Effects of mechanical ventilation with expiratory negative airway pressure on porcine pulmonary and systemic circulation: mechano-physiology and potential application.

We studied the impact of mechanically regulated, expiratory negative airway pressure (ENAP) ventilation on pulmonary and systemic circulation including its mechanisms and potential applications. Microminipigs weighing about 10 kg were anesthetized (n = 5). First, hemodynamic variables were evaluated without and with ENAP to approximately -16 cmH2O. ENAP significantly increased heart rate and cardiac output, but decreased right atrial, pulmonary arterial and pulmonary capillary wedge pressures. Second, the evaluation was repeated following pharmacological adrenergic blockade, modestly blunting ENAP effects. Third, fluvoxamine (10 mg/kg) was intravenously administered to intentionally induce cardiovascular collapse in the presence of adrenergic blockade. ENAP was started when systolic pressure was < 40 mmHg in the animals assigned to ENAP treatment-group. Fluvoxamine induced cardiovascular collapse within 4 out of 5 animals. ENAP increased systolic pressure to > 50 mmHg (n = 2): both animals fully recovered without neurological deficit, whereas without ENAP both animals died of cardiac arrest (n = 2). ENAP may become an innovative treatment for drug-induced cardiovascular collapse.

Edema pulmonar por presión negativa con máscara laríngea clásica. Presentación de un caso pediátrico / Pulmonary edema due to negative pressure with classical laryngeal mask. Presentation of a pediatric case

RESUMEN El edema pulmonar por presión negativa es una complicación rara y dramática en la anestesia general. Habitualmente ocurre como consecuencia de un laringoespasmo u otra causa de obstrucción de la vía aérea. Se presentó un caso con el objetivo de mostrar los elementos usados para el diagnóstico y tratamiento del edema pulmonar por presión negativa. Paciente de 7 años de edad, femenina, ASA I, operada de metatarso varo funcional con anestesia general balanceada y máscara laríngea clásica # 3. Desarrolló dicho evento adverso durante la recuperación anestésica. El diagnóstico se basó en la disociación toraco abdominal al restablecer la ventilación espontanea, crepitantes en ambos hemitórax, cianosis central, hipoxemia y la presencia de infiltrado difuso bilateral alveolar. Se intubó la tráquea, se controló la ventilación con presión positiva al final de la espiración y se administró furosemida. La paciente fue trasladada a la Unidad de Cuidados Intensivos donde evolucionó satisfactoriamente. Este es un síndrome cuya verdadera incidencia se desconoce debido a la escasa familiarización con el mismo. La evolución de los pacientes es favorable siempre que se establezca el diagnóstico y el tratamiento oportuno (AU).

ABSTRACT Pulmonary edema due to negative pressure is a rare and dramatic complication in general anesthetic. It usually occurs as a consequence of a laryngeal spasm or another cause of respiratory tract obstruction.A case was presented with the aim of showing the elements used for the diagnosis and treatment of the pulmonary edema due to negative pressure. An ASA I, 7-year-old female patient, was operated on a functional metatarsus varus with balanced general anesthetic and classical laryngeal mask number 3. She developed this adverse event during the anesthetic recovery. The diagnosis was based on the thoracoabdominal dissociation when recovering spontaneous ventilation, crepitation in hemithoraxes, central cyanosis, hypoxemia, and alveolar bilateral diffused infiltrate. The trachea was intubated, ventilation was controlled with positive pressure at the end of the expiration and furosemide was administered. The patient was transferred to the Intensive Care Unit where she evolved satisfactorily. This is a syndrome whose true incidence is unknown as a result of the lack of familiarization with it. Patients' evolution is favorable whenever the right diagnosis and treatment are timely established (AU).

Heat stress evaluation of two-layer chemical demilitarization ensembles with a full face negative pressure respirator.

