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
Timing of free wall rupture
Pre-lytic era - 5 days
Reperfusion era - 48hrs
STEMI acute HF
Lasix (since patient needs to lie flat during PCI)
DO NOT USE BB (can cause CV shock)
No reason for IV ACEi (enalaprit)
No lytics if awaiting urgent primary PCI
Lytics
> 75yo - load 75 plavix then 75 daily with lytics
<75yo - load 300 plavix then 75 daily with lytics
No enoxaparin as antithrombitc if CrCl<30 (use UFH)
RV infarct
hypotension after IWMI clear lung fields inc'd JVD evidence of poor perfusion tx - early reperfusion, volume/ionotrope support
Syntax
Low <22 - same outcomes pCI/CABG
Int 23-32
High >33 - lower mortaility with CABG
STEMI
FMC to PCI <120 minutes then ASA,plavix tx for PCI
Also transfer if high risk for bleed (ie on coumadin) - less good to do lytics if INR could be elevated
Facilitated PCI
Lytics then immediate tx for PCI
Selection of Reperfusion strategy STEMI
1) Time from onset sx (w/in 3 hours good for lytics)
2) Risk level of STEMI
3) Risk of bleedign
4) Time to tx to PCI facility
12-24 hrs from sx - transfer for PPCI if HD unstable, sev CHF, HD or electrical instability, persistent ischemic sx
>12 Asx - no PPCI
PPCI over lytics for high risk STEMI
TIMI>5
Pulm edema
HD/electrical instability
Contraindications to lytics
h/o ICH active bleeding suspected Ao Dissection Known cerebrovasc malformation known malignant intracranial neoplasm (primary or metastatic)
RP Bleed
Tirofiban enhanced effectiveness with dec’d renal fxn
No plts with tirofiban or eptifibide (rev binding with plts)
Abciximab - irrev binding to plt - need plt tx if bleeding
Third universal definition of MI
1) Elevation of troponins
2) Sx/Si of ischemia (new signficiant ST/T wave changes, new LBBB, new pathologic Q’s, new WMA, intracoronary thrombus
2nd Universal MI def
Supply demand mismatch (ie hypovolemia, GIB, rapid AF)
Type 1 MI
Plaque rupture
Dx criteria for STEMI
> 2mm V2-3 (1.5 for F)
1mm in other leads
Scarbossa
concordent ST elev >1mm with LBBB in 2 leads any lead with positive QRS def
discordent ST dpression >1mm V1-3
Discordent ST elev >5mm - any lead with neg QRS def
SYNTAX study
less TVR in 3vz DM patients with CABG than PCI
FREEDOM
DM & MV disease
Lower rate of death, non-fatal MI in CABG
Pre-op CV testing
Non-invasive testing should only be performed if a rationale exists to do so independent of pre-op eval OR if fxn status poor or unable to ascertain (cannot walk pre-fem pop ie)
TTE for patients with known valve disease if no TTE w/in 1 year
Revascularization should only be performed if would be done independent of propopsed non-cardiac surgery
Choice of DAPT
Prasugrel - NO if h/o CVA, >75yo, low BMI
Ticagrelor - NO if asthmatic or bradycardia, h/o ICH, liver dysfxn
CCTA
high sensitivity and NPV
rule out CAD in low to int risk patients
DO NOT USE if high pretest prob
Bayes theorum
Post test probability of CAD depends on stress results AND pre-test probability (ie neg ECG stress shifts a high pretest patient ie 60yo M Obesity, tob, HTN, HLD with typical angina - little change in probability - still very high…
Excercise Treadmill Stress Test
bad for women <60 with NON-anginal pain (low risk)
or
men >50yo with typical angina
Troponin
even if neg in first 6 hours -> trend
CPR
Epi then vasopresssin then antiarrythmics (amio)
Vasopressors before antiarrhtymics
Stent thrombosis
Resistance to clopidogrel 2/2 inability to convert drug to active form from genetic polymoprhism
Angina with CABG (LIMA) and diminished L radial pulse
r/o L SCA stenosis proximal to LIMA
Get vertebral artery duplex -> if see reversal of flow then can assume L SCA stenosis
Subclavian steal syndrome
CT Coronary for stable angina
+LAD - first start meds then consider cath…
Post CV arrest
STEMI after return of sponatenous circulation
EMERGENCY CATH
If NSTEMI with HD/electrical instability -> EMERGENCY CATH
Neuro exam post arrest unreliable (improved at 72h hours)
STEMI with afib
rate control with BB with HTN crisis or tachyarrythmia
NO SHORT ACTING NIFEDIPINE
NO CCB if systolic dysfxn
NO IBUTILIDE - no need for cardioversion
Cocaine induced MI
use only carvediolo or labetolol because block catecholamine surge (beta blockade) and prevent coronary vasosapsm (alpha blockade) Use benzo (lorazepam)
Vorapaxar
PAR-1 inhibitor - thormbin rct on plts - added to DAPT in pts with heart attack/PAD
contraindicated with h/o TIA or stroke - excessive risk of intracranial hemorrhage
Mechanical complications of MI
Pap muscle rupture - inferior MI and pulmonary edema - no murmur 2/2 sudden equalization of LA/LV pressure - 2-7 days post MI, CV shock
VSD - usually AWMI 3-5 days
RV infarct - IWMI - clear lung fields
Ticagrelor
less stent thrombosis
s/e bradycardia and dyspnea
Lipids in ACS
check lipids w/in 24hr
treat with high intensity for all patients with ASCVD <75yo (if >75yo mod intensity)
Plaque rupture
inflammation (macrophages)
integrity of fibrin cap
plaque lipid contnet
plaque location
Plaque histopathy
1) MMP degrade fibrous cap - plaque reputure
2) Majority of plaque rupture at plaque shoulder - greatest tensile force from blood flow
3) Branch points of coronaries have low shear stress allowing atheroscleortic plque formation and inflitration of monocytes that promote plque rupture
4) Neutrophils/macros - have myeloperoxidase -free radicles that promote inflammation/plque ruputre
5) Coronary calcium found in 80% ruptured plaques
Bare metal stent and urgent surgery
need to wait 4 weeks before d/c plavix
Ticagrelor
metabol by CYP450
reduced effect with rifampin,phenytoin, carbamaepine, phenobarbital, dexamethasone
Cardiac biomarkers
Use Troponin I
DO NOT USE CK-MB or myoglobin (Class III)
Risk scores
Heart - history, ECG, Age, risk factors, troponin
ER risk stratification for Chest pain - major events w/in 6 weeks
TIMI/GRACE - risk of death/MI in patients with ACS
Framingham - risk of MI in 10 years in stable patient
high pre-test ACS patient with silent ECG
check posterior leads r/o posterior MI
Out of hospital arrest
Class I hypothermia for comatose patients
Platelet reactivity testing P2Y12
not indicated (studies inconclusive)
