Fisiología respiratoria. Neumología de altura: saturación de oxígeno, edema pulmonar y pruebas de función pulmonar / Respiratory physiology - High -altitude pneumology: oxygen saturation, pulmonary edema and pulmonary function tests

En las alturas, sobre todo a 2500 metros sobre el nivel del mar, la cantidad absoluta de oxígeno va decreciendo y por lo tanto la cantidad disponible para el intercambio gaseoso disminuye, produciéndose una vasoconstricción hipóxica pulmonar (VHP). La VHP asociada a la hipoxia hipobárica de la altura produce un aumento de la presión pulmonar que es mayor en los lactantes y a mayores alturas. No hay valores únicos de saturación de oxígeno (SatO2) en la altura, porque ésta va disminuyendo según el mayor nivel de altura, aumenta con la edad, y la brecha entre la vigilia y sueño es grande (sobre todo en los primeros meses de vida). El 25% de los niños sanos que viven en altura tienen valores de SatO2 significativamente menores que el 75% restante. Los valores normales de los índices de apnea/hipopnea son distintos a los de nivel del mar. El edema pulmonar de las alturas es una patología frecuente, que se produce por un incremento desproporcionado en la VHP reflejando una hiperactividad del lecho vascular pulmonar ante la exposición aguda a la hipoxia hipobárica. Tiene cuatro fenotipos, es infrecuente en menores de 5 años y rara vez es mortal, la sospecha clínica y el manejo oportuno con oxigeno es la clave. Finalmente, en la altura los valores normales de la función pulmonar de la espirometría, oscilometría de impulso y capacidad de difusión son distintos que a nivel del mar.

At high altitude, especially > 2,500 meters above sea level, the absolute amount of oxygen decreases and therefore the amount available for gas exchange decreases, producing hypoxic pulmonary vasoconstriction (VHP). VHP associated with high-altitude hypobaric hypoxia produces an increase in pulmonary pressure that is greater in infants and at higher altitudes. There are no single values of oxygen saturation (SatO2) at altitude, because it decreases with the highest level of altitude, increases with age, and the gap between wakefulness and sleep is large (especially in the first months of life). Around 25% of healthy children living at altitude have SatO2 values significantly lower than the remaining 75%. The normal values of the apnea/hypopnea indices are different from those at sea level. High altitude pulmonary edema is a frequent pathology that is produced by a disproportionate increase in VHP reflecting hyperactivity of the pulmonary vascular bed in the face of acute exposure to hypobaric hypoxia, it has four phenotypes, it is uncommon in children under 5 years of age, and it is rarely fatal, the clinical suspicion and timely management with oxygen is the key. Finally, at high altitude, the normal values of lung function from spirometry, impulse oscillometry, and diffusing capacity are different from those at sea level.

Tiger stripes sign in acute coronary syndrome / Signo manchas de tigre en síndrome coronario agudo

Abstract The incidence of mitral regurgitation in acute myocardial syndromes is variable. Echocardiographic evaluation is fundamental in making a proper diagnosis of mechanical complications and to offer timely treatment. We present a case of a 64-year-old male who was admitted to the ER in acute pulmonary edema. The electrocardiogram showed negative ST-segment deviation from V4-V6, positive ST-segment deviation in aVR. Multivessel disease with severe mitral regurgitation was seen in catheterization. A transthoracic echocardiogram revealed important mitral regurgitation showing the "tiger stripes" sign, seen in the presence of intracardial oscillating structures, in this case, suspected papillary muscle rupture. Echocardiographic evaluation is necessary in every case of myocardial infarction who present with new-onset mitral regurgitation. Treatment is complex and must be determined with an interdisciplinary group.

