Electrocardiograms (ECGs) are commonly performed during routine anesthesia to monitor the heart rate and rhythm of your canine and feline patients. ECGs help assess the patient’s cardiovascular stability. Various arrhythmias can be encountered during an anesthetic event and ventricular arrhythmias are one of the more insidious types.
Ventricular arrhythmias are abnormal, premature beats, originating from the ventricles. These beats can be differentiated from normal sinus beats because they are not associated with a p-wave, are wide and bizarre in morphology, and occur earlier in time than the next expected beat. It is important to identify these arrhythmias to determine when medical intervention is necessary or when a procedure should be abandoned for further workup. Below are a few tips to help guide your decision making while your canine or feline patient is anesthetized.
How severe are the ventricular arrhythmias?
The first step to assess if your patients’ procedure should continue, is grading the ventricular arrhythmia. Low grade arrhythmias (grade I-II) – i.e. single, uniform, premature ventricular complexes (VPCs) do not usually cause hemodynamic compromise and are at a low risk for electrical instability. This also includes ventricular bigeminy and trigeminy (every other beat is a VPC or every other two beats are a VPC, respectively). As long as the VPCs are infrequent, and the heart rate and blood pressure remain stable, no additional treatment is necessary. It is okay to finish the anesthetic event. The patient should be reassessed once recovered to determine if a persistent arrhythmia is present that may need to be further investigated.
Figure 1. Lown and Wolf grading scheme for the severity of ventricular arrhythmias.
If your patient has multifocal VPCs (grade III), or ventricular couplets (IVa) medical intervention may be necessary. Multifocal VPCs represent more widespread conduction abnormalities. They can be identified as VPCs coming from different foci (some may be positive, some may be negative in polarity). Ventricular couplets represent two VPCs in a row. If the arrhythmia is frequent, or causes hemodynamic compromise, in a canine patient, a 2 mg/kg IV bolus of lidocaine should be administered. A clinical response should be seen within minutes. Please note that lidocaine is fast acting and if the patient responds but arrhythmias recur during the anesthetic event, a lidocaine CRI may need to be started (50 mcg/kg/min in a canine patient). The procedure should be stopped if the patient does not respond to medical intervention. Further investigation and workup should be pursued if the arrhythmia is present after recovery.
Figure 2. Lead I-III in a dog showing an underlying sinus rhythm with two, ventricular couplets.
Higher grade arrhythmias such IVb, and V warrant immediate medical intervention. Grade IVb represents ventricular triplets i.e. three VPCs in a row. Ventricular tachycardia is more than four VPCs in a row. Grade V represents R-on-T or the R wave of the VPC falls on the previous beats T wave. These arrhythmias are electrically unstable and can create hemodynamic compromise or degeneration of the arrhythmia. Medical intervention is warranted as described above (in a canine: 2 mg/kg IV bolus of lidocaine, followed by a 50 mcg/kg/min constant rate infusion). If the arrhythmia is frequent, and the procedure is elective, it should be stopped and the patient should be further assessed.
Figure 3. Lead I-III in a dog showing one sinus beat followed by ventricular tachycardia.
Why does my canine or feline patient have this arrhythmia?
This question might be more difficult to answer. First, look at your anesthetic protocol. Could it have been related to any premedications? For example, ketamine and dexmedetomidine are two preanesthetic agents that are considered arrhythmogenic. Was your patient hemodynamically compromised by anesthesia to the point that it caused myocardial hypoxia? Or, is it unrelated to the anesthetic event? Presumably full blood work has been performed prior to the anesthetic event but recheck electrolytes! Disturbances in sodium, potassium, calcium, and magnesium can all cause arrhythmias.
If unrelated to the anesthetic event, ventricular arrhythmias in canines can be caused by primary heart disease or secondary to various abdominal ailments. A good physical exam and baseline bloodwork can help you narrow your search. Arrhythmias in specific breeds such as Doberman Pinschers and Boxers may be more commonly linked to primary heart disease. In cats, arrhythmias are more pathognomonic for primary heart disease.
Should I be worried in the short / long term?
If after recovery your canine or feline patient is still having a frequent, higher grade arrhythmia, treatment is warranted, and a further workup should be done as soon as possible. This could include thoracic radiographs, repeat lab work, a point of care ultrasound, and transfer to a local ER or ideally a veterinary cardiologist. Hospitalization may be needed to stabilize and treat the patients’ arrhythmia. An echocardiogram and telemetry can help diagnose the underlying etiology and monitor the treatment effect.
Don’t forget about accelerated idioventricular rhythms
Often times we mistake an accelerated idioventricular rhythm (AIVR) for ventricular tachycardia. AIVR is usually due to myocardial depression, hypoxia, or less commonly in animal patients, myocardial infarction. We commonly see AIVR in patients’ undergoing a splenectomy or surgery for gastric dilatation and volvulus. Accelerated idioventricular rhythms are identified as abnormal, wide, and bizarre beats that do not come prematurely. A slow transition is usually noted from normal sinus beats to fusion beats to ventricular beats and back. The heart rate and blood pressure monitoring do not typically show a change. It is important to differentiate AIVR from ventricular tachycardia, because AIVR does not typically cause hemodynamic compromise and won’t respond to anti-arrhythmic medications. If AIVR is identified the procedure does not need to be stopped.
Figure 4. An example of an accelerated idioventricular rhythm in a dog (lead I-III). Note the fusion beat (third from left) and the slow transition from ventricular beat, to fusion, to sinus, to ventricular beat. The heart rate does not change.
Credit: ECG images were provided by the University of Minnesota.
References
- Bastiaenen R, Gallagher MM, Batchvarov VN. Ventricular automaticity as a predictor of sudden death in ischaemic heart disease. Europace; 2011: 1-10.
- Boujon CE, Amberger CN. Arrhythmogenic Right Ventricular Cardiomyopathy (ARVC) in a Boxer. JVC. 2003;5(1):35-41.
- Garcia TB, Miller GT. Arrhythmia Recognition 2004; 379-391.
- Gunasekaran T, Sanders R. Sudden cardiac death in a dog during Holter recording – R on T Phenomenon. JVC. 2017;19(5):455-461.
- Jackson BL, Lehmkulh LB, Adin DB. Heart rate and arrhythmia frequency of normal cats compared to cats with asymptomatic hypertrophic cardiomyopathy. 2014;16(4):215-225.
- Olgin JE, Zipes DP. Specific Arrhythmias: Diagnosis and treatment. In Braunwald’s Heart Disease: A textbook of cardiovascular medicine. Tenth Edition, 2015; 771-790.
