Syncope refers to a sudden, transient loss of consciousness due to global cerebral hypoperfusion with rapid onset, short duration and spontaneous complete recovery.
Neurally mediated reflex syncope (NMRS) is a group of related conditions in which there is symptomatic hypotension due to neural reflex vasodilation or bradycardia.
- Vasovagal syncope is a type of NMRS that is brought on by emotion, pain or stress (i.e. a common faint).
Pathophysiology
In all types of syncope, there is a transient cerebral hypoperfusion/insufficiency that occurs most commonly due to a decrease in BP → low oxygen and nutrients reaching the brain → fainting due to a loss of consciousness and loss of postural tone.
A vasovagal attack is caused by dysregulation of the ANS regulation of cerebral blood flow. When we have a strong stimulus, such as an emotional event, painful sensation or sudden change in temperature, we get PSNS stimulation → decrease in cerebral perfusion → syncope.
It is usually skeletal muscle involved, but there may also be a loss of control in non-skeletal muscle → bladder and bowel incontinence.
Some patients who go on to have severe oxygen deprivation then have jerky muscular movements, but once again this is not present in most patients.
Normally, in a healthy person, cerebral perfusion represents 12-15% of the resting cardiac output to maintain oxygen levels to sustain consciousness.
A cessation of cerebral blood flow for 6-10 seconds is enough to cause a loss of consciousness.
The cerebral perfusion pressure is the net pressure gradient allowing for cerebral blood flow.
CPP is calculated as such:
To maintain our CPP > 60mmHg we need to keep our MAP > 90mmHg or our systolic BP >110mmHg. The ICP needs to be within the normal range of 7-15mmHg. If it is raised too much, the CPP will drop as there is excessive resistance → ischaemia.
Our systemic BP is regulated by a few mechanisms:
- Arterial baroreceptors-induced adjustments - predominantly in the aortic arch and carotid sinuses. These baroreceptors monitor BP changes and relay them to the medulla oblongota (solitary nucleus via CN IX and CN X) which then adjust SVR, contractility and HR.
- Intravascular volume regulation - renal and hormonal influences to maintain the blood volume.
- ANS control - especially in short-term.
- Cerebrovascular autoregulation - the regulation of cerebral blood flow across a wide range of blood pressures by decreasing cerebrovascular resistance or vasodilation when the MAP decreases.
⚠️ Risk factors and causes
Simple faints are harmless and have no long-term implications. However, it is important to establish the cause of the syncopal episode as not all are primary syncope, meaning that they are secondary to other diseases. We will provide some of the causes of syncope in the classification section below.
The risk factors for NMRS are:
- Old age
- Illness
- Autonomic failure
- Prior syncope
- Cardiac diseases - such as arrhythmias, MI, HF, cardiomyopathy or severe aortic stenosis (with large pressure gradient).
🔢 Classification
We will not delve deep into all the causes of syncope, however, let’s mention the 3 broad groups of syncopal syndromes:
- Neurally mediated reflex syncope
- Orthostatic syncope
- Cardiovascular syncope
- Arrhythmias as primary cause
- Structural causes
- Cerebrovascular causes
😷 Presentation
- ⭐️ History of provocative factor - such as unpleasant sights, pain, stress, dehydration, prolonged standing.
- Lightheadedness
- Pallor
- Diaphoresis (sweating)
- Fatigue after the episode
- Palpitations
- Loss of vision and hearing - it is essential to consider it a true faint.
- Signs of physical injury as this may induce a vasovagal episode.
- Bradycardia
🔍 Investigations
There is no investigation that can pinpoint vasovagal syncope. However, it is important to rule out some other issues that may induce other forms of syncope, and then by exclusion and clinical background we can diagnose it asa a vasovagal episode.
Some of these include:
- ECG
- Serum haemoglobin - to rule out anaemia-induced syncope.
- Plasma glucose - to rule out hypoglycaemia-induced syncope.
- Serum B-hCG - to rule out pregnancy-induced syncope.
- Cardiac enzymes - to rule out MI if there is a suspicion.
- D-dimer levels - to rule out PE if there is a suspicion.
- Serum cortisol - to rule out syncope secondary to adrenal insufficiency.
- U&Es - to rule out dehydration-induced syncope.
This is a score that predicts risk for serious outcomes at 7 days in patients presenting with syncope or near-syncope. The reason we use it is because syncope may be relatively benign or a manifestation of serious underlying pathology.
The 5 parameters are easily remembered by the mnemonic CHESS:
C - History of congestive heart failure
H - Hematocrit < 30%
E - Abnormal ECG
S - Shortness of breath
S - Triage systolic blood pressure < 90
🧰 Management
There is not much management needed as it is a transient episode that is spoentaneous with complete recovery. However, we should focus on patient education, physical techniques and volume expansion.
- Patient education - on avoidance of triggers (prolonged standing, warm environments) and how to cope with certain settings that may induce it (hospital or dental settings). Inform them of recurrence and of potential injuries that may occur if measures are not taken.
- Physical techniques - these include physical counter-pressure movements and tilt training to promote a stronger neurovascular response to orthostatic stress.
- Volume expansion - by increasing dietary salt and electrolyte-rich drinks. This is contraindicated in hypertension, renal disease, heart failure or cardiac dysfunction.
- Fludrocortisone - may also be used for volume expansion.
- Midodrine - an alpha agonist used to increase arterial tone and prevent NMRS.