Although syncope often causes the patient to fall down, fall and syncope are basically two separate diagnoses.
Elderly patients are often not able to rexplain why they fell down. Instead of syncope they have often experienced dizziness when falling. The underlying cause of unexplained falling may be serious (but treatable) cardiac syncope.
”Drop attack”: abrupt loss of postural muscle tone without disturbance of consciousness
Causes and clinical pictures of syncope
Reflex-mediated or vasovagal syncope
Vasovagal reaction (= a simple faint) is the most common cause of syncope.
In classic cases the reason for fainting is a reflex triggered by some outside cause, the reflex leading to slowing down of pulse, lowering of blood pressure or both.
Fainting may be recurrent and the patient usually has prodromal symptoms.
The patient's heart is structurally healthy.
Precipitated by
pain, fright, unpleasant experiences (vaccination, blood test, sight of blood)
nausea and vomiting
micturition (micturition syncope), defecation
coughing (cough syncope)
standing in an upright position (particularly if the calf muscle pump is not used)
insufficient fluid or salt intake
heat or excess sweating
Prodromal symptoms
unsteadiness when standing (swaying, motor restlessness, restless eye movements)
pallor
nausea or sweating, faintness
closing in of visual field or blurred vision
So-called atypical reflex-mediated syncope, which comes without prodromal symptoms or precipitating factors, is rare. The diagnosis is made after outruling of other causes and a positive finding in carotid sinus massage or tilt test.
Oversensitivity of carotid sinus: diagnosed by sinus massage during ECG-monitoring. Syncope is usually brought on by turning of head.
Cardiac syncope
Unlike reflex-mediated syncope, cardiac syncope is always dangerous. Most often it is a symptom of a structural cardiac defect but it may also be caused by a congenital ion channel abnormality (e.g. long QT syndrome Long QT Syndrome (LQTS), Brugada syndrome).
Cardiac syncope typically presents during exercise and is often preceded by palpitation or chest pain.
Arrhythmia-induced syncope
Bradyarrhythmias: severe sinus node malfunctions and third degree atrioventricular blocks (a long PQ interval and a bundle branch block may be suggestive of short runs of complete heart block).
Tachyarrhythmias: ventricular tachycardia, extremely fast SVT (WPW syndrome) as well as AF in the elderly. A congenital long QT interval Long QT Syndrome (LQTS) and drug-induced proarrhythmia (torsade de pointes) should be remembered as a possible cause of syncope.
Malfunctioning of a cardiac pacemaker or an implantable cardioverter defibrillator
Syncope in a patient with myocardial infarction should always be presumed to have been caused by VT until proven otherwise.
Other cardiac syncope
Acute coronary event
Severe aortic stenosis (poor prognosis unless treated)
Hypertrophic cardiomyopathy (ask about family history)
Cardiac tamponade (post-pericardiotomy syndrome)
Pulmonary embolism
Atrial myxoma
There is a high risk of repeated episodes of cardiac syncope and, without treatment, the prognosis is poor and these patients should therefore be referred for specialist consultation and care.
Nitroglycerin-induced syncope is common in the elderly, particularly as the drug is often taken for vague symptoms of malaise or weakness when the blood pressure is already low.
Antihypertensive drugs
Drugs indicated in prostatic hypertrophy (alpha blockers)
Drugs indicated in erectile dysfunction (Note! Not to be taken with nitroglycerin)
Psychoactive drugs (antipsychotics: e.g. haloperidol, phenothiazine derivatives; antidepressants: e.g. amitriptyline and its derivatives)
Some antihistamines (terfenadine, astemizole have already been removed from the market)
Some antimicrobials (e.g. erythromycin, clarithromycin)
Drug interactions (concurrent use of several drugs causing prolongation of the QT interval, or use of medication inhibiting the metabolism of a QT interval-prolonging drug)
Antidiabetic drugs
Hypoglycaemia usually leads to unconsciousness and rarely to syncope.
Alcohol and illicit drugs usually lead to unconsciousness and rarely to syncope.
The mechanism of syncope induced by diuretics, phenothiazines, antiparkinson drugs and vasodilators is orthostatic, especially if the patient is dehydrated.
Syncope caused by hypovolaemia
Diuretics
Sweating
Vomiting or diarrhoea
Acute intestinal bleeding and extrauterine pregnancy may present with a low blood pressure and syncope.
Orthostatic hypotension
Long-standing bed rest and standing up quickly
Fever and dehydration
Drugs: diuretics, phenothiazines, nitrates and beta-blockers
Diabetic autonomic neuropathy
Parkinsonism and drugs used for its treatment
Carry out a brief orthostatic test (3 min) immediately during the acute phase.
