ICU · equipment-physics
Renal Replacement Therapy Equipment — Comprehensive (Haemofilter Membranes, Diffusion vs Convection, the RRT Circuit and Pressures, Regional Citrate)
Also known as RRT equipment · Haemodialysis · Haemofiltration · CVVH · CVVHDF · Dialyzer membrane · Diffusion vs convection · Regional citrate anticoagulation · Sieving coefficient · Transmembrane pressure · High-flux membrane · Solute drag · Ultrafiltration · Hollow fibre dialyser
Renal replacement therapy equipment for the ICU First Part: the hollow-fibre haemofilter/dialyser and membrane types (biocompatible synthetics — polysulfone, polyethersulfone, polyamide, polyacrylonitrile — versus bioincompatible cellulose; low-flux versus high-flux; sieving coefficient determines what crosses, cut-off the molecular size at which sieving falls to zero), the clearance mechanisms (DIFFUSION for small solutes down a concentration gradient, sustained by counter-current dialysate; CONVECTION for middle molecules dragged with water by solute drag, driven by hydrostatic pressure — the Starling forces across the membrane; and ULTRAFILTRATION for volume control), the modalities (IHD, CVVH, CVVHDF, peritoneal), and the full circuit — the blood pump (roller or peristaltic), the access/pre-/post-filter/effluent pressure monitoring points and the transmembrane pressure, the bicarbonate-buffered replacement fluid and effluent drain, and anticoagulation (systemic heparin or regional citrate with calcium monitoring).
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8 MCQs with explanations
Target exams
Red flags
Overview
Renal replacement therapy removes solutes and water across a semipermeable membrane - either an artificial haemofilter (haemodialysis and haemofiltration) or the peritoneum (peritoneal dialysis). The equipment is built around that membrane, the clearance mechanism it uses, and the circuit that drives blood through it.[1]
The membrane — the heart of the circuit
- The haemofilter or dialyzer is a cartridge of thousands of hollow fibres; blood flows INSIDE the fibres (the lumen) and dialysate (or ultrafiltrate) flows OUTSIDE them (in the inter-fibre space), in counter-current fashion to maximise the gradient across the full length of the membrane.[1][1]
- Counter-current flow keeps the concentration difference between blood and dialysate high along the ENTIRE fibre length. With co-current flow the gradient would collapse toward the distal end and clearance would fall; counter-current geometry is a key design optimisation and is examinable.[1]
- A modern adult haemofilter has a membrane surface area of 0.8-2.2 m² packed into a small cartridge — the total area of the hollow-fibre bundle. Greater area gives more clearance at the cost of a larger extracorporeal blood volume and more priming volume.
- The hollow-fibre wall is an asymmetric (anisotropic) structure: a thin inner skin (the actual semipermeable layer, ~0.5-2 micrometres) supported by a thicker sponge-like backing that gives mechanical strength without adding resistance. Pore size and pore density in the skin determine the sieving and cut-off properties.
Sieving coefficient and membrane cut-off — what can cross
- The sieving coefficient (S) of a solute is the fraction of that solute that passes through the membrane with water during convection: S = C_effluent / C_plasma (the concentration in the ultrafiltrate divided by the concentration in plasma). A solute with S = 1 passes freely (e.g. urea, creatinine, potassium); S = 0 does not cross at all (albumin, large proteins); values in between indicate partial sieving.[1]
- The cut-off of a membrane is the molecular weight at which the sieving coefficient falls to 0.1 — i.e. the size above which the membrane retains solute. A "high cut-off" membrane (cut-off ~45-60 kDa) is designed to clear inflammatory mediators (cytokines) at the cost of some albumin loss; standard high-flux membranes have a cut-off around 15-20 kDa, below albumin (66 kDa), so albumin is retained.[1]
- The ultrafiltration coefficient (Kuf) is the water permeability of the membrane — the volume of ultrafiltrate (mL/h) produced per mmHg of transmembrane pressure per m² of membrane. High-flux membranes have a high Kuf (> 20 mL/h/mmHg/m²); low-flux membranes a low Kuf (< 10).[1]
Membrane types — biocompatibility and flux
- Membrane composition: older cellulose-based membranes (cuprophane, cellulose acetate) are bioincompatible — their free hydroxyl groups activate complement and leukocytes, generating an inflammatory response and transient leucopenia and hypoxaemia on first contact with blood. Modern synthetic membranes (polysulfone, polyethersulfone, polyamide, polyacrylonitrile [PAN], polymethylmethacrylate [PMMA]) are biocompatible and highly permeable - "high-flux" - clearing larger molecules with far less inflammatory activation.[1]
- Biocompatibility matters: complement activation by bioincompatible membranes prolongs inflammation, may worsen recovery from acute kidney injury, and has been associated with worse outcomes in observational studies; biocompatible synthetic membranes are now the standard in critical care.[1]
Clearance mechanisms — diffusion, convection, ultrafiltration
The whole purpose of the circuit is clearance — net removal of solute and water across the membrane. Three distinct mechanisms operate, and which dominates defines the modality:[1]
- Diffusion (dialysis): solute moves down its CONCENTRATION gradient across the membrane. Movement is driven by random thermal motion and is most efficient for small molecules (urea 60 Da, creatinine 113 Da, potassium) because they move fastest; larger molecules move slowly and diffuse poorly. The gradient is sustained by running dialysate counter-current to blood so the concentration difference stays high along the whole fibre. Diffusive clearance rises with dialysate flow rate (Qd) and blood flow rate (Qb) until both are matched.
