Effective Tidal Volume for Normocapnia in Very-Low-Birth-Weight Infants Using High-Frequency Oscillatory Ventilation

PURPOSE: Removal of CO₂ is much efficient during high-frequency oscillatory ventilation (HFOV) for preterm infants. However, an optimal carbon dioxide diffusion coefficient (DCO₂) and tidal volume (VT) have not yet been established due to much individual variance. This study aimed to analyze DCO₂ values, VT, and minute volume in very-low-birth-weight (VLBW) infants using HFOV and correlates with plasma CO₂ (pCO₂). MATERIALS AND METHODS: Daily respiratory mechanics and ventilator settings from twenty VLBW infants and their two hundred seventeen results of blood gas analysis were collected. Patients were treated with the Dräger Babylog VN500 ventilator (Drägerwerk Ag & Co.) in HFOV mode. The normocapnia was indicated as pCO₂ ranging from 45 mm Hg to 55 mm Hg. RESULTS: The measured VT was 1.7 mL/kg, minute volume was 0.7 mL/kg, and DCO₂ was 43.5 mL²/s. Mean results of the blood gas test were as follows: pH, 7.31; pCO₂, 52.6 mm Hg; and SpO₂, 90.5%. In normocapnic state, the mean VT was significantly higher than in hypercapnic state (2.1±0.5 mL/kg vs. 1.6±0.3 mL/kg), and the mean DCO₂ showed significant difference (68.4±32.7 mL²/s vs. 32.4±15.7 mL²/s). The DCO₂ was significantly correlated with the pCO₂ (p=0.024). In the receiver operating curve analysis, the estimated optimal cut-off point to predict the remaining normocapnic status was a VT of 1.75 mL/kg (sensitivity 73%, specificity 80%). CONCLUSION: In VLBW infants treated with HFOV, VT of 1.75 mL/kg is recommended for maintaining proper ventilation.

Effect of chronic ethanol exposure on rat ventilatory responses to hypoxia and hypercapnia

OBJECTIVE: The effect of chronic ethanol exposure on chemoreflexes has not been extensively studied in experimental animals. Therefore, this study tested the hypothesis that known ethanol-induced autonomic, neuroendocrine and cardiovascular changes coincide with increased chemoreflex sensitivity, as indicated by increased ventilatory responses to hypoxia and hypercapnia. METHODS: Male Wistar rats were subjected to increasing ethanol concentrations in their drinking water (first week: 5% v/v, second week: 10% v/v, third and fourth weeks: 20% v/v). At the end of each week of ethanol exposure, ventilatory parameters were measured under basal conditions and in response to hypoxia (evaluation of peripheral chemoreflex sensitivity) and hypercapnia (evaluation of central chemoreflex sensitivity). RESULTS: Decreased respiratory frequency was observed in rats exposed to ethanol from the first until the fourth week, whereas minute ventilation remained unchanged. Moreover, we observed an increased tidal volume in the second through the fourth week of exposure. The minute ventilation responses to hypoxia were attenuated in the first through the third week but remained unchanged during the last week. The respiratory frequency responses to hypoxia in ethanol-exposed rats were attenuated in the second through the third week but remained unchanged in the first and fourth weeks. There was no significant change in tidal volume responses to hypoxia. With regard to hypercapnic responses, no significant changes in ventilatory parameters were observed. CONCLUSIONS: Our data are consistent with the notion that chronic ethanol exposure does not increase peripheral or central chemoreflex sensitivity. .

