Correspondence  |   April 2004
Hemodynamic Compensation during Acute Normovolemic Hemodilution
Author Affiliations & Notes
  • George J. Crystal, Ph.D.
  • * Advocate Illinois Masonic Medical Center, Chicago, Illinois.
Article Information
Correspondence   |   April 2004
Hemodynamic Compensation during Acute Normovolemic Hemodilution
Anesthesiology 4 2004, Vol.100, 1034. doi:
Anesthesiology 4 2004, Vol.100, 1034. doi:
To the Editor:—
Acute normovolemic hemodilution (ANH) causes a reduction in arterial oxygen content because of reduced hemoglobin concentration. The primary compensatory mechanism during ANH is an increase in cardiac output to maintain systemic oxygen delivery. 1,2 Therefore, the lower limit of an acceptable hemoglobin concentration is related to how low hemoglobin can be reduced without jeopardizing the ability of the heart to sustain an augmented pumping requirement. Previous studies have shown that the tolerance to ANH was diminished when the heart had a perfusion deficit, e.g.  , critical coronary stenosis, or when it was pharmacologically depressed with either disopyramide or isoflurane. 3–5 Not surprisingly, Van der Linden et al.  6 demonstrated similar findings during pharmacologic depression by the anesthetics halothane and ketamine. The authors found that the critical hemoglobin concentration at low anesthetic doses was approximately 3 g/dl (a value consistent with that found by us in dogs anesthetized with “low doses” of either isoflurane or fentanyl–midazolam 2,3), whereas this value was increased to approximately 5 g/dl at high anesthetic doses. They explained their findings on a complete blunting of the compensatory increases in cardiac output during ANH and attribute this effect to an enhanced cardiodepressive action of the anesthetics at the high doses.
Although the current hemodynamic findings and previous pharmacologic studies 7,8 are consistent with a more pronounced negative inotropic effect at the higher anesthetic doses, it is unlikely that this effect alone was responsible for the impaired cardiac output responses during ANH in the study of Van der Linden et al.  In the case of halothane, the impact of a reduced arterial blood pressure, i.e.  , coronary perfusion pressure, must also be considered; arterial blood pressure averaged only 43 ± 7 mmHg at the critical point during ANH (hemoglobin 4.5 ± 1.6 g/dl). Previous studies have suggested that this combination of arterial pressure and hemoglobin concentration results in a maldistribution of myocardial blood flow, i.e.  , subendocardial hypoperfusion, leading to myocardial lactate production, ischemic changes in the electrocardiogram, and ultimately impairment in global cardiac function. 2,3,9 A vulnerability of the subendocardium to hypoperfusion, secondary to reduced perfusion pressure, has been recognized for many years. 10 This tendency is enhanced during ANH because vasodilation (as evidenced by blunted reactive hyperemic responses 2,3) reduces the autoregulatory capability of the coronary circulation.
The ketamine group in the study of Van der Linden et al.  did not show a dose-related hypotensive effect during ANH; therefore, a lower arterial pressure can be ruled out as contributing to the reduced tolerance to ANH under the higher dose of ketamine. However, this condition was accompanied by a paradoxical and unexplained reduction in heart rate, which limited the cardiac output responses. This mechanism was not acknowledged by the authors.
As a method of blood conservation, ANH has unique advantages relating to cost, simplicity, and practicality. 11 Although it is safe if performed properly by an experienced team, it is contraindicated in the presence of any coexisting disease that may jeopardize vital organ oxygen delivery. As underscored by the findings of Van der Linden et al  ., ANH should not be performed if the anticipated hemodynamic compensatory mechanisms are neither possible nor desirable.
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