Presión de distensión en el síndrome de dificultad respiratoria aguda (SDRA): su relación con la injuria pulmonar inducida por el ventilador / Distension pressure in acute respiratory distress syndrome (ARDS): its relationship with ventilator-induced lung injury

Existen evidencias que la presión de distensión (ΔP) puede ser un buen predictor del riesgo de muerte en pacientes con sindrome de dificultad respiratoria aguda (SDRA), inclusive con Presión Plateau (PPlat) y volumen tidal (Vt) considerados seguros. Aunque no se pudo establecer una causalidad, se ha sugerido una probable relación entre ΔP y el desarrollo de injuria pulmonar inducida por el ventilador (VILI). Objetivo: Evaluar si ΔP correlaciona con el riesgo de VILI (barotrauma, volutrauma y atelectrauma). Materiales y Métodos: Doce pacientes con SDRA fueron ventilados en VCV con Vt: 6 ml/kg. El nivel de PEEP fue ajustado para obtener una PPlat de 30 cmH2O. Se midieron presiones transpulmonares (PTP) y posteriormente se realizó TAC de tórax en fin de inspiración y de espiración. Los volumenes pulmonares fueron evaluados a partir del análisis de las densidades tomográficas, considerandose hiperinsuflación (HI) al pulmón comprendido entre: -901 a 1000 UH, atelectrauma a la diferencia de pulmón no aireado (NA: -100 a 100 UH) entre ambos tiempos ventilatorio, y distensión pulmonar cíclica (strain) a la diferencia de pulmón hiperinsuflado. Resultados: El ΔP se relacionó de forma inversa con la Cst (r= -0,84, p= 0,0005, IC95% -0,9 a -0,5 y el riesgo de volutrauma (strain: r:-0,86, p=0,0003, IC95:-0,9 a -0,6 e hiperinsuflación: r:-0,78, p 0,002, IC95%: -0,9 a -0,4) y de forma directa con el riesgo de atelectrauma (r:0,89, p=0,0001, IC95% 0,7 a 0,9). No se observó correlación entre ΔP y barotrauma. Conclusiones: En este modelo de SDRA, la presión de distensión estuvo condicionada por la complacencia respiratoria y se encontró directamente relacionada con mayor riesgo de atelectrauma e inversamente asociada al riesgo de volutrauma.

El abordaje homeopático de la tos / The homeopathic approach cough

El organismo humano posee distintos mecanismos de defensa natural para sus diversos sistemas, los que son conocidos como signos clínicos o lo que Hahnemann llamaba en los §6 y 7 del Organon la expresión de la fuerza vital. La tos es un fenómeno producido por un mecanismo reflejo que emerge en los receptores vagales situados a lo largo del tracto respiratorio. Se han descrito tres tipos diferentes de receptores, los receptores de estiramiento de adaptación lenta (REAL), receptores de estiramiento de adaptación rápida (REAR) y las fibras C. Este reflejo tusígeno consiste en tres fases: inspiratoria, compresiva y espiratoria. Es importante tener muy en cuenta que la tos es tan sólo un síntoma de un cuadro clínico complejo e individual que se desarrolla en la totalidad del organismo. Incluso la medicina convencional reconoce que la tos, aunque puede ser un síntoma problemático, es una forma de curación del cuerpo; en este sentido, se debe hacer lo posible por no erradicarla, menos aún en menores de seis años, a través de antitusígenos de venta libre.

Human organism has different natural defense mechanisms for its various systems,these mechanisms are known as clinical signs or what Hahnemann called in § 6and 7 of Organon “expression of the vital force”. Cough is a phenomenon caused by a reflection mechanism emerges vagal receptors along the respiratory tract have been described three types of receptors, slowly adapting stretch receptors (SARs), rapidly adapting stretch receptors (RARs) and C-fibers. This cough reflex consists of three phases, the first “inspiratory”, “compression” and “expiratory”. It is important to bear in mind that the cough is just a symptom of a complex clinical picture and individual that develops in the whole organism, even conventional medicine recognizes that cough, but can be a troubling symptom, it is a form of healing the body, in this regard, it should be possible not eradicate it, even less in children under six years antitussives through counter.

