ABSTRACT
The effect of hypocapnia on regional cerebral glucose utilization (L-CMRg) was studied in 14 Sprague Dawley rats. After cannulation of femoral vessels, halothane was discontinued and anesthesia was maintained with 70% N2O in oxygen. The animals' lungs were mechanically ventilated to achieve normocapnia (PaCO2 = 40 +/- 2 mmHg) in group A or hypocapnia (PaCO2 = 25 +/- 2 mmHg) in group B. L-CMRg was measured by the 14C-2-deoxyglucose autoradiographic method. Twenty-six anatomically discrete structures representing cortical, subcortical, limbic, and brainstem areas were studied. In hypocapnic animals, mean values for L-CMRg were higher in 25 out of 26 structures studied. The increase in L-CMRg was heterogenous. The structures that had higher L-CMRg during normocapnia showed the greatest increase in L-CMRg. When the two groups were compared using a profile analysis, in six regions (lateral and ventral thalamus, inferior colliculus, lateral habenulla, medial geniculate body, and auditory cortex), a value of P less than 0.05 was obtained.
Subject(s)
Brain/metabolism , Carbon Dioxide/deficiency , Glucose/metabolism , Animals , Blood Glucose/analysis , Carbon Dioxide/blood , Carbon Radioisotopes , Deoxyglucose/blood , Halothane , Male , Nitrous Oxide , Oxygen , Rats , Rats, Inbred Strains , Respiration, ArtificialSubject(s)
Neurocirculatory Asthenia/complications , Respiratory Distress Syndrome/diagnosis , Carbon Dioxide/deficiency , Diagnosis, Differential , Dyspnea/diagnosis , Dyspnea/etiology , Humans , Hypercapnia/diagnosis , Hypercapnia/etiology , Neurocirculatory Asthenia/diagnosis , Respiratory Distress Syndrome/etiologyABSTRACT
We report significant neurological abnormality at 18 months of age in 3 of 7 very low birth weight infants (less than or equal to 1,500 g), who during mechanical ventilation inadevertently became severely hypocarbic (arterial carbondioxide tension less than 2.0 kPa (15 mmHg)) at some time during the first 24 h of life. Although the number is small the outcome was significantly worse than the outcome in two fairly similar groups of infants selected as controls (p = 0.026). The infants in one of the control groups were also mechanically ventilated but remained normocapnic. Germinal layer haemorrhage (GLH) was more frequent among these infants compared with the severely hypocarbic infants (p = 0.022). The infants in the other control group was not mechanically ventilated. In all the severely hypocarbic infants the Bayley mental developmental index uncorrected for prematurity was at or below the median for the total sample (p = 0.01). The results suggest that neonatal cerebral ischaemia, for instance due to hypocarbia, is of greater prognostic significance than GLH.
Subject(s)
Carbon Dioxide/deficiency , Developmental Disabilities/etiology , Infant, Premature, Diseases/complications , Blood Gas Monitoring, Transcutaneous , Cerebral Hemorrhage/etiology , Child, Preschool , Humans , Infant , Infant, Newborn , Prospective Studies , Respiration, Artificial/adverse effectsABSTRACT
Cerebral vascular responses to hypocapnia during hypotension to a mean arterial blood pressure (MAP) = 50 mm Hg induced with sodium nitroprusside (SNP, n = 12) or trimethaphan (TMP, n = 12) were examined in dogs. Cerebral vascular resistance (CVR) and cerebral blood flow (CBF) at PaCO2 = 40 mm Hg, and PaCO2 = 20 mm Hg were examined first at normal MAP then at hypotension in six dogs in the SNP group and six dogs in the TMP group. In both the SNP group and the TMP group, CO2 responsiveness, as indicated by increased CVR and decreased CBF, was intact at normal MAP, but absent during hypotension. In the remaining 6 of 12 dogs in the SNP group and 6 of 12 dogs in the TMP group, CO2 responsiveness at MAP = 50 mm Hg was examined without prior determination of CO2 responsiveness at normal MAP. These additional studies were performed to rule out the possibility that absent CO2 responsiveness during hypotension in the initial groups resulted from (1) physiologic deterioration of the preparation with time, or (2) adaptation of brain extracellular fluid pH to a preceding period of hypocapnia. Again, during both SNP- or TMP-induced hypotension CO2 responsiveness was absent.
Subject(s)
Carbon Dioxide/deficiency , Cerebrovascular Circulation , Hypotension/physiopathology , Animals , Bicarbonates/blood , Carbon Dioxide/physiology , Cerebrovascular Circulation/drug effects , Dogs , Hydrogen-Ion Concentration , Hypotension/chemically induced , Nitroprusside/pharmacology , Trimethaphan/pharmacology , Vascular ResistanceABSTRACT
When elevated intracranial pressure (ICP) complicates the course of various forms of cerebral edema, the likelihood of survival with full recovery is greatly diminished. Controlled mechanical hyperventilation effectively lowers ICP in some patients by causing cerebral vasoconstriction. Improved survival occurs in patients with elevated ICP from head trauma and intracranial infection treated with hyperventilation; however, no benefit has been demonstrated in patients with increased ICP from strokes or hypoxic brain damage. Proper management of the hyperventilation requires knowledge of basic cerebral circulatory physiology. Arterial Paco2 tensions should be maintained between 25 and 30 mm Hg. Vasoconstrictive effects of hyperventilation diminish after 48 to 72 hours when renal mechanisms compensate for the respiratory alkalosis. When hyperventilation is discontinued, the Paco2 must be gradually returned to normal values, since sudden changes may cause a marked rise in ICP.
