Safety lessons learned from aviation
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Transcript Safety lessons learned from aviation
Joseph P. Ornato, MD, FACP, FACC, FACEP
Professor & Chairman, Department of Emergency Medicine
Self-limited loss of consciousness and postural
tone
Relatively rapid onset
Variable warning symptoms
Spontaneous, complete, and usually prompt
recovery without medical or surgical intervention
Underlying mechanism is
transient global cerebral hypoperfusion.
Brignole M, et al. Europace, 2004;6:467-537.
Real or Apparent TLOC
Syncope
Neurally-mediated reflex
syndromes
Orthostatic hypotension
Cardiac arrhythmias
Structural cardiovascular
disease
Brignole M, et al. Europace, 2004;6:467-537.
Disorders Mimicking
Syncope
With loss of consciousness (i.e.,
seizure disorders, concussion)
Without loss of consciousness,
i.e., psychogenic “pseudosyncope”
Structural
CardioPulmonary
NeurallyMediated
Orthostatic
1
2
3
4
• Vasovagal
syndrome
• Carotid sinus
syndrome
• Situational
• Drug-induced
• Autonomic
nervous
system failure
• Bradyarrhythmia
• Acute
myocardial
ischemia
• Aortic stenosis
• Hypertrophic
cardiomyopathy
• Pulmonary
hypertension
• Aortic dissection
Cough
PostMicturition
Primary
Secondary
Cardiac
Arrhythmia
Sinus node
dysfunction
AV block
•Tachyarrhythmia
VT
SVT
• Long QT
syndrome
Unexplained Causes = Approximately 1/3
Acute intoxication (e.g., alcohol)
Seizures
Sleep disorders
Somatization disorder (psychogenic
pseudo-syncope)
Trauma/concussion
Hypoglycemia
Hyperventilation
Brignole M, et al. Europace, 2004;6:467-537.
40% will experience syncope
at least once in a lifetime1
1-6% of hospital admissions2
1% of emergency department
visits per year3,4
10% of falls by elderly are due
to syncope5
Major morbidity reported in 6%1
(fractures, motor vehicle crashes)
Minor injury in 29%1
(lacerations, bruises)
1Kenny
RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and
Treatment of Syncope. Futura;2003:23-27.
2Kapoor W. Medicine. 1990;69:160-175.
3Brignole
M, et al. Europace. 2003;5:293-298.
Blanc J-J, et al. Eur Heart J. 2002;23:815-820.
5Campbell A, et al. Age and Ageing. 1981;10:264-270.
4
Estimated hospital costs exceeded $10
billion1
Estimated physician office expenses
exceeded $470 million2
Over $7 billion is spent annually in the US
to treat falls in older adults4
1Kenny
RA, Kapoor WN. In: Benditt D, et al. eds. The Evaluation and Treatment of Syncope. Futura;2003:23-27.
v. 6.0. Solucient LLC, Evanston IL.
3Farwell D, et al. J Cardiovasc Electrophysiol. 2002;13(Supp):S9-S13.
4Olshansky B. In: Grubb B and Olshansky B. eds. Syncope: Mechanisms and Management. Futura. 1998:15-71.
2OutPatientView
100
80
73%1
71%2
60%2
60
37%2
40
20
0
1Linzer
2Linzer
Anxiety/
Depression
M. J Clin Epidemiol. 1991;44:1037.
M. J Gen Int Med. 1994;9:181.
Alter Daily
Activities
Restricted
Driving
Change
Employment
Low mortality vs.
high mortality
Neurally-mediated
syncope vs.
syncope with a
cardiac cause
Soteriades ES, Evans JC, Larson MG, et al. Incidence and prognosis of syncope.
N Engl J Med. 2002;347(12):878-885. [Framingham Study Population]
Distinguish true syncope from syncope
mimics
Determine presence of heart disease
Establish the cause of syncope with
sufficient certainty to:
Assess prognosis confidently
Initiate effective preventive treatment
Initial Examination
Detailed patient history
Physical exam
ECG
Supine and upright
blood pressure
Monitoring
Holter
Event
Insertable loop recorder (ILR)
Cardiac Imaging
Special Investigations
Head-up tilt test
Hemodynamics (cardiac cath)
Electrophysiology study
Brignole M, et al. Europace, 2004;6:467-537.
