ACS Flashcards
Dressler’s
Post-infarction pericarditis
Vulnerable plaque
large lipid core, thin fibrous cap, increased macrophages, evidence of inflammation
Post lytic cath
Resolution of symptoms, improvement of ST-segment elevation by at least 50%, and reperfusion arrhythmias (e.g., accelerated idioventricular rhythm) are indicative of epicardial coronary patency. If there is clinical uncertainty about the status of reperfusion, emergent coronary angiography is warranted (e.g., rescue percutaneous coronary intervention). Most patients following STEMI treated with lytic therapy will undergo elective coronary angiography to define the coronary anatomy within a day of presentation (Class IIa). In high-risk scenarios like shock, heart failure, or recurrent chest pain, urgent coronary angiography is recommended (Class I).
Mortality benefit of radial access
STEMI cases ONLY
Definition of MI
MI is diagnosed when there is an elevation of cardiac-specific biomarkers >99% above the upper reference limit and at least one of the following: 1) symptoms of ischemia, 2) new or presumed significant ST-segment–T wave (ST–T) changes or new left bundle branch block (LBBB), 3) development of pathological Q waves in the ECG, 4) imaging evidence of new loss of viable myocardium, 5) a new regional wall motion abnormality, or 6) identification of an intracoronary thrombus by angiography or autopsy.
Ischemic Cascade
Perfusion defect, diastolic dysfunction, systolic dysfunction, ecg changes, chest pain
Single vessel CAD
similar outcomes PCI vs CABG (cabg more stroke less TVR)
Medical Therapy Post STEMI
Class I
1) Beta blockade
2) ACEi if AWMI, HF, EF<40%
Coronary Microvascular Dysfunction
Coronary Flow reserve <2.5 in setting of normal epicardial coronary vessels= positive coronary microvascular dysfunction
Outcomes of patients with CMD evidence of ishemia on stress test, angina and normal coronaries WORSE than patients without angina
Stress with imaging
1) Pre-excitation
2) LBBB
3) paced rhythm
4) >1mm ST depression
Fibrinolytic related hemorrhagic stroke
1) cessation lytics
2) Protamine to reverse heparin
3) FFP to give FV,VIII
4) Platelets
5) Prothrombin complex concentrate
6) NSx
MC Complication of Cath
Vascular access site complication
CABG
Pt with diabetes and significant left main coronary artery disease (=50%) or severe coronary artery disease (=70%) in three major coronary arteries or involving the proximal LAD plus one other coronary artery, coronary artery bypass grafting is the recommended revascularization strategy and has been shown to improve survival but higher CVA risk
Class I to CABG for anginal improvement
IIa - cabg to improve mortality in pt with low EF, severe LV dysfxn, CAD
Viability testing
STITCH trial - viability testing didn’t identify patients with a differential survival benefit with CABG
Cocaine or methamphetamine induced MI
Give benzo(ie lorazepam)/nitro No BB - potentiates coronary vasospasm NO nifedipine in acute MI No nitro gtt in patient on sildenafil or viagra give benzo (lorazepam)
if need BB - labetolol or carvedilol - both alpha AND BB so less coronary vasospasm - no metoprolol
Prasugrel
Do not administer prior to cath
Do not give with h/o CVA/TIA
TIMI Risk score
Score >=3 benefit early invasive, IIb/IIIa, LMWH
Age ≥65 years.
Presence of ≥3 risk factors for CAD (i.e., diabetes, cigarette smoking, hypertension, hypercholesterolemia, family history of premature CAD).
Known CAD (coronary artery stenosis ≥50%).
Aspirin use in the past 7 days.
≥2 episodes of angina within 24 hours.
ST changes ≥0.05 mV.
Positive cardiac markers.
Grace score
Score >140 = early invasive strategy
Low risk patients TIMI<=2
Ischemia guided strategy - stress test ok (risk stratification) - stress test before discharge or w/in 72 hrs of d/c as outpatient
Post PCI NSVT w/in 24hrs
Reperfusion rhythm - no tx needed
Guideline for revasc of stable angina
trial of OMT
2 max tolerated anti-anginals (BB, CCB, long acting nitrates, ranolazine)
Mod to severe ischemia on Nuc
> 10% - better with revasc
U/A, NSTEMI - conseravtive tx
ASA lifetime
heparin/enox/fonda x up to 8 days
Plavix x (at least 30 days) ideally 1 year
MI VSD
Sudden hypotension after late AWMI
New murmur (holosystolic thrill)
best to repair immediately (surgically)
MI Acute MR
less likely with LAD infarct as ANTERLAT PAP has dual blood supply AND would not have murmur as acute MR has rapid equalization of LA/LV pressures
Sx flash pulm edema and hypoxia not just hypotension
more likely with IWMI - posteromedial pap has single blood supply
MI Acute Free wall rupture
Late presenting Cx MI or AWMI - first CAD in older Females Effusion on echo muffled heart sounds Clear lungs Inc'd JVP
RV infarct
usually not late presentation
STEMI within 12 hrs
Urgent reperfusion therapy PCI/lytics to prevent risk of cardiac rupture Risk factors for ruputure -female, older age, Q waves on ecg, absense of collaterals, no prior h/o MI, HTN, use of steroids or NSAIDs, lytics >14 hours after start of sx