Transcript Syncope - University of Toronto

Syncope
The only difference between syncope
and sudden death is that in one you
wake up.1
UHN/MSH AIMGP Seminar
2007
Yash Patel
1
Engel GL. Psychologic stress, vasodepressor syncope, and sudden death. Ann Intern Med 1978; 89: 403-412.
References
Neurocardiogenic Syncope. New England Journal
of Medicine 10 March 2005. 352(10): 1004-1010.
Guidelines on Management of Syncope – Update
2004. European Heart Journal 25: 2054-2072.
Vasovagal Syncope. Ann Intern Med Nov 7 2002;
133(9):714-725.
Incidence and Prognosis of Syncope. NEJM
347(12):878-85. Sept 2002.
Primary Care: Syncope. NEJM 343(25):1856-1862.
Dec 2000.
AHA Statement on Evaluation of Syncope.
Circulation 113:316-327. Jan 2006.
Outline
1. Objectives
2. Definitions
3. Differential diagnosis
4. Approach
5. Treatment
6. Extra material
Objectives
Learn to distinguish syncope from other
“non-syncopal” conditions that lead to
transient loss of consciousness
Develop an approach to the assessment
of patients with syncope
How to risk stratify patients with syncope
When to hospitalize patients with syncope
Case 1
35 Woman
Unwitnessed loss of consciousness (1st.
Event)
No palpitations or preceding symptoms
PMH: Hypothyroidism on replacement
Exam normal
No sequelae
No injuries
IS THIS SYNCOPE?
WHAT IS SYNCOPE?
Some Definitions
Syncope: sudden, transient loss of
consciousness and postural tone with
spontaneous recovery without therapeutic
intervention
Presyncope: no actual loss of consciousness
Vertigo: Dizziness accompanied by a sense
of motion
Drop attacks: spontaneous falls while
standing or walking without LOC
Is it Syncope or Seizure?
Syncope:
– Precipitant: pain,
exercise,
micturition,
defecation, anxiety
– Preceding sx:
sweating and
nausea
– Event: LOC
usually <5 min
– Followed by: prompt
recovery
Seizure:
– Preceding sx: aura,
jacksonian march
– Event: clonic or
myoclinic jerks, LOC
>5 min, incontinence
– Followed by: slowness,
neurological deficits,
postictal paresis
Epidemiology of Syncope
Population based incidence
(Framingham):
Men
Women
3% per yr.
3.5% per yr.
It increases with age:
35 - 44 y/o
> 75 y/o
0.7% per yr.
6% per yr.
Case 1
35 Woman
Unwitnessed loss of consciousness (1st. Event)
No palpitations or preceding symptoms
PMH: Hypothyroidism on replacement
Exam normal
No sequelae
No injuries
IS THIS SYNCOPE?
YES, THIS WAS PROBABLY A SYNCOPAL
EVENT
REMEMBER SYNCOPE IS A SYMPTOM NOT A
DIAGNOSIS
Case 2
70 Woman
PMH: CAD - Previous MI
CABG x 3 10 yr. Ago
Meds: Metoprolol, ASA, Fosinopril, recently
started on clarithromycin for CAP
Witnessed syncope lasting 15 sec.
Palpitations prior to event
ECG: Inferior Q waves, no arrhythmias
WHAT IS THE CAUSE OF HER SYNCOPE?
Syncope: Etiology
NeurallyMediated
1
• Vasovagal
• Carotid
Sinus
• Situational
Cough
Postmicturition
24%
Orthostatic
2
3
• Brady
• Drug
Induced
• ANS
Failure
Sick sinus
AV block
Primary
Secondary
11%
Cardiac
Arrhythmia
• Tachy
VT*
SVT
Structural
CardioPulmonary
NonCardiovascular
4
• Aortic
Stenosis
• HOCM
• Pulmonary
Hypertension
5
• Psychogenic
• Metabolic
e.g. hyperventilation
• Neurological
4%
12%
• Long QT
Syndrome
14%
Unknown Cause = 34%
Case 2
70 Woman
PMH: CAD -
Previous MI
CABG x 3 10 yr. Ago
Meds: Metoprolol, ASA, Fosinopril, recently started on clarithromycin for CAP
Witnessed syncope lasting 15 sec.
Palpitations prior to event
ECG: Inferior Q waves, no arrhythmias
WHAT IS THE APPROACH TO EVALUATING
SOMEONE WITH SYNCOPE?
Approach
1. Hx, Physical and ECG form core workup
(yields diagnosis in ~ 50 % of cases)
2. Cardiac causes carry a worse prognosis and
should be excluded first
3. Exertional syncope or existing heart disease
predicts worse outcomes and warrants more
intense investigation
4. In the elderly think of polypharmacy
History: focus on...
