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Case #1
42 year old female Chief complaint: passing out at work Works in a pharmaceutical lab. Was sitting at her desk, felt nauseated and knew she was going to pass out. Per witnesses, was slump over chair and was unconscious for a few seconds.
Case continues
No chest pain, palpitations, shortness of breath Similar episodes 10 years ago. No family history of sudden cardiac death No medications. No smoking. No alcohol. No drugs.
Case #2
82 year old male. Found unresponsive by his son Past medical historyHTN MedicationsHCTZ ExamBP 160/98. P 70. Now alert and oriented. Facial contusions. Otherwise normal exam.
Syncope: Definition
Abrupt and self-limited loss of consciousness associated with absence of postural tone Relatively rapid onset. Variable warning symptoms. Followed by rapid and complete recovery. Last only a few minutes. Absence of prolonged confusion Presyncope---prodromal symptom of fainting and typically has the same work up as syncope.
Significance of Syncope
The only difference between syncope and sudden death is that in one you wake up. [1] --anonomymous
Syncope: Epidemiology
20-50% of adults experience at least one episode of syncope during their lifetime.
Explained 53-62% Infrequent, unexplained 38-47%
500,000 new syncope patients each year. 3-5% of ER visits. 6% of hospital visits. More common in the elderly.
Up to 23% in age >70 years.
Causes of Syncope
Syncope in Children
Generally a benign event. Most common causes
Vasovagal (40%) Simple faint (29%) Breathholding (4%) Unknown (15%)
Syncope: Pathophysiology
Decreased cerebral perfusion is common to all causes of syncope Cessation of cerebral perfusion for as little as 3-5 seconds can result in syncope Decreased cerebral perfusion may occur as a result of decreased cardiac output or decreased systemic vascular resistance.
More Pathophysiology
Bilateral hemisphere dysfunction or reticular activating system (RAS) midbrain knockout. Generally acute hypoperfusion is responsible.
Regional (vasoconstriction) Systemic (global hypotension)
Loss of consciousness causes loss of postural tone leading to collapse 35% reduction in cerebral blood flow will cause syncope. Modifying factors
Cardiac output Systemic and local vascular resistance/occlusion Blood volume Ability to compensate
Syncope: Etiology
Mnemonic: PASSOUT P-ressue (hypotensive causes) A-rrthymias S-eizures S-ugar (hypo/hyper glycemia) O-utput (cardiac)/ O2 (hypoxia) U-nusual causes T-ransient (TIAs, strokes, CNS diseases)
More specifics
OUTPUT
Cardiac
AS, PA, MS,IHSS Cardiomyopathies Atrial myoxomas Cardiac tamponade Aortic dissection MI, CHF PE, acute hypoxemia Pulmonary HTN COPD exacerbation CO poisoning
UNUSUAL CAUSES
Anxiety, Panic disorder Major depressive disorder Somatization disorder (psychogenic syncope) Hyperventilation syndrome Migraine, sleep disorder
Pulmonary
TRANSIENT
TIA (vertebrobasilar), CVA, subdural hematoma Subarachnoid hemorrhage CNS mass effect (tumor) Basilar artery migraine.
Syncope
CAUSES (Head---Heart---Vessels)
Reflex mediated
Vasovagal, carotid sinus, situational
Cardiac
Mechanical , arrhythmias
Orthostatic
Drugs, autonomic failure
--what happens?