Edema pulmonar de reexpansão na doença pleural / Re-expansion pulmonary edema in pleural disease

O edema pulmonar de reexpansão é uma condição clínica rara, porém frequentemente letal. É uma complicação secundária à rápida reexpansão do pulmão colapsado em consequência a um pneumotórax ou derrame pleural de grande volume. São de fundamental importância para sua prevenção, o conhecimento da etiopatogenia e a execução de técnica adequada na drenagem pleural tubular e na toracocentese. A sua patogênese é multifatorial. O esvaziamento lento da cavidade pleural, a monitorização da oximetria e administração de oxigênio são necessários para prevenção e tratamento. AU

The reexpansion pulmonary edema (RPE) is a rare clinical condition, but often lethal. It is a secondary complication to the rapid re-expansion of the lung collapsed as a result of a pneumothorax or pleural effusion of large volume. The fundamental importance for prevention are knowledge of the pathogenesis and executing proper technique on pleural drainage and thoracentesis. Its pathogenesis is multifactorial. Its prevention is still based on slow pleuralemptying procedures, without standards to avoid RPEevolution. The oximetry monitoring and administration of oxygen are needed for treatment. AU

Hipertensión y edema pulmonar de altura: Rol de la disfunción endotelial y de la programación fetal / Pulmonary hypertensión and lung edema at high altitude: Role of endothelial dysfunction and fetal programming

La altura constituye un fascinante laboratorio natural para la investigación médica. Si bien al principio el objetivo de la investigación en la altura fue la comprensión de los mecanismos de adaptación del organismo a la hipoxia y la búsqueda de tratamientos para las enfermedades relacionadas con la altura, durante la última década el alcance de esta investigación se ha ampliado considerablemente. Dos importantes observaciones han generado las bases para el crecimiento del alcance científico de la investigación en la altura. Primero, el hecho de que el edema pulmonar agudo de la altura constituye un modelo único para estudiar los mecanismos fundamentales de la hipertensión pulmonar y el edema pulmonar en humanos. Segundo, que la hipoxia ambiental asociada con la exposición a la altura facilita la detección de disfunción vascular pulmonar y sistémica en un estadio precoz. Aquí revisaremos los estudios que, capitalizando estas observaciones, han llevado a la descripción de nuevos mecanismos subyacentes del edema pulmonar y de la hipertensión pulmonar, y a la primera demostración directa de la existencia de una programación fetal sobre la disfunción vascular en humanos.

High altitude constitutes an exciting natural laboratory for medical research. While initially, the aim of high-altitude research was to understand the adaptation of the organism to hypoxia and find treatments for altitude-related diseases, over the past decade or so, the scope of this research has broadened considerably. Two important observations led to the foundation for the broadening of the scientific scope of high-altitude research. First, high-altitude pulmonary edema (HAPE) represents a unique model which allows studying fundamental mechanisms of pulmonary hypertension and lung edema in humans. Secondly, the ambient hypoxia associated with high-altitude exposure facilitates the detection of pulmonary and systemic vascular dysfunction at an early stage. Here, we review studies that, by capitalizing on these observations, have led to the description of novel mechanisms underpinning lung edema and pulmonary hypertension and to the first direct demonstration of fetal programming of vascular dysfunction in humans.

Echocardiographic parameters associated with pulmonary congestion in outpatients with Chagas' cardiomyopathy and non-chagasic cardiomyopathy / Parâmetros ecocardiográficos associados com a congestão pulmonar nas miocardiopatias chagásica e não-chagásica

INTRODUCTION: Despite significant left ventricular (LV) systolic dysfunction and cardiomegaly, pulmonary congestion does not seem to be a major finding in Chagas' cardiomyopathy (CC). This study sought to identify echocardiographic parameters associated with pulmonary congestion in CC and in dilated cardiomyopathy of other etiologies, such as non-CC (NCC), and to compare pulmonary venous hypertension between the two entities. METHODS: A total of 130 consecutive patients with CC and NCC, with similar echocardiographic characteristics, were assessed using Doppler echocardiography and chest radiography. Pulmonary venous vessel abnormalities were graded using a previously described pulmonary congestion score, and this score was compared with Doppler echocardiographic parameters. RESULTS: NCC patients were older than CC patients (62.4 ± 13.5 × 47.8 ± 11.2, p = 0.00), and there were more male subjects in the CC group (66.2% × 58.5%, p = 0.4). Pulmonary venous hypertension was present in 41 patients in the CC group (63.1%) and in 63 (96.9%) in the NCC group (p = 0.0), the mean lung congestion score being 3.2 ± 2.3 and 5.9 ± 2.6 (p = 0.0), respectively. On linear regression multivariate analysis, the E/e' ratio (β = 0.13; p = 0.0), LV diastolic diameter (β = 0.06; p = 0.06), left atrial diameter (β = 0.51; p = 0.08), and right ventricular (RV) end-diastolic diameter (β = 0.02; p = 0.48) were the variables that correlated with pulmonary congestion in both groups. CONCLUSIONS: Pulmonary congestion was less significant in patients with CC. The degree of LV of systolic and diastolic dysfunction and the RV diameter correlated with pulmonary congestion in both groups. The E/e' ratio was the hallmark of pulmonary congestion in both groups.