Precipitating Factors
– exertion, position, neck or arm movement, specific activities
(urination, defecation) and stressful situations
Associated Symptoms:
– Nausea, diaphoresis, blurred vision - vasovagal
– Diarrhea, Vx, GI bleed - volume contraction
– Prodromal aura, incontinence - seizure
Medications:
– side effects, overdose, interactions
– antiHTN, Digoxin, diuretics, antibiotics
Family Hx: Long QT, WPW, HOCM, CAD, Brugada
Syndrome
Physical Exam: focus on...
Vitals: Orthostatic, BP in both arms
CSM (avoid if carotid bruits present)
Cardiac exam
Neurologic exam
Misc: Pulses, bruits, OB in stool
Case 2
70 Woman
PMH: CAD -
Previous MI
CABG x 3 10 yr. Ago
Meds: Metoprolol, ASA, Fosinopril, recently started on clarithromycin for CAP
Witnessed syncope lasting 15 sec.
Palpitations prior to event
ECG: Inferior Q waves, no arrhythmias
SHOULD SHE BE ADMITTED TO HOSPITAL?
WHAT INVESTIGATIONS ARE INDICATED?
When to Hospitalize?
1. For Investigation:
structural heart disease, arrhythmias or
ischemia (palpitations or chest pain), or
abnormal ECG
2. For Treatment:
obstructive HD, severe orthostasis, or
adverse drug reactions
3. Consider in all patients with injury
following syncope
Investigations for Suspected
Cardiac Syncope
Guided by history, physical and clinical suspicion
(ie/risk factors, age >60)
Echo - abnormalities found in 5-10 % but these
may not relate to sx
Stress testing if ischemic arrhythmia suspected
Prolonged ECG recording
Electrophysiologic testing
If above testing is negative and syncope
recurrent, evaluate for neurally mediated
syncope
ECG Features Suggesting
Arrhythmic Etiology
Bifasicular block
Intraventricular conduction abn (QRS>.12)
Mobitz II AV block
Sinus brady, sinus block or sinus pause >3 sec in
absence of negative chronotropes
Pre-excited QRS
Prolonged QT
Brugada Syndrome:RBBB and ST elevation V1-V3
Neg T waves in R precordial leads, epsilon waves and
ventricular late potentials (ARVD)
Q waves
Electrocardiographic Monitoring
“ECG monitoring is unlikely to be helpful in
patients who do not have clinical or ECG
features suggestion an arrhythmic
syncope and therefore should not be
performed”
Electrocardiographic Monitoring
In hospital monitoring if high risk
Holter monitoring
– True + (arrhythmias with sx) ~ 4% of tests
– True - (sx with no arrhythmia) ~ 17% of
tests
Loop recording for longer monitoring
– External if inter-symptom interval <4 wks
Consider EPS in anyone with structural heart
disease with a non-diagnostic Holter
Case 3
82 Man
PMH: HTN, BPH, Glaucoma, COPD, Depression
Meds: Diltiazem, ASA, Salbutamol, Ipratropium,
Prazosin, Paroxetine, Tyl #3, Omeprazole
Syncope while urinating in early AM, shortly after
rising
Trauma to forehead from episode
YOUR DIAGNOSIS IS NEURALLY-MEDIATED
SITUATIONAL SYNCOPE
WHAT INVESTIGATIONS DOES HE NEED?
Investigations for Suspected
Neurally Mediated Syncope
The majority of patient with single or rare
episodes do not require confirmatory tests
Investigations in patients without
suspected heart disease and recurrent or
severe syncope:
– Tilt testing
– Carotid massage
– Prolonged ECG monitoring
Case 1
Case 2
Case 3
35 Woman
Unwitnessed loss of
consciousness (1st.
Event)
No palpitations or
preceding symptoms
PMH: Hypothyroidism
on replacement
Exam normal
No sequelae
No injuries
70 Woman
PMH: CAD - Previous MI
CABG x 3 10 yr. Ago
Meds: Metoprolol, ASA,
Fosinopril, recently started
on clarithromycin for CAP
Witnessed syncope lasting
15s
Palpitations prior to event
ECG: Inferior Q waves, no
arrhythmias
82 Man
PMH: HTN, BPH,
Glaucoma, COPD,
Depression
Meds: Diltiazem, ASA,
Salbutamol, Ipratropium,
Prazosin, Paroxetine, Tyl
#3, Omeprazole
Syncope while urinating
in early AM, shortly after
rising
Trauma to forehead from
episode
WHAT IS THE PROGNOSIS FOR EACH
OF THESE PATIENTS WITH SYNCOPE?
