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Managing the military patient with syncope
  1. Iain T Parsons1,2,
  2. A T Cox2,3,
  3. I A Mollan4 and
  4. C J Boos5,6
  1. 1Department of Medicine, Chelsea and Westminster Hospital NHS Foundation Trust, London, UK
  2. 2Defence Medical Services, Royal Centre for Defence Medicine, Lichfield, UK
  3. 3Department of Cardiology, St George's Hospital NHS Trust, London, UK
  4. 4RAF Centre of Aviation Medicine, RAF Henlow, UK
  5. 5Centre for Postgraduate Medical Education, Bournemouth University, Bournemouth, UK
  6. 6Department of Cardiology, Poole Hospital NHS Foundation Trust, Poole, Dorset, UK
  1. Correspondence to Lt Col C J Boos, Department of Cardiology, Poole Hospital NHS Foundation Trust, Longfleet Road, Poole, Dorset, BH15 2JB, UK; Christopherboos{at} and christopher.boos{at}


Syncope is a relatively common occurrence in military populations. It is defined as a transient loss of consciousness due to global cerebral hypoperfusion, characterised by a rapid onset, short duration and a spontaneous and complete recovery. While the symptom of syncope is easily elicited, discovering the mechanism can be more problematic and may require a plethora of diagnostic tests. The aim of this paper is to review current evidence pertaining to the classification, investigation and management of syncope, from a military perspective. Emphasis is placed on assisting primary healthcare professionals in the assessment and management of syncope, in the UK and on operations, while providing explicit guidance on risk. The occupational limitations required in safely managing patients with syncope are stressed along with the potential long-term limitations.


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Key messages

  • Syncope is common in the general population and, while frequently of benign aetiology, can signal serious cardiac disease.

  • The cause of syncope can commonly be diagnosed with a detailed history and simple investigations.

  • When structural or disarrhythmic causes of syncope are excluded, simple management can provide effective management with little occupational restriction required.

A 20-year-old female soldier presented following an episode of collapse with transient loss of consciousness. She had a 2-month history of worsening paroxysmal dizziness and light-headedness. As a brass player in the Corps of Army Music her symptoms often occurred during prolonged standing particularly while playing instruments. Her exercise tolerance was unaffected and she was participating without symptoms in physical training. Her symptoms never occurred while lying or sitting and she described no chest pains or palpitations. There was no other relevant history.


Syncope is defined as a transient loss of consciousness (T-LOC) due to global cerebral hypoperfusion characterised by a rapid onset, short duration and a spontaneous and complete recovery. It is sometimes preceded by a prodromal period termed presyncope. Presyncope can be isolated and does not always lead to a T-LOC, although the patient will often feel this to be imminent. Syncope is common with a lifetime cumulative incidence of up to 35% in the general population1 and a similar incidence between genders.2 Syncope is particularly relevant in the younger military population as first presentation commonly occurs between 10 years and 30 years of age.3 ,4 Recurrence is common with the risk of a further episode increasing with each recurrence of syncope. In a patient with three previous episodes there is a predicted recurrence of 36% and 42% after 1 year and 2 years, respectively.5 A first episode is uncommon in patients over 40 years. A further peak occurs after 70 years of age, but this is irrelevant in the military population.6 A 17 year review of discharges due to cardiovascular disease, from the UK Armed Forces, showed syncope was the cause of 16% of discharges (107/651—rate 3.6 per 100 000 Service years).7 While commonly benign, syncope has been recognised as a frequent first symptom (18%) in soldiers that suddenly die.8

In syncope two elements are important when considering the patient's holistic management: the risk of death and life-threatening events and the risk of recurrence and consequent physical injury to themselves or others.

When primary cardiac causes of syncope are excluded, there is an excellent prognosis.2 The symptom of syncope can usually be differentiated from other causes of LOC by a detailed clinical history.9 ,10 Reaching the diagnosis and precipitating aetiology may be more challenging and require advanced investigation.


Syncope is commonly classified (Table 1) as reflex syncope, cardiac syncope (including arrhythmias and structural disease) or syncope secondary to orthostatic hypotension (OH).

