Syncope



Syncope


Humberto Butzke da Motta

Olujimi A. Ajijola



INTRODUCTION

Syncope is defined as a transient loss of consciousness (TLOC) and loss of postural tone because of cerebral hypoperfusion. It is characterized by rapid onset, short duration (minutes or less), and spontaneous recovery; is not associated with prior head trauma, use of alcohol or other substances or metabolic abnormalities; and must be differentiated from seizure.1,2 It can cause secondary traumatic injury and be the only warning sign of severe cardiac disease before sudden cardiac death.

Syncope is a common clinical problem, accounting for up to 3% of all emergency department (ED) visits3 for an estimate of over 156,000 hospital admissions in the United States in 2013, with increasing costs in the last decade.4 Among the 7814 participants in the Framingham Heart Study, in an average follow-up of 17 years, 822 patients (11%) reported having syncope, with an incidence of a first episode of 6.2 per 1000 patient-years.5 In the general population, up to 50% of people report having had at least one episode of syncope, most of whom never come to medical attention, with peaks at around 20, 60, and 80 years of age.6


PATHOGENESIS, CAUSES, AND CLASSIFICATION

Syncope is the result of a fall in systemic blood pressure (BP), leading to a global decrease in cerebral perfusion. BP is the result of the interaction between cardiac output and systemic vascular resistance—with these two mechanisms acting together in different degrees depending on the underlying cause—leading to hypotension.

The causes of syncope can be divided into three major groups: reflex syncope, orthostatic hypotension, and cardiac syncope. These are summarized in Table 61.1 and Figure 61.1.


Reflex Syncope

Reflex syncopes, also called neurally mediated syncopes or vasovagal syncopes (VVSs), are caused by a loss of sympathetic tone or increase in vagal tone. The mechanisms involved determine two hemodynamic patterns: either a vasodepressive state, with decreased systemic vascular resistance, or a cardioinhibitory state, with bradycardia and low cardiac output. These mechanisms are not associated with specific triggers and can predominate or occur simultaneously. Reflex syncopes can be subdivided into: situational—that is, associated with specific actions, such as micturition, stimulation of the gastrointestinal tract (swallowing, defecation), cough, post-strenuous exercise, laughter; vasovagal—occurring either with prolonged standing or emotional and physical stimulation (eg, pain, blood phobia, other forms of emotional stress); and associated with carotid sinus hypersensitivity. There are also cases in which no specific trigger can be identified or the patient presents with nontypical symptoms. These cases are denominated reflex syncope of unknown cause, and the diagnosis is probable if cardiac causes are excluded and/or the symptoms are reproduced in a tilt-table test. Reflex syncope is considered to have a more benign course than that of cardiac syncope or orthostatic hypotension.7















Orthostatic Syncope

Moving to an upright position is associated with a significant shift of blood to the lower segments of the body, leading to a decrease in preload. In physiologic states, this activates the sympathetic nervous system, which counteracts by increasing the systemic vascular tone, thereby restoring blood flow toward the heart and maintaining cardiac output. In pathologies that cause autonomic failure, this compensation mechanism may be impaired. In these patients, changing from a recumbent or sitting position to the upright posture may trigger syncope or presyncope. This is denominated orthostatic hypotension and is defined as a 20 mm Hg or more drop in systolic BP or a 10 mm Hg or more drop in diastolic BP after 3 minutes of standing.8 Autonomic failure may occur as a primary phenomenon in neurodegenerative diseases such as Parkinson disease, multiple system atrophy, or pure autonomic failure, as well as a secondary effect of other systemic illnesses, such as diabetes mellitus or amyloidosis. It can also be an adverse effect of drugs (eg, alpha- or beta-adrenergic antagonists, diuretics) and occur in volume-depleted states.

