Antiarrhythmics Flashcards
spontaneous depolarization is caused by inward positive current carried by ___ and ____ flow
Sodium and Calcium Ion Flow
what can cause an abnormality in cardiac rhythm
dysfunction of impulse generation or conduction
what is a slow heart rhythm
bradycardia
what is a rapid heart rhythm
tachycardia
what is a random beat of the heart
asynchronous fibrillation
myocardium responds to stimulation by ______ of the membrane; leads to shortening of the contractile proteins and then relaxation ; respond to stimuli as a unit
depolarization
how are action potentials generated
by pacemaker cells located in the SA node and AV nodes ; there are five phases
What are the five phases of the action potential
phase o: fast upstroke, phase 1: partial repolarization, phase 2: plateau, phase 3: repolarization , phase 4: forward current
in this phase , theres a rapid Na influx, through open fast Na channels
Phase o: fast upstroke
in this phae, transient K channels open and K efflux returns TMP to 0 mV
Phase 1 : partial repolarization
in this phase, influx of Ca through L type Ca channels is electrically balanced by K efflux through delayed rectifier K channels
Phase 2: plateau
IN this phase, Ca channels close and the delayed K channels remain open and return the TMP to -90 mV
phase 3: repolarization
in this phase, Na and Ca channels are closed , open K channels keep the action potential stable at -90 mV
Phase 4: forward current
T or F: the force of contraction is directly related to the concentration of unbound cytosolic Ca
T
Agents that increase Ca levels or increase Ca sensitivity _______ the force of contraction ( inotropic effect)
increase
What are some source of ic Ca
voltage sensitive channels , exchange with Na, released from sarcoplasmic reticulum and mitochondria
what would happen to cardiac muscle if cytosolic Ca levels remained high
cardiac muscle would be in a constant state of contraction
How is Ca removed
NA exchange and uptake by Sarcoplasmic reticulum and mitochondria
what are the two basic mechanisms of arrhythmias
disturbances in impulse formation and disturbances impulse conduction
these conditions : ischemia, acidosis or alkalosis, electrolyte imbalance, autonomic influences, drug toxicity, and stretching of cardiac tissue can exacerbate__________
arrhythmias
the SA node=
the pacemaker
what can lead to abnormal automaticity
- if sites other than SA node show enhanced automaticity ( generate competing stimuli)
- If myocardial cells are damaged, they may remain partially depolarized ( reach fire threshold earlier)
what are tx options for abnormal automaticity
drugs block either Na or Ca channels to reduce the ration to K ; decreases the frequency of discharge
what can lead to abnormal impulse conduction
block of nerve impulses can cause short circuit ( re entry defect, premature contraction)
what are tx options for abnormal impulse conduction
prevent re entry by slowing conduction and or increasing the refractory period
what is the aim of drug therapy for arrhythmias
modify impulse generation and conduction
These class of drugs bind to open or inactivated Na channels ; have a greater effect in frequently depolarizing ; don’t interfere with normal heart beat; subdivided into IA, IB, and IC
Class I drugs
These Class I subgroup drugs has a greater affinity for Na channels ; dissociate from Na channels slowly and they slow the rate of rise of the action potential
Class IA drugs
this type of CLass IA drug is rapidly absorbed after oral administration; extensive metabolism by P450 enzymes; has adverse effects of arrhythmia , GI disturbances, and blurred vision
Quinidine
this Class IA drug shows alpha blocking activity ; increases steady state concentration of digoxin
quinidine
this Class IA drug is a derivative of procaine; short half life; lupus like syndrome can develop; Fewer GI side effects and has CNS side effects
procainamide
This class IA drug has similar actions to Quinidine; metabolite is less active; side effects of dry mouth, urinary retention, blurred vision, and constipation
Disopyramide
This class of drugs has a greater affinity for inactivated Na channels ; shortens repolarization
Class IB drugs
This Class IB drug is also a local anesthetic; has little effect on atrial or AV junctions arrhythmias; Given IV; Large therapeutic index ; Mild CNS effects
Lidocaine
These Class IB drugs are similar to lidocaine
Mexilitine and Tocainide
this class IB drug is often used after MI
Mexilitine
This Class IB drug has pulmonary toxicity
Tocainide
this class of drugs has greater affinity for open Na channels ; depresses the rate of rise of the action potential; slowly dissociates from resting Na channels
Class IC drugs
these two Class IC drugs have minimal biotransformation; long half life,; adverse effects of dizziness, blurred vision, HA, nausea, and arrhythmia
Flecainide and Propafenone
this class of drugs are beta blockers ; diminish phase 4 depolarization ; useful in treating arrhythmias caused by increased sympathetic activity
Class II drugs
this class II drug reduces incidence of sudden arrhythmic death after MI
propanolol
this class II drug is the most widely used beta blocker to treat cardiac arrythmias; reduces the risk of bronchospasm
metoprolol
this class II drug is short acting; used IV to treat arrhythmias that occur during sx or in emergency situations
esmolol
This class of drugs diminishes the outward K current during repolarization of cardiac cells ; all have potential to induce arrhythmias
Class III K channel blockers
This Class III drug is a complex drug; it shows Class I, II , III, and IV actions; has antianginal activity; therapy of choice for atrial fibrillation; most commonly Rx’ed;
amiodarone
this Class III drug is incompletely absorbed ; half life of several weeks; adverse effects include discontinuation of tx, interstitial pulmonary effects, GI intolerance, tremor, ataxia, and dizziness, BLUE SKIN DISCOLORATION ( can manifest in the retina) , NAION and WHORL KERATOPATHY
amiodarone
this class III drug is a amiodarone derivative ; shorter half life and side effects mainly GI
dronedarone
This Class III drug has potent beta blocker activity ; lowest rate of acute or long term adverse effects
sotalol
These Class III drugs have high risk of proarrhythmia; prolongs QT interval; 80% of drug eliminated unchanged
Dofetilide and Ibutilide
this class of drugs are Ca channel blockers; they decrease inward current;
Class IV drugs
These Class IV drugs are used to treat angina and HTN; absorbed well after oral admin; adverse effects include negative inotropic properties ( CI in pts with depressed cardiac function)
Verapamil and Diltiazem
this Class IV drug is extensively metabolized by the liver
verapamil
This “other antiarrhythmic drug” is a naturally occurring nucleoside; activates an inward rectifier K current and inhibits Ca current ; inhibits AV nodal conduction and increases the AV nodal refractory period
Adenosine
This” other antiarrhythmic drug” Is less effective in presence of caffeine ( blocks adenosine receptors) ; adverse effects include flushing, shortness of breath, and chest burning
adenosine
which drug shortens the refractory period in myocardial cells
digoxin
this “other antiarryhtmic drug” can cause arryhtmia if too much ; supplementation aimed at balancing the gradients
potassium
