Antiarrhythmics Flashcards
Why do sodium, potassium, and calcium need channels?
net + charge so can’t move readily across phospholipid bilayer
What opens or closes ion channel gates?
specific transmembrane conditions such as voltage, ionic, or metabolic
What is the path of cardiac conduction?
SA node->Internodal tracts->AV node->bundle of His->L&RBB->purkinje fibers
What are 3 ways you can alter HR?
1)rate of phase 4 depolarization, 2)threshold potential, 3)RMP
What’s the intrinsic rate of the SA node?
70-80bpm
What’s the intrinsic rate of the AV node?
40-60bpm
What’s the intrinsic rate of the purkinje fibers?
15-40 bpm
Define arrhythmias.
those electrical impulses or cardiac depolarization that deviate from the normal pathway. Abnormalities in site of origin, rate/regularity, or conduction pathway
What regulates the RMP?
potassium
Most cells are impermeable to ________ at rest but highly permeable at the start of an action potential.
sodium
What happens at phase 0 of a ventricular action potential?
gates open, Na enters, fast depolarization. brief.
What happens phase 1-2 of a ventricular action potential?
Repolarization starts, Cl- in, K out (phase 1) Na stops influx, Ca moves in, K moves out (phase 2). slow development of repolarization (K+)
What happens phase 3 of a ventricular action potential?
fast repolarization, Na and Ca minimum influx, K moves out, end of phase 3 cardiac cells respond to stimulus greater than normal intensity (relative refractory period)
What happens phase 4 of a ventricular action potential?
resting potential, repolarized state, diastole, Na/K pump: 3Na out for 2K in to keep negative
What’s resting membrane potential for ventricular?
-90
What’s threshold potential for ventricular?
-70-
When’s the absolute refractory period?
phase 1-3ish
Is sodium higher inside or outside cell?
outside…flows in
Is potassium higher inside or outside of cell?
inside….flows out
Is Calcium higher inside or out of cell?
outside…flows in
What determines HR?
SA node/autonomic tone, rate of phase 4 depolarization
What’s the RMP for nodal action potential?
-60
What’s the threshold potential for nodal action potentials?
-45
What happens phase 0 of nodal action potential?
t-type Ca channels open so further depolarization/tips scales, Ca in, Na in, depolarization
What happens phase 3 of a nodal action potential?
K+ out, cell becomes more negative, Ca channels close, repolarization
What happens phase 4 of a nodal action potential?
K out, Na in, Ca in, lf=funny current activated by hyperpolarization, spontaneous depolarization
What are things that precipitate arrhythmias?
myocardial ischemia, hypoxemia, resp acidosis, electrolyte imbalances, excess catecholamine exposure, certain drugs, drug toxicity, over stretching of cardiac fibers
What are all arrhythmias a result of?
disturbances in impulse FORMATION or CONDUCTION
What is the MOA of antiarrhythmics?
Na channel blockade of depolarized cells, blockade of sympathetic autonomic effects on heart (reducing epi/ne that’s generated), prolongation of refractory period, calcium channel blockade of depolarized cells
What is the goal of therapy for arrhythmias?
reduce ectopic pacemaker activity and modify conduction of refractoriness in reentry circuits.
Do antiarrhythmics decrease automaticity of SA node or ectopic pacemakers more?
ectopic pacemakers
What during anesthesia can cause arrhythmias?
intubation, abnormal ventilation leading to hypercapnia or hypoxia, anesthetic agent
What are the 4 classes of antiarrhythmics?
No Body Kisses Cats: Na channel blockers, Beta blockers, K channel blockers, Ca channel blockers
Describe Class I antiarrhythmics.
Na channel blockers (phase 0), 1A: lengthen action potential, INTERMEDIATE with Na channels, 1B: shortens actions potential, RAPID with Na channels, 1C: no effect on action potential, SLOW interaction with channels
Describe Class II antiarrhythmics.
Beta blockers, reduce adrenergic activity in heart
Describe Class III antiarrhythmics.
K channel blockers, prolong effective refractory period
Describe Class IV antiarrhythmics.
Ca channel blockers, slow conduction, increase refractory period.
What is included in the 5th, unnamed class of antiarrhythmics?
adenosine, potassium, and magnesium
What are beta blockers used for?
efficacy of suppression of ventricular ectopic depolarization lower than sodium channel blockers. Decrease rate of spontaneous phase 4 depolarization
Is esmolol long or short acting?
short acting used primarily for intraop and acute arrhythmias
What’s the dose of esmolol?
10mg IVP, repeat q5-10 min
When should you be cautious with esmolol?
hypovolemia causing decreased BP
What’s the dose for metoprolol?
1-2mg IVP up to 15mg max dose, smaller in OR than ICUS
What is the dose of propranolol?
