23-30 are morphologically identical, are very wide ...

Michael R. O'Grady, Blair Carley, Dana G. Allen An eight-year-old spayed female Golden Retriever was presented to the Ontario Veterinary College

Veterinary Teaching Hospital about 10 hours after having been hit by a car. On physical examination the dog was depressed and was experiencing respiratory distress. Thoracic radiographs were obtained to assess the labored respiration; pulmonary contusion was diagnosed. The dog was hospitalized to monitor the status of the respiratory embarrassment. The followiing day a rhythm disturbance was suspected on physical examination. A lead II rhythm strip was obtained and is presented here. 411

5

4

3

2

6

9

8

7

branches (4). Although there are many exceptions to the following simple rule, ventricular escape beats tend to be characterized by QRS complexes that are wide and morphologically bizarre relative to the normal sinus beats. Conversely, supraventricular escape beats tend to be characterized by QRS complexes that are narrow and of a morphology very similar to the normal sinus beats.

Let us now consider the possibility of these complexes being premature beats. Premature beats represent ventricular activation initiated from cells of the

atrial or ventricular myocardium that do not possess pacemaker potential (do not have automaticity) (2,5). These cells may acquire automaticity due to the effects of

I1

1 24

13

114A

is

16

17

11

18 U 1

2

drugs, electrolyte imbalances

or

myocardial

diseases

(5). Premature beats activate the ventricles before the sinoatrial node has an opportunity to initiate the normal activation of the ventricular myocardium.

arrhythmia (varying R to R intervals) premature beats can occur after a considerable pause which can make the distinction between premature beats and escape beats very difficult. This distinction is more than a mere academic curiosity. Escape beats may give rise to an escape rhythm which may be too slow to maintain cardiac output and therefore require artificial pacemaker support. Efforts to abolish escape beats or reduce the heart rate associated with escape beats are counterproductive and dangerous. However premature beats may give rise to a rhythm composed exclusively of premature beats. This type of rhythm results in beats that cause a reduction in the efficiency of ventricular contraction. As well a rhythm of premature beats usually results in tachycardia which is often detrimental. Rhythms of premature beats are managed with anti-dysrhythmic therapy with a view to the eradication of the premature beats. Thus the treatment for one is contraindicated for the other and vice versa. In addition, the distinction between escape beats and premature beats has etiologic significance. Escape beats are a normal protective mechanism whose purpose is to prevent asystole. As well, escape beats indicate an abnormality or disease of the sinoatrial pacemaker. However premature beats indicate abnormality or disease within the atrial or ventricular myocardial cells. In the face of a marked sinus

2i

292

2

2

2

26

27

28

29

In that the grid lines are not present and the size of Ithe original ECG is altered with photographic duplica1tion, we do not expect readers to determine the dura1tion or amplitude measurements or the heart rate. The

heart rate is about 110/minute. Beats 6, 7, 17-19, and 21 are normal sinus beats. Beats 1-4, 9-15, 20, and 23-30 are morphologically identical, are very wide and bizarre relative to the sinus beats, and are not preceded by a P wave. Ventricular beats that possess these features are classified as either escape beats or premature beats (1,2). Escape beats represent ventricular activation initiated from sources other than the sinoatrial pacemaker cells. These other sources of pacemaker activity are located in the region of the coronary sinus, mitral and tricuspid valve leaflets, and cells of the peri-atrioventricular nodal region, His bundle and Purkinje network (3). These alternative sources of pacemaker activity become active when the sinoatrial pacemaker has failed to initiate the activation of the ventricles. Thus escape beats occur after a pause of about 1.5 to 2.0 seconds following a sinus beat. Escape beats may be classified as supraventricular, if they arise from a source above the bifurcation of the bundle branches, or ventricular, if they arise from a source below the bifurcation of the bundle Department of Clinical Studies, Ontario Veterinary College, of Guelph, Guelph, Ontario NIG 2W1 University 1 118

Referring to the ECG, the pause that occurs between beats 8 and 9 is about 0.6 seconds. This pause would appear to be too brief for the bizarre beats to be escape beats. Thus we believe that these bizarre beats are most

consistent with premature beats. It is the presence of the background sinus arrhythmia which is responsible Volue-32,

