Antiarrhytmics Flashcards
Review antiarrhythmics diagram.
What occurs in phase 0 of myocyte AP?
What occurs in phase 1 of myocyte AP?
What occurs in phase 2 of myocyte AP?
What occurs in phase 3 of myocyte AP?
What occurs in phase 4 of myocyte AP?
What is the effective refractory period?
Effective or absolute (phase 2) (ERP) is the longest amount of time when cells cannot be depolarized again. The longest input that fails to conduct.
What are common factors that facilitate arrhythmias?
- hypoxemia
- electrolyte/acid-base abnormalities (acidosis, alkalosis, K+, Mg++)
- myocardial ischemia
- bradycardia
- altered sympathetic nervous system various drugs
What are non-modifiable risk factors of Cardiac Arrhythmias?
- dilated cardiac diseases
- ischemic cardiomyopathy
- autonomic changes of the conduction system
- polymorphism of ion channels
- congenital long-QT syndrome (LQTS).
Most arrhythmias occurring during anesthesia do not require treatment unless ____________
hemodynamic compromise
What is the mechanism of cardiac arrhythmias?
- re-entry
- enhanced/ectopic pacemaker activity
- triggered activity
- early after depolarization
- delayed after depolarization
Mechanisms of Cardiac Arrhythmias: Define re-entry.
- Due primarily to abnormality of conduction, an impulse may recirculate in the heart and cause repetitive activation without the need for any new impulse to be generated.
- These are called reentrant arrhythmias.
Mechanisms of Cardiac Arrhythmias: Define Enhanced/ectopic pacemaker activity
Ectopic impulse may be increased pathologically in the automatic fibers or such activity may appear in ordinary fibers.
Mechanisms of Cardiac Arrhythmias: Define Triggered activity.
Secondary depolarizations accompanying a normal or premature action potential (AP).
Mechanisms of Cardiac Arrhythmias: Define Early after-depolarization.
- Repolarization during phase-3 is interrupted and membrane potential oscillates.
- If the amplitude of oscillations is sufficiently large, neighboring tissue is activated and a series of impulses are propagated.
Mechanisms of Cardiac Arrhythmias: Define Delayed after-depolarization.
After attaining resting membrane potential (RMP) a secondary deflection occurs which may reach threshold potential and initiate a single premature AP.
What are the two main causes of Mechanisms of Cardiac Arrhythmias?
- Re-entry
- Enhanced/ectopic pacemaker activity
What are the ECG changes with Hypomagnesemia?
- prolonged PR QT intervals, diminished T-wave
- Torsades
What are the ECG changes with Hypermagnesemia?
QRS widening, heart block, arrest
What does Hypomagnesemia often accompany?
hypoK+ and hypoCa
What are the ECG changes with Hypocalcemia?
Prolongation of QT
What are the ECG changes with Hypercalcemia?
- QT shortening
- widened or flattened T wave
- J waves following QRS (early repolarization
What are the effects with Hypokalemia?
- cellular level- hyperpolarizes (prolonged action potential)
- This leads to Na+/Ca++ derangements that result in increased excitability
What are the ECG changes with Hypokalemia?
- flattened T wave/inversion and U waves (repolarization)
- PVC’s
- tachyarrhythmias
- Torsades
- AF
- VT/VF
What is hypokalemia associated with?
Associated with dig toxicity
What are the ECG changes with Hyperkalemia?
- peaked T-waves
- PR prolongation
- QRS widening
- VF
- asystole
Review different classifications of arrhythmias.
Review the narrow and wide QRS complex.
What is the general MOA of Antiarrhythmic Drugs?
Block Na+, K+, Ca++ ion channels that constitute each phase of the cardiac action potential (AP)
What effects duration of Antiarrhythmic Drugs?
Duration of phase varies, atria vs ventricles
What is the inactive state?
unresponsive to a continued or new stimulus (plateau phase/repolarization
What is the resting state?
more prevalent during diastole
What is the active state?
more prevalent during systole (upstroke of the action potential)
What are the clinicsl effects of antiarrhymic drugs?
- are targeted to specific phases (ions) of the AP and the effective refractory period (ERP)
- leads to electrophysiologic effect on the myocardium
What is a component of the relative regractory period?
coincides with the T wave apex
What is the effect of Na+ blockade?
slow conduction and suppress upstroke velocity of the AP
What is the effect of K+ blockade?
prolong repolarization by increasing the duration of the AP and ERP resulting in prolonged QT (Class III agents)
What is the effect of Ca++ blockade?
by way of the α-subunits of L and T myocardial Ca++ channels
Where do Class 1 drugs exert their effect on the cardiac AP?
Na+ Channel Blocker
- Phase 0 (Na+ in)
What are examples of Class 1 antidysrhymic medications?
Na+ Channel Blocker
- 1a (moderate): Quinidine, Procainamide
- 1b (Weak): Lidocaine, Phenytoin
- 1c (strong): Flecainide, Propafenone
What are examples of Class 4 antidysrhymic medications?
Ca2++ Channel blocker
- Verapamil
- Dilitiazem
Where do Class 4 drugs exert their effect on the cardiac AP?
Ca2++ Channel blocker
- Phase 2 (Ca2+ In)
Where do Class 3 drugs exert their effect on the cardiac AP?
K+ Channel Blocker
- Phase 3 (K+ Out)
What are examples of Class 3 antidysrhymic medications?
