Syncope

Syncope is a transient loss of consciousness caused by global cerebral hypoperfusion, defined by rapid onset, short duration, and spontaneous complete recovery. Every one of those elements matters: an episode that does not recover spontaneously and completely is not syncope, and the diagnosis is as much about what recovery looks like as about the collapse.

Consciousness is lost after only six to eight seconds of interrupted cerebral blood flow, or a drop in systolic pressure to around 60 mmHg. Since cerebral perfusion is the product of cardiac output and systemic vascular resistance, syncope follows from a fall in either.

The causes divide into three groups, and distinguishing them is the whole of the clinical task — because their prognoses are entirely different.

Reflex (Neurally Mediated) Syncope

The commonest form and benign. An inappropriate autonomic reflex causes vasodilatation, bradycardia, or both.

• Vasovagal — provoked by prolonged standing, heat, pain, fear, or the sight of blood, and preceded by a recognizable prodrome of nausea, sweating, warmth, and visual greying. Rare when supine.
• Situational — triggered by a specific act: coughing, swallowing, defecation, or micturition, the last classically in men rising at night.
• Carotid sinus hypersensitivity — provoked by neck turning, tight collars or shaving, typically in older men.

Orthostatic Hypotension

A sustained fall in blood pressure on standing, defined as ≥20 mmHg systolic or ≥10 mmHg diastolic within three minutes. Causes include hypovolaemia from bleeding or dehydration; drugs, particularly antihypertensives, diuretics, nitrates, alpha-blockers and antidepressants; and autonomic failure in diabetes, Parkinson’s disease or amyloidosis. It is a common and frequently reversible cause in older people.

Cardiac Syncope

The dangerous group, and the one that must be actively excluded. Cardiac output falls abruptly.

• Arrhythmia — bradyarrhythmia from sinus node disease or high-grade AV block; or tachyarrhythmia, particularly ventricular tachycardia, long QT syndrome, and Brugada syndrome.
• Structural disease — aortic stenosis and hypertrophic cardiomyopathy, both classically causing exertional syncope; also pulmonary embolism, aortic dissection, and cardiac tamponade.

Cardiac syncope carries a materially higher mortality than the other groups, which is the reason the assessment is structured around finding it.

The episode itself is a brief loss of consciousness with loss of postural tone, followed by rapid, complete recovery without confusion.

Reflex syncope has a prodrome — light-headedness, nausea, sweating, pallor, warmth, tinnitus and tunnel or greying vision — usually lasting several seconds, giving the person time to sit or lie down. Recovery is prompt but often followed by fatigue and nausea for some time.

Cardiac syncope characteristically occurs with little or no warning. Abrupt collapse without prodrome, syncope during exertion or while supine, and syncope preceded by palpitations or chest pain are the features that should raise concern, as are injury from an unprotected fall, a family history of sudden death under 40, and known structural heart disease.

Brief myoclonic jerking is common in syncope of any cause and is frequently misinterpreted as a seizure. The distinguishing features are that the jerks are brief and follow the collapse, and that recovery is immediate rather than followed by prolonged postictal confusion.

A careful history from the patient and from a witness is the highest-yield element of assessment and establishes the cause in about half of cases. The questions that matter are: what the person was doing, whether there was a prodrome, how long they were out, whether there was confusion afterward, and whether there was any tongue-biting or incontinence.

Examination should include lying and standing blood pressure, a cardiovascular examination for murmurs — aortic stenosis in particular — and a neurological examination. A 12-lead ECG is mandatory in every case, looking for conduction disease, pre-excitation, a long or short QT interval, Brugada pattern, and evidence of prior infarction.

Further investigation follows risk. Echocardiography where structural disease is suspected, ambulatory or implantable loop recording for infrequent episodes, exercise testing for exertional syncope, and tilt-table testing for recurrent unexplained episodes suspected to be reflex. A full blood count, glucose and electrolytes are reasonable baseline tests. Neuroimaging and EEG have a very low yield in genuine syncope and should not be routine — they are for suspected seizure or focal deficit.

Syncope is a common cause of injury in older adults, and hip fracture and head injury from unprotected falls are a major source of morbidity. Recurrent episodes carry significant anxiety and functional restriction, and have implications for driving and occupation that need to be raised explicitly. Polypharmacy is a frequent and correctable contributor in older people. Underlying structural heart disease is the factor that determines prognosis, which is why its exclusion, rather than symptom control, is the priority.