Circumstances of
recent event
Eyewitness account of
event
Symptoms at onset of
event
Sequelae
Medications
Circumstances of
prior events
Concomitant disease,
especially cardiac
Pertinent family
history
Cardiac disease
Sudden death
Metabolic disorders
Past medical history
Neurological history
Syncope
Brignole M, et al. Europace, 2004;6:467-537.
Vital signs
Heart rate
Orthostatic blood pressure change
Cardiovascular exam: Is heart disease present?
ECG: Long QT, pre-excitation, conduction system disease
Echo: LV function, valve status, hypertrophic cardiomyopathy
Neurological exam
Carotid sinus massage
Perform under clinically appropriate conditions preferably
during head-up tilt test
Monitor both ECG and BP
Brignole M, et al. Europace, 2004;6:467-537.
Neurally-mediated
Vasovagal Syncope (VVS)
Carotid Sinus Syndrome (CSS)
Cardiac arrhythmia
Tachy-brady syndrome
Long QT syndrome
Torsade de pointes
Brugada syndrome
Drug-induced
Structural cardio-pulmonary disease
Orthostatic
Vasovagal syncope (VVS)
Carotid sinus syndrome (CSS)
Situational syncope
Post-micturition
Cough
Swallow
Defecation
Blood drawing, etc.
Most common form of syncope
8% to 37% (mean 18%) of syncope cases
Depends on population sampled
Young without structural heart disase, ↑
incidence
Older with structural heart disease, ↓
incidence
Useful as diagnostic
adjunct to confirm
vasovagal syncope
Useful in teaching
patients to recognize
prodromal symptoms
Brignole M, et al. Europace. 2004;6:467-537.
60° - 80°
Etiology
Drug-induced (very
common)
Diuretics
Vasodilators
Primary autonomic
failure
Multiple system atrophy
Parkinson’s Disease
Postural Orthostatic
Tachycardia Syndrome
(POTS)
Secondary autonomic
failure
Diabetes
Alcohol
Amyloid
Syncope clearly associated with
carotid sinus stimulation is rare (≤1%
of syncope)
CSS may be an important cause of
unexplained syncope/falls in older
individuals
Kenny RA, et al. J Am Coll Cardiol. 2001;38:1491-1496.
Brignole M, et al. Europace. 2004;6:467-537.
Sutton R. In: Neurally Mediated Syncope: Pathophysiology, Investigation and Treatment. Blanc JJ, et al. eds. Armonk, NY: Futura;1996:138.
Method1
Massage, 5-10 seconds
Don’t occlude
Supine and upright posture
(on tilt table)
Outcome
3 second asystole and/or
50 mmHg fall in systolic BP
with reproduction of
symptoms = Carotid Sinus
Syndrome
1Kenny
RA. Heart. 2000;83:564.
M. Ann Intern Med. 1997;126:989.
3Munro N, et al. J Am Geriatr Soc. 1994;42:1248-1251.
2Linzer
Absolute
contraindications2
Carotid bruit, known
significant carotid arterial
disease, previous CVA, MI
last 3 months
Complications
Primarily neurological
Less than 0.2%3
Usually transient
Ambulatory ECG
Holter monitoring
Insertable loop recorder (ILR)
Tilt table test
Includes drug provocation (NTG, isoproterenol)
Cardiac catheterization
Electrophysiology study (EPS)
Brignole M, et al. Europace, 2004;6:467-537.
OPTION
12-Lead 10 Seconds
1 day
Holter Monitor
Event Recorders
7-30 days
(non-lead and loop)
Up to 14
Months
ILR
0
1
2
3
4
5
6
7
8
TIME (Months)
Brignole M, et al. Europace, 2004;6:467-537.
