Syncope (Greek: synkope = cut-off) is a brief transient loss of consciousness (fainting) and postural tone (collapse) with rapid spontaneous recovery
From 1997-2000 National Health Ambulatory Medical Survey of ED visits in USA.
2.63 million ED pt.( 0.65% of all visits) with the diagnosis of syncope unrelated to injury
1.1 million pt.(40.8%) were 65 yrs or older
63.8% were female
Among pt. older than 65 yrs, admit rate for syncope was 61.8% and was the sixth most common admission diagnosis
Incidence of syncope in the Framingham Heart Study
Age-dependent morphological and physiological changes
Old patients often take drugs (sedatives, diuretics, vasodilators, anti-hypertensives)
Old patients display a higher incidence of chronic pathologies such as diabetes mellitus, congestive heart failure, coronary disease, cerebrovascular pathologies and multiple sensorial deficiency.
Age-related physiological changes that predispose to syncope
Autonomic nervous system
Other non cardiological changes
Atherosclerosis is also universally present in older humans
Impair endothelial-dependent nitric oxide release
Increase endothelin release in the ageing vessels
This impairs both the cardiac and cerebral circulation which may predispose to syncope in the elderly.
Age-related stiffening of arterial vessels produces high afterload.
Ventricular walls become more fibrotic and noncompliant leading to ventricular diastolic dysfunction.
LV systolic dysfunction is also common because of the high prevalence of HTN and IHD among the elderly
Increase incidence of age-related mitral and aortic valvular diseases.
A progressive fall in the ratio of nodal myocytes to collagenous stroma with age particularly in the SA node increases the incidence of AF, heart block and sick sinus syndrome.
Autonomic nervous system
Beta-adrenergic response to plasma noradrenaline is blunted in the elderly
Diminished beta-1 responses lead to reduced cardioacceleration and cardiac contractility
Diminished beta-2 results in increased vascular tone because of the unopposed alpha-1 vasoconstriction.
Baroreflex mediated cardioacceleration is also reduced
Autonomic nervous system
HR increase in response to stress is less effective.
Sympathetic and parasympathetic autonomic responses are reduced in health ageing
Blunted autonomic responses together with other factors including dehydration, vasodilator medications, sodium wasting may result in orthostatic hypotension, cerebral underperfusion and syncope in the elderly.
Other non cardiological change
Plasma renin and aldosterone fall with age and this results in sodium wasting.
impaired thirst response of many elderly people to hyperosmolality may cause hypovolaemia and consequent orthostatic hypotension
Causes of syncope of the elderly
- Primary cardiac arrhythmias
- Structural cardiovascular diseases—obstruction to left ventricular outflow
- Obstruction to right ventricular outflow
Neurally mediated syncopal syndromes
- Vasovagal syncope
- Situational syncope
- Carotid sinus hypersensitivity
Orthostatic and dysautonomic disturbance of blood pressure control
Cerebrovascular, neurological, and psychiatric causes
Primary cardiac arrhythmias
Probably the most common cause of syncope in patients with structural heart or vascular disease.
An age-related fall in nodal myocytes particularly in the sino-atrial node increases the incidence of atrial fibrillation, heart block and sick sinus syndrome
Conditions predisposing to a prolonged QT interval and torsade des pointes Azole antifungals + terfenadine or astemizole or cisapride Macrolide antibiotics + terfenadine or astemizole or cisapride Organophosphate overdose Hypomagnesemia Tetracyclic/tricyclic antidepressant overdose Hypocalcemia Encephalitis Butyrophenone overdose Hypokalemia Myocarditis Traumatic brain injury Phenothiazine overdose Hypothyroidism Rheumatic heart disease Cerebrovascular occlusive disease Class 1C antidysrhythmics - flecainide, encainide Bulemia, stringent dieting Congestive heart failure Subarachnoid hemorrhage Class 1A antidysrhythmics - quinidine, procainamide, disopyramide Hypothermia Ischemic coronary artery disease Neurological causes Medicinal and toxicological causes Enviromental and endocrinological causes Acquired causes
Structural cardiovascular diseases obstruction to left ventricular outflow
Aortic stenosis is the most common structural lesion associated with syncope in the elderly
- Age < 70 yr.: Congenital bicuspid valves
- Age > 70 yr.: Degenerative changes
Hypertrophic obstructive cardiomyopathy (HOCM)
Vasodilator drugs or even vasodilatation after a hot bath can induce syncope in these patients
Obstruction to right ventricular outflow
The limitations to right ventricular outflow may lead to diminished capacity to increase cardiac output.
