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Resident Version
Syncope Module
created by Dr. Teodora Konstantinova
Objectives:
1. You will be able to describe syncope and different causes of syncope.
2. You will be able to understand the diagnostic criteria for the causes of syncope.
3. You will be able to understand the preferred approach to the diagnostic work-up
in various subgroups of patients with syncope.
4. To determine how patients with syncope should be risk stratified and when they
should be hospitalized.
References:
1. Guidelines on Management ( Diagnosis and Treatment) of Syncope, Brignole M,
Alboni P, Benditt D, et al., Update 2004, The Task Force on Syncope, European
Society of Cardiology, Europace (2004)6, 467-537.
2. Syncope, Wishwa Kapoor, MD,MPH, NEJM, Volume 343-1856-1862, 12/21/2000.
3. Incidence and Prognosis of Syncope, Elpidofores S. Soteriades, MD, Jane Evans,
D. Sc., Martin Larson, Sc.D., Ming Hui Chin, MD, Leway Chin, MD, Emelia J.
Benjamin, MD, Daniel Levy, MD, NEJM, Volume 347:878-885, 9/19/2002 (table 2
copied from this article).
Case:
Patient is a 54 yo male with h/o hepatitis C and ESLD, on the transplant list. He is
followed in the clinic regularly, but presents for an unscheduled visit due to a recent
concerning episode. Per patient and partner (who witnessed event), patient was sitting on couch a
few days ago, tired from recent shopping, and all of a sudden felt blackness coming on like he
was in a tunnel, and he blacked out. Per partner, he then slumped to the side, and had a few
jerking motions. Partner got up to call 911, came back in to check on patient while on phone, and
patent had wakened, remembered what happened, and felt drained. Also noted feeling very hot
with episode, but otherwise DENIED the following: cp/sob/, change in vision other than
tunnel/blackness, palpitations, aura, loss of bladder/bowels, n/v/abd pain, new
weakness/numbness, facial droop, difficulty speaking, or headache.
EMT arrived at the house, and took vitals - pulse 47, bp 120/71, o2 sat 97% RA, blood glucose
199. Rhythm strip with sinus bradycardia. Patient declined transport to hospital. No events since
the episode 4 days ago.
Pmhx:
Hepatitis C – completed 18 weeks of therapy last year, but had to stop due to severe exacerbation
of ESLD, complicated by hepatic encephalopathy, with peak NH3 levels of 300-400.
Depression/anxiety
Peripheral neuropathy
Mitral valve prolapse
GERD
Medications:
aldactone 50 mg po q am
lasix 20 mg qam--> changed to 10 mg po qd
omeprazole 20 mg po qd
zinc 220 mg po qd
lactulose 10g/15 ml 2 oz (4 tbsp) qid
rifaximin 400 mg tid for encephalopathy
zoloft 100 mg bidpilocarpine 5 mg qid (for dry mouth)
neurontin 900 mg tid--> decreasing dose
testosterone androderm 5mg/24 hour patch
Shx: lives with partner, no etoh, very remote h/o IVDU.
Fhx: no sudden deaths, father with CAD at age 50.
PE:
Vitals: T=97.9, BP=127/72, not orthostatic, P=82, skipped beats, RR=12, O2 sat=92%RA
gen: alert, oriented, comfortable, able to give good history of event. Speech normal, face
symmetric
skin: no rashes, has spider angiomas on chest
heent: cn 2-12 symmetric/intact. Tongue midline, no scleral icterus, TM’s clear bilaterally, moist
mucus membranes, no adenopathy, nl carotid pulses, no bruits.
cv: irregular, not tachycardic, soft murmur at the apex without radiation, s1s2 present
abd: flat, soft, nl bs, nt, no evidence of ascites on exam
lungs: ctab, no crackles or wheezes, nl excursion
neuro: non-focal, negative rhomberg, able to do finger to nose, no asterixis, strength 5/5 all major
muscle groups, sensory: decreased sensation bilateral Les, reflexes: 3+ biceps, brachioradialis,
triceps, knee and ankle. Down ward going toes bilaterally, gait normal.
Recent labs from last week: NH4=72 (baseline for patient). Basic metabolic including mg2+ wnl.
CBC=wbc nl, hct 34, plate 93 (baseline). Liver enzymes – notable for alk phos 233, ast 69; alb
3.6, inr wnl. Chol 187, ldl 97.
EKG: sinus rhythm with many PAC’s, nl intervals, no QT prolongation, no block present.
Based on the above information, what is on your differential diagnosis?
Does patient need to be admitted to the hospital?
What additional studies would be helpful?
