A

The resting potential during which time K+ channels are open and Na+ and Ca++ channels are closed.

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16
Q

What is the ERP of the ventricular action potential?

A

Effective refractory period during which the cell cannot be depolarized again. (Between phase 4s of the action potential cycle)

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17
Q

How do conduction cells vs. pacer cells differ in their action potentials?

A

Conduction myocytes have “fast” APs (dependent on Na+ for phase 0); pacemaker cells have “slow” APs (dependent on Ca++ for phase 0)

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18
Q

What is the resting charge for the ventricular AP?

A

-90 mV

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19
Q

What charge does the ventricular AP depolarize to?

A

+10 mV

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20
Q

What happens during phase 0 of the pacemaker AP?

A

Depolarization. L-Type Ca++ channels open; Ca++ rushes into the cell.

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21
Q

Pacemaker AP lacks which two phases?

A

1 and 2

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22
Q

Considering the lack of phases 1 and 2 in the pacemaker AP, what event causes the cell to begin repolarization?

A

For phase 3, K+ channels open and K+ leaves the cell.

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23
Q

Why is phase 4 of the pacemaker AP never a straight line?

A

There is always a slow Na+ leak into the cell.

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24
Q

Changing what aspect of the pacemaker AP changes heart rate?

A

The rate of phase 4 depolarization; steeper slope, by NE leads to faster HR; flatter slope by ACh leads to bradycardia or asystole

