Clinical Vignette
An 11-year-old castrated shih tzu was presented with the chief complaint of collapse. The first episode of collapse occurred during exertion while bathing and others have occurred during excitement when the owner returned home from work. Physical examination revealed a moderate to severe heart murmur at the level of the left apex. The remainder of the physical examination was unremarkable.
Problem Definition and Recognition
Syncope is defined as collapse with a temporary loss of consciousness and spontaneous recovery. Given the loss of consciousness, syncope is most often confused with seizure activity. In addition, syncope must be distinguished from episodic paresis and narcolepsy.
Pathophysiology
The causes of syncope are listed in Table 22-1.
Syncope results from reduced blood flow and/or nutrients (i.e., glucose or oxygen) to the brain. Cerebral blood flow is maintained by mean arterial pressure (cardiac output × systemic vascular resistance). The resistance to cerebral blood flow is intracranial pressure. Therefore, conditions that affect heart rate (electrical disturbances), stroke volume (structural heart disease), and intracranial pressure (neurologic disease) may lead to syncope. The most common metabolic causes of syncope are hypoglycemia, hypoxemia, and anemia (Table 22-1).
Most cardiac electrical disturbances causing syncope can be detected or suspected on the basis of a static electrocardiograph (ECG). However, neurally mediated bradycardia/syncope is characterized by a sudden but transient withdrawal of sympathetic tone and concurrent parasympathetic discharge. Although the pathophysiology of neurally mediated bradycardia/syncope is incompletely understood, it results from the activation of a complex neurocardiovascular reflex that can be initiated by stimulation of a number of peripheral, chemical, and/or mechanical receptors transmitting sensory impulses through autonomic afferent fibers to the brain stem. Episodes can be triggered by activities or situations that result either in a sympathetic surge that triggers intracardiac receptors that normally respond to cardiac muscle fiber loading or stretch to evoke a reflex vagal response (neurocardiogenic bradycardia/syncope), or a parasympathetic surge where cough, emesis, micturition, and defecation stimulate receptors in the pharynx, larynx, respiratory tree, bladder, and gastrointestinal tract to evoke a vagal response and bradycardia (situational syncope). The final common pathway associated with either the sympathetic- or the parasympathetic-initiated surge is afferent vagal stimulation of the medullary vasomotor (vasodepressor) center. This center then responds with sympathetic withdrawal and a mildly to severely accentuated vagal efferent discharge resulting in bradycardia or even temporary sinoatrial arrest, decreased cardiac filling and output, a precipitous decrease in systemic blood pressure, and decreased brain perfusion.
TABLE 22-1. Conditions associated with syncope
Minimum Database
History and Physical Examination
The primary objective of the history is to distinguish syncope from seizure activity, episodic paresis, and narcolepsy (see Table 22-2). Syncope is most often associated with a flaccid rather than tonic–clonic collapse typical of seizures. Patients with seizure activity often have a postictal phase of confusion, blindness, and ataxia. Episodic paresis does not result in loss of consciousness, while narcolepsy and syncope are accompanied by loss of consciousness. However, presyncope without collapse can occur and is usually associated with arrhythmia.
Given the difficulty sometimes in distinguishing between syncope and seizure activity, often times a good history is not enough. However, there are some distinguishing features that can assist with differentiation. Episodes that are precipitated by exertion, excitement, startle, cough, vomiting, and defecation are most likely syncope. If ptyalism is observed prior to episodes and/or blindness and ataxia are observed afterward, then the episodes are most likely seizures. A common pitfall is to associate defecation, urination, and extensor rigidity with seizure activity originating from the central nervous system. Profound cardiac arrhythmias can result in hypoxic convulsive syncope with similar signs.
TABLE 22-2. Comparison of clinical signs of conditions that may be confused with syncope
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