The purpose of this study was to examine the heat stress effects of three protective clothing ensembles: (1) protective apron over cloth coveralls including full face negative pressure respirator (APRON); (2) the apron over cloth coveralls with respirator plus protective pants (APRON+PANTS); and (3) protective coveralls over cloth coveralls with respirator (PROTECTIVE COVERALLS). In addition, there was a no-respirator ensemble (PROTECTIVE COVERALLS-noR), and WORK CLOTHES as a reference ensemble. Four acclimatized male participants completed a full set of five trials, and two of the participants repeated the full set. The progressive heat stress protocol was used to find the critical WBGT (WBGTcrit) and apparent total evaporative resistance (Re,T,a) at the upper limit of thermal equilibrium. The results (WBGTcrit [°C-WBGT] and Re,T,a [kPa m(2) W(-1)]) were WORK CLOTHES (35.5, 0.0115), APRON (31.6, 0.0179), APRON+PANTS (27.7, 0.0244), PROTECTIVE COVERALLS (25.9, 0.0290), and PROTECTIVE COVERALLS-noR (26.2, 0.0296). There were significant differences among the ensembles. Supporting previous studies, there was little evidence to suggest that the respirator contributed to heat stress.

Negative pressure ventilation and positive pressure ventilation promote comparable levels of ventilator-induced diaphragmatic dysfunction in rats.

BACKGROUND: Mechanical ventilation is a life-saving intervention for patients with respiratory failure. Unfortunately, a major complication associated with prolonged mechanical ventilation is ventilator-induced diaphragmatic atrophy and contractile dysfunction, termed ventilator-induced diaphragmatic dysfunction (VIDD). Emerging evidence suggests that positive pressure ventilation (PPV) promotes lung damage (ventilator-induced lung injury [VILI]), resulting in the release of signaling molecules that foster atrophic signaling in the diaphragm and the resultant VIDD. Although a recent report suggests that negative pressure ventilation (NPV) results in less VILI than PPV, it is unknown whether NPV can protect against VIDD. Therefore, the authors tested the hypothesis that compared with PPV, NPV will result in a lower level of VIDD. METHODS: Adult rats were randomly assigned to one of three experimental groups (n = 8 each): (1) acutely anesthetized control (CON), (2) 12 h of PPV, and (3) 12 h of NPV. Dependent measures included indices of VILI, diaphragmatic muscle fiber cross-sectional area, diaphragm contractile properties, and the activity of key proteases in the diaphragm. RESULTS: Our results reveal that no differences existed in the degree of VILI between PPV and NPV animals as evidenced by VILI histological scores (CON = 0.082 ± 0.001; PPV = 0.22 ± 0.04; NPV = 0.25 ± 0.02; mean ± SEM). Both PPV and NPV resulted in VIDD. Importantly, no differences existed between PPV and NPV animals in diaphragmatic fiber cross-sectional area, contractile properties, and the activation of proteases. CONCLUSION: These results demonstrate that NPV and PPV result in similar levels of VILI and that NPV and PPV promote comparable levels of VIDD in rats.

Cytokine release, small airway injury, and parenchymal damage during mechanical ventilation in normal open-chest rats.

Lung morpho-functional alterations and inflammatory response to various types of mechanical ventilation (MV) have been assessed in normal, anesthetized, open-chest rats. Measurements were taken during protective MV [tidal volume (Vt) = 8 ml/kg; positive end-expiratory pressure (PEEP) = 2.6 cmH(2)O] before and after a 2- to 2.5-h period of ventilation on PEEP (control group), zero EEP without (ZEEP group) or with administration of dioctylsodiumsulfosuccinate (ZEEP-DOSS group), on negative EEP (NEEP group), or with large Vt (26 ml/kg) on PEEP (Hi-Vt group). No change in lung mechanics occurred in the Control group. Relative to the initial period of MV on PEEP, airway resistance increased by 33 +/- 4, 49 +/- 9, 573 +/- 84, and 13 +/- 4%, and quasi-static elastance by 19 +/- 3, 35 +/- 7, 248 +/- 12, and 20 +/- 3% in the ZEEP, NEEP, ZEEP-DOSS, and Hi-Vt groups. Relative to Control, all groups ventilated from low lung volumes exhibited histologic signs of bronchiolar injury, more marked in the NEEP and ZEEP-DOSS groups. Parenchymal and vascular injury occurred in the ZEEP-DOSS and Hi-Vt groups. Pro-inflammatory cytokine concentration in the bronchoalveolar lavage fluid (BALF) was similar in the Control and ZEEP group, but increased in all other groups, and higher in the ZEEP-DOSS and Hi-Vt groups. Interrupter resistance was correlated with indexes of bronchiolar damage, and cytokine levels with vascular-alveolar damage, as indexed by lung wet-to-dry ratio. Hence, protective MV from resting lung volume causes mechanical alterations and small airway injury, but no cytokine release, which seems mainly related to stress-related damage of endothelial-alveolar cells. Enhanced small airway epithelial damage with induced surfactant dysfunction or MV on NEEP can, however, contribute to cytokine production.