0.5-1mg IVP, longer acting
What’s special about Carvedilol?
beta blocker and alpha adrenergic blockade, blocks K, Ca, and Na, prolongs AP depolarization (phase 4)
What is carvedilol good for?
diseased hearts, prolonged use causes upregulation of Na, K, and Ca channels
What is a IIb antiarrhythmic?
Digoxin, inotropic agent in CHF
What is Digoxin for?
treat supraventricular arrhythmias
What’s the MOA of digoxin?
inhibits Na/K ATP pump, Ca cant be removed in exchange for Na, increased Ca levels and prolonged contraction of myocytes. decreased activity of SA node and prolonged conduction through AV node, increases contractility, decreases myocardial O2 consumption
What is a caution with digoxin?
dont use synchronized cardioversion if dig toxicity=Vfib
What’s the loading dose of dig?
0.5-1mg IV
What are some class III antiarrhythmics?
bretylium, sotalol, ibutilide
What’s the MOA of bretylium?
lengthens ventricular not atrial action potential duration and effective refractory period, causes initial release of catecholamine so some positive inotropic effects
What’s the dose, onset, DOA of bretylium?
54-10mg/kg over 15 min, onset 1-3 min DOA 6-24h
What’s the uses for sotalol?
SVT and ventricular arrhythmias
What’s a concern with sotalol?
torsades de pointe: major toxicity associated with beta blockade and with prolongation of repolarization
What is ibutilide used for?
acute onset Afib/flutter
What’s the MOA of Verapamil?
binds to l-type Ca channels, decrease sinus node firing, decrease AV conduction, decrease contractility, decrease smooth muscle tone.
Does Verapamil block inactivated or activated calcium channels?
both, and it’s more marked in tissues that fire frequently
Does Verapamil cause peripheral vasodilation?
yes
What happens with large doses of Verapamil?
cardiotoxic effects, AV block
How do you treat an AV block caused by Verapamil?
atropine, beta receptor stimulants, Calcium admin
What are the minor adverse effects of Verapamil?
constipation, Nervousness, Peripheral edema
What are the s/s of Ca channel blocker toxicity?
hyperglycemia, hyperkalemia, acidosis, bradycardia, progressive AV block.
How do you treat Ca channel blocker toxicity/
activated charcoal, atropine, Ca, NE/epi, inodilator to prevent reuptake of Ca in sarcoplasmic reticulum
What is Verapamil primarily used for?
treat reentry SVT
What is diltiazem also used for?
arterial vasodilator
What kind of drug is diltiazem?
benzothiazepine
What channels does amio block?
Na, Ca, K
What is amio primarily used for?
very effective against both supraventricular and ventricular arrhythmias
Does amio have a long or short half life?
extremely long: 13-103 days
What’s the dose, onset, duration of amio?
150mg IV bolus then 15mg/min x10 min, if continues repeat 150mg then 60mg/hr; onset 20-30 min, DOA 1-2 weeks
What’s the MOA of amiodarone?
very effective Na channel blocker, low affinity for activated channels…almost exclusively combines with inactivated state.
Markedly lengthens action potential duration by blocking K channels.
Weak calcium channel blocker and noncompetitive inhibitor of beta receptors
What effects does amio have on the heart?
slows sinus rate and AV conduction, prolongs QT, prolongs QRS, increases atrial, AV nodal, ventricular refractory periods, antianginal effects
What are the side effects of amiodarone?
causes peripheral vascular dilatation through its alpha blocking abilities. May cause symptomatic brady and heart block, concentrated in every tissue/organ. yellow-brown eye crystals deposit in cornea, pulmonary fibrosis/inflammation, reduces clearance of drugs: warfarin, theophylline, quinidine, procainamide, flecanide
What is the half life of adenosine?
10 seconds…push fast
What’s the MOA of adenosine?
thought to involve enhanced potassium conductance and inhibition of cAMP induced Ca influx: marked hyperpolarization and suppression of Ca dependent action potentials
What does adenosine do?
inhibition of AV nodal conduction and increases AV nodal refractory period
What are the side effects of adenosine?
flushing, SOB, chest burning possibly related to bronchospasm, headache, hypotension, nausea, parasthesias
What is adenosine used for?
treat ONLY confirmed PSVT
What is the dose, onset, and duration of adenosine?
dose 6-12mg, onset <20 sec, duration 3-7 min
What is the MOA of magnesium?
naturally occuring Ca channel blocker, influence Na/K ATPase, Na channels, K channels and Ca channels
When do you use mag?
digitalis induced arrhythmias with hypomagnesemia, torsades de pointe
What is essential for K levels?
magnesium
What effects does Potassium have on cell membrane?
Resting potential depolarizing action, membrane potential stabilizing action,
