Therapeutic Interventions for Dysrhythmias

Question 1

Coordinated Electrical Stimulation

Answer 1

• heart capable of automaticity
• two types of myocardial tissue
  (contractile/conductive)
• impulses travel through action potential superhighway)

Question 2

Etiology of Dysrhythmias

Answer 2

• 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

Question 3

Electrocardiograms (ECG or EKG)

Answer 3

• graphic recordings of the wave of electrical conduction across the myocardium
• three distinct waves: (P wave, QRS complex, T wave)

Question 4

Bradydysrhythmias

Answer 4

• 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)

Question 5

Tachyarhythmia

Answer 5

• 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)

Question 6

Management of Asymptomatic dysrhythmia

Answer 6

• little or no benefit to treatment with medications unless AFIB and then discussion regarding CHADS-2 score and anticoagulation

Question 7

Management of Acute Dysrhythmias

Answer 7

• in life-threatening cases, medications or electrocardioversion required

Question 8

Prophylaxis of dysrhythmias

Answer 8

• initiated for high-risk patients

- avoid drug combinations that increase QT interval

Question 9

Nonpharmacologic treatment

Answer 9

• 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)

Question 10

Phases and Measurement of the Cardiac Action Potential

Answer 10

• a cell with negatively charged membrane potential is polarized
• phase 4: cell is resting. membrane potential slowly increasing toward threshold potential

Question 11

Phase 0

Answer 11

• action potential begins when threshold potential is reached
• sodium rushes in, producing rapid depolarization.
• calcium enters at a slower rate

Question 12

Phase 1

Answer 12

• brief transient phase

- inside of plasma membrane reverses charge, becoming positive

Question 13

Phase 2

Answer 13

• plateau reached in which depolarization is maintained
• additional calcium enters
• contraction of cardiac muscle
• efflux of potassium from cells

Question 14

Phase 3

Answer 14

• 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.

Question 15

Therapeutic goals for drugs for dysrhythmias

Answer 15

• 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

Question 16

Sodium Channel Blockers: Class I

Answer 16

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

Question 17

Class I A prototype Drug: Sodium channel blocker
1. therapeutic effects and uses
2. mechanism of action
3 adverse effects

Answer 17

1. 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
2. blocks sodium channels in myocardial cells. reduces automaticity and slows velocity of action potential
3. Confusion and psychosis at high doses

Question 18

Class IB Sodium channel blockers

Answer 18

• shorten refractory period
• little effect on conduction velocity
• primary indications are ventricular dysrhythmias
• includes (lidocaine, mexiletine, phytoin)

Question 19

Class IC of sodium channel blockers

Answer 19

• Class IC antiarrhythmic
  (flecainide - may generate new ventricular dysrhythmias in 10% of patients)
  Propafenone (prodysrhythmic activity limits use in treating ventricular dysrhythmias)

Question 20

Class IC

Answer 20

• profoundly decrease conduction velocity
• PR, QRS, and QT intervals are often prolonged
• life-threatening ventricular dysrhthmias
• pronounced pro-arrhythmic affect

Question 21

Beta-Adrenergic Antagonists: Class II

Answer 21

• Treat HTN, MI, HF, and dysrhythmias
• block calcium channels in SA and AV nodes
• slow HR
• Decrease conduction velocity

Question 22

Potassium Channel Blockers: Class III

Answer 22

• block potassium ion channels in myocardial cells
• delay repolarization
• prolong refractory period
• limited use due to serious adverse effects

Question 23

Prototype Drug Potassium channel blocker: Amiodarone

1. therapeutic effects and uses
2. mechanism of action
3. Adverse effects
4. serious adverse effects

Answer 23

1. atrial and ventricular dysrhythmias/resistant ventricular tachycardia/recurrent fibrillation/highly toxic to multiple organs
2. exact mechanism unknown. blocks potassium channels but also blocks sodium ion channels and inhibits sympathetic activity
3. Nausea/vomiting/anorexia/fatigue/dizziness/hypotension/visual disturbances/rashes/photosensitivity
4. pneumonia-like syndrome/prodysrhythmic action

Question 24

Calcium Channel Blockers: Class IV

Answer 24

• 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

Question 25

Miscellaneous Antidysrhythmics

Answer 25

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