Ischemic heart dz

Question 1

What is ischemic heart dz?

Answer 1

Results from insufficient perfusion to meet the metabolic demands of myocardium

Question 2

Disruption of what arteries mainly result in ischemic heart disease?

Answer 2

Coronary arteries

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

Question 3

What can ischemia result in?

Answer 3

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

Question 4

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

Answer 4

Ischemic heart disease

> 90% of cases are secondary to atherosclerosis

• chronic vascular occlusion
• acute plaque change = thrombus

Question 5

What is angina pectoris?

Answer 5

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

Question 6

What are the clinical variants Angina Pectoris?

Answer 6

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

Question 7

Describe stable angina.

Answer 7

Stenotic occlusion of coronary artery

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

Induced by physical activity, stress

Question 8

Describe Prinzmetal variant angina.

Answer 8

Episodic coronary artery spasm, relieved with vasodilators

Unrelated to physical activity, HR, or BP

Question 9

Describe unstable (or “crescendo”) angina.

Answer 9

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

Question 10

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

Answer 10

Atheromatous plaque

Embolus
vasospasm
ischemia secondary to vasculitis, shock, hematologic abnormalities

Question 11

What is a classic presentation of MI?

Answer 11

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

Question 12

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

Answer 12

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

Question 13

Describe ATP and lactate levels in relation to ischemia.

Answer 13

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)

Question 14

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

Answer 14

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

Question 15

Describe how irreversible injury to the heart progresses overtime.

Answer 15

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

Question 16

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

Answer 16

Coagulative necrosis
Pyknotic nuclei
Loss of cross striations

Question 17

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

Answer 17

Loss of striations

Neutrophilic infiltration

Question 18

What is reperfusion?

Answer 18

Restoring blood flow to an area of ischemia and impending infarction

Attempt to limit infarct size by rescuing at risk myocardium

Question 19

How can you undergo reperfusion?

Answer 19

Thrombolysis
Angioplasty
Stent placement
CABG (coronary artery bypass graft)

Question 20

Why would you order labs to diagnose an MI?

Answer 20

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

Question 21

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

Answer 21

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

Question 22

Describe the changes in troponin levels during an MI.

Answer 22

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

Question 23

What is CK? Elaborate on the MB designation.

Answer 23

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)

Question 24

How do CK-MB levels change during MI?

Answer 24

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

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

Question 25

Briefly describe cardiac enzyme level changes over time.

Answer 25

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

Question 26

What are some complications of an MI?

Answer 26

``` Arrhythmia Contractile dysfunction Fibrinous pericarditis Myocardial rupture Infarct expansion Ventricular aneurysm ```

Question 27

Describe how arrhythmia is a complication of an MI.

Answer 27

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

Question 28

Describe how contractile dysfunction is a complication of an MI.

Answer 28

Dependent on size of infarct and associated loss of function

Question 29

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

Answer 29

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

Question 30

Describe how infarct expansion is a complication of an MI.

Answer 30

Muscle necrosis --> weakening, stretching, and thinning of wall Mural thrombus often seen

Question 31

Describe how ventricular aneurysm is a complication of an MI

Answer 31

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