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Tintinalli Section 7 - Cardiovascular Disease > S7C53 - ACS: acute MI and unstable angina > Flashcards

S7C53 - ACS: acute MI and unstable angina Flashcards

1
Q

LAD

A
  • goes down anterior heart, to inferior margin, anastamoses with posterior diagonal branch or RCA
  • supplies anterior and septal regions
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2
Q

Circumflex

A
  • goes through AV sulcus, anastamoses with RCA

- supples some anterior wall and most of the lateral wall

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3
Q

RCA

A
  • 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
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4
Q

Blood supply to the AV conduction system

A
  • RCA and the septal perforating branch of the LAD

- RBB and left posterior division also have a similar blood supply

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5
Q

Inferior MI and what territory it represents on ECG.

A
  • 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
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6
Q

What percentage of MI have a normal or nonspecific ECG?

A

1-5% of AMI

10% chance of unstable angina

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7
Q

ST elevation in LBBB

A
  1. ST elevation 1mm or greater and concordant (same direction as main deflection)
  2. ST depression 1mm in leads V1, V2, or V3
  3. ST elevation 5mm or greater and discordant with the QRS
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8
Q

Paced rhythms and ST elevation

A
  • 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
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9
Q

STEMI treatment

A
  • PCI or fibrinolysis

- goals for STEMI: PCI w/in 90mins or fibrinolysis w/in 30mins

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10
Q

Acute Meds for ACS

A

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

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11
Q

Fibrinolytics

A
  • 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
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12
Q

Contraindications to Fibrinolysis

A

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
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13
Q

Risk for ICH if treated with fibrinolysis:

A
  • > 65yo

- low body weight (

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14
Q

Streptokinase

A

Allergic rxn in 5% of pts

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15
Q

Alteplase / tPA (tissue plasminogen activator)

A

-binds fibrin and triggers fibrinolysis

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16
Q

Reteplase

A
  • longer half life (18mins vs 3mins)

- no benefit b/w tPA and rtPA

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17
Q

Tenectaplase

A
  • 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
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18
Q

Rescue PCI (following failed TNK?)

A
  • 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
19
Q

Other indications for PCI in NSTEMI/UA

-should be performed w/in 48h

A
  • 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
20
Q

Aspirin

A
  • 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
21
Q

Antiplatelets

A
  • ASA
  • Adenosine Diphosphate receptor antagonists (clopidogrel)
  • GP IIa/IIIb inhibitors (glycoprotein)
22
Q

Clopidogrel / prasugrel

A
  • 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
23
Q

Glycoprotein IIb/IIIa inhibitors

A
  • 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
24
Q

Antithrombins

A
  • unfractionated heparin
  • LMWH
  • fondaparinux
  • direct thrombin inhibitors (bivalirudin)
25
Q

Unfractionated heparin

A
  • 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
26
Q

LMWH

A
  • more reliable effect than heparin

- slight advantage to use it in fibrinolysis vs heparin

27
Q

Antithrombin changes

A

-should continue on whatever antithrombin was started as changing from one to another increases bleeding risk

28
Q

Fondaparinux

A
  • 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?
29
Q

Direct Thrombin Inhibitors - bivalirudin

A
  • bind to thrombin

- safe for intermediate/high risk UA/NSTEMI receiving PCI

30
Q

Meds that limit infarct size

A
  • nitrates
  • BB
  • ACEi
  • magnesium
  • CCB
31
Q

Nitrates

A
  • 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
32
Q

Beta-blockers

A
  • 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
33
Q

ACEi

A
  • 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
34
Q

Magnesium

A
  • systemic and coronary vasodilation
  • protects myocytes from Ca influx during reperfusion
  • conflicting studies
  • correct hypomagnesemia but don’t just give Mg
35
Q

CCB

A
  • 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
36
Q

Coronary steal syndrome

A

(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)

37
Q

Complications of ACS

A
  • 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
38
Q

Indications for TV PM

A
  • 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)
39
Q

Killip CHF classification

A

I. no CHF (5% mortality)
II. mild CHF (crackles and S3)
III. frank pulm edema (40% mortality)
IV. cardiogenic shock (80% mortality)

40
Q

Dressler’s syndrome

A
  • 2-10w after AMI
  • c/p, fever, pleuropericarditis
  • tx with ASA 650mg qid (ibuprofen may cause myocardial scar thinning and infarct extension)
41
Q

Re-stenosis of a stent

A

-more likely to occur in a BMS in the short term and DES in the long-term

42
Q

Cocaine-induced MI

A
  • 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
43
Q

Medical conditions associated with MI

A
  • GI bleed
  • stroke
  • sever infxn

Tintinalli Section 7 - Cardiovascular Disease (13 decks)

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