Syncope

Syncope is a broad term for transient loss of consciousness.

Syncope refers to a transient loss of consciousness. The loss of consciousness is usually due to a brief reduction in cerebral perfusion due to an abrupt fall in blood pressure. The loss of consciousness inevitably leads to a collapse with subsequent recovery as perfusion is restored (~8-10 seconds).

There are many different causes of syncope of which the most common is vasovagal syncope. Vasovagal syncope is also known as a ‘common faint’ and typically occurs in the setting of a stressful event (e.g. phlebotomy). It is characterised by prodromal symptoms (e.g. lightheadedness, sweating, palpitations) and then loss of consciousness due to alteration in activation of the autonomic nervous system. For more information see our Vasovagal syncope note.

During the assessment of a patient with syncope, it is important to differentiate between the causes based on the history, examination, and simple investigations. It is especially important to be able to recognise dangerous causes of syncope (e.g. cardiac arrhythmias, structural cardiac disease) and to differentiate from non-syncopal causes of collapse/loss of consciousness (e.g. seizures, hypoglycaemia).

Vasovagal syncope is the most common cause of syncope in young people.

The causes of syncope are broadly divided into four major categories:

• Reflex syncope (vasovagal is a form of reflex syncope)
• Orthostatic hypotension (fall in blood pressure on standing)
• Arrhythmias (e.g. ventricular tachycardia, heart block)
• Structural cardiopulmonary disease (e.g. aortic stenosis, massive pulmonary embolism)

Reflex syncope

A ‘reflex syncope’ causes loss of consciousness due to a reflex response in the autonomic nervous system. The most common type is vasovagal syncope, otherwise known as a common faint.

Types of reflex syncope:

• Vasovagal syncope: alteration in the autonomic nervous system is often due to a ‘stressful’ event with a fall in blood pressure, heart rate, or both. It is characterised by a prodromal period with symptoms of lightheadedness, sweating, feeling warm/cold, nausea, visual alteration and reduced hearing. This is followed by a collapse due to hypotension and/or bradycardia
• Situational syncope (faint in response to a specific trigger): coughing, swallowing, sneezing, micturition
• Carotid sinus syndrome: exaggerated response to carotid sinus baroreceptor stimulation. Baroreceptors are mechanoreceptors that sense arterial stretch and alter blood pressure through the autonomic nervous system. Excess external palpation or turning the head (e.g. look over the shoulder) can lead to over activation and syncope

The history of clear prodromal symptoms in response to an external trigger is very typical of vasovagal syncope. The loss of consciousness is brief and patients usually quickly recover. In the absence of an obvious trigger (more common in the elderly), it may be difficult to diagnose vasovagal syncope.

Orthostatic hypotension

In simple terms, orthostatic hypotension refers to a fall in blood pressure (BP) on standing. It is broadly defined as:

• Fall in systolic BP ≥ 20 mmHg or more (with or without symptoms)
• Fall in diastolic BP ≥ 10 mmHg with symptoms (clinically much less significant)

NOTE: It may also be considered for patients with a fall in systolic BP below 90 mmHg (even if drop less than 20 mmHg)

When we stand, there is a natural fall in blood pressure as blood pools in the lower extremities and splanchnic circulation. Less stress on baroreceptors (e.g. in the carotid sinus) leads to activation of the autonomic nervous system that increases vascular resistance, venous return, and cardiac output to limit the fall in blood pressure. Blunting of this normal response due to age, medications or autonomic failure can lead to syncope.

Factors that can increase the risk of orthostatic hypotension include:

• Older age (often due to reduced baroreceptor activity)
• Medications (e.g. antihypertensives, vasodilatory drugs, tricyclic antidepressants)
• Volume depletion
• Autonomic dysfunction (e.g. Parkinson’s disease, diabetes mellitus)

The Royal College of Physicians (RCP) outlines the correct way to assess for orthostatic hypotension.

• Lying:
  • Step 1: Ask the patient to lie down for 5 minutes
  • Step 2: Measure the blood pressure
• Standing
  • Step 3 (0-1 minute): Ask the patient to stand (assist if needed). Measure the blood pressure (1 minute)
  • Step 4 (3 minutes): Measure the blood pressure again (3 minutes)
  • Step 5 (3+ minutes): Repeat measurements of the blood pressure if still dropping
• Recovery
  • Step 6: in the instance of positive results, help back down and repeat regularly until resolves

Arrhythmias

Cardiac arrhythmias are an important cause of syncope, particularly in the elderly or those with cardiovascular risk factors. These causes are often characterised by little or no prodromal symptoms with sudden syncope. Both tachyarrhythmias (e.g. ventricular tachycardia) and bradyarrhythmias (e.g. complete heart block) can lead to syncope.

