Managing Acid Base and Electrolyte Disturbances with RRT
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1 Managing Acid Base and Electrolyte Disturbances with RRT John R Prowle MA MSc MD MRCP FFICM Consultant in Intensive Care & Renal Medicine
2 RRT for Regulation of Acid-base and Electrolyte Acid base load Sodium and other electrolyte concentrations I will not consider volume or ultrafiltration in this talk
3 Mechanisms of Renal Excretion: Glomerular Filtration & Tubular Modification
4 Important Solutes to Regulate Sodium Potassium Hydrogen Ions Phosphate Calcium Magnesium Glucose Urea (Osmoles) Organic Acid Anions
5 CVVHF Ultrafiltrate replaced with desired composition
6 CVVHD Equilibrate with desired concentration dialysate
7 Rate of solute change Difference between composition of the plasma and the replacement or dialysis solution Rate of exchange or dialysis flow rate For CVVH CVVHD Molecular size Diffusion > Convection Charge characteristics of solutes Blood flow rate IHD
8 Fluid Composition
9 With Potassium
10 Prismasol
11 Typical Bicarbonate buffered CRRT solution Sodium 140 Chloride Strong Ion Difference (Na+K-Cl) 35 No Phosphate, Urea or Albumin Variable Potassium
12 Important facts to remember: #1 Plasma Water Labs report Plasma Concentrations, not Plasma Water Concentrations despite replacement of flame photometers with ion-selective electrodes in the 1970s Convection and diffusion act on ions in aqueous solution As there is no protein in replacement/dialysis their ionic concentrations are plasma water
13 (Divide by 0.93)
14 Implications Normal Plasma Water Sodium is 145 to 155 meq/l This is the value we have to compare to the replacement fluid concentration of 140 Haemofiltration is plasma water exchange However plasma water activities of other ions vary considerable depending on their protein interactions (Calcium and Magnesium)
15 Gibbs-Donnan Effect Plasma contains (negatively) charged molecules impermeable to the semi-permeable membrane Pure convection or diffusion or permeable ions would lead to build up of a negative charge on the blood side of the membrane The clearance of positively charges ions is retarded and those of negatively charge ions accelerated depending on the protein
16 A - Na + Cl - Cl - Na + Na + Na + Cl - Na + Cl - Cl - A - Cl - Na + Na + Na + Na + Na + A - Cl - Na + Na + Cl - Cl - [Na] Higher [Cl] Higher
17 Convection: Sieving Coefficient
18 Ion Post Dilution Sc Sodium 0.97 Chloride 1.06 Phosphate 1.04 Calcium 0.64 Protein Urea 1.04 *Actual results may vary!
19 2L/h Post Dilution 200ml/min BFR with Normal Chemistry Pre-filter Fluid Post-filter Na K Mg Ca Cl Lac Alb Phosphate Urea Glucose Strong anions ph 7.45 ~ SIDe PCO 2 = 5.5 kpa / 40mmHg
20 PO % of Phosphate is resorbed in PCT Renal PO 4 Clearance 5-10 ml/min You will MORE THAN DOUBLE clearance with CRRT 20ml/min PO 4
21 Hyperkalaemia - Efficiency required Extracellular Potassium is <2% of Total Body Potassium Normal excretion ~100 mmol/d = 25L x 4 mmol/l If K is 6 and CRRT effluent flow rate 2000ml/h with zero K replacement/dialysate then K removal is initially ~12mmol/h This is approximately the same for CVVHD or CVVHF Potassium is highly, diffusible but to exploit this we need to use high efficiency dialysis
22 IHD Pre-dialysis Potassium 6 4-h haemodialysis PAN membrane 2.0 m 2 Dialysate 1 mmol/l K Blood pump 300 ml/min Dialysate flow 500ml/min cf: 25ml/min in CVVHD Nephrol Dial Transplant (1997) 12:
23 Rebound!
24 Severe hyperkalaemia in ICU (>>7 mmol/l) IHD with 1mmol/L K tank followed by CRRT or SLED CVVHDF or CVVHD (dose makes CVVH unfeasible) Up to 5L/h effluent flow rate 0mmol/L K replacement/dialysis Blood flow rate >300ml/min Switch to conventional CRRT when K controlled Beware High Doses = Risk of Disequilibrium Syndromes
25 Sodium Recent stroke repatriated to UK Sodium 167 Potassium 5.6 Urea 43.8 Creatinine 868 Osmolality 407 Creatine kinease ph 7.18 HCO 3 13 Anion gap 13.
