Transient Loss of Consciousness (TLoC) is a common reason for paramedics to be called. In lay terms it may be referred to as a faint, a fit, a spell, a turn, a collapse or one of many other names. Its causes can range from quite benign to life threatening. The role of the paramedic is to assess, treat and refer to appropriate care.
Van Dijk and colleagues (2009) define TLoC as “an apparent loss of consciousness with an abrupt onset, short duration and spontaneous and complete recovery”. 1 in 2 people will experience an episode of TLoC in their life. The UK National Institute for Healthcare and Clinical Excellence (NICE) guideline for TLoC 2011 categorises the causes as follows.
- Uncomplicated Faint or Situational Syncope
- Orthostatic Hypotension
- Dysfunction of Nervous System
- Dysfunction of Cardiovascular System
- Dysfunction of Psyche
We can further add:
- Rare causes
- Subclavian steal syndrome
- Subarachnoid haemorrhage
- Breath holding spell
(thanks to Alexandra Ulrich on Twitter for a great post that taught me about these! – @alex_ulrich1)
Note that by their nature, TLoC are brief and resolve completely. Patients who remain unconscious are not covered in this article. Also worth noting that we won’t be covering what I’ll term ‘obvious’ causes such as STEMI, dissecting AA or ectopic pregnancy – but they should be high on your list of differentials.
Uncomplicated Faint or Situational Syncope
(Also known as – reflex syncope)
Vasovagal syncope
Paramedics LOVE this diagnosis. However, it’s probably grossly overused as a catch-all for collapses, when a thorough investigation and history taking should be done. That being said, it is a common cause of TLoC, with > 85% of syncopal events in persons aged less than 40 attributable to vasovagal syncope. In elderly patients at least 50% are caused by vasovagal syncope.
So what is actually happening in a vasovagal syncope? Well like most things it’s not entirely understood, however we know there is an afferent limb (think cause/stimuli) and an efferent limb (effect). Some known triggers include emotional distress and pain, but in many cases is unknown. Distressing medical procedures (such as cannulation) are a common cause of vasovagal syncope. These triggers can be exacerbated by upright posture or dehydration, increasing the likelihood of collapse.
The efferent limb is characterised by increased vagal firing (revise neuro anatomy here!), which drives parasympathetic activity at the sinoatrial node and atrioventricular node. Remember the increased parasympathetic activity causes a slowing of heart rate, which can lead to pauses for several seconds. In addition, decreased sympathetic tone causes vasodilation, reducing venous return to the heart and therefore stroke volume. The combination of these two factors reduces mean arterial pressure, causing the patient to lose consciousness.
By achieving supine position (either by collapsing or lying down consciously) the blood no longer needs to pump ‘uphill’ to perfuse the brain – resulting in a rapid return to consciousness.
Situational Syncope
Suspected to be the same pathophysiology as vasovagal syncope, situational syncope is diagnosed where there is a known triggering event such as urination (particularly whilst standing), defecation, swallowing, coughing or vomiting.
Carotid Sinus Syndrome
We all have baroreceptors in our necks, at the bifurcation of the internal and external carotid arteries. These play a role in regulating our blood pressure and are sensitive to pressure, meaning that higher blood pressure stimulates these receptors to increase parasympathetic innervation, therefore decreasing blood pressure. In some individuals they may have increased sensitivity of their carotid baroreceptors (carotid sinus hypersensitivity), which leads to syncope.
This stimulation may occur when turning the head, looking upwards or when pressure is applied to the baroreceptors (eg. by a tumour). The resulting vagal activation causes syncope through the reflex described previously.
Carotid sinus hypersensitivity typically occurs in older males with atherosclerotic vascular disease. It is a relatively common finding however not all patients with CSH will suffer from syncope. It is diagnosed by applying carotid massage and assessing for a decrease in heart rate and blood pressure.
Orthostatic Hypotension
When moving from lying to standing, gravity causes the shifting of 500 – 800mL of blood into the lower limbs, reducing venous return, cardiac output and mean arterial pressure. In order to compensate for this, the body has several mechanisms to help it maintain orthostasis. The most important of these is the autonomic nervous system response to a drop in blood pressure.
When baroreceptors detect a decrease in blood pressure, they reduce vagal nerve stimulation and increase sympathetic innervation – resulting in vasoconstriction, increased heart rate and increased stroke volume. The renin-angiotensin-aldosterone system also plays a role in boosting blood pressure.
A normal response is an increase in heart rate 10-15 beats per minute, which will maintain systolic blood pressure and increase diastolic BP by 10mmHg (Campos Munoz et al., 2022). When this system fails to compensate, orthostatic hypotension occurs.
