Reversal of narcotic depression in the neonate by nalozone

Naloxone 40 mug was administered intravenously one minute after birth to 20 out of 44 neonates whose mother had been given pethidine in labour. These neonates were compared with 20 others whose mothers had had only lumbar epidural block. Alveolar PCO2, alveolar ventilation, and ventilatory rate were measured 10 and 30 minutes after birth. The untreated neonates of mothers who had had pethidine showed significant ventilatory depression compared with infants in the epidural and naloxone-treated groups. The naloxone-treated neonates were comparable with the epidural group, although the effects of naloxone were diminishing at 30 minutes. Naloxone is an effective narcotic antagonist which should be considered to be the drug of choice for treating narcotic depression in the neonate.     

Effect of prior O2 breathing on ventilatory response to sustained isocapnic hypoxia in adult humans

Sixteen healthy volunteers breathed 100% O2 or room air for 10 min in random order, then their ventilatory response to sustained normocapnic hypoxia (80% arterial O2 saturation, as measured with a pulse oximeter) was studied for 20 min. In addition, to detect agents possibly responsible for the respiratory changes, blood plasma of 10 of the 16 subjects was chemically analyzed. 1) Preliminary O2 breathing uniformly and substantially augmented hypoxic ventilatory responses. 2) However, the profile of ventilatory response in terms of relative magnitude, i.e., biphasic hypoxic ventilatory depression, remained nearly unchanged. 3) Augmented ventilatory increment by prior O2 breathing was significantly correlated with increment in the plasma glutamine level. We conclude that preliminary O2 administration enhances hypoxic ventilatory response without affecting the biphasic response pattern and speculate that the excitatory amino acid neurotransmitter glutamate, possibly derived from augmented glutamine, may, at least in part, play a role in this ventilatory enhancement.     

The Chinese General Health Questionnaire in a psychiatric setting: the development of the Chinese scaled version

Hydroxyzine is frequently used to tranquilize chronic obstructive pulmonary disease patients, who may be concomitantly receiving narcotic analgesics. Therefore, its effect alone and in combination with meperidine on arterial blood gases and ventilation at rest were evaluated in 44 patient volunteers, who gave informed consent. Hydroxyzine, 1.5 mg/kg i.v. caused no significant decrease in PaO2 and pH, no increase in PaCO2 at 5, 10, 20, 30 and 60 min post-infusion (n = 13, mean age = 63.4 years). Meperidine, 1.5 mg/kg i.v. caused a significant (p < 0.001) reduction in PaO2 for 20 min with concomitant increase in PaCO2 (n = 14; mean age = 49.4 years). The combination of the same doses of hydroxyzine with meperidine i.v. caused no greater decrease in PaO2 or in pH or increase in PaCO2 than did meperidine alone (n = 17; mean age = 52.6 years), indicating no greater ventilatory depression with the combination than with meperidine alone. The lack of significant pH decreases at 30 and 60 min further corroborates no potentiation of meperidine by hydroxyzine. In conclusion, hydroxyzine, even when given through the i.v. route in excess of the maximum i.m. therapeutic dose, caused no changes in PaO2, PaCO2 or pH in chronic obstructive pulmonary disease patients. Therefore, its i.m. administration resulting in lower blood levels than i.v., is not likely to cause ventilatory depression. Furthermore, hydroxyzine caused no potentiation of the ventilatory depression induced by meperidine, hence hydroxyzine may be safely employed in combination with meperidine.     

