Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Long-term tracheostomy-ventilated patients have better speech with a cuffless tracheostomy tube and a large tidal volume. Moderate day time hyperventilation from a pressure-limited ventilator is necessary in these patients to avoid hypoxia during sleep due to the variable insufflation leak. This study sought to confirm whether a dead space of 3 ml.kg-1 could help to provide normocapnic hyperventilation during waking time without causing hypercapnia and hypoxaemia during sleep. Transcutaneous blood gas studies were performed on 11 patients with high tetraplegia undergoing pressure-limited pulmonary ventilation with room air. Recordings were made for 120 min each when awake and asleep, with and without dead space. The mean derived arterial PCO2 without the dead space was 2.95 kPa awake and 3.21 kPa asleep, whilst the corresponding tensions with dead space were 3.39 kPa and 3.79 kPa. These small increases associated with the dead space, both awake and asleep, were statistically significant. There was a statistically, though not clinically significant decrease in oxygen tension when the patients without dead space went to sleep. The fact that the carbon dioxide tension was higher during sleep when dead space was in situ indicates that, despite the insufflation leak in these patients, there is significant rebreathing back through the dead space. Amelioration of hypocapnia during waking and sleeping is achievable using a dead space extension in these patients.
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PMID:Does dead space ventilation always alleviate hypocapnia? Long-term ventilation with plain tracheostomy tubes. 764 97

Humans with spinal cord injury have impaired cardiovascular function proportional to the level and completeness of the lesion. The effect on cerebrovascular function is unclear, especially for high-level lesions. The purpose of this study was to evaluate the integrity of dynamic cerebral autoregulation (CA) and the cerebrovascular reactivity in chronic tetraplegia (Tetra). After baseline, steady-state hypercapnia (5% CO(2)) and hypocapnia (controlled hyperventilation) were used to assess cerebrovascular reactivity in 6 men with Tetra (C5-C7 lesion) and 14 men without [able-bodied (AB)]. Middle cerebral artery blood flow velocity (MCAv), cerebral oxygenation, arterial blood pressure (BP), heart rate (HR), cardiac output (Q; model flow), partial pressure of end-tidal CO(2) (Pet(CO(2))), and plasma catecholamines were measured. Dynamic CA was assessed by transfer function analysis of spontaneous fluctuations in BP and MCAv. MCAv pulsatility index (MCAv PI) was calculated as (MCAv(systolic) - MCAv(diastolic))/MCAv(mean) and standardized by dividing by mean arterial pressure (MAP). Resting BP, total peripheral resistance, and catecholamines were lower in Tetra (P < 0.05), and standardized MCAv PI was approximately 36% higher in Tetra (P = 0.003). Resting MCAv, cerebral oxygenation, HR, and Pet(CO(2)) were similar between groups (P > 0.05). Although phase and transfer function gain relationships in dynamic CA were maintained with Tetra (P > 0.05), coherence in the very low-frequency range (0.02-0.07 Hz) was approximately 21% lower in Tetra (P = 0.006). Full (hypo- and hypercapnic) cerebrovascular reactivity to CO(2) was unchanged with Tetra (P > 0.05). During hypercapnia, standardized MCAv PI reactivity was enhanced by approximately 78% in Tetra (P = 0.016). Despite impaired cardiovascular function, chronic Tetra involves subtle changes in dynamic CA and cerebrovascular reactivity to CO(2). Changes are evident in coherence at baseline and MCAv PI during baseline and hypercapnic states in chronic Tetra, which may be indicative of cerebrovascular adaptation.
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PMID:Cerebrovascular reactivity and dynamic autoregulation in tetraplegia. 2008 10