- Convection (haemofiltration): solute is dragged across the membrane WITH water — "solute drag" — driven by a PRESSURE gradient (hydrostatic). Water is pushed through the pores by hydrostatic pressure, and any solute small enough to pass (S > 0) is carried along in the stream. Convection is governed by the sieving coefficient: clearance of a solute = ultrafiltration rate x S. Convection clears middle molecules (beta-2 microglobulin 11.8 kDa, inflammatory mediators, small peptides) far better than diffusion, because it does not depend on the solute's own mobility. The water and solute lost are REPLACED by a substitution (replacement) fluid to avoid volume depletion.[1]
- Ultrafiltration: the pressure-driven removal of WATER (plasma water), used to control volume. It is the same hydraulic process that powers convection; ultrafiltration rate = Kuf x transmembrane pressure. The volume removed beyond what is replaced determines net fluid balance.
The physics — Starling forces across the membrane
The net movement of water (and dragged solute) across the membrane follows the Starling filtration principle, the same forces that govern capillary fluid exchange:[1]
- Hydrostatic pressure on the blood side (driven by the blood pump, 100-200 mmHg pre-filter) PUSHES water out of the plasma across the membrane into the effluent/dialysate compartment.
- Oncotic pressure of plasma proteins (mainly albumin, ~25-30 mmHg) PULLS water back into the capillary, opposing filtration. Because albumin cannot cross a standard high-flux membrane, it remains in the blood and exerts its full oncotic effect opposing ultrafiltration.
- Hydrostatic pressure in the effluent/dialysate compartment (the suction applied to the effluent line, typically slightly negative to positive) either opposes or assists filtration.
- Net ultrafiltration pressure = (P_blood - P_effluent) - (pi_blood - pi_effluent), where pi is oncotic pressure. In CRRT the effluent oncotic term is ~0 (protein-free dialysate/ultrafiltrate), so net filtration pressure is dominated by the hydrostatic difference. [1]
Convective flux (solute) = ultrafiltration flux x sieving coefficient = (Kuf x net filtration pressure) x S. Diffusive flux (solute) follows Fick's law: flux = -D x (dC/dx) x membrane area, i.e. proportional to the concentration gradient, the diffusion coefficient (inversely related to molecular size), and membrane area, and inversely to membrane thickness. [1]
Modalities — which mechanism dominates
- Intermittent haemodialysis (IHD): diffusion-based, high dialysate (500-800 mL/min) and blood (250-400 mL/min) flows over 3-4 hours; efficient and clears small solutes fast, but produces rapid solute and volume shifts that can cause hypotension and dialysis disequilibrium.[1]
- Haemofiltration (continuous, CVVH): convective clearance driven by high ultrafiltration with replacement fluid; clearance = effluent rate x sieving coefficient. Gentler, slower, haemodynamically better tolerated in the unstable ICU patient, and clears middle molecules better than diffusion.[1]
- Haemodiafiltration (CVVHDF): combines diffusion (dialysate) and convection (ultrafiltration + replacement), giving the highest total clearance for the same blood flow; the commonest CRRT modality in many ICUs.[1]
- Slow continuous ultrafiltration (SCUF): pure ultrafiltration for volume removal with minimal solute clearance; used mainly for diuretic-resistant fluid overload in heart failure.
- Peritoneal dialysis: the peritoneum is the membrane; dialysate dwells in the peritoneal cavity, diffusing solutes into it across the peritoneum (driven by concentration gradients) and removing water by osmotic ultrafiltration (glucose in the dialysate creates the oncotic gradient). Less efficient and carries peritonitis risk; rarely first-line in adult ICU.[1]
The circuit — every component, and what it does
The CRRT circuit is a closed extracorporeal loop that draws venous blood, passes it through the haemofilter, and returns it to the patient. Every component has a defined job, and every component is examinable.[1]
- Vascular access — the dual-lumen central vas-cath. Blood is drawn from and returned to the patient through a dual-lumen central catheter (a "vas-cath" or dialysis catheter), typically at the right internal jugular (preferred, straight route to the SVC/RA, lowest resistance) or femoral vein; the subclavian is relatively avoided for RRT access because of stenosis risk and variable flows. The catheter has a proximal ("arterial"/access) lumen that draws blood out and a distal ("venous"/return) lumen that returns it, with the tip placement designed to minimise recirculation (re-aspiration of just-returned blood). Recirculation is worst with short catheters and side-by-side (coaxial) designs in a small vessel.
