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.
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.
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 severe 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 occur secondary to sudden bradycardia following bouts of tachycardia in especially 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.
Approach to the patient with syncope:
Clues as to the underlying cause of the episodes can be elicited through a thorough history and physical examination of the animal. Getting a detailed (almost dramatic) description of the events as they occurred as well as the preceding events, prodromal signs, and the animal's mentation and behavior prior to and after the event can help in differentiating cardiovascular syncope from seizure activity and other causes of collapse. In a nice human prospective study the etiology of the syncopal event was able to be correctly elicited in 32% of patients based on obtaining a thorough history and physical examination. Performing diagnostic testing in a stepwise manner is critical in diagnosing the syncopal patient.
Some questions you should consider asking when obtaining a history include:
While this is not an all inclusive list of questions and the answers may take you down different lines of questioning, answers to most of these questions may help you decide to follow the path of seizure or syncope for you next steps in diagnostic testing.
Routine database of CBC, biochemical profile, urinalysis, heartworm test and arterial blood pressure measurement should be performed. In some cases, testing for adrenal and thyroid abnormalities should also be performed. In the syncopal patient however, these tests are usually normal, however it is important to perform them to rule out non cardiogenic causes of collapse.
A resting electrocardiogram (ECG) should be obtained and the rhythm should be evaluated for at least one minute if not longer, and while the animal is calm and excited. In dogs with bradycardia, ECG should be evaluated a second time following the administration of atropine 0.04 mg/kg IV or SC. Dogs with underlying sinus node disease will show an inadequate response (heart rate increase to <140 bpm). Dogs with vagal tone as the underlying mechanism for bradycardia typically have heart rates that increase above 160 bpm. Normal heart rates on transient baseline ECG's however does not completely rule out arrhythmias as the underlying cause of the syncopal episode.
Thoracic radiographs should be performed to evaluate lungs, pleural space, mediastinum and pulmonary vasculature as well as normal cardiac size and shape. Echocardiogram should be performed even if no murmurs are ausculted on physical examination to assess global cardiac function and to rule out the present of pericardial disease and obstructive cardiac masses.
In the face of finding all of the aforementioned test to be relatively normal (blood work, ECG, radiographs, and echocardiography) the clinician should consider ambulatory ECG monitoring with either Holter or event monitoring. Ambulatory monitoring can help identify or exclude cardiac arrhythmias as a cause for syncope in some animals.
Holter monitoring is twenty-four to forty-eight hours of continuous ECG monitoring. They are most likely to be diagnostic of syncopal events in animals with multiple and frequent syncopal episodes. To make a definitive diagnosis a syncopal episode must occur while the monitoring is occurring. However, just because frequent events are occurring doesn't increase the likelihood of an event occurring during testing. Holter monitoring does allow one to identify any arrhythmia and quantitate the severity of arrhythmias that might increase the suspicion that the syncopal events are induced by arrhythmias. Because arrhythmias often occur without clinical signs this ability to evaluate the entire recording period is a very useful aspect of Holter monitoring. Holter monitors are also very useful for assessment of anti-arrhythmic therapy efficacy.
Event monitors are typically worn for 1-2 weeks periods in our patients that allow longer periods of assessment than with Holter monitoring. The event recording system does need to be activated when an event is observed. The monitor then saves to memory a portion of the recording prior to and after activation. The save recording is then transmitted via telephone to be printed. Event recorders have a higher diagnostic yield than Holter monitors however there biggest disadvantage is that they do not save recordings of potentially significant arrhythmias unless activated and they can not quantify the frequency of arrhythmias.
Therapy of animals with syncope episodes is intended to manage the underlying disease and avoidance of precipitating activities such as excitement as much as one can. In as such treatment of specific causes is sometimes obvious for example correcting anemia or treating respiratory or metabolic disorders.
In the case of heart failure patients: addressing proper management of the patient in heart failure: Institute appropriate therapy with diuretics, angiotensin converting enzyme inhibitors (ACE-I), and inotropic support if needed. In the case of patients who are already being treated with triple therapy, optimizing drug therapy dosages or stacking additional medications such as additional diuretics or vasodilators may help to place the patient in a more positive hemodynamic state and thus resolving syncopal signs.
If tachyarrhythmias are the apparent cause, treating with the appropriate anti-arrhythmic (or combination of anti-arrhythmic) will reduce or eliminate the number and severity of the arrhythmias such that the signs are eliminated. In the case of those arrhythmias that can not be eliminated such as atrial fibrillation associated with advanced heart disease, than using drug combinations that slows the number of impulses that cross the AV node to the ventricles will appropriately slow the heart rate enough to allow for appropriate ventricular filling and contraction that syncopal signs are eliminated or reduced significantly.
In the case of bradyarrhythmias, than pacemaker therapy may be warranted; especially those cases that don't respond to atropine trials. Other strategies that have been effective, at least anecdotally include using Theophylline or Aminophylline to attempt to increase heart rate. We have found that often this therapy may be effective early but becomes ineffective as time passes on. We have also successfully employed pacemaker therapy in animals where syncope was apparently induced by coughing and the cause of the cough could not be resolved (i.e. severe LA enlargement).
In the rare cases of neurocardiogenic syncope pacemaker therapy is not likely to alter the hypotension that results. In suspected cases therapy with beta-blockers can be used to blunt the initiating sympathetically-induced tachycardia and the hyperkinetic ventricular contractions that stimulate the mechanoreceptors. The concern with utilizing beta-blocker therapy along is exacerbation of the resultant bradycardia thus these patients should be monitored very closely and combination of drug and pacemaker therapy may be the most appropriate for these animals.
Syncope can be a very difficult diagnosis and hard to distinguish from seizures or other causes of collapse. An adequate physical examination and understanding of the etiology and pathophysiology along with a stepwise approach to animals presenting with this clinical complaint can expedite uncovering the underlying cause and allow for early intervention for these animals.
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