Table 1

An overview of the classification of syncope, provoking factors, clinical features and initial diagnostics

Reflex or neurally mediated syncope

Reflex syncope incorporates a group of conditions where the neurovascular reflexes, that normally control the circulation, intermittently dysfunction. This is the most frequent cause of syncope in any setting. A provoking stimuli precipitates an abrupt withdrawal of sympathetic tone and an increase in parasympathetic tone that causes vasodilation, bradycardia or both.11 Vasovagal syncope, or the ‘common faint’, is common in the young and is usually isolated and mediated by emotion or orthostatic stress such as prolonged standing. Reflex vasovagal syncope remains the most common cause of syncope irrespective of age, sex or comorbidities.2 ,12 Commonly there are preceding autonomic symptoms such as sweating or nausea. Situational syncope describes syncope associated with a specific circumstance, such as cough, micturition, defecation, post exercise or post prandial. Rarer causes of reflex syncope include carotid sinus hypersensitivity, where mechanical stimulation of the carotid sinuses triggers the hypotensive reflex.

Syncope secondary to OH

In orthostatic syncope autonomic failure is secondary to a chronic impairment in sympathetic activity. OH is an abnormal decrease in systolic BP upon standing. Classically the diagnosis of OH requires the systolic BP to decrease by >20 mm Hg and the diastolic BP to decrease >10 mm Hg, within 3 min of standing.13 Classical OH is more commonly seen in the elderly due to chronic impairment of the autonomic system by conditions such as Parkinson's disease or diabetes. In the military population, OH can be precipitated by spinal cord injuries, alcohol, drugs, diarrhoea and dehydration.

Cardiac syncope

Cardiac syncope is the second most common cause of syncope. It occurs due to structural heart disease or arrhythmias with the latter being a more frequently identified cause. In both causes cardiac function is acutely impaired resulting in a loss of cardiac output and cerebral blood flow. Structural heart disease causes syncope when the demands on the circulatory system outweigh the ability of the heart to increase cardiac output. Causes include cardiomyopathies, valvular heart disease, constrictive pericarditis or acute myocardial infarction. When due to transient bradycardia or tachycardia, arrhythmias can induce syncope before compensatory mechanisms occur. Causes of bradycardia-induced syncope include Mobitz Type II second degree or third degree AV block and sinoatrial node dysfunction. Syncope due to tachyarrhythmias is usually ventricular in origin but can, less commonly, be supraventricular. Both are reviewed in other parts of this supplement. Structural heart disease and arrhythmias can coexist with one often associated with the other.

Evaluation of syncope

On assessment by a military primary healthcare doctor the patient had completely recovered aside from superficial injuries subsequent to her impact with the ground. Her lying to standing BP, over 3 min, showed a non-symptomatic systolic drop from 110 mm Hg to 100 mm Hg. Cardiovascular and neurological examinations were unremarkable. Her 12-lead ECG was normal and showed sinus rhythm with a rate of 65 bpm. The primary healthcare doctor arranged 4 weeks of light duties and referred the patient to a cardiologist.

Initial assessment

A military patient presenting with presyncope or syncope is likely to be initially assessed by a primary healthcare (PHC) professional. Initial evaluation includes a careful history focusing on the sequence of events and identifying potential triggers. Physical examination should look for evidence of arrhythmia or structural heart disease. An orthostatic BP measurement lasting for at least 3 min should be included. If possible, an ECG should be recorded. Arrhythmia-related syncope can be diagnosed by a resting 12-lead ECG alone in certain bradycardias or tachyarrhythmias, or evidence of high-risk features of disease, such as long QT syndrome.

If there is evidence of an arrhythmic cause for syncope then ECG monitoring should be commenced and an urgent cardiology opinion sought. If there is evidence of ongoing instability, including evidence of myocardial ischaemia, hypotension, decreased consciousness or recurrent syncope then ALS principles should be initiated. Evidence of structural heart disease such as valvular stenosis, from clinical examination also warrants an urgent cardiology opinion. During operational deployment the patient should be stabilised prior to aeromedical evacuation to definitive management. Cardiology advice should be actively sought although a physical review is dependent on deployed expertise.

