Síndrome de obesidad-hipoventilación: situación hemodinámica basal e impacto de la ventilación no invasiva / Obesity-Hypoventilation Syndrome: Baseline Hemodynamic Status and Impact of non-Invasive Ventilation

INTRODUCCIÓN: El síndrome de obesidad-hipoventilación (SOH) es un factor de riesgo para presentar insuficiencia cardiaca (IC). Algunos estudios relacionan el uso de ventilación no invasiva (VNI) con la alteración de parámetros hemodinámicos. Nuestro objetivo fue describir la situación hemodinámica de un grupo de pacientes con SOH y estudiar el efecto de la VNI. PACIENTES Y MÉTODOS: Con un diseño transversal de mediciones repetidas, se incluyó a pacientes con SOH tratados con VNI en situación estable. Se estudió su hemodinámica con bioimpedancia: 30 min basales y otros 30 con VNI. Se midieron el gasto cardiaco (GC), el índice cardiaco y el volumen sistólico. Se tomó como referencia el GC calculado para cada paciente expresado como porcentaje sobre su límite inferior de normalidad (LIN) y se establecieron 2 grupos: sin IC con GC conservado (≥ 100% sobre LIN) y con IC y GC bajo (< 100% del LIN). Se utilizaron la U de Mann-Whitney para comparación de variables independientes y el test de Wilcoxon para variables apareadas, se consideró significativo p < 0,05. RESULTADOS: La muestra final fue de 36 casos, de 66 (8) años, 19 (52%) varones. En 17 (46%) detectamos IC con GC de 3,7 l/min (66%) frente al grupo sin IC con 7 l/min (107%). Tras VNI, los pacientes en IC mejoraron su GC (4,5 l/min [77%] p = 0,009) y no lo modificó el grupo sin IC: 6,8 l/min (104%), p = 0,2. CONCLUSIÓN: Un 46% de pacientes con SOH estable presenta IC. La VNI mejora su hemodinámica y no influye en los pacientes con GC conservado

INTRODUCTION: Obesity-hypoventilation syndrome (OHS) is a risk factor for heart failure (HF). Some studies associate the use of non-invasive ventilation (NIV) with changes in hemodynamic parameters. Our objective was to describe the hemodynamic status of a group of patients with OHS and to study the effect of NIV. PATIENTS AND METHODS: Patients with stable OHS treated with NIV were included in this cross-sectional repeated measurements study. Hemodynamics were measured by bioimpedance: 30minutes at baseline and another 30minutes on NIV. Cardiac output (CO), cardiac index, and systolic volume were measured. The CO calculated for each patient expressed as a percentage of the lower limit of normal (LLN) was taken as reference, and 2 groups were formed: patients without HF and normal CO (≥ 100% of LLN) and patients with HF and low CO (< 100% of LLN). The Mann-Whitney U test was used to compare independent variables and the Wilcoxon test was used for paired variables, with significance set at P < .05. RESULTS: The final sample comprised 36 patients, aged 66 (± 8) years, 19 (52%) men. In 17 (46%) patients, HF was detected with a CO of 3.7 l/min (66%) compared to the group without HF, whose CO was 7 l/min (107%). After NIV, patients with HF showed improvement in CO (4.5 l/min (77%), P = .009, while the non-HF group remained unchanged, with CO 6.8 l/min (104%), P = .2. CONCLUSION: A total of 46% of patients with stable OHS present HF; NIV improves hemodynamics and does not affect patients with normal CO

Obesity-Hypoventilation Syndrome: Baseline Hemodynamic Status and Impact of non-Invasive Ventilation. / Síndrome de obesidad-hipoventilación: situación hemodinámica basal e impacto de la ventilación no invasiva.

INTRODUCTION: Obesity-hypoventilation syndrome (OHS) is a risk factor for heart failure (HF). Some studies associate the use of non-invasive ventilation (NIV) with changes in hemodynamic parameters. Our objective was to describe the hemodynamic status of a group of patients with OHS and to study the effect of NIV. PATIENTS AND METHODS: Patients with stable OHS treated with NIV were included in this cross-sectional repeated measurements study. Hemodynamics were measured by bioimpedance: 30minutes at baseline and another 30minutes on NIV. Cardiac output (CO), cardiac index, and systolic volume were measured. The CO calculated for each patient expressed as a percentage of the lower limit of normal (LLN) was taken as reference, and 2 groups were formed: patients without HF and normal CO (≥ 100% of LLN) and patients with HF and low CO (< 100% of LLN). The Mann-Whitney U test was used to compare independent variables and the Wilcoxon test was used for paired variables, with significance set at P<.05. RESULTS: The final sample comprised 36 patients, aged 66 (± 8) years, 19 (52%) men. In 17 (46%) patients, HF was detected with a CO of 3.7 l/min (66%) compared to the group without HF, whose CO was 7 l/min (107%). After NIV, patients with HF showed improvement in CO (4.5 l/min (77%), P=.009, while the non-HF group remained unchanged, with CO 6.8 l/min (104%), P=.2. CONCLUSION: A total of 46% of patients with stable OHS present HF; NIV improves hemodynamics and does not affect patients with normal CO.

