Cribado del síndrome de apneas-hipopneas del sueño en el preoperatorio de cirugía bariátrica / No disponible

La prevalencia de síndrome de apneas-hipopneas del sueño (SAHS) en pacientes con obesidad mórbida que van a ser sometidos a cirugía bariátrica se encuentra incrementada de forma importante respecto a la población general. Los pacientes con SAHS son especialmente vulnerables durante los procesos de anestesia, sedación y analgesia y presentan un riesgo elevado de desarrollar complicaciones respiratorias y cardiopulmonares. Las guías para el cuidado perioperatorio del paciente con SAHS están basadas en la opinión de expertos, más que en la evidencia objetiva de que el SAHS es un factor de riesgo independiente para las complicaciones perioperatorias. Son necesarios estudios prospectivos aleatorizados multicéntricos casos-controles, que nos permitan identificar los beneficios del cribado rutinario del SAHS en dicha población, así como el papel del tratamiento perioperatorio con CPAP para evitar las complicaciones. Se consideraría beneficioso establecer un protocolo entre los cirujanos y anestesistas con las Unidades de Sueño (AU)

The sleep apnea hypopnea syndrome (SAHS) prevalence in severe obesity patients undergoing bariatric surgery is highly with respect to general population. SAHS patients are particularly vulnerable during anesthesia, sedation and analgesia proceedings and it´s supposed an increased risk of developing respiratory and cardiopulmonary complications postoperatively. Existing guidelines for the perioperative care of SAHS patients are based primarily on expert opinion rather than on SAHS objective evidence is actually a risk factor for perioperative complications. Randomized prospective multi-centric case-control studies are required to identify the benefits of routine SAHS diagnosis and the CPAP treatment in the perioperative of bariatric surgery to avoid postoperative complications. It´s necessary to set up some screening strategies for the surgeons, anaesthesiologists and Sleep diagnosis Units (AU)

Síndrome complejo de apneas del sueño / Complex sleep apnea syndrome

Los trastornos respiratorios del sueño se han clasificado como obstructivos, centrales o mixtos, atendiendo a la presencia o no de estímulo respiratorio. Esta clasificación puede resultar un tanto simplista, limitando la comprensión de los complejos mecanismos que subyacen en la aparición de uno u otro tipo de eventos, que podrían tener un origen común en la inestabilidad del control respiratorio. Mientras los eventos obstructivos responden a la presión positiva continua sobre la vía aérea (CPAP), es más difícil el tratamiento de los eventos centrales. La aparición o deterioro de apneas centrales y la resolución incompleta de los eventos obstructivos con la aplicación de CPAP en algunos sujetos, se reconoce como un nuevo tipo de trastorno respiratorio del sueño: el síndrome complejo de apneas del sueño. En la siguiente revisión se repasan las diferentes formas de apneas centrales, se exponen los aspectos fundamentales de la patogenia, diagnóstico y epidemiologia del síndrome complejo de apneas del sueño y se discuten las posibilidades terapéuticas (AU)

Sleep-related respiratory disorders have been classified as obstructive, central or mixed, according to the presence or nonpresence of respiratory stimulus. This classification may seem to be a bit simple, limiting it to the understanding of the complex mechanisms underlying the appearance of one type of event or another, which may have a common origin in the instability of respiratory control. While the obstructive events respond to continuous positive airway pressure (CPAP), treatment of the central events is more difficult. The appearance or deterioration of central apneas and the incomplete resolution of the obstructive events with the application of CPAP in some subjects is recognized as a new type of sleep-related respiratory disorder, the complex sleep apnea syndrome. In this review, the different forms of central apnea are studied, the fundamental pathogenic aspects, diagnosis and epidemiology of the complex sleep apnea syndrome are presented and the possible treatments are discussed (AU)

Exploración funcional pulmonar en pacientes con hipertensión arterial pulmonar / Lung function testing in patients with pulmonary arterial hypertension