Several risk assessment criteria (Box 1) and scores exist.17–21 The San Francisco Syncope rule21 may be of some use to PHC doctors. The rule states that when there is an absence of congestive heart failure or breathlessness, a normal ECG, the haematocrit is ≥30% and the systolic BP >90 mm Hg, the risk of a serious event at 7 days is very low (98% sensitive, 56% specific). Where patients satisfy these criteria and their symptoms suggest vasovagal syncope, management at PHC is appropriate. However, the requirement for a normal ECG may decrease the utility of risk scores with ECG changes being present in up to 53.7% of military aircrew, the vast majority of which (86%) are secondary to benign, training related changes.22

Box 1

Adapted guidelines for identification of high-risk features for cardiac syncope in military servicemen14–16

Severe structural or coronary artery disease

  • Heart failure, low ejection fraction or previous known coronary artery disease or myocardial infarction

Clinical features

On history

  • Syncope during exertion or supine

  • Palpitations at the time of syncope

  • Family history of sudden cardiac death

On examination

  • Anaemia

  • Non-physiological valvular murmurs

ECG features increasing risk of arrhythmic syncope

  • ECG features of myocardial ischaemia including ST segment changes (≥0.5 mm in depth) or T wave inversion (>2 mm) in two or more adjacent leads or pathological Q waves

  • Non-sustained ventricular tachycardia

  • Mobitz type II second-degree or third-degree AV block/complete heart block

  • Left axis deviation

  • Any QRS duration >120 ms including either complete LBBB or RBBB,

  • Pre-excited QRS Complex

  • Prolonged or short QT interval

  • Suggestive features of ARVC (negative T waves in right precordial leads, epsilon waves, ventricular late potentials)

  • Features of HCM (T wave inversion >1 mm in two adjacent leads, Q waves of >40 ms and >25% height of R-wave, ST depression)

  • Brugada pattern (RBBB with ST elevation V1–V3)

  • ≥two premature complexes per 10 s tracing or worsening ventricular ectopy on exercise

  • Left atrial enlargement

  • Right ventricular hypertrophy

Important comorbidities

  • Severe anaemia

  • Electrolyte disturbances and severe diarrhoea

ARVC, arrhythmogenic right ventricular cardiomyopathy; AV, atrioventricular; HCM, hypertrophic cardiomyopathy; LBBB, left bundle branch block; RBBB, right bundle branch block.


ECG monitoring is used for the diagnosis of intermittent arrhythmias causing syncope or presyncope. Monitoring modalities include in-hospital monitoring, ambulatory Holter monitors, event recorders or implantable loop recorders (ILRs). Correlation between symptoms and ECG arrhythmia recording is ideal23 although asymptomatic arrhythmias may be significant.24 If the patient's episodes of syncope are infrequent the yield of abnormal findings on a 24-h or 48-h Holter monitor is as low as 1–2%.25 External loop recorders continuously record and delete ECGs so are commonly used where the episodes of syncope are infrequent. They are activated by the patient when symptomatic and so a prodromal period is required. A period of preactivation recording can be retrieved for analysis.26 ILRs are devices subcutaneously implanted over the chest that store retrospective recordings when activated by the patient or a bystander.23 They can activate automatically if predefined arrhythmias occur. Despite high initial costs and the requirement for operative placement, ILRs reliably provide ECG-symptom correlation and are effective in investigating arrhythmic syncope.27 Remote external and internal devices with wireless transmission have recently been developed and may have a higher diagnostic yield than patient-activated devices.28 For all ECG recording devices, the absence of arrhythmia during syncope ordinarily excludes arrhythmia as the cause.

Exercise testing should be performed in patients who experience syncope during or shortly following exertion. While exertional syncope is frequently of cardiac origin, postexertional syncope is commonly secondary to reflex vasodilation. Exercise testing is diagnostic when syncope occurs during or after exertion, in the presence of ECG abnormalities or severe hypotension. If syncope doesn't occur exercise testing can still be diagnostic in the presence of Mobitz type II or third degree heart block, tachyarrythmias or with the development of the characteristic ECG findings of long-QT or Brugada syndromes (Box 1).