Capnography and ventilatory assessment during ambulatory dentoalveolar surgery

PURPOSE: The purpose of this study was to determine whether capnography is a more sensitive monitor than auscultation of breath sounds in detecting ventilatory changes consistent with hypoventilation, obstruction, or apnea and in detecting ventilatory changes that can be associated with oxygen desaturation. PATIENTS AND METHODS: Fifty-five patients received intravenous agents and supplemental oxygen to achieve a state of deep sedation or general anesthesia for removal of impacted third molars. The surgeon/anesthetist monitored respiratory status using a pretracheal stethoscope and direct observation. A blinded observer with no access to the patient or anesthetist monitored respiratory status using capnography. A second observer monitored all respiratory parameters to allow for correlation between clinical and electronic monitors. RESULTS: Ventilatory status was continuously represented by capnogaphy. The Pearson correlation coefficient showed a positive correlation between increased end-tidal CO2 (PETCO2) and decreased oxygen saturation that became stronger with greater positive changes in PETCO2. An additive relationship was found between PETCO2 and respiratory rate (RR), with increased PETCO2 and decreased RR contributing to decreased oxygen saturation. CONCLUSION: Patients with nasal ventilatory exchange maintain this exchange throughout the anesthesia so that sampling of nasal PETCO2 is an effective way to monitor ventilatory status. Respiratory depression or obstructive ventilatory changes detected by capnography showed a high sensitivity and low positive predictive value in detecting oxygen desaturation. The current technology does not show a clinically satisfactory correlation between PETCO2 and oxygen saturation. However, a combined increase in PETCO2 and decrease in RR suggested a trend of decreasing oxygen saturation.     

Contribution of peripheral chemoreceptor drive in exercise hyperpnea in humans

The peripheral chemoreceptors play a dominant role in the respiratory compensation of lactic acidosis during heavy exercise of humans. Our object was to determine the contribution of peripheral chemoreceptors to exercise hyperpnea during mild to moderate and heavy exercise above the anaerobic threshold. We used a hyperoxic suppression test in six normal male subjects. Inspired gas was abruptly changed without the subject's knowledge from air to pure oxygen for 5 to 6 breaths. The maximal ventilatory depression after O2 breathing was 5.5 +/- 1.7 L/min (BTPS) at mild exercise, and the depression increased with increasing exercise intensity up to 12.8 +/- 4.1 L/min (BTPS). The relative contribution of the peripheral chemoreceptors to ventilation in terms of percentage of the maximal ventilatory depression was maintained, being 20% throughout the entire work ranges studied. The contribution of the peripheral chemoreceptors to total ventilation is hardly altered by lactic acidosis caused by heavy exercise above the anaerobic threshold according to our data. These results suggested that the peripheral chemoreceptors may not be solely responsible for excessive hyperventilation, or residual activities of peripheral chemoreceptors still exist after O2 breathing especially during heavy exercise above the anaerobic threshold.     

Effect of meperidine on occlusion pressure responses to hypercapnia and hypoxia with and without external inspiratory resistance

In 5 normal subjects we measured ventilation and P0.1, the pressure generated by the first 0.1 sec of inspiratory effort against a closed airway, in response to hypercapnia and hypoxia with and without added inspiratory resistance before and after oral meperidine (1.1 to 1.3 mg per kg). CO2 responses were studied in the steady state, whereas progressive hypoxia was used to elicit hypoxic responses. In general, resistance decreased ventilatory responses to hypercapnia but increased P0.1 responses to both hypoxia and hypercapnia. Meperidine depressed both ventilatory and P0.1 responses, more so in hypoxia than in hypercapnia. The combination of resistance and merperidine was additive in depressing responses to hypercapnia but in hypoxia produced little more depression than did meperidine alone. In both hypercapnia and hypoxia, meperidine decreased the augmentation of P0.1 that was associated with increased resistance. Normal subjects responded to acute increases of inspiratory resistance by increasing inspiratory motor output; this increase was distinctly blunted by meperidine.     

