syncope dr yate
TRANSCRIPT
Approach to SYNCOPE
Dr yatendra singh
Syncope is defined as transient loss of consciousness due to reduced cerebral blood flow.
Syncope is associated with postural collapse and spontaneous recovery.
It may preceded by faintness or presyncope
This may include lightheadedness,dizziness without true vertigo, a feeling of warmth,diaphoresis, nausea and or visual blurring
Syncope(SING-kə-pee) is a transient, self-limited loss of consciousness with loss of postural tone due to acute global impairment of cerebral blood flow.
The onset is rapid, duration brief, and recovery spontaneous and complete without medical or surgical intervention.
Other causes of transient loss of consciousness need to be distinguished from syncope.
These include seizures, vertebrobasilar ischemia (vertigo), hypoxemia, and hypoglycemia.
The differentiation of syncope from seizure is an important, sometimes difficult, diagnostic problem.
Syncope may be benign when it occurs as a result of normal cardiovascular reflex effects on heart rate and vascular tone or
Serious when due to life threatening arrythmias.
May be single episode or recurrent
Syncope: Etiology
OrthostaticCardiac
Arrhythmia
StructuralCardio-
Pulmonary
1• VVS• CSS• Situational
CoughPost- Micturition
2• Drug-Induced• ANS FailurePrimarySecondary
3• Brady
SN Dysfunction
AV Block
• TachyVTSVT
• Long QT Syndrome
4 • Acute
Myocardial Ischemia
• Aortic Stenosis
• HCM• Pulmonary
Hypertension• Aortic
Dissection
Neurally-Mediated
Unexplained Causes = Approximately 1/3
Etiologies of Syncope
Neurocardiogenic / VasovagalMost Common
• Pain/Noxious Stimuli• Situational (micturation, cough,
defecation)• Carotid Sinus Hypersensitivity
(CSH)• Fear• Prolonged standing / heat
exposure
CardiovascularMost Dangerous
• Arrhythmia – Tachy or Brady• Valve Stenosis (outflow
obstruction)• HOCM (outflow obstruction)
Orthostatic Hypotension“ D A A D “
• Drugs: BP meds, Diuretics, TCAs• Autonomic Insufficiency
(Parkinsons, Shy-Dragger, DM, Adrenal Insufficiency)
• Alcohol• Dehydration
Neuro / Functional / Psychiatric - <5%
• Psuedosyncope• TIA or Vertibro-basilar Insufficiency
Pathophysiology
As blood pools in peripheral vessels and arterial blood pressure begins to fall, compensatory mechanisms are activated that attempt to maintain adequate cerebral blood flow.
These mechanisms include baroreceptors, which reflexely constrict peripheral blood vessels, increasing the return of venous blood to the heart, and the carotid and the aortic arch reflexes, which increases the heart rate.
These mechanisms work to increase the cardiac output and the maintenance of a close to normal blood pressure, all of which are seen during early presyncopal period
If the situation goes unmanaged these compensatory mechanisms fatigue, which is manifested through development of reflex bradycardia. ( cardioinhibitory component and vasodepressor component )
Slowing of the heart rate to less than 50 beats/min is common & leads to a significant drop of cardiac output which is precipitous fall in blood pressure to levels below the critical for maintenance of consciousness.
In such cases, cerebral ischemia results and the individual loses consciousness
Neurally Mediated (Reflex )Syncope--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)
Neurally Mediated Syncope
Dizziness, lightheadedness, and fatigue, premonitory features of autonomic activation may be present
These include diaphoresis, pallor, palpitations, nausea, hyperventilation, and yawning.
Features of Neurally Mediated Syncope
During the event proximal and distal myoclonus (typically arrhythmic and multifocal) may occur, raising the possibility of epilepsy.
The eyes typically remain open and usually deviate upward. Urinary but not fecal incontinence may occur.
Reassurance Avoidance of provocative stimuli Plasma volume expansion with fluid and
salt are the cornerstones of the management of neurally mediated syncope.
Treatment: Neurally Mediated Syncope
Isometric counterpressure maneuvers of the limbs (leg crossing or handgrip and arm tensing).
Fludrocortisone, vasoconstricting agents, and beta-adrenoreceptor antagonists are widely used by experts to treat .
Orthostatic hypotension, defined as a reduction in systolic blood pressure of at least 20 mmHg or diastolic blood pressure of at least 10 mmHg within 3 minutes of standing or head-up tilt on a tilt table.
