Supraventricular abnormalities in dogs with cardiac disorders
On electrocardiography various types of supraventricular abnormalities were observed and summarized in Fig 1, 2, 3, 4, 5 and 6. Supraventricular disorders documented as wandering pacemaker in 30.60%, followed by atrial fibrillation (fine AF and coarse AF) in 22.58%, sinus tachycardia in 12.90%, left atrial enlargement in 8.06%, sinus bradycardia in 8.06%, sinus arrhythmia in 6.45%, sinus arrest in 4.84%, atrial premature complexes in 3.22% and similar frequency
i.e. 1.61% atrial standstill and right atrial enlargement in dogs.
Atrial fibrillations were recorded as coarse atrial fibrillation (large oscillations
i.e. ‘f’ waves (Fig 2) of varying amplitude replace the normal sinus P waves) and fine atrial fibrillation, small f waves take the place of sinus P waves. Atrial fibrillation is characterized by complete electrical disorganization at the atrial level leading to the chaotic and rapid rise of depolarization
(Ettinger et al., 2000; Gugliemini et al., 2000). The electrophysiological mechanism underlying AF is re-entry, which is characterized by multiple wavelets of depolarization. Multiple wavelets can cross the atria without fusing in one normal front of depolarization only when a large atrial mass is present (
Zipes, 1997). Atrial fibrillation is a common arrhythmia in dogs
(Meurs et al., 2001; Noszczyk et al., 2008). The results of the present study also suggested that AF is a common supraventricular disorder after the wandering pacemaker. Similar findings were also found by
Varshney et al., (2011) who documented thirty cases of atrial fibrillation in dogs with unexplained illness and weakness. Atrial standstill is identified by the absence of P waves in any lead, heart rate is below 60 bpm and rhythm is regular. Atrial standstill is reported to be rare and often found associate with atrial parenchymal hypoplasia and severe hyperkalemia
(Ettinger et al., 2000). In this study, the atrial standstill may be due to hyperkalemia which is similar to the report of
Jeyaraja et al., (2004).
Atrial premature complexes were diagnosed by ectopic premature P waves, which were superimposed on the previous T wave (Fig 3) and its configuration was different from normal sinus P waves. Atrial premature complexes arise from ectopic foci in the atria and may lead to atrial fibrillation/ tachycardia. These complexes can be of normal variation in geriatric dogs. The impulse that spread through the atrium to the atrioventricular node fails to reach to ventricles (
Kumar, 2013). On examination of electrocardiogram, P wave was recorded as an abnormal shape
i.e. premature and may be “buried” or superimposed on preceding T wave (
Dhanapalan, 2003). Similar findings were also reported in other studies as 3.13% (
Priyanka, 2012) and 8.69% (
Singh, 2013).
Left atrial enlargement was recognized as P-mitrale by increasing the duration of P wave or wide P wave
i.e. more than 0.04 second (Fig 4). Mitral valve disease leads to haemodynamic problems to the left atrium that injures and destroys some cells. The increased volume load and/ or pressure lead to cellular hypertrophy and atrial dilatation which results in the death of some atrial cells with replacement (fibrosis). P mitrale could be seen in chronic mitral valve insufficiency and DCM (McEwan, 2000). Right atrial enlargement was diagnosed as P- pulmonale by increase amplitude of P wave (more than 0.4 mV). Tall P waves are referred to as P- pulmonale (as right atrial enlargement may be associated with cor pulmonale; more than 0.4 mV) (
Tilley, 1985 and
Mike, 2007). The results similar to our study are also reported by
Kumar (2012) as 3.03% in dogs.
Sinus arrest (sinoatrial block) was identified by the irregular rhythm with a pause or a lack of P-QRS-T complexes. The pause was double or greater than doubles of the normal R-R interval (Fig 5). The characteristics features of sinus arrest were variability of R-R interval that was twice of the normal preceding R-R interval as in this study, agreeing with the findings of
Changkija (2007). A similar finding of sinus arrest was also reported by
Singh (2013). Sinus arrhythmia was recognized by the normal P wave, QRS complex and PR interval whereas sinus bradycardia was diagnosed as a heart rate less than 70 bpm in small breeds or less than 60 bpm in giant breeds with regular sinus rhythm. Sinus tachycardia was recognized as a normal sinus rhythm with a heart rate above 160 bpm in giant breeds and above 180 bpm in toy breeds. The findings of present study are in agreement with the findings of
Kumar et al., (2014) who reported sinus bradycardia and sinus tachycardia as 6.09% and 7.30%, respectively. Similar findings have also been recorded by various other workers as sinus arrhythmia is one of the most common forms of arrhythmia in young animals (
Varshney and Tiwari, 2002;
Changkija et al., 2006).
