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).

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).

Edema pulmonar por presión negativa tras cirugía de hernia de disco cervical / Negative pressure pulmonary edema following cervical disc hernia surgery

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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.

Edema pulmonar por presión negativa tras septoplastia / Negative pressure pulmonary oedema after septoplasty

El edema pulmonar por presión negativa (NPPE) es una complicación anestésica por obstrucción aguda de la vía aérea superior, su principal causa es el laringoespasmo. La fisiopatología radica en una marcada presión negativa intrapleural durante una inspiración contra glotis cerrada, la cual desencadena una presión excesiva en la microvasculatura pulmonar. El diagnóstico puede ser difícil, su reconocimiento ayuda a minimizar la morbimortalidad. En este artículo se presenta un caso de NPPE por laringoespasmo postextubación (AU)

Negative pressure pulmonary oedema (NPPO) is an anaesthetic complication due to acute obstruction of the upper airway, whose main cause is laryngospasm. The pathophysiology involves a strong negative intrapleural pressure during inspiration against a closed glottis, which triggers excessive pressure in the pulmonary microvasculature. Although its diagnosis can be difficult, its recognition helps to minimise morbidity and mortality. This article presents a case of NPPO due to postextubation laryngospasm (AU)

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.

Edema pulmonar por presión negativa: a propósito de 3 casos / Negative pressure pulmonary edema: 3 cases report

El edema agudo pulmonar por presión negativa esuna complicación descrita desde 1977 tras la obstrucciónde la vía aérea respiratoria, tanto en niños comoen adultos. Aunque su etiopatogenia es multifactorial,destaca especialmente la excesiva presión intratorácicanegativa causada por la inspiración forzada espontáneade un paciente con la glotis cerrada, que resultaen trasudación de líquido de los capilares pulmonareshacia el espacio alveolointersticial. El edema pulmonarresultante puede aparecer en pocos minutos tras laobstrucción de la vía aérea o de forma diferida al cabode varias horas. Este cuadro clínico es potencialmentegrave, pero habitualmente responde bien al tratamientocon oxigenoterapia, ventilación mecánica a presiónpositiva y diuréticos. Es importante el diagnóstico desospecha para adecuar el tratamiento con presteza.Presentamos nuestra experiencia en 3 casos clínicoscon edema agudo pulmonar por presión negativa

Negative pressure pulmonary edema is a complication, ;;described since 1977, caused by upper airway ;;obstruction in both children and adults. ;;Although its aetiopathogeny is multifactorial, especially ;;outstanding is excessive negative intrathoracic ;;pressure caused by the forced spontaneous inspiration ;;of a patient against a closed glottis, that causes ;;high arteriole and capillary fluid pressures that favor ;;transudation into the alveolar space The resulting ;;pulmonary edema can appear a few minutes after the ;;obstruction of the airway or in a deferred way after ;;several hours. The clinical manifestations are potentially ;;serious, but normally respond well to treatment ;;with supplemental oxygen, positive pressure ;;mechanical ventilation and diuretics. Diagnostic suspicion ;;is important for acting promptly. We report ;;three clinical cases with acute negative pressure pulmonary ;;edema

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.