S7C53 - ACS: acute MI and unstable angina Flashcards
LAD
- goes down anterior heart, to inferior margin, anastamoses with posterior diagonal branch or RCA
- supplies anterior and septal regions
Circumflex
- goes through AV sulcus, anastamoses with RCA
- supples some anterior wall and most of the lateral wall
RCA
- runs in AV sulcus b/w RA and RV, gives off marginal branch, terminates as the right posterior descending artery
- supplies the right side of the heart and some part of the inferior aspect of the LV through the posterior descending artery
Blood supply to the AV conduction system
- RCA and the septal perforating branch of the LAD
- RBB and left posterior division also have a similar blood supply
Inferior MI and what territory it represents on ECG.
- inferior = L circumflex or RCA (L Cx if there is ST elevation in one of the lateral leads -V5,6, aVL- with isoelectric or elevation in lead I)
- if ST elevation is greater in III than in II this is more likely RCA
- if ST elevation in V1 or V4R this is more likely proximal RCA
What percentage of MI have a normal or nonspecific ECG?
1-5% of AMI
10% chance of unstable angina
ST elevation in LBBB
- ST elevation 1mm or greater and concordant (same direction as main deflection)
- ST depression 1mm in leads V1, V2, or V3
- ST elevation 5mm or greater and discordant with the QRS
Paced rhythms and ST elevation
- RV pacing causes repolarization opposite of that to the predominant QRS
- most leads will have a predominant negative QRS followed by ST elevation
- ST elevation >5mm is most indicative of AMI in leads with predominantly negative QRS
- any ST segment elevation that is concordant with the QRS in a predominantly positive QRS complex is specific for MI
- in RV pacing QRS usually neg in V1 and V3, ST depressio is 80% specific for MI in these leads
STEMI treatment
- PCI or fibrinolysis
- goals for STEMI: PCI w/in 90mins or fibrinolysis w/in 30mins
Acute Meds for ACS
Antiplatelets: ASA, clopidogrel, ticagrelor
Antithrombins: UF Heparin, enoxaparin, fondaparinux
Fibrinolytics: streptokinase, alteplase, tenecteplase, reteplase,
Glycoprotein IIb/IIIa inhibitors: abciximab, eptifibatide, tirofiban
Other agents: nitro, morphine, metoprolol, atenolol
Fibrinolytics
- plasminogen activators
- plasminogen binds directly to fibrin during thrombus formation, forms a complex, promotes fibrin proteolysis\
- > 30 lives saved per 1000 pts treated with lysis
- Indications:
- STEMI
- time to treatment is
Contraindications to Fibrinolysis
Absolute:
- any previous ICH
- known cerebral vascular lesion (AV malf.)
- known brain neoplasm
- ischemic stroke w/in past 3mo
- active internal bleeding
- suspected Ao dissection or pericarditis
Relative:
- severe uncontrolled BP (>180)
- hx of chronic severe poorly controlled HTN
- hx of prior ischemic stroke >3mo
- current use of AC with INR>2
- known bleeding diathesis
- trauma in past 2w
- prolonged CPR (>10min)
- major surgery
Risk for ICH if treated with fibrinolysis:
- > 65yo
- low body weight (
Streptokinase
Allergic rxn in 5% of pts
Alteplase / tPA (tissue plasminogen activator)
-binds fibrin and triggers fibrinolysis
Reteplase
- longer half life (18mins vs 3mins)
- no benefit b/w tPA and rtPA
Tenectaplase
- TNK
- derived from tPA, longer half life (20mins), minimal systemic fibrinogen depletion, no difference in 30d mortality or ICH b/w TNK and tPA
- easy to administer - single bolus
- weight based dosing
Rescue PCI (following failed TNK?)
