Cardio part 2 Flashcards
Transmural infarction
usu dt acute coronary thrombosis
sub endothelial ( non-transmural) infarction
- coronaries narrowed but patent
- thrombotic occlusions-> thrombolysis
- limited period of time of increased oxygen demand and/or decreased oxygen delivery
- hypotension/hypertension
- Anemia
Lab finding on an MI
- ECG changed may reflect a progression from ischemia to infarction
- specific EKG abmornalities can reflect the location of ischemia or infarction
- MI resulting from total coronary occlusion result in more homogenous tissue damage and are usu reflected b q wave MI pattern on the EKG
Labs reflective of an MI
- elevated WBC
- Elevated LDH
- Elevated Cardiac Enzymes
- Creatine phosphokinase (MB band)
- troponin (esp tromonin I an T)
define Coronary artery disease
progressive narrowing of the coronary artery d/t expansion of a fiberous plaque. impairs flow after > 50 to 70% luminal obstruction
- decreased flow leads to sx of inadequate blood supply to target organs the event of increased metabolic activity and oxygen demand or with superimposed coronary spasm
Myocardial infarction
the development of myocardial necrosis caused by prolonged critical imbalance b.n the amount of oxygen supplied to the myocardium and the metabolic demand of the myocardium
what is the most common pathogenss of AMI
plaque rupture w.in a coronary artery
what occurs after a plaque has ruptured
exposure of the sub endothelial area result in platelet agg., thrombus formation, fibrin accumulation, hemorrhage into the plaque, and varying degrees of vasospasm
what are other causes of an MI
emboli to coronary arteries- mb dt cholesterol or infection
- coronary artery spasm, if prolonged or occurring in the presence of underlying atherosclerotic dz or in poorly functioning heart muscle
- coronary anomalies
- aneurysm of the arteries
- hypoxia dt underlying pulmonary dz, carbon monoxide px,
- arteritis
what is the FX of decreased o2 flow to the myocardium
- go from aerobic to anaerobic
- ATP syn decreases w.in 1-2 min and it is reduced to 50% b 10 minuted
- reduction in ATP leads to disruption of NA/K ATPase membrane channel which causes a marked increase in the membrane permeability
- increased permeability, oocytes of the cardia muscle begin to swell and internal cellular metabolic functions begin to deteriorate
- Ca+ influx into cardia muscle cells activated various degradative enzymes which further disrupt all cellular fun
- irreversible cell death occurs in 15- 20 min
- reprofusion w/in 1-6 hours can can decrease death
Histopathology
sorry but your gunna have to writ out the chart of what happen to the heart tissue from 0->2mon gross pathology and histopathology BRS book has a good chart
what are some potential cardia complications following an MI
-hypOtension
-Arrhythmias
_CHF
-Hypoxemia
-Ventricualr wall rupture VSD, acute MR
- pericarditis
-Repeat MI
hemopericardium
blood trapped in the pericardium this can lead to cardiac tamponade
what are some potential non-cardia complications following an MI
- aspiration
- infection -pneumonia
- complications arising from prolongs immobilization ( DVT PE)
Define Pericarditis
- a fibrinous or fibrin-hemorrhagic pericarditis often develops in the 2, 3, or 4th day following a TRANSMURAL MI as a result of inflammatory epicardial response to the underlying myocardial injury
- usually resolover time w. no serious sequelae
