5.1 Anticoagulants, Antiplatelets & Thrombolytics

Anticoagulants, Antiplatelets, and Thrombolytics in the Cardiac Lab

The R.T.(CI) works in a room where a clot in a coronary artery is the disease and a clot at the sheath is the complication. ARRT Cardiac-Interventional Patient Care 1.E tests types, actions, indications, preparation, contraindications, and reactions. The highest-yield cluster is 1.E.1.a anticoagulants, 1.E.1.b thrombolytics, and the antiplatelet branch of 1.E.1.e. You are not the prescriber. You are the person who knows which bottle belongs on the table, which home drug changes access and closure, which number must be shouted, and which reaction is a stop-the-line event.

When a milligram or unit figure appears below, it is a typical teaching range used in labs, not an ARRT-published official dose. Follow the physician order and the printed protocol in your room.

Quick Answer: Unfractionated heparin (UFH) is the default procedural anticoagulant, monitored by activated clotting time (ACT) and reversed with protamine. Bivalirudin is the usual heparin-induced thrombocytopenia (HIT) alternative. Home warfarin and direct oral anticoagulants (DOACs) change access and closure. After a stent, dual antiplatelet therapy (DAPT) is aspirin plus a P2Y12 inhibitor; prasugrel is contraindicated after stroke or TIA, and ticagrelor can cause dyspnea that is not an allergy. Thrombolytics carry intracranial hemorrhage (ICH) risk after recent stroke or surgery.

Unfractionated heparin: bolus, ACT, protamine

UFH remains the workhorse anticoagulant for diagnostic work that proceeds to percutaneous coronary intervention (PCI), for most mechanical-support cases, and for heparinized flush on manifolds and sheaths. It potentiates antithrombin and thereby inhibits thrombin and factor Xa. The CI technologist's job is preparation, timing, monitoring, and recognition of bleeding or HIT — not inventing a dose while the operator is in a vessel.

Typical teaching bolus for PCI is often 70–100 units/kg (lab-protocol teaching, not ARRT-official). Diagnostic-only angiography may use a smaller bolus or heparinized flush only. Confirm the vial concentration before you draw (many labs stock 1,000 units/mL). Announce the units given in closed loop, not “heparin is in.”

ACT monitoring is the intra-case compass for UFH. Draw from a line that is not contaminated with residual flush heparin, after the bolus has circulated (many labs wait a few minutes). Typical teaching targets often sit around greater than 250–300 seconds for PCI without a glycoprotein IIb/IIIa inhibitor, and somewhat lower when a GP IIb/IIIa infusion is running — your facility card is the number you follow. Shout the ACT as soon as it prints. A still-low ACT is thrombus risk on wires and stents. An unexpectedly high ACT is bleeding risk if you are about to pull a femoral sheath or deploy a closure device.

Protamine reverses UFH by forming an inactive ion pair. Give it only on physician order, slowly, with the crash cart in mind: hypotension and anaphylactoid reactions are the exam-relevant adverse effects. Protamine does not fully reverse low-molecular-weight heparin and does not reverse bivalirudin, warfarin, or DOACs. Do not treat protamine as a universal “undo blood thinner” drug.

HIT is a hard contraindication to UFH and to heparinized flush. If the history says HIT, nothing heparin-coated or heparin-flushed belongs on the table. A heparinized manifold is still heparin. Strip the pressure bag, change the tubing, and move to the alternative anticoagulant before the first flush.

Bivalirudin: direct thrombin inhibitor, HIT alternative

Bivalirudin is a direct thrombin inhibitor. It is the common PCI alternative when HIT is documented or strongly suspected, and some labs use it as a default PCI anticoagulant. It has a short half-life, so anticoagulation falls quickly when the infusion stops — useful when a sheath must come out, dangerous if the bag runs dry during a chronic-total-occlusion case. There is no protamine reversal. Prepare the infusion with a second-person concentration check. Do not copy a heparin ACT target onto a bivalirudin protocol; follow the bivalirudin card. Watch the access site for bleeding the same way you would with any anticoagulant.

Enoxaparin: less common in lab, timing issues

Enoxaparin is a low-molecular-weight heparin (LMWH) used more on the floor than as the lab's first-line, ACT-guided drug. The exam trap is timing. A patient who received enoxaparin a few hours ago is already anticoagulated in a way ACT does not reliably display. Additional UFH or a protocol “top-up” is an operator decision based on hours since the last dose and renal function, not a reflex heparin bolus as if the patient were naive. Protamine reverses enoxaparin incompletely. Renal impairment prolongs effect. Do not treat enoxaparin as interchangeable with UFH for ACT-guided PCI.

Warfarin and DOACs: home meds that change access and closure

These agents are usually not started in the lab. They change access, closure, and bleeding risk.