Objetivo: El objetivo principal es la descripción de los hallazgos funcionales respiratorios en una serie de 120 pacientes con hipertensión arterial pulmonar (HAP), y el objetivo secundario es su comparación con los datos hemodinámicos. Pacientes y métodos: Estudio descriptivo de la función pulmonar de los 120 casos con HAP estable, de los grupos 1 y 4 de Evian/Venecia, estudiados hasta enero de 2002 en el grupo de trabajo de Hipertensión Pulmonar y Trasplante de Pulmón del Servicio de Cardiología del Hospital Universitario 12 de Octubre de Madrid. Los datos de 47 pacientes se recogieron retrospectivamente desde 1981 a 1995, y de forma prospectiva en los 73 restantes. Se incluyeron casos de hipertensión arterial idiopática y de la asociada a colagenosis, tromboembolia pulmonar crónica, shunt cardíaco y, en 30 casos, a síndrome de aceite tóxico (SAT). Resultados: En el conjunto del grupo la capacidad vital, el volumen espiratorio forzado en el primer segundo y la capacidad pulmonar total fueron normales; los valores medios mostraron un factor de transferencia bajo (media ± desviación estándar: 67,6 ± 23,2), e hipoxemia moderada (65,8 ± 15,4 mmHg). No se observaron asociaciones significativas entre los parámetros funcionales pulmonares y los hemodinámicos. El grupo con SAT tenía la edad más baja (33,7 ± 11,4 años), junto a los valores medios más altos en la escala de la New York Heart Association (3,3 ± 0,5) y de resistencias vasculares pulmonares (20,3 ± 8,1 kPa·l­-1·s). Conclusiones: En este trabajo se estudia la función pulmonar en una serie de 120 pacientes con HAP, de los grupos 1 y 4 de Evian/Venecia, entre los que se incluyó a 30 casos con SAT. No se han encontrado asociaciones significativas entre los valores funcionales respiratorios y los hemodinámicos

Objective: The main objective was to describe the results of lung function testing in a series of 120 patients with pulmonary arterial hypertension, and the secondary objective was to compare these findings with hemodynamic variables. Patients and Methods: This was a descriptive study of lung function in 120 patients with stable pulmonary arterial hypertension (Evian/Venice groups 1 and 4) studied until January 2002 in the Pulmonary Hypertension and Lung Transplant Working Group attached to the Cardiology Department of the Hospital Universtario 12 de Octubre in Madrid, Spain. Data were collected retrospectively for the first 47 patients (1981 to 1995) and prospectively thereafter for the remaining 73 patients. The diagnosis was idiopathic arterial hypertension or hypertension associated with collagenosis, chronic pulmonary embolism, cardiac shunt, or toxic oil syndrome (30 cases). Results: In the group as a whole, forced vital capacity, forced expiratory volume in 1 second, and total lung capacity were normal; mean (SD) values revealed low carbon dioxide diffusing capacity (67.6% [23.2%]), and moderate hypoxemia (65.8 [15.4] mm Hg). No significant associations were observed between lung function and hemodynamic parameters. Mean age in the toxic oil syndrome group was lower (33.7 [11.4] years), and these patients had higher mean scores on the New York Heart Association scale (3.3 [0.5]) and for pulmonary vascular resistance (20.3 [8.1] kPa·L-­1·s). Conclusions: Lung function was studied in a series of 120 patients with pulmonary arterial hypertension (Evian/ Venice groups 1 and 4), 30 of whom had toxic oil syndrome. No significant associations were found between lung function and hemodynamic parameters

Inhaled nitric oxide and arterial oxygen tension in patients with chronic obstructive pulmonary disease and severe pulmonary hypertension.

