Diagnosis and treatment of syncope (Proceedings)
Apr 01, 2008
CVC IN WASHINGTON, D.C. PROCEEDINGS
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 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 rhythms.
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.