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Anesthesia Pharm I > antidysrhythmic drugs > Flashcards

antidysrhythmic drugs Flashcards

1
Q

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

A

-16.3-84%

-

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2
Q

describe antidysrhythmic drug use

A
  • 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.
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3
Q

what are the two primary mechanisms of dysrhythmias?

A
  • automaticity

- re entry

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4
Q

describe automaticity

A

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

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5
Q

describe re-entry

A

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

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6
Q

what are factors that promote dysrhythmias?

A
  • 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
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7
Q

what is the basic MOA of antidysrhythmias?

A
  • 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
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8
Q

describe prodysrhythmias

A

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)
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9
Q

describe different antidysrhythmic classes

A

-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

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10
Q

describe Class I drugs

A

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
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11
Q

describe Class II drugs

A

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
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12
Q

describe Class III drugs

A

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
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13
Q

describe Class IV drugs

A

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
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14
Q

what are effects of antidysrhythmic drugs?

A
  • 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
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15
Q

describe Quinidine

A
  • 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
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16
Q

what are adverse effects of quinidine?

A
  • prolongs QRS, QT, PR
  • hypotension
  • may increase NMB
  • depressant effect on myocardial contractility but may offset this by an increase in HR
17
Q

describe procainamide (Procan)

A
  • Class Ia
  • blocks Na+, K+ channels; decreases automaticity; increases refractoriness
  • ventricular and atrial tachydysrhythmias; PVCs
18
Q

what are adverse effects of procainamide?

A
  • slowed conduction times
  • prolongs QRS, QT
  • hypotension d/t myocardial depression
  • lupus-like symptoms
19
Q

describe disopyramide (Norpace)

A
  • Class Ia
  • Na+ channel block; anticholinergic actions; slowed conduction
  • atrial and ventricular tachydysrhythmias; maintain sinus rhythm in Afib, Aflutter
20
Q

what are adverse effects of disopyramide?

A
  • myocardial depression
  • depresses contractility, aggravate CHF
  • prolongs QT
21
Q

describe lidocaine

A
  • Class Ib
  • delays phase 4 depolarization
  • ventricular dysrhythmias; re-entry cardiac dysrhythmias (PVCs, V tach)
  • little effect on supraventricular dysrhythmias
22
Q

what are implications of lidocaine?

A
  • may increase mortality after MI
  • more rapid than quinidine or procainamide
  • easily titrated
  • myocardial depressant
  • neurologic, seizures
  • prolonged PR, QRS
23
Q

describe beta blockers

A

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
24
Q

what are adverse effects of beta blockers?

A
  • prolonged PR, depressed myocardium
  • bradycardia, hypotension, bronchospasm
  • not for CHF, RAD (reactive airway d/t bronchoconstriction), AV block pts.
25
Q

describe amiodarone (Cordorone)

A

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)
26
Q

what are adverse effects of amiodarone?

A
  • 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)
27
Q

describe Class IV drugs

A
  • 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
28
Q

what are adverse effects of class IV drugs?

A
  • AV block, aggravates reduced LV function
  • hypotension
  • myocardial depression
  • NMB may be exaggerated
29
Q

describe digitalis

A
  • 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
30
Q

describe adenosine

A
  • 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
31
Q

describe phenytoin use for dysrhythmias

A
  • useful in ventricular but not atrial dysrhythmias
  • digitalis toxicity induced ventricular dysrhythmias
  • can depress sinus node
  • Na+ blocking potential
32
Q

describe magnesium use for dysrhythmias

A
  • useful in preventing Torsades de Pointes

- digitalis induced dysrhythmias and ventricular ectopy

33
Q

describe calcium use for dysrhythmias

A
  • moves threshold potential further away from resting potential
  • useful in hyperkalemia where resting potential is closer to threshold potential
  • protectant
34
Q

describe robinul use for dysrhythmias

A

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

35
Q

describe vasopressin use for dysrhythmias

A

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

Anesthesia Pharm I (28 decks)

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