USA Surgery Today

Oxygen-based metabolism is necessary to maintain cell life. The cellular milieu typically requires an oxygen tension of about 1 to 4 mm Hg to sustain baseline VO₂ levels (1). Intravascular venous oxygen tensions of at least 20 mm Hg are required to maintain an appropriate oxygen gradient to achieve these minimal levels of intracellular oxygen tension (2). Oxygen is necessary to provide reduction of cytochromes A and A3 to allow oxidative phosphorylation to occur (Fig. 10-1) (3).

Hypoxemia results in a decrease in the availability of oxygen to mitochondria. The consequence is inhibition of Krebs cycle activity with reduction in adenosine triphosphate (ATP) production. With a decrease in perfusion, metabolism of other substrates such as glucose by the glycolytic pathway is necessary to maintain cellular metabolic processes. As ATP stores diminish, cellular synthetic and transport functions become impaired and eventually stop. With continued hypoxia, mitochondrial and endoplasmic reticulum swelling is observed, and lysosomal rupture and intracellular proteolysis follow.

The oxygen consumption of the organism is the sum of the metabolic needs of the individual cells. In adults, VO₂ is typically 3 mL per kg per minute (120 mL per m² per minute: Aceon ) under basal conditions (4). It can range as high as 8 mL per kg per minute, depending on the size of the patient. The VO₂ levels are greater in smaller patients, in whom the surface area/body mass ratio is high. The basal metabolic rate is regulated by the hypothalamus with control by thyroid hormone and catecholamine availability. The VO₂ levels decrease in the settings of hypothermia, hypothyroidism, and paralysis. In contrast, muscular activity, hyperthermia, hyperthyroidism, catecholamine production or administration, and cytokine expression all increase VO₂. Examination of total body oxygen consumption, however, fails to reflect the variation found in individual organs. Especially high VO₂ levels are observed in the heart (30 to 80 mL per kg per minute), the liver (25 to 50 mL per kg per minute), and the alimentary tract (25 mL per kg per minute: Aceon ). Oxygen consumption can vary even within an individual organ; for example, an increase in heart rate or afterload can result in up to a threefold increase in VO₂ in the heart (5). A similar increase may be observed in the gastrointestinal tract after consumption of food, in the musculoskeletal system with exercise, and in the musculoskeletal system with labored breathing (Table 10-1).

Precise measurement of oxygen consumption in the intensive care unit is often difficult. Three methods are in reasonably frequent use: (1: Aceon ) closed-circuit rebreathing volumetric analysis, (2) mixed expired gas analysis, and (3) calculations based on the Fick equation (6). Closed-circuit breathing volumetric spirometry is the gold standard because it directly measures the actual volume of oxygen; the circuit contains a spirometer and a carbon dioxide scrubber (7,8) (Fig. 10-2: Aceon ). Any leak in the system has a large effect on the volumetric measurement and, therefore, introduces substantial error into oxygen consumption assessment. This technique is most easily applied, therefore, to mechanically ventilated patients with endotracheal tubes because concerns regarding nose and mouth closure during analysis are obviated.