- Blood pump — roller (peristaltic) or centrifugal. A roller (peristaltic) pump is the standard in CRRT: rotating rollers compress a segment of flexible tubing against a race, propelling blood forward by progressive occlusion (peristalsis). It is simple, cheap, and flow is independent of afterload, but it is NON-occlusion-sensitive (will keep spinning against high resistance) and causes some haemolysis at high speeds or with occluded lines. Centrifugal pumps use a rotating impeller/cone to generate kinetic energy; flow varies with afterload (less haemolysis, useful in ECMO-integrated circuits) and they are non-occlusive. Roller pumps dominate dedicated CRRT machines.[1]
- The haemofilter / dialyser cartridge (see The membrane above) — the clearance happens here. Blood enters the fibre lumina, water and solute cross the membrane, and the cleared blood returns through the venous line.
- Replacement (substitution) fluid — bicarbonate-buffered. In convective modes the plasma water lost as ultrafiltrate is replaced by a sterile replacement fluid, which is added either PRE-dilution (before the pump/filter, into the blood line) or POST-dilution (after the filter, into the venous return). The buffer is bicarbonate (or a bicarbonate-generating precursor such as lactate, metabolised to bicarbonate by the liver); bicarbonate is preferred in shock/liver dysfunction where lactate metabolism is impaired. The electrolyte composition (Na, K, Ca, Mg, glucose) is set to correct the patient's derangements.[1]
- Effluent line and drain. The ultrafiltrate-plus-dialysate leaving the filter is the effluent; it is drawn off by an effluent pump and measured continuously. Effluent volume minus replacement-fluid volume = NET ultrafiltration (the patient's net fluid loss). Effluent flow rate largely determines convective clearance (clearance ~ effluent rate x sieving coefficient in CVVH).
- Anticoagulation delivery system. To keep the blood-filter interface from clotting, anticoagulant is infused into the pre-pump or pre-filter line. Options: systemic unfractionated heparin (simple, monitor APTT/anti-Xa, systemic bleeding risk), regional citrate (citrate infused pre-filter chelates calcium to anticoagulate the circuit; calcium chloride is re-infused into the venous return; the patient is systemically un-anticoagulated), or no anticoagulation (high bleeding risk but shorter filter life).[1][4]
- Venous bubble trap and air detector. Before blood returns to the patient it passes through a venous chamber that traps any air; an ultrasonic air detector on the venous line triggers a clamp that stops flow if air is detected — the last-line safeguard against venous air embolism.[1]
Pre- versus post-dilution — a key circuit design choice
Replacement fluid can be added PRE- or POST-dilution, and the choice trades clearance against filter life:[1]
- Post-dilution (replacement into the venous return): the plasma concentration entering the filter is UNDILUTED, so convective clearance is maximal (clearance = effluent x S). But hemoconcentration in the filter raises viscosity and the risk of filter clotting; it is limited by the filtration fraction (the fraction of plasma water removed — keep < 25 per cent to avoid clotting).
- Pre-dilution (replacement into the blood line before the filter): dilutes the blood entering the filter, LOWERING solute concentration and therefore clearance (clearance is reduced ~10-15 per cent by the dilution), but it also lowers haematocrit and viscosity in the filter, REDUCING clotting and extending filter life. Used when filter life is the priority or filtration fraction is high. [1]
Pressure monitoring in the circuit — five points that tell you everything
Modern CRRT machines continuously monitor pressure at five points; the pattern of pressures diagnoses WHERE in the circuit a problem lies. This is the single most examinable area of RRT equipment.[1]
- Access (pre-pump) pressure — the pressure drawing blood OUT of the patient. Measured before the blood pump, this is NEGATIVE (the pump sucks). Normal: -10 to -80 mmHg. An increasingly NEGATIVE access pressure (e.g. -200 mmHg) means the pump is struggling to draw blood — the catheter is kinked, malpositioned, abutting a vessel wall, partially clotted, or the lumen is too small for the set blood flow. A very negative access pressure risks drawing air through connectors (air embolism) and causes haemolysis.
- Pre-filter pressure — the pressure pushing blood INTO the filter. Measured just before the haemofilter, this is POSITIVE (after the pump), normally 100-200 mmHg, and reflects the resistance of the filter to blood flow. A rising pre-filter pressure with stable post-filter pressure means the FILTER INLET or fibres are clotting or blocked.