INTRODUÇÃO: Na miocardiopatia chagásica, ocorre uma discrepância entre os achados de disfunção ventricular e uma menor magnitude de congestão pulmonar em relação a outras miocardiopatias. Foram associados parâmetros morfofuncionais ecocardiográficos com achados de congestão pulmonar à radiografia do tórax em pacientes portadores de miocardiopatia chagásica e não chagásica, sendo a intensidade dos achados radiológicos comparada nos dois grupos. MÉTODOS: Foram recrutados 130 pacientes portadores de miocardiopatia chagásica e não chagásica, tendo os dois grupos parâmetros ecocardiográficos semelhantes. Todos realizaram o estudo radiológico do tórax, sendo atribuída uma pontuação aos achados sugestivos de congestão pulmonar, conforme escore já previamente estabelecido, sendo este comparado com os achados ecocardiográficos de disfunção ventricular. RESULTADOS: Os pacientes não chagásicos eram mais idosos (62,4±13,5 x 47,8±11,2, p=0,0), havendo um predomínio do sexo feminino nos chagásicos (66,2% x 58,5%, p=0,4). A hipertensão venocapilar pulmonar esteve presente em 41 chagásicos (63,1%) e 63 (96,9%) não-chagásicos (p=0,0), com escore da congestão pulmonar de 3,2±2,3 e 5,9±2,6 (p=0,0) respectivamente. Na análise de regressão linear, a relação E/e' (β=0,13; p=0,0), o diâmetro diastólico do ventrículo esquerdo (β=0,06; p=0,06), o diâmetro do átrio esquerdo (β=0,51; p=0,08) e o diâmetro diastólico final do ventrículo direito (β=0,02; p=0,48) foram as variáveis que mais se associaram com a congestão pulmonar nos dois grupos. CONCLUSÕES: Os pacientes chagásicos apresentaram um menor grau de congestão pulmonar. Os parâmetros de disfunção sistólica e diastólica associaram com a intensidade da congestão pulmonar, sendo a relação E/e' a variável que mais determinou a congestão pulmonar nos dois grupos.

Echocardiographic parameters associated with pulmonary congestion in Chagas cardiomyopathy / Parâmetros ecocardiográficos associados com a congestão pulmonar na miocardiopatia chagásica

INTRODUCTION: Discrepancy between the intensity of pulmonary congestion and the grade of cardiomegaly seems to be a common finding of Chagas cardiomyopathy, in spite of significant systolic dysfunction of the left ventricle. Its mechanism has not been established. The aim of this study was to investigate pulmonary congestion and to analyze if it correlated with Doppler echocardiographic parameters in patients with Chagas dilated cardiomyopathy. METHODS: Fifty-five patients with positive serology tests for Trypanosoma cruzi and Chagas dilated cardiomyopathy were studied. Chest x-rays, Doppler echocardiogram and plasmatic brain natriuretic peptide levels were obtained in all patients. The degree of pulmonary venous vessels changes on chest x-ray was graded using a pulmonary congestion score, and then compared to Doppler echocardiographic parameters. RESULTS: Mean age was 48.5 ± 11.2 years and 29 percent were women. The majority (95 percent) of patients were in NYHA functional class I and II. Mild pulmonary congestion by chest x-ray was found in 80 percent of the patients. In a multivariate analysis, left ventricular ejection fraction, right ventricular TEI index and the color M-mode velocity correlated with the degree of pulmonary congestion. CONCLUSIONS: Pulmonary venous changes on chest x-rays are frequent, but usually mild in patients with Chagas dilated cardiomyopathy. The degree of pulmonary congestion correlates with Doppler echocardiographic left and right ventricular dysfunction and with color M-mode velocity.

