Oxygen delivery and consumption during hypothermia and rewarming in the dog.

Department of Anesthesiology, University of Washington School of Medicine, Seattle 98195.
Anesthesiology (Impact Factor: 6.17). 04/1990; 72(3):510-6. DOI: 10.1097/00000542-199003000-00020
Source: PubMed

ABSTRACT Changes in oxygen consumption (VO2) and oxygen delivery (DO2) were compared in three groups of paralyzed, sedated dogs: 1) a group (n = 5) cooled to 29 degrees C and immediately rewarmed to 37 degrees C; 2) a group (n = 5) cooled to and maintained at 29 degrees C for 24 h, and then rewarmed; and 3) a group (n = 5) maintained at 37 degrees C for 24 h. During the cooling phase, in both the acute and prolonged hypothermia animals, VO2 and DO2 decreased significantly from control values (P less than 0.05). The decrease in DO2 occurred as a result of a similar decrease in cardiac index (CI; P less than 0.05) that was associated with a significant increase in systemic vascular resistance index (SVRI; P less than 0.05). Arteriovenous oxygen content difference (C(a-v)O2), O2 extraction ratio, mixed venous oxygen tension (PVO2), pH, and base deficit (BD) were not different from control values even during prolonged hypothermia. Normothermic control dogs also demonstrated a significant decrease in CI (P less than 0.05) at 24 h. Surface rewarming increased VO2 back to control values in the acute hypothermia group and to values above control (P less than 0.05) in the prolonged hypothermia group. DO2 remained below control in both groups, resulting in a significant increase in O2 extraction (P less than 0.05) and a decrease in PVO2 (P less than 0.05) in the prolonged hypothermia animals. Following rewarming administration of sodium nitroprusside returned DO2, CI, and SVRI to control values but did not increase VO2. All animals survived the study without need for inotropic support.(ABSTRACT TRUNCATED AT 250 WORDS)

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    Critical Care 06/2012; 16(2). · 5.04 Impact Factor
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    ABSTRACT: Hypoxic-ischemic encephalopathy (HIE) is an important cause of acute neurologic injury at birth, affecting approximately two to three cases per 1000 full-term live births. Despite advancements in many aspects of neonatal intensive care, the outcome for infants with HIE remains poor. Interventions to improve outcomes in this population have been disappointing. The treatment of infants who have HIE is generally supportive and includes fluid and electrolytes homeostasis, correction of hypotension, and treatment of seizures. It is now known that severe hypoxia-ischemia may not necessarily cause immediate cell death, but can precipitate a complex biochemical cascade leading to the delayed neuronal loss. The key phases of injury include a latent phase after reperfusion, with initial recovery of cerebral energy metabolism, followed by a secondary phase characterized by accumulation of cytotoxins, seizures, cytotoxic edema, and failure of cerebral oxidative metabolism starting 6 to 15 h post insult. Studies designed around this conceptual framework have shown that moderate cerebral hypothermia initiated as early as possible before the onset of secondary deterioration, and continued for a sufficient duration has been associated with long-lasting neuroprotection. Three large controlled trials have demonstrated that post resuscitation cooling is generally safe and reduces death or disability at 18 months of age after neonatal encephalopathy. Hypothermia is now widely recommended as a standard of care for infants with HIE. However, national guidelines concerning regional organization and supportive care are necessary. A developmental follow-up must be organized. Neonatologists involved in this procedure must be encouraged joining a national data collection and registry.
    Archives de Pédiatrie 09/2010; 17. · 0.41 Impact Factor