Outcome after neonatal continuous negative-pressure ventilation: follow-up assessment.

BACKGROUND: A previous randomised trial of continuous negative extrathoracic pressure (CNEP) versus standard treatment for newborn infants with respiratory distress syndrome raised public concerns about mortality and neonatal morbidity. We studied the outcome in late childhood of children entered into the trial to establish whether there were long-term sequelae attributable to either mode of ventilation. METHODS: Outpatient assessment of neurological outcome, cognitive function, and disability was done by a paediatrician and a psychologist using standardised tests. 133 of 205 survivors from the original trial were assessed at 9-15 years of age. Of the original pairs randomly assigned to each ventilation mode, the results from 65 complete pairs were available. The primary outcome was death or severe disability. FINDINGS: Primary outcome was equally distributed between groups (odds ratio for the CNEP group 1.0; 95% CI 0.41-2.41). In unpaired analysis there was no significant difference between treatment modalities (1.05; 0.54-2.06). Full IQ did not differ significantly between the groups, but mean performance IQ was 6.8 points higher in the CNEP group than in the conventional-treatment group (95% CI 1.5-12.1). Results of neuropsychological testing were consistent with this finding, with scores on language production and visuospatial skills being significantly higher in the CNEP group. INTERPRETATION: We saw no evidence of poorer long-term outcome after neonatal CNEP whether analysis was by original pairing or by unpaired comparisons, despite small differences in adverse neonatal outcomes. The experience of our study indicates that future studies of neonatal interventions with the potential to influence later morbidity should be designed with longer-term outcomes in mind.

Negative-pressure ventilation: is there still a role?

Negative-pressure ventilation (NPV) was the primary mode of assisted ventilation for patients with acute respiratory failure until the Copenhagen polio epidemic in the 1950s, when, because there was insufficient equipment, it was necessary to ventilate patients continually by hand via an endotracheal tube. Thereafter, positive-pressure ventilation was used routinely. Since it was also observed that patients with obstructive sleep apnoea could be treated noninvasively with positive pressure via a nasal mask, noninvasive positive-pressure ventilation (NPPV) has become the most widely used noninvasive mode of ventilation. However, NPV still has a role in the treatment of certain patients. In particular, it has been used to good effect in patients with severe respiratory acidosis or an impaired level of consciousness, patients that to date have been excluded from all prospective controlled trials of NPPV. NPV may be used in those who cannot tolerate a facial mask because of facial deformity, claustrophobia or excessive airway secretion. NPV has also been used successfully in small children, and beneficial effects on the cardiopulmonary circulation maybe a particular advantage in children undergoing complex cardiac reconstructive surgery. This review is divided into two parts: the first is concerned with the use of negative-pressure ventilation in the short term, and the second with its use in the long term.

