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N Syabbalo

Publications and source records attributed to N Syabbalo.

8 recordsLinked to original sources

Assessment of respiratory muscle function and strength.

Measurement of respiratory muscle strength is useful in order to detect respiratory muscle weakness and to quantify its severity. In patients with severe respiratory muscle weakness, vital capacity is reduced but is a non-specific and relatively insensitive measure. Conventionally, inspiratory and expiratory muscle strength has been assessed by maximal inspiratory and expiratory mouth pressures sustained for 1 s (PImax and PEmax) during maximal static manoeuvre against a closed shutter. However, PImax and PEmax are volitional tests, and are poorly reproducible with an average coefficient of variation of 25%. The sniff manoeuvre is natural and probably easier to perform. Sniff pressure, and sniff transdiaphragmatic pressure are more reproducible and useful measure of diaphragmatic strength. Nevertheless, the sniff manoeuvre is also volition-dependent, and submaximal efforts are most likely to occur in patients who are ill or breathless. Non-volitional tests include measurements of twitch oesophageal, gastric and transdiaphragmatic pressure during bilateral electrical and magnetic phrenic nerve stimulation. Electrical phrenic nerve stimulation is technically difficult and is also uncomfortable and painful. Magnetic phrenic nerve stimulation is less painful and transdiaphragmatic pressure is reproducible in normal subjects. It is a relatively easy test that has the potential to become a widely adopted method for the assessment of diaphragm strength. The development of a technique to measure diaphragmatic sound (phonomyogram) during magnetic phrenic nerve stimulation opens the way for noninvasive assessment of diaphragmatic function.

Electric Stimulation↗

Chronobiology and chronopathophysiology of nocturnal asthma.

Asthma is increasing in prevalence and severity worldwide despite effective treatment and innovative research developments. Chronobiology is the study of biological rhythms and their mechanisms. Asthma is one of many diseases that exemplifies a circadian pattern in intensity, frequency of attacks and mortality. As many as 90% of asthmatics experience nocturnal symptoms severe enough to awaken them from sleep. Increased airway narrowing at night is thought to occur as a result of circadian variation in neurohormones and intensification of airway inflammation. Furthermore, vagal tone, neurogenic inflammation and airway hyperresponsiveness are increased at night. Many cells contribute to the nocturnal inflammatory process in the asthmatic airways, including mast cells, eosinophils, neutrophils and lymphocytes. These cells are capable of secreting innumerable inflammatory mediators, such as histamine, cytokines, leukotrienes, prostaglandins, neutral endopeptidase and superoxides, which are potent bronchoconstrictors and secretogogues. They also cause increased vascular permeability and airway oedema. All these chronobiological events promote nocturnal worsening of asthma and increased nocturnal deaths. Understanding the mechanisms of nocturnal asthma will help us learn more about asthma, and how to implement appropriate chronotherapeutic interventions.

Asthma↗

Measurement and interpretation of arterial blood gases.

Arterial blood gases and pH are routinely being measured in clinical practice, both to provide diagnosis and to guide therapy in critically ill patients. Oximetry is clinically useful in establishing the presence of hypoxaemia in patients with respiratory diseases. Oximetry is also a simple and reliable method for monitoring patients undergoing anaesthesia, sleep studies and cardiopulmonary exercise testing. The search continues for new innovative techniques for continuous transcutaneous and intra-arterial blood gas monitoring. This is essential in the management of critically ill patients because blood analysers provide only intermittent monitoring of arterial blood gases.

Blood Gas Analysis↗

Respiratory muscle function in patients with neuromuscular disorders and cardiopulmonary diseases.

Respiratory muscle dysfunction frequently occurs in patients with neuromuscular disorders, cardiopulmonary diseases and in patients in intensive care units. Respiratory muscle weakness and/or fatigue is responsible for dyspnoea, reduced exercise tolerance, nocturnal desaturation, and prolonged weaning from mechanical ventilation. Chronic respiratory muscle weakness may also be associated with poor quality of life and increased mortality. Patients with severe respiratory muscle weakness are at increased risk of respiratory failure due to respiratory infections, electrolyte imbalance, sedation or uncontrolled inspired oxygen therapy. Although respiratory muscle weakness is often seen in clinical practice, the consequences and the precise point at which respiratory muscle fatigue occurs remain elusive. This article reviews the pathophysiology of respiratory muscle weakness and fatigue, and therapeutic interventions for enhancing respiratory muscle function in patients with neuromuscular and cardiopulmonary diseases.

Female↗