INTRODUÇÃO: Na miocardiopatia chagásica, é considerado haver uma menor intensidade de congestão pulmonar, mesmo na vigência de disfunção ventricular esquerda importante, não havendo ainda explicação definitiva para este fenômeno. O objetivo deste estudo foi de investigar a presença de congestão pulmonar na miocardiopatia chagásica e analisar se a intensidade da congestão esteve associada com parâmetros morfofuncionais ecocardiográficos de disfunção cardíaca. MÉTODOS: Cinquenta e cinco pacientes com sorologia positiva para o Trypanosoma cruzi e portadores de miocardiopatia chagásica foram estudados. Todos os pacientes foram submetidos ao estudo radiológico do tórax, ecocardiograma e dosagem plasmática do peptídeo natriurético cerebral. O grau de congestão pulmonar foi quantificado através de um escore da congestão pulmonar, e então comparado com os parâmetros ecocardiográficos. RESULTADOS: A idade média foi de 48.5 ± 1.2 anos e 29 por cento eram mulheres. A maior (95 por cento) parte dos pacientes encontrava-se na classe funcional I e II. Discreta congestão pulmonar à radiografia do tórax foi encontrada em 80 por cento dos pacientes. Na análise multivariada, a fração de ejeção do ventrículo esquerdo, o índice de TEI do ventrículo direito e a velocidade ao color M mode foram as variáveis que mais estiveram associadas com o grau de congestão pulmonar. CONCLUSÕES: Nos pacientes com miocardiopatia chagásica, as alterações do fluxo venoso pulmonar foram frequentes, porém discretas. O grau de congestão pulmonar associou com parâmetros ecocardiográficos de disfunção ventricular esquerda e direita e com a velocidade do color M mode.

Effects of pneumonectomy on nitric oxide synthase expression and perivascular edema in the remaining lung of rats

Pneumonectomy is associated with high mortality and high rates of complications. Postpneumonectomy pulmonary edema is one of the leading causes of mortality. Little is known about its etiologic factors and its association with the inflammatory process. The purpose of the present study was to evaluate the role of pneumonectomy as a cause of pulmonary edema and its association with gas exchange, inflammation, nitric oxide synthase (NOS) expression and vasoconstriction. Forty-two non-specific pathogen-free Wistar rats were included in the study. Eleven animals died during or after the procedure, 21 were submitted to left pneumonectomy and 10 to sham operation. These animals were sacrificed after 48 or 72 h. Perivascular pulmonary edema was more intense in pneumonectomized rats at 72 h (P = 0.0131). Neutrophil density was lower after pneumonectomy in both groups (P = 0.0168). There was higher immunohistochemical expression of eNOS in the pneumonectomy group (P = 0.0208), but no statistically significant difference in the expression of iNOS. The lumen-wall ratio and pO2/FiO2 ratio did not differ between the operated and sham groups after pneumonectomy. Left pneumonectomy caused perivascular pulmonary edema with no elevation of immunohistochemical expression of iNOS or neutrophil density, suggesting the absence of correlation with the inflammatory process or oxidative stress. The increased expression of eNOS may suggest an intrinsic production of NO without signs of vascular reactivity.

Investigation of the Cause of Readmission to the Intensive Care Unit for Patients with Lung Edema or Atelectasis