A decrease of > 20 mmHg in systolic blood pressure or a systolic blood pressure < 90 mmHg coupled with weakness, dizziness, swaying and decreased muscle tone are diagnostic findings.
Loss of muscle tone, collapse and syncope, in particular, are suggestive of orthostatic hypotension.
Psychogenic causes
A psychogenic cause should be considered when no other cause is found for recurring collapse.
Syncope of unknown aetiology
The aetiology of a single syncopal attack is not always established even after comprehensive investigations (25% of cases). In such cases the cause is probably vasovagal, and the prognosis is good provided that the patient has no cardiac disease.
Diagnostic clues
Syncope in young and otherwise healthy patients is most often harmless, especially if a precipitating factor was present.
With cardiac illness and with advanced age, the probability of serious syncope increases, and more detailed investigations are warranted. Just one syncope attack in a man over 50 years of age and with cardiovascular risk factors is a serious symptom.
Signs, symptoms and details of patient history that are suggestive of dangerous syncope include
recurrent syncope and sudden deaths in members of immediate family.
The onset of cardiac syncope is sudden or induced by physical exercise. It is often associated with palpitations, chest pain or other cardiac symptoms.
Reflex-mediated syncope is often clearly preceded by a triggering factor.
Syncope brought on by head turning or a tight collar is suggestive of carotid sinus hypersensitivity.
Aural symptoms and convulsions suggest epilepsy. However, tonic-clonic convulsions of a short duration may also be associated with cardiac, or even vasovagal, syncope as a result of cerebral ischaemia. In this case the convulsions begin only after loss of conciousness.
Eyewitness evidence is often useful: convulsions, pallor, pulse, regaining of consciousness, position and predisposing factors.
When patients diagnosed as being epileptics fail to respond to antiepileptic medication and further investigations are carried out, they are often found to be, in fact, suffering from attacks of cardiac syncope.
Neurological hemilateral symptoms suggest TIA.
Psychogenic syncope should be considered in the presence of hyperventilation or a multitude of symptoms or when no witnesses are produced despite the frequency of attacks.
Repeated episodes of syncope usually require further investigations, unless the attacks are clearly vasovagal in origin and occur in a healthy young person. Vasovagal reactions, even when recurring frequently, are an innocent finding and are likely to improve spontaneously.
Recording the patient's history and the syncope setting is usually sufficient to reveal most cases of harmless syncope which do not require extensive specialized investigations.
After his/her first syncope attack the patient is advised to visit the emergency department.
Syncope in a cardiac patient almost always requires thorough specialized investigations.
The cause for cardiac syncope may often be earlier myocardial infarction, cardiac insufficiency or other structural cardiac defect. The symptoms usually present during physical exercise and the most common prodromal symptoms are palpitation and chest pain.
Other diseases (e.g. diabetes, pulmonary and neurological diseases)
Medication (keep in mind over-the-counter drugs!)
Family history: recurrent syncope, severe ventricular arrhythmia or sudden death in members of immediate family may indicate a hereditary arrhythmia tendency (e.g. long QT syndrome).
Clinical examination
Auscultation: heart murmurs and carotid bruit
Blood pressure and feeling for the pulse
Blood pressure should also be recorded with the patient standing up. If needed, an orthostatic testing and, if indicated , a nitrate tolerance test are performed.
The pulse of a fainted person is often slow and weak, and the faint can easily be mistaken for cardiac arrest. The skin is sweaty and pale. On regaining consciousness, the patient is tired and appears frightened.
Carotid sinus massage will reveal hypersensitivity of the sinus. With simultaneous ECG and blood pressure monitoring the carotid artery is massaged for about 5 seconds (only one side at a time!). The test can also be performed with the patient standing up. Significant bradycardia (< 30/min), ≥ 3 second asystole or a decrease in systolic pressure suggest hypersensitivity.
ECG
Systematic analysis of 12-lead ECG is a first-line investigation in a patient with a history of syncope.
Atrial fibrillation: syncope might be caused by cardiogenic cerebral embolism, sick sinus syndrome Sick Sinus Syndrome or intermittent atrioventricular block.
Various degrees of AV conduction disturbances and/or intraventricular conduction disturbances (long PQ interval, bundle branch block, bi- or trifascicular block)
Delta wave (WPW syndrome)
Long QT interval
LVH, infarct scar
If the ECG is totally normal, cardiac origin of the syncope is unlikely and extensive investigations are usually not needed.
Other investigations
A brief neurological examination is an essential investigation in patients with syncope, but further neurological investigations aren't usually needed unless basic and cardiac examinations have proved inconclusive.