Hipotensão pós-exercício: mecanismos e infl uências do exercício físico / Post-exercise hypotension: mechanisms and infl uences of physical exercise

Imediatamente após um período de exercício físico dinâmico, a pressão arterial diminui para níveis inferiores aos observados pré-exercício. Foi observado em indivíduos hipertensos, resposta de hipotensão pós-exercício de 11 mmHg e 4 mmHg para as pressões arteriais sistólica e diastólica, respectivamente , mas não verifi caram reduções signifi cantes nos indivíduos normotensos. Com relação ao efeito da intensidade do exercício foi verifi cado em hipertensos idosos, que o exercício físico mais intenso (70% do consumo pico de oxigênio) provocava diminuição da pressão arterial maior que uma sessão menos intensa (40% do consumo pico de oxigênio). As respostas de pressão arterial, freqüência cardíaca e resistência vascular periférica pós-exercício não apresentam sempre um padrão coerente ao esperado pelo controle barorrefl exo. Dessa forma, torna-se importante verifi car o efeito do exercício físico no controle barorrefl exo cardiopulmonar. Foi observado que após uma sessão aguda de exercício físico, ocorre diminuição da atividade nervosa simpática muscular com diminuição concomitante da resistência vascular periférica. Isto indica alteração no controle barorrefl exo arterial, pois o fl uxo simpático está diminuído para um nível de pressão arterial idêntico. Portanto, estas modifi cações na sensibilidade dos barorreceptores arteriais estão relacionados a mecanismos neurais e vasculares. Com isso, pode-se notar que a hipotensão pós-exercício pode ser infl uenciada por diversos mecanismos, sendo que os mesmos ainda necessitam de maiores investigações, por isso o intuito da realização dessa revisão.

Immediately after a dynamic physical exercise, blood pressure decreases to lower levels compared with pre-exercise. In hypertensive subjects was observed post-exercise hypotension reply of 11 mmHg and 4 mmHg for systolic and diastolic blood pressure, respectively, but was not verifi ed signifi cant reductions in normotensive individuals. In older hypertensive subjects, it was noted that the most intensive physical exercise (70% of the oxygen consumption peak) provoked a higher reduction on blood pressure than another light intensive (40% of the oxygen consumption peak). Blood pressure, heart rate and peripheral vascular resistance’s post-exercise reply do not present a coherent standard answer for the barorefl ex control expected frequently. Thus, it becomes important to verify the effect of physical exercise in cardiopulmonary barorefl ex control. It was observed that post-exercise, the sympathetic muscular nervous activity reduces with concomitant diminishes of the peripheral vascular resistance. This indicates that there is an alteration in arterial barorefl ex control, because the sympathetic fl ow is decreased for an identical level of blood pressure. So, these modifi cations in the sensibility of arterial baroreceptors are related with neural and vascular mechanisms. Therefore, we can observe that the post-exercise hypotension might be infl uenced by several mechanisms, which still need additional investigations; so, this is the intention of the present review.

Ouabain stimulates slowly adapting pulmonary stretch receptors / 生理学报

Ouabain, a Na(+)/K(+)-ATPase inhibitor, induces slowly adapting pulmonary stretch receptors (SARs) to discharge paradoxically. Paradoxical discharge is characterized by increased SAR activity during lung deflation coupled with silence during lung inflation. We hypothesized that over-excitation silences the SARs. Accordingly, if cyclic inflation pressure was reduced so as to lower SAR stimulation, paradoxical discharge would be prevented. In the present study, single-unit activity of SARs was recorded in anesthetized, open-chest and mechanically ventilated rabbits with positive-end-expiratory pressure (PEEP). After microinjection of ouabain into the receptive field, SAR activity initially increased and then gradually became paradoxical. During paradoxical cycling, SAR activity started and stopped abruptly, oscillating between high frequency discharge during lung deflation and silence during peak inflation. Removing PEEP reduced basal cyclic stimulation and returned the discharge pattern to normal, that is, SAR activity was highest at peak inflation pressure but silent during deflation. It is speculated that stretching SARs causes Na(+) influx, producing generator potential (GP). Normally, GP recovers by Na(+) extrusion via Na(+)/K(+)-ATPase. Ouabain inhibits the ATPase, which limits Na(+) extrusion, and thus sustains the GP. Therefore, after ouabain microinjection, lung inflation will further increase GP, causing over-excitation to silence the SARs.

An overview of vagal airway receptors / 生理学报

Breathing is critically depending on a variety of sensory feedbacks from multiple sources for its optimal performance. The sensory information from the lung and airways probably provides one of the most important feedbacks to adjust the respiratory controller to generate optimal breathing movements. Since Breuer and Hering made the seminal report regarding role of the vagus nerve in control of breathing in 1868, airway sensory receptors have been a subject for intensive and extensive studies. After more than a century investigation, our knowledge accumulates immensely, however, our understanding of the nature of these sensory receptors is still far from complete. This brief review provides an overview on this topic.

