An 11-year-old 5.6-kg (12.3-lb) castrated male Miniature Poodle was evaluated because of episodic weakness and tremors and an instance of collapse. The first episode, reported 7 months earlier, occurred at a boarding facility and was witnessed by the kennel staff. The dog appeared anxious and stressed while running with other dogs and was noted to suddenly sit down and tremble vigorously but did not collapse or lose consciousness. The second episode occurred at a grooming facility and was reported by the staff. When the blow dryer was turned on, the dog fell into sternal recumbency, vocalized loudly, and had tremors. The final episode also occurred at the grooming facility during use of the blow dryer and was witnessed by the owner. On the basis of recommendations from the primary care provider, the dog had received trazodone (4.4 mg/kg [2 mg/lb], PO) prior to that visit for grooming. During the episode, the dog became notably anxious, vocalized, and developed tremors before suddenly collapsing into lateral recumbency. The dog voided its urinary bladder, salivated, and became unresponsive and limp. It was brought immediately to an urgent-care hospital and appeared to recover completely during the drive.
On evaluation at the hospital, the dog was bright and alert. Physical examination revealed a grade 2/6 left apical systolic heart murmur, but findings were otherwise unremarkable. The dog was hypotensive (systolic arterial blood pressure, 76 mm Hg). Results of a urinalysis, CBC, and serum biochemical panel were unremarkable, and serum total thyroid concentration was within reference range. One hundred fifteen milliliters (20 mL/kg [9.1 mL/lb]) of fluids was administered SC; systolic arterial blood pressure was rechecked and had improved (98 mm Hg). Consultation with a board-certified neurologist revealed that the dog had no neurologic deficits. A cardiology consultation was obtained. Echocardiography revealed mild thickening and prolapse of the mitral valve with a mild eccentric jet of mitral regurgitation and trace tricuspid valve regurgitation. All chamber sizes were considered normal, and tricuspid valve regurgitation velocity did not support pulmonary hypertension (1.8 m/s; reference range, < 2.8 m/s).1 Electrocardiography was performed.
ECG Interpretation
A baseline ECG recording was obtained with the dog manually restrained in right lateral recumbency and revealed a normal sinus rhythm with a mean heart rate of 100 beats/min with normal P-wave and QRS-complex morphologies. Stress was induced by partially releasing restraint on the dog and allowing it to struggle gently in attempts to right itself while remaining in right lateral recumbency. This right lateral restraint-release procedure was repeated several times. During each of these procedures, the initial sinus rhythm became sinus tachycardia as the dog remained in lateral recumbency but struggled to attain sternal recumbency, with a mean heart rate of 260 beats/min and gradual onset and offset followed by a pause, then a regular junctional or low right atrial escape rhythm with inverse P waves in the caudal leads and a mean heart rate of 110 beats/min, and eventual recovery of the sinus rhythm (Figure 1). These findings indicated an extreme autonomic response to stress without overt bradycardia and supported a diagnosis of stress-induced vasodepressor syncope. During this period of stress, 2 complexes preceding the escape rhythm had slightly decreased P-wave amplitude and PR intervals, compared with the sinus complexes; these could have represented fusion complexes. The R-wave amplitude was decreased during the sinus tachycardia, compared with findings for the sinus and escape beats, which could have been attributable to decreased cycle length associated with less ventricular filling (the Brody effect).
Representative continuous ECG tracings obtained during a period of induced stress in an 11-year-old Miniature Poodle that had episodic weakness and tremors and an instance of collapse. The first episode reportedly occurred 7 months prior to the evaluation. To induce stress, the dog was manually restrained in right lateral recumbency, and then restraint was partially released, allowing it to gently struggle in attempts to right itself (although the dog remained in lateral recumbency at all times). Notice the initial sinus rhythm with a mean heart rate of 100 beats/min (A), followed by an artifact caused by the patient struggling (B) and resulting sinus tachycardia with a mean heart rate of 260 beats/min and gradual onset and offset (C), which was followed by a pause and then a regular junctional or low right atrial escape rhythm with inverse P waves in the caudal leads and a mean heart rate of 110 beats/min (D) and eventual recovery of the sinus rhythm (E).
Citation: Journal of the American Veterinary Medical Association 254, 2; 10.2460/javma.254.2.206
Representative continuous ECG tracings obtained during a period of induced stress in an 11-year-old Miniature Poodle that had episodic weakness and tremors and an instance of collapse. The first episode reportedly occurred 7 months prior to the evaluation. To induce stress, the dog was manually restrained in right lateral recumbency, and then restraint was partially released, allowing it to gently struggle in attempts to right itself (although the dog remained in lateral recumbency at all times). Notice the initial sinus rhythm with a mean heart rate of 100 beats/min (A), followed by an artifact caused by the patient struggling (B) and resulting sinus tachycardia with a mean heart rate of 260 beats/min and gradual onset and offset (C), which was followed by a pause and then a regular junctional or low right atrial escape rhythm with inverse P waves in the caudal leads and a mean heart rate of 110 beats/min (D) and eventual recovery of the sinus rhythm (E).
Citation: Journal of the American Veterinary Medical Association 254, 2; 10.2460/javma.254.2.206
Representative continuous ECG tracings obtained during a period of induced stress in an 11-year-old Miniature Poodle that had episodic weakness and tremors and an instance of collapse. The first episode reportedly occurred 7 months prior to the evaluation. To induce stress, the dog was manually restrained in right lateral recumbency, and then restraint was partially released, allowing it to gently struggle in attempts to right itself (although the dog remained in lateral recumbency at all times). Notice the initial sinus rhythm with a mean heart rate of 100 beats/min (A), followed by an artifact caused by the patient struggling (B) and resulting sinus tachycardia with a mean heart rate of 260 beats/min and gradual onset and offset (C), which was followed by a pause and then a regular junctional or low right atrial escape rhythm with inverse P waves in the caudal leads and a mean heart rate of 110 beats/min (D) and eventual recovery of the sinus rhythm (E).
