Cardiopulmonary Function
The next logical step in the algorithm of renal function monitoring
is the assessment of adequate cardiac function through determination of systemic
perfusion, pulse
oximetry, acid-base assessment, cardiac output monitoring, or left ventricular fractional
area of change as a surrogate for ejection fraction[90]
(see Chapter 18
and Chapter
32
).
Systemic Perfusion and Acid-Base Balance
Severe arterial hypoxemia to a partial pressure of arterial oxygen
(PaO2
) value of less than 40 mm Hg is
associated with decreased renal blood flow and renal vasoconstriction.[91]
[92]
There is no consensus on the mechanism that
underlies the antidiuresis response to hypoxia. It appears that systemic hypoxia
can produce antidiuresis and antinatriuresis independent of renal nerve innervation.
[93]
Capnometry may be a useful monitor because
hypercarbia has been associated with decreased renal blood flow in patients requiring
mechanical ventilation.[94]
Cardiac Output
The electrocardiogram is essential to detect the depolarization-repolarization
changes consistent with the electrolyte abnormalities of renal dysfunction and to
monitor for normal rate and rhythm. The synchronized atrial kick preceding ventricular
contraction may contribute significantly to cardiac output in the patient with a
noncompliant left ventricle. The clinician can assess cardiac function by using
the thermodilution technique for measuring cardiac output with the pulmonary artery
catheter and can assess global and regional myocardial function with echocardiography.
Perfusion Pressure
Stone and Stahl[95]
studied the
effect of renal hemorrhage in otherwise healthy patients and concluded that a decrease
in mean perfusion pressure from 80 to 60 mm Hg reduced renal blood flow about 30%
without an autoregulatory response of the renal vasculature. It has been suggested
that renal blood flow decreases precipitously when mean blood pressure drops below
80 mm Hg. In a study by Yao and associates,[96]
mean arterial pressure during cardiopulmonary bypass was maintained with vasoactive
drugs at 80 to 100 mm Hg in one group of patients and at 50 to 60 mm Hg in another
group during moderate hypothermic conditions. It was found that renal circulation
was maintained as long as mean arterial pressure was maintained above 50 mm Hg.
Other studies challenge evidence that demonstrates decreased perfusion pressure as
a cause of renal failure.[97]
[98]
[99]
We evaluated the relationship between preoperative isolated systolic
hypertension[10]
and wide pulse pressure hypertension
[11]
(both markers of abnormal central aortic compliance)
and postoperative renal failure. In these two separate, large, multicenter epidemiologic
studies, it was determined that preexisting central aortic disease manifesting as
systolic wide pulse pressure hypertension is associated with significant increase
risk of postoperative renal dysfunction outcomes. In the first case, preexisting
systolic hypertension predicted a 40% greater risk of renal dysfunction outcome,
and in the latter case, wide pulse pressure predicted postoperative renal dysfunction
as well (odds ratio = 2:37, 1.69–3.33, P <
.005). Mean arterial pressure less than 40 mm Hg during cardiopulmonary bypass in
patients with preoperative isolated systolic hypertension (> 160 mm Hg) predisposed
them to renal insufficiency or failure postoperatively. These observations underscore
the importance of renal physiology during surgery and perhaps pressure management
during cardiopulmonary bypass. The systolic component of blood pressure is determined
by stroke volume and the rate of ventricular ejection, whereas the pulsatile component
of blood pressure is governed by the relationships among stroke volume, ventricular
ejection, viscoelastic properties of large arteries, and peripheral vascular resistance.
The latter factors contribute to the effect of arterial wave reflection from the
periphery back to the central conduit arteries. Pulse pressure is an index of the
effects of large artery stiffness and the rate of pressure on propagation and reflection
within the arterial tree. Early return of reflected arterial waves during late systolic
rather than early diastolic (from increased propagation velocity in stiff vessels)
increases systolic blood pressure (i.e., afterload) and decreases diastolic blood
pressure (i.e., perfusion pressure). It is likely that perfusion pressure and risk
of perioperative renal dysfunction are linked by the preexisting capacity of the
vasculature to compensate for low pressure as it determines flow. Future studies
need to stratify the risk of pressure management according to specific diseases (i.e.,
systolic hypertension and wide pulse pressure hypertension groups). We might not
have assigned risk and renal dysfunction to perfusion pressure appropriately. Those
with a predisposition to low flow due to abnormal central aortic compliance may represent
patients who require higher pressure to maintain adequate flow compared with normotensive
patients.
The decision to use any monitor should depend on the patient's
functional cardiac reserve status, the extent of the proposed surgical insult, and
the capabilities of the anesthesiologist, the perioperative team, and the hospital.
Differentiation between hypovolemic hypotension and cardiogenic hypotension, for
example, is critical to properly tailor management and prevent exacerbation of renal
ischemia. The best way to prevent intraoperative renal ischemia is to maintain renal
blood flow. Although maintaining adequate cardiac output is necessary for maintaining
adequate renal blood flow, it may not guarantee adequate flow. Monitoring with invasive
devices, such as pulmonary artery catheters, arterial cannulas, and transesophageal
echocardiography, has never been demonstrated to reduce the incidence of ARF.