Dyspnea: Mechanisms and assessment

This work studies the pathophysiological mechanisms of dyspnea and describes the assessement of intensity of dyspnea. The study of mechanisms of dyspnea show that dyspnea can result from a respiratory muscle dysfunction, an excessive stimulation and/or alteration of pulmonary and extrapulmonary receptors, and a direct and excessive stimulation of respiratory centres. The assessment of dyspnea can be made generally by indirect methods based on questionnaires and direct methods based on psychophysiology techniques. The understanding of pathophysiological mechanisms and the study of the assessment of dyspnea represents the key principles in strategy and effectiveness of the dyspnea treatment

Receptores pulmonares / Pulmonary receptors

En los pulmones existen receptores sensoriales y emergentes o farmacológicos que intervienen en el control del calibre de las vías aéreas, la secreción bronquial, así como en la liberación de mediadores por las células cebadas u otras células inflamatorias. Su estudio es de vital importancia para poder explicar la fisiopatología, la sintomatología y el manejo terapéutico de las enfermedades que cursan con limitación del flujo de aire expiratorio, principalmente el asma bronquial y la enfermedad pulmonar obstructiva crónica (EPOC).

Interaction of arterial chemoreceptors and pulmonary stretch reflexes in circulatory regulations in the cat

Interactions of lung stretch receptor [LSR] activity with that of arterial chemoreceptor [ACR] stimulation on the cardiovascular system [CVS] during hypoxic hypercapnia [HH] and hypoventilation [HV] are studied in anesthetized cats. HV was induced by lowering the tidal volume to 45% of its normal value. At this condition HV with arterial blood oxygen and carbon dioxide tensions of 45 and 60 mmHg [PaO2 - 45 mmHg and PaCO2 = 60 mmHg] was induced and changes in CVS parameters were recorded. In the second run the tidal volume was kept constant and the same level of HH was induced by exposing the cat to a gas mixture of 6-8% O2, 10% CO2 in nitrogen. Results of this study revealed that stimulations of ACR during HH did not alter the heart rate but did elevate aortic flow [30%] and contractility [60%]. Despite Induction of systemic vasodilation at this stage, there was a 12% increase in mean arterial pressure [Pa]. Reduced LSR reflexes during HV increased the heart rate [20%] and contractility [90%]. Although aortic flow increased equally in both conditions, the absence of systemic vasodilation during HV caused a 40% rise in Pa. Hence it is concluded that the reduction of LSR reflexes will greatly potentiate the regulatory influences of ACR on CVS during systemic hypoxia and hypercapnia

Participación de receptores J pulmonares en reflejo cardiorespiratorio provocado por acetaldehido en ratas / Pulmonary J receptors in the cardiorespiratory response induced by acetaldehyde in rats

Anteriormente demostramos que la administración endovenosa de acetaldehido (AcH) y etanol, provoca en la rata una triple respuesta refleja caracterizada por bradicardia, hipotensión y apnea, cuya vía eferente es vagal. La activación central del vago, como un mecanismo de iniciación de esta respuesta refleja se descartó mediante la inyección intracarotídea (hacia el SNC) de (AcH), la que produce hipertensión sin bradicardia. La administración de AcH en el ventrículo izquierdo no produce reflejo, y sin embargo su administración en ventrículo derecho produce una respuesta refleja mayor y con una latencia significativamente menor que por vía endovenosa. Esto sugiere la estimulación de receptores sensitivos ubicados en la circulación pulmonar. De éstos, sólo la estimulación de los receptores J pulmonares puede producir una respuesta refleja con bradicardia, hipotensión y apnea, y dada su ubicación entre el alvéolo y capilar pulmonar, son accesibles por la circulación pulmonar y por vía respiratoria. Con el objeto de precisar la participación de estos receptores en la respuesta refleja se administró AcH mediante nebulización a ratas anestesiadas y traqueotomizadas. El AcH administrado por vía respiratoria produjo la misma respuesta refleja, caracterizada por bradicardia (-52.8ñ21.73%). hipotensión (-36,9ñ12.10%) y apnea (4/7), pero con una latencia significativamente menor (p=0.0001) que por la vía endovenosa. La frecuencia respiratoria, volumen corriente y ventilación minuto no se modificaron significativamente. La vagotomía cervical bilateral bloqueó totalmente la bradicardia y la apnea, observándose una hipotensión de menor magnitud (p=0.0001) y con una latencia mayor (p=0.0001). La nebulización de solución Ringer Locke, a 10§C y a 37§C, produjo solamente hipotensión que no se modificó con vagotomía. Los resultados sugieren que la respuesta inducida por AcH, es mediada por un aumento reflejo en el tonovagal y que los neurorreceptores involucrados en la iniciación de este reflejo se ubican a nivel pulmonar y corresponderían a los receptores J pulmonares