Orthostatic Hypotension
It is a manifestation of sympathetic vasoconstrictor (autonomic) failure .
light-headedness, dizziness, and presyncope (near-faintness)
Visual blurring may occur, likely due to retinal or occipital lobe ischemia.
Patients may report orthostatic dyspnea
Features
Neck pain—typically in the suboccipital, posterior cervical, and shoulder region (the "coat-hanger headache") most likely due to neck muscle ischemia, may be the only symptom.
Symptoms may be exacerbated by exertion, prolonged standing, increased ambient temperature, or meals
The first step is to remove reversible causes—usually vasoactive medications .
Nonpharmacologic interventions should be introduced.
Treatment: Orthostatic Hypotension
Patient education regarding staged moves from supine to upright
Warnings about the hypotensive effects of meal ingestion
Instructions about the isometric counterpressure maneuvers that increase intravascular pressure.
Intravascular volume should be expanded by increasing dietary fluid and salt.
Nonpharmacologic interventions
If these nonpharmacologic measures fail, pharmacologic intervention with fludrocortisone acetate and vasoconstricting agents such as midodrine and pseudoephedrine should be introduced.
Cardiac (or cardiovascular) syncope is caused by arrhythmias and structural heart disease.
Both cause the heart to be unable to sufficiently increase cardiac output to meet demand.
Cardiac arrythymias especially in the elderly have high mortality.
Cardiac Syncope
Approach to the Patient
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.
Diagnostic Objectives
A Diagnostic Plan is Essential
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 ◦Electrophysiology study (EPS)
.
Diagnostic Flow Diagram Initial Evaluation
Treatment
Syncope Not Syncope
Certain Diagnosis
Unexplained Syncope
Cardiac Likely
Cardiac Tests
Neurally-Mediated or Orthostatic Likely
Tests for Neurally-Mediated Syncope
Frequent or Severe Episodes
Tests for Neurally-Mediated Syncope
Single/Rare Episodes
No Further Evaluation
Confirm with Specific Test or
Specialist Consultation
Suspected Diagnosis
++/?+
- + - + -
Treatment Treatment
Re-AppraisalRe-Appraisal
Treatment
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
HISTORYEvents preceding
the syncopeProlonged standing
(vasovagal)Immediately upon
standing (orthostatic)With exertion (cardiac)Sudden without warning
or palpitations (cardiac)Aggressive dieting Heat exposureEmotional stress
Events during and after the episodeTrauma (implication
important)Chest pain (CAD, PE)Seizure (incontinence,
confusion, tongue laceration, postictal behavior)
Cerebrovascular syndrome (diplopia, dysarthia, hemiparesis)
Associated with n/v/sweating (vasovagal)
HISTORYAssociated symptoms
Chest pain, SOB, lightheadedness, incontinence
Past medical historyIdentifying risk factorsMorbidity and mortality
increases with organic causesParkinsons (orthostatic)Epilepsy (seizure)DM (cardiac, autonomic
dysfunction, glucose)Cardiac disease
MedicationsAntihypertensives,
diuretics (orthostatic)Antiarrthymics (cardiac
syncope)TCA, Amiodarone
(cardiac/prolonged QT)Family history
Sudden death (cardiac syncope/prolonged QT or Brugada)
PHYSICAL EXAMVital signs
Orthostatics—most 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
Temperature Hypo/hyperthermia (sepsis,
toxic-metabolic, exposure)
Heart rateTachy/brady, dysrhythmia
Respiratory rateTachypnea (pe, hypoxia,
anxiety)Bradypnea (cns,
toxicmetabolic)Blood pressure
High (cns, toxic/metabolic)Low (hypovolemia,
cardiogenic shock, sepsis)
PHYSICAL EXAMHEENT
Tenderness/deformity (trauma)
Papilledema (increased icp, head injury)
Breath (alcohol, dka)
NECKBruitsJVD (chf, mi, pe,
tampnade)
HEARTMurmur (valves,
dissection)Rub (pericarditis,
tamponade)LUNGS
Sounds may help distinguish chf, infection, pneumothorax
PHYSICAL EXAMABDOMEN
Pulsatile mass; AAATendernessOccult blood loss
PELVISBleeding, hypovolemiaTenderness (PID, ectopic,
torsion, sepsis)
SKINSigns of trauma,
hypoperfusionEXTREMITES
Paralysis (CNS)Pulses unequal
(dissection, embolus, steal)
PHYSICAL EXAMNEUROLOGIC
Mental status; toxic metabolic; organic disease; seizure; hypoxia.
