Syncope & Collapse Flashcards
What are three major criteria within the definition of syncope? [3]
There must be a loss of consciousness:
- an initial loss of postural tone (going floppy) is a good indication of this. If the patient did not lose postural tone, other causes should be considered first.
The loss of consciousness must be transient.
- This means it is self-limiting (i.e. no intervention is needed for the patient to fully recover). This, therefore, excludes events such as cardiac arrest and hypoglycaemic coma which do not normally involve spontaneous recovery.
It is caused by global cerebral hypoperfusion
- which almost always means a reduction in blood pressure. Focal cerebral hypoperfusion (e.g. a transient ischaemic attack from carotid artery thrombo-embolism) does not cause or constitute syncope.
To help with the diagnosis of syncope, the European Society of Cardiology (ESC) definition states that syncope is characterised by [3]?
- Rapid onset
- Short duration (typically no longer than 20 seconds, but can be several minutes)
- Spontaneous and complete recovery (although some disorientation is common with increasing age)
What questions do you need to ask about pre-syncope events? [3]
Was there a trigger?
- Establish whether there was a trigger to the event. Syncope often includes an immediately preceding trigger such as emotion, pain or exercise.
Was there a prodrome?
- Syncope often involves an immediate warning (called ‘pre-syncope’), consisting of symptoms such as feeling faint, dizzy, sick, visual disturbances and ringing in the ears (tinnitus).
- The presence of palpitations or other cardiac symptoms suggests a cardiac cause of syncope.
Did the patient change colour?
- Pallor occurs from systemic hypotension, thus indicating syncope.
- A blue colour (cyanosis) occurs from transient loss of respiratory muscle action in any seizure beginning with a tonic phase (e.g. generalised tonic-clonic seizure).
What questions do you need to ask about events during syncope [4]
How long did the unconsciousness last?
- Typically, patients are unconscious for seconds in syncope. The duration of unconsciousness is often longer in seizures.
Was there a convulsion?
- Convulsions may occur in both epilepsy and syncope and thus do not distinguish between the two. However specific patterns (e.g. tonic-clonic) may be recognisable if the eyewitness provides a detailed, reliable account.
Was there tongue biting?
- Although tongue biting can rarely happen in syncope, this is more strongly associated with seizures.
Was there urinary incontinence?
- Urinary and faecal incontinence are more strongly associated with seizures and not a typical feature of syncope (although not impossible).
What question should you ask about post-syncope? [1]
How long did it take for full recovery?
- Seizures are followed by a post-ictal fatigue lasting several hours. In contrast, syncope is usually followed by near-immediate complete recovery with no lasting effects.
What are the four classifications of syncope? [4]
SNAP:
- Structural
- Neurally mediated
- Arrhythmic
- Postural
What are the three types of neurally mediated syncope? [3]
Neurally mediated syncope is due to an inappropriate autonomic reflex in response to a trigger and hence this is also known as reflex syncope.
Vasovagal syncope:
- Vasovagal syncope. also known as a ‘simple faint’, is by far the most common type of syncope overall.
Situational syncope
- Situational syncope occurs when syncope occurs consistently after a specific trigger:
Post-micturition (the most common)
Post-cough
Post-swallow
Post-defecation
Post-prandial
Post-exercise
Carotid sinus hypersensitivity
- mechanical manipulation of the carotid sinus, which can happen accidentally whilst shaving, wearing a tight shirt collar or even head movement (e.g. looking over shoulder).
Describe different causes of postural (orthostatic hypotension) syncope [4]
Autonomic nervous failure secondary to drugs:
- this is the commonest cause of orthostatic hypotension.
- Common drugs include antihypertensives, diuretics, tricyclic antidepressants, antipsychotics and alcohol.
Hypovolaemia:
- hypovolaemia may be a key contributing factor in syncope.
- There may be a sinister underlying cause such as a gastrointestinal bleed.
Primary autonomic nervous failure:
- this is usually present to some degree in the spectrum of disorders which includes Parkinson’s disease, Lewy body dementia and multi-system atrophy.
Secondary autonomic nervous failure:
- occurs secondary to other conditions such as diabetes, uraemia and spinal cord lesions
What are the investigations should do for orthostatic syncope? [2]
Lying and standing blood pressure
Tilt table testing:this will distinguish between postural and vasovagal syncope
- Tilt table testing: recreates trigger/situation while measuring BP and other signs to confirm the diagnosis
What are the two types of arrhythmogenic syncopes? [2]
Tachyarrhythmias
Bradyarrhythmias
Which is more likely to cause syncope:
Tachyarrhythmias
Bradyarrhythmias
Which is more likely to cause syncope:
Tachyarrhythmias
Bradyarrhythmias
Describe how bradyarrhythmia syncopes occur [3]
Usually there is either failure of impulse initiation by the sinus node (sick sinus syndrome) or impulse conduction to the ventricles.
When this occurs sporadically, there is usually an ectopic site further down the pathway which will take over and continue to beat at its own slower rate.
The reduction in blood pressure responsible for the syncope occurs when there is a long pause (usually >3 secs) between the impulse conduction failure and the ectopic escape mechanism.
Name three causes of bradyarrhythmias causing syncope [3]
Sick sinus syndrome
Second-degree atrioventricular block
Third-degree (complete) atrioventricular block
Name 4 causes of tachyarrhythmias that can cause syncope
atrial fibrillation, atrial flutter, atrioventricular nodal re-entry tachycardia) or ventricular tachycardia
Structural causes of syncope are usually due to mechanical obstruction in the [] [] inflow or [] tract.
Structural causes of syncope are usually due to mechanical obstruction in the left ventricular inflow or outflow tract.