J . small Anim. Pract. (1976) 17, 149-162.
Permanent pacemaker implantation with transvenous electrode placement in a dog with complete atrioventricular heart block, congestive heart failure and Stokes-Adams syndrome E. E. M U S S E L M A N , G. P. R O U S E
AND
A. J. P A R K E R
Clinic for Small Animals, College of Veterinary Medicine, University of Illinois, Urbana, Illinois 61801
ABSTRACT A permanent asynchronous pacemaker was implanted in a 2-year-old Shetland Sheepdog with complete heart block. Electrode implantation was via the transvenous method. One year after implantation the pacemaker unit began to fail. A new pacemaker, with a 7-year battery expectancy, was substituted for the original unit. The subject is still leading a normal life, 14 years after the use of the pacemaker. INTRODUCTION Atrioventricular heart block is a disturbance in the atrioventricular conducting system, which includes the A-V node (A-V junction), the bundle of His, and the bundle branches (right bundle branch, the left anterior hemibranch, and the left posterior hemibranch) (Bellet, 1971). Heart block may be classified as partial or complete. Partial heart block is categorized as first-degree A-V block, when the conduction time of the A-V junction is prolonged; and as second-degree A-V block when some, but not all, atrial impulses are conducted to the ventricles. I n complete heart block, there is complete failure of any supraventricular impulse to activate the ventricles. Stokes-Adams seizures are commonly associated with complete heart block, and are a consequence of bradyarrhythmias that cause a marked reduction in cardiac output. Syncopal attacks and convulsive episodes are due to failure of the brain to receive adequate blood flow (Bellet, 1971). Before the advent of the electronic pacemaker, medical treatment of complete heart block in man had only limited success. Symptomatic therapy with steroids 149
150
E. E. MUSSELMAN
et al.
was used to decrease inflammatory lesions within the A-V conducting system, and isoproterenol was administered to increase the rate of the idioventricular pacemaker. Medical treatment of complete A-V block in four dogs was reported, with three subjects responding to treatment with a return to normal A-V conduction (Ettinger, 1969) The introduction of the electronic cardiac pacemaker provided a dramatic advance in the treatment of heart disease in man. Studies in animals had indicated that electrical stimulation would function as a pacemaker for the heart (Hyman, 1932), but the development of the transistor and miniaturization was necessary before the first practical pacemaker for human clinical use was described (Chardack, Gage & Greatbach, 1961 ; Zoll, 1952). Cardiac pacing was initially used for the treatment of complete he art block (Burchell, Connolly & Ellis, 1964; Castellanous, Lemberg & Berkovits, 1966; Chardack, 1966; Furman & Schwedel, 1969; Harris, 1965; Johannson, 1966; Kantrowitz, 1962; Lagergren & Johannson, 1963; Levin et al., 1970). Pacemaker therapy has been utilized in Mobitz type I1 A-V block and in symptomatic bradyarrhythmias such as ‘sick sinus syndromc’, sinus bradycardia, nodal bradycardia and sinus arrest (Burchell, Connolly & Ellis, 1964; Chawla, Rea & Shapiro, 1969). More recent uses include ‘overdrive suppression’ to abolish supraventricular and ventricular tachyarrhythmias, when medical treatment has not been effective (Arthur & Basta, 1973; DeSanctis & Kastor, 1968; Durrer, 1967; Escher, 1969; Massumi, Kistin & Tawakkal, 1967; Zipes, 1968). Pacing has proved to be effective in the prevention of bradyarrhythmias or arrest as a consequence of cardiodepressant drug administration (Chawla, Rea & Shapiro, 1969; Furman & Escher, 1970; Solomon & Escher, 1963). Human survival has been dramatically increased in heart block patients treated by pacemaker implantation (Chardack et al., 1961; Johannson, 1966; Johannson, 1969). One-year mortality in heart block patients treated by medical therapy alone is 50-60%, whereas pacemaker therapy results in a decline in mortality to within 10% of the normal population. Clinical application of the pacemaker in the dog was reported (Buchanan et al., 1968) in which a subject with complete A-V block and congestive heart failure was treated by implantation of a fixed-rate pacemaker with epicardial electrode placement. CASE R E P O R T A 2-year-old female spayed Shetland Sheepdog was admitted to the University of Illinois Clinic for Small Animals on 12 August, 1974. The subject had been examined by a veterinarian on 15 July, 1974, when it had developed signs of dyspnoea and weakness. Thoracic radiographs showed pulmonary oedema and the dog was placed on chloramphenicol and a diuretic. The subject was re-examined on 18July, and no improvement was noted. O n 25 July, the dog was febrile with
PERMANENT PACEMAKER IMPLANTATION
151
a rectal temperature of 103.5"F (39.7"C). Diuretic administration was continued and amphicillin was substituted for chloramphenicol. The dog was examined again on 5 August, and the owner stated that two 'spells' or convulsive-like episodes had occurred in the previous 72 hours. Bradycardia at a rate of 35-40 beatslmin was observed, and the dog was referred to the University Clinic as a possible neurological disorder. Physical examination upon admission (11/8/74) showed moderate dyspnoea and the mucous membranes were cyanotic. Severe, bilateral temporal muscle atrophy was present. The femoral pulses were symmetrical, full and bounding, at
FIG. I . (a) Lead I1 electrocardiogram at 25 mm/s. The atrial rate is 160 beats/min and the ventricular rate is 35 beatslmin. QRS complex duration is 0.12 s. (b) Lead I1 electrocardiogram after the initiation of isoproterenol therapy. The rS pattern and QRS widening are characteristic of the idioventricular focus originating in the left posterior hemibranch.
