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CRP- Cardiology > Clinical Myocardial Infarction > Flashcards

Clinical Myocardial Infarction Flashcards

1
Q

What classically precipitates angina?

A

exercise, stress, or cold.

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2
Q

What is stable angina?

A

angina that occurs with exertion or after a big meal. This generally means that a plaque has become large enough to produce a partial obstruction of a coronary artery. IT occurs at a relatively fixed and predictable point and can slowly change over time (ex. same thing happens every time they walk the dog).
Ischemia occurs when activity causes an increase in O2 demands to the point that is beyond the coronary blood supply.

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3
Q

What is acute coronary syndrome (ACS)?

A

A term used to describe pts with acute chest pain and other symptoms of myocardial ischemia (condition brought on by a sudden reduction or blockage of blood flow to the heart). It could be 3 things:

  1. unstable angina
  2. non ST segment elevation MI
  3. ST segment elevation MI
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4
Q

What causes acute coronary syndrome (ACS)?

A

a reduction in myocardial blood flow due to disruption of atherosclerotic plaque caps leading to platelet aggregation, or thrombus formation at site of an atherosclerotic plaque.

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5
Q

What is a STEMI?

A

ST segment elevation

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6
Q

What is a non-STEMI?

A

ST segment depression (similar to unstable angina) only this will show cardiac enzymes and unstable angina will not.

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7
Q

What are the clinical features of IHD?

A

chest pain. People define “pain” differently. So be sure to ask if they have tightness, heaviness, pressure…

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8
Q

What questions should you ask?

A

You need to ask about its severity, location, radiation, duration, and quality. Also diaphoresis, dyspnea, and syncope.

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9
Q

How many patients with AMI are clinically unrecognized?

A

30% Some have had atypical symptoms for which they didn’t pursue medical advice.

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10
Q

Who are most at risk to have clinically unrecognized symptoms?

A

women and elderly often because they have atypical symptoms such as GI symptoms.

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11
Q

What are the cardiac risk factors?

A

age over 40, male, post-menopausal women, family history with 1st degree relative, smoking, hypertension, DM

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12
Q

How helpful is the physical exam in the setting of ACS (aka MI)?

A

not very helpful actually. Instead you have to look at the person because they will look like crap.

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13
Q

What heart sounds are related to ACS (aka MI)?

A
  • S1 and S2 are often diminished due to poor myocardial contractility.
  • S3 can be present due to failing myocardium
  • S4 is common in pts with long standing HTN or myocardial dysfunction.
  • New systolic murmur is an ominous sign! This signifies papillary muscle dysfunction, flail leaflet of mitral valve or VSD.
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14
Q

What are the 5 types of MI?

he said we are only going to talk about types 1 and 2

A
  1. Type 1= typical plaque rupture.
  2. *Type 2= SUPPLY DEMAND MISMATCH: MI secondary to ischemia due to either increased O2 demand or decreased supply, coronary embolism, ANEMIA, arrhythmias, hypertension or hypotension.
  3. Type 3= sudden unexpected cardiac death
  4. Type 4a= MI associated with PCI. Type 4b= MI associated with stent thrombosis
  5. Type 5
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15
Q

What is the duration of symptoms for angina?

A

typically less than 20 mins if stable.

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16
Q

Are the symptoms similar between unstable angina and MIs (NSTEMI or STEMI)?

A

YES

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17
Q

Are the serum biomarkers (troponins) the same or different between unstable angina and MIs (NSTEMI or STEMI)?

A

different. Unstable angina will not show serum biomarkers but both NSTEMI and STEMI will show serum biomarkers.

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18
Q

How do unstable angina and NSTEMI compare on the EKG?

A

they are the same! Both show ST segment depressions with T wave inversion.

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19
Q

So what really is the difference between a type 1 and type 2 MI?

A

type 1 involves a rupture with thrombus, whereas type 2 means you can go about your normal activities, but you have fixed atherosclerosis and supply-demand imbalance, so when something changes you can’t get enough blood to the myocardium and can spill some enzymes.

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20
Q

What is the best way to determine an MI?

A

12 lead EKG (must be read within 10 mins of a pt complaining of chest pain in the hospital).
However, even though it is the best, it still has a low sensitivity of picking up an acute MI.

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21
Q

If a patient comes in complaining of chest pain and has a new LBBB, what does this mean?

A

they are having an MI until proven otherwise!

