Ischemic heart dz Flashcards

1
Q

What is ischemic heart dz?

A

Results from insufficient perfusion to meet the metabolic demands of myocardium

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
2
Q

Disruption of what arteries mainly result in ischemic heart disease?

A

Coronary arteries

Blood to myocardium is supplied by the coronary arteries, so any disruption of coronary flow may result in ischemia

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
3
Q

What can ischemia result in?

A

MI
Angina pectoris
Chronic ischemic heart dz, with heart failure
Sudden cardiac death

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
4
Q

What is the leading cause of death in the US? What is it associated with?

A

Ischemic heart disease

> 90% of cases are secondary to atherosclerosis

  • chronic vascular occlusion
  • acute plaque change = thrombus
How well did you know this?
1
Not at all
2
3
4
5
Perfectly
5
Q

What is angina pectoris?

A

Transient, often recurrent chest pain induced by myocardial ischemia insufficient to induce MI

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
6
Q

What are the clinical variants Angina Pectoris?

A

Stable angina
Prinzmetal variant angina
Unstable (or “crescendo”) angina

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
7
Q

Describe stable angina.

A

Stenotic occlusion of coronary artery

“Squeezing” or burning sensation, relieved by rest or vasodilators

Induced by physical activity, stress

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
8
Q

Describe Prinzmetal variant angina.

A

Episodic coronary artery spasm, relieved with vasodilators

Unrelated to physical activity, HR, or BP

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
9
Q

Describe unstable (or “crescendo”) angina.

A

Frank pain, increasing in frequency, duration, & severity; at progressively lower levels of physical activity, eventually even at rest

Usually rupture of atherosclerotic plaque, with partial thrombus

~50% may have evidence of myocardial necrosis, acute MI may be imminent

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
10
Q

90% of all MIs are caused by ____. What are some other causes?

A

Atheromatous plaque

Embolus
vasospasm
ischemia secondary to vasculitis, shock, hematologic abnormalities

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
11
Q

What is a classic presentation of MI?

A

Prolonged CP (>30 min)

  • crushing, stabbing, squeezing, tightness
  • radiating down left arm, or left jaw

Diaphoresis
Dyspnea
Nausea-vomiting
Up to 25% asymptomatic

*side note: info based on studies primarily w/ men

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
12
Q

The location, size, & features of an acute MI depend on what?

A

Site, degree, & rate of occlusion of the artery

Size of area perfused

Duration of occlusion

Metabolic & oxygen needs of the area at risk

Extent of collateral blood flow

Presence of arterial spasm

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
13
Q

Describe ATP and lactate levels in relation to ischemia.

A

ATP levels decline as Lactate levels increase

  • ATP levels to 50% = 10 min
  • ATP levels to 10% = 40 min

As lactate levels rise you see the onset of irreversible injury (20-40 min)

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
14
Q

Describe the frequency at which the coronary vessels are affected and which region of the heart do the affect.

A

LAD (40-50%)
-Apex, LV anterior wall, anterior 2/3 of septum

RCA (30-40%)
-RV free wall, LV posterior wall, posterior 1/3 of septum

LCX (15-20%)
-LV lateral wall

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
15
Q

Describe how irreversible injury to the heart progresses overtime.

A

Within the first 24 hrs:

  • dark mottling
  • waviness of fibers –> edema, hemorrhage –> pyknosis, hypereosinophilia, neutrophilic infiltrate

Within 7 days:

  • Yellow-tan infarct
  • coagulation necrosis –> disintegration of dead myocytes by macrophages; dying neutrophils

Within 14 days:

  • Red-gray infarct
  • well-developed phagocytosis, granulation tissue at margin –> well-established gt with new blood vessels & collagen

Within 2 mo:
-increased collagen w/ decreased cellularity –> dense collagenous scar

How well did you know this?
1
Not at all
2
3
4
5
Perfectly
16
Q

What changes to the heart are seen within the first 24 hours of an acute MI?

A

Coagulative necrosis
Pyknotic nuclei
Loss of cross striations

17
Q

What changes to the heart are seen within 1-3 days of an acute MI?

A

Loss of striations

Neutrophilic infiltration

18
Q

What is reperfusion?

A

Restoring blood flow to an area of ischemia and impending infarction

Attempt to limit infarct size by rescuing at risk myocardium

19
Q

How can you undergo reperfusion?

A

Thrombolysis
Angioplasty
Stent placement
CABG (coronary artery bypass graft)

20
Q

Why would you order labs to diagnose an MI?

A

Measure blood levels of proteins that leak out of irreversibly damaged myocytes

21
Q

What are the most useful proteins to test for MI? Which is the most sensitive and specific? What does it do?

A

Cardiac specific Troponins T and I (cTnT and cTnI)

MB fraction of creatinine kinase (CK-MB)

Most sensitive and specific = troponins
-proteins that regulate ca-mediated contraction of cardiac and skeletal muscle

22
Q

Describe the changes in troponin levels during an MI.

A

Troponins I and T are NOT normally detectable in circulation

Following MI, levels being to rise at 3-12 hours

  • cTnT peak at 12-48 hrs
  • cTnI peak at 24 hrs
23
Q

What is CK? Elaborate on the MB designation.

A

Creatine Kinase - enzyme expressed in brain, myocardium, and skeletal muscle; dimer composed of 2 isoforms = M and B

MM = predominantly in cardiac and skeletal muscle 
BB = brain, lung, and other tissue 

MB = localized to cardiac muscle (considerable lesser amounts in skeletal)

CK-MB = sensitive by NOT specific (can rise in skeletal m injury)

24
Q

How do CK-MB levels change during MI?

A

Begins to rise within 3-12 hours of onset of MI

Peaks at 24 hrs, returns to normal within 48-72 hrs

25
Q

Briefly describe cardiac enzyme level changes over time.

A

Elevation of CKMB, cTnI & T = 3-12 hrs

Both peak at 24 hrs

CK-MB normal within 3 days
cTnI = 5-10 days
cTnT = 5-14 days

26
Q

What are some complications of an MI?

A
Arrhythmia 
Contractile dysfunction 
Fibrinous pericarditis 
Myocardial rupture
Infarct expansion
Ventricular aneurysm
27
Q

Describe how arrhythmia is a complication of an MI.

A

Half of all MI death occur within 1 hour of onset, and are usually secondary to an arrhythmia

Can be long-term complication of MI, depending on site and extent of lesion

Can result form permanent damage to conducting system or from myocardial irritability following infarct

28
Q

Describe how contractile dysfunction is a complication of an MI.

A

Dependent on size of infarct and associated loss of function

29
Q

Describe how myocardial rupture is a complication of an MI. What are the risk factors?

A

Typically requires transmural infarct

2-4 days post MI, when inflammation and necrosis have weakened the wall

Risk factors = older, large transmural anterior MI, first MI, absence of LV hypertrophy

30
Q

Describe how infarct expansion is a complication of an MI.

A

Muscle necrosis –> weakening, stretching, and thinning of wall

Mural thrombus often seen

31
Q

Describe how ventricular aneurysm is a complication of an MI

A

Late complication of large transmural infarcts with early expansion

Composed of thinned wall of scarred myocardium

Also associated with mural thrombus

Rupture does not usually occur