There is no cephalocaudal gradient of computed tomography densities or lung behavior in supine patients with acute respiratory distress syndrome.

BACKGROUND: There is debate whether pressure transmission within the lungs and alveolar collapse follow a hydrostatic pattern or the compression exerted by the weight of the heart and the diaphragm causes collapse localized in the areas adjacent to these structures. The second hypothesis proposes the existence of a cephalocaudal gradient in alveolar collapse. We aimed to define whether or not lung density and collapse follow a 'liquid-like' pattern with homogeneous isogravitational layers along the cephalocaudal axis in acute respiratory distress syndrome lungs. METHODS: Acute respiratory distress syndrome patients were submitted to full lung computed tomography scans at positive end-expiratory pressure (PEEP) zero (before) and 25 cmH2 O after a maximum-recruitment maneuver. PEEP was then decreased by 2 cmH2 O every 4 min, and a semi-complete scan performed at the end of each PEEP step. RESULTS: Lung densities were homogeneous within each lung layer. Lung density increased along the ventrodorsal axis toward the dorsal region (ß = 0.49, P < 0.001), while there was no increase, but rather a slight decrease, toward the diaphragm along the cephalocaudal axis and toward the heart. Higher PEEP attenuated density gradients. At PEEP 18 cmH2 O, dependent lung regions started to collapse massively, while best compliance was only reached at a lower PEEP. CONCLUSIONS: We could not detect cephalocaudal gradients in lung densities or in alveolar collapse. Likely, external pressures applied on the lung by the chest wall, organs, and effusions are transmitted throughout the lung in a hydrostatic pattern with homogeneous consequences at each isogravitational layer. A single cross-sectional image of the lung could fully represent the heterogeneous mechanical properties of dependent and non-dependent lung regions.

Real-time ventilation and perfusion distributions by electrical impedance tomography during one-lung ventilation with capnothorax.

BACKGROUND: Carbon dioxide insufflation into the pleural cavity, capnothorax, with one-lung ventilation (OLV) may entail respiratory and hemodynamic impairments. We investigated the online physiological effects of OLV/capnothorax by electrical impedance tomography (EIT) in a porcine model mimicking the clinical setting. METHODS: Five anesthetized, muscle-relaxed piglets were subjected to first right and then left capnothorax with an intra-pleural pressure of 19 cm H2 O. The contra-lateral lung was mechanically ventilated with a double-lumen tube at positive end-expiratory pressure 5 and subsequently 10 cm H2 O. Regional lung perfusion and ventilation were assessed by EIT. Hemodynamics, cerebral tissue oxygenation and lung gas exchange were also measured. RESULTS: During right-sided capnothorax, mixed venous oxygen saturation (P = 0.018), as well as a tissue oxygenation index (P = 0.038) decreased. There was also an increase in central venous pressure (P = 0.006), and a decrease in mean arterial pressure (P = 0.045) and cardiac output (P = 0.017). During the left-sided capnothorax, the hemodynamic impairment was less than during the right side. EIT revealed that during the first period of OLV/capnothorax, no or very minor ventilation on the right side could be seen (3 ± 3% vs. 97 ± 3%, right vs. left, P = 0.007), perfusion decreased in the non-ventilated and increased in the ventilated lung (18 ± 2% vs. 82 ± 2%, right vs. left, P = 0.03). During the second OLV/capnothorax period, a similar distribution of perfusion was seen in the animals with successful separation (84 ± 4% vs. 16 ± 4%, right vs. left). CONCLUSION: EIT detected in real-time dynamic changes in pulmonary ventilation and perfusion distributions. OLV to the left lung with right-sided capnothorax caused a decrease in cardiac output, arterial oxygenation and mixed venous saturation.

N-terminal-pro-brain natriuretic peptide as a haemodynamic marker in idiopathic pulmonary arterial hypertension.

Patients with idiopathic pulmonary arterial hypertension usually undergo acute vasodilator tests with nitric oxide (NO) for haemodynamic evaluation and therapeutical planning. The aim of this study was to evaluate the link between the variation of N-terminal (NT)-pro-brain natriuretic peptide (BNP) levels and haemodynamic parameters during the acute vasodilator test. A total of 22 idiopathic pulmonary arterial hypertension patients who underwent acute vasodilator tests were studied. Blood samples were collected at baseline and after 30 and 60 min of NO inhalation. NT-pro-BNP levels were measured in each sample. A receiver-operating characteristic curve was used to evaluate the capability of the NT-pro-BNP level variation during NO inhalation in recognising nonresponders. To distinguish responders from nonresponders, the increase of the NT-pro-BNP (0% as cut-off value) determined a 50% specificity and 100% sensitivity (positive predictive value of 38% and a negative predictive value of 100%). These results suggest that N-terminal-pro-brain natriuretic peptide was able to distinguish nonresponder patients with the acute vasodilator test. N-terminal-pro-brain natriuretic peptide may be an interesting additional biological tool in the evaluation of idiopathic pulmonary arterial hypertension patients.

Effects of tracheotomy on respiratory mechanics in spontaneously breathing patients.