Influences of morphine on the ventilatory response to isocapnic hypoxia

BACKGROUND: The ventilatory response to hypoxia is composed of the stimulatory activity from peripheral chemoreceptors and a depressant effect from within the central nervous system. Morphine induces respiratory depression by affecting the peripheral and central carbon dioxide chemoreflex loops. There are only few reports on its effect on the hypoxic response. Thus the authors assessed the effect of morphine on the isocapnic ventilatory response to hypoxia in eight cats anesthetized with alpha-chloralose-urethan and on the ventilatory carbon dioxide sensitivities of the central and peripheral chemoreflex loops. METHODS: The steady-state ventilatory responses to six levels of end-tidal oxygen tension (PO2) ranging from 375 to 45 mmHg were measured at constant end-tidal carbon dioxide tension (P[ET]CO2, 41 mmHg) before and after intravenous administration of morphine hydrochloride (0.15 mg/kg). Each oxygen response was fitted to an exponential function characterized by the hypoxic sensitivity and a shape parameter. The hypercapnic ventilatory responses, determined before and after administration of morphine hydrochloride, were separated into a slow central and a fast peripheral component characterized by a carbon dioxide sensitivity and a single offset B (apneic threshold). RESULTS: At constant P(ET)CO2, morphine decreased ventilation during hyperoxia from 1,260 +/- 140 ml/min to 530 +/- 110 ml/ min (P < 0.01). The hypoxic sensitivity and shape parameter did not differ from control. The ventilatory response to carbon dioxide was displaced to higher P(ET)CO2 levels, and the apneic threshold increased by 6 mmHg (P < 0.01). The central and peripheral carbon dioxide sensitivities decreased by about 30% (P < 0.01). Their ratio (peripheral carbon dioxide sensitivity:central carbon dioxide sensitivity) did not differ for the treatments (control = 0.165 +/- 0.105; morphine = 0.161 +/- 0.084). CONCLUSIONS: Morphine depresses ventilation at hyperoxia but does not depress the steady-state increase in ventilation due to hypoxia. The authors speculate that morphine reduces the central depressant effect of hypoxia and the peripheral carbon dioxide sensitivity at hyperoxia.     

COPD: using nutrition to prevent respiratory function decline

Close to three-fourths of patients with chronic obstructive pulmonary disease (COPD) suffer from weight loss. Identifying a single cause for this is difficult, as several factors-including chronic mouth breathing, dyspnea, aerophagia, certain medications, and depression-often act in concert. Malnutrition can exacerbate symptoms of COPD by decreasing ventilatory muscle strength, exercise tolerance, and immunocompetence, and by increasing the risk of depression and anxiety. Goals of nutrition intervention are to prevent or reverse malnutrition without worsening the disease process and to improve respiratory function, thereby reducing morbidity and delaying mortality. Recommendations for intake of fats, carbohydrates, protein, and water must be individualized.     

Dextromethorphan affects ventilation differently in male and female rats

Subcutaneous administration of aspartic acid results in a long-lasting but reversible depression of ventilation in male but not in female rats. Aspartic acid acts on N-methyl-D-aspartate receptors. The present study tested the hypothesis that a noncompetitive N-methyl-D-aspartate-receptor antagonist, dextromethorphan (Dex), would depress ventilation in female rats and stimulate it in male rats. Moreover, Dex administered prior to aspartic acid should prevent the aspartic acid-induced depression of ventilation in male rats. In female rats, Dex caused a 30% depression of ventilation relative to saline at 5 and 10 mg/kg (P < 0.01) but not at the highest dose (20 mg/kg). In male rats, Dex had no effect on ventilation. At a dose of 20 mg/kg, Dex depressed oxygen consumption to 50% of the saline value at all time points in female rats (P < 0.001) and in male rats 45 and 60 min after administration. The time points when Dex depressed ventilation and oxygen consumption were different in female rats, suggesting that the depression of ventilation was not the result of a depression in oxygen consumption. During a hypercapnic challenge (7% CO2), female rats treated with 5 and 10 mg/kg of Dex exhibited a smaller increase in ventilatory response relative to saline treatment. At a dose of 20 mg/kg, the hypercapnic responsiveness of male rats was markedly stimulated (85.8 +/- 8.95 ml/min) relative to saline (50.6 +/- 9.14 ml/min; P < 0.001). Finally, Dex administered before aspartic acid prevented the aspartic acid-induced depression of ventilation in male rats. Thus, in rats, Dex has gender-specific effects on ventilation and these effects are not associated with changes in oxygen consumption.     

