DIRECT AND INDIRECT MONITORS OF RENAL FUNCTION
Means for direct, on-line evaluation of renal function are limited.
We can monitor indirectly, however, the several factors that may contribute to the
failure of compensatory
mechanisms supporting renal function perioperatively. Among obstructive causes that
may initiate ARF, an occluded or kinked urinary catheter can cause perioperative
oliguria and must be eliminated as a source of obstruction. Toxic causes precipitated
by antibiotics (e.g., aminoglycosides, amphotericin B) and radiocontrast agents also
may be responsible for the development of ARF. For example, with aminoglycosides,
nephrotoxicity is poorly correlated with kidney tissue or plasma levels of the drug
but is markedly augmented by concomitant volume depletion or liver cirrhosis.[15]
Similarly, ARF loosely correlates with the amount of radiocontrast material injected
unless the patient has preexisting diabetic nephropathy or low cardiac output syndrome.
The vigilance of the anesthesiologist is the first monitor required for preserving
renal function.
Unlike the nephrologist, who can evaluate a patient's renal function
under stable conditions over long periods, an anesthesiologist caring for hemodynamically
unstable patients in the operating room is unable to use standard tests of renal
function, such as creatinine clearance. To maintain the normal excretory functions
of the kidney (i.e., filtration, reabsorption, and secretion), adequate perfusion
is essential. The anesthesiologist often relies on indirect variables, such as urine
volume, to assess renal perfusion. Unfortunately, urine output may not reliably
reflect glomerular filtration and renal function under intraoperative conditions.
Although not practical, monitoring renal perfusion directly would be ideal. Instead,
we use monitors to ensure adequate intravascular volume (i.e., preload) and adequate
cardiac performance or systemic perfusion as an indirect means to maintain normal
renal function conditions. Serum chemistries and urinary indices may enable the
assessment of adequate distribution of cardiac output to the kidneys themselves.
Ultimately, however, only direct assessment of renal blood flow (and its regional
distribution) can tell us whether a kidney is adequately perfused. Evidence of local
renal tissue metabolism ensures that oxygen use is adequate. The combination of
blood flow (i.e., oxygen delivery) and oxygen use should reflect normal function
( Table 37-3
).
Intravascular Volume
Central Venous Pressure versus Pulmonary Capillary
Wedge Pressure
Monitoring techniques to ensure adequate intravascular volume
should be selected after consideration of the physiologic condition of the patient
in each situation
(see Chapter 32
). Epidemiologic
studies have shown that renal failure commonly develops when dehydration acts in
synergy with other chronic conditions. Diabetes mellitus and volume depletion together,
for example, increase the chance of developing ARF by 100-fold.[15]
Monitoring central venous pressure to assess adequate preload is contingent on normal
left and right ventricular function, normal pulmonary vascular resistance, and normal
mitral, pulmonary, and tricuspid valve function. Monitoring pulmonary artery pressure
or pulmonary capillary wedge pressure to assess preload assumes normal left ventricular
compliance, normal mitral valve function, and normal airway pressure.
Left Atrial Pressure
Directly measuring left atrial pressure may offer insights into
the kidney pressure-flow relationship because left atrial hypotension has been shown
to be a pwerful stimulus for renal vasoconstriction.[85]
Despite similar reductions in cardiac output and arterial blood pressure, renal
blood flow appears to decrease much less during experimental conditions of cardiogenic
shock, in which left atrial pressures are increased, compared with conditions of
hemorrhagic shock, in which left atrial pressures are decreased.[85]
It is postulated that when a decrease in cardiac output is accompanied by left atrial
hypotension, reduction in systemic arterial pressure is followed by the normal response
of renal vasoconstriction. The left atrial receptors are connected to the renal
circulation by atrial natriuretic peptide, a hormone secreted by the cardiac atria
in response to intravascular volume expansion.[86]
Atrial natriuretic hormone acts on the arterial and venous systems, the adrenals,
and the kidneys to reduce intravascular volume and decrease blood pressure.[34]
Within the kidney, the hormone increases hydraulic pressure in the glomerular capillaries
through afferent arteriolar dilation and efferent arteriolar vasoconstriction. Atrial
natriuretic peptide reduces blood pressure by relaxing smooth muscle and reducing
sympathetic vascular stimulation. It also inhibits renin and aldosterone secretion,
producing renal vasodilation, natriuresis, and diuresis.[34]
Left Ventricular End-Diastolic Area
Although the most direct way to clinically monitor for adequate
intravascular volume or preload may be during surgery by assessment of the left ventricular
end-diastolic area with echocardiography,[87]
[88]
the most practical method is by obtaining preoperative history and physical examination
and by maintaining changes in systemic blood pressure to changing conditions. An
awake patient may be observed for orthostatic changes in blood pressure, whereas
an anesthetized patient may be observed for paradoxical arterial pulse changes with
positive-pressure inspiration.[89]
The clinician
must decide which modality can most accurately reflect intravascular volume for a
patient in a particular situation.
