Myocardial infarction Flashcards
Myocardial infraction
-essentially end stage of coronary artery disease
NSTEMI
partial occlusion of a major artery
Myocardial infraction is _____ onset
acute
STEMI means…
S-T segment elevation MI
body has a few hours of oxygen deprivation before
cardiac cells die
Path of myocardial infraction
- atherosclerosis
- complicated lesion
- ischemia -therefore no oxygen to the heart (cardiac hypoxia)
- anaerobic metabolism
- acidosis (alters ph, which alters potential for heart to contract)
- arrythmias (irregular pattern beating)
- decreased ability to pump
- necrosis of heart muscle (infarction)
larger vessels are _______
smaller vessels are ______
- proximal vessels
- distal vessels
Etiology of myocardial infarction
- mostly atherosclerosis
- thrombus may be responsible (can develop there or come through as an embolus) causing ischemia
- artery may be severed (hemorhagging) causing ischemia
- coronary artery spasm
proximal occlusion is more ______ than distal occlusion
severe
The extent of the infarct depends on?
- vessel: how much tissue is affected
- duration of occlusion (time)
- complete or partial occlusion
- metabolic needs of affected tissue (sleeping vs exercising)
- existing collateral circulation in area (other vessels in area)
- HR, BP, rhythm
- risk factors present
Normal ECG waves
PQRSTU
Transmural infarct
- goes across entire thickness of ventricular wall
- proximal occlusion (primary artery obstruction)
- ST elevation (STEMI)
subendocardial infarct
- Inner part of ventricular wall
- distal occlusion (branches)
- ST depression (NSTEMI)
Typical mnfts of MI
- acute severe chest pain – that radiates typically to left arm, neck & jaw (also other areas such as tips of fingers
- anxiety & tachycardia
- nausea & vomiting (severe pain often comes with vomiting, vomiting center of brain near pain center, nociceptors activate pain center which may then activate vomiting center)
what is the primary mnfts of MI
-acute severe chest pain that radiates typically to left arm, neck & jaw
Diagnosing an MI
- ECG (will always be abnormal in case of MI)
- Serum markers (are released when cardiac muscle dies)
- Angiogram
Diagnosing an MI
- ECG (will always be abnormal in case of MI)–is basis of diagnoses
- Serum markers (are released when cardiac muscle dies)
- Angiogram
ECG for diagnosing MI
- ECG will always be abnormal in the cause of MI
- basis of diagnosis
- ST depression or elevation (ST segment is isoelectric point should be flat)
- T inversion
- loss of R wave
- abn Q
Serum markers for diagnosing MI
- are released when cardiac muscle dies
- Troponin I
Serum markers for diagnosing MI
-are released when cardiac muscle dies
-Troponin I & T, myoglobin, CKmb (creatine kinase–enzyme)
3 sub classes of creatine kinase–CKmb is restricted to heart and want to be measuring for an MI
-troponin peaks @ 3-10 hrs after MI
-CKmb is enzyme released by heart muscle and peaks 4-8 hrs after MI
angiogram for diagnosing MI
- releases dye into coronary circuit shows blockages & etc
a) could be problematic-may have atherosclerosis & knocks off some & creates an embolus
b) may insert a stent
c) may ballon “blow up” vessel to create patency