Effect of a subanesthetic minimum alveolar concentration of isoflurane on two tests of the hypoxic ventilatory response

BACKGROUND: These experiments were designed to study the effect of 0.1 minimum alveolar concentration isoflurane on the hypoxic ventilatory response as measured by two common methods of hypoxic testing: when normocapnic hypoxia was induced abruptly and when it was induced gradually. We hypothesized that any disparity in results would be due to an isoflurane effect that was manifested differently in the two tests. METHODS: After 20 min for uptake and equilibration of 0.1 minimum alveolar concentration end-tidal isoflurane or carrier gas in hyperoxia, isocapnic hypoxia was induced either abruptly over 60-80 s ("step" test) or gradually over 10 min ("ramp" test), followed by 20 min of isocapnic hypoxia at 45 mmHg end-tidal oxygen. Control of the hypoxic and isocapnic stimuli was accomplished accurately by a computer-controlled dynamic end-tidal forcing system. Eight subjects performed each test in the presence and absence of isoflurane. RESULTS: For both step tests and ramp tests, 0.1 minimum alveolar concentration isoflurane had no effect on minute ventilation during the defined periods of hypoxia. With isoflurane, delta VE45, the acute change in ventilation from hyperoxia to hypoxia, was 97 +/- 20% (mean +/- SEM) of the control response for step tests and 100 +/- 25% of the control response for ramp tests. The step tests produced significantly larger acute hypoxic responses than did the ramp tests, but by the end of 20 min of hypoxia, ventilation was similar for both tests. CONCLUSIONS: Neither method of hypoxic testing demonstrated the level of isoflurane effect reported by others. A comparison of the two methods of hypoxic testing suggests that ramp tests, as commonly performed, do not allow adequate time for full expression of the acute hypoxic ventilatory response. Step tests also better separated the opposing hypoxic effects of carotid body stimulation and central ventilatory depression.     

Airway muscle in infants with congenital diaphragmatic hernia: response to treatment

BACKGROUND/PURPOSE: Airway muscle hyperactivity and chronic lung disease frequently follow congenital diaphragmatic hernia (CDH) treatment. The aim of this study was to compare the quantity of airway muscle and alveolar ductal artery muscle in CDH infants after various treatments. METHODS: Five groups were studied postmortem: CDH, died within 24 hours, without high ventilatory assistance (n = 3); CDH, various extracorporeal membrane oxgenation (ECMO) durations, without high ventilatory assistance (n = 4); CDH, various ECMO durations, with high ventilatory assistance (n = 7); no CDH, without high ventilatory assistance (n = 12); and no CDH, with high ventilatory assistance and bronchopulmonary dysplasia (BPD) (n = 5). Sections from standardized fixed lungs were immunohistochemically stained for alpha-smooth muscle actin. Muscle surrounding conducting airways from small preterminal bronchioles to bronchi was quantitated in both the ipsilateral and contralateral lungs with computerized image analysis. Similarly, muscle mass was quantitated in alveolar ductal arteries. RESULTS: CDH infants with low ventilatory assistance, regardless of postnatal age, had the same quantity of airway muscle as low ventilatory assistance controls. Infants with CDH and prolonged high ventilatory assistance had significantly more muscle throughout the conducting airways, similar to BPD infants without CDH, even though the CDH infants had significantly less exposure to high ventilatory assistance. With both low and high ventilatory assistance, the quantity of muscle in both the ipsilateral and contralateral lungs was similar. In contrast, small acinar arteries in CDH infants have increased muscle mass at birth. This muscle is decreased by ECMO but persists in CDH infants with high ventilatory assistance. CONCLUSIONS: The authors show that postnatally, CDH infants acquire increased muscle quantity throughout the conducting airways, in both the ipsilateral and contralateral lungs, with relatively short exposure to high ventilatory assistance. The normal decrease in acinar arterial mass that occurs postnatally is delayed in CDH infants with high ventilatory assistance.     

