Atlantic Veterinary College, University of Prince Edward Island, Charlottetown, PE, Canada
The reader is referred to case examples shown in another set of notes in these proceedings (Nurse Technician program: Clinical Approach to Arrhythmias) for examples of the differential diagnosis for ventricular arrhythmias.
Historically, treating ventricular arrhythmias often was presented as a straightforward proposition: "If the rhythm is VT, or if there are more than 10/15/20/30 VPCs each minute (depending on the author), or if the rhythm has other 'criteria of malignancy' (e.g., polymorphic VT), then treatment must be instituted in order to prevent deterioration to even worse arrhythmias or cardiac arrest." Algorithms were mapped out to provide the best strategy for converting these arrhythmias, and these protocols were applied universally.
This cut-and-dried approach of yesteryear, albeit reassuring in its simplicity, has been shown in humans to be either imprecise or completely wrong. Large multi-institutional placebo-controlled, double-blinded trials in human cardiology (notably the CAST trials) have shown that although ventricular antiarrhythmic drugs can eliminate the arrhythmia and restore sinus rhythm, the human patients whose rhythm was improved this way died in significantly greater numbers than did the untreated (placebo) patients.
So whom, and when, do we treat in veterinary medicine? The axiom that pertains to treatment of all cardiac arrhythmias in small animals remains true. The two simplified reasons to treat a cardiac arrhythmia in a dog or cat are:
1. If it is making the animal sick, or
2. If the patient is at imminent risk of harm due to the arrhythmia
Step 1: Is the arrhythmia the cause of illness or one of many manifestations of a generalized problem?
Clinical signs attributable to ventricular arrhythmias can include weakness, staggering, collapse, and syncope/fainting. The presence of such signs warrants antiarrhythmic treatment.
A complete physical examination is essential, with particular attention to the cardiovascular system, to identify (and address) inciting causes of the arrhythmia.
Database: Complete electrocardiogram (ECG), complete blood count, serum biochemical profile, urinalysis, thoracic radiographs, abdominal ultrasound or radiographs or both, and echocardiogram are ideal. Rule out systemic disease and structural heart disease. Are there other disorders that secondarily cause ventricular arrhythmias - infection, trauma, neoplasia, intoxication, gastric dilation/volvulus? If so, treating these will address the arrhythmia at its source, rather than trying to mask it with antiarrhythmic drugs.
Virtually any disease, when severe enough, can secondarily produce ventricular arrhythmias.
If a disease is identified and controlled but the severity of the arrhythmia itself is worrisome, refer to Step 3, below.
Step 2: If there is no apparent underlying problem to explain the ventricular arrhythmia, is the arrhythmia itself serious enough to cause the clinical signs that are seen?
As an example, a few PVCs each minute would not be expected to reduce cardiac output by any substantial extent and should not produce clinical signs.
Conversely, rapid VT at 300 beats/minute in a giant-breed dog (a more extreme example) would most assuredly be expected to cause clinical signs. This is due to the poor diastolic filling of the ventricles between beats (inadequate time to fill), leading to reduced cardiac output.
Between these two extremes, it appears that the heart rate (specifically, ventricular rate) is a major determinant of clinical signs. A dog with an accelerated idioventricular rhythm, where all QRS complexes are wide and bizarre in shape and there is no A-V relationship, at a rate of 110 beats per minute, may have an ECG that is initially alarming (looks like "slow VT") but in fact be well-perfused and normotensive, and have none of its clinical signs due to the arrhythmia.
However, at higher ventricular rates, there comes a point where filling of the ventricles during diastole is inadequate and hemodynamic compromise begins. Rapid, sustained VT, especially in the absence of noncardiac disease to explain hypotension, and poor perfusion (regular but weak pulse, or low arterial blood pressure via manometry) subjectively are an indication for treatment of ventricular arrhythmias in this author's practice.*
Differentiating the weak pulses of hemodynamic instability (e.g., rapid VT) vs. intermittent pulse deficits (e.g., single, intermittent VPCs): the weak pulses discussed above are constant, and associated with VT that does not perfuse the body well (hemodynamically unstable). By contrast, it is expected that single PVCs will cause single pulse deficits, and this does not make a PVC "hemodynamically unstable".
Step 3: Is there a reversible or correctable disease process that could explain the arrhythmia? Common examples include anemia, hypokalemia, hypoxemia, splenic or other abdominal masses, gastric dilation and volvulus, and severe inflammatory states.
If so, and if the patient is hemodynamically stable, then treating the systemic abnormality is logical, and the arrhythmia can be expected to normalize. going on at the moment but it doesn't seem severe enough to be causing this arrhythmia.
If not, the recommended approach is:
Still establish nature of disease affecting this animal (other than the arrhythmia) and address it as best as can be done.
Assess peripheral perfusion, blood pressure, mentation to determine hemodynamic impact of the arrhythmia.
Evaluate serum electrolytes and correct imbalances appropriately, especially K+.
Expect improvement of pulse quality and perfusion with control of underlying disease. If rate of ventricular arrhythmia is not controlled or disease resolution does not bring expected clinical and ECG improvements, consider antiarrhythmic treatment.
Successful conversion to sinus rhythm should bring a visible, marked improvement in pulse quality, mentation, and mobility, if the arrhythmia was the sole cause of clinical signs. These changes should occur quickly (i.e., within minutes of conversion to sinus rhythm), although chronically affected dogs may take longer.
If conversion is successful but clinical signs persist, investigation of underlying disease should be pursued further.
If conversion is not successful, the opportunity to do harm becomes greater because of the temptation to administer more and more antiarrhythmic drug while staring only at the ECG monitor. When given in very high dosages, most antiarrhythmic drugs have proarrhythmic effects. That is, they can cause arrhythmias on top of the ones that already exist. Furthermore, the class Ib antiarrhythmics, notably lidocaine and mexiletine, also can cause neurologic disturbances (e.g., seizures). Repeat dosing of antiarrhythmic drugs is often valid, but the pharmacodynamics of the drugs must be kept in mind.
If giving IV drugs (e.g., lidocaine), keep in mind that the effect of the drug may disappear before its blood level decreases (i.e., the arrhythmia returns despite the continued presence of drug in the blood - potential for intoxication if re-dosing too frequently).
Drugs We Commonly Use
In dogs, draw up 4 mg/kg. Give 1/2 as IV bolus, then the other 1/2 over 5 min slow IV. Onset of action = 2 min or less. Duration of action = 10–20 min.
If needed, IV infusion is 25–80 µg/kg/min. Recipe: For a 50 µg/kg/min infusion, remove 27 mL of sterile 0.9% NaCl from a 500 mL bag and replace with 27 mL of 2% lidocaine (which does not contain epinephrine). Administer at maintenance (60 mL/kg/day).
In cats (caution because risk of toxicosis): 0.25–0.75 mg/kg slow IV bolus. If needed, IV infusion at 10–40 µg/kg/min.
"Broader spectrum" antiarrhythmic with both beta- and potassium-channel blocking properties. Drug of choice for VT in boxers with arrhythmogenic right ventricular cardiomyopathy. Typical dosage: 4–6 mg/kg PO q 12 h.