CRRT Flashcards
SCUF: Slow Continuous Hemofiltration
Hemofiltration convection
Primary therapeutic goal: safe removal of fluids (Solute control not a primary goal)
No dialysate or replacement fluids
Blood enters the extracorporeal circuit through the access line, passes through the hemofilter, and returns to the patient via the return line. As blood passes through the filter, ultrafiltration takes place and effluent collects in the effluent bag. Pumps control blood flow and fluid removal rates
UF rate up to 2 L/hr
Blood flow rate 10-180 mL/min
CVVH: Continuous V-V hemofiltration
Hemofiltration convection
Maximizes CONVECTIVE removal of small and middle molecules
Replacement solution required to aid convection. The replacement fluid enters the blood flow path as it circulates through the hemofilter. This has a dilutional effect on the blood and facilitates the removal of large volumes of ultrafiltrate without dehydrating the patient or causing other hemodynamic shifts.
No dialysate
UF Rate >500 mL/hr
CVVHD Continuous VV Hemodialysis
Hemodialysis diffusion
Addition of dialysate on fluid side of the filter to increase solute exchange by diffusion
Primary therapeutic goal: solute removal by diffusion, safe fluid volume management
* Requires dialysate solution
* No replacement solution
UF rate ~300 mL/hr
Dialysate rate 1-3 L/hr
Blood flow rate 10-180 mL/min
CVVHDF: Continuous VV Hemodialafiltration
HEMODIAFILTRATION CONVECTION AND DIFFUSION
Combines CVVH and CVVHD therapies to:
Give high volumes of fluid to maintain diffusive solute removal and convective solute removal
Solute and fluid removal
UF rate ranges 12-20L/24hr
Blood Flow rate = 10-180ml/min
Dialysate Flow rate = 15-45 ml/min
Risk of injury (RIFLE)
Cr increased x1.5
GFR decrease > 25%
UO < 0.5 mL/kg/hr for 6 hours
Injury (RIFLE)
Cr increased x2.0
GFR decrease >50%
UO <0.5 mL/kg/hr x 12 hours
Failure (RIFLE)
Cr increased x3.0
GFR decrease >75%
UO <0.3 mL/kg/hr x24 hours
OR
anuria 12 hr
Loss (RIFLE)
Persistent acute renal failure x4 weeks
Need to consider renal replacement therapies
ESRD (RIFLE)
ESRD >3 months
Prerenal AKI
decreased effective circulating arterial volume –> kidney perceives less fluid
Filtration lost but not perfusion. GFR goes down, but kidney is not “injured”
Causes: volume loss (bleeding, GI loss, diuretics), extravasation, venous pooling (CHF, cirrhosis, pulmonary edema)
Dx: Evidence of volume loss or altered volume distribution
BPs, daily weights, I/Os, cardiac function
BUN: Cr ratio (>10:1)
Urine: Normal UA because kidney’s ability to concentrate unchanged, very concentrated urine, high SpGr, retention of urine so expect low urine Na and fractional excretion of Na
Tx: Give volume if depleted, stop diuretics/ACEIs/ARBs, correct hypotension, avoid nephrotoxins
ATN
Loss of perfusion and filtration (function)
Early on, normal hemodynamics but accelerated apoptosis of tubular cells –> tubular cells “drop out” and move downstream so normal filtration at first but back leak with reabsorption of Cr/Urea via peritubular system.
As solute moves distally, tubular osmolarity is higher than normal. Signals macula densae to secrete neurohumoral signal to glomerulus to decrease filtration.
Causes: severe/prolonged volume loss, shock, toxins (aminoglycosides, IV contrast, rhabdomyolysis)
Dx: high urine Na, high FeNa (>1%), muddy brown granular casts and renal tubular epithelial cells
*Does not immediately reverse w/ fluid admin
Renal failure phase—usually lasts 7-21 days
Recovery (diuretic) phase –watch for high UO and electrolyte disorders
80-90% recover
Acute glomerulonephritis
Autoimmune reaction in the kidney (idiopathic, secondary, infectious)
Causes: lupus, vasculitis
HDs ok. Infiltration of immunoglobulins and decreased glomerular basement membrane permeability (so diminished glomerular filtration).
Classifications:
Focal glomerulonephritis - Active urine sediment without renal insufficiency or nephrotic syndrome
Diffuse glomerulonephritis - Active urine sediment with renal insufficiency and variable proteinuria, which can include nephrotic syndrome
Nephrotic syndrome - Heavy proteinuria, bland sediment although some hematuria allowed
Dx: RBC casts on UA, proteinuria, HTN, renal biopsy
May require RRT
Obstructive uropathy
Filtration fine, but downstream blockage –> microscopic obstruction
Causes: kinked foley, BPH, stones, anticholinergics, strictures, infections, carcinoma
Dx: bland UA, confirm w/ renal US
Broad waxy casts (signals chronic injury)
Vasomotor neuropathy
Abnormalities in afferent/efferent pressures = decrease in filtration
Ex: Patient on RAAS blocker for HTN has a loss of EF d/t cardiac injury and subsequent loss of CO. This loss of CO perceived by kidneys as decreased effective circulating volume –> attempts Efferent vasoconstriction BUT this is inhibited by RAAS blocker –> GFR declines