The postural orthostatic tachycardia syndrome (POTS), a condition related to orthostatic hypotension, is defined as an increment of 30 bpm in heart rate within 10 minutes of standing or after being tilted head-up, in the absence of hypotension. Patients may complain of symptoms of cerebral hypoperfusion or autonomic reactivity. It is associated with recent viral illness, deconditioning, chronic fatigue, or restricted autonomic neuropathy. Symptoms tend to be relieved by returning to the recumbent position.


Cardiac Syncope

Cardiac or cardiopulmonary syncopes, which occur when the cardiac output is dramatically decreased, can be subdivided into two categories: arrhythmic syncope and structural cardiac disease. The most frequent form of arrhythmic syncope is that caused by bradyarrhythmias, usually happening when the ventricular rate is lower than 30 bpm for 15 to 30 seconds.9 Tachyarrhythmias, notably ventricular tachycardia but also supraventricular tachycardia, can also present with syncope. Particular heart diseases that lead to syncope are covered in depth in specific chapters in this book.

Some conditions may be confused with syncope. Generalized epileptic seizures, with concomitant disorganized electrical activity of both cerebral hemispheres, cause TLOC, but generally last longer and present with one-sided limb movements, tongue bites, and more prolonged postictal mental confusion and somnolence. Psychogenic pseudosyncope does not have the characteristic changes in BP and heart rate that accompany syncope; it usually has increased frequency, longer duration, and patients tend to maintain their eyes closed, which is unusual in syncope.
Cerebrovascular disease, notably subclavian steal syndrome, which was previously described as a cause of syncope, does not fit the more modern definition. This syndrome, as well as transient ischemic attacks (TIAs) arising from carotid obstructions or vertebrobasilar ischemia, does not present without focal neurologic signs, being relatively easy to distinguish from syncope in general practice. Cataplexy, a rare diagnosis, can be distinguished because of the fact that patients with this condition do not have amnesia, being able to describe the event after recovering conscience.




DIAGNOSIS

The most important part of the diagnostic evaluation is a careful and thorough patient history. It should ascertain the presence of any prodromal symptoms such as light-headedness, palpitations, sweating, tunnel and faded vision, chest pain, dyspnea, and neurologic symptoms (eg, focal weakness, tonic-clonic movements). An eyewitness account is also valuable, in order to establish the duration of the attack and any movement the patient may have done while unconscious, as well as to provide a description of the recovery period. The presence of previous episodes of syncope should also be evaluated, as well as possible triggers. The physical examination should focus on measuring the BP while the patient is in a supine position, after sitting, immediately after standing, and after being upright for 3 minutes. Also, the physician should pay attention to heart rate and rhythm and any signs of possible structural heart disease, such as gallops, murmurs, rubs, or bruits. A summary neurologic examination looking for focal signs is also warranted.

All patients presenting with syncope should have a 12-lead electrocardiogram (ECG) performed. An abnormal ECG in the context of syncope is associated with increased all-cause mortality.10

According to the most recent guidelines on the diagnosis and management of syncope,1,2 the initial evaluation should answer four questions, which will guide the subsequent management:



  • Was the event a TLOC?


  • Was it syncopal or nonsyncopal in origin?


  • In the case of syncope, is there a clear etiology?


  • Is there evidence to suggest a high risk of cardiovascular events or death?

Clinical and ECG features associated with higher risk are summarized in Table 61.2. Patients who do not have structural heart disease, ECG abnormalities, family history of sudden cardiac death, and no evidence of supine or exertional syncope or palpitations at the time of syncope are considered to be at low risk for cardiac syncope and should be managed in the outpatient setting.11

Routine comprehensive laboratory testing is not recommended. Selected tests should be ordered according to clinical suspicion. The usefulness of high-sensitivity troponin and B-type natriuretic peptide is uncertain when not guided by a specific clinical hypothesis, such as a clinical suspicion of ischemia or heart failure.







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May 8, 2022 | Posted by in CARDIOLOGY | Comments Off on Syncope

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