Card - Path (Part 3: Ischemic Heart Disease & MI) Flashcards Preview

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Flashcards in Card - Path (Part 3: Ischemic Heart Disease & MI) Deck (44):
1

What defines angina? Include what causes it and whether angina causes myocyte necrosis.

Chest pain due to ischemic myocardium secondary to coronary artery narrowing or spasm; no myocyte necrosis

2

What are 3 types of angina?

(1) Stable (2) Variant angina (Prinzmetal) (3) Unstable/Crescendo

3

To what is stable angina usually secondary?

Usually secondary to atherosclerosis

4

Characterize the pain and ECG findings of stable angina.

Exertional chest pain in classic distribution (usually with ST depression on ECG), resolving with rest

5

What is another name for Variant angina? When does it occur, and to what is it secondary?

Occurs at rest secondary to coronary artery spasm

6

What ECG finding characterizes Variant angina (Prinzmetal)?

Transient ST elevation on ECG

7

What are 3 known triggers of Variant angina (Prinzmetal)? What is often the case in terms of the trigger?

Known triggers include tobacco, cocaine, and triptans, but trigger is often often

8

How can Variant angina (Prinzmetal) be treated?

Treat with calcium channel blockers, nitrates, and smoking cessation (if applicable).

9

What defines Unstable/Crescendo angina?

Thrombosis with incomplete coronary artery occlusion

10

Describe the chest pain and ECG finding of Unstable/Crescendo angina.

ST depression on ECG (increase in frequency or intensity of chest pain; any chest pain at rest).

11

What are 5 types of ischemic heart disease manifestations?

(1) Angina (2) Coronary steal syndrome (3) Myocardial infarction (4) Sudden cardiac death (5) Chronic ischemic heart disease

12

What defines Coronary steal syndrome? Give 2 examples of the type of substance involved. What is an important clinical correlation for this?

Distal to coronary stenosis, vessels are maximally dilated at baseline. Administration of vasodilators (e.g., dipyridamole, regadenoson) dilates normal vessels and shunts blood toward well-perfused areas => decreased flow and ischemia in the poststenotic region; Principle behind pharmacologic stress

13

What most often defines and causes myocardial infarction?

Most often acute thrombosis due to coronary artery atherosclerosis with complete occlusion of coronary artery and myocyte necrosis

14

What will the ECG show in transmural versus subendocardial myocardial infarction?

If transmural, ECG will show ST elevation; if subendocardial, ECG may show ST depressions.

15

What is used to diagnose myocardial infarction?

Cardiac biomarkers are diagnostic

16

What defines sudden cardiac death, and what most commonly causes it?

Death from cardiac causes within 1 hour of onset of symptoms, most commonly due to a lethal arrhythmia (e.g., ventricular fibrillation).

17

What are 3 conditions associated with sudden cardiac death, and what is important to relate to each?

Associated with CAD (up to 70% of cases), cardiomyopathy (hypertrophic, dilated), and hereditary ion channelopathies (e.g., long QT syndrome).

18

What defines chronic ischemic heart disease?

Progressive onset of CHF over many years due to chronic ischemic myocardial damage.

19

What are the 3 most commonly occluded arteries leading to MI? List them in order of most to least common.

LAD > RCA > Circumflex

20

What 7 symptoms characterize MI?

Symptoms: (1) diaphoresis (2) nausea (3) vomiting (4) severe retrosternal pain (5) pain in left arm and/or jaw (6) shortness of breath (7) fatigue

21

What gross myocardial changes occur at the following time periods after an MI: (1) 0-4 hr (2) 4-12 hr (3) 12-24 hr (4) 1-3 days (5) 3-14 days (6) 2 weeks to several months?

(1) None (2) & (3) [Occluded artery]; Infarct, Dark mottling; Pale with tetrazolium stain (4) Hyperemia (5) Hyperemic border; central yellow-brown softening - maximally yellow and soft by 10 days (6) [Recanalized artery], Gray-white (scar)

22

What changes can be seen under light microscope at the following time periods after an MI: (1) 0-4 hr (2) 4-12 hr (3) 12-24 hr (4) 1-3 days (5) 3-14 days (6) 2 weeks to several months?

(1) None (2) Early coagulative necrosis, release of necrotic cell contents into blood; edema, hemorrhage, wavy fibers (3) Neutrophil migration starts. Reperfusion injury may cause contraction bands (due to free radical damage) (4) Extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation with neutrophils. (5) Macrophages, then granulation tissue at margins (6) Contracted scar complete

23

Again, what microscopic change(s) occur(s) 0-4 hr after onset of an MI? What are 4 complications that may occur in this time frame? What is important to know about these complications?

None; (1) Arrhythmia (2) HF (3) Cardiogenic shock (4) Death; These are the 4 complications that can occur within the first 24 hours after onset of an MI

24

Again, what microscopic change(s) occur(s) 4-12 hr after onset of an MI? What are 4 complications that may occur in this time frame? What is important to know about these complications?

Early coagulative necrosis, release of necrotic cell contents into blood; edema, hemorrhage, wavy fibers; (1) Arrhythmia (2) HF (3) Cardiogenic shock (4) Death; These are the 4 complications that can occur within the first 24 hours after onset of an MI

25

Again, what microscopic change(s) occur(s) 12-24 hr after onset of an MI? What are 4 complications that may occur in this time frame? What is important to know about these complications?