Cardiac imaging using echocardiography (echo), cardiac MR or CT remain key investigations to identify structural disease. Transthoracic echocardiography alone can be diagnostic in valvular disease, obstructing cardiac tumours, tamponade, aortic dissection and congenital anomalies and it is usually the first imaging modality of choice. To identify structural diseases, such as anomalous coronary artery origins or aortic dissection, CT can be invaluable. Myocardial scarring is frequently found in cardiomyopathies or sarcoidosis and as the sequelae of infarction or myocarditis. The differentiation between normal myocardium and scar tissue is a particular strength of cardiac MR.

Electrophysiology studies are invasive investigations that record surface and intracardiac ECG during sinus rhythm, in response to intracardiac pacing and during arrhythmia. Some diagnoses may also precede to ablation of abnormal intracardiac conduction pathways. Prolonged monitoring techniques have decreased the utilisation of electrophysiology studies 29 although there is still efficacy in patients with known structural heart disease.16

Tilt testing is used to confirm a diagnosis of reflex syncope where initial evaluation has been inconclusive.30 ,31 The test can be performed using different protocols30 but all aim to induce orthostatic stress. Usually the patient lies horizontal for a period followed by moving the patient to an upright, vertical position. Commonly medication is administered such as sublingual nitroglycerine or low dose intravenous isoprenaline.32 Blood pooling and decrease in venous return secondary to orthostatic stress trigger hypotension and bradycardia secondary to impaired vasoconstriction and vagal stimulation. Tilt testing remains useful in discriminating between reflex syncope and delayed OH.33 When the history is unclear, such as in epilepsy or psychiatric manifestations, it may assist to rule out reflex mediated syncope.34

Pressure applied to the common carotid bifurcation can be diagnostic where it induces bradycardia and hypotension and syncope. Carotid sinus syncope remains uncommon and an unlikely diagnosis in patients under 40 years.35 In patients with symptomatic long QT secondary to psychoactive or other medications an alternative pharmacological strategy is indicated. Military populations have long suffered from somatisation disorders36 secondary to the brutality of warfare and this should be considered in patients that remain a diagnostic quandary despite comprehensive investigation.

A service cardiologist reviewed the patient and confirmed the General Practitioner's (GP's) findings. There had been no further episodes of syncope although the patient still described infrequent episodes of presyncopal symptoms particularly during prolonged orthostatic stress. The patient was diagnosed with neutrally mediated syncope. An echocardiogram was requested to rule out structural heart disease. As the symptoms were infrequent a Holter monitor was not thought to be helpful and was not undertaken. 


The management aims are to prevent mortality secondary to cardiac disease and injury resulting from syncope in particular occupational environments. In the military population temporary or permanent occupational restrictions (Table 2) are often required to protect the patients and their colleagues from harm. Consideration should also be given to high-risk activities such as diving, driving, using firearms or flying. With respect to driving, consideration should be given to the type of license held. Group II licenses (heavy goods vehicles such as lorries or buses) carry greater restriction compared with that of group I (car and motorcycle). The Driver and Vehicle Licensing Agency produce up-to-date guidelines for cardiac conditions38 although military driving may carry greater occupational restriction than civilian dependent on occupational risk assessment.

Table 2

Syncope occupational recommendations for Role 1 GPs

Reflex syncope

Reflex syncope is a generally benign condition though the occupational and social implications can sometimes be significant. Non-pharmacological management should include education and reassurance of the military patient. General education includes early recognition of prodromal symptoms and avoidance of likely triggers. For military personnel the trigger is frequently standing on parade in hot weather with inadequate hydration. Avoidance of BP lowering agents and alcohol should also be discussed.

Physical counter pressure manoeuvres (PCMs) should be used as first line treatment in reflex syncope. The manoeuvres, performed by leg crossing, squatting and hand grip arm tensing (Figure 1), cause a BP increase often sufficient to delay or abort LOC when syncope is imminent39 ,40 with a relative risk reduction of 39%.41 It is worthwhile for Role 1 clinicians to become well versed in PCMs so they can be used as an immediate and effective treatment. In motivated military populations, with recurrent vasovagal syncope secondary to orthostatic stress, a prescription of progressively prolonged periods of enforced upright posture (termed ‘tilt training’) can also be beneficial.42

Figure 1

Graphic illustration of physical counterpressure manoeuvres to reduce the burden of reflex syncope.