Hemodynamic and ventilatory response to different levels of hypoxia and hypercapnia in carotid body-denervated rats

OBJECTIVE: Chemoreceptors play an important role in the autonomic modulation of circulatory and ventilatory responses to changes in arterial O2 and/or CO2. However, studies evaluating hemodynamic responses to hypoxia and hypercapnia in rats have shown inconsistent results. Our aim was to evaluate hemodynamic and respiratory responses to different levels of hypoxia and hypercapnia in conscious intact or carotid body-denervated rats. METHODS: Male Wistar rats were submitted to bilateral ligature of carotid body arteries (or sham-operation) and received catheters into the left femoral artery and vein. After two days, each animal was placed into a plethysmographic chamber and, after baseline measurements of respiratory parameters and arterial pressure, each animal was subjected to three levels of hypoxia (15, 10 and 6% O2) and hypercapnia (10% CO2). RESULTS: The results indicated that 15% O2 decreased the mean arterial pressure and increased the heart rate (HR) in both intact (n = 8) and carotid body-denervated (n = 7) rats. In contrast, 10% O2did not change the mean arterial pressure but still increased the HR in intact rats, and it decreased the mean arterial pressure and increased the heart rate in carotid body-denervated rats. Furthermore, 6% O2 increased the mean arterial pressure and decreased the HR in intact rats, but it decreased the mean arterial pressure and did not change the HR in carotid body-denervated rats. The 3 levels of hypoxia increased pulmonary ventilation in both groups, with attenuated responses in carotid body-denervated rats. Hypercapnia with 10% CO2 increased the mean arterial pressure and decreased HR similarly in both groups. Hypercapnia also increased pulmonary ventilation in both groups to the same extent. CONCLUSION: This study demonstrates that the hemodynamic and ventilatory responses varied according to the level of hypoxia. Nevertheless, the hemodynamic and ventilatory responses to hypercapnia did not depend on the activation of the peripheral carotid chemoreceptors.

The effect of hypercapnic acidosis preconditioning on rabbit myocardium / 华中科技大学学报（医学）（英德文版）

This study observed the protective effect of hypercapnic acidosis preconditioning on rabbit heart suffered from ischemia-reperfusion injury. Hypercapnic acidosis was established in animals with mechanical hypoventilation before ischemia-reperfusion. Thirty-two rabbits were randomly divided into 4 groups, with each having 8 animals in term of the degree of acidification: hypercapnic acidosis group A (group A), hypercapnic acidosis group B (group B), hypercapnic acidosis group C (group C), ischemia and reperfusion group (group IR). Animals in group IR were ventilated normally (tidal volume: 15 mL/kg, breathing rate 35 bpm). The PETCO(2) was maintained at the level of 40-50 mmHg for 30 min. Animals in groups A, B, C received low-frequency, low-volume ventilation to achieve hypercarbonic acidosis and the target levels of PETCO(2) were 75-85,65-75, 55-65 mmHg, respectively, with levels being maintained for 5 min. The animals then were ventilated normally to lower PETCO(2) to 40-50 mmHg. The left anterior branch artery of all the animals was ligated for 30 min and reperfused for 180 min. Then the infarct size was calculated. The cardiomyocytes were morphologically observed and ECG and hemodynamics were monitored on continuous basis. Acid-base balance was measured during procedure. Our results showed that the infarct size was (48.5+/-11.5)% of the risk area in the control group and (42.4+/-7.9)% in group C (P>0.05). Mean infarct size was significantly smaller in group B (34.5%+/-9.4%) (P<0.05 vs control group) and group A (31.0%+/-9.1%) (P<0.01 vs control group). It is concluded that HA-preconditioning can effectively protect the myocardium.

Quantitative aspects of brain perfusion dynamic induced by BOLD fMRI / Aspectos quantitativos da dinâmica perfusional do cérebro induzida pelo BOLD fMRI

The increase of relative cerebral blood flow (rCBF) may contribute for a change in blood oxygenation level dependent signal (BOLD). The main purpose of this study is to investigate some aspects of perfusional alterations in the human brain in response to a uniform stimulation: hypercapnia induced by breath holding. It was observed that the BOLD signal increased globally during hypercapnia and that it is correlated with the time of breath holding. This signal increase shows a clear distinction between gray and white matter, being greater in the grey matter.

