Cardiology Clinical Practice Guidelines: 2018 Midyear Review

John Anello; Brian Feinberg; John Heinegg; Yonah Korngold; Richard Lindsey; Cristina Wojdylo; Olivia Wong, DO

Disclosures

June 28, 2018

In This Article

Syncope

European Society of Cardiology

Transient loss of consciousness (TLOC) has four specific characteristics: short duration, abnormal motor control, loss of responsiveness, and amnesia for the period of LOC.

TLOC is probably syncope when: (1) there are signs and symptoms specific for reflex syncope, syncope due to orthostatic hypertension (OH), or cardiac syncope, and (2) signs and symptoms specific for other forms of TLOC (head trauma, epileptic seizures, psychogenic TLOC, and/or rare causes) are absent.

When epileptic seizures or psychogenic attacks are likely, appropriate steps should be taken. By using a detailed clinical history, physicians can differentiate syncope from other forms of TLOC in approximately 60% of cases.

The starting point of the diagnostic evaluation of TLOC of suspected syncopal nature is the initial syncope evaluation, which consists of careful history taking concerning present and previous attacks, as well as eyewitness accounts, in person or through a telephone interview; physical examination, including supine and standing blood pressure (BP) measurements; and an electrocardiogram (ECG).

Additional examinations may be performed when needed: immediate ECG monitoring when there is a suspicion of arrhythmic syncope; echocardiogram when there is previous known heart disease, data suggestive of structural heart disease, or syncope secondary to cardiovascular cause; carotid sinus massage (CSM) in patients aged >40 years; head-up tilt testing when there is suspicion of syncope due to OH or reflex syncope; blood tests when clinically indicated (eg, hematocrit or hemoglobin when hemorrhage is suspected, oxygen saturation and blood gas analysis when hypoxia is suspected, troponin when cardiac ischemia-related syncope is suspected, or D-dimer when pulmonary embolism is suspected).

Reflex syncope

Clinical features that can suggest a diagnosis on initial evaluation:

Long history of recurrent syncope, in particular occurring before the age of 40 years

After unpleasant sight, sound, smell, or pain

Prolonged standing

During a meal

Being in crowded and/or hot places

Autonomic activation before syncope: pallor, sweating, and/or nausea/vomiting

With head rotation or pressure on the carotid sinus (as in tumors, shaving, tight collars)

Absence of heart disease

Syncope due to OH

Clinical features that can suggest a diagnosis on initial evaluation:

While or after standing

Prolonged standing

Standing after exertion

Post-prandial hypotension

Temporal relationship with start or changes of dosage of vasodepressive drugs or diuretics leading to hypotension

Presence of autonomic neuropathy or parkinsonism

Cardiac syncope

Clinical features that can suggest a diagnosis on initial evaluation:

During exertion or when supine

Sudden onset palpitation immediately followed by syncope

Family history of unexplained sudden death at young age

Presence of structural heart disease or coronary artery disease

ECG findings suggesting arrhythmic syncope

Patients with low-risk features: These patients do not need further diagnostic tests in the emergency department (ED) as they are likely to have reflex, situational, or orthostatic syncope. They may benefit from reassurance, or counseling.

Patients with high-risk features: These patients should be classified as HIGH RISK; they require an intensive diagnostic approach and may need urgent treatment and admission. These patients should be monitored (although it is unclear for how long this should be, most studies suggesting up to 6 hours in the ED and up to 24 hours in hospital) in a setting where resuscitation can be performed in case of deterioration.

Patients that have neither high- nor low-risk features: These patients will require expert syncope opinion, which can probably be safely managed in an outpatient setting. There is no direct evidence that admitting patients to hospital changes their outcome, while there is evidence that management in an ED observation unit and/or fast-track to a syncope outpatient unit is beneficial.

There is strong consensus that the diagnosis of carotid sinus syndrome (CSS) requires both the reproduction of spontaneous symptoms during carotid sinus massage (CSM) and clinical features of spontaneous syncope compatible with a reflex mechanism.

