Page 707 - Fluid, Electrolyte, and Acid-Base Disorders in Small Animal Practice
P. 707
694 SPECIAL THERAPY
sequestered in the intracellular compartment, and the
155 mmol/L
excessive potassium load must transfer from this compart-
150 mmol/L ment. Consequently, serum potassium concentration may
not be corrected adequately during short dialysis sessions
145 mmol/L if a standard dialysate is used in animals with severe
Dialysate sodium
hyperkalemia or during treatments using slow blood flow
BV% Change in blood volume rates. Similarly, the extracellular potassium load in animals
35
30 treated medically for severe hyperkalemia before dialysis
25 may become sequestered in cells and not accessible for
20 dialytic removal during short dialysis treatments.
15
10 Consistent evidence in human patients suggests large
5 dialysis potassium gradients or rapid changes in serum
0 potassium concentration during sessions employing a
5
10 dialysate potassium <1.0 mmol/L can alter the intracel-
Ultrafiltration: 500 mL
15 lular/extracellular potassium ratio and resting
20
cell membrane potential to increase the risk for
Figure 29-7 Relative percent changes in blood volume (DBV%) ventricular arrhythmias and sudden cardiovascular
assessed by an in-line blood volume monitor in response to stepped death. 88,103,132,134,135 Sudden intradialytic cardiovascu-
sodium profiling and simultaneous ultrafiltration during lar death is uncommon in animals perhaps due to the
hemodialysis in an uremic dog. The concentration and duration of acute versus chronic nature of the patient populations
each dialysate sodium step are indicated by the bars at the top of
the figure. The sodium profiling supports a positive blood volume andtherelativedifferencesincardiovascularcomorbidities
during the simultaneous ultrafiltration. between animals and humans. Nevertheless, these
identified risks should prompt reconsideration of current
recommendations. At a minimum, the appearance of
ventricular arrhythmias during the treatment warrants
400 20 mOsm/kg 160 changing to a dialysate containing 2 or 3 mmol/L of
Serum urea nitrogen (mg/dl) 250 Serum urea (~60 mg/dl urea) 155 Dialysate sodium (mmol/L) potassium should be prescribed with caution.
potassium. Until additional evidence becomes available,
350
the future use of dialysate solutions with 0 mmol/L of
300
89 mOsm/kg
200
Buffer Formulation
150
Hydrogen ions are at too low a concentration for the acid
100
50
acid load can be buffered by base equivalents supplied in
0 Dialysate sodium 150 burden to be disposed by dialysis alone. Alternatively, the
the dialysate. High-flux and high-efficiency dialysis
0 1 2 3 4 5
procedures require a bicarbonate-based dialysate that
Dialysis time (hours)
Figure 29-8 Hypothetical plot of the changes in serum urea has replaced virtually all use of acetate as a source of base
nitrogen and dialysate sodium concentration during a dialysis equivalents in both human and animal dialysis. Bicarbon-
treatment employing low-to-high sodium profiling from 150 to ate is formulated to a concentration higher than that of
160 mmol/L. The 20 mOsm/kg (NaCl) change in serum osmolality plasma to cause accrual of new buffer by the patient
resulting from the sodium modeling could help offset, in part, the and to replenish the deficits caused by production and
89 mOsm/kg change in serum osmolality resulting from the dialytic retention of metabolic acids. The amount of base
change in urea of 250 mg/dL during the treatment. The osmotic equivalents transferred depends on the dialysate buffer
buffer provided by dialysate sodium profiling is equivalent to the concentration, choice of dialyzer, the blood and dialysate
approximately 60 mg/dL change in blood urea nitrogen. flow rates, and the distribution of hydrogen ions during
the dialysis session. 58,75
from low to high promoted a 50% reduction in the prev- Many delivery systems can proportion dialysate bicar-
alence of hyperkalemia compared with dialysis with stan- bonate concentration from 20 to 40 mmol/L. Use of a
dard dialysate. 122 Severe hypertension can been seen in low dialysate bicarbonate concentration (25 mmol/L)
animals in association with prolonged use of high sodium has been suggested for animals with severe metabolic aci-
dialysate profiling, and the profile must be adjusted to dosis (serum bicarbonate <12 mmol/L) on the premise a
produce neutral sodium balance, or an isonatric dialysate higher bicarbonate concentration may correct the bicar-
should be used if these signs are recognized. bonate deficit too rapidly, increase cerebrospinal fluid
A standard dialysate potassium concentration of (CSF) PCO 2 , decrease CSF pH, and precipitate paradoxi-
3 mmol/L can be used for most animals with acute or cal cerebral acidosis, cerebral edema, and dialysis disequi-
chronic renal failure. Essentially all potassium is librium syndrome. 9,11,34 In practice, it is difficult to