Arrhythmias can significantly reduce the cardiac output leading to reduced cerebral perfusion and syncope. If severe or persistent, they can lead to cardiac arrest (i.e. the abrupt loss of heart function). The abnormal rhythm may be transient leading to syncope with recovery and no detectable abnormality on the electrocardiogram (ECG). These patients may need cardiac monitoring in case the abnormal rhythm returns.

Structural cardiopulmonary disease

Cardiac outflow obstruction (i.e. reduced blood exiting the heart) can lead to reduced cerebral perfusion and syncope. These causes are often characterised by little or no prodromal symptoms with sudden syncope.

Clinically important structural cardiac defects include aortic stenosis (narrowing of the aortic valve limiting blood flow) and hypertrophic cardiomyopathy (abnormal cardiac muscle hypertrophy that can limit the outflow of blood into the aorta). On the contrary, low flow states (i.e. poor cardiac output) secondary to severe heart failure or valvular regurgitation can result in syncope, especially during increased demand (e.g. on exertion).

A clinical examination is critical to aid the diagnosis of structural cardiac defects, which may show a murmur, features of heart failure, or cardiac hypertrophy (e.g. heave, displaced apex).

Syncope may also occur from major cardiopulmonary events such as massive pulmonary embolism, acute myocardial infarction, or aortic dissection. These causes are usually associated with severe chest pain, systemic symptoms, and hypotension. They can cause a sudden fall in blood pressure with reduced cerebral perfusion leading to syncope.

Non-syncopal attacks

It is important to differentiate true syncope from other causes of collapse/loss of consciousness that do not occur from cerebral hypoperfusion. Some of these causes may cause a partial or complete loss of consciousness due to other mechanisms, which include:

• Seizures
• Non-epileptiform seizures
• Intoxication
• Metabolic disturbances (e.g. hypoglycaemia, hypoxia)

Other causes may lead to collapse without impaired consciousness, but without proper history and examination, may be confused with syncope, which includes:

• Cataplexy: sudden loss of muscle tone
• Drop attacks: sudden spontaneous fall without external physical trigger
• Falls

The history is vital to help differentiate between causes of collapse (e.g. syncopal and non-syncopal causes).

The history is vital to get a good description of the event and confirm the presence of syncope. This may be very difficult if the patient was alone but greatly helps when a relative, caregiver, or bystander can give a witness account. It is important to determine the history leading up to the event, the event itself (usually a collapse), and then symptoms afterward.

Before the event

Enquire about what the patient was doing before the event. Did they stand up from a lying position, were they having their blood taken? This can often point to specific triggers for a syncopal episode.

The position of the patient during the episode is important. A reflex syncope almost never occurs when lying down. Syncope during sitting or lying is more concerning for a cardiac cause. Symptoms on standing followed by syncope are suggestive of orthostatic hypotension.

It is important to ask about any prodromal symptoms (e.g. nausea, dizziness, visual changes, feeling hot/cold) that are suggestive of reflex syncope. Sudden collapse without warning is concerning for a cardiac cause. Some patients, particularly the elderly, may have amnesia of the event leading to a report of sudden collapse despite a prodromal period. This makes differentiating between causes hard.

Enquire about any concerning features that may have proceeded the event such as chest pain, palpitations, or shortness of breath that may point towards a concerning cardiopulmonary disease.

During the event

It may be very difficult to decipher what happened during the event, which is usually a collapse, without a witness. This should always be obtained, if possible, by liaising with the ambulance crew or calling the carer or next of kin.

Establish whether there was a confirmed loss of consciousness, how long this lasted, and what they looked like during the episode. A collapse or fall may occur without a complete loss of consciousness due to a drop attack, trip, or vertigo. Syncope is usually a brief episode lasting 8-12 seconds followed by recovery. The exact time of unconsciousness may be inaccurately reported by the patient or bystander.

Vital to enquire whether any physical movements occurred during the collapse (e.g. limb shaking) with associated features like incontinence and tongue biting. These features may indicate a seizure.

After the event

Syncope is classically associated with a quick recovery. Compare this to a seizure that has a post-ictal period of reduced consciousness and altered mental status. Key questions include: Did the patient immediately recover? Were they able to get themselves up?

Vasovagal syncope may be associated with a brief period of fatigue that delays an immediate recovery but there should be no confusion or significant delay. Cardiac syncope is classically associated with rapid recovery.

Additional history

Other factors in the history help to establish the possible cause:

• Past medical history: does the patient have a history of epilepsy, diabetes, or heart disease that may point towards a specific cause. Has this happened before and what were they previously diagnosed with? Many elderly patients will get recurrent falls due to a dysfunctional baroreceptor reflex or autonomic dysfunction
• Drug history: does the patient take any medications that increase the risk of orthostatic hypotension (e.g. antihypertensives). Do they take or have they started any medications that can precipitate an arrhythmia (e.g. prolonged QTc).
• Family history: is there any history of collapse or sudden cardiac death that may suggest an underlying cardiac disease (e.g. long QT syndrome).

