Anticoagulation and ACT Management
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Direct answer
Bypass without anticoagulation is a pumping thrombosis — contact between blood and the artificial surfaces of the circuit activates the intrinsic pathway within minutes, so heparin 300-400 U/kg precedes cannulation and the activated clotting time (ACT) must exceed 400 seconds, with many centres demanding 480, before flow begins. Management is a closed loop rather than a single dose: recheck every 30-60 minutes, supplement 50-100 U/kg as the value drifts, work up failure to respond as heparin resistance (antithrombin deficiency first), know that hypothermia and haemodilution prolong the ACT independently, and reverse at the end with protamine about 1 mg per 100 units of heparin remaining. Heparin-induced thrombocytopenia replaces heparin with bivalirudin, monitored by ACT or ecarin-based assays with no reversal agent available.
What you must remember
- Dose and target: heparin 300-400 U/kg intravenously via a verified central lumen; ACT above 400 seconds (commonly 480) against a baseline of 90-120 seconds before cannulation.
- The loop: ACT every 30-60 minutes on pump; a drift toward the floor triggers 50-100 U/kg supplements into the reservoir, with recheck 15-20 minutes later.
- ACT confounders: hypothermia and haemodilution prolong it (overstating anticoagulation), profound thrombocytopenia shortens it, and celite ACT is spuriously prolonged by aprotinin — use kaolin.
- Heparin resistance algorithm: unexpected ACT below target — first confirm delivery (right lumen, sample from a different site), then treat antithrombin deficiency with antithrombin concentrate or fresh frozen plasma; piling on heparin is not the answer.
- Anti-Xa as the modern cross-check: heparin assay 0.8-1.2 IU/mL or a heparin dose-response monitor exposes both resistance and over-anticoagulation where ACT is distorted.
- HIT pathway: bivalirudin is the usual bypass alternative (bolus plus infusion per haematology protocol, ACT-monitored, no reversal), argatroban second-line; clot risk in the stagnant corners of the circuit is the perfusionist's specific worry.
- Reversal discipline: protamine 1 mg per 100 units of heparin remaining (titration-guided, not the original dose), slow infusion, never into the circuit; protamine overdose is itself anticoagulant and antiplatelet.
- Heparin-coated circuits dampen complement activation but never substitute for systemic anticoagulation.
A resistance workup, step by step
A 62-year-old for redo CABG receives 24,000 units of heparin; the four-minute ACT returns 340 against a 480-second institutional target. Step one, verify delivery: the anaesthetist confirms the lumen aspirated blood before injection and the sample came from the radial line, not the heparinised lumen. Step two, repeat after five minutes with a fresh cartridge: 355 — real, not artefact. Step three, think mechanism: recent preoperative heparin infusion (platelet factor 4 neutralisation) and possible consumptive antithrombin deficiency. Step four, treat: antithrombin concentrate where available (fresh frozen plasma as the Indian-practice fallback in many centres), wait, recheck. Step five, if still short, a second heparin bolus of 100 U/kg under guidance. The ACT crosses 520, bypass proceeds, and the case is recorded as documented heparin resistance — which matters for every future operation this patient has. Contrast the branch where the number was simply a misdrawn sample: correcting delivery costs two minutes and no money; diagnosing resistance without excluding it costs the programme both.
How the exam frames it
Theory papers pair this topic with the short note "heparin resistance" and the viva probes sequence: what is checked before the diagnosis is made, what replaces heparin in HIT, and why the ACT rather than aPTT guides bypass (aPTT is unmeasurably prolonged at surgical heparin levels — off-scale, useless). The mark-losing answer remains "give more heparin" for any low ACT. A second favourite: "Why does the ACT rise during cooling even without extra heparin?" — hypothermia slows enzyme kinetics of the cascade itself; the anticoagulation has not truly increased, which is why anti-Xa cross-checking matters in deep hypothermia. Indian viva boards also expect the cost-and-availability answer: antithrombin concentrate where funded, plasma where not.
Frequently asked questions
What is the first step when the ACT fails to reach target after heparin?
Confirm the drug reached the circulation and the sample was drawn correctly, repeat the ACT, and only then diagnose heparin resistance and treat with antithrombin concentrate or fresh frozen plasma.
Which anticoagulant allows bypass in heparin-induced thrombocytopenia?
Bivalirudin in most programmes (argatroban second-line), given by bolus and infusion with ACT or ecarin-based monitoring and no reversal agent.
What anti-Xa level corresponds to adequate surgical heparinisation?
Roughly 0.8-1.2 IU/mL during bypass, used as a cross-check where ACT is confounded by hypothermia, haemodilution or thrombocytopenia.
How is protamine dosed at the end of bypass?
About 1 mg per 100 units of heparin remaining — guided by heparin-protamine titration where available — infused slowly through a patient line, never the circuit.
Why does the ACT prolong during hypothermia without extra heparin?
Cold slows the enzymatic reactions the ACT measures, so the number overstates true anticoagulation — one reason anti-Xa or dose-response monitoring is added in deep hypothermia.