Making change happen: learning from "positive deviancts"
Syncope-for-Residents-08.26.ppt
1. Diagnosis and Management of
Syncope
Robert Helm, M.D.
Assistant Professor of Medicine
Boston University School of Medicine
August 2013
2. Case 1
53 year-old obese gentleman with diabetes, hypertension and
hyperlipidemia who presented with syncope. This occurred
after working at the boat yard on a very hot day. He was taking
a break and drinking a cold slurpee, when he suddenly felt pins
and needles in his neck, peri-oral numbness, and tingling of his
forehead. As he was calling for wife, he lost consciousness and
fell to the ground. According to his wife, he was unconscious
for about a minute and his entire body was quivering. Upon
regaining consciousness, he was confused and disoriented.
His wife reports that he was cold, clammy, and very
diaphoretic. He sustained some minor bruising of left shoulder
but no head injuries.
3. No prior syncope but two weeks ago he did a “pirouette”
due to sudden brief episode of lightheadedness and loss of
balance. He did not lose consciousness. He consulted
with his internist, who found relative low blood pressure
(100/54 mmHg) and reduced his Lisinopril by half (40 to 20
mg daily). His blood sugars have been well controlled.
Case 1
4. Past Medical History
Diabetes (HgBA1C 5.8)
Hypertension
Hyperlipidemia
? myocardial infarction
Obstructive sleep apnea
Social History
Non-smoker
No alcohol or drugs
Family History
Mother had MI at 60
Brother died suddenly at 48
Review of system
Negative. Good functional
capacity.
Allergies
None
Medications
Cardizem cd 120 mg daily
Lisinopril 20 mg daily
Lantus 40 units at night
Novalog 12 units with meals
Aspirin 81 mg daily
Lasix 80 mg daily
Simvastatin 80 mg at night
Fenofibrate 134 mg daily
Percocet 5/325 mg as needed for pain
Viagra 100 mg – last used 2 days prior
Nitroglycerin 0.4 mg SL – never used
Case 1
5. Physical examination
BP 124/62 mmHg. Not orthostatic. Normal carotid
palpation and auscultation. Normal cardiovascular exam.
Bruised right hip.
Laboratory
BUN 27 ng/dl Creatinine 1.47 ng/dl. Electrolytes and blood
count normal.
Echocardiogram – normal 1 month ago.
Case 1
7. Case 1
Admitted for 24 hour observation and hydration.
Diagnosis: “Vaso-vagal syncope”
8. Poll
The correct statement is:
A. The patient has been correctly diagnosed.
B. The patient should be referred for urgent pacemaker.
C.The patient should be referred for electrophysiologic
study.
D.The patient should be referred for 30 day event
recorder.
E. The patient should be referred for tilt-table study.
9. 61 year old gentleman with history of cocaine use who
presented with syncope. “He was in kitchen making
Thanksgiving dinner and developed lightheadedness. He
sat on a step stool and the next thing he remember is being
on the floor and his son calling his name. He felt like he
couldn’t move. The kitchen was really hot and and he had
missed lunch. He reports using cocaine “months ago”.
Case 2
10. Past Medical History
none
Social History
history of cocaine
Family History
no premature CAD or SCD
Review of system
Negative.
Allergies
None
Medications
None
Case 2
11. Physical examination
BP 145/91 mmHg. Not orthostatic. Normal carotid
palpation and auscultation. Normal cardiovascular exam.
Minor bruise on elbow.
Laboratory
BUN 26 ng/dl Creatinine 1.1 ng/dl. Electrolytes and blood
count normal.
Case 2
13. a. Check toxicology screen. If positive then
attribute syncope to cocaine use.
b. Continuous-loop event monitoring.
c. Increase fluid intake and reassure patient.
d. Electrophysiology study to assess for inducible
VT
e. Tilt-table study.
f. Implant loop recorder (ILR).
g. Echocardiogram.
h. B and then D if event monitoring is negative.
i. B and then F if event monitoring is negative.
j. G and if ejection fraction is < 35% then D
Poll
The correct next step is:
14. Why is syncope a difficult problem?
• Physiologic response to a wide variety of medical conditions
• By definition it is a transient condition
• Occurs with unpredictable and random pattern
• Difficult to establish definitive “diagnosis”
• “Another patient with syncope….”