Análise do efeito das manobras de pressäo negativa e da sustentaçäo máxima da inspiraçäo dos volumes pulmonares / Analysis of negative pressure maneuver effect and the inspiration maxima sustentation in the lung volume

O objetivo deste trabalho foi verificar o efeito das manobras de pressäo negativa (MPN) e compará-la com a sustentaçäo máxima da inspiraçäo (SMI) em pacientes que apresentam diminuiçäo da capacidade vital (CV). Foram estudados 5 pacientes paraplégicos do sexo masculino, com lesäo nível T2-T6, há no mínimo 1 ano e com ausência de patologias pulmonares. Cada participante foi submetido a MPN e SMI aleatoriamente em diferentes dias. Antes e após a terapia foi realizada a espirometria e a mensuraçäo da frequência respiratória e durante a terapia foi registrada a saturaçäo de oxigênio (SatO2) e frequência cardíaca. Na MPN foram realizadas 3 séries de 15 repetiçöes. Todas as técnicas foram feitas com o indíviduo na posiçäo sentada, com duraçäo média de 15 minutos. Os pacientes submetidos a MPN näo apresentaram diferenças espirométricas significativas, porém os pacientes submetidos a SMI apresentaram aumento do volume de reserva inspiratório (VRI), queda do volume de reserva expiratório (VRE), queda do volume corrente (VC) e queda do fluxo inspiratório (VC/Ti). A SatO2 näo variou durante as terapias. A SMI mostrou-se mais efetiva do que a MPN em pacientes com reduçäo da CV.

Hyperventilation induces release of cytokines from perfused mouse lung.

Artificial mechanical ventilation represents a major cause of iatrogenic lung damage in intensive care. It is largely unknown which mediators, if any, contribute to the onset of such complications. We investigated whether stress caused by artificial mechanical ventilation leads to induction, synthesis, and release of cytokines or eicosanoids from lung tissue. We used the isolated perfused and ventilated mouse lung where frequent perfusate sampling allows determination of mediator release into the perfusate. Hyperventilation was executed with either negative (NPV) or positive pressure ventilation (PPV) at a transpulmonary pressure that was increased 2.5-fold above normal. Both modes of hyperventilation resulted in an approximately 1.75-fold increased expression of tumor necrosis factor alpha (TNFalpha) and interleukin-6 (IL-6) mRNA, but not of cyclooxygenase-2 mRNA. After switching to hyperventilation, prostacyclin release into the perfusate increased almost instantaneously from 19 +/- 17 pg/min to 230 +/- 160 pg/min (PPV) or 115 +/- 87 pg/min (NPV). The enhancement in TNFalpha and IL-6 production developed more slowly. In control lungs after 150 min of perfusion and ventilation, TNFalpha and IL-6 production was 23 +/- 20 pg/min and 330 +/- 210 pg/min, respectively. In lungs hyperventilated for 150 min, TNFalpha and IL-6 production were increased to 287 +/- 180 pg/min and more than 1,000 pg/min, respectively. We conclude that artificial ventilation might cause pulmonary and systemic adverse reactions by inducing the release of mediators into the circulation.

Negative extrathoracic pressure ventilation--evaluation of the neck seal.

The effect of the neck seal used in the application of negative extra-thoracic pressure ventilation was studied using near infrared spectroscopy. Changes in cerebral blood volume (CBV) were monitored during discontinuation of negative pressure and during removal of the neck seal. CBV increased by 0.17 ml 100 ml brain-1 (95% CI +0.0875 to +0.481) when negative pressure was discontinued. Removal of the neck seal had no significant effect on CBV. It is concluded that the neck seal does not cause significant jugular venous occlusion.

Sleep-disordered breathing in patients with Duchenne muscular dystrophy using negative pressure ventilators.