Acute Non-neurogenic Orthostatic Hypotension
Volume depletion (dehydration) is a common cause of orthostatic hypotension. Disease processes such as infection or myocardial infarction can also cause it. Certain medications may contribute to dehydration (such as diuretics) or may impair the body’s orthostatic mechanisms (anti-hypertensives).
Chronic Neurogenic Orthostatic Hypotension
Neurologic diseases which impair autonomic function are a common cause of orthostatic hypotension. These include diseases of the CNS such as brain stem lesions, Lewy body dementia and Parkison’s disease, as well as peripheral diseases such as diabetic neuropathy and pure autonomic failure.
Practice Point: Heart rate can provide a clue about the aetiology of orthostatic hypotension. If the postural change is less than 15 beats per minute, that suggests neurogenic cause (ie. not mounting a compensatory response). If the change is over 20 bpm that suggests volume depletion, and if its greater than 30 bpm suggests postural tachycardia syndrome.
Dysfunctions of the Nervous System
Epilepsy is a common seizure condition which is caused by an imbalance in the excitatory and inhibitory mechanisms of the brain. During a seizure, neurons within the brain begin discharging rapidly. This may be occurring in a discrete area of the brain (causing focal seizures) or may occur involve the entire brain (causing more generalised, tonic-clonic seizures). Focal seizures may progress to generalised seizures.
The sudden, uncontrolled discharge of neurons leads to unconsciousness and collapse, usually associated with obvious muscle contraction. However absence seizures (formally called petit mal) cause loss of consciousness without muscle contraction. Majority of seizures self resolve within seconds to minutes, through an unclear mechanism. Patients recovering from seizures are typically dazed and confused, referred to as the post-ictal period. Seizures which do not self resolve are known as status epilepticus, and managed with IM Midazolam.
Dysfunctions of the Cardiovascular System
Cardiac syncope results from inadequate cardiac output which is not related to reflexes such as vasovagal syncope. A cardiac cause of syncope is highly concerning and increases risk for sudden death. The causes can be further described as structural and arrhythmogenic.
Structural
Structural abnormality of the left ventricle obstructs blood flow and typically causes syncope during exertion. This is typically caused by aortic valve stenosis, hypertrophic obstructive cardiomyopathy (HOCM) or prosthetic valve dysfunction.
Arrhythmogenic
Disturbances of cardiac rhythm are a frequent cause of syncope and can be life threatening. Arrhythmogenic syncope is typically caused by ventricular tachycardia, accounting for 11% of all syncope episodes. Patients with myocardial ischaemia or poor left ventricular ejection fraction are at heightened risk. Other causes include atrial fibrillation with Wolff-Parkinson-White syndrome (which causes rapid ventricular response) and polymorphic VT secondary to long QT syndrome.
Bradyarrhythmias may cause syncope in older patients, who are less able to compensate for decreased cardiac output. Sick sinus syndrome may cause syncope when the rhythm changes from a tachyarrhythmia to a bradycardic one (bradycardia-tachycardia syndrome), resulting in a prolonged sinus pause. Atrioventricular blocks may also cause syncope.
Dysfunctions of the Psyche
Another poorly understood cause of transient loss of consciousness are psychological causes. Two diagnoses used are psychogenic non-epileptic seizures (PNES) and psychogenic pseduosyncope (PPS). Both are suspected to be caused by the same psychogenic mechanism, however PNES is characterised by jerking movements whilst PPS is not.
Rare Causes
Subclavian Steal Syndrome
A condition caused by stenosis of the subclavian artery, it causes syncope due to retrograde blood flow through the vertebral artery. This results in a sudden decrease in cerebral blood flow, causing collapse. It is typically characterised by;
- Unilateral arm pain/soreness, particularly when exercising
- Numbness, tingling or pallor of one arm
- SBP difference between arms > 15mmHg
- Pulse discrepancy between arms
- Symptoms worsen with upper body exercise
Subarachnoid haemorrhage
Bleeding into the subarachnoid space can result from trauma, or in non-traumatic cases from the rupture of an underlying aneurysm. In majority of cases it will present with sudden onset ‘thunderclap’ headache, photosensitivity, neck stiffness, nausea and altered conscious state. However in some cases it can present with transient loss of consciousness and headache alone. Loss of consciousness is thought to occur due to a rise in intracranial pressure secondary to intracranial haemorrhage.