Neutrophil migration starts. Reperfusion injury may cause contraction bands (due to free radical damage).; (1) Arrhythmia (2) HF (3) Cardiogenic shock (4) Death; These are the 4 complications that can occur within the first 24 hours after onset of an M

26

Again, what microscopic change(s) occur(s) 1 to 3 days after onset of an MI? What are is a complication that may occur in this time frame?

Extensive coagulative necrosis. Tissue surrounding infarct shows acute inflammation with neutrophils.; Fibrinous pericarditis

27

Again, what microscopic change(s) occur(s) 3-14 days after onset of an MI? What are 4 complications that may occur in this time frame?

Macrophages, then granulation tissue at margins; (1) Free wall rupture => tamponade; (2) Papillary muscle rupture => mitral regurgitation; (3) Interventricular septal rupture due to macrophage-mediated structural degradation (4) LV pseudoaneurysm (mural thrombus "plugs" hole in myocardium => "time bomb")

28

Again, what microscopic change(s) occur(s) 2 weeks to several months after onset of an MI? What are 4 complications that may occur in this time frame?

Contracted scar complete; (1) Dressler syndrome, (2) HF, (3) arrhythmias, (4) true ventricular aneurysm (outward bulge during contraction, "dyskinesia")

29

What is the gold standard for diagnosis of MI in the first 6 hours?

In the first 6 hours, ECG is the gold standard

30

Give 2 cardiac biomarkers used for diagnosis of MI and their timelines and advantages/limitations.

CARDIAC TROPONIN I rises after 4 hours and is increased for 7-10 days; more specific than other protein markers. CK-MB is predominately found in myocardium but can also be released from skeletal muscle. Useful in diagnosing reinfarction following acute MI because levels return to normal after 48 hours.

31

What are 3 ECG changes that may be seen with MI, and what causes each?

ECG changes can include (1) ST elevation (STEMI, acute transmural infarct), (2) ST depression (subendocardial infarct), and pathologic Q waves (evolving or old transmural infarct).

32

What are the 2 major types of infarcts?

(1) Transmural infarcts (2) Subendocardial infarcts

33

Distinguish between transmural infarcts and subendocardial infarcts in terms of the degree of necrosis caused.

TRANSMURAL INFARCTS: Increased necrosis; SUBENDOCARDIAL INFARCTS: Due to ischemic necrosis of < 50% of ventricle wall

34

Distinguish between transmural infarcts and subendocardial infarcts in terms of the extent of area affected.

TRANSMURAL INFARCTS: Affects entire wall; SUBENDOCARDIAL INFARCTS: Subendocardium especially vulnerable to ischemia

35

Distinguish between transmural infarcts and subendocardial infarcts in terms of their ECG findings.

TRANSMURAL INFARCTS: ST elevation on ECG, Q waves; SUBENDOCARDIAL INFARCTS: ST depression on ECG

36

For each of the following infarct locations, give the ECG leads with (patholologic) Q waves that could be used to diagnose MI: (1) Anterior wall (LAD) (2) Anteroseptal (LAD) (3) Anterolateral (LAD or LCX) (4) Lateral wall (LXC) (5) Inferior wall (RCA).

(1) V1-V4 (2) V1-V2 (3) V4-V6 (5) I, aVL (6) II, III, aVF; Think: "Lateral wall (LCX) = I, aVL" & "inFerior wall (RCA) = II, III, aVF"

37

What are 7 kinds of MI complications?

(1) Cardiac arrhythmia (2) LV failure and pulmonary edema (3) Cardiogenic shock (4) Rupture (e.g., ventricular free wall, papillary muscle, or interventricular septum) (5) Ventricular pseudoaneurysm formation (6) Postinfarction fibrinous pericarditis (7) Dressler syndrome

38

What is an important cause of death in MI patients before reaching the hospital? When is it common?

Cardiac arrhythmia - important cause of death before reaching hospital; common in first few days

39

What kind of infarct is associated with cardiogenic shock as a complication of MI? What risk does this complication increase?

Cardiogenic shock (large infarct - high risk of mortality)

40

What are 3 types of ruptures that can occur as complications of MI? What effect can/does each rupture have?

(1) Ventricular free wall rupture => cardiac tamponade (2) Papillary muscle rupture => severe mitral regurgitation (3) Interventricular septum rupture => VSD

41

When is the greatest risk for rupture (e.g., ventricular free wall, papillary muscle, interventricular septum) as a complication of MI?

Greatest risk 6-14 days postinfarct

42

What hemodynamic change, risk, and pathology are associated with ventricular pseudoaneursym formation as a complication of MI? When is the greatest risk for this post-MI?

Decreased CO, Risk of arrhythmia, Embolus from mural thrombus; Greatest risk approximately 1 week post-MI

43

What is a sign of postinfarction fibrinous pericarditis as a complication of MI? When does it occur?

Friction rub (1-3 days post-MI)

44

What is Dressler syndrome? When does it occur as a post-MI complication?

Autoimmune phenomenon resulting in fibrinous pericarditis (several weeks post-MI)