Focal findings (hemorrhagic/ischemic stroke, trauma, tumor, or other primary neurologic disease
Cranial nervesCerebellar testing
EKG---Cornerstone of workup◦ Arrhythmia, long QT, WPW, conduction abn.
Routine Blood work—limited value Radiology---limited value except if
abnormal exam Other tests—depending of history and
exam◦ Glucose - -hemoglobin --troponin
--CK (syncope vs seizure)
If young adult and No comorbid conditions or symptoms
Most likely VASOMOTOR or ORTHOSTATIC .
*Clinicians may forego the ECG in young, healthy patients with an obvious cause of syncope.
Starting the “Workup”
Young adult, no comorbidity, normal ECG, absent orthostatics
VasomotorTry carotid massage
(+) carotid sinus sensitivity
(-) reflex or neurocardiogenic
MetabolicCheck chemistry. R/O
hypoglycemia, adrenal insufficiency
NeurologicCT head (tia, cva, sah)EEG (if suspect Sz)
CardiovascularIf Outflow obstruction,
check CT chest, Echo (PE, valvular, HOCM)
If venous return, check HCG, Echo (pregnancy, tamponade)
Guidelines recommend EKG in the evaluation of all patients with syncope.
Exception: young healthy patients with an obvious cause of syncope
Abnormal ECG in 90% of patient with cardiac syncope
Only 6% of patients with reflex mediated syncope have abnormal ECG.
Syncopal patient with negative cardiac history and normal ECG—unlikely to have a cardiac cause
The ECGKey Points
If Abnormal ECG◦ Ischemia/injury◦ Dysrhythmia
Sinus brady, BBB, AV block, prolonged QT, WPW, HOCM, Brugada
If Normal ECG◦ Consider holter or event recorder if dysrhythmia
suspected
The ECG patient older, +comorbid signs/symptoms
Carotid Sinus Massage (CSM)Method1
Massage, 5-10 secondsDon’t occludeSupine and upright
posture (on tilt table)
Outcome3 second asystole and/or
50 mmHg fall in systolic BP with reproduction of symptoms = Carotid Sinus Syndrome
Absolute contraindications2
Carotid bruit, known significant carotid arterial disease, previous CVA, MI last 3 months
Complications Primarily neurologicalLess than 0.2%Usually transient
24-48 hour monitor—limited value because of intermittent nature of arrhythmias
Event recorder—more helpful. Patient must be conscious in order to activate unit.
Establishes diagnosis in only 2-3% of patients with syncope if ECG is normal.
Indicated in patients at highest risk for arrhythmia ie, abnormal ecg, palpitations, CAD history, syncope when supine or with exertion.
Holter Monitoring
Provides longer monitoring—weeks to months
Can activate the monitor after symptoms occur, thereby freezing in its memory the readings from the previous 2-5 minutes and the subsequent 1 minute
In patients with recurrent syncope, arrhythmias were found during symptoms in 8-20%.
Limitations: compliance, use of device, transmission
Loop Event Recorders
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 ECG ---history of heart disease◦ Murmur ---exercise assoc.
syncope
ECHOCARDIOGRAM
Aortic Stenosis◦ Most common structural lesion associated with
syncope in the elderly Hypertrophic Obstructive Cardiomyopathy
◦ Vasodilatation (drugs/hot bath) can induce syncope
Obstruction to Right Ventricular Outflow◦ PE, pulmonary stenosis, pulmonary htn
Structural Heart Disease
Syncope during exercise is more likely to be related to an arrhythmia
Post-exertional syncope is usually neurally mediated.
Echocardiogram should be done prior to EST to r/o structural abnormality.
INDICATION◦Syncope during or shortly after exercise
(exertional syncope)
EXERCISE STRESS TEST
TILT TABLE TEST
Changes in position to reproduce symptoms of the syncopal event.
Positive tilt table test◦ Induction of bradycardia
and hypotension◦ Considered diagnostic
for vasovagal syncope
Indications for Tilt table testUnexplained
recurrent syncope or syncope associated with injury in absence of structural heart ds.
Unexplained recurrent syncope or syncope associated with injury in setting of organic heart disease after exclusion of potential cardiac cause of syncope
Identification of neurally mediated syncope could alter treatment
Evaluation of recurrent unexplained falls.