The basic laboratory investigations include basic blood count with platelets, partial pressure of oxygen in the arterial blood (or pulse oximetry), electrolytes, blood glucose and additionally, if the patient presents with chest pain, cardiac enzymes (troponins or CK-MB).
Other useful laboratory investigations often include plasma CRP, D dimer which aids in diagnosing pulmonary embolism and atrial natriuretic peptide which is used to diagnose cardiac insufficiency.
Ambulatory ECG recording if warranted by symptoms or by clinical or ECG findings. An event ECG monitor (activated by the patient during symptoms) often reveals arrhythmias that cause presyncopal symptoms, but the underlying cause of syncope is seldom found with it.
An exercise tolerance test is indicated in exertional syncope or if the patient has coronary heart disease.
Suspected valvular dysfunction, myocardial infarction or cardiac insufficiency should be further evaluated by echocardiography.
Tilt table testing should be considered if vasodepressive syncope is suspected. However, it is a very non-specific test and has rather little influence on treatment.
The need for invasive studies (angiography, electrophysiological studies) is decided according to history and the findings of other cardiological investigations.
In rarely occurring syncope or otherwise problematic cases an implantable loop recorder may be considered. The device is implanted under the skin in the same way as is a pacemaker. The device automatically records both slow and fast heart rates for up to 3 years. Moreover, the patient may also activate the device himself/herself on symptom onset.
CT scan of the head, an EEG and other more specific neurological investigations should be considered if the patient presents with neurological deficits or the symptoms are suggestive of epilepsy.
Treatment
Vasovagal reaction (= simple faint)
As a first aid, lay the patient down with the legs elevated.
Rapid response to presyncopal symptoms: when the patient experiences prodromal symptoms, he/she may achieve a rise in blood pressure by isometric tensing of muscles (e.g. forceful clenching of fists, crossing and opening of legs while tensing buttocks and stomach, stretching arms apart while holding hands tightly together) and thus avoid fainting.
A single simple faint due to pain, fear or anxiety is considered a normal phenomenon and requires no special treatment.
Patient education is important in preventing further episodes.
Adequate fluid and salt intake
Avoidance of vasodilators and diuretics
Avoidance of accident-prone situations
Avoidance of situations that trigger an attack
Avoidance of standing-up too quickly in cases of orthostatic hypotension
Numerous different drugs have been tried for the prevention of reflex-mediated syncope. Despite positive preliminary results, almost all of them have proved to be disappointing.
Beta blockers may actually prolong the reflex and make bradycardia worse.
Only midodrine has been more effective than placebo. It may be tried, if lifestyle counselling is not sufficient to control the symptoms.
Daily standing exercises (“desensitization to upright position”) may help young motivated patients who have frequent symptoms. The effect is small for others.
A pacemaker may be indicated in cases associated with prolonged asystole or an AV block.
Treatment with a pacemaker seems to be most beneficial for patients over 40 years of age whose syncope results from a severe cardioinhibitory reaction.
In the elderly, orthostatic hypotension is a common ailment. These patients often have comorbidities with relevant medication which hinder the diagnosis.
Other forms of syncope
In other cases, treatment is aimed at the patient's underlying disease. For example, the patient may require a pacemaker, an implantable cardioverter defibrillator, coronary artery revascularization or valvular surgery.
Syncope and operating motor vehicles
After a patient has had a bout of syncope, he/she is immediately banned from operating motor vehicles. The ban is temporary and lasts until the cause of syncope has been identified and the symptoms are controllable. Follow the local regulations.
References
Kapoor WN. Syncope. N Engl J Med 2000 Dec 21;343(25):1856-62. [PubMed]
Calkins H, Shyr Y, Frumin H, Schork A, Morady F. The value of the clinical history in the differentiation of syncope due to ventricular tachycardia, atrioventricular block, and neurocardiogenic syncope. Am J Med 1995 Apr;98(4):365-73. [PubMed]
Zaidi A, Clough P, Cooper P, Scheepers B, Fitzpatrick AP. Misdiagnosis of epilepsy: many seizure-like attacks have a cardiovascular cause. J Am Coll Cardiol 2000 Jul;36(1):181-4. [PubMed]
Martikainen K, Seppä K, Viita P, Rajala S, Laippala P, Keränen T. Transient loss of consciousness as reason for admission to primary health care emergency room. Scand J Prim Health Care 2003 Mar;21(1):61-4. [PubMed]
Task Force for the Diagnosis and Management of Syncope, European Society of Cardiology (ESC), European Heart Rhythm Association (EHRA) et al. Guidelines for the diagnosis and management of syncope (version 2009). Eur Heart J 2009;30(21):2631-71. [PubMed]