Syncope (fainting) is defined as a sudden and transient loss of consciousness due to deprivation of the brain of energy substrate, be it oxygen or glucose, causing brief impairment of cerebral metabolism. The brain’s energy supply is limited to glucose as provided from cerebral blood flow. Presyncope occurs when the animal does not experience a complete loss of consciousness. The causes of syncope are manifold and often elude accurate diagnosis. Furthermore, it can be exceedingly difficult to differentiate syncope from neurologic seizure in veterinary patients. Clinical signs in humans typically entail “lightheadedness,” vertigo and falling over with flaccid, brief paralysis. Animals may become suddenly weak or wobbly, and may manifest opisthotonus. This may be followed by uncoordinated muscle activity (jerky movements), which can be difficult to differentiate from tonic-clonic movements associated with generalized seizures, and involuntary micturition/defecation. The animal then usually becomes flaccid and briefly unresponsive. Rapid and complete recovery with a brief period of confusion is a hallmark of syncope. This is in contrast to a neurologic seizure, which is typically preceded by a pre-ictal period with anxiety or hiding behavior, and is marked by tonic-clonic movements, chattering of the teeth and hypersalivation. This is then followed by post-ictal period during which the animal does not behave normally, may be apparently blind, etc., which may last for hours. Animals having a syncopal event often vocalize, which is the result of central nervous system activity, not from pain or fear, which is how most owners interpret it. Rule-outs include neurologic seizures, narcolepsy, cataplexy, episodic weakness, acute hemorrhage and diseases associated with decreased alertness. The main categories of maladies that may produce syncope include cardiac dysfunction, peripheral vascular dysfunction, metabolic disturbances, as well as some miscellaneous disorders.
Many forms of cardiac dysfunction may produce syncope. The most common include reduced cardiac output from arrhythmias, systolic myocardial disease, diastolic impairment from cardiac tamponade and hypoxemia from pulmonary arterial hypertension.
Arrhythmias that result in syncope are generally classified as bradyarrhythmias or tachyarrhythmias. Bradyarrhythmias cause problems because the cardiac output drops as a function of the decreased heart rate. Pauses in the ventricular rhythm for 6-8 seconds may produce syncope. Bradyarrhythmias most often associated with syncope include atrioventricular block (AVB), specifically Type II 2nd degree, 3rd degree AVB and transient ventricular asystole. Atrial standstill from atrial muscular dystrophy or hyperkalemia are less common causes of syncope. So-called “Stokes-Adams attacks/syncope” is a syndrome associated with incomplete or complete AVB, and includes sinus arrest, sinoatrial pause/block and sick sinus syndrome. Three basic mechanisms are at play. Transient ventricular asystole is most common, and occurs when there are sudden extended periods without a ventricular contraction. Changing block (i.e. 2nd degree to 3rd degree) also results in prolonged ventricular asystole. Ventricular tachycardia can also develop following periods of asystole, which may also precipitate syncope. Tachyarrhyhmias decrease the diastolic filling of the left ventricle, leading to decreased cardiac output. Tachycardia of 300+ beats-per-minute frequently results in syncope. Syncope may occur during the period of elevated heart rate or at the end of a paroxysm if asystole follows, which is the result of overdrive suppression. Sudden onset of atrial fibrillation may precipitate syncope. Sustained supraventricular and ventricular tachycardia (e.g. Boxers and Dobermans) are the most common. If an arrhythmia is the cause of syncope, most patients are overtly arrhythmic on presentation.
Cardiac dysfunction can also be the result of myocardial failure, cardiac tamponade, pulmonary arterial hypertension and congenital right-to-left (R-L) shunts. Syncope associated with cardiac dysfunction commonly occurs with physical exertion or shortly thereafter. Patients with dilated cardiomyopathy may experience syncope because they really have little to no systolic reserve and develop forward failure with hypotension. Hypertrophic obstructive cardiomyopathy or restrictive cardiomyopathy may decrease left ventricular output enough to precipitate syncope as well. Patients with congenital subaortic stenosis often experience syncope associated with exercise, and is generally attributed to hypotension due to the fixed/reduced cardiac output and increased intraventricular pressure that overstimulates mechanoreceptors resulting in reflex activation of cardiac afferent vagal fibers. This results in bradycardia and vasodilation (via nitric oxide and other metabolites), which is similar to that seen with neurocardiogenic (vasovagal) syncope, and referred to as the Bezold-Jarisch reflex. This reflex may also be triggered by massive hemorrhage. Furthermore, severe left ventricular hypertrophy associated with subaortic stenosis predisposes these patients to malignant ventricular arrhythmias which also may cause syncope. Cardiac tamponade associated with pericardial effusion results in diastolic dysfunction via reduced filling/preload which in turn decreases cardiac output. Pulmonary hypertension frequently results in syncope from the intrapulmonary shunting and subsequent hypoxemia. Congenital R-L shunts similarly may produce syncope and include ventricular septal defects with Eisenmenger’s physiology, R-L patent ductus arteriosus and Tetralogy of Fallot. Intracardiac masses or thrombi may act like a ball-valve over mitral or aortic orifices, causing transient obstruction of blood flow, decreased cardiac output and syncope. Herniation of an auricle through a defect in the pericardium has also been reported to be associated with syncope.
