B4-015 Big Case: Cardiac Arrest Flashcards
sudden, irreversible cessation of all biologic functions
sudden cardiac death
abrupt cessation of cardiac activity such that victim becomes unresponsive
sudden cardiac arrest
sudden loss of effective blood flow because of cardiac/vascular factors that may reserve spontaneously or require interventions
cardiovascular collapse
prodrome of cardiac arrest
new/worsening cardiac symptoms:
* chest pain
* palpitations
* dyspnea
* fatigability
symptoms at onset of cardiac arrest
abrupt change in clinical status:
* arrhythmia
* hypotension
* chest pain
* dyspnea
* lightheadedness
symptoms of cardiac arrest
sudden collapse:
* loss of effective circulation
* loss of consciousness
biologic death
- failure of resuscitation OR
- failure of electrical, mechanical, or CNS function after intial resuscitation
arrhythmias preceding SCD
- monomorphic VT
- polymorphic VT
- birectional VT
- torsades de pointes
- ventricular flutter
- ventricular fibrillation
most common substrate of SCD
ischemic heart disease
cause up to 70% of SCD
CAD
development of artherosclerosis
adaptive intimal thickening
foam cells
lipid pools
fibrous cap
calcification
- comes on with activity
- brief in duration (minutes)
- relieved with nitrates
stable angina
- comes on at rest
- recent increase in frequency or duration)
unstable angina
- nonthrombotic plaque
- ST segment elevation absent
- no increase in biomarker level
unstable angina
demand related
- nonthrombotic plaque
- ST segment elevation absent
- increased biomarker level
non STEMI type 2
- partially occluding thrombus
- ST elevation absent
- no increase in biomarker level
unstable angina
thrombosis mediated
- partially occluding thrombus
- ST elevation absent
- increased biomarker level
Non-STEMI
type 1
- fully occluding thrombus
- ST elevation present
- increased biomarker level
STEMI type 1
non Q wave MI
non-STEMI
Q wave MI
STEMI
modifiers to MI survival
- ischemic burden
- hemodynamic fluctuations
- autonomic variations
- drugs/electrolytes
- genetic profile
MI pathology:
1 day
wavy fibers
MI pathology:
3-4 days
- extensive coagulation necrosis
- acute inflammation with neutrophils
MI pathology:
7-10 days
- macrophages
- granulation tissue
MI pathology:
2 weeks to several months
contracted collagenous scar
lowers O2 levels in the heart and decreases ATP formation
ischemia
ischemia impairs […] channels
L type Ca+ channels
ischemia causes K+ to accumulate, causing
local hyperkalemia
local hyperkalemia causes the resting postential to be
more positive than normal
results in scar with adjecent border zones
MI
post MI scarring may still be ischemic. This can cause
- abnormal conduction
- abnormal refractory
- altered excitability
- automaticity
- foci of re-entry
- foci of impulse origin
risk stratification post MI depends largely on
LV function
high risk markers for SCD
- arrhythmic
- hemodynamic
moderate risk marker for SCD
acute coronary syndromes
main causes of SCD in young people
Hypertrophic cardiomyopathy
commotio cordis
coronary artery anomalies
causes syncope during exercise and may lead to SCD due to ventricular arrythmia
hypertrophic cardiomyopathy
in older patients with SCD think
ischemic diease
in younger patients with SCD,
keep broad ddx
