ECG Myocardial infarction Flashcards
what are the two different types of leads and how are they viewing the heart
Limb leads: show the depolarization of the heart in the frontal or coronal plane
Precordial leads: show the depolarization of the heart in the horizontal (axial aka transverse) plane
in determining the cardiac axis is determined by looking at what two leads and what is normal and abnormal
leads I and AVF
positive in I and AVF = normal axis
positive in I and negative in AVF = Left axis deviation
-MI, large stomach
negative in I and positive in aVF = right axis deviation
-chronic lung disease
Coronary Heart disease history and symptoms
STEMI accounts for 30percent of all MIs
chest discomfort (more severe than angina)
- heavey, crushing pressure
- retrosternam, left, across chest; radiating into neck, jaw, left arm/shoulder
- epigastrium or between shoulder blades
associated Sxs
-nausea, vomiting, diaphoresis, dyspnea
20 percent of acute myocardial infarctions are painless (silent) in diabetics and elederly women
symptoms can be atypical especially in women and diabetics
Pathophysiology of Coronary heart disease
Narrowing of coronary arteries secondary to Erosion, fissuring or rupture of plaque; thrombus (platelet, fibrin rich thrombus is generated)
if partial occlusion = unstable angina or NSTEMI
if coronary flow is occluded = STEMI
Most MI caused by athersclerosis and other causes include vasospasms, vascuulitis, dissection, genetics
What is the progression of Coronary artery disease
Normal heart
Stable angina: plaque with fibrous cap
Unstable angina: cap ruptures
NSTEMI: blood clot forms blocking artery
STEMI: dead heart tissue at site of blockage
what are the zones of infarction
Ischemia: deficient blood supply impaired repolarization
-T wave changes
then
Injury: Deficient blood supply inability to fully polarize
-ST segment shifts
then
Infarction: Dead tissue lacks depolarization
-Q waves
during NSTEMI where in the cardiac tissue is the injury happening, and how does it transition to the STEMI
subendocardial injury and myocardial ischemia (no infarction yet)
then
for STEMI the ischemia and injury extend to the epicardial surface, subendocardial muscle dying in area of most severe injury
when seeing issues with the T waves, what could it mean
Myocardial Ischemia: inverted T waves, tall peaked T waves, or depressed
Myocardial Injury
-ST elevation
Myocardial infarction: Q waves
What are some cardiac biomarkers of Necrosis
Troponin I (cTnI) or T(cTnT)
- thisis 1-4 hours detectable after onset of AMI
- 10 to 24 hours its at its peak
- will persist fr 5-14 days
Renal failure can cause false positive cTnT
other markers:
- Myoglobin
- CK
- CK-MB
what are some signs of a NSTEMI
Elevated troponin, CK, and CK/MB but no ST segment elevation
usually a ST depression or T wave inversion but could be anything
-changes usually found in contiguous leads
signs of STEMI
ST elevation of 2mm or greater at J point for leads V2-V3 in men or 1.5mm in women
an absence of LVH or 1 mm or greater in 2 or more contiguous chest or limb leads
also can be called a Acute myocardial infarction
Complete interruption of blood flow
-will eventually show leak of troponin and cardiac enzymes
Localization of Myocardial infarction/ischemia, Area and leads for artery: Left anterior descending A
LAD or anterior interventricular A
Area: Anterior wall infarction
leads V1-V7
Localization of Myocardial infarction/ischemia, Area and leads for artery: Right Coronary Artery
area: Inferior wall infarction (Right Ventricular infarction)
leads: II, III, aVF, V3R - V6R
Localization of Myocardial infarction/ischemia, Area and leads for artery: Circumflex artery
area: lateral wall
leads: I, aVL, V5-V6
Localization of Myocardial infarction/ischemia, Area and leads for artery: Posterior descending artery
or called posterior interventricular artery
area: Posterior wall infarction
leads: V1-V3