Page 230 - Feline Cardiology

Chapter 18: Arrhythmias and Other Electrocardiographic Abnormalities 235

lowering of heart rate may trigger congestive heart thetic stimulation of the clinical environment makes
failure or even hypotension (possibly hypotensive hospitalization of cats solely for ECG monitoring a con-
shock) if the improvement in diastolic filling from a troversial issue, and Holter monitors may be unwieldy
lower heart rate is counterbalanced by the large for a cat with severe cardiac disease. As Holter monitor
decrease in heart rate, resulting in a lower, not higher, technology leads to further miniaturization, pre- and
cardiac output. Drugs that can suppress heart rate, like posttreatment monitoring to assess drug efficacy is likely
beta blockers or calcium channel blockers, should to increase and bring greater accuracy to antiarrhythmic
never be initiated when the patient is in fulminant diagnosis and therapy.
congestive heart failure, unless extreme tachycardia Antiarrhythmic drugs may be administered intrave-
(HR >280 beats/minute) is present and then only judi- nously or orally. Intravenous antiarrhythmic drugs are
ciously and with concurrent initiation of intravenous indicated in patients with VT that show persistent, severe
diuretics. clinical signs thought possibly to be life-threatening,
• Goal of treatment. Repeated dosing aimed at achiev- such as collapse (syncope with poor or only partial
ing a perfect ECG should be avoided. The goal is to recovery), repeated cardiogenic generalized seizures
establish a perfusing rhythm, not permanent sinus (caused by cerebral hypoperfusion), or obtundation.
rhythm in every case. Thus, success of treatment is The advantage of rapid serum levels and fine-tuning of
judged based on clinical signs (mentation, ability to drug administration with IV use must be weighed
ambulate), mucous membrane color, pulse strength, against the drawbacks of the patient’s sympathetic stim- Arrhythmias
blood pressure, and other parameters of cardiovascu- ulation while in intensive care; the personnel, expertise,
lar stability, not just the ECG. and equipment needs required for monitoring; expense;
• Emphasis on tractability and ease of compliance. For and the lack of proven therapeutic benefit of antiar-
the small proportion of cats that accept oral medica- rhythmic drugs in cats. The pharmacokinetics of intra-
tions undisguised, compliance is reasonable. Cats that muscular administration of lidocaine, beta blockers, and
resist medications should have them hidden in other injectables are poorly understood in cats, and the
purpose-made treats (e.g., “Pill Pockets”) or home- variable perfusion of skeletal muscle in a patient with
prepared foods (e.g., small quantity of low-salt soft severe cardiovascular disease makes the intramuscular
cheese). Forceful medication administration is detri- route a poor choice.
mental on at least three counts: owner’s frustration; Lidocaine is used as a first-line antiarrhythmic in
patient’s sympathetic stimulation, with cardiac detri- many species. It is a class Ib compound metabolized
ment; and likelihood of tablet fragment remaining in principally by the liver; marked first-pass elimination
esophagus if not swallowed with food or water. explains its lack of clinically effective oral bioavailability.
Asymptomatic cats with ventricular arrhythmias Lidocaine’s effects include sodium channel blockade-
should not be treated chronically if treatment involves mediated slowing of conduction, decrease in dispersion
such noncooperation on the patient’s part. of refractoriness, decrease in action potential duration
(reducing triggered activity), increase in effective refrac-
The goal of antiarrhythmic treatment is to reach a tory period, decrease in excitability (more so in diseased
rhythm that is hemodynamically stable, providing con- myocardium), and reduction in the rate of phase 4
sistently adequate perfusion/oxygen delivery to organs depolarization (Moïse 1999; Muir et al. 1999). It is
of the body. Knowing whether antiarrhythmic therapy widely reported that as a species, cats may be especially
has worked is a challenge: a spontaneous daily variation intolerant to lidocaine (Fox and Harpster 1999; Muir
in numbers of PVCs of up to 85% is observed in et al. 1999). Interestingly, most clinical references in the
untreated humans and dogs with PVCs, meaning (by current literature pertaining to lidocaine as an antiar-
extrapolation from these species) that a cat may have rhythmic drug in cats with heart disease stem from a
1000 PVCs on a Holter monitor recording one day and series of 7 cats described qualitatively in 1977; some cats
150 PVCs the next day, with no influence from antiar- suffered adverse neurologic effects but “the majority of
rhythmic treatment. It can be understood from this these reactions were cardiovascular, including conduc-
observation that no conclusions can be drawn regarding tion disturbances, bradyarrhythmias, and hypotension,
success or failure of antiarrhythmic drugs using periodi- with sudden death in 4 of the 7 cats (Tilley and Weitz
cally obtained ECG strips alone. Therefore, in the cat, 1977).” The cardiovascular nature of complications, par-
efficacy of antiarrhythmic treatment is gauged based on ticularly in an era when taurine-deficient dilated cardio-
improvement in clinical signs (e.g., syncope), if any were myopathy was widespread, is noteworthy, since high-dose
occurring, and continuous ECG monitoring, either in- lidocaine (10 mg/kg) produces a negative inotropic
hospital or via portable monitors. Currently, sympa- effect even in a healthy dog ventricle (Tsuboi and Chiba