K+ Channel Blocker
- Amiodarone
- Sotalol
Where do Class 2 drugs exert their effect on the cardiac AP?
Beta-Blocker
- Phase 4 (K+ rectifier)
What are examples of Class 2 antidysrhymic medications?
Beta blocker
- Propranolol
- metoprolol
Review cardiac antiarrhythmic drugs overview.
Review efficacy of individual antiarrhythmic drugs.
What is the MOA of Class I drugs?
These drugs inhibit fast sodium channels during depolarization (phase 0) of the cardiac AP
What are the different types of Class I Drugs?
- Class 1A
- Class IB
- Class IC
What are the effects of Class 1A antidysrhythmics?
lengthen cardiac AP & ERP, Na+ channel inhibition, prolonged repolarization d/t K+ channel blockade
What are the effects of Class 1B antidysrhythmics?
shorten the cardiac AP duration & refractory period
What are the effects of Class 1C antidysrhythmics?
potent Na+ channel blockers, decrease rate of phase 0 depolarization & speed of conduction of cardiac impulses; little effect on AP or ARP; proarrhythmic effects
What do class II drugs block?
These drugs primarily beta adrenergic blockers
What are the effects of Class II drugs on the AP?
- Decreased rate of spontaneous phase 4 depolarization
- decreased autonomic nervous system activity
What effect do Class II drugs have on the myocardial oxygen requirements?
Class 2: Beta Blockers
- Drug-induced slowing of HR reduces myocardial oxygen requirements
What affect do Class II Drugs have on the conduction of the heart?
Beta Blocker
- Slows speed of conduction of impulses through atrium
- prolongs PR interval on ECG
- doesn’t alter duration of cardiac AP
What is the MOA of Class III drugs?
K+ channel blocker
- Block potassium ion channels, results in prolongation of cardiac depolarization, AP duration, & ERP
What does Class III drugs decrease?
Decreases proportion of cardiac cycle during which myocardial cells are excitable & susceptible to a triggering event
When are class III drugs useful?
Useful in suppressing reentrant tachycardias making the AP duration to be longer than that generated within the tachycardia circuit
What are the effects of Amiodarone?
- exhibits class III effects, class I, class II, and class IV effects
- used in tx of supraventricular & ventricular arrhythmias
What is the effects of Sotalol?
long acting, noncardioselective β-blocking drug w/ class III effects
What are the effects of Dofetilide?
class III drug prescribed by cardiologists
What are class IV drugs?
verapamil & diltiazem
What is the MOA of Class IV drugs?
act by inhibiting inward slow calcium ion currents that may contribute to development of tachycardias
Which Ca++ triggers contraction?
The L-type Ca++ channel is most abundant and is responsible for Ca++ entry into the cell that triggers contraction.
What are T type Ca channels?
T-type Ca channels are most prevalent in the conduction system and are probably involved in automaticity
What are Class IV drugs useful in treating?
Useful in tx of SVTs and idiopathic ventricular tachycardia
Which CCBs do not possess Class IV drugs?
Dihydropyridine CCBs do not possess antiarrhythmic action (nifedipine, nicardipine, nimodipine)
What is a Torsade de pointes more likely to develop?
- More likely to develop with prolonged QTc
- Drugs that increase duration of refractoriness; prolong the QTc d/t K+ channel blockade
What medications likely to cause Torsades?
Class IA (quinidine, disopyramide); Class III (amiodarone)
What is torsades often associated with?
Often asso/w bradycardia b/c the QTc interval is longer at slower heart rates
What can exacerbate torsades de pointes?
Exacerbated by hypoK+, hypoMg++, poor LV function, and other QT prolongation drugs
How does ventricular tachycardia occur?
Slowed conduction that allows for ventricular re-entry impulse
What is the medications often associated with ventricular tachycardia?
Class IA (quinidine, procainamide), Class IC (flecainide, propafenone); (rarely class IB)
What is true about ventricular tachycardia?
Tends to be slower and resistant to drug or electrical therapy
What is true about wide complex ventricular rhythms?
re-entrant tachycardia that can degenerate into VF
What drug class is associated with wide complex ventricular rhythms?
Class IC drugs (flecainide, propafenone)
Chronic suppression of ventricular ectopy does not prevent future occurrence of ______________
life-threatening arrythmias
What medication can prevent prevent future occurrence of life-threatening arrythmias?
Except amiodarone
What precludes the use of Class IA/IC in CHF patients?
- Proarrhythmic and negative inotropic effects
- Amiodarone ok
What increases mortality of with Class IA/IC?
Hx of MI and ventricular arrythmias: Mortality increased with Class IA/IC
What decreases mortality of with Hx of MI and ventricular arrythmias?
Decreased with amiodarone and β-blockers
What is not recommended in early stages of MI?
- Lidocaine not recommended for prophylactic Tx in early stages of MI
- CCB not recommended as first-line tx for acute MI
What is treatment of torsades de pointes?
Magnesium
What is true about amiodarone and heart failure patients?
Little role for drugs other than amiodarone for prevention of cardiac sudden death in patients with heart failure
What is a common complication after cardiac surgery? What is prophylactic therapy?
Atrial fibrillation after cardiac surgery a common complication: Prophylactic therapy to reduce occurrence (& risk of stroke) often uses amiodarone, β-blockers, sotalol and Mg++
The benefits of using an antiarrhythmic other than for ______ does not always outweigh the risks
acute use