If the reflex syncope is frequent, there is a short prodrome exposing the patient to trauma or the syncope occurs during high-risk activities, occupational restrictions should be instigated in the first instance pending further occupational advice, cardiac review and initiation of effective management. Examples of high-risk activities include driving, operating machinery, firing live weapons, flying or controlling aircraft such as unmanned or remotely piloted aircraft systems. Frequent syncope of any cause remains incompatible with flying until symptom-free for 12 months and/or the instigation of effective management (Table 2).43

Pharmacological therapy with α-agonists like oral midodrine44 and β-blockers45 has proven to be largely ineffective. While oral fludrocortisone has been used widely in adults for reflex syncope there is no trial evidence to support this and it is ineffective in children.46 Paroxetine was effective in one study,47 possibly through decreasing anxiety that may exacerbate the syncope. Permanent cardiac pacing, while sometimes effective in patients with severe bradycardia or documented asystole, remains incompatible with service.

Orthostatic hypotension

In patients with OH with prodromal symptoms PCMs are also effective.48 Patients should be instructed to drink 2–3 L of water a day and increase their oral salt intake to 10 g per day.49 The rapid ingestion of cold water can be effective in combating orthostatic intolerance and postprandial hypotension.50 In drug-induced autonomic dysfunction management involves recognition and elimination of the culprit agent. In contrast to reflex syncope, midodrine is effective51 in patients with autonomic failure, although the underlying cause of autonomic dysfunction may preclude further military service. Fludrocortisone was also shown to be effective in OH.52 Any reliance on medication will require a review of the patient's occupational status. A Military Aeromedical Examiner is required to oversee the use of any medications in aircrew with consequent potential flying status restrictions.43

Cardiac syncope: structural and electrical heart disease

The management of structural heart disease and arrhythmias are beyond the scope of this article but are covered elsewhere in this edition. As a general rule, patients presenting with cardiac syncope are at greater risk of sudden cardiac death than those with non-cardiac causes.15 Patients with cardiac syncope usually therefore require specialist investigation, diagnosis and management. Patients with syncope due to structural or electrical heart disease, whether acquired or congenital, are often unsuitable for continued military service. It is important patients with cardiac syncope are risk assessed appropriately for high-risk activities such as driving38 or flying.43 ,37 Patients with a reversible cause for their syncope may be fit for continued service once the cause is fully corrected.

The echocardiogram was unremarkable and the patient improved with advice on physical counter-measures, maintaining hydration and adequate salt intake coupled with a phased return to prolonged periods of orthostatic stress.


While syncope may be relatively common in a young military population, for the vast majority, it remains a benign symptom. With the exclusion of cardiac causes, syncope is usually amenable to simple measures and causes few occupational restrictions. With the introduction of more sensitive cardiac screening of recruits the burden of cardiac disease may even fall further. Clinicians should remain vigilant for features that could be attributed to underlying cardiac disease. A comprehensive initial assessment to identify high-risk features, make an accurate diagnosis and trigger appropriate management or specialist referral, remain the cornerstones of effective syncope management. Diagnostic tests are likely to be required due to the nature of particular occupational roles in the military. Lifestyle measures such as hydration, adequate salt ingestion and PCMs are simple and effective and should suffice for the majority. For diagnostic quandaries, where an arrhythmic cause is suspected, referral for implantation of an ILR may be the fastest and most cost-effective method of investigation and should be exploited. While more complex management in syncope is effective it may impact on further military service.



  • Contributors ITP was responsible for researching and drafting of the article. ATC planned the review and contributed towards review of content and editing. IAM has given expert advice and contributed towards the review on occupational aspects of the paper. CJB gave overarching review of the content.

  • Competing interests None declared.

  • Provenance and peer review Commissioned; internally peer reviewed.