Citation: Journal of the American Veterinary Medical Association 254, 2; 10.2460/javma.254.2.206
Results of subsequent 24-hour Holter monitoring revealed a mean heart rate of 73 beats/min. Recordings of the minimum heart rate (31 beats/min) and maximum heart rate (216 beats/min) were associated with sinus rhythm and correlated with appropriate diary entries (ie, when the dog was sleeping and excited because of the owner's return home, respectively). One single ventricular premature complex was noted. A diagnosis of suspected vasovagal syncope was made. The owner was advised to discontinue prestress treatments with trazodone and avoid triggers for stress, if possible. If stressful events were anticipated, the owner was advised to encourage the dog to eat salty treats, provide it with free access to water, and administer a dose of atenolol (1.1 mg/kg [0.5 mg/lb], PO). The owner elected to avoid all stressful triggers and reported during a follow-up conversation that the dog had no additional collapse episodes.
Discussion
Syncope—sudden and transient loss of consciousness with rapid spontaneous recovery—can have various causes, which influence cardiac output or vascular tone and thereby alter cerebral perfusion. Such causes include poor systolic function, severe mitral valve regurgitation, pulmonary hypertension, cardiac tamponade, bradyarrhythmias, tachyarrhythmias, or vasovagal mechanisms.2–6 Vasovagal syncope, also referred to as neurally mediated syncope or neurocardiogenic syncope, involves an autonomic signal cascade, which is typically initiated by a triggering stimulus that elicits fear, stress, or pain or is related to adjustment to upright posture (orthostatic hypotension).2,3 These central stimuli cause postganglionic sympathetic fiber activation and result in increased chronotropy and in-otropy.2,3 Subsequently, baroreceptor stimulation results in sudden withdrawal of sympathetic tone and increased vagal tone via the dorsal efferent nuclei of the medulla oblongata and vagus nerve, which serves as a protective mechanism and slows sinoatrial and atrioventricular nodal conduction.2,3 Hypovolemia can exacerbate this reflex (which has been referred to as the Bezold-Jarisch reflex, although this term is often reserved for human patients experiencing myocardial infarction) because of marked stimulation of myocardial C fibers.2–4 Hemodynamic assessments in humans with vasovagal syncope have revealed that serum catecholamine concentration, heart rate, and arterial blood pressure typically increase immediately before the onset of symptoms, followed by decreases in heart rate and blood pressure during the syncopal episode.5 This may represent an overzealous baroreceptor response as a cause for syncope and forms the basis for use of isoproterenol to provoke an episode during tilt-table testing of humans with suspected vasovagal syncope.6,7
Classification of autonomic dysfunction by subtypes has been used to specify the mechanism of neurally mediated syncope; subtypes include vasodepressor (vasodilation), cardioinhibitory (bradycardia), or mixed (vasodilation with bradycardia).5 Suggested treatments for vasovagal syncope have included medical treatment and permanent pacemaker implantation. Previously investigated medications include β-adrenoreceptor blockers, disopyramide, and serotonin reuptake inhibitors, all of which are intended to blunt the neural reflexes involved in modulating heart rate and vascular tone. Of these treatments, β-adrenoreceptor blockers are most commonly prescribed for human patients because treatment with these drugs may attenuate heart rate and decrease C fiber stimulation; however, success of treatment is variable and inconsistent.4 Prospective randomized studies4,5 in human patients are limited, and results have been generally unhelpful. Fludrocortisone has been proposed as a potential treatment to increase blood volume, but data are limited and have not shown clear clinical benefit.5 On the basis of results of small nonblinded studies,8,9 pacemaker implantation has been historically touted as a viable treatment for vasovagal syncope with the intent to target the cardioinhibitory mechanism. However, more recent blinded studies10,11 have not revealed a clear treatment benefit, perhaps suggesting that bradycardia is merely a sentinel of autonomic dysfunction and that vasodepressor mechanisms are intrinsic to clinical signs for most patients.2,5
The dog of the present report had ECG changes that supported marked sympathetic stimulation (sinus tachycardia) with abrupt withdrawal (sinus pause followed by junctional escape). Autonomic modulation of the sinoatrial node is independent of that of the atrioventricular node and may account for the disparity in vagal response that allows the junctional escape to predominate.12 The dog did not become overtly bradycardic during periods of stress; therefore, the dog was suspected to have a profound autonomic response to stress that resulted in neurally mediated vasodepressor syncope. Although there are descriptions of vasovagal syncope in dogs secondary to cough, micturition, and defecation among other triggers, stress-induced vasovagal syncope is not widely reported.2,13 There has been 1 anecdotal report13 of presumptive excitement-induced vasodepressor syncope in a dog; that diagnosis was based on a lack of palpable femoral pulses without a change in heart rate during an episode of excitement. Additional recommendations for patients with vasovagal syncope include facilitation of adequate cardiac preload by positioning to increase venous return (eg, by crossing legs) and by increasing sodium and water intake (hence, the recommendations for provision of salty treats and water for the dog of the present report). However, these recommendations have not undergone extensive prospective investigation.5,6 Treatment with trazodone causes vasodilation and has been correlated with orthostatic hypotension in humans; for the dog of the present report, it was recommended that administration of this medication be discontinued in case it was exacerbating vasodilation.14 Given the lack of clear treatment benefits for patients with vasovagal syncope, avoidance of stress triggers and reassurance regarding the non-life-threatening nature of the episodes should be emphasized.
Acknowledgments
The authors declare that there were no conflicts of interest.
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