PURPOSE: For patients with acute respiratory failure due to lung edema or atelectasis, Surplus lung water that is not removed during an initial stay in the Intensive Care Unit (ICU) may be related to early ICU readmission. Therefore, we performed a retrospective study of patient management during the first ICU stay for such patients. MATERIALS AND METHODS: Of 1,835 patients who were admitted to the ICU in the 36 months from January, 2003 to December, 2005, 141 were patients readmitted, and the reason for readmission was lung edema or atelectasis in 21 patients. For these 21 patients, correlations were investigated between body weight gain at the time of initial ICU discharge (weight upon discharge from the ICU ÷ weight when entering the ICU) and the time to ICU readmission, between body weight gain and the P/F ratio at ICU readmission, between the R/E ratio (the period using a respirator (R) ÷ the length of the ICU stay after extubation (E)) and the time to ICU readmission, between the R/E ratio and body weight gain, and between body weight gain until extubation and the time to extubation. RESULTS: A negative linear relationship was found between body weight gain at the time of initial ICU discharge and the time to ICU readmission, and between body weight gain at the time of ICU discharge and the P/F ratio at ICU readmission. If body weight had increased by more than 10% at ICU discharge or the P/F ratio was below 150, readmission to the ICU within three days was likely. Patients with a large R/E ratio, a large body weight gain, and a worsening P/F ratio immediately after ICU discharge were likely to be readmitted soon to the ICU. Loss of body weight during the period of respirator support led to early extubation, since a positive correlation was found between the time to extubation and body weight gain. CONCLUSION: Fluid management failure during the first ICU stay might cause ICU readmission for patients who had lung edema or atelectasis. Therefore, a key to the prevention of ICU readmission is to ensure complete recovery from lung failure before the initial ICU discharge. Strict water management is crucial based on body weight measurement and removal of excess lung water is essential. In addition, an apparent improvement in respiratory state may be due to respiratory support, and such an improvement should be viewed cautiously. Loss of weight at the refilling stage of transfusion prevents ICU readmission and may decrease the length of the ICU stay.

The extracellular matrix of the lung and its role in edema formation

The extracellular matrix is composed of a three-dimensional fiber mesh filled with different macromolecules such as: collagen (mainly type I and III), elastin, glycosaminoglycans, and proteoglycans. In the lung, the extracellular matrix has several functions which provide: 1) mechanical tensile and compressive strength and elasticity, 2) low mechanical tissue compliance contributing to the maintenance of normal interstitial fluid dynamics, 3) low resistive pathway for an effective gas exchange, d) control of cell behavior by the binding of growth factors, chemokines, cytokines and the interaction with cell-surface receptors, and e) tissue repair and remodeling. Fragmentation and disorganization of extracellular matrix components comprises the protective role of the extracellular matrix, leading to interstitial and eventually severe lung edema. Thus, once conditions of increased microvascular filtration are established, matrix remodeling proceeds fairly rapidly due to the activation of proteases. Conversely, a massive matrix deposition of collagen fiber decreases interstitial compliance and therefore makes the tissue safety factor stronger. As a result, changes in lung extracellular matrix significantly affect edema formation and distribution in the lung.

A matriz extracelular é um aglomerado tridimensional demacromoléculas composta por: fibras colágenas (principalmente, tipos I e III), elastina, glicosaminoglicanos e proteoglicanos. No pulmão, a matriz extracelular tem várias funções, tais como: 1) promover estresse tensil e elasticidade tecidual, 2) contribuir para a manutenção da dinâmica de fluidos no interstício, 3) propiciar efetiva troca gasosa, 4) controlar a função celular através de sua ligação com fatores de crescimento, quimiocinas, citocinas e interação com receptores de superfície, e 5) remodelamento e reparo tecidual. A fragmentação e a desorganização da matriz extracelular pode acarretar edema intersticial e, eventualmente, edema alveolar grave. Logo, quando há aumento da filtração microvascular ocorre rápido remodelamento da matriz por ativação de proteases. Destarte, a deposição de fibras colágenas reduz a complacência intersticial limitando o edema. Em conclusão, modificações na matriz extracelular podem afetar a formação e distribuição do edema no pulmão.

