Weight-Based Heparin Nomogram Calculator
Weight-Based Heparin Nomogram Calculator
Adjust an unfractionated heparin infusion from the aPTT ratio using the Raschke weight-based nomogram — and check first that the ratio target belongs to your laboratory, because a target borrowed from another hospital can be materially wrong.
Weight-based heparin nomogram
aPTT ratio → new infusion rate80 kg, running at 1,440 units/hour, aPTT ratio 1.4
The Raschke weight-based nomogram
Adjustment: new rate = current rate + (change in units/kg/hour × weight in kg)
- ratio below 1.2
- rebolus 80 units/kg, increase by 4 units/kg/hour
- ratio 1.2 to 1.5
- rebolus 40 units/kg, increase by 2 units/kg/hour
- ratio 1.5 to 2.3
- no change — the therapeutic band in the original trial
- ratio 2.3 to 3.0
- decrease by 2 units/kg/hour
- ratio above 3.0
- hold the infusion for one hour, then decrease by 3 units/kg/hour
- actual body weight
- the trial used actual rather than ideal body weight. Many protocols cap the bolus and initial rate in obesity; follow the local one
- the ratio target is local
- the 1.5 to 2.3 band corresponded to 46 to 70 seconds on the 1993 study's reagent. Current reagents differ widely in heparin responsiveness, so the therapeutic ratio has to be established locally against an anti-Xa of 0.3 to 0.7 IU/mL
Worked example
80 kg, running at 1,440 units/hour, aPTT ratio 1.4
A ratio of 1.4 falls in the 1.2 to 1.5 band
Raschke: rebolus 40 units/kg and increase by 2 units/kg/hour
Bolus = 40 × 80 = 3,200 units
Rate change = 2 × 80 = 160 units/hour
New rate = 1,440 + 160 = 1,600 units/hour
Recheck the aPTT six hours after the change — sooner and the result still reflects the old rate
The Raschke nomogram in full
| aPTT ratio | aPTT in the original study | Bolus | Rate change |
|---|---|---|---|
| Below 1.2 × control | Below 35 s | 80 units/kg | Increase by 4 units/kg/hour |
| 1.2 to 1.5 × control | 35 to 45 s | 40 units/kg | Increase by 2 units/kg/hour |
| 1.5 to 2.3 × control | 46 to 70 s | None | No change |
| 2.3 to 3.0 × control | 71 to 90 s | None | Decrease by 2 units/kg/hour |
| Above 3.0 × control | Above 90 s | None | Hold for 1 hour, then decrease by 3 units/kg/hour |
Why the target ratio is a local number
| Issue | Consequence |
|---|---|
| aPTT reagents differ severalfold in heparin responsiveness | The same plasma gives ratios of 1.6 on one reagent and 2.6 on another. A ratio target is a property of the reagent, not of heparin |
| The therapeutic range should be calibrated against anti-Xa 0.3 to 0.7 IU/mL | Each laboratory derives the aPTT ratio that corresponds to that anti-Xa band on its own analyser. A borrowed target can over- or under-anticoagulate |
| Lupus anticoagulant | Prolongs the baseline aPTT and makes the ratio uninterpretable. Monitor with anti-Xa instead |
| Antithrombin deficiency or consumption | Heparin works through antithrombin. A low level produces apparent heparin resistance — escalating doses with a stubbornly short aPTT |
| Acute-phase rise in factor VIII and fibrinogen | Shortens the aPTT independently of heparin, so the ratio understates the true heparin effect. Common in sepsis and post-operatively |
| Sampling from the infusion line | Gives an absurdly long aPTT. Always draw from the opposite limb |
A nomogram, a weight, and a laboratory-specific target
Before weight-based dosing, unfractionated heparin was started at a fixed dose and adjusted by impression, and most patients spent the first day sub-therapeutic — which is the day recurrent thromboembolism is most likely. Raschke and colleagues tested a nomogram tied to body weight against standard care in a randomised trial published in 1993, and it reached the therapeutic range far faster and more reliably. The scheme is simple: 80 units/kg as a bolus, 18 units/kg/hour as the infusion, and adjustments in steps of 2 to 4 units/kg/hour with a further bolus whenever the aPTT is below target. Doses are calculated on actual body weight, not ideal, though many hospitals cap the bolus and the initial rate in severe obesity.