We studied the occurrence of nocturnal disordered breathing events and O2 desaturations in 12 patients with late-stage Duchenne muscular dystrophy (DMD) using negative pressure ventilators. We also assessed the effects of O2 supplementation and nasal continuous positive airway pressure (CPAP) on disordered breathing events in selected patients and examined sleep quality in a small subgroup. Average age was 23 + 2 years and FVC was 293 + 33 ml. Eleven of the 12 patients had more than five disordered breathing events per hour during nocturnal monitoring, and the lowest O2 saturation was < 85 percent in nine patients. Nasal O2 (2 L/min) during negative pressure ventilation in four patients did not alter the frequency of disordered breathing events, prolonged the mean and maximum durations of events, and failed to eliminate severe O2 desaturations in two patients. Nasal CPAP was used in two patients during negative pressure ventilation and completely eliminated disordered breathing events in both. Overnight polysomnography during negative pressure ventilation in three patients demonstrated frequent awakenings that fell in frequency following elective tracheostomy in two patients and use of nasal CPAP in one. We conclude that negative pressure ventilation in patients with late-stage DMD is associated with frequent disordered breathing events and severe O2 desaturations in many patients. Concomitant use of O2 supplementation may prolong the events, but a switch to positive pressure ventilation or addition of nasal CPAP is effective therapy.

Induction of sleep apnoea with negative pressure ventilation in patients with chronic obstructive lung disease.

BACKGROUND: Negative pressure ventilation provides intermittent non-invasive ventilatory assistance for patients with advanced chronic obstructive lung disease. Upper airway obstruction during sleep, a reported complication of the technique, may, however, limit its clinical applicability. METHODS: The effects of nocturnal negative pressure ventilation on ventilation and on indices of sleep quality were investigated in five patients with severe chronic obstructive lung disease (mean (SE) FEV1 31% (3%) predicted) who had completed three months of nightly negative pressure ventilation. Subjects underwent overnight polysomnography on consecutive nights, the first night serving as a control and negative pressure ventilation being provided on the second night. Ventilators were adjusted to result in maximum suppression of the peak phasic electromyogram signal from the diaphragm. RESULTS: Negative pressure ventilation resulted in substantial increases in episodes of obstructive apnoea and hypopnoea (mean (SE)/h 59.3 (19.8) v 3.2 (1.3) on control nights). Most obstructive events, however, were associated with under 3% oxygen desaturation, and the lowest recorded values for overnight oxygen saturation were similar on the two study nights. Negative pressure ventilation was also associated with significant increases in the frequencies of movement arousals and changes in sleep stage. CONCLUSIONS: Negative pressure ventilation applied during sleep to patients with advanced chronic obstructive lung disease may result in the development of recurrent episodes of apnoea and hypopnoea as well as altered sleep quality, which could limit its clinical applicability.

Hemodynamic effects of continuous negative chest pressure ventilation in heart failure.

We have previously shown improved cardiac output (QT) with external continuous negative-pressure ventilation (CNPV) compared with continuous positive-pressure ventilation (CPPV) in dogs with low pressure pulmonary edema (1). The current study was done to determine if this effect was reversed in high pressure pulmonary edema. Seven supine, anesthetized dogs were fluid-loaded and treated with disopyramide (3.5 to 7.0 mg/kg) and propranolol (0.25 to 1.5 mg/kg). This produced a mean pulmonary wedge pressure (Ppaw) of 21.0 mm Hg on intermittent positive-pressure ventilation (IPPV). CPPV and CNPV were then alternated at 30-min intervals. Ventilators were matched for oxygen concentration, frequency, tidal volume (VT), and the increment in FRC (delta FRC) produced by a given positive (PEEP) or negative (NEEP) end-expiratory pressure. During 20 cm H2O of PEEP, QT values were significantly depressed from IPPV control values (2.13 +/- 0.2 versus 1.27 +/- 0.2 L/min, p less than 0.05) but not during CNPV with equivalent NEEP (1.66 +/- 0.2 L/min). Although arterial oxygen saturations were similar, mixed venous oxygen saturations were depressed by CPPV with PEEP of 15 and 20 cm H2O (67.9 +/- 3.8% during IPPV versus 54.1 +/- 4.9 and 51.9 +/- 5.8%, respectively, p less than 0.05 in both instances) but not during equivalent CNPV (59.9 +/- 4.3 and 58.7 +/- 4.5%). Despite potentially increased left ventricular afterload, external negative chest wall ventilation with NEEP does not appear to significantly depress QT compared with CPPV even when Ppaw is high and myocardial contractility is impaired.