Stress causes an abnormal autonomic reflex Normal increased sympathetic tone replaced by increased vagal tone Variable contribution of vasodilation and bradycardia. Examples include syncope from: Pain and/or fear Carotid sinus hypersensitivity situational (cough, micturition, defecation syncope)
Vasovagal syncope
Most common cause of syncope in young adults Precipitating event is often identifiable
Stress, trauma, pain, sight of blood, prolonged standing, heat exposure
Vasovagal Syncope
3 PHASES --Prodrome
Diaphoresis, epigastric discomfort, weakness, nausea, dizziness Lasts about 2 minutes
--Loss of consciousness
Usually lasts 5-20 seconds
--Postsyncopal phase
Nausea, dizziness, general sense of poor health If present, confusion which lasts no more than 30 seconds
Drug therapies
Pacing (DDD pacing)
Class II indication if positive tilt test and cardioinhibitory or mixed reflex
Disopyramide SSRIs
1 controlled study Use if hx of depression
Beta-adrenergic blockers
1 positive control study using atenolol Use if hx of htn
Outcome
3 sec asystole and/or 50mmHg fall in systolic blood pressure with reproduction of symptoms ==CAROTID SINUS SYNDROME
Method
Massage, not occlusion. Right followed by left, pause between Duration:5-10 seconds Posture: supine and erect
Contraindications
Carotid bruit, known but significant carotid arterial disease, previous CVA, MI last 3 months.
Risks
1/5000 massages complicated by TIA
Situational Syncope
Related to micturition, defecation, swallowing or coughing Induced by baroreceptor and mechanoreceptors causing vagal stimulation Circumstances of the event are typically diagnostic
Orthostatic syncope
When vertical, blood follows gravity and pools. Increased sympathetic tone counteracts this. If the response is inadequate, syncope occurs. Drop in BP: 20 systolic or 10 diastolic within 3 minutes of standing Present in 40% of patients over 70 years old May be due to
Drugs Volume loss Neurologic damage
Medications
Seen in elderly 45% of time
Situational
Micturition, cough, postprandial, carotid sinus sensitivity, defecation, laughing
Adrenal insufficiency
Cardiac Syncope
Two basic types
Dysrhythmia mediated Structural cardiopulmonary lesions
Both cause the heart to be unable to sufficiently increase cardiac output to meet demand
Double the risk of mortality compared with other syncopal patients. Up to 50% mortality. Patients with underlying cardiac disease are at greatest risk for cardiac syncope. Only 3% have no previous heart disease. Cardiac arrythymias especially in the elderly have high mortality.
Neurologic Syncope
Rarely the primary cause of syncope Ischemia to the RAS in the brainstem may cause drop attacks
Results from Vertebrobasilar insufficiency due to TIA (sometimes basilar migraine) Usually accompanied by vertigo, ataxia, dysarthia, diplopia
Other examples
Subclavian stealoccurs with arm activity. Systolic BP in arms (difference of 10mmHg) Subarachnoid hemorrhage
Psychiatric causes
Most commonly associated with
Anxiety Panic Major depressive disorders
Syncope-like States
Migraine Acute hypoxia Hyperventilation Somatization disorder (psychogenic syncope) Acute intoxication (ie alcohol) Seizures Hypoglycemia Sleep disorders
An Approach to Syncope
History Physical Exam EKG
Neurological Evaluation
ENT Evaluation
Cardiovascular Evaluation
Endocrine Evaluation
Psychological Evaluation
HISTORY
RAPID ASSESSMENT
Identify Life-Threatening causes
Dysrhythmias cardiac ischemia Critical aortic stenosis Aortic dissection Pulmonary embolus CVA SAH Toxic-metabolic derangement
HISTORY
HISTORY alone identifies the cause up to 85% of the time POINTS
Previous episodes Character of the events, witnesses Events preceding the syncope Events during and after the episode
HISTORY
Events preceding the syncope
Prolonged standing (vasovagal) Immediately upon standing (orthostatic) With exertion (cardiac) Sudden without warning or palpitations (cardiac) Aggressive dieting Heat exposure Emotional stress
