Cardiopulmonary Bypass
CPB (see Chapter
50
) induces hypotension with nonpulsatile flow, which promotes renal vasoconstriction
and decreased RBF. Norepinephrine levels increase progressively during bypass, and
the renin-angiotensin system is activated. Acute renal failure has been associated
with persistent elevation of plasma renin levels.[114]
Thromboxane, released from activated platelets, and vascular elaboration of endothelin
could add to renal vasoconstriction during extracorporeal circulation. Tubular enzymuria
and microalbuminuria, an index of subclinical injury to the nephron, are consistently
observed during CPB.[119]
Despite these observations,
acute renal failure occurs in less than 2% of all patients. Nonetheless, when it
does occur after cardiac surgery, acute renal failure is associated with a forbidding
mortality rate—60% to 90%.
Renal Protection during Cardiopulmonary Bypass
As yet, no evidence has been presented that pulsatile perfusion
during CPB offers an advantage with respect to RBF, catecholamine release, or renal
outcome. Although plasma renin activity is suppressed by pulsatile perfusion, microalbuminuria
persists.[120]
Badner and colleagues[121]
found no difference in postoperative renal function in a group of patients with normal
kidneys undergoing pulsatile or nonpulsatile CPB. Case series claiming that pulsatile
CPB confers protection to patients with chronic renal insufficiency who are undergoing
cardiac surgery do exist, but unfortunately they are neither randomized nor prospective.
[122]
It has been observed in animal studies of CPB that RBF is dependent
on renal perfusion pressure and that infusion of dopamine does not increase RBF during
low-pressure states.[9]
This observation suggests
that autoregulation may be impaired during CPB. However, Hilberman and associates
[123]
found no relationship between low flow
(<50 mL/kg/min) or low mean arterial pressure (<50 mm Hg) and postoperative
acute renal failure. Instead, the severity of postoperative renal dysfunction and
its outcome correlated with the severity of cardiac dysfunction after CPB.[124]
Other important risk factors for postoperative renal dysfunction
after cardiac surgery include the complexity of the surgery (e.g., combined procedures
versus simple revascularization) and preoperative renal function. In a prospective
review of more than 4000 cases at the Cleveland Clinic, Higgins and coworkers[125]
observed that the risk of renal morbidity and mortality increases exponentially when
the preoperative serum creatinine level is greater than 1.9 mg/dL.
There is little evidence that the "prophylactic" administration
of low-dose dopamine has a protective role during CPB in patients with normal[126]
or impaired renal function[127]
who are undergoing
cardiac surgery. Moreover, dopamine may induce tachycardia even in the low-dose
range and is associated with a higher incidence of postoperative supraventricular
and ventricular arrhythmias.[128]