Tracheotomy is a method of intubating the trachea, which is employed in several clinical settings, including the treatment of head and neck neoplasms. Tracheotomy is believed to facilitate weaning through changes in respiratory mechanics. Existing information concerning functional changes associated with tracheotomy are limited to comparisons with orotracheal intubation. In this study, respiratory mechanics were monitored in seven spontaneously breathing patients, before and after an elective tracheotomy was performed for surgical treatment of cancer. Campbell diagrams were constructed by plotting pressure, obtained with an oesophageal balloon catheter, against volume, obtained from a pneumotachograph placed at the airway opening. Work of breathing was calculated as the internal area of the Campbell diagram and was partitioned into its elastic and inspiratory and expiratory resistive components. Oesophageal pressure was also used to quantify intrinsic positive end-expiratory pressure (PEEPi) and the pressure-time product (PTP), which is considered to be proportional to the oxygen cost of breathing. PTP was divided into its resistive and elastic components. Inspiratory resistive work, PEEPi, inspiratory PTP, as well as its resistive and elastic components were significantly reduced by tracheotomy. Tracheotomy significantly reduces work of breathing and pressure-time product in spontaneously breathing patients.

Interação cardiopulmonar durante a ventilação mecânica / Cardiopulmonary interaction during mechanical ventilation

As interaçöes cardiopulmonares durante a ventilação mecânica são complexas e dependem do estado volêmico do paciente (hipovolemia, normovolemia e hipervolemia), das funçöes dos ventrículos direito e esquerdo, assim como de sua pós-carga, do estado funcional dos pulmöes (normal, restritivo, ou obstrutivo) e da complacência do sistema toracoabdominal. Nos estados hipovolêmicos, a adição de pressão positiva intratorácica prporciona diminuição do retorno venoso e conseqüente dominuição do débito cardíaco. Esse efeito encontr-se exacerbado nas disfunçöes do ventrículo direito presentes no tromboembolismo pulmonar e na doença pulmonar obstrutiva crônica e, em menor grau, do ventrículo esquerdo. Nos estados de hipervolemia, a pré-carga de ambos os ventrículos está aumentada. Quando a pressão capilar pulmonar ultrapassa 18 mmHg em pulmöes normais ocorre o extravasamento de líquido para o interstício pulmonar e interior dos alvéolos. Esse efeito está exacerbado nas alteraçöes de permeabilidade da membrana alveolocapilar (síndrome do desconforto respiratório agudo). Nos estados hipervolêmicos, a adição de pressão intratorácica positiva não costuma ocasionar a diminuição do débito cardíaco. Nas disfunçöes de ventrículo esquerdo com pressão capilar acima de 18 mmHg, a adição de pressão intratorácica positiva mantém os alvéolos abertos, melhorando a oxigenação e diminuição a pós-carga do ventrículo esquerdo, o que proporciona a melhora do desempenho ventricular. Assim observando-se e compreendendo-se essas complexas interaçöes cardiopulmonares, poderemos otimizar as condiçöes cardiorrespiratórias nas diferentes situaçöes clínicas.

Chronic amiodarone ingestion induces pulmonary toxicity in rats

Patients who receive amiodarone may develop interstitial pulmonary disease. The objective of the present study was to develop an experimental model of interstitial pulmonary disease in rats based on the chronic oral administration of amiodarone diluted in water ad libitum. A total of 97 three-month old male. Wistar rats weighing 133-167g (control and intoxicated) were studied after daily administration of amiodarone (about 50 mg/Kg) for 3 weeks and 3,6, and 13 months. We carried out conventional histopathologic evaluation, morphometric studies of the alveolar wall, transmission electron microscopy measurement of pulmonary volumes and forced expiratory flows, and computed respiratory system resistance and elastance during spontaneous breath cycles. Chronic ingestion of amiodarone by rats produced pulmonary disease that started as a phospholipidosis, as early 3 weeks after the use of the drug. After 6, and mainly after 13 months, a focal inflammatory reation with reactive alveolar epithelium was observed . Signals of a comcomitant repair process were also present, but fibrosis was visible only by electron microscopy. The physiologic dysfunction could be identified after 13 months; expiratory flow (ml/sec) limitation and an increased respiratory system elastance (cmH2O/ml) were the main functional changes, respectively 10.8 (forced expiratory mean flow between 0-25 per cent of forced vital capacity) and 5.36 in treated animals vs 13.3 and 3.65 in controls, reported as mean + SD for 6 animals in each group. A body of evidence suggests that amiodarone may cause changes in lung phospholipid metabolism that may be responsible for a part of the functional derangement observed in this study.

Estenose bronquica de etiologia tuberculosa: patogenia e tratamento / Bronchial stenosis of tuberculous etiology: pathogenesis and treatment

Descrevemos quatro casos de estenose bronquica, uma complicacao rara de tuberculose pulmonar. No primeiro caso, uma mulher de 18 anos, sem tratamento previo para tuberculose, apresentou estenose bronquica como resultado da cicatrizacao de complexo primario. Nao havia lesao de parenquima ao raio X. Nos outros tres pacientes a estenose bronquica foi atribuida a tuberculose ativa com pesquisa positiva para bacilo alcool-acido resistente em escarro. Estes receberam tratamento para tuberculose. Em um deles isto foi suficiente para a resolucao da estenose, mas nos outros dois pacientes ocorreu estenose bronquica devido a fibrose.