Acute Coronary Syndrome Flashcards
Unstable angina pain characteristics
New or changing chest pain
- emergency–call 911
- get diagnosed with this if come in with chest pain until resolved
NSTEMI
- partial blockage
- depressed or normal ST
- QRS normal
- inverted T wave
- elevated troponin
- smaller infarct, better outcomes
STEMI
- complete blockage
- elevated ST
- wide QRS
- peaked then inverted T wave
- elevated troponin
- larger infarct, worse outcomes
Differentiating factor between STEMI and NSTEMI
EKG changes for STEMI
Acute coronary syndrome
umbrella term for blockage of blood to the heart–tissue dying
Prinzmetal variant angina char and tx
- vasospasm often from damage to the endothelium or coronary vessel
- may be at rest at night, not from exertion
- CAD may/may not be present
- may have elevated ST
- beginning or cause of dysrhythmias
- tx with nitrates and relaxes the spasm
Unstable plaque
- large lipid core with thin fibrous cap
- lots of inflam and smooth muscle cell proliferation into the intima–risk of rupture
- can use to monitor progress
What lab measures unstable plaque
CRP
Unstable angina
- ruptured plaque and thrombus
- occlusion is partial or thrombus dissolves–no infarction
- may be transient ECG changes
- cardiac enzymes not elevated
- more severe than chronic angina
Theory of plaque rupture
Inc SNS activity–inc BP, HR, force of ctx–inc force of coronary artery BP–inc force exerted against injured endothelium–ruptured plaque–plt adhere to ruptured plaque (bc abnormality)–release subs that attract more plt and contribute to vasospasm–thrombus forms
ACS vs stable angina
- ACS lasts beyond 15 minutes
- relief with nitrates when stable
ACS symptoms
impending doom, sweaty, tight chest, N?V
Unstable angina symptoms in women
dizzy, heartburn, cold sweat, tired
MI symptoms
diaphoretic, dyspnea, anxiety, restless, pallor, retrosternal crushing chest pain to shoulder, arm, jaw, back, weak pulse, Levine’s sign (fist to chest)
Which artery is the widowmaker
Left anterior descending; supplies blood to the heart
Acute MI
Ruptured plaque with thrombus
- ACS with prolonged ischemia w/o recovery
-BF disruption is prolonged OR BP disruption is total
- EKG chx that doesn’t go back to normal
- cardiac enzymes elevated
- prolonged ischemia w/o recovery or healing
- irreversible ischemic necrosis to myocardial cells
Ischemia
O2 supply not meeting metabolic demands
- full recovery possible
Infarction
Irreversible tissue death (necrosis)
- begins within 30 min to 4h
Can ATP be stored?
No
Cycle of ischemia to infarction
- lack ATP w/i 1-2 min of poor oxygen supply
- irreversible injury w/i 30min-4h (infarct)
- tissue necrosis w/i 4h
- necrotic tissue cleared in 1-2W
- tough fibrous scar tissue replaces necrotic tissue in 6W
Cardiac injury
- some recovery possible
- can still perfuse it and restore to become viable
- not dead yet–inc oxygen and dec demand of heart
What does extent of heart muscle damage depend on…
- location of level of occlusion in coronary artery
- length of time that artery has been occluded
- heart’s availability of collateral circulation
Immediate pharm for MI
- oxygen first!
- morphine to dec pain and inc dilation, dec preload and afterload
- chewable aspirin–plt less sticky
- nitroglycerin (IV if possible) to dec preload and afterload, limit infarct size
- beta blockers if HR able to handle
Giving thrombolytics
Need w/i 4-6h of chest pain if have a clot
Alteplase
- fibrinolytic therapy for STEMIs
- converts plasminogen to plasmin
- use w/i 30-70min of MI sx
- main risk is bleed
- CI with brain bleed
What meds can be given with alteplase?
Heparin and clopidogrel
Nitroglycerin NC and SE
- SE hypotension, HA, flush
- CI with sildenafil for severe hypotension
Reperfusion injury
Injured tissue gets blood again suddenly and it shocks the tissue, causing heart failure
- from oxidized free radicals generated by WBCs and cell response to restored BP
What can reperfusion injuries lead to?
Reperfusion dysrhythmias like v fib and v tach
