Emergency Department Management of Syncope Emilia McGhee Sept 2010
Syn.co.pe A transient loss of consciousness and inability to maintain postural tone due to global cerebral hypoperfusion. Characterised by a rapid onset, short duration and spontaneous complete recovery
Incidence 1-3 % Emergency Dept visits 6 % of hospital admissions USA, Japan and Europe Occurs in up to 50% during lifetime (only 5% after 40 yrs) Recurs in 30%
Cerebral perfusion maintained by: Due to cerebral hypoperfusion causing lack of oxygen and glucose supplly to brain Cerebral perfusion maintained by: Cardiac output Systemic vascular resistance Mean arterial pressure Intravascular volume Cerebrovascular resistance with intrinsic autoregulation Metabolic regulation
What is not syncope Transient LoC without global cerebral hypoperfusion Seizure TIA Metabolic disorders Intoxication Loss of postural tone without LoC Cataplexy Drop attacks Falls TIA of carotid origin Functional - psychogenic
Syncope vs Seizure Triggering factor Prodrome Convulsion after LoC, and <15 secs Short duration Quick recovery Ongoing lethargy but no confusion Pt history Aura Automatisms Convulsions at onset of LoC Longer duration Post-ictal phase Tongue biting, incontinence
Classification Reflex – neurally mediated – 30% Orthostatic hypotension – 10-15 % Cardiac – electrical and mechanical – 10%
Reflex Vasovagal Situational Carotid sinus syncope Emotional stress Orthostatic stress Situational Coughing, micturition GI stimulation Post exercise, post prandial Carotid sinus syncope Uncommon, caused by pressure on carotid sinus Head turning, tight collars shaving
Orthostatic Hypotension Primary autonomic failure Pure auntonomic failure, multisystem atrophy, Parkinson’s Disease, Lewy body dementia Secondary autonomic failure Diabetes, amyloidosis, uraemia, spinal cord injuries Drug induced Alcohol, vasodilators, diuretics, phenothiazines, antidepressants Volume depletion Vommitting, diarrhoea, dehydration, haemorrhage
Wyatt W. Decker, M.D. “Syncope and sudden death are the same, except that in one you wake up” SYNCOPE: Critical Questions
Cardiac - Electrical Ventricular arrhythmias VT, Torsades Sudden onset, little prodrome Elderly pts with known cardiac disease Supraventricular arrhythmias SVT, AF with fast ventricular response Assoc with palpitations, chest pain, dyspnoea May occur on attempting to stand or walk Look for evidence of WPW, Brugada, Long QT Bradyarrhythmias Sick sinus, sinus brady, high grade AV block, adverse medication reactions, pacemaker malfunction Chest pain, dyspnoea, decreased ET, fatigue
Cardiac - Mechanical Low CO output states Cardiac outflow obstruction Cardiomyopathy, CCF, valvular insufficiency Cardiac outflow obstruction Sudden onset, no prodrome Exertional in nature, murmur present Aortic stenosis, HOCM, Mitral stenosis, pulmonary stenosis, pulmonary embolism, Lt atrial myxoma
HOCM Causes of syncope: Self terminating ventricular arrhythmias SVT Severe outflow tract obstruction Bradyarrhythmia Hypotension in response to exercise Reflex syncope
Emergency Department Assessment 45% can be diagnosed on history and exam alone A cause will not be found for around 37% Management is moving away from firm diagnosis to risk stratification of patients
Aim in ED Recognise life threatening conditions Recognise low risk conditions for discharge Chose appropriate FU for those who need further diagnostic testing Recognise those who do not need further investigation Moving away from diagnosis to risk stratification
History – High Yield Questions What were they doing - at rest (arrhythmia) - exercise / post-exercise (AS, HOCM) - laughing, micturition etc Was there a prodrome? - vasovagal Did they have palpitations? - an arrhythmia
Were they SOB? - PE - tamponade Did they have chest pain? - ACS and an arrhythmia - dissection Did they have abdominal pain? - AAA - ectopic Did they have a headache? - SAH
Sudden or unexplained deaths in family Known CCF Medications Previous arrythmias Known CAD Sudden or unexplained deaths in family Known CCF Medications - QT prolonging medications - vasodilators - anti-hypertnesives
Red Flags Syncope during exertion Syncope in lying position Absence of external factors Family hx of SCD Slow recovery from syncope
Examination and bedside tests Cardiorespiratory exam Abdominal exam Neurological exam BSL Orthostatic BP A drop of 20mmHg systolic, 10mmHG diastolic or increase in HR >20 Systolic BP <90mmHg Meaningful if they become symptomatic
Ix that are helpful ECG Consider on case to case basis: FBC, EUC Troponin, D.dimer, bHCG UA CXR Echo CSM Tilt table EPS EST
Ix that are generally low yield CTB MRI Holter monitor Carotid dopplers EEG
Important ECG findings Evidence of AV conduction disorder Prolonged PR Mobitz 1 or 2 CHB RBBB or LBBB Evidence of underlying cardiac disease Rt or Lt axis deviation Significant ST or T wave changes Rt or Lt ventricular hypertrophy
ECG findings associated with high risk of sudden cardiac death Hypertrophic cardiomyopathy Long QT Ventricular pre-excitation (WPW) Brugada Syndrome Short QT Arrhythmogenic Rt ventricular dysplasia