O aumento relativo do fluxo cerebral sangüíneo (relative Cerebral Blood Flow - rCBF) pode contribuir para uma mudança no sinal dependente da oxigenação do sangue (Blood Oxygenation Level Dependent - BOLD). O objetivo principal deste trabalho foi estudar alguns aspectos da alteração perfusional no cérebro humano em resposta a um estímulo uniforme: hipercapnia, causada por um estado de apnéia induzida. Foi observado um aumento global no sinal BOLD durante a hipercapnia. Este aumento é correlacionado com a duração da apnéia e mostra uma clara distinção entre a substância branca e cinzenta, sendo maior na substância cinzenta.

Trocas gasosas intrapulmonares sob respiração em ar ambiente em pacientes hipercapneicos / Pulmonary gas exchange under room air respiration in hypercapneic patients

A diferença alvéolo-arterial de oxigênio ou P(A-a)O2 é importante no estudo de disfunções nas trocas gasosas alvéolo-capilares, entretanto não fornece resultados confiáveis em pacientes hipercapneicos, ao contrário do cálculo da mistura venosa que, embora pouco prático, é potencialmente capaz de diagnosticar a existência de distúrbio de trocas alvélo-capilares de qualquer natureza. OBJETIVO: Conferir o grau de confiabilidade da diferença alvéolo-arterial de oxigênio para avaliar distúrbio das trocas alvéolo-capilares na presença de hipoventilação alveolar, utilizando o cálculo da mistura venosa como padrão. MÉTODOS: Oitenta e três gasometrias de pacientes hipercapneicos foram submetidas ao cálculo da mistura venosa e da diferença P(A-a)O2 obtida com a PaCO2 medida e com a PaCO2 fixada em 40 mmHg. Os resultados foram comparados por teste de correlação simples. RESULTADOS: A pressão parcial de oxigênio e de gás carbônico arterial média foi de 50,8±10,4 e 51,7±6,4 mmHg, respectivamente. As médias da P(A-a)O2, da P(A-a)O2 "corrigida" e da mistura venosa foram respectivamente 26,6±10,2 mmHg; 40,4±10,8 mmHg e 37±15,2 por cento. O coeficiente de correlação entre a mistura venosa e a P(A-a)O2 foi de 0,61 (p<0,00001) e mistura venosa e P(A-a)O2 "corrigida" foi de 0,89 (p<0,00001). CONCLUSAO: A utilização do cálculo da diferença alvéolo-arterial de oxigênio em pacientes cronicamente hipercapneicos tem alcance clínico limitado, porque ele deixa de expressar o diagnóstico de distúrbio das trocas alvéolo-capilares que freqüentemente está associado à hipoventilação alveolar.

Assessment of ventilatory neuromuscular drive in patients with obstructive sleep apnea

The presence of abnormalities of the respiratory center in obstructive sleep apnea (OSA) patients and their correlation with polysomnographic data are still a matter of controversy. Moderately obese, sleep-deprived OSA patients presenting daytime hypersomnolence, with normocapnia and no clinical or spirometric evidence of pulmonary disease, were selected. We assessed the ventilatory control and correlated it with polysomnographic data. Ventilatory neuromuscular drive was evaluated in these patients by measuring the ventilatory response (VE) the inspiratory occlusion pressure (P.1) and the ventilatory pattern (VT/TI, TI/TTOT) at rest and during submaximal exercise, breathing room air. These analyses were also performed after inhalation of a hypercapnic mixture of CO2 (deltaP.11/deltaPETCO2, deltaVE/deltaPETCO2). Average rest and exercise ventilatory response (VE: 12.2 and 32.61/min, respectively), inspiratory occlusion pressure (P.1: 1.5 and 4.7 cmH2O, respectively), and ventilatory pattern (VT/TI: 0.42 and 1.09 1/s; TI/TTOT: 0.47 and 0.46 1/s, respectively) were within the normal range. In response to hypercapnia, the values of ventilatory response (deltaVE/deltaPETCO2: 1.51 lmin(-1) mmHg(-1)) and inspiratory occlusion pressure (deltaP.1/deltaPETCO2: 0.22 cmH2O) were normal or slightly reduced in the normocapnic OSA patients. No association or correlation between ventilatory neuromuscular drive and ventilatory pattern, hypersomnolence score and polymnographic data was found; however a significant positive correlation was observed between P.1 and weight. Our results indicate the existence of a group of normocapnic OSA patients who have a normal awake neuromuscular ventilatory drive at rest or during exercise that is partially influenced by obesity.

