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CPR-2 > Lecture 10: STEMI and NSTEMI > Flashcards

Lecture 10: STEMI and NSTEMI Flashcards

1
Q

What is the underlying condition/ECG changes called if coronary flow is fully occluded vs. partial occlusion?

A
  • Fully occluded = STEMI
  • Partial = Unstable Angina or NSTEMI
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2
Q

Which type of MI is sympathetic hyperactivity (↑ HR, ↑ BP) vs. parasympathetic hyperactivity (↓ HR, ↓ BP) seen in?

A
  • Sympathetic = anterior MI
  • Parasympathetic = inferior MI
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3
Q

What are 4 PE findings associated with HF?

A
  • S3
  • Crackles
  • ↑ JVD
  • New murmur
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4
Q

Everything as far as presentation and ECG will be the same for NSTEMI and NSTE ACS, except for what?

A

NSTEMI will have elevated cardiac enzymes

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5
Q

Which cardiac conduction abnormality can obscure ST elevation analysis and may hide the manifestations of a STEMI?

A

New LBBB

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6
Q

Which ECG changes will be seen in the early acute phase of a STEMI?

A
  • T wave increase in amplitude (like seen in hyperkalemia)
  • Hyper-acute pattern
  • Convex upward ST pattern
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7
Q

Besides STEMI, what are 3 other causes of ST segment elevation?

A
  • Pericarditis
  • LVH w/ J point elevation
  • Normal variant (early repolarization) common in young males and african americans
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8
Q

If a patient with no chest pain and who seems normal has this ECG, what is one characteristic that tells you it’s likely not a STEMI?

A
  • ST elevations are concave (if convex that would be early/acute MI)
  • This is early repolarization a normal variant in young males
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9
Q

In the chronic phase following STEMI, if there is persistent ST elevation (after 2 weeks) what complication should you suspect?

A

LV aneurysm

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10
Q

Q waves shouldn’t be more than how many seconds in width?

A

No more than .03 sec in width

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11
Q

Which lead is the T wave normally inverted and may be variable in which?

A
  • Inverted in aVR
  • Variable in lead III
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12
Q

Which waves/segments of the ECG represent ischemic pattern, injury pattern, and pattern of necrosis/infarction?

A
  • Ischemia –> impaired repolarization –> T waves changes (inverted/tall/peaked)
  • Injury –> inability to fully polarize –> ST elevations
  • Infarction/necrosis –> lacks depolarization –> Q wave or QS complex
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13
Q

Since there are no posterior leads, how do we view a posterior wall infarction and look for what?

A
  • Look at V1-V3 (anterior leads) and will be a mirror image
  • So looking for ST depression and a prominent R
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14
Q

After several weeks or months following an MI what Q, R, T and ST changes will exist?

A
  • Significant Q wave usually persists
  • Some R wave may return
  • T wave often less inverted
  • ST elevation may persist IF aneurysm develops
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15
Q

What does this ECG signify and how can you tell?

A
  • Recent MI of LAD (leads V1-V6)
  • Massive Q waves + T wave inversion + ST elevation
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16
Q

What is your interpretation of this ECG?

A

STEMI - Anterior Wall (LAD)

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17
Q

What is the ECG indicative of?

A
  • Anterior wall STEMI w/ left anterior hemiblock
  • The L.A.D and small R waves in II, III, and aVF meet criteria for left anterior hemiblock
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18
Q

Patient presents with what appears to be an MI and this is his ECG, where is the infarction and why?

A
  • TRUE Posterior infarct
  • Based on the reciprocal changes in anterior leads;
  • V1 shows large R (reciprocal of posterior Q) and upright T wave (reciprocal of posterior T inversion)
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19
Q

What type of MI is this indicative of?

A

Posterior wall infarction

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20
Q

Pt presents w/ chest pain and what looks do be an MI, this is his ECG, what do you suspect?

A

NSTEMI or NSTE ACS

*Need enzymes*

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21
Q

Failure of which organ can give false positive elevations of Troponin T (CTnT)?

A

Renal failure, since is excreted by kidneys

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22
Q

For patient with acute STEMI what are the reperfusion strategies if hospital has cath lab and how soon?

A
  • Primary percuteanous coronoary intervention (PCI) w/ angioplasty and stenting
  • Cath lab within 90 minutes (goal)
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23
Q

If hospital does not have cath lab or there isn’t time to get to one what is done for acute STEMI and how quickly?

A
  • Give fibrinolytic or thrombolytic
  • Begun in ED within 30 mins. (goal)
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24
Q

After beginning fibrinolysis therapy in pt with acute STEMI if there is failure of ST elevation to resolve by >50-70% within 1-2 hours this suggests what?

A

Failure of fibrinolysis

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25
Q

If your hospital does not have a cath lab (non PCI capable) how soon must patient with acute STEMI be transferred?

A

Within 120 minutes

26
Q

What is the primary reperfusion therapy for STEMI with sx’s <12 hours?

A

Primary PCI

27
Q

What is a benefit of primary PCI vs. fibrinolytics for STEMI?

A

Lower mortality rate and less chance of intracerebral hemorrhage

28
Q

Fibrinolytic therapy for reperfusion is useful in what instances, but carries what risk?

A
  • For STEMI or new LBBB within 12 hours of onset of sx’s
  • Major risk = ICH
29
Q

What are the major contraindications for administering fibrinolytic therapy?

A
  • Active bleeding (menses is excluded!)
  • Prior hemorrhagic stroke
  • Severe uncontrolled HTN
  • Recent major trauma/surgery
  • Acute peptic ulcer
  • Pregnancy
30
Q

Which drug should be given on presentation/immediately for STEMI, unless contraindicated?