Risk Stratification and Prognosis in
Syncope
Structural heart disease is the most
important predictor of mortality and
sudden death in patients with syncope
Poor Prognosis
Structural heart disease
Excellent Prognosis
Young, healthy, normal ECG
Neurally-mediated syncope
Orthostatic hypotension
Unexplained syncope
Prognosis in Syncope
(from Framingham database)
Etiology
Total Mortality
1yr
5yr
Cardiac
Noncardiac
15%
40%
5%
2%
30%
15%
5%
25%
2%
15%
Neurologic
Vasovagal/Others
Unknown
Controls w/o syncope
NEJM 2002;347:878
Summary
Syncope is a common symptom
History/Physical can establish a diagnosis
in 50% of cases
The approach involves risk assessment for
the presence of cardiac disease
Investigations and Treatment are tailored
to the suspected etiologic cause of
syncope
Extras...
Driving after syncope
Treatment of syncope
Mechanism of Vasovagal syncope
Tilt-table testing
Neurologic evaluation
Psychiatric evaluation
Driving and Syncope
Driving and Syncope
Physicians are obliged to disclose risk of
driving to patients and advise them not to
drive
7 provinces (including Ontario) and all
territories have mandatory reporting
legislation
Single episode of
vasovagal
Dx and tx cause
(ie/ PPM)
Reversible cause
(ie/ hemorrhage)
Situational
w/avoidable
trigger
Unexplained
Single episode
Recurrent
Recurrent
Private
Commercial
No restriction
No restriction
Wait 1 week
Wait 1 month
No restriction
No restriction
Wait 1 week
Wait 1 week
Wait 1 week
Wait 3 months
Wait 12 months
Wait 12 months
Wait 1 week
Wait 12 months
Syncope and Driving
Further guidelines exist for patients with
arrhythmia, MI, valvular heart disease and
devices
See CCS Consensus Conference 2003:
Assessment of Cardiac Patients for
Fitness to Drive and Fly. Canadian
Journal of Cardiology, 2004, 20(13):
1313-1323.
Treatment of Syncope
Treatment
Identifiable arrhythmia, structural heart
disease, or non-syncopal event: Rx
accordingly
Treatment: Neurally-Mediated
Education and reassurance usually
sufficient
Additional treatment may be warranted if:
– Very frequent
– Unpredictable and exposes pts to trauma
It may be valuable to assess the relative
contribution of cardioinhibition and
vasodepression
Treatment: Nonpharmacologic
Avoid trigger events
Modify or discontinue hypotensive drugs
Other
–
–
–
–
–
Increase fluid intake (2L water/day)
Salt supplements
Isometric leg and arm counter-pressure maneuvers
Tilt training
Compression Stockings
Treatment: Drugs
Beta-blockers discouraged in 2004 ESC
guidelines
Other meds with limited evidence:
– Fludricortisone
– Midodrine
– SSRIs
– Others
Treatment: Devices
Permanent dual chamber pacing may
have a role in:
– Those with no prodrome
– Failure of other therapies
– Profound bradycardia or asystole during
syncope
>5 attacks per year
Age >40
Mechanism of Vasovagal Syncope
Mechanism of Vasovagal
Syncope
Bezold–Jarisch Reflex: Excessive venous
pooling triggers a chain of events that
culminates in vasodilatation and bradycardia
(instead of the physiologic compensatory
responses of vasoconstriction and
tachycardia)
This in turn leads to the hypotension and loss
of consciousness associated with vasovagal
syncope.
Common Triggers in Situational
Syncope
Defecation
Micturition (especially in elderly men with BPH that
wake up at night and strain to pass urine)
Heavy straining
Cough
All situations that induce valsalva =>
– decreased preload +
– cardioinhibitory and vasodepressor reflexes
produced by central baroreceptors
Tilt-Table Testing
Vasovagal Syncope
Test = Head Up Tilt-table
testing using a provocative
agent (Isoproterenol or
Nitroglycerin):
Sn and Sp difficult to
evaluate because of lack of
gold standard
ACC has guidelines on
testing (JACC 1996:28 pg
263-275)
Head-up Tilt table testing
Indicated in:
1. Recurrent syncope
2. Single syncopal event
resulting in injury or
occurring in high risk
setting
3. Where the treatment of
syncope may be
complicated by vasovagal
symptoms
Contraindicated in
presence of obstructive
heart disease or
cerebrovascular stenosis
Neurologic and Psychiatric Testing
Neurologic Testing
Low yield:
– EEG ~ 2%
– CT head ~ 4%
– Doppler carotids (no studies)
The majority of positives can be identified
by history: e.g. seizure events
Bottom line: only indicated if suspicion of
seizure or neuro deficits present
Psychiatric evaluation
Syncope can be a feature of:
– Anxiety disorders: Gen anxiety or panic
– Somatization
– Substance abuse
These tend to occur recurrently in younger
patients without heart disease
In elderly patients organic (i.e. cardiac)
causes must be excluded