Abstract
BackgroundLow hemoglobin concentration (Hb) and low mean arterial blood pressure (MAP) impact outcomes in critically ill patients. We utilized an experimental model of “normotensive” vs. “hypotensive” acute hemodilutional anemia to test whether optimal tissue perfusion is dependent on both Hb and MAP during acute blood loss and fluid resuscitation, and to assess the value of direct measurements of the partial pressure of oxygen in tissue (PtO2).MethodsTwenty-nine anesthetized rats underwent 40% isovolemic hemodilution (1:1) (or sham-hemodilution control, n = 4) with either hydroxyethyl starch (HES) (n = 14, normotensive anemia) or saline (n = 11, hypotensive anemia) to reach a target Hb value near 70 g/L. The partial pressure of oxygen in the brain and skeletal muscle tissue (PtO2) were measured by phosphorescence quenching of oxygen using G4 Oxyphor. Mean arterial pressure (MAP), heart rate, temperature, arterial and venous co-oximetry, blood gases, and lactate were assessed at baseline and for 60 min after hemodilution. Cardiac output (CO) was measured at baseline and immediately after hemodilution. Data were analyzed by repeated measures two-way ANOVA.ResultsFollowing “normotensive” hemodilution with HES, Hb was reduced to 66 ± 6 g/L, CO increased (p < 0.05), and MAP was maintained. These conditions resulted in a reduction in brain PtO2 (22.1 ± 5.6 mmHg to 17.5 ± 4.4 mmHg, p < 0.05), unchanged muscle PO2, and an increase in venous oxygen extraction. Following “hypotensive” hemodilution with saline, Hb was reduced to 79 ± 5 g/L and both CO and MAP were decreased (P < 0.05). These conditions resulted in a more severe reduction in brain PtO2 (23.2 ± 8.2 to 10.7 ± 3.6 mmHg (p < 0.05), a reduction in muscle PtO2 (44.5 ± 11.0 to 19.9 ± 12.4 mmHg, p < 0.05), a further increase in venous oxygen extraction, and a threefold increase in systemic lactate levels (p < 0.05).ConclusionsAcute normotensive anemia (HES hemodilution) was associated with a subtle decrease in brain tissue PtO2 without clear evidence of global tissue hypoperfusion. By contrast, acute hypotensive anemia (saline hemodilution) resulted in a profound decrease in both brain and muscle tissue PtO2 and evidence of inadequate global perfusion (lactic acidosis). These data emphasize the importance of maintaining CO and MAP to ensure adequacy of vital organ oxygen delivery during acute anemia. Improved methods of assessing PtO2 may provide an earlier warning signal of vital organ hypoperfusion.
Highlights
Low hemoglobin concentration (Hb) and low mean arterial blood pressure (MAP) impact outcomes in critically ill patients
Acute hypotensive anemia resulted in a profound decrease in both brain and muscle tissue PtO2 and evidence of inadequate global perfusion. These data emphasize the importance of maintaining Cardiac output (CO) and MAP to ensure adequacy of vital organ oxygen delivery during acute anemia
We demonstrated a significant interaction between low Hb concentration and low MAP with respect to limiting tissue oxygen delivery in brain and muscle, in a model of normotensive vs. hypotensive hemodilution
Summary
Low hemoglobin concentration (Hb) and low mean arterial blood pressure (MAP) impact outcomes in critically ill patients. The optimal care of critically ill patients often involves management of multiple risk factors for inadequate organ perfusion, including hypotension and anemia. Interoperative hypotension has been associated with increased brain [1, 2], heart [3,4,5], and kidney injury [3, 6, 7] and mortality [8,9,10] These outcomes often depend on the magnitude and duration of hypotension; for example, a 40% drop in mean arterial pressure (MAP) from baseline for more than 30 min has been associated with myocardial injury [5]. Perioperative and acute interoperative anemia have been associated with similar patterns of adverse events; including evidence of brain [11, 12], heart [13, 14], and kidney injury [15, 16] and mortality [14, 16,17,18]. Experimental models of acute anemia suggest that inadequate microcirculatory perfusion and tissue hypoxia contribute as a mechanism of vital organ injury and mortality [19,20,21]
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