Syncope is the sudden temporary loss of consciousness that is associated with loss of postural tone as a result of an abrupt
decrease in cerebral perfusion or decreased delivery of essential nutrients (i.e. glucose) to the brain. The true incidence
of syncope is unknown however it has been reported to occur in a referral database in 0.15% of dogs and 0.03% of cats. This
number may be due to the fact that one it is a referral database and two that often to both the trained and untrained eye
it may be difficult to distinguish syncope from seizure activity.
During a syncopal event, animals will usually collapse into lateral recumbency and may have concurrent stiffening of the limbs,
opisthotonous, urination and vocalization. However it is uncommon to see persistent facial fits, persistent tonic/cloned motion,
defecation, postictal dementia and neurologic deficits with cardiovascular mediated syncope. What may often confuse one who
witnesses a syncopal event is that on occasion some animals may have "convulsive syncopal episodes" (CSE) that results from
severe hypotension or asystole. Typically CSE are preceded by loss of muscle tone whereas seizure activity is usually preceded
by atypical limb or facial movement or even staring spells prior to the loss of body tone.
Etiology And Pathophysiology:
The mechanisms underlying syncope are usually rather acute in nature. These mechanisms usually involve reduced cardiac output
resulting from arrhythmias or decreased cardiac filling, obstruction of blood flow from the heart, hypoxia or hypoglycemia
(with normal cerebral flow) or severe decreased vascular resistance related to neurocardiogenic reflexes. There are numerous
diseases that can result in any one or a combination of these mechanisms. A partial list is presented in Table 1.
The vast majority of syncopal events in veterinary medicine are due to a transient reduction in brain blood flow. A sudden
decrease in cardiac output (CO) or vascular resistance reduces mean arterial pressure may both result in reduction of cerebral
blood flow. The most common causes we see in our patients are cardiogenic in nature. Two-thirds of dogs and cats with syncope
also have a cardiac disease. Most of these are related to rhythm disturbances which are secondary to inherent cardiac disease.
Underlying cardiac functional or structural abnormalities exacerbate the negative effect of arrhythmias on cardiac output.
Poor myocardial contractility, impaired filling as with pericardial disease or outflow obstructions can all result in an inability
of the heart to maintain sufficient cardiac output to meet increased demand during excitable states; even under normal cardiac
Non-cardiogenic diseases such as those that result in increased intracranial pressure can result in syncope also by reducing
cerebral perfusion pressure by compressing intracranial vessels. While the majority of animals with severe hypoglycemia will
present with weakness or seizures, a fair number may present with syncope or CVE while maintaining normal cardiac output.
Hypoxia as a result of right to left shunts, severe acute anemia or pulmonary disease can result in insufficient cerebral
oxygen delivery and syncope.
Another common occurrence that we see is cough (tussives) syncope. Some like to use the term 'cough drop' to describe syncope
induced in this manner. This form of situational syncope occurs most often in bracheocephalic dogs however is also common
in dogs with airway disease, tracheal collapse or those with sever left atrial (LA) enlargement causing compression of the
left maintstem bronchus. Coughing results in increased intrathoracic pressure which decreases venous return (preload) and
cardiac output. It also decreases intracranial pressures both of which may cause a decease in cerebral perfusion if severe
enough coughing occurs. Coughing may also induce reflexive bradycardia by stimulation of the vagal nerve.
Neurocardiogenic (vasovagal) reflex resulting in syncope is less common in animals than in people however there are reports
of syncope that occurs secondary to sudden bradycardia following bouts of tachycardia in especially in small breed dogs with
advanced valvular disease. In cases of neurocardiogenic syncope acute sympathetic activity (induced by excitement) provokes
a strong reflex vagal response that results in bradycardia. Ventricular mechanoreceptors play a huge role in this reflex in
that their activation due to forceful contraction results in a surge in afferent neural traffic stimulating paradoxical brainstem
response to vagal activation.