HISTORY
Associated symptoms
Chest pain, SOB, lightheadedness, incontinence
Medications
Antihypertensives, diuretics (orthostatic) Antiarrthymics (cardiac syncope) TCA, Amiodarone (cardiac/prolonged QT)
Family history
Sudden death (cardiac syncope/prolonged QT or Brugada)
PHYSICAL EXAM
Vital signs
Orthostaticsmost important
Drop in BP and fixed HR >dysautonomia Drop in BP and increase HR -> volume depletion/ vasodilatation Insignificant drop in BP and marked increase in HR -> POTS
Heart rate
Tachy/brady, dysrhythmia
Respiratory rate
Tachypnea (pe, hypoxia, anxiety) Bradypnea (cns, toxicmetabolic)
Blood pressure
High (cns, toxic/metabolic) Low (hypovolemia, cardiogenic shock, sepsis)
Temperature
Hypo/hyperthermia (sepsis, toxic-metabolic, exposure)
PHYSICAL EXAM
HEENT
Tenderness/deformity (trauma) Papilledema (increased icp, head injury) Breath (alcohol, dka)
HEART
Murmur (valves, dissection) Rub (pericarditis, tamponade)
NECK
Bruits JVD (chf, mi, pe, tampnade)
LUNGS
Sounds may help distinguish chf, infection, pneumothorax
PHYSICAL EXAM
ABDOMEN
Pulsatile mass; AAA Tenderness Occult blood loss
SKIN
Signs of trauma, hypoperfusion
PELVIS
Bleeding, hypovolemia Tenderness (PID, ectopic, torsion, sepsis)
EXTREMITES
Paralysis (CNS) Pulses unequal (dissection, embolus, steal)
PHYSICAL EXAM
NEUROLOGIC
Mental status; toxic metabolic; organic disease; seizure; hypoxia. Focal findings (hemorrhagic/ischemic stroke, trauma, tumor, or other primary neurologic disease
Seizure or Not?
SEIZURE
Frothing at mouth Tongue biting Disorientation/ postictal Age < 45 year LOC over 5 minutes
*tongue biting found only in seizure
(99% specificity); absence did not exclude the possibility of a seizure (24% sensitivity)
NOT A SEIZURE
Sweating prior to episode Nausea prior to episode Oriented after event Age > 45 years
Ancillary Studies
EKG---Cornerstone of workup
Arrhythmia, long qt, WPW, conduction abn.
Routine Blood worklimited value Radiology---limited value except if abnormal exam Other testsdepending of history and exam
Glucose Ua/culture --hemoglobin --troponin --CK (syncope vs seizure)
Normal EKG
If Normal EKG:
Check orthostatics Check hemoglobin
If low---Anemia If normal or high--Volume loss, dehydration, drug induced
Neurologic
CT head (tia, cva, sah) EEG (if suspect Sz)
Cardiovascular
If Outflow obstruction, check CT chest, Echo (PE, valvular, HOCM) If venous return, check HCG, Echo (pregnancy, tamponade)
Metabolic
Check chemistry. R/O hypoglycemia, adrenal insufficiency
The EKG
patient older, +comorbid signs/symptoms If Abnormal EKG
Ischemia/injury Dysrhythmia
Sinus brady, BBB, AV block, prolonged QT, WPW, HOCM, Brugada
If Normal EKG
Consider holter or event recorder if dysrhythmia suspected
sinus bradycardia
ventricular tachycardia
3 or more beats
WPW
Prolonged QT interval
Other: sinus pause> 2 sec, SVT, afib, 2nd or 3rd AV block, PM malfunction
Echocardiogram EPS
< 30 days
Positive
Negative
Treat
Holter Monitoring
24-48 hour monitorlimited value because of intermittent nature of arrhythmias Event recordermore helpful. Patient must be conscious in order to activate unit. Establishes diagnosis in only 2-3% of patients with syncope if EKG is normal. Indicated in patients at highest risk for arrhythmia ie, abnormal ekg, palpitations, cad history, syncope when supine or with exertion, +FH
Holter results--summary
PACs and PVCs
Usually not significant Exception: ie 3 consecutive 3 PVCs at 100 bpm
ECHOCARDIOGRAM
Access structural causes of cardiac syncope
AS, MS, HOCM, atrial myoxoma
Unlikely to be helpful in the absence of known cardiac disease or an abnormal ekg. INDICATIONS
Abnormal EKG Murmur ---history of heart disease ---exercise assoc. syncope
EPSIntracardiac EPS
Rarely indicated in patients with structurally normal hearts and normal ekg. Diagnostic yield greatest in patients with known heart disease but nondiagnostic ekg monitoring.