Neumonía grave por Rhodococcus equi con diseminación hematógena al sistema nervioso central en un paciente inmunodeprimido / Severe Pneumonia Caused by Rhodococcus equi with Hematogenous Spread to the Central Nervous System in an Immunocompromised Patient

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Niveles elevados de carboxihemoglobina: fuentes de exposición a monóxido de carbono / Elevated Carboxyhemoglobin: Sources of Carbon Monoxide Exposure

Introducción: La inhalación de monóxido de carbono (CO) puede producir intoxicación, ocasionando desde una sintomatología inespecífica hasta la muerte. Muchas veces hay infradiagnóstico ya que exponerse a concentraciones bajas pasa inadvertida, y los valores umbral de normalidad para la carboxihemoglobina varían según distintos autores. El objetivo de nuestro trabajo fue analizar los niveles de carboxihemoglobina (COHb) en una población no seleccionada y detectar las fuentes de exposición al monóxido de Carbono Métodos: Con un diseño transversal y descriptivo, se analizaron consecutivamente las gasometrías arteriales procesadas en nuestro laboratorio. Se seleccionaron aquellos que tenían una COHb ≥ 2,5% en no fumadores y ≥ 5% en fumadores. A los casos seleccionados se realizó entrevista telefónica estructurada. Resultados: De 306 valoraciones iniciales, 64 casos (20%) tenían valores elevados de COHb y se obtuvieron datos de 51, 31 (60%) varones, de 65 ± 12 a˜nos. La media de COHb fue de 4,0%. Cuarenta pacientes (78%) eran no fumadores con niveles de COHb de 3,2% y 11 fumadores con niveles de COHb de 6,7%. En 45 pacientes (88,2%) se detectó exposición a al menos una fuente de producción de CO ambiental distinta al humo del tabaco. Conclusiones: Un porcentaje relevante de individuos de una muestra no seleccionada tiene valores elevados de COHb. Posiblemente las principales fuentes de exposición estén en el domicilio particular, por lo que debe explorarse esta posibilidad, alertar sobre los riesgos y estimular la toma de medidas preventivas

Introduction: Inhalation of carbon monoxide (CO) can result in poisoning, with symptoms ranging from mild and nonspecific to severe, or even death. CO poisoning is often underdiagnosed because exposure to low concentrations goes unnoticed, and threshold values for normal carboxyhemoglobin vary according to different authors. The aim of our study was to analyze carboxyhemoglobin (COHb) levels in an unselected population and detect sources of CO exposure Methods: In a cross-sectional descriptive study, we analyzed consecutive arterial blood gas levels processed in our laboratory. We selected those with COHb≥2.5% in nonsmokers and ≥ 5% in smokers. In these cases a structured telephone interview was conducted. Results: Elevated levels of COHb were found in 64 (20%) of 306 initial determinations. Of these, data from 51 subjects aged 65 ± 12 years, 31 (60%) of which were men, were obtained. Mean COHb was 4.0%. Forty patients (78%) were non-smokers with mean COHb of 3.2%, and 11 were smokers with COHb of 6.7%. In 45 patients (88.2%) we detected exposure to at least one source of ambient CO other than cigarette smoke. Conclusions: A significant proportion of individuals from an unselected sample had elevated levels of COHb. The main sources of CO exposure were probably the home, so this possibility should be explored. The population should be warned about the risks and encouraged to take preventive measures

Elevated carboxyhemoglobin: sources of carbon monoxide exposure.

INTRODUCTION: Inhalation of carbon monoxide (CO) can result in poisoning, with symptoms ranging from mild and nonspecific to severe, or even death. CO poisoning is often underdiagnosed because exposure to low concentrations goes unnoticed, and threshold values for normal carboxyhemoglobin vary according to different authors. The aim of our study was to analyze carboxyhemoglobin (COHb) levels in an unselected population and detect sources of CO exposure METHODS: In a cross-sectional descriptive study, we analyzed consecutive arterial blood gas levels processed in our laboratory. We selected those with COHb≥2.5% in nonsmokers and ≥5% in smokers. In these cases a structured telephone interview was conducted. RESULTS: Elevated levels of COHb were found in 64 (20%) of 306 initial determinations. Of these, data from 51 subjects aged 65±12 years, 31 (60%) of which were men, were obtained. Mean COHb was 4.0%. Forty patients (78%) were non-smokers with mean COHb of 3.2%, and 11 were smokers with COHb of 6.7%. In 45 patients (88.2%) we detected exposure to at least one source of ambient CO other than cigarette smoke. CONCLUSIONS: A significant proportion of individuals from an unselected sample had elevated levels of COHb. The main sources of CO exposure were probably the home, so this possibility should be explored. The population should be warned about the risks and encouraged to take preventive measures.

Reversible pre-capillary pulmonary hypertension due to dasatinib.

Pulmonary arterial hypertension and secondary pleural effusion have been reported in association with long-term therapy with the multi-tyrosine kinase inhibitor dasatinib, approved for the treatment of chronic myeloid leukemia. Here, we present the case of a 50-year-old man, diagnosed with chronic myeloid leukemia in August 2003, who developed pulmonary arterial hypertension after > 4 years of treatment with dasatinib. The complete remission of pulmonary arterial hypertension following dasatinib discontinuation suggests an etiological role of the drug in its development, although the administration of sildenafil may have played a therapeutic role.