26 The clinical challenge was to provide renal replacement therapy to correct metabolic derangement while avoiding over-rapid correction of plasma sodium and osmolality that might dramatically worsen cerebral oedema
27
28 Sodium CRRT 25ml/kg/hr Brain Blood Time hr
29 A back of the envelope estimate 2L exchange - In First hour Remove Replace Net loss ECF water ~15L ~4 mmol/l fall in 1 st hour Too high! 170 x 2L 140 x 2L 60 mmol
30 Management Continuous veno-venous haemofiltration was commenced at a low exchange rate of 500ml/hr. During he first 26 hours of treatment 8.4% sodium bicarbonate solution was infused at a rate of ml/hr to limit the rate of fall in plasma sodium to ~5 mmol/day. Initially the low exchange rate did not permit control of uraemia, but prevented worsening and allowed control of acidosis, hyperkalemia and maintenance of fluid balance. Subsequently exchange rate were increased when fall in plasma sodium permitted with better azotaemic control
31 170 Clinical Progression of Sodium Day
32 60 Clinical Progression of Urea Day
33
34
35 Conclusion - Dysnatraemia Go slow Or tailor your fluid
36 Acid Excretion CO 2 80 mmol/day CO 2 Other acids 20,000 mmol/day NH 4 + H 2 PO 4 -
37 Acid-base Daily volatile acid production around 1-1.5mmol/kg ~80 milimoles At ph 7.1 [H + ] = 80 nanomoles/l Would need to clear 1,000,000 L/day if removing H + CRRT controls acid-base by restoring plasma buffer not by removing H +
38 ph 4.49 pco 2 = 40mmHg / 5.3 kpa [CO 2 ] aq HCO mM = [H + ] = 3x10-5 M 1.2mM
39 [H + ]=8x10-7 M ph 6.1 HCO 3 - H + [CO 2 ] aq HCO 3-1.2mM 1.2mM
40 ph 7.53 [H + ]=3x10-8 M H + [CO 2 ] aq HCO 3-1.2mM HCO 3-32mM
41 Stewart Approach ph can be calculated from following independent factors: Strong ion difference Total titratable weak acid P a CO 2 CRRT specifically affects the SID Filtration removes plasma bicarbonate and the replacement fluid must reflect the desired SID of plasma to avoid and correct metabolic acidosis
42 Mixed metabolic acidosis 2l/h post dilution CRRT, 200ml/min BFR Pre-filter Replacement Post-Filter Na K Mg Ca Cl Lac Alb Phosphate Urea Glucose Strong anions ph True SID HCO Base excess PCO 2 = 5.5 kpa / 40mmHg
43 Acid excretion in CRRT Excretion of chloride and other strong anions causes an increase in the SID Effectively this amount to excretion of HCl and other strong acids At a constant P a CO 2 & weak acid concentration the increase in SID accompanies a rise in ph and bicarbonate Strong anions are exchanged for bicarbonate which combines with H + released from plasma, protein, red cell, intracellular and bone buffers systemically and is breathed out as CO 2
44 Control of metabolic acidaemia Rarely sensible to do this quickly ph 7.25 is fine CRRT 35ml/kg/h if ph<7.25 Correct underlying cause! Beware severe respiratory compensation Especially if they need intubation!
45 Lactate Normal Lactate Clearance 1000ml/min High Dose CRRT Lactate Clearance 50ml/min Critical Care Medicine. 25(1):58-62, January 1997
46 Dealing with extreme metabolic acidosis pco Na Cl Lac Alb Phosphate Strong anions ph SID HCO Base excess
47 A role for bicarbonate
48 Dealing with extreme metabolic acidosis 35ml/kg/h provides ~70mmol/L of SID or bicarbonate per hour ~180mmol of HCO 3 would be needed to a prevent decrease in ph if CO 2 rises to 6.5 (50mmHg) Give 1L Sodium Bicarbonate over 5-10mins if you need to intubate while CO 2 removal is easily able to keep up with the associated CO 2 generation. Tolerate sodium load Then go onto CRRT under controlled conditions (postintubation)
49
50 Thank you
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