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104 Cards in this Set
- Front
- Back
causes of arrhythmia
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coronary ischemia.tissue hypoxia.electrolyte disturbances.Over stimulation of SNS.General anesthetics.Any other condition or drug that may affect cardiac transmembrane potentials and lead to abnormal impulse formation or conduction.
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Digitalis glycosides can cause what?
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cause after depolarizations by increasing Calcium influx into cardiac cells; also impair AV node conduction and can cause AV block.
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“torsade de pointes” caused by what drugs
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Caused by certain antiarrhythmic drugs, psychotropic drugs, antibiotics and other miscellaneous drugs like cisapride.
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after polarization caused by what drugs
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digitalis.
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abnormal impulse formation After depolarizations occur when and definition
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abnormal impulses resulting from spontaneous generation of action potentials during or immediately after phase 3 repolarization "ob#
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Abnormal impulse CONDUCTION example
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reentry process
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Sympathomimetics can cause arrhythmias how?
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increase automaticity of SA node, AV node or His-Purkinje fibers
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Non-pharmacological therapy for arrhythmias
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cardiac ablation.implantable defibrillator.
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fluoroquinolones are known to cause what in the heart?
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arrhythmias. Especially with longer term use.
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type 1 / class 1 MOA?
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a. bind to Na channels when they are open and inactivated, dissociate from the channel during the resting state. More pronounced effect on cardiac tissue that is rapidly firing.
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type 1 / class 1 are called what?
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Na channel blockers
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types 1b within type 1 or class 1 antiarrhythmic drugs?know for your own benefit
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greater affinity for inactivated state and slow recovery. More pronounced effect on ischemic tissue. Depress phase 0 selectively in abnormal/ischemic tissue, shorten repolarization
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types 1a within type 1 or class 1 antiarrhythmic drugs?know for your own benefit
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. greater affinity for open state with slow recovery.Depress phase 0, prolonging repolarization
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types 1c within type 1 or class 1 antiarrhythmic drugs?know for your own benefit
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greater affinity for open state and very slow recovery. Greater effect on ventricular conduction . Markedly depress phase 0, minimal effect on repolarization.
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Type II/Class II are what kind of drugs
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b-adrenergic receptor blockers a. Decrease slope of phase 4.
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Type IA drugs MOA?
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block Na+ channel and K+ channel. Suppress abnormal automaticity but do not significantly affect SA node automaticity and heart rate. All have some antimuscarinic (atropine-like) activity and may inhibit PNS effects on SA node and AV node. Depress phase 0, prolonging repolarization.
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quinidine is an example of? typle/class?
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type 1A
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ADR's of quinidine which are type 1A's?
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hypotension, GI effects (diarrhea 30-40%), thrombocytopenia, cinchonism (ASA toxicity -tinnitus, blurred vision, dizziness) headache, confusion, torsades de pointes. cinchonism cinchonism
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DDI's of quinidine which are type 1A's?
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i. –CYP450 substrate and inhibitor. Several interactions.
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procainamide is made from what?
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lidocaine
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how is procainamide made active in the body?
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Absorbedfrom gut and converted to active metabolite N-acetylprocainamide(NAPA)
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i. Indications-of procainamide?
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Tx most types of supraventricular and ventricular arrhythmias. Produces less hypotension than quinidine IV – so more often used IV for TX of acute ventricular arrhythmias.
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ADR's of procainamide
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hypotension, GI effects, CNS effects,hematologic (thrombocytopenia), anticholinergic effects, liver toxicity, lupus-like syndrome. (50%) lupus-like syndrome. (50%)
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DDI of procainamide
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i. CYP2D6 substrate
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Disopyramide is what class / type
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type 1A/Class 1A
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Disopyramide indications
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ventricular arrhythmias
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Disopyramide ADR's
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hypotension,anticholinergic effects(blurred vision, urinary retention), CHF, CNS effects including hallucinations.
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Type IB drugs MOA?
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Electrophysiological properties make them particularly suitable for ventricular arrhythmias. Strong affinity for Na channels in depolarized ischemic tissue, but lack of effect on Na channels in normal cardiac tissue. Depress phase 0 selectively in abnormal/ischemic tissue, shorten repolarization
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why does lidocaine work in the ventricles???
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lidocaine does work in ischemia, which is why it works well in the ventricles.
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lidocaine indications
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i. Ventricular tachycardia and other acute ventricular arrhythmias. Not useful for supraventricular arrhythmias. Also a local anesthetic.
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lidocaine first pass effect stuff I should know
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i. Extensive first pass hepatic inactivation after PO, therefore must be given IV.
