3.3 Coagulation Studies & Arterial Blood Gas

Coagulation Studies & Arterial Blood Gas

Patient Care B.8.c and B.8.d are the clotting and ventilation labs. One set tells you whether a femoral stick or a coronary stent is legal from a bleeding-and-thrombosis standpoint. The other tells you whether the sedated patient is acidotic from shock or from not breathing. The R.T.(CI) does not write the protocol, but you draw the activated clotting time (ACT), you recognize a dangerous international normalized ratio (INR), and you know when an arterial blood gas (ABG) and capnography disagree.

Quick Answer: Prothrombin time (PT)/INR for warfarin; activated partial thromboplastin time (aPTT) for a heparin drip; ACT for heparin in the room. Baseline ACT is often about 80–120 seconds; many heparin PCI protocols target about 250–300 seconds. If ACT is 180 seconds at stent deployment, do not deploy—give more unfractionated heparin (UFH) and recheck. Reverse heparin with protamine carefully. ABG: pH 7.35–7.45, PaCO2 35–45 mmHg, HCO3 22–26 mEq/L.

Coagulation (B.8.c): PT, PTT, INR, ACT

These four names are not interchangeable. They use different samples, different machines, and different clinical questions.

PT and INR — warfarin

PT and INR measure the extrinsic pathway and are the outpatient and pre-op tests for warfarin. A typical teaching INR in a patient not on warfarin is about 0.8–1.2. The INR is unitless so that labs with different thromboplastin reagents can be compared.

For elective femoral access, many labs want the INR at or below about 1.7–2.0. That band is protocol-dependent, not a number ARRT publishes as a national cutoff. Radial access is often more forgiving of a moderately elevated INR because the wrist is compressible, but it is still not a license to ignore a 3.5 INR on a patient who also needs dual antiplatelet therapy. If the case can wait, wait; if it cannot (STEMI), the operator weighs bleed versus occlusion and may still go radial with a closure plan.

Trap: A point-of-care INR of 1.1 does not mean the ACT will be 300 seconds after heparin. INR is not the cath-lab heparin test.

aPTT — heparin infusion

aPTT (the outline's PTT) measures the intrinsic pathway on a citrated plasma sample sent to the lab. It is how a floor or CCU UFH infusion is titrated. It is a poor real-time tool in the middle of PCI because turnaround is too slow and the range is reagent-specific. If a patient arrives from the unit on a heparin drip, know the last aPTT, but do not use it as the stent-deployment number. Once you bolus heparin in the room, you switch mental models to ACT.

ACT — the cath-lab clotting test

ACT is a whole-blood clotting time run in the room (Hemochron, i-STAT, or similar). Blood comes from the manifold, sheath, or a dedicated draw into the cuvette—follow the device instructions, because air, contrast, and a half-filled cuvette all fake the result.

Teaching numbers, labeled as typical, not as fake ARRT law:

• Baseline ACT is often about 80–120 seconds before heparin.
• Many heparin PCI protocols target about 250–300 seconds before balloon or stent. Some protocols run lower (about 200–250 seconds) when a glycoprotein IIb/IIIa inhibitor is on board.
• Bivalirudin protocols differ. Some use a weight-based bolus and infusion with little ACT titration; others check ACT and aim higher. The concept the exam wants is: the target is protocol- and device-specific. Memorize the idea, then follow the card on the wall.

Scenario — ACT 180 seconds at stent deployment. The operator is on the stent, the lesion is open, and the ACT prints 180 seconds. For a typical UFH PCI target of 250–300 seconds, 180 seconds is subtherapeutic. Coronary stent thrombosis is the risk. Hold deployment, give additional UFH, recheck the ACT, then deploy when the protocol target is met. Do not reverse with protamine and then deploy. Do not treat 180 seconds as close enough because it is above the 80–120 second baseline. Baseline is unheparinized blood; 180 seconds in a coronary artery with a stent about to be placed is still a clot risk.

If the ACT is unexpectedly low after a documented bolus, think missed vein injection, short dwell time, antithrombin III deficiency, or a bad cuvette—then repeat, do not stack huge extra boluses blindly.

Protamine — reversing heparin

Protamine binds UFH and reverses the ACT toward baseline. A common teaching dose is about 1 mg protamine per 100 units of heparin remaining, given slowly intravenously. Rapid dumping causes hypotension. Patients with NPH insulin exposure or fish allergy have a higher risk of anaphylaxis. Excess protamine can itself act as an anticoagulant and is associated with paradoxical thrombosis and pulmonary hypertension. Protamine does not reverse warfarin, direct oral anticoagulants, or reliably reverse bivalirudin. If the bleed is a surgical nightmare after heparin, protamine is the tool; if the problem is an INR of 3.8, protamine is the wrong bottle.

Arterial blood gas (B.8.d): pH, PaCO2, HCO3

The outline lists pH, PaCO2, and HCO2/HCO3. HCO3 is bicarbonate; older notations sometimes write HCO2 for the same idea. Typical arterial teaching values:

Two patterns you will actually see:

• Metabolic acidosis in shock or arrest. Low pH, low HCO3, PaCO2 that may be low if the patient is compensating or high if they have also stopped breathing. Lactic acid from hypoperfusion is the usual cath-lab story—hypotension, tamponade, massive infarction, prolonged arrest. An ABG that is 7.10 / 38 / 12 is not a ventilator problem first; it is a perfusion problem.
• Respiratory acidosis from oversedation. Low pH, high PaCO2, HCO3 still near normal in the acute minute. The patient received too much opioid or benzodiazepine, the jaw fell back, and they are not exchanging. This is why you watch capnography continuously during sedation: end-tidal CO2 (ETCO2) trends with PaCO2 (usually a few mmHg lower) and alarms before the ABG comes back. Treat the airway and the reversal agents; do not wait for the printer.

ABG sample is arterial, heparinized, and run promptly (ice if delayed). A venous stick labeled as an ABG will look more acidotic and more hypercarbic than the arterial truth. Do not chase a venous pH of 7.28 with a bicarbonate bolus if the pulse oximeter and ETCO2 are normal and the patient is talking.

Test / sample / typical target / CI use

Exam traps

• ACT 180 seconds is above baseline and still too low for typical heparin stent deployment.
• aPTT is not the machine on the cath-lab counter. ACT is.
• Protamine anaphylaxis risk is NPH insulin and fish allergy, not iodine contrast allergy.
• High PaCO2 with a falling pH in a snoring patient is respiratory acidosis from hypoventilation. Low HCO3 with a falling pH in a crashing, hypotensive patient is metabolic acidosis. Mixing those two is the classic wrong answer.
• Do not invent a national ARRT INR cutoff. Say protocol-dependent, then know why femoral cares more than radial.