HLSC 220 Notes-127-132 PDF

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HLSC 220 Notes-127-132...

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Antidysrhythmic Drugs A Beating Heart Rate: frequency/unit time o 70 beats/min Rhythm: the regularity or irregularity of the beating Electrical activity spreads throughout heart tissue in a co-ordinated manner o ion channels in cell membrane Electrical activity leads to mechanical activity o co-ordinated contraction of cardiac muscle

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Definition Dysrhythmia o Any deviation from the normal rate/rhythm of the heart Arrhythmia “no rhythm” o Asystole – no heartbeat

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Dysrhythmias Tachydysrhythmias o HR is increased o MUCH more common o Drugs and other treatments Brady dysrhythmias o HR is slowed o Electrical pacing o Atropine

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Many causes of dysrhythmias o ischemic heart disease o myocardial infarction o cardiomyopathy o myocarditis o electrolyte imbalances (eg abnormal K+ level) Antidysrhythmics (antiarhythmics) o drugs used for the treatment and prevention of disturbances in cardiac rate and/or rhythm o most suppress abnormal electrical impulse formation or conduction

Cardiac Electrical Activity • • • • •

SA node cells AV node cells Purkinje cells Ventricular cells Electrical activity

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differs with each cell type

AP and Cardiac Muscle Contraction • •

Movement of ions across the cardiac cell membrane results in AP generation AP leads to contraction of the myocardial muscle

Cardiac Electrical Activity •

Cardiac physiology o Action potentials differ between cardiac cell types

SA and AV Node Cells • •

AP depends on Ca2+ influx via Ca channels

Ventricular/Atrial Cardiac Muscle Cell • •

AP starts with Na+ influx = depolarization o via Na channels AP ends with K+ efflux = repolarization o via K channels

Cardiac Electrical Activity

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Dysrhythmias •

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Symptoms o palpitations o dizziness o fainting o dypsnea Some are asymptomatic Supraventricular tachycardia (SVT 120-250 beats/min) o Where is the problem? Supraventricular tachycardia o Paroxysmal § episodic, start suddenly and returns to normal (within ~24 hours) o Persistent § episodes longer than seven days § usually treatment is needed to return the heart to a normal rhythm o Permanent § dysrhythmia lasts for more than a year despite medications and other treatments Supraventricular tachycardia o Atrial flutter Supraventricular tachycardia o Atrial fibrillation § most common Ventricular Tachycardia (VT) Problem with ventricular muscle o eg non-sustained (30 sec) Ventricular fibrillation o Why is this bad? Supraventricular dysrhythmias affect ventricular contraction rate o A-V block desirable Ventricular dysrhythmias more dangerous than supraventicular

Antidysrhythmic Drugs : Mechanism of Action •

Large variety of drugs o Categorized according to how drugs alter heart function o Vaughan Williams Classification

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ALL antidysrhythmics can cause dysrhythmias! o Create new and/or worsen existing ones

Antidysrhythmic Drugs - Vaughan Williams Classification •

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Class I – Na channel blockers o Class Ia o Class Ib o Class Ic Class II – b blockers Class III – K channel blockers (+ others) Class IV - Calcium channel blockers Other (adenosine, digoxin)

Class I: Na Channel Blockers

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AP starts with Na+ influx = depolarization all block Na channels o slow depolarization o Subdivided due to differing pharmacological effects Class Ia : quinidine , procainamide, disopyramide o Block sodium channels Slows atrial and ventricular rates Also delay repolarization (Class III action) Increase the APD Used for ACU ACUTE TE onset atrial fibrillation o premature atrial contractions (PAC) o premature ventricular contractions (PVCs) o ventricular tachycardia o Wolff-Parkinson-White syndrome (usually tachy, may cause atrial fib/flutter) Class Ib : lidocaine (IV) o Block sodium channels Accelerate repolarization Decrease the APD Used for ventricular dysrhyt dysrhythmias hmias only o premature ventricular contractions (PVC) o ventricular tachycardia o fibrillation after MI Class Ic: flecainide, encainide, propafenone o Block sodium channels

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Little effect on APD or repolarization Used for: o severe ventricular dysrhythmias o atrial fibrillation

Class II: b-adrenoceptor Antagonists • • • • • •

In SA & AV AP depends on Ca2+ influx B-adrenergic receptors increase Ca influx therefore B-blockers reduce cell activity Class II : b-adrenoceptor antagonists (beta blockers) Metoprololl, esmolol (IV), propranolol, sotalol (also Class III) o Metoprolo Reduce or block sympathetic nervous system stimulation o AV Block General myocardial depressants for both supraventricular and ventricular dysrhythmias

Class III: Potassium Channel Blockers • • •

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AP ends with K+ efflux = repolarization o Potassium channels blockers prolong AP Class III : amiodarone, dofetilide, sotalol, bretylium Prolong repolarization o prolong cardiac AP § extends refractory period of cells Amiodarone also affects SA node, contractility Amiodarone – very effective drug o but ~ 75% have serious AE if used for 6 months eg lung fibrosis, thyroid o 10% are fatal o Used for o Ventricular tachycardia or fibrillation, atrial fibrillation or flutter § resistant to other drugs o Sustained ventricular tachycardia

Class IV: Calcium Channel Blockers • • • • • • •

In SA & AV AP depends on Ca2+ influx Ca channel blockers reduce cell electrical activity Class IV : diltiazem , verapamil Calcium channel blockers - CCBs o Inhibits Ca cell entry o “Cardio-active” Act on AV node – reduce conduction velocity o AV Block Used for paroxysmal (“periodic attack”) SVT o Rate control for atrial fibrillation and flutter Not for ventricular dysrhythmias

Unclassified Antidysrhythmics •

Digoxin and adenosine

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o Do not fit into Classes I – IV o Both decease AV conduction and SA automaticity Digoxin o AV block o Slows HR o See ionotropics class for other actions of digoxin Adenosine o Slows conduction through the AV node § AV block o Used to convert paroxysmal supraventricular tachycardia to sinus rhythm o Short half-life — 10 to 20 sec o Only administered as fast IV push o May cause asystole for a few seconds

Antidysrhythmic Drugs: Adverse Effects l ALL antidysrhythmics can cause dysrhythmias!

Nursing Implications •

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Ensure that the client knows to notify health care provider of any worsening of dysrhythmia and: o Shortness of breath o Edema o Dizziness o Syncope o Possible signs of toxicity of the drug Clients taking B-Blockers or digoxin, and other agents should be taught how to take their own radial pulse for 1 full minute notify their physician if the pulse is less than 60 beats/minute before taking the next dose of medication Monitor for therapeutic response o Decreased BP in hypertensive clients o Decreased edema o Regular pulse rate o Pulse rate without major irregularities o Improved cardiac output

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