9
10
11
12
13
14
Initial Evaluation
History, Physical Exam, ECG, Cardiac Massage
Yield (%)
38-40
Other Tests/Procedures
Head-Up Tilt
External Cardiac Monitoring
Insertable Loop Recorder (ILR)
EP Study
Exercise Test
EEG
27
5-13
43-883-5
<2-5
0.5
0.3-0.5
EEG
Head CT
Brignole M, et al. Europace. 2004;6:467-537.
Includes cardiac arrhythmias and structural heart
disease
Often life-threatening
Suspect if syncope exercise-induced
May be warning of critical CV disease
Tachy and brady arrhythmias
Myocardial ischemia, aortic stenosis, pulmonary
hypertension, aortic dissection
Assess culprit arrhythmia or structural abnormality
aggressively
Initiate treatment promptly
Bradyarrhythmias
Sinus arrest, exit block
High grade or acute complete AV block
Can be accompanied by vasodilatation (VVS, CSS)
Tachyarrhythmias
Atrial fibrillation/flutter with rapid ventricular rate
(eg, pre-excitation syndrome)
Paroxysmal SVT or VT
Torsade de pointes
Cardiovascular pathology
Coronary artery disease
Severe left ventricular dysfunction
Cardiomyopathy
Hypertrophic cardiomyopathy
Arrhythmogenic right ventricular cardiomyopathy
Congenital heart disease, especially coronary artery anomalies
Valvular heart disease
Cardiac pacemaker and conducting system disease
Hereditary channelopathies (Sudden Arrhythmic Death Syndrome (SADS))
Brugada syndrome
Early repolarization syndrome (ERS)
Long QT syndrome (LQTS)
Short QT syndrome (SQTS)
Catecholaminergic polymorphic ventricular tachycardia (CPVT)
Often present as recurrent syncope or brief seizures
in children or young adults before sudden death
occurs
May have young relatives who have had sudden
death
ECG findings are often diagnostic
Effective preventive treatment is available (ICD)
Astute emergency physician may be the ONLY
healthcare provider who can make the diagnosis and
prevent tragic loss of a young life
Male predominance
Autosomal dominant
Common in Asians
40-60% prevalence of
life-threatening ventricular
arrhythmias and SCD
Presents as syncope
Downsloping ST-segment
elevation in ECG leads V1–3
Type I – 43% ↑ in SCD
Male predominance
1-2% of adults
Normalizes with
exercise
Type II – no ↑ in SCD
Hereditary
Autosomal recessive (Jervell
Lange-Nielsen syndrome) with
hereditary nerve deafness
Autosomal dominant (Romano
Ward syndrome w/out deafness)
Syncope, VF, SCD
Acquired causes
Hypocalcemia
Hypokalemia
Hypomagnesemia
Ischemia
Anorexia
CNS pathology
QT-prolonging drugs (www.azcert.org)
𝑄𝑇𝑐𝑜𝑟𝑟𝑒𝑐𝑡𝑒𝑑 =
𝑄𝑇𝑚𝑒𝑎𝑠𝑢𝑟𝑒𝑑
𝑅𝑅𝑖𝑛𝑡𝑒𝑟𝑣𝑎𝑙
Bazett Formula
QTc = 0.35-0.44 at HR= 60
Hereditary
Acquired causes
Autosomal dominant
Hypercalcemia
Atrial fibrillation
Hyperkalemia
Syncope, VF, SCD
Acidosis
Early repolarization inferolateral
leads in 65%
Systemic inflammatory
syndrome
Myocardial ischemia
Increased vagal tone
Anomalous L coronary artery off the pulmonary
artery
Hypertrophic cardiomyopathy
Severe aortic stenosis
Catecholaminergic polymorphic ventricular
tachycardia
Hereditary defect in myocardial calcium handling
Stress-related syncope, VF, SCD
ECG – unexplained sinus bradycardia at rest
50% carry a diagnosis of epilepsy before correct
diagnosis established
Syncope is a common symptom with
many causes
Deserves thorough investigation and
appropriate treatment
Clinical decision (observation) unit at
VCU is an appropriate location to
initiate the evaluation