Warfarin: last dose and current international normalized ratio (INR) matter. An elevated INR on an elective femoral case may delay the procedure, push the operator toward radial access, or cancel a closure device that needs a clean common-femoral puncture against bone. Mechanical valves and recent venous thrombus are why the patient is anticoagulated — do not treat holding warfarin as if the indication were optional.

DOACs (apixaban, rivaroxaban, dabigatran, edoxaban): document last-dose time and renal function. Emergency primary PCI generally proceeds; you plan a compressible or radial stick, cautious closure, and a longer postprocedure hold rather than inventing complete reversal on the table. Hospital reversal agents exist for some DOACs; they are not routine cath-lab inventory. Protamine does not reverse a DOAC. Intra-case UFH or bivalirudin for PCI is a separate decision from the capsule taken this morning.

Antiplatelets: loading versus maintenance, surgery delay, class traps

Coronary stents require DAPT — aspirin plus a P2Y12 inhibitor — because stent thrombosis is a platelet problem as much as a thrombin problem.

Aspirin. Typical teaching load in ACS is 162–325 mg chewed if the patient is not already on aspirin; maintenance is a daily low dose per protocol. True aspirin allergy must reach the operator before a stent is deployed.

Clopidogrel. Oral thienopyridine P2Y12 inhibitor. Typical teaching load 300–600 mg, then daily maintenance. Onset is slower than prasugrel or ticagrelor. Surgery delay is often about 5 days so platelet function recovers. Your job is last-dose time and whether the load was actually swallowed — a missed load is a stent-thrombosis pathway.

Prasugrel. More potent thienopyridine. Typical teaching load 60 mg. Prior stroke or TIA is a contraindication. Extra bleeding caution in older and low-body-weight patients is standard teaching. Surgery delay is often about 7 days. Do not substitute prasugrel “because it is stronger” in a patient with a remote cerebrovascular event.

Ticagrelor. Reversible, non-thienopyridine P2Y12 inhibitor, twice-daily maintenance after a typical teaching load of 180 mg. Dyspnea is a known effect and is not, by itself, anaphylaxis. Do not stop DAPT for “shortness of breath” without the physician. Surgery delay is often about 3–5 days.

Cangrelor. Intravenous P2Y12 inhibitor with a very short half-life. Used when the patient cannot take oral drug (intubated STEMI, vomiting) or as a bridge to oral therapy. When the drip stops, antiplatelet effect falls fast — plan the oral overlap as ordered. Cangrelor is not a heparin substitute and is not monitored by ACT.

GP IIb/IIIa inhibitors: thrombocytopenia and bleeding

Eptifibatide and tirofiban block the final common pathway of platelet aggregation. They appear as bailout therapy for large thrombus, no-reflow, or high-risk ACS per operator. Thrombocytopenia and bleeding are the reactions to watch: check platelets as protocol requires, watch the access site, and do not assume a closure device erases bleeding risk. Infusions are often renal-adjusted. Older stems may still name abciximab as the GP IIb/IIIa agent classically tied to acute profound thrombocytopenia.

Thrombolytics: ICH, recent stroke, recent surgery

Alteplase and tenecteplase convert plasminogen to plasmin and lyse fibrin. In current practice, primary PCI is preferred for STEMI when it can be delivered rapidly. Systemic lytics remain the reperfusion option when PCI is not available in time, and intracoronary lytic is sometimes used for heavy thrombus. ARRT still tests the class.

ICH is the feared complication. Strong contraindications in teaching lists include recent stroke, recent major surgery or trauma, active bleeding, known intracranial neoplasm or aneurysm, and severe uncontrolled hypertension. After any lytic, every puncture is a hemorrhage risk — minimize sticks, avoid noncompressible sites, and watch neurologic status. A “small brain bleed last month” is not a green light for tenecteplase.

Drug / class / typical lab use / key trap

Scenario

A 59-year-old STEMI patient has documented HIT from 2021 and took apixaban this morning for atrial fibrillation. Do not hang heparin “because it is a STEMI.” Prepare bivalirudin, strip heparin from the flush, tell the operator the last DOAC time, prefer a compressible or radial access plan, and have DAPT loading ready after the stent — aspirin plus an oral P2Y12, or cangrelor if the patient cannot swallow.

Exam traps

• ACT monitors UFH, not enoxaparin, warfarin, or apixaban.
• Protamine is not a universal reversal agent.
• Prasugrel plus prior TIA is a contraindication, not a trivia dose reduction.
• Ticagrelor dyspnea is on the teaching profile; treating it as anaphylaxis and withholding DAPT can cause stent thrombosis.
• Heparin flush counts as heparin in HIT.