ischemic heart disease II

Question 1

what causes symptomatic ischemia

Answer 1

-when intramyocardial vessels are maximally dilated, coronary flow becomes the main determinant of flow of oxygen, an increased demand or temporary decrease in flow results in symptomatic ischemia

Question 2

symptoms of ischemia/infarction

Answer 2

• chest pain

- diaphoresis

Question 3

chest pain symptoms

Answer 3

crushing pain over sternum radiating to left arm or back

• usually not sharp or fluctuating
• severe pain is accompanied by sweating, nausea, and vomitting
• pain patterns in diabetics or persons with previous chest/heart surgery may be altered due to decreased innervation

Question 4

diaphoresis symptom

Answer 4

shortness of breath, sweating, nausea, are usual signs of severe cardiac pain or insufficiency

Question 5

troponins

Answer 5

• Rises first
• remains elevated for 7 days
• specific for myocardium

Question 6

what are toponins used to diagnose?

Answer 6

occurrence of acute coronary syndrome

-confirm infarction

Question 7

creatinine kinase

Answer 7

• peaks in 12-24 hours
• decreases after that
• NOT specific for myocardium
• MB isoenzyme required to confirm cardiac origin

Question 8

what can creatinine kinase be used to diagnose?

Answer 8

• it decreases after 24 hours

- can be used to detect repeated infarctions following initial event

Question 9

LDH

Answer 9

rises after 24 hours

• peaks in several days
• requires isoenzymes to detect cardiac origin

Question 10

what can LDH diagnose?

Answer 10

can confirm infarction

• can confirm infarction somewhere else
• essentially obsolete

Question 11

in ischemia/infarction: leukocytosis appears within?

Answer 11

few hours

-persists for 3-7 days

Question 12

in ischemia/infarction: ESR

Answer 12

increases slowly

-persists 1-2 weeks

Question 13

MI etiology: acute coronary syndrome

Answer 13

acute interruption of blood flow to the myocardium

• unstable angina/NSTEMI
• STEMI

Question 14

what is not sufficient enough to cause acute MI

Answer 14

narrowing of blood vessels alone is not sufficient to cause acute infarction

• pre-existing coronary disease + thrombus formation
• coronary spams
• sudden loss vascular volume
• hemopericardium/cardiac tamponade

Question 15

Pathophysiology MI: initiating events

Answer 15

1. rupture atherosclerotic plaque and subsequent thrombus formation
   - rupture can occur with exertion resulting in sudden increase in blood pressure, coronary pressure
   - thrombus usually forms within first few cm of vessel distribution
2. thromboemboli along coronary distribution

Question 16

where is a common place for thrombus formation to occur?

Answer 16

first 2cm of vessels

• near ostia for right and left main coronaries
• just distal to bifurcations for LAD, RCA, and circumflex
• proximal 1/3 of RCA

Question 17

MI patho

Answer 17

• ischemia rapidly progresses to infarction over 20-40 minutes, time is myocardium
• distribution is transmural
• infarction leads to coagulative necrosis of myocardial fibers
• necrosis sets up inflammatory reaction at margin of infarction that migrates into area of infarction with time
• eventually necrotic fibers are replaced by scar

Question 18

morphological correlations: irreversible injury

Answer 18

1. Microscopic
   - evolution through many stages beginning with necrosis of myocytes
   * wavy, eosinophilic fibers (first thing to see)
   * nuclear pyknosis and karryorhexis
   - inflammation, infiltrates with inflammatory cells
   - clean up of necrotic debris
   - replacement of myocardium with scar tissue

