B4.015 Sudden Cardiac Death

Question 1

sudden cardiac death

Answer 1

sudden, irreversible cessation of all biological functions

Question 2

sudden cardiac arrest

Answer 2

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

Question 3

cardiovascular collapse

Answer 3

sudden loss of effective blood flow because of cardiac and/or peripheral vascular factors that may reverse spontaneously or require interventions

Question 4

time references in sudden cardiac death

Answer 4

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

Question 5

“the enemies in SCD”

arrhythmias you don’t want to see

Answer 5

v-tac
TdP
ventricular flutter
v-fib

Question 6

what % of CV deaths are SCD?

Answer 6

50%

• 25% first events
• 230,000-350,000 deaths/year
• 70% at home

Question 7

influencers on survival rates from SCD

Answer 7

home: 6%
best: organized systems, early defibrillation
age (but not linear)

Question 8

most common substrate of SCD

Answer 8

ischemic heart disease

cardiomyopathies with fibrosis or LV hypertrophy

Question 9

usual causes of SCD in adolescents

Answer 9

myocarditis
hypertrophic CM
LQT and SQT
RV dysplasis
anomalous CA
brugada syndrome
idiopathic VF, CPVT

Question 10

usual causes of SCD in pts with advanced heart disease

Answer 10

coronary artery disease

Question 11

usual causes of SCD in general population

Answer 11

coronary heart diseased

dilated cardiomyopathy

Question 12

describe development of atherosclerosis

Answer 12

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

Question 13

what happens initially in the progression of atherosclerosis as a compensatory mechanism?

Answer 13

expansion of the vessel to maintain lumen size

eventually this expansion is overcome and the lumen narrows

Question 14

outcomes of plaque erosion/rupture

Answer 14

healing
embolism
thrombosis (non-occlusive or occlusive)

Question 15

classic stable angina

Answer 15

symptom of myocardial ischemia
comes on with activity
brief in duration
relieved with nitrates

Question 16

unstable angina

Answer 16

comes on at rest with recent increase in frequency or duration (without classical biomarkers for MI)

Question 17

characterize nonSTEMI type 1

Answer 17

acute coronary syndrome
partially occluding thrombus
no ST elevation
increased biomarker levels

Question 18

characterize nonSTEMI type 2

Answer 18

supply demand imbalance
nonthrombotic plaque
no ST elevation
increased biomarker levels

Question 19

characterize STEMI

Answer 19

acute coronary syndrome
partially occluding thrombus
ST elevation on ECG
increased biomarker levels

Question 20

how does unstable angina differ from nonSTEMI

Answer 20

no biomarker elevation in angina

Question 21

in what ways can an MI induce SCD?

Answer 21

transient ischemic events
acute MI
scar formation due to chronic closure
ischemic cardiomyopathy

Question 22

modifiers which influence risk of cardiac arrest/SCD

Answer 22

ischemic burden
hemodynamic fluctuations
autonomic variations
drugs/electrolytes
genetic profile

Question 23

discuss the implications of ischemia on the heart

Answer 23

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

Question 24

MI scar + ischemia = ?

Answer 24

abnormal refractoriness
abnormal conduction
altered excitability
automaticity
foci of re-entry
foci of impulse origin

Question 25

greatest risk factor for SCD following MI

Answer 25

LV dysfunction

30% or lower EF is the marker of high risk for SCD

Question 26

predictors of mortality after CPR

Answer 26

pre-low BP, pneumonia, CRF, CA
duration >15 min
intubation
post coma
pressors

Question 27

what is commotion cordis?

Answer 27

getting hit in the chest and dying

rate of survival increasing due to increasing awareness

Question 28

top 5 causes of SCD in young athletes

Answer 28

hypertrophic cardiomyopathy
commotion cordis
coronary artery anomalies
left ventricular hypertrophy of indeterminate causation
myocarditis

Question 29

what is interesting about hypertrophic cardiomyopathy

Answer 29

strong genetic basis in about 50% of cases
variable genetic causes
no clear pattern between genetic cause and outcome

Question 30

what characteristics can help distinguish and athletes heart from one with pathologic cardiomyopathy

Answer 30

LV cavity size
frequent or complex ventricular tachyarrhythmias
LV wall thickness
distinctly abnormal electrocardiogram

Question 31

what individuals with coronary artery anomalies are most susceptible for SCD? why?

Answer 31

athletes

arteries can get pinched off by the expansion of the aorta and pulmonary arteries during times of high CO (exercise)