CPB & Renal Failure

• Renal failure of varying degrees occurs in 1.2 to 13% of post CPB patients
• Renal failure is twice as common in valvular surgery than CABG
• Renal failure correlates with:bypass time; infection; low cardiac output.; use of IABP; excessive blood loss; use of vasopressors before CPB; perioperative MI; emergency operation; excessive transfusion; chronic renal disease
• Factors contributing to perioperative renal dysfunction are: endocrine changes; diminished renal blood flow; alterations of cellular & humoral blood components; nephrotoxic drugs; preexisting renal disease
• Development of renal failure depends more on the preoperative and post operative haemodynamic state than on various manipulations used to maintain urine output during CPB
• Acute renal failure is a recognizable complication of CPB, occuring in 2.5 to 31% of cases. Acute renal failure is related to preoperative renal function as well as to the presence of coexisting disease. CPB may also affect renal function adversely due because of the unphysiological state of nonpulsatile blood flow may upset the normal autoregulatory mechanisms of renal blood flow

Mechanisms of Renal Failure & CPB

a) Hormones

• Associated with the precipitous fall in BP upon commencement of CPB [due to haemodilution & dilution of catecholamines], is the stimulation of the renin-angiotensin-aldosterone system
• The renin-angiotensin-aldosterone system causes an increase in renal vascular resistance
• Increased aldosterone levels persist longer after cardiac surgery then other surgery
• High levels of ADH observed during CPB may also contribute to renal vasoconstriction + drop in urine output
• Rises in plasma cortisol levels may also contribute to sodium retention and potassium depletion seen after CPB

b) Haemodilution

• Haemodilution is one of the most important factors in protecting renal function during CPB
• Hemodilution —> reduced blood viscosity —> increased renal blood flow —> increased electrolyte, creatinine & water clearances

c) Plasma Colloid Osmotic Pressure

• A reduced plasma oncotic pressure improves renal function during CPB — as the plasma oncotic pressure is a significant antagonist to glomerular filtration during hypotensive states

d) Hypothermia

• Hypothermia constricts renal arterioles —> reduced blood flow [most of the adverse effects of hypothermia are reversed by hemodilution]
• Tubular function is depressed by hypothermia alone

e) Haemolysis

• Haemolysis —> free haemoglobin —> limit to amount of free Hb resorbed from tubules —> haemoglobinuria —> may precipitate in tubule in acidic environment —> renal failure
• The acute tubular necrosis 2° haemoglobinuria may be due to: a) precipation of pigment in renal tubules with subsequent blockage of tubular flow; b) glomerular-tubular injuries caused by red cell stroma and other substances from lysed rbc

f) Microemboli

• High levels of renal blood flow secondary to haemodilution predispose the kidneys to microembolic damage

g) Renal blood flow

• global renal blood flow usually decreases during CPB 2° diminished flow rates and pressures or loss of pulsatility

h) Significance of urine output during CPB

• Urine output is a crude indicator of renal function. There is no correlation between the amount of urine outputduring CPB and the incidence of postoperative renal failure
• Urine output is greater when mean arterial pressures are higher, when pulsatile perfusion is used and when mannitol is added to CPB prime