HEART 2.2 Flashcards
usually used in thrombolytic therapy
streptokinase or tissue-type plasminogen activator
factors that contribute to reperfusion injury include:
Mitochondrial dysfunction Myocyte hypercontracture Free radicals Leukocyte aggregation Platelet and complement activation
Microscopically, irreversibly damaged myocytes after
reperfusion develop
contraction band necrosis
intense eosinophilic bands of
hypercontracted sarcomeres are created by an influx
of calcium across plasma membranes that heightens
actin myosin interactions
contraction bands
state of prolonged contractile
dysfunction induced by short-term ischemia that
usually recovers after several days
stunned myocardium
Myocardium that is subjected to chronic, sublethal
ischemia can also enter into a state of lowered
metabolism and function called
hibernation
restoration of blood flow to
ischemic myocardium threatened by infarction; the
goal is to salvage cardiac muscle at risk and limit
infarct size
reperfusion
can remove a thrombus occluding a
coronary artery, but does not alter the underlying
atherosclerotic plaque
thrombolysis
percutaneous transluminal coronary
angioplasty with stent placement not only emanates a
thrombotic occlusion but also relieved some of the
original obstruction and instability caused by the
underlying disrupted plaque
angioplasty
provides a new conduit for flow by passing the area of blockage
coronary artery bypass graft
clinical diagnosis (MI)
troponin and CK MB (elevated)
The tempo and magnitude of appearance of these
serum markers after MI depends on several factors,
including the
volume of damaged myocardium, blood flow and lymphatic drainage in the area of the infarct,
the rate of elimination of the marker from the blood
STEMI
transmural
NSTEMI
subendocardial
earliest marker to become abnormal
myoglobin
CK-MB begins to rise within ______ hours of the onset
of MI, peaks at about __ hours, and returns to normal
within approximately ______hours
3-12 hrs;24hrs; 48-72 hrs
is more sensitive than CK MB in coronary syndromes
troponin
to induce vasodilation and reverse vasospasm
nitrates
to decrease myocardial oxygen demand and to
reduce the risk of arrhythmias, unless contraindicated
such as in heart failure
b blockers
to salvage myocardium, by either fibrinolytic
medications or transcatheter interventions
prompt perfusion
recommended initial therapy
o2 supplementation Nitrates Antiplatelet agents Anticoagulant therapy Bblockers Prompt perfusion Improve balance of supply vs demand for oxygen
Early arryhthmia monitorung
morphine
ace inhibitors
complications of MI
contractile dysfunction Papillary muscle dysfxn Right ventricular infarction Myocardial rupture Arryhthmia Pericarditis Chamber dilatation Mural thrombus Ventricular aneurysm Progressive heart failure
Chaotic depolarization without functional
ventricular contraction
ventricular fibrillation