Edema pulmonar de altura: Modelo de estudio de la fisiopatología del edema pulmonar y de la hipertensión pulmonar hipóxica en humanos / High altitude pulmonary edema. An experiment of Nature to study the underlying mechanisms of hypoxic pulmonary hypertension and pulmonary edema in humans

La altura, fascinante laboratorio natural de investigación médica, provee resultados con importantes implicancias para la comprensión de enfermedades que afectan a millones de personas que viven en ella, asi como para el tratamiento de enfermedades ligadas a la hipoxemia en pacientes que viven en baja altitud. El edema pulmonar de altura (EPA) es una entidad que pone en peligro la vida y que ocurre en sujetos predispuestos pero sanos. Esto permite estudiar los mecanismos subyacentes del edema pulmonar en humanos, sin la presencia de factores que presten a la confusión como enfermedades concomitantes. El EPA resulta de la conjunción de dos defectos mayores: acumulación de líquido en el espacio alveolar debido a una hipertensión pulmonar hipóxica exagerada, y alteración en la eliminación del mismo por un defecto en el transporte transepitelial alveolar de sodio. En esta revisión, describimos brevemente las características clínicas y revisaremos este novedoso concepto. Proveemos evidencia experimental de como la síntesis alterada de óxido nítrico y/o la disminución de su biodisponibilidad representan el defecto central que predispone a la vasoconstricción pulmonar hipóxica exagerada y a la acumulación de líquido en el espacio alveolar. Mostramos que la hipertensión pulmonar hipóxica exagerada, per se, no es suficiente para producir un EPA, y que una alteración en la eliminación del fluido del espacio alveolar representa un segundo mecanismo fisiopatológico importante. Finalmente, describimos cómo los nuevos aportes obtenidos de los estudios del EPA pueden ser trasladados al manejo de otros estados patológicos ligados a la hipoxemia.

High altitude constitutes an exciting natural laboratory for medical research. Over the past decade, it has become clear that the results of high-altitude research may have important implications not only for the understanding of diseases in the millions of people living permanently at high altitude, but also for the treatment of hypoxemia-related disease states in patients living at low altitude. High-altitude pulmonary edema (HAPE) is a life-threatening condition occurring in predisposed, but otherwise healthy subjects, and, therefore, allows to study underlying mechanisms of pulmonary edema in humans, in the absence of confounding factors. Over the past decade, evidence has accumulated that HAPE results from the conjunction of two major defects, augmented alveolar fluid flooding resulting from exaggerated hypoxic pulmonary hypertension, and impaired alveolar fluid clearance related to defective respiratory transepithelial sodium transport. Here, after a brief presentation of the clinical features of HAPE, we review this novel concept. We provide experimental evidence for the novel concept that impaired pulmonary endothelial and epithelial nitric oxide synthesis and/or bioavailability may represent the central underlying defect predisposing to exaggerated hypoxic pulmonary vasoconstriction and alveolar fluid flooding. We demonstrate that exaggerated pulmonary hypertension, while possibly a condition sine qua non, may not be sufficient to cause HAPE, and how defective alveolar fluid clearance may represent a second important pathogenic mechanism. Finally, we outline how this insight gained from studies in HAPE may be translated into the management of hypoxemia related disease states in general.

O Treinamento físico por natação atenua o remodelamento miocárdico e congestão pulmonar em ratas wistar com insuficiência cardíaca secundária a infarto do miocárdio / Swim training attenuates myocardial remodeling and the pulmonary congestion in wistar rats with secondary heart failure to myocardial infarction

OBJETIVO: Avaliar os efeitos da natação sobre teor de água pulmonar de ratas com insuficiência cardíaca (IC) após infarto do miocárdio (IM). MÉTODOS: Após oclusão coronária, animais com 20 por cento 40 por cento do VE grandes. Os animais treinados (TR) nadaram durante 60 min/dia, 5 dias/semana, durante 8 semanas. Foram determinados os pesos úmidos do pulmão direito, lobo direito do fígado, átrios, VE e ventrículo direito (VD) e os pesos secos do fígado e pulmão. Utilizou-se ANOVA e teste de Tukey para as análises estatísticas. RESULTADOS: Verificou-se aumento da relação massa dos átrios/peso corpóreo nos animais sedentários com IM moderados (IMmod-SED: n=8) e grandes (IMgr-SED: n=10) em relação às ratas controles sedentárias (C-SED: n=14) e treinadas (C-TR: n=16). Aumento da relação VD/peso corpóreo e VE/peso corpóreo nos animais IMgr-SED em relação aos controles. A relação coração/peso corpóreo foi maior nos IMgr-SED do que nos demais. Os animais infartados treinados exibiram atenuação da hipertrofia. O teor de água pulmonar maior (p<0,05) nas ratas IMgr-SED (x±epm: 81±0,4 por cento) do que nas C-SED (79±0,4 por cento) indicou congestão pulmonar não verificada nas infartadas treinadas (IMmod-TR: 80±0,6 por cento; IMgr-TR: 79±0,7 por cento). CONCLUSÃO: Os aumentos da massa cardíaca e teor de água pulmonar em animais IMgr-SED foram atenuados em animais submetidos a treinamento físico por natação, sugerindo que a realização de exercício físico pode atenuar os indicadores de IC e contribuir para remodelamento cardíaco favorável.

