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Cardio > Acute Coronary Syndromes II > Flashcards

Acute Coronary Syndromes II Flashcards

1
Q

Paradigm for treating STEMI

A

“Time is muscle” Goal is immediate restoration of blood flow to occluded vessel.

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2
Q

Therapy that all MI patients get

A

Anti-coagulation, anti-platelet, anti-ischemic, adjunctive

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3
Q

Anti-ischemic Rx

A

Beta-blockers (relieve ischemic pain by decreasing cardiac work and oxygen demand. Reduce infarct size and arrhythmias. Mortaility benefit.)

Nitrates (enhance blood flow by coronary vasodilation and decrease preload. But don’t give to STEMI patients early, or with RV infarct)

CCB (NonDHP’s reduce HR and contractility. No mortality benefit in ACS.)

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4
Q

Antithrombotic therapy

A

Antiplatelets and anticoagulants.

Antiplatelets decrease platelet aggregation and are effective in arterial circulation.

Anticoagulants limit blood from clotting.

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5
Q

Aspirin

A

Effective across entire spectrum of ACS. Should be given as soon as possible to all patients with suspected ACS. Has rapid anti-platelet effect and reduces coronary occlusion and recurrent ischemic events after fibrinolytic therapy.

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6
Q

Clopidogrel/Prasugrel

A

Thienopyridine derivative that is an IRREVERSIBLE inhibitor of the P2Y12 Receptor. Indicated in all patients with USA/NSTEMI unless surgery planned. Takes 5 days to recover.

Prasugrel has more even effect. Newer generation.

Lots of interindividual variability in response to clop.

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7
Q

Glycoprotein IIb/IIIa inhibitors

A

Super potent, inhibit the final common pathway of platelet aggregation, but use has declined with antiplatelet drugs.

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8
Q

Anticoagulation therapy

A

Heparin
Bivalirudin
Factor Xa inhibitor

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9
Q

Heparin

A

Standard anticoagulant

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10
Q

Bivalrudin

A

Direct thrombin inhibitor. Can be used instead of heparin

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11
Q

Factor Xa inhibitor

A

Similar efficacy to LMWH but less bleeding

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12
Q

How does heparin work?

A

Unfractionated heparin: Binds to antithrombin, causes conformational change that causes it to bind to thrombin more avidly, also factor Xa.

LMWH: Binds to antithrombin, binds to just factor Xa more avidly.

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13
Q

Conservative treatment of USA/NSTEMI patients

A

Medications alone with angio/revasc only if clinical worstening or evidence of ischemia

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14
Q

Invasive treatment of USA/NSTEMI patients

A

Urgent cardiac cath.

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15
Q

How to determine risk of USA/NSTEMI

A

TIMI risk score. Risk of adverse outcomes increases with each point

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16
Q

What is ideal time to start PCI with STEMI?

A

<90 minutes.

17
Q

Can lytic agents be used for coronary artery occlusion

A

Yeah! TPA is good.

18
Q

What is better for STEMi in high risk patients: PCI or Fibrinolysis?

A

PCI

19
Q

When is fibrinolysis preferred to PCI for STEMI?

A

If there is a huge delay to get to a cath lab.

20
Q

If presentation is < 3 hours and there is no delay to an invasive strategy, what should be done?

A

No preference for either.

21
Q

Why are ACEi given in MI

A

Prevent ventricular remodeling.

Greatest benefit in anterior MI and systolic dysfunction

22
Q

What is a major complication of MI?

A

Arrhythmias.

23
Q

VFIB

A

Can cause sudden cardiac death early in MI, but can be aborted with rapid defibrillation. Take to CCU

24
Q

Supraventricular arrhythmias

A

Bradycardia, tachycardia, afib

25
Q

Pseudoaneurysm

A

Hole causes blood to pool outside LV. Communication between LV and pericardium

26
Q

True aneurysm

A

Develop months to weeks after MI. No communication between LV cavity and pericardium. Can cause arrhythmia. Tissue bulges

27
Q

Papillary muscle rupture

A

If RCA occluded, papillary muscle can rupture.

28
Q

Pericarditis after MI

A

Acute can occur if inflammation extends from myocardium to pericardium

29
Q

Dressler syndrome

A

Autoimmune process that happens 6-8 weeks post MI. Causes pericarditis,

Cardio (23 decks)

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