Blackouts

Blackouts is a term that is used very loosely by patients, with great variety of meanings. It is a symptom rather than a diagnosis - causes are numerous and varied, and work-up can be difficult. European guidelines may be of help,¹ but there are no UK consensus guidelines.²

Obtain as precise a history as possible about the exact circumstances of the event or events. If there has been loss of consciousness, an eye-witness account will be of great value.
The true story may be one of:

• Syncope
• Epilepsy
• Dizziness or vertigo without loss of consciousness
• Sudden and transient loss of vision
• It is also sometimes used to suggest a period of amnesia. The most common cause for this is alcohol abuse.

The diagnosis and management of syncope is dealt with in greater detail in the separate dedicated article Syncope.

History is of the utmost importance and, if the patient is a poor historian, this may be challenging. The GP who sees the patient soon after the event is in a better position to obtain reliable history than the consultant who may see the patient several weeks later. The first question to ask is, "What exactly happened?"

• What was the patient doing at the time? (Getting up, exercising, straining at stool, standing in a hot room).
• Was there any premonition of anything about to happen?
  • There may have been an aura as before a fit.
  • The term "dizziness" needs expansion. Was there a feeling of rotation?
  • Were there palpitations? If so, were they rapid, irregular or just a hard pounding?
  • If the patient was desperately short of breath, this might imply hyperventilation.
• Did the patient fall?
• If so, did any injury result?
• Was there incontinence of urine?
• Was the tongue bitten?
• For how long was the patient unconscious? This really requires the testimony of a third party as the subjective opinion of the patient is unreliable. Even the third party is likely to overestimate the time, as a just a minute seems a very long time in such circumstances.
• Did the patient lie flaccid or was there a tonic/clonic component?
• Was recovery fairly sudden or gradual?
• How did the patient feel afterwards? Was there confusion or disorientation?

If this was not an isolated event:

• How often does it happen?
• It is getting more frequent?
• Is there any common factor that may be precipitating such attacks?

With regard to the last, enquire about changes in posture that may predispose to orthostatic hypotension. If a man has a "blackout" when getting up in the night to pass urine, it may be postural hypotension if it occurs when he arises or it may be micturition syncope if it occurs as he passes urine.

Past medical history and medication

Note past medical history and current medication, as this may hold a clue; however, do not forget other possibilities:

• A history of heart disease is very important
• A history of vascular disease or stroke may suggest vertebro-basilar insufficiency or transient ischaemic attacks (TIAs)
• Diabetes predisposes to vascular disease and, especially if the patient takes insulin, there could be hypoglycaemia
• Previous complaints of palpitations may suggest a dysrhythmia
• Recent treatment for breast cancer or lung cancer may suggest cerebral metastasis
• Complaints of forgetfulness may suggest dementia that can be associated with late onset epilepsy
• Drugs may be responsible for postural hypotension

Examination may be unremarkable or it may give the aetiology.

Examine the cardiovascular system.

• Examining the pulse is discussed more fully elsewhere. See separate article Examining the Pulse (Different Types). Irregularities may suggest atrial fibrillation, ectopic beats or dropped beats from variable heart block.
• Examination of the jugular venous pressure is also discussed more fully elsewhere. It may suggest heart failure. Cannon waves occur with complete heart block.
• Check the blood pressure - sitting and standing. Reflex-mediated syncope or orthostatic hypotension are the most common causes of syncope and account for at least one third of all episodes.⁴ Orthostatic hypotension is defined as ≥ 20 mmHg drop in systolic blood pressure or a systolic blood pressure <90 mmHg.
• Auscultation may also give clues. It is sometimes easier to detect or analyse irregularities of rhythm by listening than by palpation. A murmur of aortic stenosis may also be relevant. If a young person develops syncope on exertion this is highly suggestive of aortic stenosis or cardiomyopathy.

Also perform a brief neurological examination. Even in the presence of a primarily neurological problem such as epilepsy, it may be completely normal.

Loss of consciousness is usually neurological or cardiovascular in origin but the history may be misleading in differentiating between the two. Thus, loss of consciousness due to inadequate cardiac output may produce convulsions and a fit may produce pallor.