Tracheobronchomalacia in preterm infants with chronic lung disease

Tracheobronchomalacia is a treatable cause of persisting ventilatory requirements in the preterm neonate, and warrants a high index of suspicion. Five preterm infants with persisting ventilatory requirements with evidence of tracheobronchomalacia are reported. Four were diagnosed by tracheobronchogram and one by flexible endoscopy. All were successfully managed by continuous positive airway pressure (CPAP) via a tracheostomy. One infant died of unrelated causes. The oldest child in this series at the age of 2 years requires no further ventilatory support. Tracheobronchial anomalies should be considered in all preterm infants with persisting ventilatory requirements.     

A historical perspective on the use of noninvasive ventilatory support alternatives

This article traces the development of mechanical ventilatory support methods from the use of body ventilators to tracheal cannulation to the use of noninvasive ventilatory support and airway secretion management alternatives. Although it has been known that tracheostomy tubes could be used for ventilatory support and airway secretion management since 1869, body ventilators continued to be the main methods of long-term ventilatory support in the United States, with tracheostomy performed only for patients with severe bulbar muscle dysfunction, until the late 1950s. Recent technological developments, however, have created renewed interest in noninvasive alternatives.     

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 (delta P.1/delta PETCO2, delta VE/delta PETCO2). Average rest and exercise ventilatory response (VE: 12.2 and 32.6 l/min, respectively), inspiratory occlusion pressure (P.1: 1.5 and 4.7 cmH2O, respectively), and ventilatory pattern (VT/TI: 0.42 and 1.09 l/s; TI/TTOT: 0.47 and 0.46 l/s, respectively) were within the normal range. In response to hypercapnia, the values of ventilatory response (delta VE/delta PETCO2: 1.51 l min-1 mmHg-1) and inspiratory occlusion pressure (delta P.1/delta PETCO2: 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 polysomnographic 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.     

Kyphosis secondary to tuberculosis osteomyelitis as a cause of ventilatory failure. Clinical features, mechanisms, and management

STUDY OBJECTIVES: To investigate the relationship of thoracic kyphosis following tuberculosis to the development of ventilatory failure and to assess the efficacy on nocturnal noninvasive ventilatory support. DESIGN: Retrospective consecutive case series with crossover from a phase without noninvasive ventilatory support to a phase with this treatment. SETTING: The Respiratory Support and Sleep Centre, Papworth, Hospital, Cambridge, England. PATIENTS: Seven patients with thoracic kyphosis following tuberculous osteomyelitis which had been contracted by the age of 4 years were studied. Their mean age was 53 (SD 7.1) years and the mean angle of kyphosis was 113.60. All patients were in ventilatory failure. INTERVENTIONS: The patients were treated with nocturnal noninvasive ventilation with either an individually constructed cuirass shell and a negative pressure pump or nasal intermittent positive pressure ventilation using a volume preset ventilator. MEASUREMENT AND RESULTS: Each patient underwent an initial clinical assessment along with radiologic studies of the spine, pulmonary function tests, daytime arterial blood gas tensions, and overnight recordings of arterial saturation, and transcutaneous carbon dioxide tension. They were reassessed in detail at a mean of 5 years after starting ventilatory support. Symptoms, vital capacity, daytime carbon dioxide tension, and overnight oximetry had all improved following treatment. Temporary withdrawal of ventilatory support led to severe sleep fragmentation in four patients and the appearance of central apneas and hypopneas in the other three. Six of the 7 patients were alive at a mean of 5.7 years after starting nocturnal ventilation. CONCLUSION: These results show that ventilatory failure may develop, after an interval of many years, in patients with a severe thoracic kyphosis due to tuberculosis in childhood. Noninvasive nocturnal ventilatory support can control the symptoms of ventilatory failure, improve the physiologic abnormalities, and is associated with prolonged survival.     

