antidysrhythmic drugs

Question 1

what is the incidence of arrhythmias during cardiac and non cardiac surgery? what is the incidence of serious arrhythmias?

Answer 1

-16.3-84%

-

Question 2

describe antidysrhythmic drug use

Answer 2

• used in surgery to control dysrhythmias
• not utilized as much d/t new therapies such as ablation, AICD
• myocardial depressant effects, decreased LV function
• can trigger new dysrhythmias (prodysrhythmias)
• seen mostly with maintenance therapy for refractory A fib, A flutter and frequently shocked AICD pts.

Question 3

what are the two primary mechanisms of dysrhythmias?

Answer 3

• automaticity

- re entry

Question 4

describe automaticity

Answer 4

condition where spontaneous depolarizations occur d/t abnormal impulse generation in sinus or ectopic foci (electrolyte imbalance; irritation from line insertion, etc.)

Question 5

describe re-entry

Answer 5

impulses propagate more than one pathway

ex: Wolff-Parkinson-White syndrome
* seen more with volatile anesthetics b/c of suppression of SA node and conduction pathway

Question 6

what are factors that promote dysrhythmias?

Answer 6

• electrolyte imbalance: Na+, K+, Cl-, Mag++
• hypoxemia (PVCs)
• acid base imbalance: alkalosis > acidosis (PVCs from alkalosis/hypokalemia most)
• myocardial ischemia
• bradycardia
• increased mechanical stretch of myocardium
• SNS stimulation
• Drugs

Question 7

what is the basic MOA of antidysrhythmias?

Answer 7

• most work directly or indirectly by blocking various ion channels
• differing action potentials in ventricular vs. nodal tissue illustrate various drug effects
• Na+ blockers affect velocity of AP upstroke
• K+ blockers affect refractory
• Ca+ blockers affect slope of phase 4 in nodal tissue

Question 8

describe prodysrhythmias

Answer 8

newly developed brady or tachydysrhythmias resulting from chronic antidysrhythmic therapy

• mainly caused by Class I drugs (Na+ blockers)
• Torsades de Pointes (polymorphic V-tach; V-fib)
• Incessant Ventricular Tachycardia (drugs that slow conduction can allow re-entry impulses; Ia & Ib)
• Wide Complex Ventricular Rhythm (usu. seen with class Ic drugs d/t slow conduction)

Question 9

describe different antidysrhythmic classes

Answer 9

-Class I: membrane stabilizer (manipulate Na+)
Ia, Ib, Ic
-Class II: beta adrenergic antagonist
-Class III: refractory prolongers (manipulate K+)
-Class IV: Ca+ channel blockers

Question 10

describe Class I drugs

Answer 10

decrease depolarizations and conduction velocity; blocking Na+ moves threshold potential farther away from resting potential

• Ia: lengthen action potential by Na+ block; lengthen repolarization by K+ block
• Ib: blocks Na+ but weaker than Ia; shorten AP duration and refractory period
• Ic: Potent Na+ channel blocker; decrease rate of phase 0 depolarization; decrease speed of conduction (lengthening AP, widening QRS; myocardial depression)
• *increases risk of mortality and prodysrhythmias

Question 11

describe Class II drugs

Answer 11

beta adrenergic blockers

• decrease magnitude of Ca+ influx current
• decrease K+ current (Na+/K+ pump)
• decreased pacemaker current (decreases sinus rate)
• decrease rate of phase 4 depolarization
• decrease automaticity
• decrease epinephrine induced hypokalemia
• decrease myocardial O2 requirements
• increase energy required to fibrillate heart in ischemic tissue; useful in ischemic r/t dysrhythmias
• increase AV nodal conduction time and refractoriness, which terminates re-entrant dysrhythmias
• shown to reduce mortality weeks after MI

Question 12

describe Class III drugs

Answer 12

refractory prolongers

• block K+ channels
• increase refractoriness (absolute)
• increase AP duration
• reduces automaticity
• reduce re-entrant dysrhythmias
• interact with beta blockers
• used a lot now in a fib and flutter

Question 13

describe Class IV drugs

Answer 13

cardiac Ca+ channel blockers

• work primarily on sinus and AV nodal tissues
• generally slow HR
• decrease velocity of AV nodal conduction (HR)
• useful in re-entrant dysrhythmias
• useful in rate control for rapid ventricular response w/ a fib and a flutter, PSVT
• useful in V tach
• not shown to reduce mortality after MI like beta blockers and amiodarone

Question 14

what are effects of antidysrhythmic drugs?

Answer 14

• may increase mortality risk
• increased risk of prodysrhythmias
• Class Ia and Ib increase mortality and vent dysrhythmias
• amiodarone and beta blockers decrease mortality after MI
• Class Ia and Ic can complicate CHF
• lidocaine increases bradydysrhythmias and mortality after MI
• many physicians choose not to treat ventricular ectopy if asymptomatic

Question 15

describe Quinidine

Answer 15

• Class Ia
• decreases phase 4 slope, prolongs conduction
• blocks Na+, K+, alpha block, vagal inhibition
• prevent Supraventricular dysrhythmias, PVCs; maintain sinus rhythm in Afib, Aflutter

Question 16

what are adverse effects of quinidine?

