Critical level of rbc count before periodontal surgery
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Abstract
The terminology and fundamental aspects of the delivery, consumption, and deficits of oxygen are recalled. In chronic and acute, nonseptic states, red blood cell (RBC) transfusion is capable of increasing oxygen consumption (VO2). In acute septic states, the response of VO2 to RBC transfusion is variable and unpredictable, but attempts to increase oxygen delivery (DO2) should be made if the clinical picture raises the suspicion of a potentially lethal oxygen deficit. Therapeutic interventions raising the cardiac index to "supranormal" values in critically ill patients improve their chances of survival; and maintenance of hemoglobin or hematocrit values around 11 g/dl or 33%, respectively, is one part of such interventions. Opinions differ on the general tolerance of anemia, as witnessed by postulated "critical levels" of the hemoglobin concentration between approximately 11 and 4 to 5 g/dl or hematocrit values between 33% and 12% to 15%, respectively. The common denominator underlying these vastly different opinions is the variable behavior of several "non-Hb variables," which influence the venous oxygen tensions apart from the hemoglobin or hematocrit. Abnormalities of these non-Hb variables-typically encountered in the critically ill-increase the dependence of patients on hemoglobin or hematocrit levels that suffice to protect them against an oxygen deficit. For this reason, the "critical" hemoglobin or hematocrit is an individual value, and a generally valid "transfusion trigger" does not exist. Finally, the entity now known as silent myocardial ischemia (SMI) is a decisive factor for the tolerance of anemia. Solid clinical evidence is now available to support the concept that patients over age 40 should not, as an elective procedure, be subjected to levels < 10 g/dl or < 30%, respectively, without prior exclusion of SMI by appropriate investigations.
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The terminology and fundamental aspects of the delivery, consumption, and deficits of oxygen are recalled. In chronic and acute, nonseptic states, red blood cell (RBC) transfusion is capable of increasing oxygen consumption (VO2). In acute septic states, the response of VO2 to RBC transfusion is variable and unpredictable, but attempts to increase oxygen delivery (DO2) should be made if the clinical picture raises the suspicion of a potentially lethal oxygen deficit. Therapeutic interventions raising the cardiac index to "supranormal" values in critically ill patients improve their chances of survival; and maintenance of hemoglobin or hematocrit values around 11 g/dl or 33%, respectively, is one part of such interventions. Opinions differ on the general tolerance of anemia, as witnessed by postulated "critical levels" of the hemoglobin concentration between approximately 11 and 4 to 5 g/dl or hematocrit values between 33% and 12% to 15%, respectively. The common denominator underlying these vastly different opinions is the variable behavior of several "non-Hb variables," which influence the venous oxygen tensions apart from the hemoglobin or hematocrit. Abnormalities of these non-Hb variables-typically encountered in the critically ill-increase the dependence of patients on hemoglobin or hematocrit levels that suffice to protect them against an oxygen deficit. For this reason, the "critical" hemoglobin or hematocrit is an individual value, and a generally valid "transfusion trigger" does not exist. Finally, the entity now known as silent myocardial ischemia (SMI) is a decisive factor for the tolerance of anemia. Solid clinical evidence is now available to support the concept that patients over age 40 should not, as an elective procedure, be subjected to levels < 10 g/dl or < 30%, respectively, without prior exclusion of SMI by appropriate investigations.