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Arrhythmias

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Abstract

Electrical impulses control the intracellular movement of calcium ions that regulate contraction and relaxation of cardiac myocytes. Organization of these impulses therefore determines the pattern and timing of contraction and relaxation, which is important to optimize cardiac output. Coordinated electrical activity is vital for this and is achieved by the cardiac conduction system. This section considers the Cardiac conduction system; Normal heart rhythms; Bradyarrhythmias; Sinus tachycardia; Supraventricular arrhythmias; Ventricular arrhythmias; Cardiac arrest rhythms; Intraventricular conduction defects; and Electrical alternans.

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Figures

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16.1 Normal sinus rhythm. Mixed-breed dog (heart rate 125 beats/minute; lead II shown). Paper speed 50 mm/s; gain 1 cm/mV. Domestic Shorthaired cat (heart rate 190 beats/minute; lead II shown). Paper speed 50 mm/s; gain 1 cm/mV.
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16.2 Sinus arrhythmia in a 10-year-old West Highland White Terrier (lead II shown). Note the variable amplitude P waves, with taller P waves (arrowed) during faster heart rates. This is a wandering pacemaker and indicates a varying site of origin of the sinus impulse. Paper speed 25 mm/s; gain 1 cm/mV.
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16.3 Sinus bradycardia. A trained Greyhound at rest (heart rate 60 beats/minute; lead II shown). Paper speed 25 mm/s; gain 1 cm/mV. A 1-year-old Domestic Shorthaired cat with signs of lethargy, anorexia and vomiting, indicating probable gastrointestinal disease (heart rate 130 beats/minute; lead II shown). Paper speed 50 mm/s; gain 1 cm/mV.
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16.4 Sick sinus syndrome. Sinus arrest for 5 seconds in a 12-year-old West Highland White Terrier with syncope and exercise intolerance (leads I–III shown). Note the second-degree AV block with 3:2 conduction prior to the sinus pause (arrows indicate non-conducted P waves). Paper speed 25 mm/s; gain 1 cm/mV.
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16.5 Second-degree AV block (Mobitz type I) in a 3-year-old Lurcher (lead II shown). Non-conducted P waves are indicated by arrows (second-degree AV block). Prolongation of the PR interval for the conducted sinus complexes is also present (first-degree AV block). Paper speed 50 mm/s; gain 1 cm/mV.
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16.6 Third-degree AV block in a 10-year-old Golden Retriever with concurrent signs of right-sided CHF (lead I shown). A ventricular escape rhythm of rate 60 beats/minute is present. A non-conducted P wave is seen to be superimposed on the ST segment of the last escape complex (arrowed). Paper speed 50 mm/s; gain 1 cm/mV.
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16.7 Atrial standstill in a dog with severe hyperkalaemia due to hypoadrenocorticism (lead II shown). Note the flat baseline indicating lack of atrial activity. A sinoventricular rhythm is present at a rate of about 50 beats/minute. Paper speed 50 mm/s; gain 1 cm/mV. Atrial standstill in a cat with severe hyperkalaemia due to urinary obstruction (lead II shown). A wide complex, sinoventricular rhythm is present at a rate of 60 beats/minute. This is a very unstable rhythm that requires urgent treatment. Paper speed 25 mm/s; gain 1 cm/mV.
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16.8 Sinus tachycardia of 250 beats/minute in a racing Greyhound immediately after finishing a race (lead II shown). The P wave of each sinus complex occurs on the terminal portion of the preceding T wave. Paper speed 25 mm/s; gain 1 cm/mV. (Courtesy of A. Boswood.)
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16.9 APCs in a 9-year-old Doberman pinscher with dilated cardiomyopathy (lead II shown). The 4th and 7th complexes are APCs and have similar QRS morphology to sinus complexes. Ectopic P waves (P’ waves) are negative and superimposed on the T wave of preceding sinus complexes. Paper speed 50 mm/s; gain 1 cm/mV.
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16.10 Atrial fibrillation in a 6-year-old Dobermann with dilated cardiomyopathy and CHF (lead II shown). Note the absence of detectable P waves and irregular RR intervals, which are the hallmarks of atrial fibrillation. Ventricular rate is rapid at 240 beats/minute. Paper speed 50 mm/s; gain 1 cm/mV.
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16.11 Focal junctional tachycardia in a 9-year-old Labrador Retriever with myocardial failure and CHF (lead II shown). Note that at the beginning of the trace no P or Q waves are visible, as they are superimposed. Both become visible towards the end of the trace (arrowed) as the ventricular rate slows from 220 to 180 beats/minute. This indicates separate atrial and ventricular rhythms and is termed isorhythmic AV dissociation. Paper speed 50 mm/s; gain 1 cm/mV.
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16.12 Ventricular pre-excitation in a 3-year-old Labrador Retriever with SVT (Wolff–Parkinson–White syndrome) (lead II shown). The SVT was treated successfully with diltiazem and this recording was taken during the following 24 hours. The fourth complex is a sinus complex with conduction through the AV node; all other complexes exhibit pre-excitation – short PR interval, delta wave (arrowed) in the upstroke of the R wave, and abnormal QRS complex morphology. This is consistent with an accessory pathway between the atria and ventricles. Paper speed 50 mm/s; gain 1 cm/mV.