Breath Holding Spell
Involuntary breath holding which typically occurs in children aged 6 months to 6 years of unknown cause. Around 1/3 children with breath holding have a family history of the same, and may go on to be more likely to faint as adults. Can be categorised as cyanotic or pale breath holding spell
| Cyanotic Breath Holding Spell – Most common type – Usually occurs when very upset or frightened – Begins with cry/scream and forceful exhalation, then will breath hold, turn blue and faint | Pallid Breath Holding Spell – Less common and may be mistaken for seizure – Usually follows a minor injury or upsetting moment – Child becomes bradycardic, pale and faints – May become stiff and lose bladder control |
So, how do we narrow down the differential diagnosis of transient loss of consciousness?
Assessment
- Complete set of vital signs
- 12 lead ECG
- BGL
- Stroke screen
- History taking – particularly focussing on events leading up to collapse and any previous collapses
- Ambulation assessment
- Postural blood pressure assessment if orthostatic hypotension suspected
Then consider the following points about each cause of TLoC
Uncomplicated Faint
- Prodromal symptoms such as sweating, feeling hot or nauseated
- Provoking factor such as pain or medical procedure
- Situational syncope may be diagnosed when it is clearly and consistently provoked by straining (usually whilst standing up) or by coughing or swallowing
Orthostatic Hypotension
- Affected by posture – prolonged standing or changing position causes syncope, which is prevented by lying down
- Orthostatic hypotension typically presents with a postural drop of 20mmHg difference between lying and standing
- May have a recent history of dehydration or medications which impact orthostasis (anti-hypertensives, diurectics)
Dysfunction of the Nervous System (Epilepsy)
- May have pre-seizure aura
- Classical seizure behaviour such as unusual posturing and prolonged jerking of limbs
- Head turning to one side
- Tongue biting
- Post-ictal confusion
- No memory of abnormal behaviour witnessed before, during or after TLoC
Dysfunctions of the Cardiovascular System
- ECG abnormality, particularly
- Inappropriate persistent bradycardia
- Ventricular arrhythmia
- Long QT (QTC > 450ms) or short QT (QTC < 350ms)
- Brugada Syndrome
- Ventricular pre-excitation (Delta wave/WPW)
- Ventricular hypertrophy
- Abnormal T Wave inversion
- Pathological Q waves
- Sustained atrial arrhythmia
- Paced rhythm
- History of heart failure
- TLoC occurs during exertion
- Family history of sudden cardiac death (age < 40) and/or inherited cardiac condition
- New or unexplained breathlessness
- Heart murmur
Dysfunctions of the Psyche
- Generally need to rule out other causes of TLoC with specialist testing such as tilt table
- Psychogenic causes of TLoC tend to last several minutes, whilst reflex syncope lasts around 20 seconds
- 97% of patients with psychogenic TLoC have their eyes shut, whilst only 7% of vasovagal syncope do
- Increased heart rate and blood pressure during TLoC
Bottom Line
Most of the time transient loss of consciousness (TLoC) will be caused by a reflex syncope, which is fairly benign. However we can’t allow this to lull us into a false sense of security – all patients with a TLoC must be thoroughly assessed, and will usually require investigations which aren’t possible in the paramedic space. Vasovagal syncope, orthostatic hypotension and known epilepsy are not significantly concerning, however cardiovascular syncope should send alarm bells ringing. Finally psychological causes of syncope cannot be diagnosed without ruling out other causes – and this is outside the scope of assessment tools we have in the ambulance.
References:
Bromfield EB, Cavazos JE, Sirven JI, editors. An Introduction to Epilepsy [Internet]. West Hartford (CT): American Epilepsy Society; 2006. Chapter 1, Basic Mechanisms Underlying Seizures and Epilepsy. Available from: https://www.ncbi.nlm.nih.gov/books/NBK2510/
Campos Munoz A, Vohra S, Gupta M. Orthostasis. [Updated 2022 Jan 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK532938/
Holmes, J., & Gokdogan, Y. (2019). Subarachnoid haemorrhage: a sinister cause of transient loss of consciousness during oral sex. BMJ case reports, 12(3), e228014. https://doi.org/10.1136/bcr-2018-228014
Jeanmonod R, Sahni D, Silberman M. Vasovagal Episode. [Updated 2021 Oct 7]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2022 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK470277/
Rogers, G., & O’Flynn, N. (2011). NICE guideline: transient loss of consciousness (blackouts) in adults and young people. The British journal of general practice : the journal of the Royal College of General Practitioners, 61(582), 40–42. https://doi.org/10.3399/bjgp11X548965
van Dijk, J., Thijs, R., Benditt, D. et al. A guide to disorders causing transient loss of consciousness: focus on syncope. Nat Rev Neurol 5, 438–448 (2009). https://doi.org/10.1038/nrneurol.2009.99