18% of elderly pts admitted to an acute geriatric ward had pulmonary embolism in one study ( Impallomehi et al., 1995 )
Myoxma, pulmonary stenosis and pulmonary hypertension
Vasovagal syncope The mechanism of tilt or haemorrhage-induced vasovagal syncope
Peripheral receptors similar to ventricular mechanoreceptors are found in lung, bladder, GI tract
Cough or micturition related syncope
Carotid sinus hypersensitivity
20% of older people who presented with unexplained syncope ( Parry and Eltrafi ).
Defined as asystole of 3 s or more and/or a decrease in systolic pressure of 50 mmHg or more during carotid sinus massage.
Orthostatic and dysautonomic disturbance of BP control
30% of community-dwelling adults over 75 years of age have orthostatic hypotension ( Lipsitz, 1989 ).
Autonomic failure such as multiple system atrophy and diabetes mellitus.
The combination of the blunted age-related autoregulatory changes, medications (diuretic, vasodilators), and chronic diseases predispose older adults to orthostatic hypotension.
8% of syncope cases in older nursing home patients in one study ( Jansen et al., 1995 ).
Defined as 20 mmHg or greater decline in systolic blood pressure within 90 min after a meal.
Common in older adults and can coexist with orthostatic hypotension in the same individual ( Jansen and Lewis, 1995 ).
Pathophysiological mechanism of postprandial hypotension is still a matter of debate.
Cerebrovascular, neurological, and psychiatric causes
Syncope is rarely due to cerebrovascular disease unless there are accompanying focal neurological deficits.
Transient posterior circulation ischaemia can result in loss of consciousness and there are usually brain stem signs present including diplopia, vertigo, dysarthria, or hemiparesis.
Vasovagal syncope may mimic seizures
Psychiatric disturbances including hysterical reaction, panic attack with hyperventilation can either mimick or may lead to true syncope
Differentiating syncope from seizure Present Absent Increase in CK enzyme Present common Absent rare Disorientation after event Minutes Seconds Duration of event Common Rare Urinary incontinence Common Absent Tongue biting lateral Common Absent Forced conjugate deviation of eyes Uncommon Common Upturning of eyes GTC movements- coincidence with LOC Uncoordinated myoclonic jerks & twitches after LOC Pattern of convulsion Common & longer-lasting Infrequent & short-lived Jerking movements Sometimes purple Sometimes pale Color at onset of event Absent Sometimes present Dizziness prodome Rarely present Absent Aura Seizure Syncope Feature
An emergency physician, when faced with a syncope-patient in an ED setting, should first seek to exclude life-threatening causes of syncope, which require immediate diagnostic evaluation/treatment + hospital admission
active internal bleeding
malignant cardiac arrhythmias
carotid artery/vertebral artery dissection
If there are no overt life-threatening causes of syncope, then an emergency physician should attempt to identify patients with situational syncope, vasovagal syncope and benign orthostatic (postural) syncope - who are candidates for home discharge after any necessary stabilization treatment in the ED
If the cause of the syncope is not readily apparent after initial clinical evaluation in the ED, then an emergency physician should attempt to decide whether certain categories of syncope-patients require admission to hospital
An eye-witness account is very important
mode of onset and progression of event
Body position at onset of event
Depth of altered consciousness
Duration of the syncopal episode
Rate of recovery of consciousness
Identify any precipitants including meals, pain, cough, micturition, defaecation, swallowing, postural change, neck movement and exercise
Associated symptoms such as palpitation, dyspnoea, chest pain
History of panic attack and hyperventilation
pscyhological triggering events (painful stimuli, sudden bad news)
Drug history is obviously important.