Two features of the nomogram are easy to skip and shouldn't be. The first is the rebolus. When the aPTT is below range, increasing the infusion alone takes several hours to reach a new steady state, and the bolus is what closes the gap in the meantime. The second is the hold. Above three times control, the nomogram stops the infusion for an hour before restarting at a lower rate, which is a different instruction from simply turning the rate down — the rate this page shows for that band is the restart rate, not the rate to continue running.
The part that travels least well is the target itself. The 1.5 to 2.3 times control band corresponded to an aPTT of 46 to 70 seconds on the reagent that study used, and modern aPTT reagents differ severalfold in how strongly they respond to heparin. The same plasma can give a ratio of 1.6 on one analyser and 2.6 on another. The correct approach, and the one every current guideline takes, is for each laboratory to establish the aPTT ratio that corresponds to an anti-Xa heparin level of 0.3 to 0.7 IU/mL on its own reagent and analyser. A ratio target carried over from a previous hospital, a textbook or a printed nomogram may therefore over- or under-anticoagulate, and the error is invisible because the number looks familiar.
Several situations break the aPTT as a monitoring tool altogether. A lupus anticoagulant prolongs the baseline aPTT so the ratio means nothing. An acute-phase rise in factor VIII and fibrinogen shortens the aPTT independently of heparin and makes the patient look under-anticoagulated when they are not. Antithrombin deficiency or consumption produces genuine heparin resistance, since heparin acts by potentiating antithrombin, and shows up as escalating doses with a stubbornly short aPTT. In all three, switch to anti-Xa monitoring. And a rising aPTT alongside a falling platelet count should prompt a 4Ts assessment for heparin-induced thrombocytopenia rather than a further rate reduction. This calculation supports a prescriber's decision against the local anticoagulation protocol and does not replace it. The dose that is given is the one the responsible clinician writes on the chart, against that hospital's own nomogram and its own laboratory's calibration.
Frequently asked questions
What is the Raschke weight-based heparin nomogram?
An 80 units/kg bolus followed by an infusion at 18 units/kg/hour, adjusted from the aPTT: below 1.2 times control, rebolus 80 units/kg and increase by 4 units/kg/hour; 1.2 to 1.5, rebolus 40 units/kg and increase by 2; 1.5 to 2.3, no change; 2.3 to 3.0, decrease by 2; above 3.0, hold one hour then decrease by 3.
Why is the target aPTT ratio different between hospitals?
Because aPTT reagents differ severalfold in heparin responsiveness, so the same plasma gives different ratios on different analysers. Each laboratory should establish the ratio corresponding to an anti-Xa heparin level of 0.3 to 0.7 IU/mL on its own system. A ratio target borrowed from elsewhere can materially over- or under-anticoagulate.
When should the aPTT be rechecked after a rate change?
Six hours afterwards, which is roughly the time needed to reach a new steady state, then every six hours until two consecutive results are in range, and daily thereafter. Checking sooner reports on the old rate and invites an unnecessary second adjustment.
What causes apparent heparin resistance?
Most often antithrombin deficiency or consumption, since heparin works by potentiating antithrombin. Also a high factor VIII or fibrinogen from an acute-phase response, which shortens the aPTT independently of heparin. Measure an anti-Xa level and an antithrombin activity rather than escalating the infusion indefinitely.
How is unfractionated heparin reversed?
Usually by stopping the infusion, because its half-life is only about 60 to 90 minutes. For serious bleeding, protamine sulfate neutralises roughly 1 mg per 100 units of heparin given in the preceding two to three hours, to a maximum of 50 mg. Protamine itself can cause hypotension and anaphylaxis, so it is given slowly.
Related calculators
References
- Raschke RA, Reilly BM, Guidry JR, Fontana JR, Srinivas S. The weight-based heparin dosing nomogram compared with a standard care nomogram: a randomized controlled trial. Ann Intern Med. 1993;119(9):874–881.
- Garcia DA, Baglin TP, Weitz JI, Samama MM. Parenteral anticoagulants: antithrombotic therapy and prevention of thrombosis, 9th ed: American College of Chest Physicians evidence-based clinical practice guidelines. Chest. 2012;141(2 suppl):e24S–e43S.
- Olson JD, Arkin CF, Brandt JT, et al. College of American Pathologists Conference XXXI on laboratory monitoring of anticoagulant therapy: laboratory monitoring of unfractionated heparin therapy. Arch Pathol Lab Med. 1998;122(9):782–798.
Medical Disclaimer: The tools and content provided here are for educational and reference purposes only. They are not intended to substitute for professional medical advice, diagnosis, or treatment. Clinical decisions should always be based on the comprehensive assessment of a qualified healthcare professional.