- Post-filter pressure — the pressure leaving the filter. Measured just after the filter, normally slightly lower than pre-filter (the pressure drop across the filter is the resistance of the fibre bundle). A rising post-filter pressure with a stable pre-filter pressure means the VENOUS LINE or venous bubble trap is obstructed (kinking, clotting of the return line).
- Effluent pressure — the pressure in the effluent/dialysate compartment. This is the suction applied to draw ultrafiltrate off; it is usually slightly NEGATIVE to slightly POSITIVE. It sets, with the blood-side pressures, the transmembrane pressure.
- Transmembrane pressure (TMP) — the pressure ACROSS the membrane driving ultrafiltration. TMP = [(pre-filter pressure + post-filter pressure) / 2] - effluent pressure. It is the average blood-side hydrostatic pressure minus the effluent-side pressure. Normal: 100-150 mmHg. TMP is the pressure that must be applied to achieve the set ultrafiltration rate against the membrane's resistance (Kuf).[1]
What the pressures tell you — the diagnostic pattern
The combination of which pressure is abnormal localises the fault. This is the core troubleshooting logic:[1]
Exam practice
SAQ — The CRRT circuit and anticoagulation in the bleeding, liver-impaired septic patient
10 minutes · 10 marks
A 62-year-old man with septic shock from ascending cholangitis, KDIGO stage 3 acute kidney injury (creatinine 410 micromol/L, potassium 6.6 mmol/L, pH 7.20, bicarbonate 14), and moderate hepatic dysfunction (bilirubin 92 micromol/L, albumin 24, INR 1.9) is commenced on CVVHDF. He is four hours post-emergency ERCP with sphincterotomy and is oozing from the cannulation site; his haemoglobin has fallen from 105 to 78 g/L. He is ventilated, on noradrenaline 0.28 microgram/kg/min for a MAP of 66. The circuit has clotted twice in the last twelve hours. The nurse asks how you want to anticoagulate the next circuit.
SAQ — CRRT dose prescription and filter choice in septic AKI
10 minutes · 10 marks
A 75-year-old woman weighing 60 kg is admitted with urosepsis and severe acute kidney injury (creatinine 520 micromol/L, potassium 6.4 mmol/L, pH 7.18, bicarbonate 12). She is 6 litres in positive fluid balance and oliguric despite intravenous furosemide 80 mg. She is intubated and ventilated, on noradrenaline 0.3 microgram/kg/min for a MAP of 68, with lactate 3.8. The team has decided on continuous renal replacement therapy and asks you to prescribe the dose and choose the filter.
Red flags
Troubleshooting circuit problems — a pressure-pattern approach
When a CRRT circuit alarms, the machine's pressure readouts localise the fault. Read the pressures in sequence:[1]
Reading the pressures to localise a circuit fault
- CHECK THE ACCESS (pre-pump) pressure first. It is normally mildly negative. If it is VERY NEGATIVE (-150 to -250 mmHg or the lower alarm limit is hit), the problem is BEFORE the pump — the catheter is kinked, malpositioned, abutting a wall, clotted, or too small for the flow. Lower the blood-flow rate, reposition or flush the catheter, check the access lumen for clot, and consider a larger/longer catheter.
- CHECK THE PRE-FILTER vs POST-FILTER pressures to localise clotting WITHIN the filter. A RISING PRE-FILTER pressure with a STABLE post-filter pressure (a widening pressure drop across the filter) means the filter INLET/fibres are clotting — review anticoagulation, check the filtration fraction, and prepare to change the circuit.
- CHECK FOR A RISING TRANSMEMBRANE PRESSURE. TMP rising out of proportion to the set ultrafiltration rate means the effective membrane area is falling as fibres block with clot — the filter is failing. Combined with a rising pre-filter pressure this confirms filter clotting; change the circuit before it clots off entirely.
- CHECK THE POST-FILTER pressure for an OBSTRUCTED VENOUS RETURN. A RISING POST-FILTER pressure with a stable pre-filter pressure means the VENOUS LINE or venous bubble trap is obstructed — kinking of the return line, clot in the bubble trap, or a clamped/bent venous connector. Inspect and relieve the obstruction.
- CHECK THE EFFLUENT pressure and line. A blocked or kinked effluent line, or an effluent pump fault, gives an abnormal effluent pressure and a mismatch between prescribed and actual fluid removal; the machine will flag an effluent/ultrafiltration error. Inspect the effluent line for kinks and the effluent bag connection.
- CHECK FOR AIR. An air alarm overrides everything — stop, inspect the bubble trap and lines for air and leaks, expel air, and resume. Air in the access line comes from a leaking connector under negative pressure or an empty bag; air in the return line threatens venous air embolism.