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22
Q

**What leads on the EKG correspond to specific coronary arteries?

A
  • leads II, III, aVF= RCA or LCX
  • leads I, aVL= LCX or diagonal branch of LAD
  • V1-4= LAD
  • V5-6= LCX or LAD
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23
Q

If you have ST depressions, can you figure out what coronary artery we are dealing with?

A

NO!! Only with ST elevations can we distinguish between coronaries.

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24
Q

**What will you see on an EKG with an anterior MI?

A

STEMI V1-4

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25
Q

**What will you see on an EKG with an inferior wall MI?

A
  • ST segment elevation in II, III, and AVF
  • ST segment depression in I, AVL, or both (reciprocal changes)
  • Inferior wall is supplied by RCA and LCX
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26
Q

**What will a lateral wall MI look like on an EKG?

A
  • ST elevation in I, AVL, V5-6
  • high lateral wall (I and AVL)
  • low lateral wall (V5-6)
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27
Q

**What will a posterior wall MI look like on an EKG?

This one is different

A
  • ST DEPRESSION (V1-4)
  • duration of R wave to S wave >1 (V1 or 2)
  • can even place leads around the back (V7-9) and see ST elevations in these.
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28
Q

What 3 differentials should go through your head when you see anterior ST depressions in leads V7-9?

A
  1. reciprocal changes
  2. concomitant anterior ischemia
  3. posterior infarction
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29
Q

What will you see in a right ventricular MI?

A

RCA occlusions.
You will see ST elevations in V4 RIGHT when using RIGHT SIDED LEADS.
- Look also for Q waves in leads II, III, and aVF.

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30
Q

How often do pts having MIs show up with elevated enzymes?

A

50% because in order to spill cardiac enzymes, you must have ongoing ischemia for at least 20 mins and it can take up to 6-12 hours for these enzymes to show up in the blood tests.

31
Q

What markers are used most often clinically?

A

CPK-MB and troponins.

32
Q

How long will troponins last?

A

7-10 days in the blood stream (so they are less useful in detecting RECURRENT MIs during this time).

33
Q

What enzyme level is considered diagnostic for acute MI?

A

elevated troponin I or T

34
Q

With what do low levels of troponins correlate?

A

risk for CV complications in CAD and renal failure

35
Q

When is CPK-MB more useful?

A

If you get recurrent pain after you’ve already been infarcted because it’s useful in detecting recurrent infraction after the initial 24-48 hours by noting a repeat elevation in the level (because these rise and fall more quickly).

36
Q

How do we treat ACS?

A
  • beta blockers, nitrates, and sometimes Ca++ channel blockers. These reduce O2 demand on the heart and increase O2 supply :)
  • antiplatelet therapies: aspirin, clopidogrel
  • GpIIb/IIIa inhibitors
  • statin
  • ACE inhibitors
37
Q

What is the first decision when treating STEMI ACS?

A

catheter lab (PCI) or not… The sooner you get there, the more tissue you salvage. If you are not within 90 mins of a cath lab, you can get lytic therapy (rural area).

38
Q

What is the first decision when treating non-STEMI ACS?

A

conservative vs. invasive approach. Most times cath lab is the best approach, however recent research shows high risk pts (esp. DM) should be treated medically rather than invasively.

39
Q

What is the first thing you should do if a person is complaining of chest pain (STEMI)?

A

immediately give 162-325 mg of aspirin (CHEWED). If aspirin allergy, give 300 mg clopidogrel (plavix).
- also Thienopyridines: Ticagrelor (Brillenta)= newer agent but when using this, only give 81 mg of aspirin after the initial aspirin dose.

40
Q

What is important to remember about Ticagrelor?

A

it works on the adenosine receptors and can cause SOB.

41
Q

When should heparin be given?

A
  • 1-2 days IV after PCI or lysis with tPA to prevent DVT.

- Also if atrial fibrillation, LV thrombus, or new anterior MI

42
Q

Why are nitrates important?

A
  • they reduce pain/ischemia and reduce pulmonary congestion in heart failure.
  • only use I.V. or sublingually with frequently reoccurring chest pain associated with ischemia
43
Q

Can you give a nitrate to someone who has taken Sidenafil (Viagra)?

A

NO, because it causes an unsafe drop in BP.

44
Q

Why are ACE inhibitors important?

A

they decrease remodeling, decrease afterload (therefore improving forward flow) decreasing heart failure and decreasing death :)
- use captopril or lisionopril

45
Q

Why are statins important?

A

they reduce reinfarction and death, regardless of LDL levels. Better when given early.
- use crestor, lipitor, or zocor

46
Q

What is a ventricular septal defect (VSD)?

A

left to right shunting at the ventricular level causing right volume overload.

