Myocardial Infarction Flashcards
1
Q
Ischemic Heart Disease
- Ischemia
- Infarction
- Ischemic heart disease
A
- Ischemia
- Compromised blood supply or increased oxygen demand (supply-demand mismatch)
- Infarction
- Cell death due to ischemia
- Ischemic heart disease
- Chronic ischemia +/- infarction
2
Q
Ischemic Heart Disease
- Causes
- What happens
A
- Causes
- Coronary atherosclerosis
- Hypertension
- Heart failure
- Obesity
- Chronic pulmonary disease
- Anything that decreases O2 delivery or increases O2 demand
- What happens
- Supply-demand mismatch
- Myocardial ischemia in affected region
- Myocaridla infarction
- Other complications
3
Q
Blood Supply
- Right coronary artery
- Left anterior descending
- Left circumflex
A
- Right coronary artery
- RV
- Posterior LV / septum (75% of cases)
- Posteromedial papillary muscle
- SA & AV nodes
- Left anterior descending
- Anterior LV / septum
- Apex
- Left circumflex
- Lateral LV
- Posterior LV / septum (25% of cases)
4
Q
Quality of Myocardial Ischemia Depends On…
A
- Degree of arterial occlusion
- Collateral circulation
- Overall “health” of the heart
- Arrhythmia
5
Q
A patient has an acute right coronary artery thrombus. Where is the infarct most likely to occur?
A
Posterior septum
6
Q
What Happens in Acute MI
A
- Acute change in coronary artery plaque
- Rupture
- Hemorrhage
- Thrombosis
- Thrombosis
- Ischemic damage to myocardium
- Myocyte necrosis
- Other complications
7
Q
MI: Timing & Cellular Changes after Arterial Occlusion
- 2 mins
- 30 mins
- 1 hour
- 2-4 hours
A
- 2 mins = loss of contractility
- 30 mins = irreversible cell injury
- 1 hour = microvascular injury
- 2-4 hours = permanent damage
8
Q
Myocardial Infarction
- Progression of ischemia
- Predominance of occluded arteries
- Rare infarcts
A
- Progression of ischemia
- Typically begins in subendocardial region
- Can progress outward to transmural injury
- Predominance of occluded arteries
- LAD 40-50%
- RCA 30-40%
- LCx 15-20%
- Rare infarcts
- Isolated RV infarcts are rare
- Atrial infarcts rae even more rare
9
Q
Infarct Histology
- General
- Cells involved
- Early changes
- Middle changes
- Later changes
- Healing
A
- General
- Series of progressive changes
-
Cells involved
- Neutrophils
- Macrophages
- Fibroblasts (granultaion tissue)
-
Early changes (<24 hours)
- Initially no visible histology
- Then coagulative necrosis: “contraction band necrosis”
- Then neutrophil response
-
Middle changes (1-3 days)
- Initially neutrophils
- Then cellular debris
- Then macrophages
-
Later changes (3-7 days)
- Initially macrophages
- Then phagocytosis
- Then fibroblasts (granulation tissue)
- Greatest risk of myocardial rupture
-
Healing (7 days - weeks)
- Initially fibroblasts
- Then neovascularization
- Then collagen / fibrin
- Result: myocardial scar
10
Q
Post-Infarct Complications
A
- Arrhythmia
- Myocardial rupture
- Pericarditis
- Mural thrombus
- Ventricular aneurysm
- Ventricular remodeling
11
Q
What complication is most likely to occur 3-7 days after acute infarction?
A
Papillayr muscle rupture
12
Q
Arrhythmia
A
- Myocardial irritability
- Heart block (depending on location)
- Bradycardia, ventricular tachycardia, premature ventricular contractions
13
Q
Myocardial Rupture
A
- Free wall
- Hemopericardium
- Septum
- Causes acute VSD w/ left-to-right shunt
- Pappillary muscle
- leads to acute mitral valve insufficiency
14
Q
Dressler’s Syndrome
- aka
- After acute MI
- After bypass graft surgery
A
- aka
- Fibrinous pericarditis
- After acute MI
- 1-7 days later: acute inflammatory exudate
- 6-8 weeks later: autoimmune
- After bypass graft surgery
- Post-pericardotomy syndrome
15
Q
Mural Thrombus
A
-
Akinesis / hypokinesis of infarcted myocardium
- Blood pools on endocardial surface
- Thrombus forms
- Complication: embolization of thrombus
- Leads to stroke or gangrene