Ischemic Heart Disease Flashcards

1
Q

What is the primary cause of ischemic heart disease/MI?

Other causes?

A
  • atherosclerosis (>90%)
  • vasospasm (due to platelet aggregation or drugs, ie. cocaine and ephedrine)
  • emboli (formed in LA due to a-fib)
  • vasculitis/hematologic abnormalities
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2
Q

How long does it take for loss of contractility and irreversible myocardial damage to occur in an MI?

A
  • loss of contractility <2 min
  • permanent, irreversible damage ~30 mins
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3
Q

What are the classic symptoms of an MI?

A
  • “crushing/stabbing” substernal chest pain
  • possible radiation to back, shoulder, or jaw
  • diaphoresis
  • N/V
  • dyspnea
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4
Q

What serum marker can be used to detect an MI?

A
  • troponin (T/I); most sensitive and specific
  • CK-MB; sensitive, no specific
  • myoglobin; not specific
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5
Q

What is important to note about using serum marker in diagnosing an MI?

A

serum marker may not be elevated in the first 3 hours of an MI

  • serial draws are necessary to rule out MI
  • CK-MB returns to normal within 2-3 days of infarction; can be used to assess reinfarction
  • troponin remains elevated for >5 days
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6
Q

What are the most common coronary vessels affected by MI?

What porions of the heart are affected with each?

A

left anteiror descening (LAD):

  • apex, anterior LV wall, and anteiror 2/3 of septum
  • most common (40-50%)

right cornary artery (RCA):

  • (posterior descending branch only) posterior LV wall, posterior 1/3 of septum
  • (proximal, in RCA) entire RV wall, + posterior descending
  • 30-40%

left circumflex:

  • lateral LV wall
  • 15-20%
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7
Q

How does damage during an MI progress?

A
  • intial damage occurs to inner most myocardium; most distant from coronary arteiries
  • damage progresses externally until it is transmural with increased duration of infarction

if reperfusion occurs, damage may be limited to a subendocardial infarct

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8
Q

How does the appearance of the heart and cardiac tissue change following MI?

A

first 30 mins -> no change

30 mins - 4 hrs -> wavy fibers

4 - 12 hrs -> edema, early necrosis

12 - 24 hrs -> dark mottling; progressive necrosis (pyknosis, hypereosinophilia), early neutrophils

1 -3 days-> yellow-tan mottling; loss of nuclei, neutrophil infiltrates

3 - 7 days -> hyperemic border; macrophages

7 - 10 days -> depressed margins; granulation tissue

10 - 14 days -> collagen deposition

2 - 8 wks -> gray-white scar; continued collagen deposition

>2 mo -> complete scar

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9
Q

What is the first microscopic sign of irreversible myocardial injury?

When is it seen?

A

wavy fibers; viabale fibers at border of infarct pull adjacent dead fibers

-seen within 30 mins - 4 hrs

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10
Q

What is the first gross sign of irreversible myocardial injury?

When is it seen?

A

staining of myocardium with triphenyltetrazolium which binds lactate dehydrogenase (only found in live myocardium) turning it bright red

  • infarcted areas and scars are not stained
  • 2 - 3 hours
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11
Q

When is dark mottling first seen following an MI?

A

12 hrs - 1 day, by 1 day

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12
Q

When is central yellow infarct seen first seen following an MI?

A

1 - 3 days, by day 3

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13
Q

When is neutrophillic infiltration first seen following an MI?

A

1 - 3 days, by day 3

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14
Q

When is loss of myocardial nuclei first seen following an MI?

A

1 - 3 days, by day 3

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15
Q

When is a macrophage infiltrate first seen following an MI?

A

3 - 7 days, by 1 week

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16
Q

When is granulation tissue first seen following an MI?

A

1 - 2 wks, by 2 weeks

17
Q

When is scaring/repair comlete following an MI?

A

by 2 months

18
Q

What complications are seen with an MI and when?

A

Early (within 24 hours):

  • lethal arrhythmia
  • cardiogenic shock

Intermediate (>2-4 days):

  • rupture of wall, septum or papillary muscles
  • acute pericarditis (during neutrophil/macrophage infiltration)

Late (>2wks):

  • chronic/immune pericarditis (Dressler syndrome)
  • ventricular aneurysm
  • heart failure
  • arrhythmia
19
Q

What is the most common cause of death due to an MI?

A

fatal arryhthmia, V-fib, within 24 hours of onset

20
Q

What arrhythmias can be seen following an MI?

How does MI cause them? (some of the explanations are my best guesses to help understand why)

A

caused by conduction delays or irritabililty

  • sinus bradycardia (conduction delay, SA/AV node damage?)
  • A-fib (conduction delays, catches post-refractroy period)
  • heart block (septal involvement, LAD and RCA/PDA?)
  • tachycardia (compensatory for decreased CO?)
  • V-tach (can progress to V-fib)
  • V-fib (lethal) (conduction delays, catches post-refractroy period)
21
Q

How does MI lead to cardiogenic shock?

A

too large of a portion of the mycardium is damaged to sustain adequate systemic perfusion

22
Q

How does MI cause rupture?

What complications can occur due to this?

A

necrosis following MI weakens wall

Free wall rupture:

  • blood into pericardium -> cardiac tamponade
  • most common rupture, common cause of intermediate death (still after arrhythmia)

Septal rupture:

-VSD formation -> L-to-R shunt

Papillary muscle rupture:

  • mitral incompitanc/regurgitation
  • least common rupture
23
Q

What is Dressler syndrome and how does MI cause it?

A

chronic, immune-mediated fibrinous pericarditis

damage of myocytes releases myocardial proteins which the immune system may recognize

24
Q

How does Dressler sydrome present?

A
  • pleuritic chest pain + friction rub
  • dry cough
  • fever
25
Q

What is angina pectoris?

A

transient, possibly recurrent ischemia that is insufficient to cause infarction

-usually last for seconds to 15 mins

26
Q

What are the types of angina pectoris?

(compare)

A

Stable angina:

  • predictable, induced by activity/stress
  • relieved by rest and vasodilators

Prinzmetal angina:

  • induced by cornary A. vasospasm
  • relieved by vasodilators
  • not induced by activity/stress; not relieved by rest

Unstable angina:

  • unpredictable, can occur at rest
  • “crescendo pattern”; progressively worse and more frequent -> can evolve into NSTEMI
  • caused by ruptured or growing plaque
27
Q

What conditions are associated with increased risk of ischemia but may also obscure the perception of ischemic pain?

A
  • diabetes (neuropathy)
  • age