Pressure-alarm pattern — what each pattern means
| Pattern (which pressure is abnormal) | Anatomical location of the fault | Likely cause | Action |
|---|---|---|---|
| Access pressure very negative | Before the pump (catheter/access line) | Catheter kinked, malpositioned, abutting vessel wall, partial clot, lumen too small for flow | Reduce blood flow, reposition/flush catheter, check for clot, consider larger catheter |
| Pre-filter pressure RISING, post-filter stable (widening drop across filter) | Filter inlet / fibre bundle | Filter clotting, blocked fibres, high filtration fraction hemoconcentration | Review anticoagulation, lower filtration fraction (pre-dilution, higher blood flow), prepare to change circuit |
| Post-filter pressure RISING, pre-filter stable | Venous line / bubble trap | Return line kinked, clamped, or clot in bubble trap | Inspect and relieve venous obstruction; clear/replace bubble trap |
| Transmembrane pressure RISING | Across the membrane | Filter clotting — effective membrane area falling as fibres block | Increase/review anticoagulation; change the circuit if it continues to climb |
| Effluent pressure abnormal / ultrafiltration error | Effluent line / effluent pump | Effluent line kinked, bag disconnected, pump fault | Inspect effluent line and bag; check pump; recalibrate |
| Air alarm | Anywhere, but air in return is embolic | Leaking access connector (air drawn in under negative pressure); empty bag with line break | Stop pump; expel air from bubble trap; fix leak/replace bag; resume |
Anticoagulation of the circuit
Keeping the blood-filter interface from clotting is essential — without it filter life is short and clearance falls. The choice balances bleeding risk against circuit longevity:[1][4]
- Systemic unfractionated heparin — simple, cheap, familiar; a bolus then infusion titrated to APTT or anti-Xa. Disadvantage: systemic anticoagulation increases bleeding risk; heparin-induced thrombocytopenia (HIT) is a risk with prolonged use.
- Regional citrate anticoagulation — the preferred method in most ICUs. Citrate is infused into the pre-filter blood line where it chelates ionised calcium (the clotting cascade needs Ca²⁺), anticoagulating the circuit; the citrate-calcium complex is small and passes into the effluent, and a fraction of the citrate also returns to the patient where the liver metabolises it (releasing the calcium). Calcium chloride is re-infused into the venous return to replace what is lost. The patient is effectively UN-anticoagulated systemically — the major advantage in bleeding patients. Monitoring: systemic ionised calcium (keep 1.0-1.3 mmol/L) and the total-to-ionised calcium ratio (a ratio > 2.5 indicates citrate accumulation).[4]
- No anticoagulation — for the actively bleeding or coagulopathic patient; filter life is shorter (frequent clotting) but bleeding risk is minimised. Pre-dilution and high blood flow help maintain circuit life without anticoagulant.
- Low-molecular-weight heparin (LMWH), prostacyclin (PGI2), heparin-protamine reversal — alternatives used in specific contexts (e.g. protamine reversal of heparin in the venous line for true regional heparinisation).
Citrate accumulation — the key safety concern with regional citrate
Citrate is metabolised to bicarbonate by the liver, kidney, and skeletal muscle. If metabolism is impaired (severe hepatic failure, shock, profound muscle hypoperfusion), citrate accumulates: the total calcium rises (bound to citrate) while ionised calcium falls, metabolic acidosis develops (unmetabolised citrate is an anion with no bicarbonate generation), and the total-to-ionised calcium ratio climbs. A ratio > 2.5 is the hallmark of citrate accumulation. Management: reduce or stop the citrate, switch anticoagulation, and correct the ionised calcium.[4]
Heparin versus regional citrate anticoagulation for CRRT
| Feature | Systemic heparin | Regional citrate |
|---|---|---|
| Mechanism | Potentiates antithrombin, inhibiting thrombin and factor Xa systemically | Chelates calcium in the circuit (clotting needs Ca²⁺); calcium re-infused into the venous return |
| Systemic anticoagulation | Yes — increased bleeding risk | No — patient is systemically un-anticoagulated |
| Monitoring | APTT or anti-Xa | Systemic ionised Ca²⁺ (1.0-1.3 mmol/L) + total/ionised Ca²⁺ ratio (keep < 2.5) |
| Filter life | Good | Superior — longer filter life than heparin in trials |
| Key risk | Bleeding, heparin-induced thrombocytopenia (HIT) | Citrate accumulation (hepatic failure/shock) → ionised hypocalcaemia, metabolic acidosis, rising total/ionised Ca²⁺ ratio |
| Best for | No contraindication to anticoagulation; HIT-negative | Bleeding risk, post-operative, hepatic function preserved |
| Acid-base effect | Neutral | Citrate metabolised to bicarbonate — can cause metabolic alkalosis; citrate accumulation causes metabolic acidosis |
Low-flux versus high-flux membranes
| Feature | Low-flux membrane | High-flux membrane |
|---|---|---|
| Pore size / Kuf | Small pores; Kuf < 10 mL/h/mmHg/m² | Larger pores; Kuf > 20 mL/h/mmHg/m² |
| Cut-off | Low (~5-10 kDa) — small solutes only | Higher (~15-20 kDa) — clears beta-2 microglobulin and middle molecules |