Pre-syncope

This is a commonly utilised term that refers to a ‘near-faint’ or ‘near blacking out’. It is essentially a prelude to syncope with exactly the same symptoms (e.g. lightheadedness, dizziness) that lasts for a few seconds, but the actual loss of consciousness (i.e. the syncope) is aborted.

As these symptoms (e.g. dizziness) are usually non-specific, it is important to distinguish true pre-syncopal symptoms from other causes such as vertigo.

The examination is important to look for clues to the underlying cause and for any consequences of the collapse.

A full clinical examination should be performed to determine the cause of syncope.

• Cardiopulmonary examination: look for features suggestive of a cardiac cause (e.g. murmur, raised JVP, irregular pulse, bradycardia). Pay particular attention to features of heart failure (e.g. lung crackles, peripheral oedema, displaced apex beat) and valve disease (e.g. ejection-systolic murmur of aortic stenosis)
• Neurological examination: look for any changes in mentation and behaviour, focal neurological signs (e.g. hemiparesis), or post-ictal features. These are usually suggestive of a non-syncopal cause of the collapse (e.g. seizure, stroke). Assess for global neurological symptoms that may imply autonomic dysfunction (e.g. bradykinesia, tremor, and rigidity suggestive of Parkinson’s disease)
• External injuries: Patients are at risk of serious injuries during the loss of consciousness. Look for any head injuries, lacerations, or broken bones. These may be less obvious in the elderly and require a detailed assessment of each joint

Bedside investigations can give you loads of information about the potential cause of syncope.

Bedside investigations are vital or determining the cause of syncope and excluding non-syncopal causes:

• Capillary blood glucose: exclude hypoglycaemia as a non-syncopal cause
• Lying-standing blood pressure: exclude orthostatic hypotension
• Electrocardiogram: may be normal if the ECG is not performed during the event (i.e. it has already normalised). There may be subtle features on the ECG suggestive of a potential cardiac cause (e.g. long QTc, q waves, heart block). If there is a high index of suspicion then longer ECG monitoring may be required
• Venous blood gas (if available – hospital setting): gives a rapid indication to the biochemical picture of the patient. A significantly raised lactate may be seen following a seizure or profound cardiac dysfunction (e.g. massive myocardial dysfunction, aortic dissection)

If observations are taken during the event, it may help to indicate the possible cause. Remember, vasovagal syncope is associated with hypotension and/or bradycardia during the event and does not necessarily indicate a bradyarrhythmia.

Other investigations

Patients being investigated for syncope in the hospital setting may undergo a series of other investigations including blood tests (e.g. FBC, renal profile, CRP), x-rays, CT, and echocardiography to look for any precipitating factors, underlying cause or complications arising from the syncope. Some of these are standard (e.g. blood tests), whereas others depend on the clinical assessment of the patient (e.g. echocardiography for suspected cardiac cause).

Monitoring

In patients with unexplained syncope, monitoring in the hospital setting may be required if there is concern about a dangerous cause (e.g. cardiac arrhythmia) and the risk of recurrence is felt to be high. These patients will often be admitted to a bed with cardiac monitoring to observe over a period of time (typically 24 hours). If the patient remains well and no abnormality is detected, they may be discharged with follow-up investigations arranged.

Follow-up investigations

In patients with unexplained syncope, follow-up investigations are often requested to help determine the underlying cause. Examples include:

• Tilt table testing: completed in patients with suspected vasovagal syncope or orthostatic hypotension not detected on a lying/standing blood pressure
• Cardiac monitoring: refers to continuous ECG monitoring to detect an abnormal rhythm. It may be performed over hours, days, or even months/years with implantable devices
• Cardiac imaging: specialised imaging may be requested to look for structural defects that may predispose to syncope (e.g. echocardiography, cardiac MRI)

Always be concerned about a possible cardiac cause in the elderly or those with cardiac risk factors.

A cardiac cause of syncope is potentially life-threatening, and if not recognised, could occur again leading to severe complications including secondary injuries or cardiac arrest. A cardiac cause should be suspected in elderly patients or those with cardiovascular risk factors. This is because cardiac disease can lead to structural alteration in the heart that predisposes to arrhythmias.

Features supportive of a cardiac cause include:

• No prodromal symptoms
• Sudden collapse
• Quick recovery
• Examination findings (e.g. murmur)
• History of cardiac disease
• Family history of sudden cardiac death
• ECG abnormalities