BACKGROUND: Inhaled nitric oxide (NO) is a selective pulmonary vasodilator which can improve gas exchange in acute lung injury. However, it is uncertain that this effect on arterial oxygenation can be generalised to all lung diseases. METHODS: The effects of inhaled NO on gas exchange were studied in nine patients with chronic obstructive pulmonary disease (COPD), 11 patients with severe pulmonary hypertension, and 14 healthy volunteers. A randomized sequence of 40 ppm of NO or air was inhaled for 20 minutes through an orofacial mask. RESULTS: Inhaled NO reduced mean (SE) transcutaneous arterial oxygen tension (TcPO2) from 9.6 (0.3) to 8.9 (0.4) kPa in healthy volunteers and from 7.4 (0.6) to 7.0 (0.5) kPa in patients with COPD. There was no change in TcPO2 in patients with severe pulmonary hypertension. During inhalation of NO and air no change occurred in transcutaneous arterial carbon dioxide tension (TcPCO2), arterial oxygen saturation (SaO2) measured by pulse oximeter, or cardiac output determined by the transthoracic impedance method. CONCLUSIONS: Inhaled NO does not improve TcPO2 nor increase cardiac output in normal subjects and patients with COPD, suggesting that inhaled NO worsens gas exchange. This could represent inhaled NO overriding hypoxic pulmonary vasoconstriction in COPD. The finding that TcPO2 also fell when normal subjects inhaled NO suggests that a similar mechanism normally contributes to optimal gas exchange. Whilst inhaled NO can improve oxygenation, this effect should not be considered to be a general response but is dependent on the type of lung disease.

Persistence of respiratory abnormalities four years after the onset of toxic oil syndrome.

We studied a random sample of 436 subjects with TOS aged 18 to 60 years, to assess the prevalence of respiratory involvement four years after onset of the syndrome. Clinical evaluation together with chest roentgenograms, electrocardiogram and functional respiratory tests were carried out. Respiratory involvement occurred in 390 (89.4 percent) individuals and was the most common abnormality detected, followed by neurological disorders in 289 (66.3 percent), osteoarticular symptoms in 171 (39.2 percent), psychiatric disorders in 96 (22 percent), hepatic involvement in 91 (20.9 percent), and sclerodermatous sequelae in 89 (20.4 percent). Among patients with respiratory involvement, dyspnea and cough were the most common complaints. Decreased VC was observed in 151 (34.6 percent) patients and reduced transfer factor of CO in 95 (21.8 percent) patients. Airway obstruction and alveolar hypoventilation were observed only in nine (2.1 percent) patients. Six (1.4 percent) patients suffered from pulmonary artery hypertension.

Dynamic pulmonary arterial hypertension: a new form of pulmonary hypertension in patients with impaired pulmonary diffusing capacity due to toxic oil syndrome.

The authors studied the pulmonary haemodynamic response to exercise in eleven patients with toxic oil syndrome (TOS) (mean age 38.3 +/- 15.7 years; 10 women, 1 man) and abnormal pulmonary diffusing capacity (39.1 +/- 10.3% of predicted value) without clinical evidence of pulmonary hypertension. Eight patients had normal pulmonary pressure at rest (mean PAP less than 25 mmHg) and three showed mild pulmonary hypertension. After exercise the mean PAP rose to 35.3 +/- 11.5 mmHg from a basal value of 20.72 +/- 3.8 mmHg (p less than 0.01). Only four patients did not develop pulmonary hypertension during exercise. Pulmonary artery oxygen saturation decreased from 72.9 +/- 1.9% at rest to 52.3 +/- 10.1% during exercise (p less than 0.01). In conclusion, in this subset of TOS patients, an early diagnosis of their subclinical pulmonary hypertension can be made on the basis of the presence of dyspnoea and abnormal pulmonary diffusing capacity for carbon monoxide and can be then confirmed with the exercise haemodynamic test.

Pulmonary hypertension due to toxic oil syndrome. A clinicopathologic study.

Clinical and pathologic findings in seven patients who died of severe pulmonary artery hypertension due to toxic oil syndrome are assessed. These cases correspond to a late stage of evolution of the disease characterized by progressive deterioration in clinical features--increasing dyspnea, chest pain, syncope, and death (in low-output heart failure). The main pathologic pulmonary vascular findings consisted of plexiform lesions, thromboses, and venous lesions. Endothelial damage induced by the toxic agents is suggested as an initial causative mechanism, perpetuated by intimal proliferation and in situ thrombosis. Plexiform lesions appear late and active histologically. This new cause of pulmonary artery hypertension, with pathologic findings similar to those found in primary pulmonary hypertension, may help in understanding the pathophysiology of this unknown disease.