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A-CardioPulm Rosen's > ACS > Flashcards

ACS Flashcards

1
Q

Type 2 MI is caused by what?

Seen in what conditions?

A

MI 2/2 ischemia caused by increased oxygen demand or decreased supply

Coronary artery spasm, embolism, severe anemia, arrhythmia, HoTN

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2
Q

What is type 3 MI?

A

SCD w/new STE or LBBB

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3
Q

What is type 4 MI?

Type 5?

A

MI associated w/instrumentation like PCI

MI associated w/CABG

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4
Q

When does coronary arterial vessel stenosis cause ischemic symptoms?

What about during exercise?

A

When CAD exceeds 95% obstruction to flow

60% vessel stenosis

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5
Q

What is the MC angina equivalent symptom presentation?

A

Dyspnea

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6
Q

Where does reciprocal STD occur in inferior MI?

Anterior MI?

A

aVL

II, III, aVF

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7
Q

Where should T waves always be upright?

Inverted?

A

Left-sided leads: I, II, V3-V6

aVR, V1 (usually)

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8
Q

STE in leads I and aVL indicate lesion where?

A

1st diagonal branch of LAD

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9
Q

What favors RV infarction in an inferior STEMI?

A

STE in V1 with STE in lead III > II

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10
Q

Inferior STEMI has what reciprocal changes?

A

STD in I, aVL

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11
Q

Why is it important to diagnose RV infarction with right-sided EKG?

A

They have larger infants w/higher mortality rates and complications

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12
Q

Name the 5 ACS mechs of pathophysiology

A
  1. Endothelial damage through: plaque disruption, irregular luminal lesions/shear injury
  2. Platelet aggregation
  3. Thrombus formation —> occlusion
  4. Coronary artery vasospasm
  5. Reperfusion injury via ROS, Ca, neutrophils
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13
Q

How can excessive oxygen therapy increase rate of ADVERSE outcomes in ACS?

A

Increases coronary vasoconstriction and oxidative stress

AVOID trial —> O2 increased myocardial injury, dysrhythmias increased

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14
Q

How do nitrates effect myocardium?

How?

A

Decrease preload (and some afterload)

Inc venous capacitance and induces venous pooling

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15
Q

Why is IV BB use in the ED discouraged?

What is the benefit?

A

Inc risk of adverse events including: higher rate of cardiogenic shock, inc rate of development of HF, persistent HoTN and bradycardia

Minimal reduction of re-infarction and VFib

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16
Q

Ticagrelor (Brillinta) MOA and dosing?

Peak serum [ ] reached when?

Major SE?

What clinical trial states “good value for the money” when used with ASA?

A

P2Y12 receptor inhibitor that does NOT require hepatic activation, 180mg loading dose

2.5 hours

Nonprocedure-related bleeding, inc ICH

PLATO study

17
Q

What is the standard loading dose of Clopidogrel for STEMI?

A

300mg but can do 600mg

18
Q

What is the ACC/AHA class I recommendation regarding clopidogrel/ticagrelor?

What if CABG is preformed w/in 5 days of clopidogrel use?

A

Withhold for at least 24 hours before urgent on-pump CABG

Inc rate of op and postop hemorrhage, need for transfusion, postop mortality

19
Q

What is Cangrelor (kenreal)?

A

IV P2Y12 receptor inhibitor w/IMMEDIATE action and half life of 4-6 minutes

20
Q

What about prasugrel (Effient) 60mg compared to ticagrelor 180mg?

Adverse SE of prasugrel?

A

ISAR-REACT5 trial in Germany 2019 showed prasugrel was superior to ticagrelor

Pts > 75 y/o,weighing more than 60kg, previous TIA have higher bleeding risk

21
Q

LMWH (Enoxaparin) dosing is what?

If GFR < 30?

A

Bid at 1 mg/kg

QD

22
Q

Dose of tPA for STEMI?

A

100mg bolus

23
Q

What time frame is considered a contraindication to fibrinolytic therapy?

How was this proved?

A

> 12 hours after symptom onset

LATE trial found 26% decrease in 35 day mortality in pts treated w/tPA from 6-12 hours sx onset with NO decrease in mortality after 12 hours

24
Q

What BP is an absolute contraindication to tPA for STEMI?

What are 2 additional contraindications?

A

> 200/120 in the ED

Previous ICH
CPR for > 10 minutes

25
Q

What does the term ACS include?

A

Unstable Angina
AMI (NSTEMI and STEMI)
SCD - sudden cardiac death

26
Q

Type 1 MI is spontaneous MI related to ischemia from what?

A

Plaque erosion rupture
Thrombus formation that is eroding, fissuring, dissecting
Vasospasm

A-CardioPulm Rosen's (7 decks)

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