Pharmacological

Treatment of Arrhythmias
Do I need to treat?

Is there haemodynamic instability/compromise?

Could this be a premonitory sign of a more serious arrhythmia or of
sudden death?

TREAT UNDERLYING CAUSE FIRST – e.g. electrolyte imbalance,

CHF, GDV, sepsis, autonomic imbalance, inflammation, toxins,
hypo/hyperthermia, respiratory disease……..

Always consider the possible adverse

effects of treatment.

Drugs alter the shape of action potentials in

cardiac tissue with the aim of making
arrhythmogenesis less likely…………
Cardiac Action Potentials
Sympathetic fibres innervate the entire heart.
Stimulation of beta-1 receptors leads to
•increase in HR,
•increased AVN conduction,
•shortening of AP,
•increased contractile force.
This increases cardiac work, pacemaker currents, oxygen demand etc.
And are therefore potentially arrhythmogenic.

Parasympathetic fibres (from the vagus) innervate the SAN and AVN.
Stimulation of muscarinic receptors by Ach leads to decreased heart rate
due to decreased rate of depolarisation and hyperpolarisation of the
membrane.
Lidocaine – 1st choice for ventricular tachyarrhythmias

Inhibits fast Na channels - therefore slows conduction in Purkinje and

working myocytes.
Preferential inhibition on cells with less –ve resting potential – and
therefore targets diseases cells first.
Rapid first pass metabolism so i/v is best. Multiple boluses (2mg/kg
over 1-2mins, 1-2mins between each bolus to check for resolution.
Consider CRI or switch to per os Mexiletine for chronic therapy.

No effect on nodal tissue so rarely useful in supraventricular

tachyarrhythmias.
S/e – mainly neurological inc seizures, muscle tremors.
Beta Blockers – supraventricular tachyarrhymias
Atenolol, propanolol, metoprolol.

Inhibit atrial ectopy, slow conduction at AVN.

Decrease ventricular rate in AF.
Increase refractory period in atria.

BUT reduce contractility and relaxation. So avoid in patients with

systolic dysfunction and poorly controlled CHF.
Diltiazem – supraventricular tachyarrhymias

Ca channel blocker. Therefore, slows sinus rate, and AVN

conduction

Good for animals in CHF (especially cats) – few adverse effects at

therapeutic doses. At higher doses begin to see negative inotropic
effects.

Highly protein bound so frequent administration required.

Digoxin

Many actions but most important to combat arrhythmias is

activation of vagal (parasympathetic tone).

Slows sinus rate, decreases AVN conduction.

Also inhibits Na/K/ATPase, leading to increased Ca in the cells

(as the Ca level is governed by a Na/Ca transporter) – which
leads to increased contractility. UNTIL Ca levels become too
high, when tachyarrhythmias can result.

Agent of choice in atrial tachyarrhythmias in dogs with CHF.

Monitor renal parameters – due to blockade of renal Na/K.

Interacts with a lot of other drugs.

Amiodarone

Numerous mechanisms of action, acts on all parts of the heart.

Slow and variable onset, long half life, numerous extra-cardiac

actions.

Seems most useful at cardioversion following AF, or to maintain

sinus rhythm following electrical cardioversion. Used for
ventricular arrhythmias in dogs with CHF (questionable?).

Appetite suppression, GI disturbances, +ve Coombs test,

hypotension, hypersensitivity reactions.
 Underlying CHF Digoxin
Diltiazem

Supraventricular

No underlying CHF Beta blocker

Ventricular

Lidocaine (or Amiodarone

associated drug)