Acute Myocardial Infarction
1.25 million MIs in the US every year
Early diagnosis and treatment are key!
- 30% of patients die before reaching the hospital
- another 10% die in the hospital
- yet another 10% die within a year of their first MI
- and 4% die per year following the first year of survival
Stable angina an occluded coronary artery that doesnt allow enough blood flow in for exercise but is fine at rest
Unstable angina an ongoing process that leads to Þ MI necrosis and death of tissue
Plaque rupture Þ exposed collagen Þ activated platelets release TXA2 Þ vasospasm and platelet aggregation Þ thrombus Þ obstruction of coronary blood flow.
Evidence of platelet involvement
(1) ASA and IIb IIIa inhibitors stop the process of thrombus formation
(2) Ý [TXA2] measured during MIs
(3) thrombolysis works
Diagnosis of Mis
- History Chest pain (like an elephant sitting on the chest), however can have silent ischemia
- Cardiac Enzymes enzymes released into the blood during the death of myocytes
- Myoglobin nonspecific marker of muscle injury appears first within 2 hours
- Troponin cardiac-specific isoenzymes of TnI and TnT are detectable next, 3 hours after the onset of chest pain
- CK-MB cardiac-specific creatine kinase starts to rise 4 - 8 hours after infarction
- LDH LDH1 is the most cardiac specific of the 5 isoenzymes of LDH. A LDH1/LDH2 ratio > 1.0 is indicative of myocardial necrosis. Serum levels of LDH peak 3-5 days after an acute MI.
EKG Changes in MI
Complications of MI
CHF diastolic dysfunction because the heart becomes stiffer
Cardiogenic shock ischemia Þ impaired contractility Þ ß CO Þ ß BP Þ ß coronary perfusion
RV infarction ß ß BP, ß CO, Ý Ý venous pressure. Treatment is fluids to maintain BP and therefore CO
Arrhythmias the MOST COMMON CAUSE OF DEATH IN MI, V tach and V fib are the biggies, but any other arrhythmia could happen. CCUs monitor patients to quickly shock them out of V Fib.
Heart Block if the infarction involves the conduction tissue a heart block may result
Aneurysm the weak, damaged wall may balloon out during systole
Ruptured septum leading to communication between the ventricles
Ruptured papillary muscles results in mitral regurgitation
Ruptured free wall death from cardiac tamponade
Thrombus stasis leads to thrombus formation, which can result in stroke. Treatment is anti-coagulation.
- 90% mortality of patients in Cardiogenic shock. Only treatment that makes an impact is Angioplasty
- must get the coronary artery open!