a rate of 38 beatslmin. Periodic jugular pulsations (cannon waves) were observed. Auscultation of the thorax disclosed bilateral pulmonary oedema, characterized by fine-to-medium moist rales, a grade I1 of V regurgitant mitral murmur, and a grade I1 of V pulmonary ejection murmur. The first heart sound varied in intensity and fourth (atrial) heart sounds were heard at a rapid rate at the base of the heart. An electrocardiogram showed complete heart block with an atrial rate of 160 beats/min and an idioventricular rhythm of 35 beatslmin (Fig. la). A 2 mg dose of atropine sulphate was administered intravenously with no effect on atrioventricular conduction.
152
E . E. M U S S E L M A N
et al.
FIG. 2. (a) Lateral thoracic radiograph taken on the day of admission. Note bilateral ventricular enlargement and left atrial enlargement (b) Dorso-ventral radiograph obtained upon admission. Pulmonary oedema is present and bi-ventricular enlargement is seen.
PERMANENT PACEMAKER IMPLANTATION
153
TABLE 1. Results of clinical pathology tests Test Haemogram RBC Haemoglobin Haematocrit WBC Neut segs Lymph Mono Biochemical profile BUN Calcium SGPT Creatinine Glucose Phosphorus Total protein Alkaline phosphatase LDH CPK
Result
7.39 x 106 14.7 gm% 43 % 13.7 103 86 % 12%
2% 42 mg% 10.0 mg% 51 Hycell units 1.8 mg% 106 mg% 4.7 mg% 5.9 mg% 11 Hycell units 90 Hycell units 3 Hycell units
(normal
Permanent pacemaker implantation with transvenous electrode placement in a dog with complete atrioventricular heart block, congestive heart failure and Stokes-Adams syndrome E. E. M U S S E L M A N , G. P. R O U S E
AND
A. J. P A R K E R
Clinic for Small Animals, College of Veterinary Medicine, University of Illinois, Urbana, Illinois 61801
ABSTRACT A permanent asynchronous pacemaker was implanted in a 2-year-old Shetland Sheepdog with complete heart block. Electrode implantation was via the transvenous method. One year after implantation the pacemaker unit began to fail. A new pacemaker, with a 7-year battery expectancy, was substituted for the original unit. The subject is still leading a normal life, 14 years after the use of the pacemaker. INTRODUCTION Atrioventricular heart block is a disturbance in the atrioventricular conducting system, which includes the A-V node (A-V junction), the bundle of His, and the bundle branches (right bundle branch, the left anterior hemibranch, and the left posterior hemibranch) (Bellet, 1971). Heart block may be classified as partial or complete. Partial heart block is categorized as first-degree A-V block, when the conduction time of the A-V junction is prolonged; and as second-degree A-V block when some, but not all, atrial impulses are conducted to the ventricles. I n complete heart block, there is complete failure of any supraventricular impulse to activate the ventricles. Stokes-Adams seizures are commonly associated with complete heart block, and are a consequence of bradyarrhythmias that cause a marked reduction in cardiac output. Syncopal attacks and convulsive episodes are due to failure of the brain to receive adequate blood flow (Bellet, 1971). Before the advent of the electronic pacemaker, medical treatment of complete heart block in man had only limited success. Symptomatic therapy with steroids 149
150
E. E. MUSSELMAN
et al.