A wandering pacemaker (WPM) was identified by gradual change in configuration of the P wave (Fig 6) without changing its polarity (due to shifting of pacemaker within the SA node). Shifting of the pacemaker causes a gradual change in the configuration of the P wave, which becomes positive, biphasic, isoelectric and negative. A wandering pacemaker was characterized by a ‘P’ wave of varying amplitude and morphology. It is a common non-pathological condition in dogs. The finding of
Kumar (2012) is contrary to our findings who recorded wandering pacemaker in one dog (1.51%) and
Jafari et al., (2011) reported 5.1%.
Ventricular abnormalities in dogs with cardiac disorders
On electrocardiographic examination of affected dogs, different types of ventricular alterations were recorded
i.e. left ventricular enlargement, right ventricular enlargement and biventricular enlargement as 41.67%, 37.49% and 8.33%, respectively. However, ventricular premature complex (VPCs), ventricular fibrillation and ventricular tachycardia were recorded in the same frequency (4.17%) in dogs suffering from cardiac disorders. Results are summarized in Fig 7, 8, 9, 10 and 11.
Right ventricular enlargement was recognized by deep Q wave (amplitude; greater than 0.7 mV, Fig 8) and deep S wave (more than 0.35 mV) in lead II. Left ventricular enlargement was identified by ST coving (displacement of the ST segment in the opposite direction of QRS deflections, Fig 9). In volume overload both wall thickness and cavity size increases; wall thickness may be only moderately increased but the cavity size is the main dimension contributed to ventricular muscle mass. Due to increased muscle mass in hypertrophy or enlargement the height of the R wave is increased, the QRS complex is delayed or altered in conduction, the ST segment is depressed
i.e. endocardial ischaemic change. These myocardial ischaemic changes may be due to neoplasia, renal disorders, blood parasites, immune mediated haemolytic anaemia, myocardial infarction and mitral valve insufficiency
(Mahendran et al., 2021). Sarita (2008) and Kumar
et al.,
(2011) also documented ST coving 8.3% and 3.91%, respectively. The findings of biventricular enlargement (Fig 11) of the present study are similar to
Tilley (1985) and
Kumar (2012) and characterized either by the presence of a tall ‘R’ wave (left ventricular enlargement; Fig 4) and deep ‘Q’ wave (right ventricular enlargement) or deep Q-wave (right ventricular enlargement) and deep-T wave (left ventricular enlargement).
Ventricular premature complexes (VPCs) were recognized by the premature, bizarre and large amplitude of the QRS complex with irregular rhythm and the T wave is directed opposite to the QRS complex.
Gupta et al., (2005) documented ventricular premature complexes with bizarre QRS complexes in dogs suffering from congestive heart failure. Similar findings of VPCs 2.08% and 6.41% were reported by
Kumar et al., (2011) and
Varshney et al., (2013), respectively. Our findings are contrary to
Knight (1999); who found that the VPCs were ubiquitous; however,
Tilley (1985) reported incidence of VPCs as high as 26% to 45%. Ventricular premature complexes originate from the ventricles and are commonly seen in chronic mitral valve insufficiency and dilated cardiomyopathy.
Ventricular fibrillation was diagnosed by rapid heart rate with irregular, chaotic and bizarre waves. The P waves, QRS and T deflections were unrecognized (Fig 10).
Varshney et al., (2013) documented the prevalence rate of ventricular fibrillation (0.98%) and ventricular tachycardia (2.76%) similar to our study. Ventricular tachycardia was recognized by a wide and bizarre pattern of QRS complex with a rate more than 120 bpm, however, the normal configuration of P waves.
