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39 Cards in this Set

  • Front
  • Back
Two physiologic mechanisms that can cause ectopic cardiac dysrhythmias
Enhanced automaticity
Factors associated with

Enhanced automaticity
Arterial hypoxemia
Electrolyte (Alkalosis > Acidosis)
Myocardial ischemia
Increased sympathetic activity ( threshold for V-fib)
Certain drugs
acid-base abnormalities (hypo-kalemia/mag)
When to treat cardiac dysrhythmias?
Can not be corrected by removing the precipitating cause.

Homodynamic function is compromised.

Disturbance predisposes the patient to a more serious cardiac dysrhythmias.
General Mechanism of Action
Cardiac antidysrhythmics drugs produce pharmacologic effects by blocking passage of ions across sodium, potassium, and calcium ion channels present in the heart.”
Ventricular Muscle Action Potential
phase 0- Fast Na+ channels open then slow Ca++ channels = Class 1 antidysrhythmics
phase 1- K+ channels open
phase 2- Ca++ channels open more
phase 3- K+ channels open more
phase 4- Resting membrane potential
Classification 1
Inhibit fast sodium channel during depol. (phase 0)
Classification 2
Beta-adrenergic antagonists = decrease rate of spontaneous phase 4 depolarization.
Classification 3
Block potassium ion channels resulting in prolongation of cardiac depol, AP duration, and the effective refractory period.
Classification 4
Act by inhibiting inward slow calcium ion currents.
Class 1A Drugs



Acute/chronic supraventricular dysrhythmias
Prevent recurrence SVT or suppress PVC
SVT associated with Wolff-Parkinson-White
Quinidine notes
Of note:
Occasional paradoxical increase in the rate of ventricular response. *****give Digitalis prior*****
Can displace digoxin from myocardial and peripheral tissue stores.
Limited IV use due to peripheral vasodilatation and myocardial suppression.
Quinidine MOA
blocking the fast inward sodium current
Decrease the slope of phase 4 depolarization = enhanced automaticity
Increases atrial and ventricular fibrillation threshold
Can abolish reentry dysrhythmias by prolonging conduction of cardiac impulses in an area of injury.
Has antimalarial and antipyretic effects.
Hydroxylated in the liver to inactive metabolites
Excreted in the urine
20% unchanged
80-90% in plasma is bound to albumin
Accumulates rapidly in most tissues except the brain.
Quinidine S/A
At plasma concentration of greater than 2ug/ml
Prolonged P-R, QRS, and QTC
Quinidine syncope due to vent. Dysrhythmias
Depress myocardial contractility
Interfere with neuromuscular transmission =
**********accentuate the effects of neuromuscular blocking drugs************
Procainamide Metabolism and Excretion
Hepatic metabolism
Acetylated to N-acetyl procainamide (NAPA) which is a cardiac active metabolite.
Highly resistant to hydrolysis by plasma cholinesterase.
15% bound to plasma protiens
Renal excretion
40-60% unchanged
Procainamide MOA
Blocks open sodium channels

prolongs the cardiac action potential (outward potassium currents may be blocked).

This results in slowed conduction, and ultimately the decreased rate of rise of the action potential, which may result in widening of QRS on EKG. (wikipedia)
Procainamide notes
Can be given IV at a rate not exceeding 100mg every 5 minutes until cardiac dysrhythmia is controlled.
********Very limited use in anesthesia due to propensity to produce hypotension*********
Procainamide use/class
Treatment of ventricular tachydysrhythmias.
Suppression of PVC and paroxysmal ventricular tachycardia.
Procainamide S/A
Ventricular asystole or fibrillation may occur if given in presence of heart block
Chronic administration may be associated with syndrome that resembles systemic lupus.
Drug fever
Myocardial deppression
The Cardiac Action Potential

Phase 4 is
the resting membrane potential
The Cardiac Action Potential

Phase 0 is
the rapid depolarization phase
The Cardiac Action Potential

Phase 1 occurs with
the inactivation of the fast Na+ channels
The Cardiac Action Potential

Phase 2 "plateau” is
sustained by a balance between inward movement of CA and outward movement of K+
The Cardiac Action Potential

Phase 3...
Ca channels close, while the K+ channels are still open. This ensures a net outward current, corresponding to negative change in membrane potential, thus allowing more types of K+ channels to open
Class II agents are
anti-sympathetic nervous system agents. All agents in this class are beta blockers.
Class I agents interfere with
the sodium (Na+) channel.
Class III agents
affect potassium (K+) efflux.
Class IV agents affect
the AV node.
Class V agents work by
other or unknown mechanisms.
Class I-a antiarrhythmic agents MOA
Class I-a agents block the fast sodium channel. Blocking this channel depresses the phase 0 depolarization (reduces Vmax), which prolongs the action potential duration by slowing conduction

class 1a effect on AP?

Class I-b antiarrhythmic agents MOA
Sodium channel blockers
Little or no effect at slower heart rates, more effects at faster heart rates
Shorten the action potential duration and reduce refractoriness

class 1b effect on AP
Class I-c antiarrhythmic agents MOA
Markedly depress the phase 0 depolarization (decreasing Vmax). They decrease conductivity, but have a minimal effect on the action potential duration
Most potent Na+ blockers

Class II antiarrhythmic agents MOA
Class II agents are anti-sympathetic nervous system agents
Are conventional beta blockers
Act by selectively blocking the effects of catecholamines at the beta-1 adrenergic receptors, thereby decreasing sympathetic activity on the heart
Decrease conduction through the AV node

Class III antiarrhythmic agents MOA
Class III agents affect potassium (K+) efflux, thereby prolonging repolarization
prolongation of the action potential duration and refractory period, combined with the maintenance of normal conduction velocity, prevent re-entrant arrhythmias

Class IV antiarrhythmic agents MOA
Class IV agents affect the AV node.
Are slow calcium channel blockers.
They decrease conduction through the AV node
Include verapamil and diltiazem
Class V antiarrhythmic agents MOA
Class V agents work by other or unknown mechanisms
Include digoxin and adenosine.
Digoxin increases vagal activity via its central action on the central nervous system, thus decreasing the conduction of electrical impulses through the AV node