Summary Pharmacy Pharmacology Anti Arrythmics (Key points) Medical School

ANTI ARRHYTHMICS

States of Na+ channels:  Ventricular myocyte:
1. Open – during upstroke (P0) Na blockers have inc. affinity a) slow down or reduce slope of or ↓upstroke (P0) – this is the main “Na+ channel blockade”
2. Inactivated – during plateau (P2) function
3. Resting/Closed – as the membrane repolarizes (P3) IA - moderate
IB – weak IC > IA > IB
Na & Ca blockers – alter threshold potential (TP) aka the CFL IC – strong
K blockers (class III function) – prolongation of repolarization (P3) → prolong (APD) action potential
duration → prolonged ERP b) some prolongs repolarization (P3) ---- additional potassium channel blockade ↑ APD →
increases ERP
Sodium channel blockade (Class I) IA - increase
 SA node: ↓ automaticity by ↑TP (hard to create an action potential) & ↓slope of P4 or slow IB - shortens
P4 (slow spontaneous depolarization) IC – no effect

Class I: SODIUM Channel Blockers
Class IA (“PaQ, Die”) MODERATE Na+ blockade + ↑ ERP Anti-cholinergic/anti-muscarinic/Atropin-like effects : D > Q > P
DRUG CARDIAC EXTRACARDIAC EFFECTS CARDIAC EXTRACARDIAC TOXICITY KINETICS USES
EFFECTS TOXICITY
Procainamide SA nodal effect:  Ganglion blocking  Excessive slowing of  Lupus-like syndrome (25  Different routes:  Atrial and ventricular
 Slows P4 depolarization properties conduction – 30 %) IV, IM, PO arrhythmias
→ ↓ abnormal  ↓ peripheral  Precipitation of new (arthralgia, pleuritis, (good absorption)
automaticity vascular resistance* arrhythmias such as pericadtitis, parenchymal  NAPA metabolite - Class
 ↑ threshold for  Orthostatic torsades de pointes lung dse., ↑ ANA) III activity (reason for
excitation in atrium and Hypotension (esp.IV) (TDP)  Nausea & Diarrhea TDP)  Sustained ventricular
ventricles – direct  Syncope 10%  Liver metabolism and arrhythmias with acute
depressant action WEAK ANTICHOLINERGIC  Hepatitis renal excretion MI (second choice)
Ventricular myocyte effects EFFECTS  Fever
mentioned above: Constipation  Rash  Half-life is 3-4 h (frequent
 ↓ PO Dry mouth  Agranulocytosis dosage)
 ↑P3 → ↑APD → ↑ERP Tachycardia (Cardiac)  Dose reduction in renal
Urinary retention failure and heart failure
Blurred vision
Quinidine  Similar to procainamide  Excessive slowed  Diarrhea, nausea,  Rapid absorption after Occasional:
 More cardiac anti- conduction vomiting oral intake Atrial flutter/fib
muscarinic effects than  TDP  Hepatitis  Binds to albumin and  (supraventricular)
procainamide  Excessive QT interval  Fever glycoprotein
prolongation  Cinchonism  (less free active)
Dizziness
DizTinHea  Hepatic metabolism
Tinnitus
(Destiny)
Headache  Half-life: 6-8 hrs
 Thrombocytopenia  Slow release formulations
 Angioneurotic edema

Disopyramide  Similar to procainamide  Similar to quinidine:  ATROPINE-LIKE  Oral  Ventricular arrhythmias
& quinidine  Excessive slowed EFFECTS  Reduced dose in renal
least appropriate/ most  Greater cardiac anti- conduction Constipation failure
dangerous class I drug muscarinic effect than  TDP Dry mouth
quinidine (drug that  Excessive QT interval Tachycardia (Cardiac)
slows AV conduction is prolongation Urinary retention
given with it)  Precipitation of heart Blurred vision
failure Glaucoma worsening