B4.015 Sudden Cardiac Death Flashcards
sudden cardiac death
sudden, irreversible cessation of all biological functions
sudden cardiac arrest
abrupt cessation of cardiac activity such that the victim becomes unresponsive
presumed to be cardiac unless it is known to have been caused by trauma, drowning, asphyxia, electrocution
rare spontaneous reversions but reversible with interventions
cardiovascular collapse
sudden loss of effective blood flow because of cardiac and/or peripheral vascular factors that may reverse spontaneously or require interventions
time references in sudden cardiac death
prodromes: new or worsening cardiovascular symptoms (chest pain, palpitations, dyspnea, fatigability)
days to months
onset of terminal event: abrupt change in clinical status (arrhythmia, hypotension, chest pain, dyspnea, lightheadedness)
up to an hour
cardiac arrest: sudden collapse, loss of circ, loss of consciousness
minutes to weeks
death
“the enemies in SCD”
arrhythmias you don’t want to see
v-tac
TdP
ventricular flutter
v-fib
what % of CV deaths are SCD?
50%
- 25% first events
- 230,000-350,000 deaths/year
- 70% at home
influencers on survival rates from SCD
home: 6%
best: organized systems, early defibrillation
age (but not linear)
most common substrate of SCD
ischemic heart disease
cardiomyopathies with fibrosis or LV hypertrophy
usual causes of SCD in adolescents
myocarditis hypertrophic CM LQT and SQT RV dysplasis anomalous CA brugada syndrome idiopathic VF, CPVT
usual causes of SCD in pts with advanced heart disease
coronary artery disease
usual causes of SCD in general population
coronary heart diseased
dilated cardiomyopathy
describe development of atherosclerosis
adaptive intimal thickening accumulation of foam cells formation of lipid pools fibrous cap growth over necrotic core angiogenesis into necrotic fat cells calcification within core
what happens initially in the progression of atherosclerosis as a compensatory mechanism?
expansion of the vessel to maintain lumen size
eventually this expansion is overcome and the lumen narrows
outcomes of plaque erosion/rupture
healing
embolism
thrombosis (non-occlusive or occlusive)
classic stable angina
symptom of myocardial ischemia
comes on with activity
brief in duration
relieved with nitrates
unstable angina
comes on at rest with recent increase in frequency or duration (without classical biomarkers for MI)
characterize nonSTEMI type 1
acute coronary syndrome
partially occluding thrombus
no ST elevation
increased biomarker levels
characterize nonSTEMI type 2
supply demand imbalance
nonthrombotic plaque
no ST elevation
increased biomarker levels
characterize STEMI
acute coronary syndrome
partially occluding thrombus
ST elevation on ECG
increased biomarker levels
how does unstable angina differ from nonSTEMI
no biomarker elevation in angina
in what ways can an MI induce SCD?
transient ischemic events
acute MI
scar formation due to chronic closure
ischemic cardiomyopathy
modifiers which influence risk of cardiac arrest/SCD
ischemic burden hemodynamic fluctuations autonomic variations drugs/electrolytes genetic profile
discuss the implications of ischemia on the heart
lower O2 levels and thus decreased ATP formation
impairs L-type Ca2+ current during APs
accumulation of K+ due to decreased blood flow results in local hyperkalemia
depolarization of resting membrane potential, so phase 4 resting membrane potential will be more positive than normal
impairment of Na+ current
MI scar + ischemia = ?
abnormal refractoriness abnormal conduction altered excitability automaticity foci of re-entry foci of impulse origin
greatest risk factor for SCD following MI
LV dysfunction
30% or lower EF is the marker of high risk for SCD
predictors of mortality after CPR
pre-low BP, pneumonia, CRF, CA duration >15 min intubation post coma pressors
what is commotion cordis?
getting hit in the chest and dying
rate of survival increasing due to increasing awareness
top 5 causes of SCD in young athletes
hypertrophic cardiomyopathy commotion cordis coronary artery anomalies left ventricular hypertrophy of indeterminate causation myocarditis
what is interesting about hypertrophic cardiomyopathy
strong genetic basis in about 50% of cases
variable genetic causes
no clear pattern between genetic cause and outcome
what characteristics can help distinguish and athletes heart from one with pathologic cardiomyopathy
LV cavity size
frequent or complex ventricular tachyarrhythmias
LV wall thickness
distinctly abnormal electrocardiogram
what individuals with coronary artery anomalies are most susceptible for SCD? why?
athletes
arteries can get pinched off by the expansion of the aorta and pulmonary arteries during times of high CO (exercise)