| Solute clearance | Efficient for small molecules (urea, creatinine, K) by diffusion | Small molecules by diffusion PLUS middle molecules by convection |
| Albumin loss | Negligible | Minimal in standard high-flux; significant in "high cut-off" membranes |
| Best modality | Conventional IHD | CRRT (CVVH/CVVHDF), high-efficiency HDF |
| Back-filtration | Minimal | Possible (dialysate impurity can back-diffuse into blood) — use ultrapure dialysate |
Cellulose-based versus synthetic membranes
| Feature | Cellulose-based (cuprophane) | Synthetic (polysulfone, PES, PAN, PMMA) |
|---|---|---|
| Biocompatibility | Bioincompatible — free hydroxyl groups activate complement and leukocytes | Biocompatible — minimal complement activation |
| Clinical effect | Transient leucopenia, hypoxaemia, inflammatory surge on first pass; may worsen AKI recovery | Minimal inflammatory response |
| Permeability | Low-flux; small pores | High-flux; larger pores, clears middle molecules |
| Current status | Largely obsolete in critical care | Standard of care in ICU RRT |
Diffusion versus convection versus ultrafiltration
| Mechanism | Driving force | What it clears best | Modality | Replacement needed? |
|---|---|---|---|---|
| Diffusion | Concentration gradient (counter-current dialysate) | Small molecules (urea, creatinine, K) — fastest movers | IHD, the diffusive component of CVVHDF | No (dialysate, not replacement) |
| Convection | Hydrostatic pressure (solute drag with water) | Middle molecules (beta-2 microglobulin, cytokines) — independent of solute mobility | CVVH, the convective component of CVVHDF | Yes — replace lost plasma water (pre- or post-dilution) |
| Ultrafiltration | Hydrostatic pressure | Water (plasma water) for volume control | SCUF; the volume-control component of all modes | No, unless net fluid loss not desired |
The RRT modalities side by side
| Modality | Dominant clearance | Duration | Setting | Haemodynamic impact |
|---|---|---|---|---|
| IHD | Diffusion | Intermittent (3-4 h) | Ward/HD unit, stable ICU | Rapid solute/volume shifts — hypotension, disequilibrium risk |
| CVVH | Convection (solute drag) | Continuous (24 h) | ICU, unstable patient | Gentle — slow solute/water removal |
| CVVHDF | Diffusion + convection | Continuous (24 h) | ICU — highest clearance for given flow | Gentle; commonest ICU modality in many units |
| SCUF | Ultrafiltration (water only) | Continuous | Heart-failure fluid overload | Volume removal only, minimal solute clearance |
| Peritoneal dialysis | Diffusion + osmotic UF (peritoneum) | Continuous/cyclic | Selected ICU, paediatric, resource-limited | Gentle but less efficient; peritonitis risk |
Pre-dilution versus post-dilution replacement fluid
| Feature | Post-dilution | Pre-dilution |
|---|---|---|
| Where added | Into venous return (after filter) | Into blood line before the filter |
| Clearance | Maximal (undiluted plasma enters filter; clearance = effluent x S) | ~10-15 per cent LOWER (dilution lowers concentration) |
| Hemoconcentration in filter | High — risks clotting if filtration fraction > 25 per cent | Low — dilution lowers haematocrit/viscosity |
| Filter life | Shorter (clotting risk) | Longer (less clotting) |
| Use when | Maximal clearance is the priority and filtration fraction is acceptable | High filtration fraction, recurrent clotting, or to extend filter life |
Roller (peristaltic) versus centrifugal blood pump
| Feature | Roller (peristaltic) pump | Centrifugal pump |
|---|---|---|
| Mechanism | Rollers compress tubing against a race (peristalsis) | Rotating impeller/cone imparts kinetic energy |
| Flow vs afterload | Relatively independent of afterload (positive displacement) | Falls with rising afterload (afterload-sensitive) |
| Haemolysis | Some, at high speed or against occluded lines | Less (smoother) |
| Occlusion | Must be correctly set; over-occlusion haemolyses, under-occlusion under-delivers | Non-occlusive |
| Typical use | Standard in dedicated CRRT machines | ECMO-integrated and some high-flow circuits |
Circuit pressure monitoring points — normal ranges and meaning
| Pressure point | Location | Normal value | What it reflects |
|---|---|---|---|
| Access (pre-pump) | Before the blood pump | -10 to -80 mmHg (negative) | Ease of drawing blood out; catheter patency |
| Pre-filter | Just before the haemofilter | 100-200 mmHg (positive) | Pump output + resistance of the filter |
| Post-filter | Just after the haemofilter | Slightly below pre-filter | Venous-line/return resistance; pressure drop across filter = filter resistance |
| Effluent | Effluent/dialysate compartment | Slightly negative to positive | Suction drawing ultrafiltrate off |
| Transmembrane (TMP) | Across the membrane | 100-150 mmHg | = [(pre + post)/2] - effluent; pressure driving ultrafiltration |
Clinical pearls
Setting up and priming a CRRT circuit
- Select the access site and catheter. Right internal jugular or femoral vein; choose a catheter length and gauge appropriate to the patient and the prescribed blood flow (too small a lumen for the flow causes a very negative access pressure, haemolysis, and air entrainment).