47
Q

What will you hear with a VSD?

A

loud holosystolic murmur over the sternum. It won’t respond to maneuvers. You will feel a thrill and this requires surgical repair.

48
Q

What occurs in a free wall rupture?

A

part of the LV blows out. Occurs commonly in the hypertensive elderly and is fatal. Occasionally walls off to form pseudoaneurysm.
Urgent surgery is best chance.

49
Q

What occurs commonly with an inferoposterior MI?

A

papillary muscle infarction leading to acute MR. This will cause left heart failure/pulmonary edema.

50
Q

How do you fix a papillary muscle infarction?

A

reperfuse it, stent the artery and repair the valve.

51
Q

Does the posteromedial or anterolateral papillary muscle tend to rupture more often?

A

POSTEROMEDIAL because it only has one blood supply (PDA). The anterolateral on the other hand has two blood supplies (LAD and LCX) so the odds are better in its favor.

52
Q

Can you lie flat with an MR or VSD?

A

VSD. You cannot lie flat with an MR because all the fluid is going into your lungs since the left ventricle can’t pump as much blood (as some of it is going back into the left atrium through the mitral valve).

53
Q

Should your O2 sats be higher in your RV than your pulmonary artery?

A

NO. If it is, you have oxygenated blood entering from the left ventricle and thus a VSD. Seen with PA catheter.

54
Q

Will diastolic pressures be equal with a VSD?

A

YES :(

55
Q

What are some other complications to consider if a pt presents to the ER after recent discharge from the hospital?

A

LV thrombus formation, arterial embolization, pulmonary embolism, postinfarction angina, or infarct extension

56
Q

What is the difference between a true aneurysm and a pseudoaneurysm?

A

the wall of the ventricle can be seen in a true aneurysm and will occur late. Ir also is an infarct EXPANSION, not an infarct extension.
In a pseudoaneurysm has a narrow base with walls composed of thrombus and pericardium and has a high risk of myocardial rupture.

57
Q

In what type of infarct is a true ventricular aneurysm more likely?

A

LAD infarct

58
Q

In what type of MI is a thromboembolism more likely?

A

large anterior MI. This can cause embolic stroke.

59
Q

How do you treat a thromboembolism?

A

aggressive anticoagulant therapy

60
Q

What will you see with pericarditis?

A

fever, sharp pain with pleuritic tendency, and friction rub. This is more common in non-reperfused STEMI pts.

61
Q

What is pericarditis?

A

localized area of pericardial inflammation over site of infarct.

62
Q

In what type of MI is pericarditis more common?

A

anterior or transmural MI

63
Q

How do you treat pericarditis?

A

aspirin.

NOT steroids

64
Q

What is Dressler’s syndrome?

A

postinfarction syndrome (3-6 weeks after infarction): autoimmune resposne causing pericardial effusions with pericardial pain (pleuritic; when you breath) + fever + WBC + join pain + pulmonary infiltrates

65
Q

How do you treat Dressler’s syndrome?

A

Aspirin

66
Q

What is post cardiotomy syndrome?

A

autoimmune response like Dressler’s but only in patients post CABG (3-6 weeks after surgery).

67
Q

How do you treat cardiotomy syndrome?

A

NSAIDS

68
Q

Can you see pleural effusion with pericarditis?

A

YES, but usually resolves on its own.

69
Q

What do you want to do after an MI?

A
  • Get an echo to see what their LV ejection fraction is, and - Get pts on ACE inhibitors and beta blockers.
  • Also get a treadmill test.
  • You may need to recath them if they are still having problems.
70
Q

Is it common to see arrhythmias post-MI?

A

YES

71
Q

What is the standard discharge RX for patients after an MI?

A
  • Aspirin
  • clopidogrel/ticagrelor/prasugrel
  • beta blocker
  • ACE for CHF
  • Warfarin if needed
  • Cardiac rehab
  • nitro
  • smoking cessation
72
Q

What are the 6 life-threatening etiologies (causes) of chest pain that must be ruled out in the emergency department?

A
  1. aortic dissection
  2. pulmonary embolus
  3. perforating ulcer
  4. tension pneumothorax
  5. Boerhaave syndrome (esophageal rupture with mediastinitis) * VERY PAINFUL
  6. MI
73
Q

*How can I remember MI complications?

A 
ACT RAPID:
Arrhythimas
Cardiac Failure
Thromboembolic disorder
Rupture (ventricle)
Aneurysm (ventricle)
Pericarditis
Infection
Death/Dressler's syndrome

CRP- Cardiology (49 decks)

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