Pharm: Mgmt of Electrical Cardiac Dysfunction Flashcards
Na+ channel blockers (2)
class I/V
Quinidine and Lidocaine
Beta blockers
class II/V
Atenolol (any -olols)
K+ channel blockers (2)
class III/V
Amiodarone; sotalol
Ca2+ channel blocker
class IV/V
Diltiazem
Na+ channel class 1A blockers __?__ PR and QRS, slowing the rate in rise of phase __?__
Pronlong PR and QRS; slow the rate in rise of phase 0
What drug is most commonly used to treat A-fib/flutter in horses?
Quinidine
Na+ channel blocker
What arrhythmia can Quinidine cause and how?
Supraventricular tachycardia via anti-vagal tone effect (atropine-like)
How can quinidine be used in favor of digoxin?
Quinidine inhibits p-glycoprotein pumps –> increased digoxin serum concentrations by two-fold
recall: p-glycoprotein enhances elimination of drugs in kidneys/liver via excretion thru urine/bile
Class 1b Na2+ channel blocker indication
lidocaine, mexiletine
acute ventricular tachycardias
MoA of beta blockers
reduce sympathetic activity; reduce sinus atrial node rate and AV conduction
Atenolol works at what receptor?
Seletively blocks Beta-1 (resulting in decreased cardiac contractility, HR and CO)
Why should beta blockers be avoided in CHF patients?
esp Atelolol
B/c in CHF, the SNS is stimulated as a compensatory response –> sudden blockade of this response with beta blocker can lead to decompensation & worsen CHF
Sotalol MoA/uses
- non-selective beta-blocking activity + delay repolarization (phase 3) –> increase AP duration and the refractory (recovery in b/w consec. beats) period
- long-term tx for ventricular arrhythmias with sig. hemodynamic aspect
Describe Diltiazem’s MoA as a Ca2+ channel blocker
blocks calcium channels at at SA and AV nodes, reducing sinus rate
Clinical use of Diltiazem in dogs/cats
rate control of supraventricular arrhythmias ONLY (e.g., atrial fibrillation)
