Electrocardiographs (ECGs) are a helpful tool that can assist with the diagnosis, treatment and management of arrhythmias in veterinary practice.
Key checks
The first step is to ensure the ECG is attached correctly to the patient. A poor ECG trace can, at best, hamper interpretation and, at worst, cause misinterpretation.
Ideally, the patient should be in right lateral recumbency, with the cables untangled and coming away from the patient (ie not crossing the thorax). If specific measurements from the ECG are not being taken, such as analysis of the mean electrical axis, sternal recumbency may be preferred in nervous dogs, cats and dyspnoeic patients.
ECG interpretation
Once a good ECG trace has been established, interpretation can begin. A recommended place to start is determining the heart rate; an algorithmic approach can be helpful in this (Figure 1).
Next, the P-QRS relationship needs to be established. A sinus complex should consist of a P wave followed by a QRS complex. They should be reasonably and consistently related in every complex. An algorithm can also help here (Figure 2).
The final aim is then to assess the appearance, or morphology, of the QRS complex (Figure 3). If the complex is tall and narrow (Figure 3A), it is likely to be atrial in origin. If it is wide and bizarre (Figure 3B), it is most likely to have originated in the ventricles.
Test your knowledge with case studies
Case 1: “Tommy”
Tommy, a 10-year-old male neutered domestic shorthair, presented for his annual routine health check when the veterinary surgeon detected pauses on auscultation and requested an ECG (Figure 4). The ECG showed a predominant sinus rhythm, with multiform ventricular premature complexes (VPCs) (arrowed).
The veterinary surgeon then recommended echocardiography, which showed significant left ventricular hypertrophy, consistent with the feline phenotype hypertrophic cardiomyopathy. It also showed marked left atrial enlargement.
Blood pressure was also measured and was within the normal range.
The veterinary surgeon started treatment with the anti-platelet drug clopidogrel. The owners were instructed to record his sleeping respiratory rate and inform the VS when it increased to over 30 breaths/min.
Because Tommy was very scared of coming to the veterinary practice, it was agreed that a telephone check-up would suffice at one month post-diagnosis unless he showed any signs of heart failure or exercise intolerance before then.
ECG findings
Figure 4 shows a predominant sinus rhythm, interspersed with wide and bizarre complexes. These complexes are VPCs, and in this ECG trace, they originate at different loci, so there is some variety in morphological appearance.
The complexes look abnormal because the ventricles prematurely fired before the sinus complex began, meaning the impulse had to depolarise the myocardium cell by cell. This takes longer, and therefore the complex appears wide and bizarre.
Case 2: “Daphne”
Daphne, a 12-year-old female neutered Cavalier King Charles Spaniel, was diagnosed with myxomatous mitral valve disease (MMVD) at the age of six. At the time, a grade II/VI left-sided apical heart murmur was detected – she was assessed to be at stage B1 of MMVD (Table 1).
| Stage | Classification criteria | Description |
|---|---|---|
| A | At risk | Dogs at high risk of developing MMVD due to their breed but have no evidence of heart disease |
| B | Heart disease present, but no heart failure (Two distinct categories in this stage) | B1 – audible heart murmur on auscultation but no echocardiographic or radiographic changes |
| B2 – Audible heart murmur on auscultation, but echocardiographic and/or radiographic changes associated with mitral valve disease present, such as left-sided enlargement | ||
| C | Heart failure | Either past or current heart failure |
| D | Refractory heart failure | Routine heart failure medication no longer effective |
Three years later, she progressed to stage B2 and was treated with pimobendan. After 18 months, she developed heart failure (stage C), and furosemide was added to her treatment. A few months later, she presented collapsed and dyspnoeic. (Her ECG can be seen in Figure 5.)
Her collapse was the result of a ruptured chordae tendineae, which can occur as a result of severe degeneration of the mitral valve leaflet. This extra myocardial stress resulted in atrial fibrillation (AF), which was enough to cause weakness and collapse for a heart already working at maximum.
AF is the most common persistent arrhythmia in small animal practice and is usually the result of structural heart disease. Physiologically, AF is characterised by rapid and irregular depolarisations across the atria, some of which make it through the atrioventricular (AV) node. It is not unusual for the atria to contract at a rate over 300bpm, but what is conducted through the AV node may be 200bpm. On auscultation, the heart sounds chaotic and irregular. There is often a marked difference between heart rate and pulse rate, so pulse deficits are a common finding.
AF is usually present with heart failure; therefore, patients often show signs of left-sided congestive heart failure and are usually exercise intolerant.
ECG findings
AF is a normal to fast rhythm depending upon treatment or the efficacy of treatment, and the interval between R waves is irregular. There are no obvious P waves associated with the QRS complexes, and QRS complexes often vary in amplitude (size).
The complexes are tall and narrow because they originated in the atria.