Question 19

neutrophils peak at

Answer 19

48 hours

Question 20

macrophages infiltrate in

Answer 20

72 hours

Question 21

lymphcyotes infiltrate in

Answer 21

4-5 days

Question 22

MI has to occur within

Answer 22

24 hours in order to see things

Question 23

edema happens in

Answer 23

12 hours

Question 24

cell infiltrate after

Answer 24

24 hours

Question 25

first phase

Answer 25

ischemia to injury to infarction | 0-4 hours

Question 26

over the first few hours

Answer 26

cells begin to change from acute cell injury to necrosis

Question 27

hallmark of coagulative necrosis

Answer 27

loss of nuclei | hyper-eosinophilic fibers

Question 28

second phase

Answer 28

inflammation

Question 29

second phase: earliest changes

Answer 29

show only edema (wavy fibers) 4-24 hours -first signs of inflammation

Question 30

why are the characteristic features of inflammation delayed by 24-48 hours

Answer 30

inflammation is initiated at borders and process must migrate into the necrotic area

Question 31

cellular infiltrate to be prominent

Answer 31

2-4 days

Question 32

secondary phase: subacute phase includes

Answer 32

macrophages and lymphocytes | 3-5 days

Question 33

third phase consist of

Answer 33

removal of debris and initiation of fibrosis | -tissue integrity decreases as necrotic tissue is lysed and removed by inflammation cells

Question 34

tissue is the weakest at

Answer 34

4-5 days

Question 35

replacement by granulation tissue

Answer 35

5-10 days

Question 36

replacement of myocardium with fibrous scar

Answer 36

> 2 weeks

Question 37

what can be identified on morphological features of MI: Early

Answer 37

edema | -between 4-12 hours

Question 38

what can be identified on morphological features of MI: microscopic

Answer 38

early inflammation 1-3 days subacute inflammation 3-5 days early fibrosis 5-10 days old infarct > 2 weeks

Question 39

irreversible injury: gross (early)

Answer 39

pallor +/- hyperemic border

Question 40

irreversible injury: gross, 3-7 days later

Answer 40

hyperemic border with central, yellow-brown softening, possible hemorrhage -eventual replacement with red-brown, depressed, scarred areas, scar may actually appear grey and fiber-like

Question 41

time course: 20 mins

Answer 41

arrhythmias

Question 42

time course: 1 hour

Answer 42

increased troponins only

Question 43

time course: 2 hours

Answer 43

hyper-eosinophilic fibers

Question 44

time course: 8 hours

Answer 44

wavey fibers

Question 45

time course: 48 hours

Answer 45

acute inflammatory infiltrate

Question 46

time course: 96 hours

Answer 46

ventricular rupture

Question 47

time course: 5-10 days

Answer 47

chronic inflammatory infiltrate and debris

Question 48

time course: 10-21 days

Answer 48

replacement of fibrosis

Question 49

complications of MI

Answer 49

early 1-3 days -myocardial dysfunction earliest complication, dysfunction of conduction system due to ischemia of myocardial fibers in pathway or node

Question 50

most common cause of death with complications of MI

Answer 50

myocardial dysfunction

Question 51

complications of MI

Answer 51

extension of infarct - continued loss of non-perfused tissue - re-formation of thrombi, emboli

Question 52

Late complications of MI

Answer 52

4-5 days - mural thrombus formation - aneurysm/dilatation - ventricular rupture (septal or free wall) - papillary muscle infarction - pericardial effusion/pericarditis

Question 53

aneurysm/dilatation or ventricular rupture occurs

Answer 53

until 4-5 days with softening of necrotic tissue

Question 54

aneurysm leads to

Answer 54

to acute failure (decreased outlfow and mural thrombus formation)

Question 55

free wall rupture can lead to

Answer 55

hemopericardium and cardiac tamponade | -electromechanical dissociation

Question 56

what can ventricular rupture lead to?

Answer 56

acute volume overload and heart failure

Question 57

reperfusion injury: morphological correlates

Answer 57

- additional myocyte injury with free radical formation - influx of Ca - hemorrhage

Question 58

what is characteristic of reperfusion injury?

Answer 58

by presence of contraction bands in damaged myocytes

Question 59

MI from thrombus

Answer 59

would be transmural

Question 60

mural thrombus indicates

Answer 60

stasis