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Purpose: Current Brain Trauma Foundation guidelines recommend avoiding hypoxemia after severe pediatric traumatic brain injury (TBI). Yet, recent studies on optimum admission oxygenation and ventilation parameters associated with discharge survival in pediatric TBI are lacking., Materials and Methods: After IRB approval, a retrospective study involving pediatric patients ages ≤14 years with severe TBI (head Abbreviated Injury Scale (AIS) score of ≥3, Glasgow Coma Scale score of ≤8 on admission) admitted to Harborview Medical Center (level 1 pediatric trauma center), Seattle, WA, during 2003 to 2007 was performed. Admission demographics, clinical data, and laboratory characteristics were abstracted. Hypoxemia was defined as PaO2 < 60 mmHg, hypocarbia was defined as PaCO2 ≤ 35 mmHg, and hypercarbia was defined as PaCO2 ≥ 46 mmHg., Results: One hundred ninety-four patients met inclusion criteria of which 162 (83.5 %) patients survived. Admission hypoxemia occurred in nine (5.6 %) patients who survived and eight (25 %) patients who died (p < 0.001). Children with admission PaCO2 between 36 and 45 mmHg had greater discharge survival compared with those with both admission hypocarbia (PaCO2 ≤ 35 mmHg) and hypercarbia (PaCO2 ≥ 46 mmHg). Admission PaO2 301-500 mmHg (adjusted odds ratio (AOR), 8.02 (95 % confidence interval (CI), 1.73-37.10); p = 0.008) and admission PaCO2 = 36-45 mmHg (AOR, 5.47 (95 % CI, 1.30-23.07); p = 0.02) were independently associated with discharge survival., Conclusions: Discharge survival after severe pediatric TBI was associated with admission PaO2 301-500 mmHg and PaCO2 = 36-45 mmHg. Admission hypocarbia and hypercarbia were each associated with increased discharge mortality.

Unpressurized aircraft routinely operate at altitudes where hypoxia may be of concern. A systematic literature review was conducted regarding hypoxic impairment, including mental functions, sensory deficits, and other pertinent research findings that may affect aviation-related duties at moderate altitude (8000 to 15,000 ft/2438 to 4572 m). The results of this review suggest that cognitive and psychomotor deficits may include learning, reaction time, decision-making, and certain types of memory. However, results are difficult to quantify and reliably reproduce. Inconsistency of results may be related to the subtlety of deficits compared to high altitude, differences among individual compensatory mechanisms, variation in methodology or sensitivity of metrics, presence or absence of exercise, heterogeneous neuronal central nervous system (CNS) response, and interindividual variation. Literature regarding hypoxic visual decrements is more consistent. Rod photoreceptors are more susceptible to hypoxia; visual degradation has been demonstrated at 4000 to 5000 ft (1219 to 1524 m) under scotopic and 10,000 ft (3048 m) under photopic conditions. Augmented night vision goggle resolution demonstrates more resilience to mild hypoxic effects than the unaided eye under starlight conditions. Hypocapnia enhances visual sensitivity and contrast discrimination. Hyperventilation with resulting respiratory alkalosis and cerebral vasoconstriction may confound both cognitive/ psychomotor and visual experimental results. Future research should include augmentation of validated neuropsychological metrics (surrogate investigational end points) with actual flight metrics, investigation of mixed gas formulations, contribution of hypocapnic vasoconstrictive effects on hypoxic performance, and further investigation into cellular- and systems-level approaches for heterogeneous CNS response. Research is also required into the contribution of mild-moderate hypoxia in human factors- and spatial disorientation-related mishaps.

We hypothesized that chronic intermittent hypoxia (CIH) would induce a predisposition to apnea in response to induced hypocapnia. To test this, we used pressure support ventilation to quantify the difference in end-tidal partial pressure of CO(2) (Pet(CO(2))) between eupnea and the apneic threshold ("CO(2) reserve") as an index of the propensity for apnea and unstable breathing during sleep, both before and following up to 3-wk exposure to chronic intermittent hypoxia in dogs. CIH consisted of 25 s of Pet(O(2)) = 35-40 Torr followed by 35 s of normoxia, and this pattern was repeated 60 times/h, 7-8 h/day for 3 wk. The CO(2) reserve was determined during non-rapid eye movement sleep in normoxia 14-16 h after the most recent hypoxic exposure. Contrary to our hypothesis, the slope of the ventilatory response to CO(2) below eupnea progressively decreased during CIH (control, 1.36 +/- 0.18; week 2, 0.94 +/- 0.12; week 3, 0.73 +/- 0.05 l.min(-1).Torr(-1), P < 0.05). This resulted in a significant increase in the CO(2) reserve relative to control (P < 0.05) following both 2 and 3 wk of CIH (control, 2.6 +/- 0.6; week 2, 3.7 +/- 0.8; week 3, 4.5 +/- 0.9 Torr). CIH also 1) caused no change in eupneic, air breathing Pa(CO(2)); 2) increased the slope of the ventilatory response to hypercapnia after 2 wk but not after 3 wk compared with control; and 3) had no effect on the ventilatory response to hypoxia. We conclude that 3-wk CIH reduced the sensitivity of the ventilatory response to transient hypocapnia and thereby increased the CO(2) reserve, i.e., the propensity for apnea was reduced.