Hypoxic ventilatory responsiveness in Tibetan compared with Han residents of 3,658 m

Lifelong high-altitude residents of North and South America acquire blunted hypoxic ventilatory responses and exhibit decreased ventilation compared with acclimatized newcomers. The ventilatory characteristics of Himalayan high-altitude residents are of interest in the light of their reportedly lower hemoglobin levels and legendary exercise performance. Until recently, Sherpas have been the only Himalayan population available for study. To determine whether Tibetans exhibited levels of ventilation and hypoxic ventilatory drives that were as great as acclimatized newcomers, we compared 27 lifelong Tibetan residents of Lhasa, Tibet, China (3,658 m) with 30 acclimatized Han ("Chinese") newcomers matched for age, body size, and extent of exercise training. During room air breathing, minute ventilation was greater in the Tibetan than in the Han young men because of an increased respiratory frequency, but arterial O2 saturation and end-tidal PCO2 did not differ, indicating similar levels of effective alveolar ventilation. The Tibetan subjects had higher hypoxic ventilatory response shape parameter A values and hypercapnic ventilatory responsiveness than the Han subjects. Among the Han subjects, duration of high-altitude residence correlated with the degree of blunting of the hypoxic ventilatory drive. Paradoxically, hyperoxia (inspired O2 fraction 0.70) increased minute ventilation and decreased end-tidal PCO2 in the Tibetan but not in the Han men. We concluded that lifelong Tibetan residents of high altitude neither hypoventilated nor exhibited blunted hypoxic ventilatory responses compared with acclimatized Han newcomers, suggesting that the effects of lifelong high-altitude residence on ventilation and ventilatory response to hypoxia differ in Tibetan compared with other high-altitude populations.     

Sleep-induced breathing instability. University of Wisconsin-Madison Sleep and respiration Research Group

We present a view of the neuromechanical regulation of breathing and causes of breathing instability during sleep. First, we would expect transient increases in upper airway resistance to be a major cause of transient hypopnea. This occurs in sleep because a hypotonic upper airway is more susceptible to narrowing and because the immediate excitatory increase in respiratory motor output in response to increased loads is absent in non-REM sleep. Secondly, sleep predisposes to an increased occurrence of ventilatory "overshoots", in part because abruptly changing sleep states cause transient changes in upper airway resistance and in the gain of the respiratory controller. Following these ventilatory overshoots, breathing stability will be maintained if excitatory short-term potentiation is the prevailing influence. On the other hand, apnea and hypopnea will occur if inhibitory mechanisms dominate following the ventilatory overshoot. These inhibitory mechanisms include: a) hypocapnia-if transient, will inhibit carotid chemoreceptors and cause hypopnea, but if prolonged will inhibit medullary chemoreceptors and cause apnea; b) a persistent inhibitory effect from lung stretch; c) baroreceptor stimulation, from a transient rise in systemic blood pressure immediately following termination of apnea or hypopnea may partially suppress the accompanying hyperpnea; d) depression of central respiratory motor output via prolonged brain hypoxia. Once apneas are initiated, reinitiation of inspiration is delayed even though excitatory stimuli have risen well above their apneic thresholds, and these prolonged apneas are commonly accompanied by tonic EMG activation of expiratory muscles of the chest wall and upper airway.     