• It is important first to decide if this is truly syncope. This is based almost exclusively on the history and this may include information from a third party.
• If the history is suggestive of a cardiac cause, including a history of cardiac disease, this is helpful but 50% will still have other causes.⁶
• If there is no suggestion of a cardiac cause and there is no known heart disease, this almost excludes a cardiological problem.⁷ Paroxysmal tachycardia, especially supraventricular tachycardia, can occur without known heart disease but palpitations are usually reported.

• Neurally mediated causes include vasovagal syncope and carotid sinus sensitivity.
• Orthostatic hypotension occurs on taking an upright position and is due to dysfunction of the autonomic nervous system (ANS) or hypovolaemia.
• Cardiac arrhythmias, including heart block. Stokes-Adams attacks are episodes of syncope, usually of between 10 and 30 seconds' duration, that are usually due to heart block.
• Structural heart defects are a problem when the heart is unable to meet demands.
• Straining can so impair venous return as to impair cardiac output and cause a faint. Examples are cough syncope and micturition syncope.
• Steal syndromes, such as the subclavian steal syndrome (SSS), are rare.

Hypotension can result from failure of the ANS as may occur in multiple system atrophy, some cases of Parkinson's disease, diabetic neuropathy, amyloidosis causing peripheral neuropathy, use of vasoactive drugs, after exercise and after a meal when much blood is directed towards the alimentary canal.⁸

Volume depletion may occur from haemorrhage or from fluid loss, as from diarrhoea or in Addison's disease.

Drugs may cause volume depletion or an increase in the size of the vascular bed, causing relative hypovolaemia. The old-fashioned antihypertensive drugs were more notorious than modern drugs for causing postural hypotension but the latter are not innocent and, with more aggressive management of hypertension, it may be more of a problem. Diuretics, ACE inhibitors and calcium channel blockers may all be implicated. Beta blockers may cause undue bradycardia.

Obstruction to flow will impair cardiac output, as with significant valvular stenosis or cardiomyopathy, especially hypertrophic obstructive cardiomyopathy (HOCM). An atrial myoma can also impede flow. A large pulmonary embolism (PE) will impair the heart's ability to pump enough blood to the circulation.

Diagnostic indicators

The following may suggest that neurally mediated syncope is involved:

• No known cardiovascular disease
• Long history
• Response to a sudden, unexpected, unpleasant experience including pain or the sight of blood
• Prolonged standing in a hot environment
• Nausea or vomiting with syncope
• Postprandial
• After exertion
• Rotation of the head and tight collars

Compression of the carotid sinus by starched wing-collars has not been a problem in the many years since they have fallen from fashion. However, carotid sinus syndrome (CSS) should be considered in old people with non-accidental falls.⁹

The following suggest orthostatic hypotension:

• It occurs on standing
• Medication has been recently started or the dose increased
• Hot flushes
• Autonomic neuropathy, e.g. diabetic neuropathy or Parkinson's disease
• After exertion

The following suggest a structural lesion of the heart:

• Known severe structural heart lesion
• Occurs on exertion or when supine
• Palpitations or chest pain
• Family history of sudden death

Steal syndromes, usually SSS, are rare. The trigger is energetic use of the arm. The blood pressure may be different in the two arms.

If the underlying problem is syncope, the investigation is orientated towards the cardiovascular rather than nervous system. As explained in the article on the diagnosis of epilepsy, the history is much more important than investigations. In syncope, a good history, followed by ECG, will indicate what other tests should be performed. Routine performance of a battery of tests has a low yield.¹⁰ In principle, non-invasive tests should be performed before invasive tests.¹¹

• The EEG can be normal in many people with epilepsy and abnormal in some who do not have the disease.
• An American study of the use of CT scanning in emergency department patients who had suffered syncope showed that, whilst it was frequently requested, it almost never showed pathology.¹²

Investigation of the cardiovascular system is far more likely to be rewarding:

• The first test is a simple ECG. There are many abnormalities that may raise suspicion
  • Any conduction defect, including bundle branch block, short PR or long QT intervals¹³
  • Pre-excitation phenomena
  • Q waves suggestive of myocardial infarction (MI)
• Carotid sinus massage has been used to diagnose CSS
• Echocardiogram may show valve defects, poor function or atrial myxoma
• An implantable loop recorded can help to exclude a cardiac aetiology in cases of syncope of unknown cause
• A tilt table requires specialist expertise¹⁴ "Head up" tilt testing using glyceryl trinitrate as a provoking factor is less time-consuming then the conventional method and gives more accurate results.¹⁵

Routine blood tests should include FBC, ESR, U&E, LFTs. Perform urinalysis too, as both undiagnosed diabetes and chronic renal failure can cause polyuria and dehydration.

A study of a systematic approach to the investigation of syncope¹⁶ showed that it was possible to classify the cause in nearly all cases:

• Neurally mediated (vasovagal) 66%
• Orthostatic hypotension 10%
• Primary arrhythmias 11%
• Structural cardiac or cardiopulmonary pathology (e.g. MI or PE) 5%
• Non-syncopal attack 6%
• Unclassified 2%

A diagnosis is first necessary to determine management.

• If drugs are implicated they need to be reviewed to ascertain if it is possible to find a better regimen. Slow titration of dose, especially in the elderly, should reduce such problems.¹⁷ Elderly patients on certain medications are much more likely to experience syncope.¹⁸
• If there is heart block, a demand pacemaker may have a great effect on quality of life.
• The management of tachycardias is discussed in their own articles.
• Structural defects such as valvular stenosis or atrial myxoma usually require surgery.
• A young person with aortic stenosis or HOCM should avoid severe exertion as they are a cause of sudden cardiac death in young people. Otherwise, syncope in children and adolescents tends to be benign.¹⁹
• The Brugada syndrome is a rare inherited disorder characterised by right bundle branch block, ST segment elevation and sudden, unexpected ventricular fibrillation.²⁰ Prolonged QRS duration in precordial leads is a useful ECG marker may be useful for distinguishing high- from low-risk patients.
  It can be treated by implantation of a defibrillator.²¹
• In many cases, especially those of neurally mediated origin, reassurance and avoidance of situations likely to precipitate syncope are to be advised.²²
• Orthostatic training (daily 30-minute sessions of upright standing against a vertical wall 6 days a week for at least 4 weeks) may be helpful.²²
• Squatting may prevent an attack of vasovagal syncope but the manoeuvre must be followed by lower body tensing to avoid precipitating a further attack on standing up.²³
• If there is epilepsy it needs treatment as discussed in the article on the subject but if there is psychogenic pseudo-epilepsy, the optimum management is uncertain.²⁴ Explanation and cognitive behavioural therapy are the mainstays of management.²⁵

In otherwise healthy people, isolated syncope does not appear to be associated with any excess of stroke (including TIA) or MI. There is no excess of all-cause or cardiovascular mortality (including sudden death).²⁶ Syncope related to driving is usually neurally mediated and one study found a low incidence of recurrence.²⁷

1. Guidelines for the diagnosis and management of syncope (version 2009): The Task Force for the Diagnosis and Management of Syncope of the European Society of Cardiology (ESC).; Eur Heart J. 2009 Aug 27
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19. Driscoll DJ, Jacobsen SJ, Porter CJ, et al; Syncope in children and adolescents. J Am Coll Cardiol. 1997 Apr;29(5):1039-45. [abstract]
20. OMIM 601144; Brugada syndrome
21. Sacher F, Probst V, Iesaka Y, et al; Outcome after implantation of a cardioverter-defibrillator in patients with Brugada syndrome: a multicenter study. Circulation. 2006 Nov 28;114(22):2317-24. Epub 2006 Nov 20. [abstract]
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• Brignole M, Alboni P, Benditt DG, et al; Guidelines on management (diagnosis and treatment) of syncope--update 2004. Europace. 2004 Nov;6(6):467-537.
• Morag R; Syncope; eMedicine, August 2008.