• History from patient may not be reliable.
15. Amnesia for Loss of Consciousness in
Carotid Sinus Syndrome
Falls
(n=34)
Syncope
(n=34)
P value
Mean max asystole (s) 5.1 5.4 0.42
Right Positive CSM 24 (71%) 29 (85%) 0.92
CSM positive upright 20 (59%) 9 (26%) 0.24
LOC during CSM 22 (64%) 15 (44%) 0.144
Amnesia for LOC 21 (95%) 4 (27%) <0.001
Perry S, et al: J Am Coll Cardiol 2005;45:1840
16. Neurally mediated reflex syncopal syndromes
Vasovagal (common) faint
Carotid sinus syndrome
Situational faint
Acute hemorrhage
Cough, sneeze
Gastrointestinal stimulation (swallow, defecation,
visceral pain)
Micturition (postmicturition)
Postexercise
Other (e.g. brass instrument playing, weightlifting,
postprandial)
Glossopharyngeal and trigeminal neuralgia
Orthostatic
Primary autonomic failure syndromes (e.g. pure
autonomic failure, multiple system atrophy,
Parkinson’s disease with autonomic failure)
Secondary autonomic failure syndromes (e.g.
diabetic neuropathy, amyloid neuropathy)
Volume depletion
Hemorrhage, diarrhea, Addison’s disease
Cardiac arrhythmias as primary cause
Sinus node dysfunction (including
bradycardia/tachycardia syndrome)
AV conduction system disease
Paroxysmal supraventricular and ventricular
tachycardias
Inherited syndromes (e.g. long QT syndrome,
Brugada syndrome, short QT, arrhythmogenic
dysplasia)