was used to decrease inflammatory lesions within the A-V conducting system, and isoproterenol was administered to increase the rate of the idioventricular pacemaker. Medical treatment of complete A-V block in four dogs was reported, with three subjects responding to treatment with a return to normal A-V conduction (Ettinger, 1969) The introduction of the electronic cardiac pacemaker provided a dramatic advance in the treatment of heart disease in man. Studies in animals had indicated that electrical stimulation would function as a pacemaker for the heart (Hyman, 1932), but the development of the transistor and miniaturization was necessary before the first practical pacemaker for human clinical use was described (Chardack, Gage & Greatbach, 1961 ; Zoll, 1952). Cardiac pacing was initially used for the treatment of complete he art block (Burchell, Connolly & Ellis, 1964; Castellanous, Lemberg & Berkovits, 1966; Chardack, 1966; Furman & Schwedel, 1969; Harris, 1965; Johannson, 1966; Kantrowitz, 1962; Lagergren & Johannson, 1963; Levin et al., 1970). Pacemaker therapy has been utilized in Mobitz type I1 A-V block and in symptomatic bradyarrhythmias such as ‘sick sinus syndromc’, sinus bradycardia, nodal bradycardia and sinus arrest (Burchell, Connolly & Ellis, 1964; Chawla, Rea & Shapiro, 1969). More recent uses include ‘overdrive suppression’ to abolish supraventricular and ventricular tachyarrhythmias, when medical treatment has not been effective (Arthur & Basta, 1973; DeSanctis & Kastor, 1968; Durrer, 1967; Escher, 1969; Massumi, Kistin & Tawakkal, 1967; Zipes, 1968). Pacing has proved to be effective in the prevention of bradyarrhythmias or arrest as a consequence of cardiodepressant drug administration (Chawla, Rea & Shapiro, 1969; Furman & Escher, 1970; Solomon & Escher, 1963). Human survival has been dramatically increased in heart block patients treated by pacemaker implantation (Chardack et al., 1961; Johannson, 1966; Johannson, 1969). One-year mortality in heart block patients treated by medical therapy alone is 50-60%, whereas pacemaker therapy results in a decline in mortality to within 10% of the normal population. Clinical application of the pacemaker in the dog was reported (Buchanan et al., 1968) in which a subject with complete A-V block and congestive heart failure was treated by implantation of a fixed-rate pacemaker with epicardial electrode placement. CASE R E P O R T A 2-year-old female spayed Shetland Sheepdog was admitted to the University of Illinois Clinic for Small Animals on 12 August, 1974. The subject had been examined by a veterinarian on 15 July, 1974, when it had developed signs of dyspnoea and weakness. Thoracic radiographs showed pulmonary oedema and the dog was placed on chloramphenicol and a diuretic. The subject was re-examined on 18July, and no improvement was noted. O n 25 July, the dog was febrile with
PERMANENT PACEMAKER IMPLANTATION
151
a rectal temperature of 103.5"F (39.7"C). Diuretic administration was continued and amphicillin was substituted for chloramphenicol. The dog was examined again on 5 August, and the owner stated that two 'spells' or convulsive-like episodes had occurred in the previous 72 hours. Bradycardia at a rate of 35-40 beatslmin was observed, and the dog was referred to the University Clinic as a possible neurological disorder. Physical examination upon admission (11/8/74) showed moderate dyspnoea and the mucous membranes were cyanotic. Severe, bilateral temporal muscle atrophy was present. The femoral pulses were symmetrical, full and bounding, at
FIG. I . (a) Lead I1 electrocardiogram at 25 mm/s. The atrial rate is 160 beats/min and the ventricular rate is 35 beatslmin. QRS complex duration is 0.12 s. (b) Lead I1 electrocardiogram after the initiation of isoproterenol therapy. The rS pattern and QRS widening are characteristic of the idioventricular focus originating in the left posterior hemibranch.
a rate of 38 beatslmin. Periodic jugular pulsations (cannon waves) were observed. Auscultation of the thorax disclosed bilateral pulmonary oedema, characterized by fine-to-medium moist rales, a grade I1 of V regurgitant mitral murmur, and a grade I1 of V pulmonary ejection murmur. The first heart sound varied in intensity and fourth (atrial) heart sounds were heard at a rapid rate at the base of the heart. An electrocardiogram showed complete heart block with an atrial rate of 160 beats/min and an idioventricular rhythm of 35 beatslmin (Fig. la). A 2 mg dose of atropine sulphate was administered intravenously with no effect on atrioventricular conduction.
152
E . E. M U S S E L M A N
et al.
FIG. 2. (a) Lateral thoracic radiograph taken on the day of admission. Note bilateral ventricular enlargement and left atrial enlargement (b) Dorso-ventral radiograph obtained upon admission. Pulmonary oedema is present and bi-ventricular enlargement is seen.
PERMANENT PACEMAKER IMPLANTATION
153
TABLE 1. Results of clinical pathology tests Test Haemogram RBC Haemoglobin Haematocrit WBC Neut segs Lymph Mono Biochemical profile BUN Calcium SGPT Creatinine Glucose Phosphorus Total protein Alkaline phosphatase LDH CPK
Result
7.39 x 106 14.7 gm% 43 % 13.7 103 86 % 12%
2% 42 mg% 10.0 mg% 51 Hycell units 1.8 mg% 106 mg% 4.7 mg% 5.9 mg% 11 Hycell units 90 Hycell units 3 Hycell units
(normal
