Thrombolytics / Fibrinolytics
Mechanism of Action
Convert plasminogen to plasmin, which actively dissolves the fibrin mesh of an existing clot. Unlike antiplatelets and heparin (which prevent new clots or stop a clot from extending), thrombolytics break down clots that have already formed — making them emergency reperfusion drugs. Because plasmin degrades fibrin systemically and cannot be aimed, the dominant danger is hemorrhage anywhere in the body, with intracranial hemorrhage the most lethal complication.
Fibrinolytic decision + safety sequence
- Confirm ischemic onset within windowischemic stroke: alteplase within 3–4.5 h of last-known-well; STEMI: door-to-needle 30 min when PCI >120 min away
- Screen absolute contraindicationsactive internal bleeding, recent intracranial surgery or stroke, intracranial neoplasm, uncontrolled severe hypertension
- Administer fibrinolyticafter head CT rules out hemorrhage for stroke
- Monitor for bleedingneuro checks q15min, watch all puncture sites, keep aminocaproic acid available
Common Medications
Indications
Side Effects
Contraindications & Interactions
Contraindications
Interactions
Administration & Monitoring
Patient Teaching
Clinical Pearl
tPA is a wrecking ball for clots — it can't aim, so every fibrin strand in the body is a target and bleeding can happen anywhere. Screen the absolute contraindications before you give it, watch the brain for the most lethal bleed, and keep aminocaproic acid as the emergency brake.