Implanted device (pacemaker, ICD) malfunction
Drug-induced proarrhythmias
Structural cardiac or cardiopulmonary disease
Cardiac valvular disease
Acute myocardial infarction/ischemia
Obstructive cardiomyopathy
Atrial myxoma
Acute aortic dissection
Pericardial disease/tamponade
Pulmonary embolus/pulmonary hypertension
Cerebrovascular
Vascular steal syndromes
Causes of Syncope
17. Classification of Syncope
Common and benign
Orthostatic
Neurocardiogenic
Common and not so benign
Sinus node dysfunction, carotid sinus hypersensitivity
Paroxysmal AV block
Less common, lethal
Ventricular tachycardia, ventricular fibrillation
Torsade de pointes
Everything else
18. Emergency Visits with Syncope
European Society of Cardiology Guidelines
Cause Number Percent
Neurally mediated 309 66
Orthostatic
Hypotension
46 10
Cardiac Arrhythmias 53 11
Cardiovascular 21 5
Unknown 11 2
Non-syncopal attack 25 5
Brignole M, et al. European Heart Journal 2006;27:76-82
465 patients
20. Reflex Mechanism - Bezold Jarisch
Chang-Sing P. Cardiol Clinics. 1991;9(4):641-651
Inotropy
Contractility
Venous return
Trigger
BP
Sympathetic
tone
Arterial
tone
BP
HR
Vasodilation
BP
Syncope
Vagal
efferent
Small ventricle
Vagal
afferent
Sympathetic
withdrawal
Wall stretch
Reflex
C-fibers
21. When is History and Physical Sufficient
• Young patient with single presentation or clear
situational dependency
• Normal physical examination
• Normal ECG
• No significant injury
• Low risk occupation
22. What about the rest of the patients?
History & physical exam including CSM
ECG
Tilt table test
Echocardiogram
Electrophysiology study
Holter monitor / Event recorder / Implantable Loop
Recorder (ILR)
Neurological evaluation
Psychiatric evaluation
23. Role of history in differentiating NMS from
cardiac syncope
Warm Place Abdominal Discomfort Weakness
Feeling warm
Awareness about to
faint
Yawning
Syncope while
standing
Nausea Feeling tired
Standing in one place Vomiting Feeling cold
Lightheadedness Prodrome History > 4 yrs
341 patients
Alboni P, et al: J Am Coll Cardiol 2001;37:1921-28
24. Abdominal Discomfort
Standing in one place Feeling cold
History > 4 yrs
341 patients
Alboni P, et al: J Am Coll Cardiol 2001;37:1921-28
Role of history in differentiating NMS from
cardiac syncope
25. Warm Place Abdominal Discomfort Weakness
Feeling warm
Awareness about to
faint
Yawning
Syncope while
standing
Nausea Feeling tired
Standing in one place Vomiting Feeling cold
Lightheadedness Prodrome History > 4 yrs
191 patients with cardiac disease
Alboni P, et al: J Am Coll Cardiol 2001;37:1921-28
Role of history in differentiating NMS from
cardiac syncope
26. History > 4 yrs
191 patients with cardiac disease
Alboni P, et al: J Am Coll Cardiol 2001;37:1921-28
Role of history in differentiating NMS from
cardiac syncope
27. Case 2
53 year-old obese gentleman with diabetes, hypertension and
hyperlipidemia who presented with syncope. This occurred
after working at the boat yard on a very hot day. He was taking
a break and drinking a cold slurpee, when he suddenly felt pins
and needles in his neck, peri-oral numbness, and tingling of his
forehead. As he was calling for wife, he lost consciousness and
fell to the ground. According to his wife, he was unconscious
for about a minute and his entire body was quivering. Upon
regaining consciousness, he was confused and disoriented.
His wife reports that he was cold, clammy, and very
diaphoretic. He sustained some minor bruising of left shoulder
but no head injuries.
29. Functional
Vagal tone
Medications
Structural
AV nodal or His Purkinje fibrosis
Mitral annular calcification
Infiltrative
Genetic
Prolonged PR / heart blocks
Short PR
Bundle branch blocks
Long QT
Short QT
ECG – Abnormal conduction
AV node His
Intra-cardiac recording
AH HV
PR interval
30. What about the rest of the patients?
History & physical exam including CSM
ECG
Tilt table test
Echocardiogram
Electrophysiology study
Holter monitor / Event recorder / Implantable Loop
Recorder (ILR)
Neurological evaluation
Psychiatric evaluation
32. Tilt Table Response consistent with NMS
Sra JS. Ann Intern Med. 1991;114:1013-1019.
Pretest 1 min 12.5 min Recovery
ECG
Blood
Pressure
(mmHg)
Tilt 0 70 70 0
HR (BPM) 77 94 40 46
BP (mmHg) 115/70 125/80 55/30 98/55
Syncope
33. Echocardiogram
• Strongly consider for all patients
• Screen for hypertrophic cardiomyopathy
• Stratification for EP study
Ejection fraction < 30% - meet criteria for ICD
35-50% - test for inducibility of VT
34. Electrophysiology Study
• Risk stratification of ventricular arrhythmias – assess
for inducibility
• It is poor at diagnosing bradycardic arrhythmias
• It is highly sensitive for tachycardias.
35. Holter Monitor
Yield: Arrhythmia with symptoms = 2%
Symtoms without arrhythmia = 15%
Gibson TC et al Am J Cardiol 1984;53:1013-17
36. Comparison of Loop Recorders versus
Holter Monitor (COLAPS)
Sivakumaran S, et al. Am J Med 2003;115:1-5
38. Implantable Loop Recorders (ILR)
ILR
Patient
Assist Device
Automatically detects
bradycardia
tachycardia
asystole
Records rhythm at
time of trigger
45. A. Syncope resulting in injury
B. Syncope during exercise
C. Syncope in the supine position
D. Suspected or known structural heart disease
E. ECG abnormality
Pre-excitation (WPW)
Long QT
Bundle-branch block
HR<50 bpm or pauses > 3 seconds
Mobitz I or more advanced heart block
Documented tachyarrhythmia
Myocardial infarction
F. Family history of sudden death
G. Frequent episodes (>2 per year)
H. Implanted pacemaker or defibrillator
I. High risk occupation (bus driver, pilot etc.)
Syncope – red flags
46. Case 1 - review
Discharged after 24 observation with diagnosis of “Vaso-vagal syncope”
2 days later…
Witnessed collapse while seated.
Episode of syncope with complete heart block noted on telemetry.
Dual chamber pacemaker implanted.
Discharged home the next day.
47. Case 1
Suspected or known structural heart disease - prior MI
Abnormal EKG – trifasicular block
Family history of sudden death – brother died at 45
Frequent episodes – “pirouette” 2 weeks prior
48. Case 2 - review
Discharged after 24 observation with diagnosis of “Vaso-vagal syncope”
3 month later..
