acute coronary syndrome Flashcards
umbrella term
unstable angina, non ST segment elevation MI, ST segment elevation MI
situations where blood supply to heart muscle suddenly blocked or compromised (sudden and complete or come and go) -> cardiac tissue dying, medical emergency
NSTEMI: narrowed with clot, some blood gets through
STEMI: completely occluded
angina: printzmetal’s variant angina
CA vasospasms -> decreased o2 blood to cardiac tissue, increased r/o myocardial ischemia
unstable angina
small clot, blood supply maintained
rupture of plaque -> thrombus -> occlude vessel
new or changing chest pain caused by ischemia
angina
unstable and printzmetals can be at rest and the pain is different with stable angina
always dx as unstable first until cause is determined
similar patho, presentation, and early management -> look at ecg to determine course of action (meds? cath lab for reperfussion?)
stable angina
fixed plaque
stable plaque = small lipid core with thick fibrous cap
variant/vasospastic angina: prinzmetal angina - cause
CA spasm -> narrows artery
underlying cause? endothelial dysF
variant/vasospastic angina: prinzmetal angina - characteristics
unique
CAD may/may not be present
onset timing: rest, minimal exertion, night
ecg changes: elevated ST (monitor closely)
variant/vasospastic angina: prinzmetal angina - tm
usually benign but can cause serious dysR
nitrate to relax spasm
unstable plaque
large lipid core - more unstable, thin fibrous cap, measure with dye to see narrowing
active inflam - CRP level
SM cells proliferate into intima (middle lining of BV) -> increased r/o plaque rupture
unstable angina
chest pain occurring for 1st time -> myocardial ischemia, med emergency, unstable
chest pain more severe than normal with chronic angina -> or radiate somewhere new
new regions of heart undergoing myocardial ischemia, emergency
unstable angina: patho
rupture plaque and thrombus (clot) -> size of thrombus and amount of blockage determines BF past
no infarction? -> partial occlusion or thrombus dissolves (ecg back to normal)
ecg changes: ischemia change, transient -> back to normal
no cardiac enzymes elevated
theory of plaque rupture
increased SNS: psych stress, exercise, circadian rhythms
plaque rupture
thrombus formation
theory of plaque rupture: increases SNS stim
increased BP, HR, force of contraction -> heart works harder
increased F or coronary BF
increased F exerted against ruptured epithelium
theory of plaque rupture: plaque rupture
plt adhere to ruptured plaque
release substances that attract more plt and contribute to vasospasm
ACS v stable angina
severity and duration -> lasts longer >15 min
no relief from nitro
pain descriptors -> elephant on chest, not just tight
other s/s: diaphoresis, SOA, n/v, impending doom (cant pinpoint)
these can be similar to stable but worry with change
males: discomfort/tingle in arms, back, neck, shoulder, jaw; chest pain, SOB
females: sudden dizzy, heart burn, cold sweat, n/v, unusual tiredness
MI s/s
diaphoresis, dyspnea, extreme anx (cant sit still, dont know whats wrong), levine’s sign (fist to chest), pallor, retrosternal crushing chest pain that radiates to shoulder, arm, jaw, back; weak pulse
acute MI
ACS with prolonged ischemia w/o recovery
ruptured plaque and thrombus
infarction bc BF disruption prolonged or total -> irreversible tissue ischemic necrosis of myocardial cells, amount depends on location
will see ecg changes (that dont got back to normal - classify stemi v nstemi)
will see increase in cardiac enzymes (troponin- serial labs, trend up, normal after occlusion rectified)
ischemia
O2 supply doesnt meet demands
infarction
tissue death, irreversible (30 min - 4 hr)
from ischemia to infarction
necrosis by 4 hr (reperfussion therapy done by 4hr mark)
necrotic tissue cleared 1-2 wk -> myocardium weak and susceptible to rupture
replaced by tough fibrous scar by 6 wk -> ecg change bc electrical impulse doesnt move through this as well
ATP
myocardial cells dont store
need constant O2 to make ATP
decreased ability to contract in 1-2 min
zones of damage
infarction = necrosis: MI, dead cells, cant recover but can stop from increasing by increasing O2 supply and decreasing demands
injury: some recovery possible, can still perfuse and restore it to become viable, not dead yet
ischemia: full recovery possible
acute MI -> damage
extent of damage determined by…
location/level of occlussion in CA -> small v large vessel
L of time CA occluded
availability of collateral circulation
L anterior descending artery
LAD
supply LV, most commonly involved in LV
STEMI
ST: elevation (tombstone)
QRS: usually pathologic (wide), dev over hours
T wave: peak, then inverted over time
troponin I: elevated (continue after 2hr), sharper
size of infarct: larger
outcomes: poor, depends on time till care
NSTEMI
ST: depression or normal
QRS: normal
T wave: inverted
troponin: elevated
size of infarct: smaller
outcomes: better
