Cardiac Module 5 Flashcards
Describe myocardial ischemia
- Myocardial cells become oxygen deprived
- Results in loss of contractility, conduction changes, lactic acid accumulation
- If flow is NOT restored, infarction occurs
MC cause of myocardial ischemia?
Atherosclerosis in the form of CAD
Stable angina
- Transient episode of blood flow impairment
- Recurrent episodes lasting 3-5 mins
- Relieved with rest
- Classic symptom = angina pectoris
Angina pectoris
Substernal chest discomfort (heaviness, pressure, pain)
Silent angina
- Ischemia that does not cause obvious signs/symps
- Common following conditions/surgical procedures (transplant, CABG, emotional stress, etc)
Acute coronary syndromes include:
- Unstable angina
- MI
Unstable angina
- Thrombus breaks up before cell death, allows for reperfusion
- “Reversible” ischemia (no cell damage)
- 20% will have MI or death from MI within 30 days
MI
- Thrombus occludes blood flow causing irreversible necrosis/cell death
- Damaged cells release “markers”
Changes immediately to 10-20 minutes after acute MI
- Loss of contractility (hypokinesis)
- Dysrhythmia (EKG changes w/in 30-60 secs)
- Lactic acid accumulation
- Increased catecholamine release
- AT II release
Why does lactic acid accumulation occur during an MI?
After 6-10 secs, anaerobic metabolism takes over (producing lactic acid) for survival until blood flow is restored
When does hyperglycemia occur in relation to an MI?
72 hours s/p MI
What occurs within 15-30 minutes after MI?
Process of necrosis (cell death) begins
Where does myocardial necrosis begin within the tissue?
Usually in sub-endothelium
When are cellular/histological changes of necrosis visible?
Not until 6 hours after
What occurs 3-6 hours post MI?
Necrosis expands “outward” toward epicardium
What is a transmural infarct?
Infarct affects the complete thickness of ventricular wall
What is the basis for classifying a STEMI?
Transmural infarct
What occurs 6-12 hours after MI?
- Degree of cell damage becomes increasingly irreversible
- Biomarkers begin to be released into bloodstream (myoglobin, troponin T and I, CK-MB)
What are the biomarkers for MI?
- Myoglobin
- Troponin T and I
- CK-MB
What is the biomarker of choice to assess MI?
- Troponins
- Best predictor
Myoglobin
- Very early marker of MI
- Rises within 2 hours
Troponins T and I
- Marker of choice for MI
- Rises within 3 hours, peaks at 18-48 hours depending on MI size
- Best predictor
CK-MB
- Used to be marker of choice prior to troponins
- May begin to rise within 3 hours, peak 18-24 hours
What occurs 3-4 days after MI?
- Soft scar formation
* At risk of fatal rupture during first 1-2 weeks! Accounts for 10% of MI mortality
What occurs 2-3 months after MI?
Mature scar formation
*Dilation and hypertrophy may result
Myocardial stunning
- Cell unable to contract after reperfusion
- Occurs even though the cell hasn’t suffered irreversible damage
- Transient (may last hours to days)
Hibernating myocardium
- Contractile function is reduced in a “healthy” myocardial cell that is experiencing ischemia
- Returns to normal after perfusion is restored
Ischemic preconditioning
Myocardial cell adapts to brief episodes of ischemia by increasing “tolerance” to infarction
Reperfusion injury
- May occur after a hypoxic area is re-perfused
- Reintro of blood flow may create excess oxygen free radical production leading to inflammation cascade
What does a reperfusion injury contribute to?
“Final” size of infarct (area of permanent damage)
4 stages of plaque development
- Endothelial injury
- Fatty streaks
- Fibrous plaque formation
- Complicated/unstable plaques
What is the earliest gross pathological lesion in atherosclerosis?
Fatty streaks (full of LDL)
What makes a plaque “complicated”?
If it ruptured
What is prinzmetal angina?
- Coronary spasm
- A cause of myocardial ischemia
What are the acute coronary syndromes (ACS)?
Unstable angina
Myocardial infarction
What are the clinical manifestations of myocardial ischemia?
Stable angina
Silent angina