Cardiac arrest at home and successfully defibrillated but prolonged down
time.
Had slow neurologic recovery.
ICD implanted for secondary prevention.
50. Which of the following historical findings are useful for
predicting neurally-mediated syncope in patients with heart
disease and recurrent syncope?
a. Feeling warm.
b. Awareness of being about to faint.
c. Recovery duration lasting longer than 60 minutes.
d. Confusion during recovery.
e. Time (years) between first and last syncopal
episodes.
Test questions
51. Which of the following historical findings are useful for
predicting neurally-mediated syncope in patients with heart
disease and recurrent syncope?
a. Feeling warm.
b. Awareness of being about to faint.
c. Recovery duration lasting longer than 60 minutes.
d. Confusion during recovery.
e. Time (years) between first and last syncopal
episodes.
52. An 80 year-old frail woman presents to you after falling while
ambulating to the bathroom at night. This is the second time
she has fallen in the last month. Echocardiogram shows
diastolic dysfunction and moderate mitral annular
calcification. ECG is essentially normal with exception of
first degree AV block. After her first fall one month ago, she
was told by her physician that she needs to use a cane and
to rise slowly out of bed. Her daughter is very concerned
and wants a second opinion. You recommend which of the
following:
a. Discontinuing evening dose of Lasix.
b. Tilt-table study to diagnosis the etiology of
falls and reassure her daughter.
c. Electrophysiologic test to assess for
bradyarrhythmias.
d. Continuous-loop event monitoring.
53. An 80 year-old frail woman presents to you after falling while
ambulating to the bathroom at night. This is the second time
she has fallen in the last month. Echocardiogram shows
diastolic dysfunction and moderate mitral annular
calcification. ECG is essentially normal with exception of
first degree AV block. After her first fall one month ago, she
was told by her physician that she needs to use a cane and
to rise slowly out of bed. Her daughter is very concerned
and wants a second opinion. You recommend which of the
following:
a. Discontinuing evening dose of Lasix.
b. Tilt-table study to diagnosis the etiology of
falls and reassure her daughter.
c. Electrophysiologic test to assess for
bradyarrhythmias.
d. Continuous-loop event monitoring.
54. A 16 year-old girl presents to you after a syncopal event
while playing field hockey on an unusually hot day. She
was running when she developed profound lightheadedness
just prior to losing consciousness. Upon regaining
consciousness, she was diaphoretic and confused to
surroundings. She felt nauseated for the rest of the day.
She has no cardiac history and her exam is unremarkable
except for mild orthostasis. Her EKG is normal. You
recommend which of the following:
a. Genetic testing for long QT channelopathy.
b. Continuous-loop event monitoring.
c. Increasing fluid intake and reassure parents.
d. Refer to electrophysiology.
e. Tilt-table study.
55. A 16 year-old girl presents to you after a syncopal event
while playing field hockey on an unusually hot day. She
was running when she developed profound lightheadedness
just prior to losing consciousness. Upon regaining
consciousness, she was diaphoretic and confused to
surroundings. She felt nauseated for the rest of the day.
She has no cardiac history and her exam is unremarkable
except for mild orthostasis. Her EKG is normal. You
recommend which of the following:
a. Genetic testing for long QT channelopathy.
b. Continuous-loop event monitoring.
c. Increasing fluid intake and reassure parents.
d. Refer to electrophysiology.
e. Tilt-table study.
Editor's Notes
Physiologic response to a wide variety of medical conditions ranging from benign to lethal. By definition it is a transient condition - underlying trigger and physiology not always present. Occurs with unpredictable and random pattern. Difficult to establish definitive “diagnosis”. Emphasis is on diagnosis rather than treatment
Many of our patients present after falling; particularly the elderly population. For example patient # 1 who reported that she had tripped over a plastic bag. If fact this patient was adament about not passing out or losing consciousness. Perry and colleagues evaluated 34 patients with carotid sinus syndrome. They were divided in 2 groups those that had falls and those that had syncope. Loss of consciousness was induced with carotid sinus massage. Patient with history of falls were more likely to have amnesia for loc that those that present with syncope. This is particular important to keep in mind particularly when we are evaulating the elderly patient with frequent so call falls that are truly syncopal events.