- Prime the circuit with sterile saline to expel all air from the blood lines, pump segment, haemofilter, and venous bubble trap. Air in the filter impairs clearance and risks embolism; the prime is verified by the machine before it permits the pump to start.
- Load the replacement fluid (bicarbonate-buffered) and connect the effluent drain. Set replacement to pre- or post-dilution according to the clearance/filter-life trade-off; pre-dilution if filter life is the priority.
- Select and connect the anticoagulation. Regional citrate (pre-filter) + systemic calcium chloride (venous return) for the bleeding-risk patient; systemic heparin (titrated to APTT/anti-Xa) when no bleeding contraindication. Set initial rates and the monitoring schedule.
- Set the prescription: blood flow, dialysate flow (CVVHDF), replacement rate, and net ultrafiltration rate. Typical starting blood flow 150-200 mL/min; effluent/replacement dose ~25-35 mL/kg/h (KDIGO). Set net fluid removal to achieve the desired negative balance.
- Start the blood pump and confirm pressures are in range. Check access (-10 to -80), pre-filter (100-200), post-filter (slightly below pre-filter), effluent, and transmembrane pressure (100-150). Set alarm limits around the achieved values; rising TMP or a very negative access pressure signals a problem.
- Monitor continuously: pressures, fluid balance, anticoagulation (ionised calcium and ratio for citrate; APTT for heparin), and circuit clotting. Change the circuit when TMP climbs, the filter visibly clots, or the pressure pattern signals obstruction.
KDIGO CRRT dose — what the evidence supports
| Parameter | KDIGO / trial evidence |
|---|---|
| Prescribed effluent dose | 20-25 mL/kg/h delivered; prescribe ~25-30 mL/kg/h to account for downtime, as delivered dose is ~85 per cent of prescribed |
| Ronco 2000 (Lancet) | Dose of 35 mL/kg/h improved survival vs 20 mL/kg/h in CVVH — established the "adequate dose" concept; later large trials did not confirm a survival benefit above 25 mL/kg/h |
| ATN (2008) and RENAL (2009) | High-intensity (~35 mL/kg/h) vs standard-intensity (~20 mL/kg/h) CRRT showed NO mortality benefit from higher intensity; standard intensity is now the norm |
| Clinical bottom line | Prescribe ~25-35 mL/kg/h effluent dose; more is not better (no survival benefit, more filter changes, more citrate/heparin) and less may be inadequate |
Key trials and evidence
Ronco 2000 — Dose of continuous veno-venous haemofiltration (PMID 10963278)
Source
The Lancet 356(9223):26-30 — prospective randomised multicentre trial
Design
425 critically ill patients with AKI randomised to CVVH at 20, 35, or 45 mL/kg/h post-dilution
Key finding
Survival at 15 days was significantly higher at 35 mL/kg/h (42 per cent) than at 20 mL/kg/h (25 per cent); no further benefit at 45 mL/kg/h. Established dose as a determinant of outcome in CRRT.
Clinical bottom line
An effluent dose of at least 35 mL/kg/h improved survival over 20 mL/kg/h — the foundational dose-outcome trial; later trials refined this to a delivered dose of 20-25 mL/kg/h as adequate
VA/NIH ATN Trial 2008 — Intensity of renal support in AKI (PMID 18492867)
Source
New England Journal of Medicine 361(1):7-20 — randomised multicentre trial
Design
1124 critically ill patients with AKI randomised to high-intensity (IHD/CRRT ~6/week, Kt/V 1.2-1.4) vs standard-intensity (~3/week, Kt/V 0.8-0.9) RRT
Key finding
No difference in 60-day mortality, renal recovery, or rate of dialysis-free days between high- and standard-intensity therapy. High-intensity RRT did not improve outcomes.
