The machine cannot tell you what is wrong. It can only tell you which pressure changed. Reading alarms is pattern recognition against circuit anatomy.
6.1 The Pressure Map
Four pressures, each measured at a specific point:
Pressure | Where measured | Normally | Reflects |
Access (arterial) | Pre-blood-pump | Negative | Ability to draw blood from the patient |
Filter (pre-filter) | Post-pump, pre-filter | Positive | Resistance of the filter + return path |
Return (venous) | Post-filter, pre-patient | Positive | Resistance of returning blood to the patient |
Effluent | Effluent line | Variable | Used with the above to derive TMP |
Two derived values carry most of the diagnostic weight:
TMP = [(P_filter + P_return) / 2] − P_effluent — membrane permeability (device-specific formula)
Pressure drop across the filter (ΔP) = P_filter − P_return — resistance within the fibre bundle
💡 The differential that separates the two clotting patterns:
• Rising TMP with a stable ΔP → membrane fouling — protein layering on the membrane surface. Gradual, expected, end-of-filter-life.
• Rising ΔP (with or without rising TMP) → clot within the fibre bundle, obstructing flow through the hollow fibres. More acute, more ominous.
6.2 Alarm Troubleshooting
Alarm | Meaning | Common causes | Actions |
Access pressure too negative | Cannot draw blood | Catheter tip against vessel wall; kink; patient position; hypovolaemia; catheter thrombus; intra-abdominal hypertension (femoral lines) | Reposition patient/limb; check for kinks; assess volume status; reduce Qb temporarily; consider catheter lock/exchange. Line reversal increases recirculation and reduces delivered dose — a temporising measure only. |
Return pressure high | Cannot return blood | Kinked return limb; clotted venous chamber; catheter tip malposition or thrombus; clamped line | Inspect the entire return path; check chamber for clot; reduce Qb; imaging if catheter malposition suspected |
Return pressure low | Loss of circuit integrity | Disconnection, leak, or line separation | Immediate visual inspection of every connection. Treat as urgent. |
TMP high | Membrane no longer permeable at prescribed UF | Fouling; clotting; excessive filtration fraction; high haematocrit; hypoalbuminaemia effects | Reduce Q_uf; increase Qb; increase pre-dilution fraction; review anticoagulation; anticipate circuit change |
ΔP (filter pressure drop) high | Obstruction within fibre bundle | Clotting in the fibres | Review anticoagulation and access. Circuit change usually needed. |
Air detected | Air in the return limb | Loose connection; empty fluid bag; deaeration chamber level low | Stop, identify source, de-air per protocol. Never bypass the air detector. |
Blood leak | Blood detected in effluent | Membrane rupture | Stop and change the circuit. Do not return blood through a ruptured filter. |
💡 A general heuristic: alarms that involve the access limb are usually patient or catheter problems. Alarms involving the filter/TMP are usually prescription or anticoagulation problems. Alarms involving the return limb are usually mechanical problems. This directs where to look first.
6.3 Metabolic and Nutritional Complications
Hypophosphataemia
The most predictable metabolic complication of CRRT. Phosphate (~96 Da) is efficiently cleared by both diffusion and convection, and standard replacement fluids have historically been phosphate-free.
✅ RENAL demonstrated this directly: hypophosphataemia was significantly more common in the higher-intensity (40 mL/kg/h) arm than the lower-intensity arm — approximately 65% vs 54%. Dose-dependent, and unavoidable without repletion.
Consequences: respiratory muscle weakness impairing ventilator weaning, myocardial dysfunction, arrhythmia, rhabdomyolysis, and haemolysis at extremes.
Management: monitor at least daily on high-dose CRRT; replete proactively; use phosphate-containing CRRT solutions where available.
Hypothermia
The extracorporeal circuit is a large-surface-area heat exchanger running continuously.
- Clinical consequences: shivering with increased oxygen consumption; impaired platelet function and coagulation; and — the most clinically treacherous — masking of fever, blunting a key clinical signal of sepsis in exactly the population most at risk of it.
- Management: blood warmers or fluid warmers per device; continuous core temperature monitoring; maintain a high index of suspicion for infection despite normothermia.
💡 Do not let a normal temperature reassure you in a patient on CRRT. The circuit can conceal a febrile response entirely.
Micronutrient, amino acid and drug losses
- Amino acids are small, largely unbound, and readily cleared. Amino acid losses on CRRT are well described and clinically meaningful for nutritional prescribing.
⚠️ Declared gap: while amino acid loss is a consistent kinetic observation, the optimal protein prescription for patients on CRRT is not established by randomised evidence. Guidance in this area is derived from balance studies and consensus, and recommended targets vary between critical care nutrition societies. State the uncertainty rather than quoting a single figure as settled.
- Water-soluble vitamins (thiamine, folate, vitamin C, other B vitamins) and trace elements (selenium, zinc, copper) are cleared. Thiamine deficiency in particular is clinically consequential and easily overlooked; supplementation is common practice. Trace element repletion regimens on CRRT are not standardised by trial evidence.
- Antimicrobials and other drugs — Chapter 7.
Acid–base and electrolyte derangements
Derangement | Mechanism |
Metabolic alkalosis | Excess buffer delivery — most often citrate (Ch. 5), also high-bicarbonate solutions |
Metabolic acidosis with widened gap | Citrate accumulation (Ch. 5); inadequate dose; ongoing acid generation |
Hypokalaemia | Efficient clearance with potassium-poor solutions |
Hypomagnesaemia | Efficient clearance, plus citrate chelation |
Hypocalcaemia | Citrate chelation; inadequate calcium replacement |
Hypernatraemia | Hypertonic citrate formulations |
Hypoglycaemia / hyperglycaemia | Glucose is freely cleared; direction depends on solution glucose content |
6.4 Catheter Dysfunction and Access Complications
Insertion-related: pneumothorax, arterial puncture, haemothorax, arrhythmia, malposition.
Delayed: thrombosis, fibrin sheath formation, catheter-related bloodstream infection, and — for subclavian access — central venous stenosis, which is why KDIGO ranks the subclavian vein last for patients who may later need permanent access.
✅ AKIKI recorded more catheter-related bloodstream infections in the early-initiation arm — a concrete reminder that a catheter placed for RRT that a patient never needed is not a neutral act (Ch. 3).
Recirculation — blood returned through the venous port re-entering the arterial port — silently reduces delivered dose without triggering any alarm. It is increased by line reversal, by femoral catheters that are too short, and by catheter malposition. Suspect it when delivered clearance is disappointing despite an apparently normal-running circuit.
6.5 Circuit Downtime — The Quiet Complication
Every clotted filter, circuit change, trip to CT and return to theatre subtracts from delivered dose. This is precisely why KDIGO pairs a 1A recommendation to deliver 20–25 mL/kg/h with a 2B recommendation that the prescription will usually need to be higher (Ch. 4).
💡 Audit delivered dose, not prescribed dose. A unit that prescribes 25 mL/kg/h and loses six hours a day to downtime is delivering under 19.
6.6 Chapter Summary
- Access alarms are patient/catheter problems; TMP alarms are prescription/anticoagulation problems; return alarms are mechanical problems.
- Rising TMP with stable ΔP = fouling. Rising ΔP = clot in the fibres.
- Hypophosphataemia is dose-dependent and demonstrated by RENAL — monitor and replete.
- Hypothermia masks fever. Never let normothermia on CRRT reassure you.
- Recirculation and downtime reduce delivered dose invisibly. Audit the delivered number.