EXAM #2: COMPLICATIONS OF MI Flashcards

1
Q

When are arrhythmias most common in the setting of MI?

A

Acute phase b/c of ischemia

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2
Q

Do PVCs require specific management in the post-MI setting?

A

No

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3
Q

What is an accelerated idioventricular rhythm?

A

Ventricular rhythm with a rate of 60-110 caused by ischemia induced automaticity of purkinje fibers

*Most often seen post-cath. and an indication of reperfusion

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4
Q

What kind of VT is associated with ischemia and how does this differ from VT associated with a post-MI scar?

A

Ischemia= Polymorphic

Scar= Monomorphic

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5
Q

What is the treatment for VT?

A

1) Immediate cardioversion

2) Amiodarone

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6
Q

Late VT/VF occurring 48 hours post-MI is associated with _____?

A

Increased risk of sudden cardiac death

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7
Q

What are the two indications for sudden cardiac death prophylaxis post-MI?

A

1) Late VT/VF

2) EF less than 35%

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8
Q

What causes sinus bradycardia in the acute phase of a MI?

A

1) Sinus node ischemia
2) High PNS tone
- Associated with inferior wall MI

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9
Q

When an inferior MI causes a heart block, what level of the conduction pathway is being most affected? Is a permanent pacemaker required?

A

AV node

Typically, a permanent pacemaker is NOT required b/c this is due to high vagal tone that is TRANSIENT

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10
Q

How does an anterior MI leading to heart block differ from inferior?

A

Anterior is:

1) Below the AV node
2) Requires permanent pacemaker

*Also much more rare

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11
Q

What is the difference between Killip class 2 and 3?

A

Class 2= mild pulmonary edema

Class 3= fulminant pulmonary edema

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12
Q

What is the difference between acute and chronic phase MI associated HF?

A

Acute= diastolic and/or systolic dysfunction

Chronic= systolic dysfunction

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13
Q

How is HF managed in the acute phase of a MI?

A

1) Vasodilator i.e. NTG
2) Judicious morphine
3) BiPap

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14
Q

How is HF managed in the post-acute phase of a MI?

A

1) Diuretic
2) ACE-inhibitors
3) Aldosterone antagonists

*In contrast to the acute phase, these patients are retaining fluid

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15
Q

What is a cardioembolism? What is this most commonly associated with?

A
  • Anterior wall dysfunction leads to emboli formation
  • Embolism is a cause of “cardioembolic stroke”

*Note that these can embolize to other locations as well e.g. bowels, legs…etc.

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16
Q

How are cardioembolisms treated?

A

Anticoagulation with warfarin

17
Q

When is percarditis typically seen post-MI?

A

Early= within the first week
- Focal inflammation of pericardium overlying the involved myocardium

Late= 1-8 weeks

18
Q

What is the treatment for early pericarditis? What treatments must be AVOIDED?

A

1) ASA
2) Colchicine as an adjunct

*Avoid NSAIDs and sterodis

19
Q

What is Dressler’s Syndrome?

A
  • Autoimmune disease
  • Autoantibodies against the percardium
  • Associated with malaise, arthralgias, pleural/ pericardial effusion
20
Q

What labs are associated with Dressler’s Syndrome?

A

High ESR and CRP

21
Q

What increases the risk of an Acute VSD post-MI?

A

1) Delayed or absent reperfusion
2) Elderly
3) Female
4) HTN
5) First MI

22
Q

List the sx. of an Acute VSD s/p MI.

A

Chest pain
Dyspnea
Hypotension
Biventricular failure

23
Q

What are the PE findings associated with an Acute VSD?

A
  • New murmur
  • Left low sternal border
  • Thrill in 1/2 of patients
24
Q

How is an Acute VSD diagnosed?

A

1) Echo*
2) Right heart catheterization

*Gold standard

25
Q

What is an oxygen saturation “step up” on right heart cath. pathogoominic for?

A

Acute VSD

26
Q

What is the most common etiology of acute mitral regurgitation?

A

Papillary muscle dysfunction

27
Q

In the setting of inferior MI, what papillary muscle is damaged to cause acute mitral regurgitation?

A

Posteromedial papillary muscle rupture

28
Q

What are the symptoms of acute mitral regurgitation?

A

1) HF sx.

2) Hemodynamic collapse

29
Q

How does acute mitral valve rupture differ from Acute VSD?

A

VSD= thrill in 1/2

Mitral Valve Regurg.= no thrill

30
Q

How do the murmurs of VSD and MR differ?

A

VSD= loud at LSB

MR= faint

*Note that VSD is associated with both acute and inferior MI vs. MR that is associated with inferior

31
Q

When does free wall rupture most commonly occur post MI?

A

1-5 days post MI

32
Q

How does free wall rupture present?

A
  • Sudden hemodynamic collapse
  • Cardiac tamponade
  • Feeling of impending doom
33
Q

How is free wall rupture diagnosed?

A

1) Echo

2) PA cath. with blunted Y-descent (emptying is impaired)

34
Q

What is the difference between a LV true and pseudoaneurysm?

A

True= 3x walls bulge out
- No rupture

Pseudo= tear of endocardium, myocardium–epicardium is the only thing holding this together
- Likely to rupture and require immediate surgical repair