Evaluation of near syncope or dizziness
Tilt Table Test
Unmasks Vasovagal syncope susceptibility
Reproduces symptoms Positive Tilt Test
*Prophylaxis treatment—beta blockers or disopyramide as well as SSRIs
*Recurrent symptoms and bradycardia may require pacemaker
Syncope Evaluation Flow Chart
--CLUES
Symptoms DiagnosisOccurs after sudden unexpected pain, sound, smell, or sightProlonged StandingAthletes post exertion
Vasovagal attack
Occurs after micturition, defecation, cough or swallowing
Situational Syncope
Event occurs in association with severe throat or facial pain
Glossopharyngeal or trigeminal neuralgia
Occurs with head rotation or pressure on the carotid sinus-tumors, tight collars or shaving
Carotid Sinus Syncope
Episodes occur immediately on standing
Orthostatic hypotension
Headaches are associated with the event
Migraines
Medications taken before Drug induced syncopeEvent is associated with vertigo, dysarthria or diplopiaEvent is associated with arm exercize
TIA/Subclavian Steal Syndrome
Pulse/BP differences between armsAortic dissection/SSS
Syncope occurs without prodrome and patient has underlying structural heart dz.
Arrythmia
v/s SEIZURES
SYNCOPE
Upright posture Pallor present Unconscious-seconds Recovery-rapid Post-ictal confusion,
amnesia, headache-ABSENT
Injury-UNCOMMON Tongue biting-NEVER
SEIZURE
Any posture Pallor absent Unconscious-minutes/
hrs Recovery-slow Post-ictal confusion,
amnesia, headache-PRESENT
Injury-COMMON Tongue biting-
COMMON
Risk Factors◦ C History of CHF◦ H Hematocrit less than 30◦ E Non-sinus rhythm or new changes in EKG◦ S Systolic BP less than 90◦ S Shortness of breath------------- is a simple rule for evaluating the
risk of adverse outcomes in patient who present with syncope.
San Francisco Syncope Rule
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.
SUMMARY
Case 1
71y/o M presents after he passed out while walking up the stairs. He felt slightly lightheaded just prior to the event. Wife saw him fall but was able to quickly arouse him. He had no incontinence or tongue biting. Similar event occurred 2 weeks prior while he was doing yard-work for which he did not seek medical care. He has a long history of DM, and hypertension for which he takes Glipizide, Amlodipine, Lisinopril, and HCTZ. He does not drink. Vitals, orthostatics, and blood sugar are unremarkable. ECG shows left axis deviation and LVH. Exam shows 1+ bilateral edema and 4/6 ejection murmur radiating to the carotids.
What risk category is this patient and how would you proceed with workup?
Case 1
H/P, Orthostatics, ECG, Meds◦ ECG shows evidence of structural heart disease and
exam shows murmur. No orthostasis or suspicious history of vasovagal syncope. Patient has had multiple episodes.
Based on initial workup, patient is High Risko Needs Admission and Cardiac Work-up including
Echocardiogram and Stress Test Dx: Aortic Stenosis
Case 2
35y/o healthy M presents with an episode of syncope while standing. He did not experience any prodrome symptoms. This has never happened before. He has no medical history and uses no medications, drugs, or EtoH. Physical exam and ECG are normal. No orthostasis. Carotid massage is negative. Routine labs are unremarkable.
What risk category is this patient and how would you proceed with workup?
Case 2
H/P, Orthostatics, ECG, Meds - normal with no obvious cause of syncope
Patient is Low Risk and has had only a Single Episode of syncope No Further Work-up Indicated
What if the same patient presented with syncope while working out at the gym and physical exam showed a grade III systolic murmur that increased with Valsalva?o Patient is now High Risk given possible structural heart
disease and exertional syncope Admit to telemetry for cardiac work-up including
Echocardiogram to evaluate for Hypertrophic Cardiomyopathy.
Key Points
• Key Differential Dxo Vasovagal/Neurocardiogenic - most commono Cardiac – HIGH RISK PATIENTS, most dangerouso Orthostatic – “D A A D”o Other - Neurologic, Functional, Psych
• Work-up and Risk Stratificationo H/P, Orthostatics, Meds, ECG, +/- Carotid Massageo Risk Stratify
High Risk - Admit w/ cardiac work-up Low Risk - Outpatient workup based on frequency of episodes
• Brain Imaging ONLY if focal Neuro Deficits or Head trauma
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