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lidocaine ADRs
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CVS (bradycardia, hypotension, heart block), CNS(drowsiness, paresthesias, disorientation, muscle twitching- may lead to seizures). May also cause psychosis and respiratory depression
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Type IC drugs MOA
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block Na+ channels and block the rate of rise of the action potential during phase 0 to a greater extent than other class I drugs. They slow conduction velocity throughout the heart and especially in His-Purkinje system. Markedly depress phase 0, minimal effect on repolarization.
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flecamide indications
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i. Treatment of supraventricular arrhythmias and documented life threatening ventricular arrhythmias.
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flecamide ADR's
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reentry ventricular tachycardia, CHF, GI, CNS,blurred vision
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flecamide DDI's
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CYP450 substrate, CYP2DR inhibitor
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Propafenone MOA
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– block Na+ channels and block the rate of rise of the action potential during phase 0 to a greater extent than other class I drugs. They slow conduction velocity throughout the heart and especially in His-Purkinje system. Markedly depress phase 0, minimal effect on repolarization . Similar effects as flecainide except less effects on QT interval. Also has some beta blocking activity.l
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flecamide MOA
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– block Na+ channels and block the rate of rise of the action potential during phase 0 to a greater extent than other class I drugs. They slow conduction velocity throughout the heart and especially in His-Purkinje system. Markedly depress phase 0, minimal effect on repolarization
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Propafenone indications
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i. Treatment of supraventricular arrhythmias and documented life threatening ventricular arrhythmias
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Propafenone ADR's
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– reentry ventricular tachycardia. -same as flecainide but also hematological.
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Propafenone DDi's
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CYP450 substrate, CYP1A2, 2D6 inhibitor
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TYPE II/CLASS II DRUGS MOA
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1. inhibitsSNS activation of cardiac automaticity and conduction. Slow heart rate,decrease AV node conduction velocity and increase AV node refractory period
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TYPE II/CLASS II DRUGS Indications?
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1. Used for prevention and treatment of supraventricular arrhythmias and for their ability to reduce ventricular ectopic depolarizations and sudden death in pts with myocardial infarction
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Esmolol indications?how?how long?Who gets it?
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acute SVT tx. rapidly metabolized, short half life.Only hospital patients get it IV. No PO form.
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Metoprolol and Propranolol tx what?
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a. Both available PO or INJ for treatment and suppression of supraventricular and ventricular arrhythmias
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Metoprolol indications?
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i. given IV in early phase of MI followed by PO – protects the heart against the damage caused by ischemia and free radicals that may be formed during reperfusion of coronary arteries when fibrinolytics are used.
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Acebutolol can be used in preg when
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B/D in 2nd & 3rd trimester
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Amiodarone MOA
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block K+ channels and prolong the ventricular action potential depolarization and refractory period. i. Type III, but also blocks Na channels, Ca channels and b-adrenergic receptors. Decreases SA node automaticity, decreases AV node conduction velocity and prolongs AV node and ventricular refractory periods.q=iO
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Amiodarone properties
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i. organic iodine compound similar to thyroid hormones. Unusual kinetics, very long half-life (40 days).
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amiodarone indications
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POfor supraventricular and ventricular arrhythmias incl AF, atrial flutter, SVT and life threatening ventricular tachycardia. IV for acute life-threatening VF or sustained VT.
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amiodarone ADR's
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Several.GI effects, CV effects (hypotension, AV block, arrhythmias incl torsades (less torsades than other Class III agents), visual disturbances, thyroid dysfunction,pulmonary fibrosis and pneumonitis, blue-gray skin discoloration
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amiodarone DDI
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CYP450 substrate and inhibitor of almost all isoenzymes. Several DDI which increase levels of other important drugs like digoxin, phenytoin, warfarin skin
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Dronedarone properties
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i. –structurally similar to amiodarone but with shorter half-life, less lipophilicity and no iodine group so les risk of thyroid, pulmonary and neurological side effects
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Dronedarone MOA
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block K+ channels and prolong the ventricular action potential depolarization and refractory period. i. Type III, but also blocks Na channels, Ca channels and b-adrenergic receptors. Decreases SA node automaticity, decreases AV node conduction velocity and prolongs AV node and ventricular refractory periods.
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Dronedarone indications
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– to reduce risk of CV hospitalization inpatients with Afib or A-flutter with certain CV risk factors
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Dronedarone ADR's
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Like amiodarone but w/ less thyroid, pulmonary and neurological (visual) ADRs
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Dronedarone DDI's
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several CYP450 DDIs esp w digoxin, CCBs and warfarin. Watch warfarin carefully.