Past medical history and risk factors for ischaemic heart disease
CLINICAL CLUE TABLE Leaking AAA, ectopic pregnancy Preceding or accompanying abdominal pain Dissecting aortic aneurysm, leaking AAA Preceding or accompanying back pain AMI, PE, cardiac tamponade, dissecting aneurysm, tension pneumothorax, mitral valve prolapse Preceding or accompanying chest pain PE, tension pneumothorax, cardiac tamponade, air embolism Preceding or accompanying dyspnea Cardiac arrhythmia Preceding palpitations Vasovagal syncope, orthostatic hypotension Preceding "lightheadness" prodrome when erect Aortic stenosis, HOCM, atrial myxoma, malignant cardiac arrhythmia Sudden syncope on exertion Cardiac arrhythmia, atrial myxoma Sudden syncope at rest when non-erect Suggest Clinical clue
CLINICAL CLUE TABLE Postprandial hypotensive syncope Recent meal Orthostatic hypotension Recent fluid loss (diarrhea, vomiting, sweating) Orthostatic syncope Polypharmacy, recent sialdenafil use Vasovagal syncope, prolonged QT interval and torsade Occurring after emotional upset Vasovagal syncope Occurring after prolonged standing Situational syncope Occurring during (or immediately after) coughing, laughing, vomiting, swallowing, urination, defecation, combing hair, stretching Subclavian steal syndrome Occurring when exercising upper arm Carotid sinus syncope Occurring when turning head to side, or looking up Suggest Clinical clue
CLINICAL CLUE TABLE Pacemaker failure Pacemaker HOCM, prolonged QT syndrome Family history of syncope or sudden death Cardiac arrhythmia, carotid sinus syncope, atrial myxoma, aortic stenosis, subclavian steal syndrome, prolonged QT interval - torsade History of recurrent syncope Orthostatic hypotension secondary to autonomic neuropathy History of autonomic dysfunction (impotence, anhydrosis, sphincter dysfunction) Pulmonary embolism Recent history of cancer, prolonged immobilization, leg injury or surgery Thrombosis of valve History of mechanical heart valve Cardiac arrhythmia, pro-arrhythmia drug effect, valve dysfunction History of known cardiac ischemia or structural heart disease Suggest Clinical clue
Search for trauma and assessment of severity
- Pulse volume
- Neck bruits
- Apex beat, Heart sounds
Difference in BP between lt. and rt. upper limbs > 20mmHg is abnormal (suggests dissecting aortic aneurysm or subclavian steal syndrome)
Difference in BP between upper and lower limbs > 20mmHg when recumbent is abnormal (suggests a dissecting aortic aneurysm)
Orthostatic vital signs : positive test is defined as a SBP decrease of > 20 - 30mmHg, a DBP decrease of >10 - 15mmHg and/or HR increase of greater than 30 bpm when standing
A significant drop in BP + fixed HR suggests dysautonomia
A significant drop in BP + increased HR suggests volume depletion and/or excessive vasodilatation
An insignificant drop in BP + marked increase in HR suggests postural tachycardia syndrome (history of frequent fainting, symptoms of autonomic overactivity - palpitations, diaphoresis, tremulousness, visual blurring, non-anginal chest pain, "spaced-out" feelings, inability to concentrate, inability to breathe, sensations of impending doom)
Decreased and delayed upstoke (aortic stenosis/hypertrophic obstructive cardiomyopathy)
traditional approach to syncope of unknown etiology with low yield
only 17% of patients with syncope undergoing 24-h monitoring experience symptoms and 2% have an arrhythmia-related symptom in one study ( Gibson and Heitzman, 1984 )
extending the continuous ambulatory electrocardiograhic monitoring to 72 hours results in a slightly higher yield
if no symptoms/arrhythmias are detected, arrhythmogenic syncope cannot be excluded
Tilt table testing
Provocative test used to determine a patient's susceptibility to neurally mediated syncopal syndrome.
An important non-invasive investigation for syncope particularly for those with no structural heart disease
The details of tilt table testing technique and protocol are beyond the scope of this review.
Indication for admission
Admit patients with syncope and any of the following:
1. A history of congestive heart failure or ventricular arrhythmias 2. Associated chest pain or other symptoms compatible with acute coronary syndrome 3. Evidence of significant congestive heart failure or valvular heart disease on physical examination 4. ECG findings of ischemia, arrhythmia, prolonged QT interval, or bundle branch block
Consider admission for patients with syncope and any of the following:
1. Age older than 60 years 2. History of coronary artery disease or congenital heart disease 3. Family history of unexpected sudden death 4. Exertional syncope in younger patients without an obvious benign etiology for the syncope