Answer 16

• prolongs QRS, QT, PR
• hypotension
• may increase NMB
• depressant effect on myocardial contractility but may offset this by an increase in HR

Question 17

describe procainamide (Procan)

Answer 17

• Class Ia
• blocks Na+, K+ channels; decreases automaticity; increases refractoriness
• ventricular and atrial tachydysrhythmias; PVCs

Question 18

what are adverse effects of procainamide?

Answer 18

• slowed conduction times
• prolongs QRS, QT
• hypotension d/t myocardial depression
• lupus-like symptoms

Question 19

describe disopyramide (Norpace)

Answer 19

• Class Ia
• Na+ channel block; anticholinergic actions; slowed conduction
• atrial and ventricular tachydysrhythmias; maintain sinus rhythm in Afib, Aflutter

Question 20

what are adverse effects of disopyramide?

Answer 20

• myocardial depression
• depresses contractility, aggravate CHF
• prolongs QT

Question 21

describe lidocaine

Answer 21

• Class Ib
• delays phase 4 depolarization
• ventricular dysrhythmias; re-entry cardiac dysrhythmias (PVCs, V tach)
• little effect on supraventricular dysrhythmias

Question 22

what are implications of lidocaine?

Answer 22

• may increase mortality after MI
• more rapid than quinidine or procainamide
• easily titrated
• myocardial depressant
• neurologic, seizures
• prolonged PR, QRS

Question 23

describe beta blockers

Answer 23

Class II

• decrease spontaneous phase 4 depolarization; decrease conduction through AV node
• effective in dysrhythmias r/t increases in SNS; ventricular rate control for a fib, a flutter

Question 24

what are adverse effects of beta blockers?

Answer 24

• prolonged PR, depressed myocardium
• bradycardia, hypotension, bronchospasm
• not for CHF, RAD (reactive airway d/t bronchoconstriction), AV block pts.

Question 25

describe amiodarone (Cordorone)

Answer 25

Class III - blocks Na+; reduces currents of K+, Ca+ - prolongs AP, refractory and conduction - alpha and beta antagonist (vasodilation) - dilate coronary arteries (antianginal) * resistant V tach, V fib, A fib, WPW * acute termination of V tach, V fib (1st line treatment)

Question 26

what are adverse effects of amiodarone?

Answer 26

- hypotension r/t vasodilation, LV depression (pushed too fast) - pulmonary toxicity (lipophilic, slow elimination) - altered thyroid function (resembles thyroid hormone) - marked QT prolongation, bradycardia, AV block - resistant to catecholamines - reduce oxygen concentrations (leads to more pulmonary toxicity)

Question 27

describe Class IV drugs

Answer 27

- verapamil and diltiazem - block Ca+ in cardiac cells - decreases spontaneous phase 4 depolarization - vasodilation or coronary and peripheral arteries - depress AV node; negative chronotropic SA node * PSVT; re-entrant tachy * ventricular rate control in a fib, a flutter * good to prevent arterial spasm (neuro) * not effective in reducing ventricular ectopy

Question 28

what are adverse effects of class IV drugs?

Answer 28

- AV block, aggravates reduced LV function - hypotension - myocardial depression - NMB may be exaggerated

Question 29

describe digitalis

Answer 29

- treat atrial tachydysrhythmias - slow AV node conduction which slows ventricular response in A fib - enhance assessor pathway conduction - cardiac glycosides ultimately increase Ca+ which increases cardiac contractility (increase SV) * can cause any cardiac dysrhythmia

Question 30

describe adenosine

Answer 30

- slows sinus rate and conduction through AV node - not effective in A fib, A flutter, V tach - effective if rapid bolus through CVL, short half life of 6-10 seconds - transient asystole

Question 31

describe phenytoin use for dysrhythmias

Answer 31

- useful in ventricular but not atrial dysrhythmias - digitalis toxicity induced ventricular dysrhythmias - can depress sinus node * Na+ blocking potential

Question 32

describe magnesium use for dysrhythmias

Answer 32

- useful in preventing Torsades de Pointes | - digitalis induced dysrhythmias and ventricular ectopy

Question 33

describe calcium use for dysrhythmias

Answer 33

- moves threshold potential further away from resting potential - useful in hyperkalemia where resting potential is closer to threshold potential * protectant

Question 34

describe robinul use for dysrhythmias

Answer 34

-muscarinic antagonist prevents Ach from producing negative chronotropic, inotropic and dromotropic (conduction velocity) effects

Question 35

describe vasopressin use for dysrhythmias

Answer 35

produces negative lusitropic (myocardial relaxation) effects and potent coronary vasoconstriction