Morphological changes in the rat carotid bodies 1, 2, 4, and 8 weeks after the termination of chronically hypocapnic hypoxia (10% O2 for 8 weeks) were examined by means of morphometry and immunohistochemistry. The rat carotid bodies after 8 weeks of hypoxic exposure were enlarged several fold with vascular expansion. The carotid bodies 1 and 2 weeks after the termination of 8 weeks of hypoxic exposure were diminished in size, although their diameter remained larger than the normoxic controls. The expanded vasculature in chronically hypoxic carotid bodies returned to the normoxic control state. In the carotid bodies 1 week after the termination of chronic hypoxia, the density of NPY fibers was remarkably increased and that of VIP fibers was dramatically decreased in comparison with the density in chronically hypoxic carotid bodies. In the carotid bodies 2 and 4 weeks after the termination of hypoxia, the density of SP and CGRP fibers was gradually increased. In the carotid bodies 8 weeks after the termination of hypoxia, the appearance of the carotid body returned to a nearly normoxic state, and the density of SP, CGRP, VIP, and NPY fibers also recovered to that of normoxic controls. These results suggest that the morphological changes in the recovering carotid bodies start at a relatively early period after the termination of chronic hypoxia, and a part of these processes may be under the control of peptidergic innervation.

The effects of adaptation to cold-and-hypoxic exposure on the cardiovascular system, lipid peroxidation and concentrations of adaptogenesis involved hormones were studied in male students. The two weeks cold- and hypoxic training was shown to be accompanied by a significant increase of apnea duration, reduced velocity of bradycardia development and a more rapid ECG post-cold and- hypoxic exposure normalization, as well as by inhibition of activation of adrenal cortex and thyroid gland after stress of different nature. The changes of the character of influences between the indices under study, were demonstrated. The correlation analysis showed an increase of the human's adaptive potential and a decrease of its dependence on the adrenal cortex hormones.

The hypoxic ventilatory response during hypocapnia has been studied with divergent results. We used volume-cycled ventilation in spontaneously breathing normal subjects to study their hypoxic ventilatory response under conditions of stable hypocapnia. Subjects were studied at three different levels of end-tidal (partial) carbon dioxide pressure (PETCO2), eucapnia and 6 and 12 mm Hg below eucapnia (mild and moderate hypocapnia, respectively). The response to hypoxia was assessed by changes in muscle pressure output (Pmus) and respiratory rate. Compared with the Pmus response at eucapnia (0.53 +/- 0.59 cm H2O/percentage oxygen saturation [% O2sat]), the response at mild hypocapnia was attenuated (0.26 +/- 0.33 cm H2O/% O2sat), whereas the response at moderate hypocapnia was negligible (0.003 +/- 0.09 cm H2O/% O2sat). Similar reductions were seen with the respiratory rate (eucapnia, 0.17 +/- 0.2 breaths/minute/% O2sat; mild hypocapnia, 0.11 +/- 0.11 breaths/minute/% O2sat; moderate hypocapnia, 0.01 +/- 0.06 breaths/minute/% O2sat). The Pmus and respiratory rate responses at the three levels of PETCO2 were significantly different (p < 0.05, analysis of variance). The responses at moderate hypocapnia were not significantly different from zero. We conclude that when apnea occurs under conditions in which central PCO2 is well below the CO2 setpoint, subjects are at risk of developing dangerous hypoxemia due to absence of a hypoxic ventilatory response.

Background: Using the renal clearance of lithium as an index of proximal tubular outflow, this study tested the hypothesis that acute hypocapnic hypoxemia decreases proximal tubular reabsorption to the same extent as hypocapnic normoxemia (hyperventilation) and that this response is blunted during normocapnic hypoxemia., Methods: Eight persons were studied on five occasions: (1) during inhalation of 10% oxygen (hypocapnic hypoxemia), (2) during hyperventilation of room air leading to carbon dioxide values similar to those with hypocapnic hypoxemia, (3) during inhalation of 10% oxygen with the addition of carbon dioxide to produce normocapnia, (4) during normal breathing of room air through the same tight-fitting face mask as used on the other study days, and (5) during breathing of room air without the face mask., Results: Hypocapnic and normocapnic hypoxemia and hyperventilation increased cardiac output, respiratory minute volume, and effective renal plasma flow. Glomerular filtration rate remained unchanged on all study days. Calculated proximal tubular reabsorption decreased during hypocapnic hypoxemia and hyperventilation but remained unchanged with normocapnic hypoxemia. Sodium clearance increased slightly during hypocapnic and normocapnic hypoxemia, hyperventilation, and normocapnic normoxemia with but not without the face mask., Conclusions: The results indicate that (1) respiratory alkalosis with or without hypoxemia decreases proximal tubular reabsorption and that this effect, but not renal vasodilation or natriuresis, can be abolished by adding carbon dioxide to the hypoxic gas; (2) the increases in the effective renal plasma flow were caused by increased ventilation rather than by changes in arterial oxygen and carbon dioxide levels; and (3) the natriuresis may be secondary to increased renal perfusion, but application of a face mask also may increase sodium excretion.

A physician's assessment of the probable outcome of an episode of respiratory failure should be based on a combination of survival data from large studies and specific knowledge about the individual case in question. Clearly, mortality rates in cases of ARF are influenced by a number of factors. In general, only a minority of patients with ARF complicating COPD require mechanical ventilation. In these cases, mortality often is related to the nature of the precipitating illness and the severity of the patient's underlying chronic respiratory disease. The long-term prognosis in patients with COPD who survive an episode of ARF is related primarily to the severity of the patient's underlying disease. Acute mortality is higher in patients with ARDS than in patients with ARF complicating COPD. Although a significant number of ARDS patients die of their underlying illness, mortality in others more commonly appears to be related to sepsis and multiple organ failure rather than end-stage respiratory disease. Pulmonary function in survivors of ARDS is quite variable, and may be related to the severity of the acute episode. ARF has a particularly poor prognosis when associated with certain underlying illnesses such as hematologic malignancy.