Therapeutic Interventions for Dysrhythmias Flashcards
Coordinated Electrical Stimulation
- heart capable of automaticity
- two types of myocardial tissue
(contractile/conductive) - impulses travel through action potential superhighway)
Etiology of Dysrhythmias
- some are asymptomatic
- others require immediate treatment
- occur in all age groups, in healthy and diseased hearts
- atrial arrhythmias can cause significant morbidity whereas Ventricular arrhythmias have higher mortality
Electrocardiograms (ECG or EKG)
- graphic recordings of the wave of electrical conduction across the myocardium
- three distinct waves: (P wave, QRS complex, T wave)
Bradydysrhythmias
- HR less than 60 bpm
- common in older adults
- major indication for pacemakers
- common bradyarrhythmia (sinus bradycarida, sinoatrial node dysfunction, atrioventricular conduction block or delay)
Tachyarhythmia
- HR over 100 bpm
- incidence increases in older adults and those with preexisting cardiac disease
- common tachyarrhythmia (atrial tachycardia, atrial fibrillation, atrial flutter, ventricular tachycardia, ventricular fibrillation, torsades de pointes)
Management of Asymptomatic dysrhythmia
- little or no benefit to treatment with medications unless AFIB and then discussion regarding CHADS-2 score and anticoagulation
Management of Acute Dysrhythmias
- in life-threatening cases, medications or electrocardioversion required
Prophylaxis of dysrhythmias
- initiated for high-risk patients
- avoid drug combinations that increase QT interval
Nonpharmacologic treatment
- cardioversion or defibrillation - electrical stimulation of the heart reserved for symptomatic patients with changes in their cardiac output status
- identification and destruction of myocardial cells responsible for abnormal conduction
- cardiac pacemakers
- implantable cardioverter defibrillator (ICDs)
Phases and Measurement of the Cardiac Action Potential
- a cell with negatively charged membrane potential is polarized
- phase 4: cell is resting. membrane potential slowly increasing toward threshold potential
Phase 0
- action potential begins when threshold potential is reached
- sodium rushes in, producing rapid depolarization.
- calcium enters at a slower rate
Phase 1
- brief transient phase
- inside of plasma membrane reverses charge, becoming positive
Phase 2
- plateau reached in which depolarization is maintained
- additional calcium enters
- contraction of cardiac muscle
- efflux of potassium from cells
Phase 3
- calcium channels close
- additional potassium channels open
- repolarization returns negative resting membrane potential
- refractory period (brief period where depolarization cannot occur. ensures myocardial cell finishes contracting before another action potential begins.
Therapeutic goals for drugs for dysrhythmias
- terminate existing dysrhythmia
- prevent abnormal rhythms
- restoration of sinus rhythm
- rate versus rhythm control
Classification is based on stage at which they affect action potential
Sodium Channel Blockers: Class I
largest group of antiarrhythmics
- similar in structure and function to local anesthetics
- includes
Quinidine
Disopyramide (Norpace)
Procainamide
- block sodium ion channels during phase 0 of action potential
Class I A prototype Drug: Sodium channel blocker
1. therapeutic effects and uses
2. mechanism of action
3 adverse effects
- ventricular tachycardia during CPR/refractory ventricular fibrillation during CPR/pulseless ventricular tachycardia during CPR/PAT, atrial flutter, atrial fibrillation/prophylaxis of PSVT/drug of last choice for ACLS
- blocks sodium channels in myocardial cells. reduces automaticity and slows velocity of action potential
- Confusion and psychosis at high doses
Class IB Sodium channel blockers
- shorten refractory period
- little effect on conduction velocity
- primary indications are ventricular dysrhythmias
- includes (lidocaine, mexiletine, phytoin)
Class IC of sodium channel blockers
- Class IC antiarrhythmic
(flecainide - may generate new ventricular dysrhythmias in 10% of patients)
Propafenone (prodysrhythmic activity limits use in treating ventricular dysrhythmias)
Class IC
- profoundly decrease conduction velocity
- PR, QRS, and QT intervals are often prolonged
- life-threatening ventricular dysrhthmias
- pronounced pro-arrhythmic affect
Beta-Adrenergic Antagonists: Class II
- Treat HTN, MI, HF, and dysrhythmias
- block calcium channels in SA and AV nodes
- slow HR
- Decrease conduction velocity
Potassium Channel Blockers: Class III
- block potassium ion channels in myocardial cells
- delay repolarization
- prolong refractory period
- limited use due to serious adverse effects
Prototype Drug Potassium channel blocker: Amiodarone
- therapeutic effects and uses
- mechanism of action
- Adverse effects
- serious adverse effects
- atrial and ventricular dysrhythmias/resistant ventricular tachycardia/recurrent fibrillation/highly toxic to multiple organs
- exact mechanism unknown. blocks potassium channels but also blocks sodium ion channels and inhibits sympathetic activity
- Nausea/vomiting/anorexia/fatigue/dizziness/hypotension/visual disturbances/rashes/photosensitivity
- pneumonia-like syndrome/prodysrhythmic action
Calcium Channel Blockers: Class IV
- limited number approved as antidysrhythmics (diltiazem, verapamil)
- effects similar to those of beta-adrenergic antagonists
- safe and well tolerated by most patients
- monitor for bradycardia and hypotension
Miscellaneous Antidysrhythmics
Adenosine:
- naturally occuring nucleoside
- activates potassium channels in SA and AV nodes
- terminates tachycardia
- primary indication is PSVT
- 10-second half-life, so adverse effects are self-limiting
Digoxin
- primarily used for HF
- can be prescribed for atrial flutter, fibrillation, or PSVT
- not effective against ventricular dysrhythmias
- patients must be carefully monitored for toxicity, drug interactions, and adverse effects
