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SAQIB RANA
03/12/15
 “symptom complex comprising a brief loss of
consciousness associated with an inability to maintain
postural tone that resolves spontaneously without
medical intervention”
CARDIAC
REFLEX
MEDIATED
NEUROLOGIC UNKNOWN
 Many other names : IHSS, ASH, HOCM
 Characteristic anatomic abnormalities
- Hypertrophied, non-dilated LV (normal CXR)
- Thickened usually prominent in septum
 Familial incidence in 55% of cases
 Average age at diagnosis is 30-40 y
 Mortality 3.5% per year
 Pathophysiology (theories)
- Inherited abnormality in myocardium’s response to
adrenergic stimulation
- Abnormal diastolic function
- Subaortic obstruction to cardiac flow
- Anterior mitral leaflet obstructs LV outflow
 Clinical features
- Syncope, chest pain, palpitations, dyspnoea, sudden
death
 Often associated with exertion (not always!!!)
 Attributable to dysrhythmias or sudden reductions in
cardiac output
 Systolic murmur at apex or LLSB
- Increases with valsalva, standing
- Decreases with trendelenburg and squatting
 ECG abnormalities present in 85-93%
 Definitive diagnosis – DOPPLER ECHO
- Doppler helps assess severity of obstruction at rest
and with provocative maneuvers
 Treatment
- Beta blockers, calcium channel blockers
- Amiodarone if ventricular dysrhythmias
 First described in 1992 by Pedro and Josep Brugada
 Associated with sudden cardiac death
 Individuals are usually healthy with structurally
normal hearts
 Generally considered a hereditary disease
 Mortality ~ 10% per year if not treated with Internal
cardioverter- defibrillator (ICD)
-Anti arrythmics have NO effect on prognosis
 Syndrome characterized by
-ECG abnl in leads V1-V3
- Polymorphic or monomorphic VT
- Structurally normal heart
- Familial occurrence in ~ half of patients
 ECG findings in V1-V3
- RBBB or IRBBB pattern
- ST segment elevation – 2 types
-Coved type (most common)
- Saddle type
- Findings can vary depending on many factors
 Definitive diagnosis - EPS
 Ventricular pre-excitation
- 0.1-3% population
- Classic triad
. Shortened PR interval
. Widened QRS interval
. Delta wave
 Atrial fibrillation
- Very rapid irregularly irregular tachycardia (rates
may approach 300 beats/min)
- Often misdiagnosed as SVT, VT or atrial fibrillation
with BBB
- Misdiagnosis and treatment with AVN blockers can
be deadly
 ECG appearance
- Irregularly irregular tachycardia
- Wide QRS complexes
- QRS morphologies vary
- Rates may approach 300 BPM
 QT interval vary based on rate
 Corrected QT interval (QTc) based on Bazett formula
 How long is too long?
- Major risk occurs in patients when QTc >= 500msec
- Major concern : Development of Torsade de
pointes
 What do you do with a prolonged QT?
- Search for and treat underlying cause
- Congenital/ idiopathic: beta blockers
 Treatment of torsade de pointes
- cardiovert/defibrillate
- magnesium bolus and infusion
- Overdrive pacing rarely needed
- Avoid amiodarone, procainamide, lidocaine
 Hypokalemia (due to U wave)
 Hypomagnesemia
 Hypocalcemia
 Sodium-channel blockers (e.g. Type Ia anti –
arrhytmics, TCAs, etc.)
 Miscellaneous : Elevated ICP, ACS, hypothermia,
hereditary, etc)
 Acute coronary syndrome
 Tachyarrythmias
 Bradyarrhtymias and AV blocks
 HOCM
 Brugada syndrome
 WPW syndrome
 Long QT interval
History of heart failure
Abnormal ECG
Hematocrit less than 30
Shortness of breath
SBP <90 in emergency department
Diagnosis
established
YES
Serious
diagnosis(cardiac,
neurologic)
Non serious
diagnosis (Reflex
mediated)
NO
UNEXPLAINED
SYNCOPE (risk
stratify)
Syncope, sudden death and ekg

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Syncope, sudden death and ekg

