ACS Tx and Complications

Question 1

tx for STEMI vs UA/NSTEMI

Answer 1

STEMI: open vessel immediately

UA/NSTEMI: anti ischemic, anti platelet, anti coag, maybe invasive

Question 2

UA NSTEMI anti ischemic agents

Answer 2

beta blockers first line, then CCBs, nitrates

Question 3

contra for CCBs

Answer 3

LV dysfn, can increase mortality

Question 4

contra for nitrates

Answer 4

RV infarction, pts are preload dependent so dont want to lower preload too much

Question 5

UA /NSTEMI anti platelet

Answer 5

ASA (give immediately) and clopidogrel

often together, reduces mortality

IV GP IIB/IIIA inhib (abciximab) have higher bleeding risk, used in cath lab

Question 6

anticoag tx NSTEMI UA

Answer 6

UFH, LMWH (reduced events than UFH, harder to monitor), fondaparinux (when no PCI), bivalirudin (used in cath lab)

Question 7

required tx for pts w/ stents

Answer 7

dual antiplatelet: ASA and plavix

Question 8

contrast early invasive vs conservative tx for UA /NSTEMI

Answer 8

EI: when high risk, coronary angiography and revascularization

conservative: medical tx, only cath w/ more ischenia or positive stress test

Question 9

2 important TIMI factors for invasive approach to UA/NSTEMI

Answer 9

ST change, elevated Tn

Question 10

tx goals w/ STEMI

Answer 10

restore blood flow (PCI, fibrinolytics), prevent further thrombus (anti platelet anti coag) and restore supply and demand balance (nitrates, B blockers, CCB)

Question 11

time frame for fibrinolysis

Answer 11

given w/i 120 mins of sx onset

need to transfer to PCI hospital

Question 12

fibrinolysis contra

Answer 12

ulcer disease, bleeding, recent, CVA or surgery, HTN, very old

Question 13

time frame for PCI

Answer 13

w/i 90 min of hosp pres

Question 14

mech of arrhythmias after MI

Answer 14

impaired perfusion to conduction system, accumulation of toxic metabolites (acid), autonomic stim, drugs

Question 15

early vs late arrhythmias from MI

Answer 15

early due to transient electrical changes, will go away

late from structural disease like scars, risk remains high

Question 16

conduction blocks from MI, most susceptible?

Answer 16

AV node- RCA
bundle of His- LAD
RBB- LAD, distal from RCA
LBB-anterior fascicle by LAD (most susceptible to ischemia)

Question 17

sinus brachy from MI

Answer 17

most pts have SA (and AV) supply from RCA, so SA node ischemia associated w/ inferior MI

Question 18

effects of IABP

Answer 18

inflates during diastole to increase aortic pressure and coronary perfusion

deflates during systole to facillitate LV unloading, improving SV and CO

Question 19

signs of right heart failure

Answer 19

high JVP, hypotension, clear lungs

Question 20

tx of RV infarction

Answer 20

volume, reperfusion

Question 21

pap muscle rupture

Answer 21

causes acute mitral regurg (holosystolic murmur), more common w/ RCA, 3-5 days post MI

Question 22

ventricular septal rupture

Answer 22

3-7 days post MI, holosystolic murmur (dx w/ echo), leads to HF from pulmonary overload

Question 23

free wall rupture

Answer 23

w/i 14 days, blood in pericardial space, causes tamponade or pseudoaneurysm if thrombus plugs rupture

Question 24

ventricular aneurysm

Answer 24

weeks to months after MI, wall was weakened from phagocytic clearance of necrotic tissue

thrombus formation, arrhythmias, wasted SV and HF

Question 25

ventricular aneurysm on ECG

Answer 25

ST elevations weeks after STEMI

Question 26

pericarditis w/ MI, acute vs long term, tx

Answer 26

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

Question 27

thromboembolism w/ MI

Answer 27

from stasis in regions of impaired LV, requires anticoag, seen w/ LV aneurysm

Question 28

other ACS therapies post hospital

Answer 28

ACEi esp w/ LV dysfn, reduces mortality

statins to stabilize endothelium and reduce mortality