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16.13 Narrow complex tachycardia in a 2-year-old Labrador Retriever (lead II shown). Ventricular rate is very rapid at 300 beats/minute. Orthodromic AV reciprocating tachycardia was later confirmed, but focal atrial tachycardia can have a similar ECG appearance. Paper speed 50 mm/s; gain 1 cm/mV.
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16.14 VPCs in two dogs (leads I–III shown). In the sixth complex is a VPC; in the fourth complex is a VPC. The morphology of each VPC differs, indicating different sites of origin within the ventricles. However, both are of wide and bizarre conformation compared with their respective sinus complexes. Note the presence of compensatory pauses for both VPCs (VPC is flanked by sinus complexes separated by a period of two RR intervals). Paper speed 25 mm/s; gain 1 cm/mV.
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16.15 Complex ventricular ectopy. Ventricular arrhythmia in a 4-year-old Dogue de Bordeaux (lead III shown). A triplet (filled arrow), couplet (open arrow) and ventricular run/salvo of six complexes (arrowhead) are seen. Ventricular complexes exhibit R-on-T phenomenon. An idiopathic ventricular arrhythmia was diagnosed as no underlying cardiac or systemic disease was detected. Paper speed 50 mm/s; gain 1 cm/mV. Ventricular bigeminy in a Boxer with cardiomyopathy (lead II shown). Sinus complexes alternate with ventricular complexes (bigeminy). Paper speed 25 mm/s; gain 1 cm/mV. (Courtesy of V. Luis Fuentes.)
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16.16 Rapid ventricular tachycardia (350 beats/minute) in the same dog as in Figure 16.15 a (lead II shown). The trace starts with a couplet of different QRS morphology to the tachycardia, followed by a sinus complex, then the tachycardia. Ventricular complexes exhibit R-on-T phenomenon. This is a dangerous arrhythmia that requires immediate treatment. Paper speed 50 mm/s; gain 1 cm/mV.
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16.17 Fusion complex in a 6-year-old Golden Retriever with monomorphic VPCs (leads I–III shown). The fusion complex (arrowed) is flanked by sinus beats and occurs midway between two VPCs. This timing is suggestive of ventricular parasystole, in which an ectopic ventricular focus fires at a regular rate irrespective of the concurrent sinus rhythm. VPCs or fusion complexes will occur if the ventricular focus fires during diastole (between sinus T wave and QRS complex). If the ventricular focus fires during systole, no ectopic complexes are seen as the ventricle is depolarized by the sinus rhythm. Paper speed 25 mm/s; gain 1 cm/mV.
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16.18 AIVR in an 8-year-old mixed-breed dog 3 days after abdominal surgery to remove a ruptured splenic haemangiosarcoma (lead II shown). An ectopic ventricular focus and the sinus node are firing at about the same rate of 100 beats/minute, but they are unrelated. Note that P waves (arrowed) are visible, superimposed on the upstroke of the ectopic R waves, and appearing to move in and out of the ectopic ventricular complexes. This is another example of isorhythmic AV dissociation (see Figure 16.11 ). Paper speed 25 mm/s; gain 1 cm/mV.
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16.19 Ventricular standstill (asystole) in a cat (lead II shown). The first half of the trace shows AV dissociation with an irregular ventricular escape rhythm. Only P waves are present during the second half of the trace as no ventricular electrical activity occurs. Paper speed 25 mm/s; gain 1 cm/mV.
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16.20 Ventricular fibrillation. Fine ventricular fibrillation in a dog (lead II shown). Note the absence of coordinated electrical activity and replacement with baseline oscillations of variable contour and amplitude (fibrillatory waves). The amplitude of these oscillations is low, <0.2 mV (fine). Attempts to resuscitate were unsuccessful. Paper speed 25 mm/s; gain 1 cm/mV. Coarse ventricular fibrillation in a dog with dilated cardiomyopathy (lead II shown). In comparison with (a) the amplitude of these oscillations is high, >0.2 mV (coarse). Paper speed 25 mm/s; gain 1 cm/mV
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16.21 RBBB in a dog. QRS complex duration is prolonged (0.08 seconds) with deep S waves and right axis deviation (lead II shown). Paper speed 25 mm/s; gain 1 cm/mV. Intermittent LBBB in an 8-year-old Boxer with paraparesis (lead II shown). The first three sinus complexes are conducted normally, the next five with LBBB. The development of aberrant conduction in complexes with a short RR interval following a long RR interval is called Ashman’s phenomenon (or long–short aberrancy). Paper speed 25 mm/s; gain 1 cm/mV.
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16.22 Electrical alternans in Bulldog with pericardial effusion secondary to a heart base mass (lead II shown). There is one taller R wave alternating with two shorter R waves. This is 3:1 QRS alternans. Paper speed 25 mm/s; gain 1 cm/mV. Electrical alternans (2:1 QRS alternans) in the Labrador Retriever with narrow complex tachycardia shown in Figure 16.13 (lead II shown). Electrical alternans developed when the heart rate exceeded 350 beats/minute. Paper speed 50 mm/s; gain 1 cm/mV.

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