acute coronary syndrome

Question 1

umbrella term

Answer 1

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

Question 2

angina: printzmetal’s variant angina

Answer 2

CA vasospasms -> decreased o2 blood to cardiac tissue, increased r/o myocardial ischemia

Question 3

unstable angina

Answer 3

small clot, blood supply maintained
rupture of plaque -> thrombus -> occlude vessel
new or changing chest pain caused by ischemia

Question 4

angina

Answer 4

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?)

Question 5

stable angina

Answer 5

fixed plaque
stable plaque = small lipid core with thick fibrous cap

Question 6

variant/vasospastic angina: prinzmetal angina - cause

Answer 6

CA spasm -> narrows artery
underlying cause? endothelial dysF

Question 7

variant/vasospastic angina: prinzmetal angina - characteristics

Answer 7

unique
CAD may/may not be present
onset timing: rest, minimal exertion, night
ecg changes: elevated ST (monitor closely)

Question 8

variant/vasospastic angina: prinzmetal angina - tm

Answer 8

usually benign but can cause serious dysR
nitrate to relax spasm

Question 9

unstable plaque

Answer 9

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

Question 10

unstable angina

Answer 10

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

Question 11

unstable angina: patho

Answer 11

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

Question 12

theory of plaque rupture

Answer 12

increased SNS: psych stress, exercise, circadian rhythms
plaque rupture
thrombus formation

Question 13

theory of plaque rupture: increases SNS stim

Answer 13

increased BP, HR, force of contraction -> heart works harder
increased F or coronary BF
increased F exerted against ruptured epithelium

Question 14

theory of plaque rupture: plaque rupture

Answer 14

plt adhere to ruptured plaque
release substances that attract more plt and contribute to vasospasm

Question 15

ACS v stable angina

Answer 15

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

Question 16

MI s/s

Answer 16

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

Question 17

acute MI

Answer 17

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)

Question 18

ischemia

Answer 18

O2 supply doesnt meet demands

Question 19

infarction

Answer 19

tissue death, irreversible (30 min - 4 hr)

Question 20

from ischemia to infarction

Answer 20

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

Question 21

ATP

Answer 21

myocardial cells dont store
need constant O2 to make ATP
decreased ability to contract in 1-2 min

Question 22

zones of damage

Answer 22

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

Question 23

acute MI -> damage

Answer 23

extent of damage determined by…
location/level of occlussion in CA -> small v large vessel
L of time CA occluded
availability of collateral circulation

Question 24

L anterior descending artery

Answer 24

LAD
supply LV, most commonly involved in LV

Question 25

STEMI

Answer 25

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

Question 26

NSTEMI

Answer 26

ST: depression or normal
QRS: normal
T wave: inverted
troponin: elevated
size of infarct: smaller
outcomes: better