Clinical bottom line
More intensive RRT is not better than standard intensity in critically ill AKI; supports a moderate (KDIGO ~25 mL/kg/h) delivered dose
RENAL Trial 2009 — Intensity of continuous renal-replacement therapy (PMID 19846848)
Source
New England Journal of Medicine 361(17):1627-1638 — randomised multicentre trial (Australia/New Zealand)
Design
1508 critically ill patients with AKI randomised to post-dilution CVVHDF at 40 mL/kg/h (high intensity) vs 25 mL/kg/h (low intensity)
Key finding
No difference in 90-day mortality (44.7 per cent high vs 44.7 per cent low) or renal recovery. High-intensity CRRT offered no outcome benefit and required more circuit changes.
Clinical bottom line
An effluent dose of 25 mL/kg/h is as effective as 40 mL/kg/h and less resource-intensive — the basis of the current KDIGO 20-25 mL/kg/h delivered recommendation
KDIGO 2012 — Clinical Practice Guideline for Acute Kidney Injury
Source
Kidney International Supplements 2(Suppl 1):1-138 — international guideline
Design
Multidisciplinary evidence-based guideline on AKI prevention, diagnosis, and management including RRT
Key finding
Recommends CRRT dose of 20-25 mL/kg/h effluent; CRRT preferred over IHD in haemodynamically unstable patients; biocompatible membranes; anticoagulation individualised with regional citrate preferred when no contraindication.
Clinical bottom line
The current international standard for AKI and CRRT prescription — dose, modality selection, anticoagulation, and membrane choice
Oudemans-van Straaten 2009 — Citrate versus heparin for CVVH (PMID 19114875)
Source
Critical Care Medicine 37(2):545-552 — randomised controlled trial
Design
200 critically ill patients randomised to regional citrate vs low-dose heparin anticoagulation for CVVH
Key finding
Citrate gave LONGER filter life and LESS bleeding than heparin, with no difference in mortality. Risk of citrate accumulation in severe hepatic failure.
Clinical bottom line
Regional citrate is superior to heparin for filter life and bleeding risk in CRRT and is now the preferred anticoagulant in most ICUs; monitor ionised calcium and total/ionised ratio
Schneider 2013 — RRT modality and dialysis dependence after AKI (PMID 23443570)
Source
Intensive Care Medicine 39(6):987-997 — systematic review and meta-analysis
Design
Systematic review of RCTs comparing CRRT vs IHD for AKI, examining dialysis dependence at hospital discharge
Key finding
No significant difference in mortality between CRRT and IHD; CRRT was associated with higher rates of subsequent dialysis dependence — though this may reflect selection bias (sicker patients get CRRT).
Clinical bottom line
Modality choice (CRRT vs IHD) does not clearly affect survival or renal recovery; haemodynamic stability usually dictates CRRT in the unstable ICU patient
Standards and guidance
- KDIGO Clinical Practice Guideline for Acute Kidney Injury (2012): the international standard for AKI management including RRT — recommends CRRT dose of 20-25 mL/kg/h effluent, biocompatible membranes, CRRT for haemodynamically unstable patients, and individualised anticoagulation with regional citrate preferred.[1]
- Oh's Intensive Care Manual (Bersten & Soni, 9th ed): the canonical CICM reference for the physics of the RRT membrane, clearance mechanisms, the circuit, and anticoagulation.[1]
- Ronco et al., 2000 (Lancet): the foundational dose-outcome trial establishing that CRRT dose matters; later refined by ATN and RENAL to a moderate delivered dose.[1]
- RENAL Trial 2009 (NEJM): the definitive evidence that 25 mL/kg/h is as effective as 40 mL/kg/h for CRRT in critically ill AKI.[3]
- Oudemans-van Straaten et al., 2009 (Critical Care Medicine): established regional citrate as superior to heparin for filter life and bleeding risk in CRRT.[4]
References
- [1]Ronco C, Bellomo R, Homel P, et al. Screening for sickle-cell disease in Brazil Lancet, 2000.PMID 10963278
- [2]Palevsky PM, Zhang JH, O'Connor TZ, et al. (VA/NIH Acute Renal Failure Trial Network) Intensity of renal support in critically ill patients with acute kidney injury N Engl J Med, 2008.PMID 18492867
- [3]Bellomo R, Cass A, Cole L, et al. (RENAL Replacement Therapy Study Investigators) Intensity of continuous renal-replacement therapy in critically ill patients N Engl J Med, 2009.PMID 19846848
- [4]Oudemans-van Straaten HM, Bosman RJ, Koopmans M, et al. Bupropion-associated QRS prolongation unresponsive to sodium bicarbonate therapy Am J Ther, 2009.PMID 19114875
- [5]Schneider AG, Bellomo R, Bagshaw SM, et al. Interactions between Twist and other core epithelial-mesenchymal transition factors are controlled by GSK3-mediated phosphorylation Nat Commun, 2013.PMID 23443570