2. “symptom complex comprising a brief loss of
consciousness associated with an inability to maintain
postural tone that resolves spontaneously without
medical intervention”
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
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
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
A reduction of cerebral perfusion by 35% or complete disruption for 5-10 seconds will cause most people to loose consciousness or develop symptoms.
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)
AJMALINE TESTING IN LAB
NA chanelopathy, exacerbated by anti-cholinergics, anti depressants, anti arrythmics, fever, hot ambient temperature
Coved type : More sensitive, more specific, typically terminates in inverted T waves
Saddle type: less sensitive, less specific
Atrial fibrillation with WPW syndrome
AVRT with orthodromic (left) and antidromic (right) AV nodal conduction