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Cardiovascular > EXAM #2: MI I & II > Flashcards

EXAM #2: MI I & II Flashcards

1
Q

What does a MI typically result from?

A

Rupture/erosion of a VULNERABLE PLAQUE and the inflammation/pro-coagulation that follows

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2
Q

What is Acute Coronary Syndrome (ACS)?

A

Spectrum of clinical events that follow plaque rupture:

1) Unstable angina
2) Non-STEMI
3) STEMI

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3
Q

Do most plaque ruptures result in clinical events?

A

NO

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4
Q

What is the difference between NSTEMI and STEMI, in terms of the severity of coronary occlusion?

A

NSTEMI= partial occlusion of the coronary artery

STEMI= complete occlusion of coronary artery

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5
Q

What are the lab and ECG features that are diagnostic for an acute MI?

A

1) Elevation of cTn in setting of ischemia

2) ST changes or new onset LBBB

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6
Q

What are the ECG and echo features of a prior MI?

A

1) Q-waves

2) Evidence of loss of ventricular wall function

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7
Q

What are the three classifications/types of an MI?

A

1) Spontaneous MI caused by primary coronary event
2) MI secondary to supply/demand mismatch
3) Sudden cardiac death in setting of suspect MI

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8
Q

What are the characteristics of a stable atherosclerotic plaque?

A
  • Thick fibromusuclar cap
  • Few inflammatory cells
  • Intact endothelium
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9
Q

What are the characteristics of an unstable/vulnerable atherosclerotic plaque?

A
  • Thin fibromuscular cap
  • Copious inflammatory cells
  • Eroded endothelium
  • Protruding Ca++
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10
Q

Where does atherosclerotic plaque rupture typically occur?

A

“Shoulder region” of the plaque

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11
Q

What “background” predisposes a vulnerable atherosclerotic plaque to ACS?

A
  • Proinflammatory

- Procoagulant

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12
Q

How does a coronary artery remodel in response to atherosclerosis?

A

“Positive remodeling”

*Diameter of artery gets bigger to accommodate the plaque

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13
Q

What are the possible manifestations of a MI on cardiovascular physical exam?

A

1) Paradoxically split S2 from LV dysfunction
2) S4 from stiff LV
3) S3 with LV dysfunction/HF
4) New onset of MR

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14
Q

What is the Killip Classification?

A

Risk stratification tool for decompensated HF from acute MI

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15
Q

What is a Killip Class I?

A
  • No rales

- No S3

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16
Q

What is a Killip Class II?

A
  • Rales over less than 50%

or

-S3

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17
Q

What is a Killip Class III?

A

Rales in over 50% of lung fields

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18
Q

What is a Killip Class IV?

A

Shock

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19
Q

In what patient populations do you need to have an increased index of suspicion for acute MI?

A

1) DM
2) Women
3) Elderly

All present atypically and with more dyspnea, nausea/vomiting, or fatigue

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20
Q

What do you need to do for any DM patient that is “just not feeling right?”

A

ECG

21
Q

What are the major lethal differential diagnoses for chest pain?

A

1) MI
2) PE
3) Pneumothroax
4) Acute aortic syndromes
- Dissection
- Perforated ulcer
- Intramural hematoma

22
Q

What is the most sensitive and specific serum biomarkers of myocyte injury?

A

Cardiac specific troponin (cTn)

23
Q

What is the clinical utility of CK-MB as a biomarker?

A

Differentiating timing

E.g. if a patient has chest pain a week ago and today–CK-MB elevation will correlate with acute MI today

24
Q

What imaging should you get for a patient with chest pain?

A

1) CXR– r/o pneumothorax
2) Echo– wall motion and r/o aortic dissection
3) Nuclear SPECT
4) CT Cornary Angiography

25
Q

On CXR, what is an indication of an aortic dissection?

A

Widened mediastinum

26
Q

What is the first thing to do with a patient complaining of chest pain?

A

ECG

Goal is to obtain within 10 minutes of arrival and dictates further decision-making

27
Q

What do you need to remember about the differences between ST depression and ST elevation?

A

ST depression does NOT correlate/ localize to an anatomic territory

28
Q

What is the current guideline for the immediate treatment of a-fib with with re-entry tachycardia (underlying WPW)?

A
  • Amiodarone (stable)

- Cardioversion (unstable)

29
Q

If a patient presents with STEMI, what do you need to plan for?

A

Plan for IMMEDIATE reperfusion

30
Q

What anti-platelet medication should all patients with STEMI get?

A

4x 81mg ASA

31
Q

What are the main classes of medical therapy for acute MI?

A

1) Anti-platelet
2) Anticoagulant
3) Anti-ischemic

32
Q

Practically, what should happen for every patient with acute MI?

A

1) Oxygen–lowest flow to keep O2 sat. at 90-92%
2) ASA (325mg)
3) Sublingual NTG
4) Anticoagulant e.g. Clopidogrel

33
Q

What is the second line medication to consider in a patient with angina refractory to NTG?

A

Beta-blockers e.g. IV metoprolol

*Best for patient that is tachycardic and hypertensive

34
Q

What are the three zones in a MI?

A

1) Zone of infarct
2) Zone of injury
3) Zone of ischemia

35
Q

What is the most common cause of inferior MI? What is secondary?

A

1) RCA

2) LCX

36
Q

What can result in transient AV block in inferior MI?

A
  • Inferior MI is associated with high vagal tone

- Vagotonia can induce AV block that is transient

37
Q

What infarction is associated with inferior MI?

A

RV

38
Q

What PE sx. are seen with RV infarction?

A

1) JVD
2) Hypotension
3) Clear lung fields

Note that LAD occlusion with impaired wall function will caused CRACKLES in the lung fields

39
Q

What can you do to confirm a RV infarction?

A

V4R

40
Q

What medications should be avoided or used with caution in a RV infarction?

A

1) NTG
2) Beta-blockers

Note that trying IV fluid initially can be helpful–be sure that lung are clear

41
Q

What is the clinical utility of thrombolytic therapy?

A

Cath. lab not available within 90 min of first medical contact

42
Q

What are the absolute contraindications to thrombolytic therapy?

A

1) Prior ICH
2) Known cerebral vascular lesion
3) Known malignant intracranial neoplasm
4) Ischemic stroke within 3 months
5) Active bleeding/ bleeding diathesis (NOT menses)
6) Head/facial trauma within 3 months
7) Intracranial or intraseptal surgery within 2 months
8) Severe uncontrolled HTN

43
Q

Should you give patients thrombolytics in NSTEMI?

A

NO–these are CONTRAINDICATED

44
Q

How does the medical management of NSTEMI differ from STEMI?

A

1) More aggressive with initial Beta-blocker therapy

2) GP IIb/IIIa inhibitor for refractory angina

45
Q

How does the clot type differ between STEMI and NSTEMI?

A

STEMI= fibrin rich “red’

NSTEMI= platelet rich “white”

46
Q

What are the factors that would make you send a patient with NSTEMI to the cath lab?

A

1) Elevated cTn
2) Dynamic ST changes
3) Recurrent sx.
4) Low EF

47
Q

What should be done for patients post-MI?

A

1) Assess EF with transesophageal echo
2) Assess/address risk factors
3) Educate about event and new lifestyle
4) Cardiac rehab

48
Q

Outline post-MI medical therapy.

A

1) ASA for life
2) P2Y12 inhibitor for 1x year
3) Beta-blocker
4) ACE inhibitor if EF under 40%
5) Aldosterone antagonist for EF less than 40%
6) High intensity statins
7) PRN NTG

Cardiovascular (38 decks)

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