- pts in cardiogenic shock >75yo
- severe heart failure or pulm edema
- hemodynamically compromising ventricular arrhythmias
- failed fibrinolytic tx with moderate/large are of myocardiu, at risk
Other indications for PCI in NSTEMI/UA
-should be performed w/in 48h
- recurrent angina
- elevated trops
- new ST depression
- high-risk findings on stress test
- depressed LV fxn
- hemodynamic instability
- sustained v-tach
- PCIs w/in previous 6mo or prior coronary artery bypass
Aspirin
- antiplatelet
- 162-325mg ASAP for all ACS (not enteric coated)
- prevents formation of thromboxane A2, an agonist of pletelet aggregation
- lasts 8-12 days (life of platelet)
- reduces mortality rate by 23% in STEMI
- inhibits thromboxane A2
Antiplatelets
- ASA
- Adenosine Diphosphate receptor antagonists (clopidogrel)
- GP IIa/IIIb inhibitors (glycoprotein)
Clopidogrel / prasugrel
- adenosine diphosphate receptor antagonists (AD)
- omeprazole reduces the effect of plavis
- pts with variant CYP2C19 can not metabolize plavix to its active form
- withold 5d before CABG if possible
Glycoprotein IIb/IIIa inhibitors
- abciximab (reopro)
- irreversibly binds to the GP IIb/IIIa antagonists
- when used with ASA and antithrombin there is an 40% reduced risk of death or AMI in 30d (13% of 3y)
- best used in pts undergoing PCI
- usually used when there is a large clot burden and concern for a lot of downstream microvascular occlusion
Antithrombins
- unfractionated heparin
- LMWH
- fondaparinux
- direct thrombin inhibitors (bivalirudin)
Unfractionated heparin
- forms a complex with antithrombin III which then inactivates circulating thrombin and activated factor X
- not effective against clot-bound thrombin
- used acutely in ACS it has a short-term reduced risk of death or AMI of 56%
- initial bolus of 60units/kg (max 4000 units (AHA) or 5000 units according to ESC guidelines)
- infusion of 12units/kg/h (max 1000/h)
- should be stopped 48h to reduced risk of HIT
LMWH
- more reliable effect than heparin
- slight advantage to use it in fibrinolysis vs heparin
Antithrombin changes
-should continue on whatever antithrombin was started as changing from one to another increases bleeding risk
Fondaparinux
- binds to AT-III to form an antithrombin complex, specific for factor X inhibition
- lower risk of bleeding than enoxaparin in UA/NSTEMI pts
- good for medical management
- if used for PCI, UFH or bivalirudin should be added?
Direct Thrombin Inhibitors - bivalirudin
- bind to thrombin
- safe for intermediate/high risk UA/NSTEMI receiving PCI
Meds that limit infarct size
- nitrates
- BB
- ACEi
- magnesium
- CCB
Nitrates
- relax vascular smooth muscle
- decreases pulm cap wedge pressure, systemic BP, LV end-systolic/diastolic volumes, decreased afterload
- decreases cardiac work and O2 demand
- IV nitro infusion should be titrated up to BP reduction (decrease MAP by 10% if normotensive, 30% if hypertensive)
- end goal is not symptom resolution but BP reduction
- AHA guidelines recommend IV nitro for first 24-48h for STEMI, CHF, HTN
- do not give if pt has rcvd sildenafil in past 24h or tadalafil in past 48h
Beta-blockers
- antiarrhythmic, anti-ischemic and antihypertensive
- decrease myocardial demand by lowering HR, systemic resistance and contractility
- no benefit for early therapy (reduces reinfarction but increases cardiogenic shock)
- start w/in 24h if: no signs of CHF, no evidence of decreased CO, no increased risk for cardiogenic shock (age>70, BP110 or
ACEi
- reduce LV dysfxn and LV dilatation
- reduces mortality in AMI pts
- 4.6 fewer deaths per 1000 pts
- contraindications: HoTN, renal stenosis, reanl failure, hx of cough or angioedema
Magnesium
- systemic and coronary vasodilation
- protects myocytes from Ca influx during reperfusion
- conflicting studies
- correct hypomagnesemia but don’t just give Mg
CCB
- antianginal, vasodilation, antihypertensive
- no effect on mortality rate, may cause coronary steal syndrome
- increased mortality in CHF with diltiazem
- do not use if LV dysfxn, AV block
Coronary steal syndrome
(coronary perfusion pressure reduced due to disproporionate dilatation of the coronary arteries next to the ischemic zone +/- reflex activation of sympathetic nervous sytem with increase in myocardial O2 demand)
Complications of ACS
- dysrhythmias (CHB can be a predictor of poor outcomes)
- CHF - diastolic or systolic dysfxn (systolic dysfxn leads to decr EF)
- mechanical complications: papillary rupture (MR), free wall rupture, septal rupture, pericarditis
- RV infarct: shock, if doesn’t improve after 1-2L of NS start dobutamine, if LV dysfxn also present nitroprusside may be reqd to reduce afterload
- other: LV thrombus, PE, infarct extension, angina
Indications for TV PM
- asystole
- unresponsive symptomatic brady
- mobitz II or higher
- new LBBB
- alternating BBB
- RBBB or LBBB with 1st deg block
- RBBB with left anterior or posterior hemiblocks
- unresponsive recurrent sinus pauses (>3s)
Killip CHF classification
I. no CHF (5% mortality)
II. mild CHF (crackles and S3)
III. frank pulm edema (40% mortality)
IV. cardiogenic shock (80% mortality)
Dressler’s syndrome
- 2-10w after AMI
- c/p, fever, pleuropericarditis
- tx with ASA 650mg qid (ibuprofen may cause myocardial scar thinning and infarct extension)
Re-stenosis of a stent
-more likely to occur in a BMS in the short term and DES in the long-term
Cocaine-induced MI
- ECG not as useful for predicting
- trops are very important
- tx: ASA, nitrates, benzos
- BB are contraindicated
- PCI is definitive tx, may also give antithrombins and antiplatelets
Medical conditions associated with MI
- GI bleed
- stroke
- sever infxn