  • 2.  “symptom complex comprising a brief loss of consciousness associated with an inability to maintain postural tone that resolves spontaneously without medical intervention”
  • 4.
  • 5.  Many other names : IHSS, ASH, HOCM  Characteristic anatomic abnormalities - Hypertrophied, non-dilated LV (normal CXR) - Thickened usually prominent in septum  Familial incidence in 55% of cases  Average age at diagnosis is 30-40 y  Mortality 3.5% per year
  • 6.  Pathophysiology (theories) - Inherited abnormality in myocardium’s response to adrenergic stimulation - Abnormal diastolic function - Subaortic obstruction to cardiac flow - Anterior mitral leaflet obstructs LV outflow
  • 7.  Clinical features - Syncope, chest pain, palpitations, dyspnoea, sudden death  Often associated with exertion (not always!!!)  Attributable to dysrhythmias or sudden reductions in cardiac output  Systolic murmur at apex or LLSB - Increases with valsalva, standing - Decreases with trendelenburg and squatting
  • 8.  ECG abnormalities present in 85-93%  Definitive diagnosis – DOPPLER ECHO - Doppler helps assess severity of obstruction at rest and with provocative maneuvers  Treatment - Beta blockers, calcium channel blockers - Amiodarone if ventricular dysrhythmias
  • 9.
  • 10.  First described in 1992 by Pedro and Josep Brugada  Associated with sudden cardiac death  Individuals are usually healthy with structurally normal hearts  Generally considered a hereditary disease
  • 11.  Mortality ~ 10% per year if not treated with Internal cardioverter- defibrillator (ICD) -Anti arrythmics have NO effect on prognosis  Syndrome characterized by -ECG abnl in leads V1-V3 - Polymorphic or monomorphic VT - Structurally normal heart - Familial occurrence in ~ half of patients
  • 12.  ECG findings in V1-V3 - RBBB or IRBBB pattern - ST segment elevation – 2 types -Coved type (most common) - Saddle type - Findings can vary depending on many factors  Definitive diagnosis - EPS
  • 13.
  • 14.
  • 15.  Ventricular pre-excitation - 0.1-3% population - Classic triad . Shortened PR interval . Widened QRS interval . Delta wave
  • 16.
  • 17.
  • 18.
  • 19.
  • 20.
  • 21.
  • 22.
  • 23.
  • 24.  Atrial fibrillation - Very rapid irregularly irregular tachycardia (rates may approach 300 beats/min) - Often misdiagnosed as SVT, VT or atrial fibrillation with BBB - Misdiagnosis and treatment with AVN blockers can be deadly
  • 25.  ECG appearance - Irregularly irregular tachycardia - Wide QRS complexes - QRS morphologies vary - Rates may approach 300 BPM
  • 26.
  • 27.  QT interval vary based on rate  Corrected QT interval (QTc) based on Bazett formula  How long is too long? - Major risk occurs in patients when QTc >= 500msec - Major concern : Development of Torsade de pointes
  • 28.  What do you do with a prolonged QT? - Search for and treat underlying cause - Congenital/ idiopathic: beta blockers  Treatment of torsade de pointes - cardiovert/defibrillate - magnesium bolus and infusion - Overdrive pacing rarely needed - Avoid amiodarone, procainamide, lidocaine
  • 29.  Hypokalemia (due to U wave)  Hypomagnesemia  Hypocalcemia  Sodium-channel blockers (e.g. Type Ia anti – arrhytmics, TCAs, etc.)  Miscellaneous : Elevated ICP, ACS, hypothermia, hereditary, etc)
  • 30.  Acute coronary syndrome  Tachyarrythmias  Bradyarrhtymias and AV blocks  HOCM  Brugada syndrome  WPW syndrome  Long QT interval
  • 31. History of heart failure Abnormal ECG Hematocrit less than 30 Shortness of breath SBP <90 in emergency department

Editor's Notes

  1. A reduction of cerebral perfusion by 35% or complete disruption for 5-10 seconds will cause most people to loose consciousness or develop symptoms.
  2. LVH in age >45, Criteria for LVH: R wave in V5 or V6 + S in V1 >35mm OR Max R wave + Max S wave in precordial leads >45mm OR R wave in aVL >11mm. LVH produces assymetric TWI and assymetric STD/E (MI produces symmetric)
  3. AJMALINE TESTING IN LAB NA chanelopathy, exacerbated by anti-cholinergics, anti depressants, anti arrythmics, fever, hot ambient temperature
  4. Coved type : More sensitive, more specific, typically terminates in inverted T waves Saddle type: less sensitive, less specific
  5. Atrial fibrillation with WPW syndrome
  6. AVRT with orthodromic (left) and antidromic (right) AV nodal conduction
  7. Adenosine, calcium channel blockers, beta blockers, digoxin
  8. Reverts to normal sinus rhythm after treatment with adenosine
  9. Regular wide tachycardia, VT shock
  10. Irregular wide complex QRS
  11. All AVN blockers in Afib with WPW are contra indicated, will cause Vfib
  12. Recently started on anti-psychotics, Long QT syndrome
  13. QT interval shortens at faster heart rates, QTc = QT/<RR
  14. Dysrhythmias can produce syncope or seizure like activity (myoclonic jerks often misdiagnosed as seizures)