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Ibutilide MOA
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-Different MOA than other Type III drugs. Promotes influx of Na+ through slow inward Na channels which counteracts the outward K+ current thereby prolonging repolarization.oral chemical cardioversion.
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Sotalol MOA?
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i. non-selective beta-blocker with ability to block K+ current during ventricular action potential.
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Dofetilide indications and MOA
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chemical cardioversion and blockK+ channels.prolong the ventricular action potential depolarization andrefractory period
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Bretylium MOA
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prolongs ventricular action potential in normal tissue more than ischemic tissue
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TYPE IV DRUGS are what?
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CCB's non DHP
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CCB's MOA
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1. decrease AV node conduction velocity and increase AV node refractory period (blocks Ca+from entering slow channels during depolarization)
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CCB's indications
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IV for acute PSVT, PO for AF (avoid if coexisting HF).
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non DHP- CCB's examples
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verapamil and diltiazem
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Adenosine MOA
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activates specific G protein-coupled adenosine receptors resulting in hyperpolarization and slowing of AV node conduction velocity.
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adenosine indications
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SVT or PSVT
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adenosine ADR's
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a. flushing,dizziness, bradycardia, syncope
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digoxin MOA
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a. increases vagal tone, slows AV node conduction velocity and increases AV node refractory period
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digoxin gives you an arrhythmia how do you tx it?
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lidocaine
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indications for quinidine
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i. TX most types of supraventricular and ventricular arrhythmias
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ADR's of quinidine
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cinchonism, hypotension,GI effects (diarrhea 30-40%), thrombocytopenia, cinchonism (ASA toxicity - tinnitus, blurred vision,dizziness) headache, confusion, torsades de pointes.
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Mexiletine metabolism
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do not undergo first pass effect therefore used PO
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Mexiletine indications
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long term basis for suppression of ventricular arrhythmias
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ADR's of mexilentine
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GI and CNS effects, agranulocytosis with tocainide
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Moricizine unusuualy properties
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phenothiazine analogue.
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Moricizine indications
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documented life-threatening ventriculararrhythmias. (Long term use may be associated with increased mortality rate inpts with history of MI)
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abnormal conduction example? and what causes them?
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reentry arrythmias.re-excitation caused by same impulse that already went through that part.
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sotalol indications
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ventricular arrhythmias, a fib (avoid in Heart failure)
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sotalol ADR's
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dosedependent torsades de pointes, hypotension, bradycardia, bronchospasm
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dofetilide ADR's
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dose dependant torsades de pointes, CNS effects.
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bretylium indications and ADR's
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indications VF.ADR's GI effects, orthostatic hypotension, CNS effects
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digoxin indications
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AF, PSVT.
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digoxin ADR's
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GI, CNS, arryhthmias (you can tx arrhythmias with lidocaine)
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MagnesiumSulfate MOA?
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slowsrate of SA node impulse formation and prolongs conduction time
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MagnesiumSulfate indications
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VT , VF, and torsades de pointes
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MagnesiumSulfate ADR's?
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diarrhea, CNS depression, flushing
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how to manage A fib?
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first control rate with BB's, CCB's or digoxin. Rhythm control you can do electrical cardioversion, cardiac ablation, pharmacological conversion. with cardioversion make sure to anticoag for 3 weeks prior to cardioversion.Perform a TEE to check for thrombi.
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risk factors for A fib induced stroke on the chad2 scale and how many points each has?
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CHF= 1HTN= 1Age >75 = 1DM= 1Previous stroke =2
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stroke rate for chad 2 scores?0123456
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0= 1.92= 2.83= 44=8.55=12.56=18.2
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Chad2 score tx from points.012 or more
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0 aspirin 81-325 mg daily.1 aspirin 81-325 mg daily or warfarin with INR 2-3 based on patient preference.2 or more is warfarin INR 2-3 unless they need to avoid warfarin.
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Lupus like syndrome
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Procainamide
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Cinochism
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Quinidine.
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Anticholinergic effects
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Disopyramide
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Psychosis
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Lidocaine
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Blue/green skin.
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Amiodarone
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Arrhythmia
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Digoxin
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Pulmonary fibrosis
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Amiodarone
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Dose dependant torsades de pointes
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Dofetilide
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Thyroid dysfunction
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Amiodarone
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Hematologic effects
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Propafenone
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Diarrhea in 30 to 40% of patients
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Quinidine
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Agranulocytosis
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Mexilitine
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Phenothiazine analogue
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Moricizine
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