If one does decide to use streptokinase as a last, life-saving option, how should it be administered? I assume the usual method of diluting in 100mls fluid won't work well if circulation is impaired by cardiac arrest.
hello,
@shashikiran, excellent discussion, thank you!
@medstudent: apart from what shashikiran has excellently elaborated, another reason why thrombolytics(streptokinase)
is not used in nstemi is probably as follows:
Lets go back to the pathophysiology of nstemi. Atheromatous plaque ruptures, leading to a thrombus is the basic pathophysiology
of ACS. Now in NSTEMI, what is proposed is that components of the ruptured plaque and/or platelet aggregates get embolised(away
from the primary site of rupture and thrombus) causing microemboli, leading to microinfarcts.
Hence, management of NSTEMI includes STABILITY of the plaque. Thrombolytic therapy can lead to more microinfarcts, hence is
contraindicated as it can cause more damage.
hope this was helpful,
STEMI is ST-segment elevation and elevation MI NSTEMI non-ST myocardial infarction. Because STEMI is caused by the sudden thrombotic occlusion (formation of a blood clot) of a coronary artery, the mainstay of treatment is thrombolytic therapy (treatment to dissolve the clot). NSTEMI caused by unstable plaque with platelet aggregation.
STEMI is when there is a transmural infartion of the myocardium - which just means that the entire thickness of the myocardium has undergone necrosis - resulting in ST elevation. While NSTEMI is when there is a partial dynamic block to coronary arteries (non-occlusive thrombus). There will be no ST elevation or Q waves on ECG, as transmural infarction is not seen. This is the main difference between STEMI and NSTEMI.