Injuria pulmonar aguda post-resección pulmonar / Acute lung injury post pulmonar resection

Antecedentes: La injuria pulmonar aguda post-resección pulmonar es una complicación grave y de mal pronóstico que aparece en el postoperatorio inmediato de la cirugía de resección pulmonar. Objetivos: Presentación de 3 casos clínicos de injuria pulmonar aguda post-resección pulmonar con revisión de los posibles mecanismos fisiopatológicos que participan en su génesis y descripción de las principales pautas terapéuticas. Lugar: Hospital Privado de Comunidad, Mar del Plata, Buenos Aires, Argentina. Base de datos: Base electrónica MEDLINE y revisión de los principales trabajos sobre el tema en revistas de anestesiología, medicina crítica y neumonología.

Alteraçäo da funçäo pulmonar e papel do edema intersticial pulmonar nos pacientes com insuficiência cardíaca crônica no exercício / Change of pulmonary function and the role of interstitial pulmonary edema in patients with chronic heart failure during exercice

O objetivo desta tese foi o de evidenciar as alteraçoes da funçao pulmonar e o papel do edema intersticial pulmonar (EI) nos pacientes com insuficiência cardíaca crônica (ICC), no exercício cardiorespiratório, através de uma metodologia nao-invasiva. Para isto estudamos grupos de sujeito controle, de pacientes cardíacos (graus I, II e III da Classificaçao funcional da New York Heart Association) e de pacientes broncopneumopatas. Os parâmetros espiroergométricos, a capacidade pulmonar de difusao (DLCO) corrigida pela ventilaçao (DLCONA), o débito cardíaco (Q) pelo método da reinalaçao pelo C02, e a tomodensitometria de alta resoluçao (TDM-AR), foram recolhidos e estudados no repouso e no exercício. Nós encontramos no exercício máximo, uma inadaptaçao do Q, uma DLCO diminuída no repouso e uma nao-elevaçao da DLCO e da DLCONA nos pacientes cardíacos após o exercício em relaçao aos sujeitos controles. Os resultados ainda apontaram na determinaçao de índice simples na prática clínica que permitissem diferenciar, durante o exercício, entre a origem cardíaca ou pulmonar de uma dispnéia. Este índice foi: a diferença da relaçao da frequência respiratória e o volume corrente nos pacientes cardíacos e nos pacientes com doença pulmonar obstrutiva crônica enquanto que os dados do regime ventilatório foram similares nos dois grupos. O edema intersticial foi colocado em evidência através da TDM-AR após o exercício no grupo cardíaco, utilizando os seguintes critérios: espessamentos das paredes brônquicas, a acentuaçao da linha vascular periférica, o edema peribrônquico e a relaçao do diâmetro artéria/brônquio >1 no lobo superior. O El foi máximo aos 12 minutos após o exercício, e aos 20 minutos, este edema praticamente desapareceu, em resposta a uma drenagem linfática mais ativa no espaço intersticial. Em conclusao, nós mostramos a importância e a eficácia de nossa metodologia empregada ao evidenciarmos um edema intersticial nos pacientes cardíacos crônicos. A DLCO foi bem aceita e de fácil realizaçao nos pacientes cardíacos após o exercício. A TDM-AR pode ser um instrumento indispensávem na avaliaçao do edema pulmonar