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

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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.