February1991

Can Vet J Volume 32,

February 1991

Can

Vet

J

for these premature beats occurring after a considerable delay; that is, had the sinus rate been faster these premature beats would not have occurred. Premature beats may be classified as supraventricular or ventricular. There are several criteria that are useful to assist with the differentiation of supraventricular and ventricular premature beats (4). Although there are numerous exceptions to the following rule it has remained useful for classifying premature beats. Premature beats that are wide and morphologically bizarre relative to the normal sinus beats are usually ventricular premature beats. Conversely, premature beats that are narrow and morphologically similar to the normal sinus beats are usually supraventricular in origin. Another criterion indicative of the presence of ventricular premature beats (VPB's) is the presence of fusion beats (6). Fusion beats represent QRS complexes which result from simultaneous ventricular activation via impulses from the normal sinus node and from a ventricular premature focus (such as beats 5, 8, 16, and 22). Therefore fusion beats represent a mixture of two waveforms of activation that are washing across the ventricular myocardium simultaneously. Thus fusion beats indicate the presence of a focus producing VPB's. The morphology of the fusion beat is dependent upon the relative amount of the ventricular myocardium activated by each of the two colliding waves of activation. That is, the QRS will more closely resemble the sinus beat if the majority of the ventricle is activated by the sinoatrial originating impulse (such as beat 8) or it will closely resemble the ventricular premature beat in appearance if the majority of the ventricle is activated by the impulse originating in the ventricular ectopic focus (such as beat 22). Fusion beats that result from depolarization of approximately equal amounts of ventricular mass from both pacemaker sources will create a beat with a morphology intermediate between both types of QRS shapes (such as beats 5 and 16). Fusion beats must have a normal P wave and a normal or slightly shortened PR interval. When more than three ventricular beats occur in sequence this is known as ventricular tachycardia (VT).

Management of ventricular premature beats

dysrhythmic therapy is necessary if the abnormal rhythm is likely to deteriorate to ventricular fibrillation. Since the development of ventricular fibrillation results in circulatory collapse and sudden death, it behooves us to recognize criteria in the setting of VPB's and VT that suggest the impending development of ventricular fibrillation. It should be noted that there is a plethora of activity in humans attempting to identify risk factors to distinguish a lethal rhythm disturbance from a benign rhythm disturbance. The emerging evidence indicates that VPB's or VT that occur in the face of congestive heart failure or cardiomyopathy have the potential to deteriorate to ventricular fibrillation (8-10). One might ask "Why not just treat all cases of VPB's and VT?" To consider the previous question, we must know if there is an adverse side to antidysrhythmic therapy. In the face of significant left ventricular dysfunction many anti-dysrhythmic agents have been shown to result in increased mortality (11). This occurs because all anti-dysrhythmic agents are proarrhythmic and reduce contractility (12-14). The proarrhythmic effect refers to the ability of these agents to actually promote or exacerbate dysrhythmias. In the past it has been suggested that the following criteria indicate a high risk of deterioration of VPB's or VT to ventricular fibrillation and thus warrant therapy (2,7). These include: 1. VPB's of multiple morphologies. The presence of this finding suggests multiple areas of myocardial disease each responsible for a different morphology of VPB. 2. Frequent VPB's. The presence of more than 15 to 20 VPB's per minute. 3. Presence of VT. 4. Presence of R on T phenomenon. This refers to VPB's that occur so prematurely that they encroach on the T wave of the preceding beat

(2,7).

Once again, definitive criteria to indicate the potential lethal degree of VPB's or VT have not yet been established. It is our impression at this time that VPB's or VT that occur only in the following settings warrant immediate attention: 1. result in signs of reduced cardiac output, 2. occur in the presence of cardiomyopathy or severe morphologic heart disease, 3. result in a marked increase in the ventricular rate. Because this dog had a slow rhythm associated with the ventricular tachycardia, there was no evidence of reduced cardiac output, and there was no evidence of morphologic heart disease, we decided not to treat this dysrhythmia. The rhythm disturbance spontaneously resolved within 48 hours.

As a rule, the class I anti-dysrhythmic agents are the drugs of choice to abolish VPB's and VT. These agents include lidocaine, and the oral lidocaine derivatives mexiletine and tocainide, procainamide and quinidine (7). In the event that these drugs are ineffective, the beta adrenergic blockers may be effective to abolish the VPB's. At times the use of class I anti-dysrhythmic agents in conjunction with beta blockers may be effective. We have encountered several situations where References calcium channel blockers (e.g. verapamil, diltiazem) 1. Tilley LP. Essentials of Canine and Feline Electrocardiography. were effective in abolishing VPB's or VT. 2nd ed. Philadelphia: Lea & Febiger, 1985: 150-151. We ask the question "Why do we as clinicians 2. ibid: 152-157. attempt to abolish VPB's?". There are in essence 3. ibid: 272. two reasons to abolish VPB's and VT. If the presence 4. Crowe DT, Calvert CA. Cardioarrhythmias: recognition and management. In: Zaslow IM, ed. Veterinary Trauma and of these abnormal rhythms results in clinical evidence Critical Care. Philadelphia: Lea & Febiger, 1984: 128-129. of reduced hemodynamic performance, then anti- 5. Tilley LP. Essentials of Canine and Feline Electrocardiography. 2nd ed. Philadelphia: Lea & Febiger, 1985: 273. dysrhythmic therapy is required. As well, antiCan Vet J Volume 32, February 1991

119

6. ibid: 153. 7. Bonagura JD, Muir WW. Antiarrhythmic therapy. In: Essentials of Canine and Feline Electrocardiography. Tilley LP, ed. 2nd ed. Philadelphia: Lea & Febiger, 1985: 281-316. 8. Swerdlow CD, Winkle RA, Mason JW. Determinants of survival in patients with ventricular tachycardia. N Engl J Med 1983; 308: 1436-1442. 9. Ruskin JN, DiMarco JP, Garan H. Out-of-hospital cardiac arrest: electrophysiologic observations and selection of longterm antiarrhythmic therapy. N Engl J Med 1980; 303: 607-613. 10. Meinertz T, Hofmann T, Kasper W, et al. Significance of ventricular arrhythmias in idiopathic dilated cardiomyopathy. Am J Cardiol 1984; 53: 902-907.