A

Aspirin

31
Q

After aspirin, what other drugs should be given alongside fibrinolytic agents for STEMI?

A
  • IV Heparin
  • Antiplatelet agent (clopidogrel)
32
Q

If STEMI pt receives PCI w/ stenting which drugs should be given for at least 1 year to prevent stent stenosis?

A
  • Aspirin

AND

  • Antiplatelet agent (clopidogrel)
33
Q

What is the initial standard tx while hospitalized for STEMI?

A
  • Morphine
  • O2
  • Nitroglycerin
  • Aspirin
  • Beta-blocker if ↑ BP or ↑ HR
  • ACEI = helpful if EF ↓, ↑ BP; prevent remodeling
34
Q

Tx for NSTEMI will depend first on assessment for high risk pt, which includes what factors?

A
  • Age >65 w/ >3 CAD risk factors
  • Prior stenosis
  • ST deviation
  • >2 anginal events <24 hrs
  • Elevated cardiac enzymes
35
Q

In pt’s at highest risk for complications presenting with NSTEMI what should be done and how soon?

A

Cardiac cath lab within 48 hrs (consider PCI or CABG if indicated)

36
Q

For high-risk unstable pt’s with NSTEMI who undergo PCI, which type of drug should be considered?

A

IV GP IIb/IIIa antagonist

37
Q

Which anti-ischemic therapies should be given for NSTEMI?

A
  • Nitroglycerin (don’t use if recently taken PDE-5 inhibitor)
  • Beta-blocker if HR is ↑
38
Q

After admitting/monitoring pt with NSTEMI what are some additional drugs to consider giving?

A
  • Morphine for refractory chest pain
  • High dose statin initially
  • Consider ACE-I
39
Q

If there is recurrent chest pain that may be atypical for them, 2-4 days post-MI, what complication should be considered?

How about recurrent chest pain 2-10 weeks post-MI?

A
  • 2-4 days = acute pericarditis
  • 2-10 weeks = could be Dressler Syndrome (immune mediated)
40
Q

Treatment for acute pericarditis/Dressler syndrome as a post-MI complication?

A

Aspirin, NSAIDs

41
Q

After performing reperfusion on pt with MI you see this on ECG, what is your interpretation and what should be done?

A
  • Accelerated idioventricular rhythm (60-100 BPM)
  • Indicates reperfusion following fibrinolytic and is a good sign
  • Benign
42
Q

Which type of heart block is often associated with an inferior wall MI?

A

2nd degree AV block (Wenckebach)

43
Q

How does the tx for 3rd degree AV block differ if associated with anterior or inferior wall MI?

A
  • Anterior wall MI will require a pacemaker
  • Inferior wall MI will usually be transient and NOT require a pacemaker and if it does it will only be a temporary pacemaker
44
Q

RV infarction is a potential complication of an MI where and presents how?

A
  • Inferior MI
  • ↓ BP, clear lungs, and ↑ JVP
  • Kussmaul sign (distention of jugular vein on inspiration)
45
Q

What is tx for RV infarction as complication of inferior STEMI?

A

IV fluids

46
Q

What are complications of the LV/septum which can arise post-anterior wall STEMI?

A
  • Septal rupture –> VSD
  • LV free wall rupture (typically 7 days) –> causes tamponade
  • LV aneurysm (persistent ST elevation weeks after MI)
47
Q

Tx for LV free wall rupture post-MI?

A

Surgery

48
Q

What are thromboembolic complications which can arise from a LV aneurysm?

A

Arterial emboli —> stroke or ischemic bowel

49
Q

Proximal occlusion of RCA before acute marginal branch can cause an MI where?

Use what leads and look for what?

A
  • Acute inferior wall MI —> RV infarction
  • Use R precordial leads (V4R- V6R) for RV
  • ST elevation of 1mm or > in V4-V6R
50
Q

List 4 conditions which can present like STEMI and should be differentials?

A
  • Pericarditis
  • Myocarditis
  • Stress induced (takotsubo) syndrome
  • Early repolarization
51
Q

How should you treat ventricular tachycardia after an MI?

A

1 mg/kg bolus of lidocaine

use procainamide or amiodarone if that doesn’t work

52
Q

How do you treat ventricular fibrillation?

A

electrically

if unresponsive –> amiodarone and repeat cardioversion w/ CPR

53
Q

What defines first degree AV block?

A

PR interval >0.2 sec (one little block)

54
Q

What is wenckebach 2nd degree block?

A

PR interval keeps increasing in length until finally there is a P wave w/ no QRS response

(PR interval is long, but QRS is normal)

55
Q

What is Mobitz 2nd degree block?

A

multiple P waves followed by 1 QRS response in a ratio (2:1)

QRS is widened, but PR interval is normal

56
Q

In pts w/out ST-segment elevation, what lets you know there is an MI?

A

elevated CK-MB or troponin

57
Q

What is the universal definition of myocardial infarction?

A

rise of cardiac biomarkers with at least one value above the 99th percentile w/ evidence of MI w/ at least one of the following:

sx of ischemia

ECG changes of new ischemia

new Q waves

imaging evidence of loss of myocardium

58
Q

What did the CURE trial find?

A

20% reduction in death, MI, and stroke w/ addition of clopidogrel to aspirin in pts w/ non-STE acute coronary syndroms

59
Q

Who is clopidogrel reserve for?

A

pts who cannot receive either ticagrelor or prasugrel

ticagrelor and prasugrel are both faster and more potent, work better

60
Q

What did the EARLY-ACS trial show?

A

IV abciximab reduces ischemic events by about 25% when undergoing PCI w/ high risk sx

CPR-2 (28 decks)

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