There are numerous etiologies of syncope. I have enumerated a few of the more common ones here. Certainly, it would be difficult to rule out every single etiology every time we evaluate a patient. I prefer to classify them all under two groups.
Another way to classify cardiac etiologies is shown here. One can group them as common and benign. Common and not so benign. Less common and potentially lethal. Remember people with syncope and lethal etiology have had an aborted sudden death. It is critical that we identify those patients and treat them prior to a subsequent event that they may not survive. And then finally there is everything else.
A more recent study in 2006, Brignole and colleagues performed a prospective systematic evaluation on 465 patients presenting to the emergency room of 11 general hospitals. Decision, making was based-on strict guideline-based diagnostic pathway. Unlike older studies a definative diagnosis was established in 98% leaving only 2% undiagnosed. Neuro-mediated accounted for 66%, cardiac etiologies accounted for about 16 %. In this group of 465 patients, 50% were diagnosed with just history, physical examination, and ECG alone. No further diagnostic testing was required. I will discuss diagnostic yield of various tests later.
I am now going to discuss a little about neuro-mediated syncope. This can be subdivided into Reflex syncope: Vasovagal, Carotid sinus,Situational (micturition, defecation, swallow, visceral pain etc),Post-exercise,Glossopharyngeal and trigeminal neuralgia. Orthostatic syncope , Primary autonomic failure , Secondary autonomic failure , Volume depletion (hemorrhage, diarrhea etc), Drugs and alcohol
The reflex mechanism is fairly well elucidated. A trigger such as prolonged upright posture results decreased venous return and reduced intracardiac volume. The resultant arterial hypotension is sensed in the carotid sinus baroreceptors and efferent fibers from these receptors trigger autonomic signals that increase cardiac rate and contractility by increasing sympathetic tone and decreasing vagal tone. Arterial tension is also increased. The combined effect is a rise in blood pressure. This is a physiologic and normal response. However, in some patients a hypersensitive reflex mechanism mediated by C-fibers results in syncope. Pressure receptors (C-fibers) in the inferoposterior wall of the underfilled left ventricle may then sense increased wall stress leading increase vagal afferent stimuli and consequently a sudden withdrawl of sympathetic tone. This leads to a paradoxical bradycardia, decreased contractility and vaso-dilitation. The result is sudden hypotension and syncope.
When is history and physical sufficient? Young patient with single presentation or clear situational dependency, with a normal physical examination, ECG and without significant injury. Particularly if they have a low risk occupation
What do we do about the other 40 or so percent of patients that do not have neurally-mediated syncope. We have a number of diagnostic tools that we can use. The history and physical exam is important but some studies suggest that we should be cautious in over relying on historical findings.
Alboni and colleagues enrolled 341 patients with syncope and evaluated the diagnostic value of various historical findings. Each patient answered a standard questionaire with 46 possible findings. Only 15 are shown here. Of these 46 only 4 were helpful in differentiating NMS from cardiac etiology.
But among patients with cardiac disease only history of recurrent syncope > 4 years was sufficient for differentiating NMS from cardiac etiology.
Recall our second case. The admitting physician did a fantastic job in describing the patients symptoms. I have highlighted them here. It sure sounded like a vaso-vagal event. But remember the patient has significant cardiac risk factors and possible history of MI. We can not rely on these historical findings to make our diagnosis.
In the work of syncope it is important to assess for conduction abnormalities including prolonged PR and heart block. Prolongation of PR interval can be function due to vagal tone or medication or structure due to fibrosis of the AV node or HIS purkinje network, It may also be due to mitral annular calcification, infitrative processes, or genetic. Determining the location of conduction system disease is important. During the PR interval not only are the atrium depolarized but also the AV node and His Purkinje network. The PR contains the time it takes for depolarization of the AV node (the AH interval) and the time it takes to depolarize the HIS purkinje network (HV interval). We can measure these at the time on a EP study by placing a multipolar recording catheter adjacent to HIS. With 1st degree AV block and 2nd degree type I delay is usually occurring in the AV node and therefore prolongation of the AH interval is usually observed. This function block thus is generally considered to be benign. This is not always the case and certainly 1st degree AV block can be due to delay in the HV interval (i.e His Purkinje network). This is more typical of long PR interval like the 380 msec in our 1st patient (Only so much delayed conduction can occur in the AV node). With 2nd degree type II and III degree heart block the conduction abnormality is typically within the HIS purkinje network and we observe a prolongation of the HV interval. This type of heart block is more pathologic and usually requires a pacemaker. PR interval can be too short. Short PR syndomes with norrmal or prolonged QRS duration for instance WPW. These typically manifest as tachycardias but can result in sudden death or in the case of syncope aborted sudden death. Bundle branch blocks is indicative of long QT and short QT syndromes. While I am highlighting conduction abnormalities, it is equally important to assess for myocardial injury, pulmonary embolism etc.
