Syncope in Elderly

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Syncope in Elderly
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SYNCOPE

• Syncope (Greek synkope cut-off) is a brief
  transient loss of consciousness (fainting) and
  postural tone (collapse) with rapid spontaneous
  recovery

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SYNCOPE

• 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

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Incidence of syncope in the Framingham Heart
Study
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SYNCOPE

• 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.

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Age-related physiological changes that predispose
to syncope

• Blood vessel
• Heart
• Autonomic nervous system
• Other non cardiological changes

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Blood vessel

• 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.

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Heart

• 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.

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Heart

• 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.

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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

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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.

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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

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Causes of syncope of the elderly

• Cardiac diseases
• - Primary cardiac arrhythmias
• - Structural cardiovascular
  diseasesobstruction 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
• Postprandial hypotension
• Cerebrovascular, neurological, and psychiatric
  causes

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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
• Polypharmacy

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Drugs predisposing to syncope

• Vasodilators nitrates, CCB, hydralazine, ACEIs
• AntiHT clonidine, BB
• Prolongation of QT(torsade de pointes)
• - Antiarrhythmic agent class IA,III
• - ATB macrolide(erythromycin), bactrim
• - Others terfenadine,TCA, cisapride,
  phenothiazines, probucol

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Conditions predisposing to a prolonged QT
interval and torsade des pointes
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Structural cardiovascular diseases obstruction to
left ventricular outflow

• Aortic stenosis is the most common structural
  lesion associated with syncope in the elderly
• - Age lt 70 yr. Congenital bicuspid
  
  
  valves
• - Age gt 70 yr. Degenerative changes
• Hypertrophic obstructive cardiomyopathy (HOCM)
• Vasodilator drugs or even vasodilatation after a
  hot bath can induce syncope in these patients

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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

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Vasovagal syncope
The mechanism of tilt or haemorrhage-induced
vasovagal syncope
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Situational syncope

• Peripheral receptors similar to ventricular
  mechanoreceptors are found in lung, bladder, GI
  tract
• Cough or micturition related syncope

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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.

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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.

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Postprandial 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.

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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

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Differentiating syncope from seizure
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Diagnostic evaluation

• 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

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Diagnostic evaluation

• AMI
• PE
• aortic dissection
• cardiac tamponade
• tension pneumothorax
• leaking AAA
• active internal bleeding
• malignant cardiac arrhythmias
• SAH
• carotid artery/vertebral artery dissection

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Diagnostic evaluation

• 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

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History

• 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

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History

• 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

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CLINICAL CLUE TABLE
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CLINICAL CLUE TABLE
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CLINICAL CLUE TABLE
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Physical examination

• Search for trauma and assessment of severity
• Cardiovascular examination
• - BP
• - Pulse volume
• - Neck bruits
• - JVP
• - Apex beat, Heart sounds
• Abdomen
• Neuro exam

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BP

• Difference in BP between lt. and rt. upper limbs
  gt 20mmHg is abnormal (suggests dissecting aortic
  aneurysm or subclavian steal syndrome)
• Difference in BP between upper and lower limbs gt
  20mmHg when recumbent is abnormal (suggests a
  dissecting aortic aneurysm)
• Orthostatic vital signs positive test is
  defined as a SBP decrease of gt 20 - 30mmHg, a DBP
  decrease of gt10 - 15mmHg and/or HR increase of
  greater than 30 bpm when standing

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BP

• 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)

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Pulse volume

• Decreased and delayed upstoke (aortic
  stenosis/hypertrophic obstructive cardiomyopathy)
  
• Positive pulsus paradoxus (cardiac tamponade,
  massive pulmonary embolism)
• Absent pulses (dissection of the aorta, cardiac
  emboli)

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Heart sounds

• Decreased (pericardial tamponade)
• 3rd/4th heart sounds (ventricular failure or LV
  overload)
• Loud second heart sound (pulmonary embolism or
  pulmonary hypertension)
• Ejection systolic murmurs (aortic stenosis or
  hypertrophic cardiomyopathy - increased murmur
  when standing, decreased when squatting)
• Machinary murmur (air embolism)
• "tumor plop" or diastolic murmur (atrial myxoma)
• Varying heart sounds/murmurs (thrombotic
  occlusion of a prosthetic valve)

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Abdomen

• Pulsatile masses (abdominal aneurysm)
• Rectal exam for melena or heme-occult positive
  stools (gastro-intestinal bleeding)
• Absent/decreased femoral pulses (dissection of
  the aorta)

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Investigation

• EKG
• Echocardiography
• Carotid sinus massage
• Exercise stress test
• Ambulatory continuous electrocardiography
• Event and memory loop ambulatory electrocardigram
  recording
• Signal-averaged electrocardiography
• Invasive electrophysiological studies
• Tilt table testing

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EKG

• an abnormal ECG may be etiologically significant,
  although the 'definitive' diagnostic yield is low
  (lt 5)
• ECG abnormalities include-
• previous or acute cardiac ischemic changes
• signs of pericarditis or electrical alternans
  (cardiac tamponade)
• LVH (hypertension, aortic stenosis, HOCM)
• RVH (PE or pulmonary hypertension)
• classical/non-specific ECG signs of PE
• WPW syndrome
• LBBB or bifasicular block (conducting system
  disease)
• bradyarrythmias or tachyarrhythmias
• long QT interval
• Brugada syndrome (partial RBBB with elevated ST
  segments in leads V1-3 and peculiar downsloping
  of the elevated ST segments inverted T waves in
  those leads)
• arrhythmogenic right ventricular dysplasia (RBBB,
  QRS complex gt 110 msec in leads V 1-3, inverted T
  wave or epislon wave

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Carotid sinus massage

• first performed on the right side for a minimum
  of 5 seconds (preferably 15 seconds) gt measure
  pulse rate and blood pressure gt wait 120 seconds
  gt repeat test on the left side
• positive response longer than 3 seconds of
  asystole, and/or systolic blood pressure drop of
  gt 50 mmHg when supine
• borderline positive response slowing of heart
  rate gt 30 - 40 and/or systolic blood pressure
  drop of gt 30mmHg when supine

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Carotid sinus massage

• Carotid sinus syncope can only be definitively
  diagnosed when syncope or near-syncope occurs
  during carotid massage
• Carotid sinus massage is contra-indicated in
  patients with a history of a CVA, a recent AMI or
  when a neck bruit is present

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24-hour Holter (continuous ambulatory
electrocardiographic) monitoring

• 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

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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.

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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

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