ACS Tx and Complications Flashcards
tx for STEMI vs UA/NSTEMI
STEMI: open vessel immediately
UA/NSTEMI: anti ischemic, anti platelet, anti coag, maybe invasive
UA NSTEMI anti ischemic agents
beta blockers first line, then CCBs, nitrates
contra for CCBs
LV dysfn, can increase mortality
contra for nitrates
RV infarction, pts are preload dependent so dont want to lower preload too much
UA /NSTEMI anti platelet
ASA (give immediately) and clopidogrel
often together, reduces mortality
IV GP IIB/IIIA inhib (abciximab) have higher bleeding risk, used in cath lab
anticoag tx NSTEMI UA
UFH, LMWH (reduced events than UFH, harder to monitor), fondaparinux (when no PCI), bivalirudin (used in cath lab)
required tx for pts w/ stents
dual antiplatelet: ASA and plavix
contrast early invasive vs conservative tx for UA /NSTEMI
EI: when high risk, coronary angiography and revascularization
conservative: medical tx, only cath w/ more ischenia or positive stress test
2 important TIMI factors for invasive approach to UA/NSTEMI
ST change, elevated Tn
tx goals w/ STEMI
restore blood flow (PCI, fibrinolytics), prevent further thrombus (anti platelet anti coag) and restore supply and demand balance (nitrates, B blockers, CCB)
time frame for fibrinolysis
given w/i 120 mins of sx onset
need to transfer to PCI hospital
fibrinolysis contra
ulcer disease, bleeding, recent, CVA or surgery, HTN, very old
time frame for PCI
w/i 90 min of hosp pres
mech of arrhythmias after MI
impaired perfusion to conduction system, accumulation of toxic metabolites (acid), autonomic stim, drugs
early vs late arrhythmias from MI
early due to transient electrical changes, will go away
late from structural disease like scars, risk remains high
conduction blocks from MI, most susceptible?
AV node- RCA
bundle of His- LAD
RBB- LAD, distal from RCA
LBB-anterior fascicle by LAD (most susceptible to ischemia)
sinus brachy from MI
most pts have SA (and AV) supply from RCA, so SA node ischemia associated w/ inferior MI
effects of IABP
inflates during diastole to increase aortic pressure and coronary perfusion
deflates during systole to facillitate LV unloading, improving SV and CO
signs of right heart failure
high JVP, hypotension, clear lungs
tx of RV infarction
volume, reperfusion
pap muscle rupture
causes acute mitral regurg (holosystolic murmur), more common w/ RCA, 3-5 days post MI
ventricular septal rupture
3-7 days post MI, holosystolic murmur (dx w/ echo), leads to HF from pulmonary overload
free wall rupture
w/i 14 days, blood in pericardial space, causes tamponade or pseudoaneurysm if thrombus plugs rupture
ventricular aneurysm
weeks to months after MI, wall was weakened from phagocytic clearance of necrotic tissue
thrombus formation, arrhythmias, wasted SV and HF
ventricular aneurysm on ECG
ST elevations weeks after STEMI
pericarditis w/ MI, acute vs long term, tx
acute: early inflammation from injured myocardium to pericardium- sharp pain w/ fever and pericardial friction rub, avoid anticoag and tx w/ ASA
Dressler syndrom weeks later, immune process against necrotic tissue, tx w/ ASA, NSAIDs
thromboembolism w/ MI
from stasis in regions of impaired LV, requires anticoag, seen w/ LV aneurysm
other ACS therapies post hospital
ACEi esp w/ LV dysfn, reduces mortality
statins to stabilize endothelium and reduce mortality