Peripheral vascular dysfunction basically involves an abnormal reflex or physiologic reflex that results in syncope. The most common syndrome is neurocardiogenic (“vasovagal” or vasodepressor) syncope. This may occur in otherwise healthy animals, but is very common in patients in or near congestive heart failure (typically secondary to chronic mitral valvular disease). It is usually preceded by a period of immobility, pupillary dilation, followed by peripheral arterial vasodilation and venoconstriction. Vasovagal syncope is usually precipitated by a sudden onset of extreme fright/excitement. Vagal overactivity results in characteristic bradycardia. Mixed vasodilation and bradycardia is most common in humans as a result of postural hypotension, and head-up tilt table testing is generally required for diagnosis. Holter monitoring in animals may document bradycardia, but hypotension from vasodilation is typically undocumented and assumed to be at play. Postural hypotension occurs when a fall in both systolic and diastolic blood pressure happens when animals rise with variable changes in the heart rate. This may occur secondary to diabetes mellitus, Addison’s disease, decreased intravascular volume (hypovolemia), dysautonomia or iatrogenic causes such as excessive diuresis, or drug administration (beta-blockers, vasodilators, antihypertensives, tranquilizers). Patients with hyperventilation syndrome are usually anxious/hyperexcitable and will faint following overbreathing. Overactivation of the alveoli results in a fall of alveolar and arterial PCO2 levels, leading to cerebral arterial vasoconstriction and peripheral vasodilation. Some animals have carotid sinus hypersensitivity, which is basically neurogenic dysfunction in which afferent impulses from the carotid sinuses are transmitted by glossopharyngeal nerves to vasomotor and cardioinhibitor centers in the medulla. Vagal stimulation slows the heart rate, leading to bradycardia, potentially with variable degrees of heart block. This in turn leads to decreased cardiac output, cerebral anoxia and syncope. This may be exacerbated in patients wearing tight-fitting collars and may be triggered by vomiting, sneezing, swallowing, micturition, or defecation.
Metabolic disorders may also result in syncope. Generally, the longer the duration of a syncopal attack is, the more likely a metabolic disorder is the cause. Hypoglycemia, severe anemia, hyperventilation, calcium imbalances, liver and renal dysfunction may occasionally be associated with syncope.
Miscellaneous causes of syncope may include tussive syncope, pulseless disease and acute, transient hypoxia. Well recognized in dogs, but poorly defined, tussive syncope is thought to occur when coughing raises the intrathoracic and cerebrospinal fluid (CSF) pressure. When the CSF pressure exceeds that of the intracranial capillary pressure, the brain experiences decreased blood flow, leading to syncope. Pulseless disease is the result of major obstructions to one or more of the vessels supplying the head. Syncope is typically preceded by activity in these cases. Upper airway obstruction (i.e. laryngeal paralysis, tracheal collapse or foreign bodies) may produce syncope associated with acute and transient hypoxia.
Patients that have known or suspected syncope should have a minimum of diagnostic tests. These would include a complete blood cell count, complete serum chemistry panel, blood pressure, electrocardiogram and chest x-rays. These tests quickly exclude anemia, hypoglycemia/metabolic disease, sustained hypotension, arrhythmias and pulmonary/airway disease as potential causes of syncope. If the cause is still unknown following these tests, then further testing such as upper airway examination to rule out laryngeal paralysis, echocardiography to rule out cardiac disease, pericardial effusion and pulmonary arterial hypertension, as well Holter/Event monitoring to rule out transient arrhythmias should be considered. In cases where neurologic seizure cannot be excluded, magnetic resonance imaging of the brain and CSF analysis may be warranted.