ECG changes in HOCM Normal in up to 15% Left axis deviation LVH and strain flipped T’s big voltage R waves and deep, narrow Q’s in lateral leads (I, aVL, V5 and V6) - infarct Q’s are > 1 small square where as HOCM Q’s are less than 1 small square
Risk Scores Risk scores should be applied once other identifiable causes have been considered Do not replace clinical judgment and using your brain Risk scores may miss rare causes with most serious outcomes
San Francisco Syncope Rule C H E S Congestive Cardiac Failure Haematocrit <30% ECG abnormal Shortness of breath SBP <90 at triage Any one of these factors predicts high risk and therefore pt should be admitted and investigated further
SFSR Endpoint was ‘serious outcome’ or any condition causing return to the hospital and admission Sensitivity 96% and Specificity 56% for serious outcome at 7 days Revalidated by external study in Canadian ED finding sensitivity 90%, Specificity 33% Other studies found Sensitivity 52-77% Blanket application to all syncopes and not just those with no diagnosis after ED evaluation
ROSE Criteria Predictors of serious outcome at 30 days Raised BNP Positive stool haemoccult Anaemia Hypoxia Prescence of Q waves on ECG Sensitivity 87%. Negative predictive value 95.5%
ACEP Recommendations Level A Level B Level C Hx and exam suggesting CCF consistent with high risk Elderly, structural heart disease and coronary artery disease high risk Perform ECG Echo, CT and other lab tests should not be routinely performed in absence of specific findings Admit CCF and structural heart disease. Other high risk: ECG abnormalities, haematocrit <30
What the studies agree on Identified risk factors: Age >65yrs Hx of CCF Abnormal ECG Normal ECG may include sinus tachy, first degree HB, non-specific ST/T wave changes.
Syncope in the Elderly Most common causes Orthostatic hypotension 25% ‘Age related’ 75% Medication related Reflex CCS cause in 20% Cardiac arrhythmias Advanced age, underlying cardiac disease and comorbidities
Prolonged QT Prolonged QT syndrome
Brugada – type 1 – coved type ST elevation with >2mm J point elevation with downsloping AT and negative T. ST elevation in V1-V3 with RBBB appearance but without terminal S waves in lateral leads. PR may be prolonged. Changes over time, with exrecise, fever, medications etc. Brugada Syndrome
WPW. Note Delta wave and short PR. ST and T wave changes. WPW syndrome
HOCM. LVH, large R waves in lateral leads with narrow Qs
ECG changes in HOCM Normal in up to 15% Left axis deviation LVH and strain flipped T’s big voltage R waves and deep, narrow Q’s in lateral leads (I, aVL, V5 and V6) - infarct Q’s are > 1 small square where as HOCM Q’s are less than 1 small square
Epsilon waves in arrhythmogenic right ventricular cardiomyopathy Epsilon wave, seen in 50% of Arrythmogenic Rt ventricular dysplasia. May also have inverted T waves V1-V3 and RBBB, reflecting slow conduction through myocardium rather than real BBB. 90% will have abnormal ECG but my be subtle. Epsilon waves in arrhythmogenic right ventricular cardiomyopathy
Bifasicular block. RBBB and Lt anterior or posterior hemiblock Bifascicular block
Trifasicular block. Prolonged PR, RBBB, LAD Trifascicular block
ECG Sinus progressing to CHB. Complete ventricular pause, until ventricular rhythm kicks in CHB
ECG Tachy-bradycardia syndrome Atrial tachycardia progressing to long sinus pauses Tachy-bradycardia syndrome
ECG Long QT progressing to Torsades Torsades des pointes
Disposition of patients Manage indentified cause as appropriate Admit high risk for monitoring and investigation Consider withdrawing medication likely to be responsible Advise pts on how to avoid further syncope: VVS – avoid stimulus OH – medication change, good hydration, standing slowly CSS – avoidance of tight collars, pressure on CS
Future plans for Emergency Assessment – Recommendations from Europe Falls and syncope service Run by geriatrics, cardiology, neurology Direct access to investigation and clinic Tilt tables, Echo Syncope observation unit As part of MAU 6 hr telemetry, hourly orthostatic BPs Echo
Assessing fitness to drive – National Transport Commission, Australia Unexplained syncope: Private drivers refrain from driving for 3 months. Commercial for 6 months. Recurrent syncope not responsive to treatment: criteria for conditional license not met Cause of syncope identified and assessed as temporary – NO effect on driving status In the first 2 instances it is the responsibility of the patient to inform the RTA
Driving fitness - Research ESC: Data suggests that risk of a accident in pts with syncope is not different to those without Prospective study of 3877 pts with syncope. Recurrence whilst driving occurred only in 10 pts. Risk of syncope related driving accidents is 0.8% per year.
Summary A syndrome encompassing many physiological and pathological processes Our role is to identify those at risk of sudden cardiac death Benign syncope, while having minimal mortality, has associated morbidity Remember – Cardiac BAD, Non-cardiac Not so bad
Thank You