Syncope is a symptom, not a diagnosis
Syncope (derived from the Greek words ‘syn’ meaning ‘with’ and the verb ‘kopto’
meaning ‘I cut’ or more appropriately in this case ‘I interrupt’)
* Self-limited, loss of consciousness and postural tone
* Rapid onset
* Variable warning symptoms
* Spontaneous complete recovery
The pathophysiology of all forms of syncope consists of sudden decrease in or brief
cessation of cerebral blood flow. Experience from tilt testing showed that a decrease in
SBP to 60 mmHg is associated with syncope. Further it has been estimated that as little as
20% drop in cerebral oxygen delivery is sufficient to cause syncope. In this regard, the
integrity of a number of control mechanisms is crucial for maintaining adequate cerebral
oxygen delivery:
a) Cerebrovascular capability which permits cerebral blood flow to be maintained over a
relatively wide range of perfusion pressures
b) Local metabolic and chemical control which permits cerebral vasodilation to occur in
the presence of either diminished pO2 or increase pCO2
c) Arterial baroreceptor-induced adjustments of HR, cardiac contractility and systemic
vascular resistance
d) Vascular volume regulation in which renal and hormonal influences help to maintain
central circulating volume
Causes:
1. Reflex-mediated (vasovagal, situational)
2. Carotid sinus
3. Orthostatic hypotension
4. Medications
5. Psychiatric
6. Neurological
7. Cardiac arrythmias: bradycardia (sick-sinus, AV block); tachycardia (VT, SVT), long
QT syndrome
8. Organic heart disease (AS, HOCM, pulmonary HTN)
8. Unknown (approximately 34 %)
Diagnostic objectives:
3 key questions should be addressed during the initial evaluation: is loss of consciousness
attributable to syncope or not; is heart disease present or absent; are there important
clinical features in the history that suggest the diagnosis
* distinguish “true” syncope from other “loss of consciousness spells” (seizures,
psychiatric disturbances).
* establish the cause of syncope with sufficient certainty.
* initial evaluation (detailed history, PE, serum electrolytes, glucose, 12-lead ECG,
ECHO, event monitor or Holter).
Among cardiac investigations, ECHO, prolonged electrocardiographic monitoring, stress
test, electrophysiologic study and implantable loop recorder are most useful.
Among neurally-mediated investigations, tilt test, carotid sinus massage, and implantable
loop recorder are most useful.
When a cardiac diagnosis cannot be confirmed, neurally-mediated tests are usually
performed.
Unexplained syncope: the strategy of evaluation varies according to the severity and
frequency of the episodes. In patients with unexplained syncope the likely diagnosis is
neurally-mediated.
Once the evaluation is competed and no cause of syncope is determined re-appraisal of
the work-up is needed since subtle findings or new historical information may change the
entire differential diagnosis. In theses circumstances consultation with specialty may be
needed. An additional consideration is psychiatric illness.
Conventional diagnostic methods/yield:
H & P (49-85%)
ECG (2-11%)
Electrophysiology without SHD (11%)
Electrophysiology with SHD (49%)
Tilt table test without SHD( 11-87%)
Ambulatory ECG monitors:
Holter (2%)
External loop recorder (2-3 weeks) (20%)
Insertable loop recorder (up to 14 months) (65-88%)
Neurological:
CT head, Carotid Doppler (0-4%)
Risk stratification and disposition for patients
1. High risk: hospitalization
History of PE or ECG evidence of structural heart disease, arrythmias, prolonged QT,
current use of antiarrhythmic medications or major trauma.
2. Intermediate risk:
Further evaluation in EACU or hospitalization. Usually these are patient with no high risk
features, along with recurrent syncope, age >40 yo, abnormal ECG without evidence of
prior MI, unexplained orthostatic hypotension, mild trauma, carotid hypersensitivity
3. Low risk: treatment and discharge home with follow up with PCP
Review Questions
1. You are asked to evaluate a 26 yo male who recently had a brief syncopal episode
while playing football. He denies any palpitation, SOB/CP. The physical exam reveals
BP 130/80, P-76 with a rapid carotid upstroke. CVS: S4, grade 4/6
crescendo/decrescendo systolic murmur heard best over the left sternal border. The
murmur becomes louder with Valsalva and standing and decreases in intensity with
squatting.
The most likely diagnosis is:
A)
B)
C)
D)
AS
VSD
ASD
Hypertrophic cardiomyopathy
2. A 16 yo female with recurrent loss of consciousness and most recent attack occurred
when she was awakened by an alarm clock. The physical exam reveals P- 60, BP 120/80,
no focal neuro findings and cardiac exam reveals normal heart sounds and no murmurs.
EKG: prolonged QTc.
The most important questions to ask:
A)
B)
C)
D)
History of cocaine abuse
History of ETOH abuse
History of sudden death in the family
Family history of seizures
Post Module Evaluation
Please place completed evaluation in an interdepartmental mail envelope and address to
Dr. Wendy Gerstein, Department of Medicine, VAMC (111).
1) Topic of module:__________________________
2) On a scale of 1-5, how effective was this module for learning this topic? _________
(1= not effective at all, 5 = extremely effective)
3) Were there any obvious errors, confusing data, or omissions? Please list/comment
below:
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
________________________________________________________________________
4) Was the attending involved in the teaching of this module? Yes/no (please circle).
5) Please provide any further comments/feedback about this module, or the inpatient
curriculum in general:
6) Please circle one:
Attending
Resident (R2/R3)
Intern
Medical student