Heart disease-------5080% No heart disease---1850%
Difficult to correlate spontaneous events and laboratory findings Ineffective for assessing bradyarrhythmias Often must settle for an attributable cause
Abnormal finding on EPS does not guarantee that this was what caused the patients syncope. EPS is abnormal in 1868% of patients with syncope of unknown cause.
NEUROLOGIC TESTING
Tend to be overused Includes EEG, CT head, MRI head, Carotid dopplers In contrast, Cardiovascular tests are underused. INDICATION
Only if history and physical exam suggests a neurologic cause or testing for other causes is complete.
EEG
Not a first line of testing To differentiate syncope from seizure Abnormal EEG in the interval between two attacks -> Epilepsy Normal EEG -> does not tell us anything
11
49 11-87 (syncope pt +TTT 24-75%) 2 20 65-88 0-4
Ambulatory EKG
holter loop recorder 2-3wks implantable LR upto 14mo Neurological (ct, carotid)
When to Admit
Consider admitting if age greater than 40 years Discharge if benign etiology
Vasovagal, micturition, psychogenic syncope
Admit if
Suspected or known significant heart disease ie cardiac ischemia, CHF, structural heart ds or +family hx of SCD EKG suggestive of arrhythmia or syncope during exercise Stroke Syncope causing severe injury Severe orthostatic hypotension ACEP guidelines
Clinical Risk Score for Predicting 1 year Mortality in Patients with Syncope
Risk Factors
Abnormal ekg Age >45 years History of CHF History of ventricular arrhythmia
2
3/4
16
27/80
Stratified in low (0), intermediate (1-2) and High (>2) risk groups. CHF was not associated with increased risk Even low risk group2.5% risk Needs validation Annals Emerg Med 2009.
Case #1 Continues
Physical exam: Normal Orthostatics: Normal EKG: Normal Labs: no anemia. Glucose normal. ECHO: Normal Tilt Table Test: after 7 minutes of 70 degrees upright, HR 36, BP 51/41, LOC. Regained consciousness with supine position.
Case #1 Conclusion
DIAGNOSIS----Vasovagal Syncope TREATMENT---Florinef, Ted hose, Fluids OUTCOME---No reoccurence of symptoms when followed up at 3 months, 6 months, and 1 year later.
Case #2 Continues
Emergency Room workupnegative. Electrolytes, CBC normal. EKG showed NSR with occasional PVCs. Decision made to ADMIT. 2 hours later---Nonsustained Vtach. EP studyInducible Vtach. Automated internal defibrillator placed. Cardiac cath---diffuse coronary artery disease.
SUMMARY
Syncope is a transient loss of consciousness due to decreased cerebral blood flow. Most common causes: vasovagal, cardiac (cardiac arrhythmia), and orthostatic hypotension. Seizures are rare. Patients with cardiac syncope are at increased risk of death. History and Physical exam are the MOST important to identify the cause Orthostatic BPs should be done on all pts.
SUMMARY
Shotgun approach is Not helpful. EKG should be considered in all patients. Tilt table test can diagnosis vasovagal syncope. Neurologic testing is low yield and often overused. Holter monitoring, Echo, EST, EP considered in patients at high risk for cardiac syncope. Patients remain undiagnosed in 34% of cases.
REFERENCES
Engel. Ann Internal Med. 1978. 89; 403412 Kapor, W. Medicine. 1990. 69; 160-175. Krahn. Cardiology Clinic. 1997 ACEP Clinical Policy on Syncope. Ann Emerg Med. 2009. Mayo Clinic Proceedings. Nov 2008.