Dormir en los Andes: contribución del sueño en la etiopatogenia de la enfermedad de Monge / Sleep at the Andes: contribution to dream at etiopathogeny from Monge`s disease

En las grandes alturas se han estudiado los efectos del sueño y su influencia en la etiopatogenia del soroche crónico o Enfermedad de Monge. Se hizo cateterismo cardíaco derecho durante la noche y se midió la ventilación pulmomar en voluntarios adultos normales (adaptados y en pacientes con enfermedad de Monge (desadaptados). En niños sólo se midió la ventilación pulmonar. A 4540 y a 4330 msnm. durante el sueño se producen los siguientes efectos agudos: hipoventilación, hipoxemia moderada y severa, hipercapnia, hipertensión pulmonar moderada y severa, disminuyendo el consumo de oxígeno, el débito cardíaco y el volumen de expulsión ventricular, leve incremento de la frecuencia cardíaca, acidemia y, en los desadaptados, además, se observa hipertensión diastólica sistémica. Los cambios son más acentuados en los desadaptados. En los niños el sueño ocasiona una disminución de la ventilación pulmonar siendo ésta de mayor magnitud que en los adultos. Al despertar, los residentes altoandinos están normales y sin signos, síntomas, ni ninguna condición neurológica patológica. Durante el sueño los adaptados adquieren las características que tienen los desadaptados en vigilia. Hipoventilación, hipoxemia y policitemia acentuadas, hipercapnia, hipertensión pulmonar moderada y severa son las principales características de la Enfermedad de Monge, siendo la hipoventilación el principal factor causal de ellos. Por la hipoxemia aguda durante el sueño los residentes altoandinos, teóricamente ascienden a una altura mayor que aquella en la cual están durmiendo. Desde los recién nacidos hasta la senectud la hipoventilación e hipoxemia se acentúan por el sueño, por el envejecimiento, por la mayor altitud de residencia, y más aún en las grandes alturas, la hipoxemia también se acentúa por el peculiar comportamiento fisiológico de la curva de disociación de la oxihemoglobina y, probablememte, por los mecanismos mediante los cuales la policitemia ocasiona anoxemia y viceversa y por la precoz desensibilización hipóxica de los quimiorreceptores periféricos. De esta manera, ya sea en forma aislada o asociada, el sueño y las otras variables contribuyen en la etiopatogenia de la enfermedad de Monge, condicionando que algunos adaptados vayan adquiriendo lenta y progresivamente las características que tienen los pacientes con Enfermedad de Monge. Así, la Enfermedad de Monge sería la resultante de un proceso bio-ecológico y no la de un proceso patológico

Insuficiência respiratória / Respiratory failure

A expressao "Insuficiência Respiratória" é utilizada para caracterizar condiçao clínica, na qual o aparelho respiratório é incapaz de elevar a níveis satisfatórios a oxigenaçao do sangue arterial associada (insuficiência ventilatória) ou nao à retençao de dióxido de carbono (insuficiência hipoxêmica). É freqüente estar associada à presença de doenças broncopulmonares e/ou cardíacas, ma também pode ocorrer na presença de pulmoes normais (doenças do sistema nervoso central, neuromusculares e da caixa torácica). Embora ocorram, as manifestaçoes clínicas da insuficiência respiratória sao inespecíficas e o diagnóstico depende da análise da gasometria arterial e do pH. Assim sendo, o conhecimento dos processos intrapulmonares envolvendo as trocas gasosas é essencial para o entendimento de sua fisiopatologia nas diferentes condiçoes clínicas que pode estar presente.