What do we do about the other 40 or so percent of patients that do not have neurally-mediated syncope. We have a number of diagnostic tools that we can use. The history and physical exam is important but some studies suggest that we should be cautious in over relying on historical findings.
In patients with intermediate pre-test suspicion for neuro-mediated syncope, provocative testing may be helpful. The protocol is to tilt patients at 70 degree for 15-45 minutes. Normal individual compensate for such tilt by increasing both alpha and beta adrenergic tone as a result of baroreceptor stimulation and thus compensate for decrease in venous return. In susceptible patients compensatory mechanism eventually collapse. A sudden withdrawal of sympathetic tone results in syncope. Thus, positive tilt table study identifies a patient who is prone to vasodepressor syncope. Of note: tilt table testing has been reported to be positive in about 7% of normal individuals without syncope and If left suspended long enough eventually everyone would pass out.
Here is an example data set from a tilt table test in a patient with NMS. The pre-test vitals are normal. The patient raised from a supine position to 70 degrees. After minute the heart rate is slightly elevated and blood pressure has increase somewhat. This is normal. But after 12.5 minutes there is an abrupt withdrawal of sympathetic activity and increased vagal efferent stimulation resulting in bradycardia HR 40 and hypotension due to vasodilation. Syncope occurs. The patient is then immediately brought to a supine position and recovered.
Especially those over 35 years old, any patient with abnormal ECG or physical exam or positive family history
When do we perform an electrophysiology study. It is helpful for risk stratification of ventricular arrhythmias – assess for inducibility . Invasive testing is poor at diagnosing bradicardic arrhythmias; therefore, monitoring devices are preferred. It is highly sensitive for tachycardias.
What about Holter monitor. Gibson enrolled 1512 patients with syncope. 24 hour holter monitor was performed. During 24 hour monitoring only 15 patients had syncope and 7 were related to arrhythmia. 241 patients had pre-syncope and 24 patients were found to have an arrhythmia. Thus Holter monitoring rarely results in identifying relevant syncope related arrhythmias. Obvious on of the limitations of holter monitoring is frequency of syncopal spells. I rarely order a holter on someone with syncope.
Prospective Randomized Comparison of Loop Recorders versus Holter Monitor in patients with syncope or syncope. (COLAPS) Enrolled 100 patients with syncope and randomized to 48 hour Holter or 30 day loop recorded. The 30 day event recoder because eof the longer monitoring period had a higher diagnostic yield. But loop recorders were limit be inabiliity to activate them appropriately.
Here is an event recording in a patient with and event recorder. With the spontaneous termination of flutter, the patient had a prolonged sinus node recovery time resulting in syncope. A pacemaker was recommended.
Syncopal events are often too infrequent and unpredictable for detection by conventional ambulatroy monitoring. Therefore, we use an implantable loop recorder or monitor. This is a wireless device that is implanted under the skin similar to pacemaker. Continuous loop monitoring for about 3 years. Events may be automatically triggered or patient triggered.
Leads to more implants of PPM and ICDs
Pool data from 9 studies to a total of 506 patients. Correlation between syncope and underlying rhythm was found in 35% of patients for a diagnostic yield of 35%. Of these 56% had asystole of bradycardia 11% had tachycardia and 33% had no-arrhythmia. Diagnostic yield was hampered in 5-9% of patients due to failure of syncope relapse.
Instead I prefer to identify high-risk features suggest cardiac etiology. Patients with the following characteristics should be admitted to Telemetry for evaluation and EP consult should be obtained. Mass law prohibits operating a motor vehicle for six months after a syncopal episode unless the cause is definitively reversed.