Clinical applications of cardiopulmonary interactions

The hemodynamic consequences of both spontaneous and positive-pressure ventilation may be profound and may have opposite effects on cardiovascular stability in differing patient populations. Thus, no firm rules apply as to the specific response that will be seen in all patients and under all conditions. Some generalities, however, are probably reasonable. In patients with markedly increased work of breathing, hypervolemia, or impaired LV pump function, the institution of mechanical ventilatory support can be lifesaving because of its ability to support the cardiovascular system, independent of any beneficial effects that mechanical ventilation may have on gas exchange. In patients with decreased pulmonary elastic recoil, increased pulmonary vascular resistance, hypovolemia, or airflow obstruction, the institution of mechanical ventilatory support may induce cardiovascular instability, which, if not corrected, can lead to total cardiovascular collapse. Similarly, withdrawal of ventilatory support invariably increases intrathoracic blood volume and LV afterload and can be thought of as a type of cardiovascular stress test. Patients who pass this test easily can usually be successfully weaned from mechanical ventilatory support, whereas those who fail often are not ready to be weaned. Some patients who fail weaning trials do so because of the cardiovascular effects of spontaneous ventilation, not because the work of breathing is too great. Identification of such patients early on may improve their treatment by directing supportive therapies toward cardiovascular rather than ventilatory endpoints. However, in many situations, it will be difficult to single out a primary process determining cardiovascular instability, because multiple factors are compounded to create the observed situation and the patient's response to initiation of ventilatory support or weaning. Thus, the clinician is left with a series of therapeutic options, which if depending on the patient's response, suggest specific origins of the ventilatory and cardiovascular dysfunction. In that regard, the initiation and withdrawal of ventilatory support can be seen as a ventilatory probe into the determinants of cardiovascular homeostasis in the ventilatory-dependent patient.     

Noninvasive management of pediatric neuromuscular ventilatory failure

OBJECTIVE: To evaluate the use of mouth piece/nasal intermittent positive-pressure ventilation (IPPV) as an alternative to intubation or to permit extubation for patients with primarily neuromuscular ventilatory impairment and no ventilator-free breathing ability. DESIGN: A case control study. INTERVENTIONS: Using a protocol in which oxyhemoglobin desaturation was prevented or reversed by the continuous use of noninvasive IPPV and manually and mechanically assisted coughing as needed, patients with neuromuscular ventilatory failure and no ventilator-free breathing ability were managed noninvasively or extubated to continuous use of noninvasive IPPV for ventilatory support on room air. MEASUREMENTS AND MAIN RESULTS: Four of ten patients who presented in acute ventilatory failure were managed without intubation, despite becoming dependent on continuous ventilator use. The six intubated patients were extubated successfully to continuous noninvasive IPPV once normal arterial oxygen saturation levels could be maintained on room air, despite their having no ventilator-free breathing ability. CONCLUSIONS: The use of inspiratory and expiratory aids can decrease the need for intubation for patients with neuromuscular ventilatory failure in the absence of significant lung disease. It can also permit extubation, despite the need for continuous ventilatory support and, thereby, decrease the need to resort to tracheostomy.     

Neuromuscular ventilatory insufficiency: effect of home mechanical ventilator use v oxygen therapy on pneumonia and hospitalization rates

The purpose of this study was to determine rates of pneumonia and hospitalization for patients receiving oxygen therapy, patients having indwelling tracheostomy tubes, and those using tracheostomy or noninvasive methods of home mechanical ventilation. Six hundred eighty-four users of assisted ventilation for 13,751 patient-years or 19.8 years per patient were surveyed by mail and twice by telephone over a span of four years. Pneumonia and hospitalization rates were significantly higher for ventilator users with chronic obstructive pulmonary disease or with neuromuscular ventilatory insufficiency and gastrostomy tubes than for ventilator users with neuromuscular ventilatory insufficiency without gastrostomy tubes. Of the latter group, more than 90% of the pneumonias and hospitalizations were triggered by otherwise benign intercurrent upper respiratory tract infections. Oxygen therapy was associated with a significantly (P < 0.001) higher rate of pneumonias and hospitalizations than that seen for untreated patients after initial episodes of respiratory distress or during the use of either tracheostomy intermittent positive pressure ventilation or noninvasive ventilatory assistance methods. The lowest pneumonia and hospitalization rates (P < 0.001) were by full-time, noninvasive intermittent positive pressure ventilation users. We conclude that oxygen therapy is not an effective substitute for assisted ventilation for patients with primarily ventilatory insufficiency. Noninvasive ventilatory aids can be used effectively for up to full-time ventilatory support for patients with neuromuscular conditions whose bulbar muscle function is adequate to avert the need for gastrostomy tube placement.