11. Pratt CM, Eaton T, Francis M, et al. The inverse relationship between baseline left ventricular ejection fraction and outcome of antiarrhythmic therapy: a dangerous imbalance in the riskbenefit ratio. Am Heart J 1989; 118: 433-440. 12. Slater W, Lampert S, Podrid PJ, Lown B. Clinical predictors of arrhythmia worsening by antiarrhythmic drugs. Am J Cardiol 1988; 61: 349-353. 13. Ravid S, Podrid PJ, Lampert S, Lown B. Congestive heart failure induced by 6% of the antiarrhythmic drugs. J Am Coll Cardiol (in press). 14. Podrid PJ, Lampert S, Gravoys TB, et al. Aggravation of arrhythmia by antiarrhythmic drugs-incidence and predictors. Am J Cardiol 1987; 59: 38E-44E.

BOOK REVIEWS RECENSIONS DE LIVRES Blood DC, Radostits OM. Veterinary Medicine. 7th ed. Toronto, Bailliere Tindall, 1989. 1502 pp. Price $99.95.

The authors have again produced a remarkably comprehensive text on the diseases of food animals and horses. The book is intended to prepare veterinary students and practitioners for the most economical methods of diagnosis, monitoring of animal health, advice on nutrition, and competence in the field pathology of diseases of food-producing animals. The authors first provide sound principles on historytaking and clinical examination of the individual patient, then expand to provide a conceptual framework for examination of the herd, therapeutic decision-making, and computer diagnostics. The chapter on general systemic states addresses the pathogenesis of disease syndromes we recognize in day-today practice. The descriptions of endotoxemia, anaphylaxis, dehydration, fever, and electrolyte balance are substantive, but for the person with a passion for pathophysiology the sections on sepsis, immune deficiency, renal failure, poor performance and shock might be considered superficial. Tremendous efforts went into updating the chapter on diseases of the newborn, and this provides an excellent source for those wishing to study the causes of periparturient losses, especially in calves. Practical antimicrobials are discussed thoroughly from a mechanistic and applied point of view, as are the current issues on drug withdrawal and extra-label use of antimicrobials. Details on newer antimicrobials (e.g. quinilones, beta-lactamase resistant), mechanisms of resistance, susceptibility testing, and the treatment of anaerobic infections may, however, require further reading. The strongest features of the new edition are the discussions on the general epidemiology, clinical findings, and pathogenesis of specific diseases. Epidemiologically, diseases with the highest incidence rates in food animals (e.g. bovine respiratory disease, mastitis, undifferentiated calf diarrhea, anaplasmosis), zoonoses (e.g. rabies, brucellosis), and diseases with worldwide distribution (e.g. malignant catarrhal fever, bovine viral diarrhea, foot-and-mouth disease) are emphasized, and reflect the authors' unique global perspective on these conditions. Likewise, the coverage of exotic diseases has expanded (e.g. trypanosomiasis, theileriosis, East Coast fever). Reference lists are extensive and current to 1986. 120

The discussions on the pathogenesis of specific diseases have undergone marked revision, especially with regard to bacterial virulence factors (e.g. Pasteurella haemolytica), immunologic mechanisms (e.g. BVDV), and genetic determinants of disease resistance (e.g. bovine leukosis). Clinical descriptions are, as always, illustrative, and concise tables are provided which correlate clinical signs with potential causes and differential diagnoses, and these are indexed adequately. Clearly, the greatest shortcoming of Veterinary Medicine is coverage of equine medicine, although this was not a primary objective of the book. The sections on critical care of the foal, equine colitis, neonatal maladjustment syndrome, poor performance, and rhabdomyolysis are considerably updated, but do not contain sufficient information for many equine practitioners. In the next couple of years, Veterinary Medicine will most likely be compared to Large Animal Internal Medicine (1990), edited by Bradford P. Smith. Large Animal Internal Medicine is a problem-oriented text authored by a consortium of academic 'specialists', principally from North America, which has deeper coverage of general pathophysiology, ancillary diagnostic methods, current therapeutics, and equine medicine (swine diseases are not included). On the other hand, the artful aspects of epidemiological diagnosis, specific herd diagnostic methods (e.g. Compton metabolic profiling, evaluation of trace mineral status, and mastitis problems), and diseases caused by viruses, toxic plants, and chemical agents are more thoroughly discussed in Veterinary Medicine. In the end, for the food animal practitioner with a bent toward applied epidemiology and those interested in diseases of international importance, Veterinary Medicine is an extremely valuable text. Reviewed by Andrew M. Hoffman, DVM, D. V.Sc. candidate and resident in large animal medicine, Department of Clinical Studies, Ontario Veterinary College, University of Guelph, Guelph, Ontario NIG 2WL.

Can Vet J Volume 32, February 1991