Tilt testing is widely accepted as a useful tool to demonstrate susceptibility of the patient to reflex syncope, especially a hypotensive (vasodepressive) tendency, and thereby to initiate treatment. The endpoint of tilt testing is the reproduction of symptoms along with the induction of reflex hypotension/bradycardia, OH, postural orthostatic tachycardia syndrome (POTS), or psychogenic pseudosyncope (PPS).

There is strong evidence that the absence of a BP overshoot and an absence of a heart rate (HR) increase during the Valsalva is pathognomonic for neurogenic OH.

Deep breathing test: There is strong consensus that blunted or abolished variation is suggestive of parasympathetic dysfunction.

The gold standard for the diagnosis of arrhythmic syncope is when there is a correlation between the symptoms and an ECG recording. The presence of asymptomatic significant arrhythmias—defined as prolonged asystole (≥3 s), rapid supraventricular tachycardias (SVTs) (ie, >160 bpm for >32 beats), or ventricular tachycardias (VTs)—has been considered by several authors to be a diagnostic finding.

Even if the quality of evidence is moderate, there is strong consensus that a positive electrophysiologic study (EPS) indicates that the likely mechanism of syncope is paroxysmal atrioventricular (AV) block.

Angiography alone is not diagnostic of the cause of syncope. Therefore, cardiac catheterization techniques should be carried out in suspected myocardial ischemia or infarction with the same indications as for patients without syncope.

The efficacy of therapy aimed at preventing syncope recurrence is largely determined by the mechanism of syncope rather than its etiology. Bradycardia is a frequent mechanism of syncope. Cardiac pacing is the most powerful therapy for bradycardia, but its efficacy is less if hypotension coexists.

Syncopal recurrences often decrease spontaneously after medical assessment, even in the absence of a specific therapy; in general, syncope recurs in <50% of patients within 1–2 years.

Despite its benign course, recurrent and unpredictable reflex syncope may be disabling. The cornerstone of management of these patients is non-pharmacological treatment, including education, lifestyle modification, and reassurance regarding the benign nature of the condition.

Careful avoidance of agents that lower BP (ie, any antihypertensive agents, nitrates, diuretics, neuroleptic antidepressants, or dopaminergic drugs) is key in the prevention of recurrence of syncope.

There is moderate evidence that discontinuation/reduction of hypotensive therapy targeting an SBP of 140 mmHg should be effective in reducing syncopal recurrences in patients with hypotensive susceptibility.

There is moderate evidence that fludrocortisone may be effective in reducing syncopal recurrences in young patients with low–normal values of arterial BP and without comorbidities.

There is sufficient evidence from multiple trials that beta-blockers are not appropriate in reducing syncopal recurrences. Desirable and undesirable effects are closely balanced.

There is sufficient evidence that dual-chamber cardiac pacing should be considered to reduce recurrence of syncope when the correlation between symptoms and ECG is established in patients ≥40 years of age with the clinical features of those in the ISSUE studies.

Despite the lack of large randomised controlled trials (RCTs), there is sufficient evidence that dual-chamber cardiac pacing should be considered to reduce syncopal recurrences in patients affected by dominant cardioinhibitory carotid sinus syndrome (CSS).

There is strong consensus that reduction or discontinuation of hypotensive drugs and psychotropic drugs clearly outweighs the undesirable effects (eg, complications) of high BP.

Pediatric patients

Syncope in childhood is common, the majority being of reflex origin, with only a minority having a potentially life-threatening cause.

Discriminating benign from serious causes is made primarily by history, physical examination, and ECG results.

Children with a history suggesting vasovagal syncope (VVS), a normal ECG, and no family history of arrhythmia should not undergo further cardiac investigations.

The cornerstone of therapy for young patients with reflex syncope includes education and reassurance.

Reference

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