ACS Flashcards
acute coronary syndrome (ACS)
a progression of coronary events
stable angina or unstable angina
STEMI or NSTEMI
unstable angina EKG
can be:
- normal
- inverted T waves
- ST depression
unstable angina etiology
chest pain caused by ruptured or thickened plaque with platelet and fibrin thrombus causing increased coronary obstruction
unstable angina symptoms
irregular/unpredictable chest pain of increasing intensity, frequency, or duration
occurs at rest or with minimal activity
unresponsive to NTG
unstable angina pharmological treatment
NTG beta blockers tissue plasminogen activators (tPA) O2 clopidogrel morphine statins aspirin
coronary artery disease (CAD)
leading global cause of death
number 1 cause of death in US
leading cause of death for women
acute coronary syndrome (ACS) patho
clinical manifestation of coronary disease
development of fatty plaques in artieries
narrows coronary vasculature and limits blood flow and oxygen delivery to coronary muscle
acute coronary syndrome modifiable risk factors
alcohol/tobacco use HTN sedentary lifestyle/obesity dyslipidemia DM
acute coronary syndrome innate risk factors
age gender heredity stress menopause
angina pectoris
“strangling chest”
chest pain caused by myocardial ischemia
ischemia
occurs when oxygen supply > oxygen demand
angina pectoris precipitating caues
exertion temperature extremes emotional stress large meal tobacco sexual activity stimulant use circadian rhythm patterns
stable angina etiology
myocardial ischemia
stable angina symptoms
episodic pain lasting 5-10 minutes
aggravated by exertion, cold, eating, emotional stress
relieved by rest, NTG
stable angina pharmacological treatment
NTG aspirin beta blockers calcium channel blockers ACE inhibitors
variant angina causes
coronary vasospasm
variant angina symptoms
occurs at rest without provocation
triggered by smoking
occurs with or without the presence of CAD
transient ST-segment elevation during pain
often associated with AV block or ventricular arrhythmias
variant angina treatment
calcium channel blockers
myocardial infarction (MI)
occurs when heart muscle is abruptly deprived of oxygen
ischemia is the first phase
injury occurs when tissue is injured from lack of O2
necrosis = death of myocardium tissue
location of MI
mostly occurs in left ventricle and categorized by the wall of left ventricle it occurs upon
anterior wall is caused by occlusion left anterior descending artery (LAD) and is 25% of MIs with highest mortality rate
lateral wall occurs with occlusion of circumflex artery
inferior wall occurs with occlusion of right coronary artery (RCA)
NSTEMI
associated with ST segment depression or T wave inversion on ECG
occurs as a result of subtotal occluding thrombus
may be undistinguishable from unstable angina without serologic evidence of myocardial necrosis
NSTEMI assessment and treatment
admission serial EKGs, cardiac enzymes rest 24-48 hrs continuous bedside EKG analgesics supplemental O2 pharmacological therapy
STEMI
ST segment is elevated
most common cause is reduced myocardial perfusion 2/2 occlusive thrombus
reperfusion therapy should be initiated within 12 hours of symptom onset
APQRST
Associated sx Precipitating factors Quality Region/radiation/risk factors Severity Timing
ACS nursing actions
place pt in semi-Fowlers EKG within 10 minutes draw blood, start IV initiate treatment frequent vitals
ACS nursing actions (meds)
NTG if systolic >90 supplemental O2 morphine IV beta blockers ACE inhibitors
ECG manifestations
crucial within 10 min
deviation of ST segment will determine amt of damage to heart muscle
prolonged ST elevation, new LBBB or new Q waves indicate STEMI
NSTEMI may present with ST depression or T wave inversion
ischemia ECG changes
T wave inversion
ST depression > 0.5mm
ST that remains at baseline for > 0.12 seconds
injury ECG
ST segment elevation of 1mm or more above baseline
T wave may be taller and pointed
infarction ECG
> 3mm ST segment elevation in 2 contiguous leads
troponin I
most accurate marker of myocardial injury
increase in blood 4-12 hrs
peaks in 12 hrs and remains elevated for 4-10 days
troponin T
may be predictive of MI size
>0.01 ng/mL considered elevated
exercise testing
focuses on ECG during exercise
gives info about dysrhytmias, HR, BP, exertion rate, exercise capacity, myocardial O2 update, VO2, ventilator threshold
cardiac catheterization
used to determine exact location of the myocardial injury and specific obstructions to coronary vasculature
anti-ischemic meds
NTG
morphine
beta blockers
anti-thrombotic therapy
aspirin
P2Y12 inhibitor (clopidogrel or ticagrelor)
unfractionated heparin
low molecular weight heparin
percutaneous transluminal coronary intervention (PTCI)
placement of stent into narrowed coronary artery
percutaneous balloon angioplasty (PTCA)
reperfuse myocardium
antiplatelet therapy required