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25
What are the Class I antidysrhythmic drugs known as?
Membrane Stabilizers; inhibit fast sodium channels
26
What are the Class II antidysrhythmic drugs known as?
Beta Adrenergic Antagonists; decrease rate of depolarization (phase 4)
27
What are the Class III antidysrhythmic drugs known as?
Refractory Prolongers; inhibit potassium ion channels
28
What are the Class IV antidysrhythmic drugs known as?
Ca+ Channel Blockers; inhibit slow calcium channels (calcium creep of SA cells)
29
What is the MOA of Class I antidysrhythmics?
Decrease depolarizations & conduction velocity by blocking Na+, moving the threshold potential farther away from the resting potential.
30
What is the MOA of Class II antidysrhythmics?
Beta adrenergic antagonist; decreases magnitude of Ca+ influx, decreases K+ current (Na+/K+ pump), decreases pacemaker current (dec sinus rate), decrease rate of phase 4 depolarization, decrease epinephrine induced hypokalemia, decrease automaticity, *decrease myocardial oxygen requirements*, *increase energy required to fibrillate the heart in ischemic tissue (dec ischemia related dysrhythmias)*, lengthen AV nodal conduction time and refractoriness which terminates re-entrant dysrhythmias, *reduce mortality after MI*
31
What is the MOA of Class III antidysrhythmics?
Block K+ channels, increase absolute refractoriness, increase action potential duration, reduce automaticity, reduce re-entrant dysrhythmias, interact with beta blockers
32
What is the MOA of Class IV antidysrhythmics?
Work primarily on sinus and AV nodal tissues; slow heart rate; decrease velocity of AV nodal conduction; useful in re-entrant dysrhythmias, rate control in RVR with a-fib and a-flutter, PSVT; v-tach; NOT been shown to reduce mortality after MI
33
What risks must be considered when deciding whether to initiate antidysrhythmic therapy?
May increase risk of mortality Risk of prodysrhythmias Class Ia & Ib increased mortality and vent dysrhythmias Class Ia & Ic can complicate CHF (weaken pump) Lidocaine increases bradydysrhythmias & mortality after an MI
34
Which antidysrhythmic drugs decrease mortality after MI?
**Amiodarone & beta-blockers**
35
Indication for Quinidine
Prevent SVT, PVCs, maintain sinus rhythm in a-fib/a-flutter
36
Quinidine MOA
Class I Decrease phase 4 slope, prolong conduction Blocks Na+, K+, alpha block, vagal inhibition
37
Adverse effects of quinidine
Prolongs QRS, QT, PR, hypotension, may increase NMB | Depressant effect on contractility but may offset by increase in HR
38
What class is procainamide?
Class I
39
Indications of procainamide?
* *ventricular and atrial tachydysrhythmias** | * *PVCs**
40
MOA of procainamide?
Blocks Na+, K+ channels | Decreases automaticity, increases refractoriness
41
Adverse effects of procainamide?
Slowed conduction times Prolonged QRS, QT Hypotension d/t myocardial depression Lupus-like symptoms
42
What class is disopyramide?
Class I
43
Indications for disopyramide
* *Atrial and ventricular tachydysrhythmias** | * *Maintain sinus rhythm in a-fib, a-flutter**
44
MOA of disopyramide
Na+ channel block, anticholinergic actions | Slowed conduction
45
Adverse effects of disopyramide
Myocardial depression Depresses contractility, aggravates CHF Prolongs QT
46
What class is lidocaine?
Class I
47
What are the indications for lidocaine?
Ventricular dysrhythmias, re-entry dysrhythmias (PVCs, V-tach) Little effect on supraventricular dysrhythmias
48
What is the non-dysrhythmic use for lidocaine?
ERAS multi-modal pain control Infusion shown to be effective in colon surgery Local anesthesia and IV regional blocks
49
Lidocaine MOA
Delays phase 4 depolarizations (inhibits Na+ channels)
50
What quality of lidocaine makes it appropriate for infusion?
Easily titrated
51
What are some adverse implications of lidocaine use?
**May increase mortality after MI** Myocardial depressant (bad for CHF) Neurologic/seizures with toxicity **Prolonged PR, QRS**
52
**Indications for beta adrenergic antagonists**
Effective in dysrhythmias r/t increases in SNS | Ventricular rate control for a-fib, a-flutter
53
**Beta adrenergic antagonist MOA**
Class II Decrease spontaneous phase 4 depolarization Decreased conduction through AV node
54
**Adverse effects of beta adrenergic antagonists**
Prolonged PR, depressed myocardium | Bradycardia, hypotension, bronchospasm (since beta2 causes bronchodilation)
55
**Contraindications for beta adrenergic antagonists**
CHF, reactive AW disease, AV block patients
56
What class is amiodarone?
Class III
57
Indications for amiodarone
Resistant v-tach, v-fib, a-fib, WPW | Acute termination of v-tach, v-fib (FIRST LINE TREATMENT)
58
MOA of amiodarone
Blocks Na+, reduces currents of K+, Ca+ Prolongs AP, refractory, and conduction Alpha and beta antagonist = vasodilation Dilates coronary arteries (antianginal)
59
Adverse effects of amiodarone
Hypotension (vasodilation, LV depression) **Pulmonary toxicity (d/t lipophilic, slow elimination)** Altered thyroid function (resembles thyroid hormone) Marked QT prolongation, bradycardia, AV block Resistant to catecholamines Reduce O2 concentrations
60
Describe dronedarone
Derivative of amiodarone (Class III) Prevents return to a-fib/a-flutter (ONLY if pt is currently in sinus rhythm/after EP lab) Potential to increase HF
61
Drug class of verapamil and diltiazem
Class IV - Ca+ channel blockers
62
Indications for verapamil and diltiazem
Rapid HRs - paroxysmal SVT, re-entrant tachydysrhythmias Ventricular rate control in a-fib, a-flutter NOT effective in reducing ventricular ectopy (bc dealing with SA tissue)
63
MOA of verapamil and diltiazem
Block Ca+ in cardiac cells Decreases spontaneous phase 4 depolarization Vasodilation or coronary and peripheral arteries Depresses AV node, negative chronotropic SA node
64
Adverse effects of verapamil and diltiazem
AV block, aggravates reduced LV function Hypotension Myocardial depression NMB may be exaggerated
65
OTHER: Digitalis
Used to treat atrial tachydysrhythmias; slow AV node conduction slowing VR in a-fib; enhance accessory pathway conduction; increase Ca+ which enhances contractility Risk of toxicity Can cause any cardiac dysrhythmia
66
OTHER: Adenosine
Slows sinus rate and conduction through AV node NOT effective in a-fib, a-flutter, v-tach RAPID BOLUS thru CVL Transient asystole less than 5 seconds
67
OTHER: Phenytoin
An anticonvulsant drug Useful in VENTRICULAR but not atrial dysrhythmias and digitalis toxicity-induced ventricular dysrhythmias Can depress sinus node
68
OTHER: Magnesium
Prevent Torsades, digitalis-induced dysrhythmias, ventricular ectopy ERAS analgesic effect, enhances opioid analgesia
69
OTHER: Calcium
Increases threshold potential, protective against hyperkalemia dysrhythmias
70
OTHER: Robinul/Glycopyrrolate
Muscarinic antagonist prevents ACh from producing negative chronotropic, inotropic, and dromotropic (conduction velocity) effects
71
OTHER: Vasopressin
Produces negative lusitropic (myocardial relaxation) effects and **potent coronary vasoconstriction** (bad for CAD)

NUNA 680 - Pharm (8 decks)

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