lecture 12 - acute MI Flashcards
what is the definition of acute myocardial infarction?
commonly known as aheart attack, is the interruption of blood supplyto part of the heart, causing some heart cells to die.
what is believed to be triggering mechanism for development of thrombus in most patients with an MI ?
plaque rupture
how does plaque rupture result in MI?
when the plaque ruptures, a thrombus is formed at the site that can occlude blood flow, thus resulting in an MI
what plays an important role in rupture?
vulnerability more than triggers because exercise stress testing of patients with advanced coronary artery disease rarely triggers a rupture/ thrombus-related acute heart attack
describe NSTEMI vs STEMI
NSTEMI is when there is a partial occlusion of a major coronary artery previously by atherosclerosis and particle thickness damage to heart muscle
STEMI occurs by developing a complete occlusion of a major coronary artery previously affected by atherosclerosis and causes a full thickness damage of heart muscle
what does the shorter the time between coronary occlusion and coronary perfusion mean?
the less damage and greater amount of myocardial tissue that may be salvaged
how long does it take for irreversible damage to the myocardium?
20 - 40 minutes after interruption of blood flow
where does cellular death occur and where does it spread?
cellular death may occur fist in the subendocardial layer and spreads like a ‘wavefront’ throughout the thickness of the wall of the heart
what are cellular changes associated with the initial MI onset of coronary occlusion ?
the cellular changes associated with the initial MI may be followed with
1. the development of infarct extension (new myocardial necrosis)
2. infarct expansion (a disproportionate thinning and dilation of the infarct zone) or
3. ventricular remodelling (a disproportionate thinning and dilation of the ventricle), resulting in an enlarged heart
what are symptoms of mi?
chest pain, nausea, vomiting, stating, breathing difficulty
- siting on chest sensation
- pain radiates to the neck, left arm, back or jaw
- pain of MI os often more prolonged and not relieved by rest or sublingual GTN
what are biochemical markers that are associated with clinical diagnosis of MI?
a rise and gradual fall (troponin) or more rapid rise and fall (creatine Kinase MB) are biochemical markers of myocardial necrosis if associated with:
a. ischemic symptoms (shortness of breath, chest pain)
development of pathogenic Q waves on the ECG
electrocardiographic changes indicative of ischemia (ST segment elevation or depression)
what are troponin released from and what do each category of them rise and fall in?
troponin released from damaged muscle, release prolonged with actin and myosin damage
troponin I levels rise in about 3 hours, peak at 14 to 18 hours and remain elevated for 5 to 7 days
troponin T levels rise 3 to 5 hours and remain elevated for 10 to 14 days
what are high sensitivity troponin measurements used for?
major method of detection of MI and early rule out; e.g., Elecsys Troponin T high sensitive and ARCHITECT STAT high-sensitive Troponin I assays
describe creatine kinase in the serum and when are serial samplings performed?
CK-MB appears in the serum in 6 to 12 hours, peaks between 12 and 28 hours, and returns to normal levels in about 72 to 96 hours.
Serial samplings are performed every 4 to 6 hours for the first 24 to 48 hours after the onset of symptoms.
what is myoglobin and why is it not specific for diagnosis of MI?
Myoglobin: Myoglobin is an oxygen-binding protein found in skeletal and cardiac muscle. Myoglobin’s release from ischemic muscle occurs earlier than the release of CK.
The myoglobin level can elevate within 1 to 2 hours of acute MI and peaks within 3 to 15 hours.
Because myoglobin is also present in skeletal muscle, an elevated myoglobin level is not specific for the diagnosis of MI. Subsequently, its diagnostic value in detecting an MI is limited
