Recovery of costal and crural diaphragmatic contractility from partial paralysis. (73/124)

Since the two muscles (costal and crural) that constitute the diaphragm are separate and histologically different, their individual recovery pattern from neuromuscular blockade also may be different. Therefore, we studied the recovery of force and shortening in the in vivo diaphragm from atracurium-induced neuromuscular blockade in seven pentobarbital anesthetized dogs to assess segmental differences. Transdiaphragmatic pressure (Pdi), shortening of costal and crural segments, integrated electromyogram (EMG), and tidal volume (VT) were measured during spontaneous breathing. After atracurium had reduced VT to 30% of control, breathing parameters were followed until recovered to 90% of control values. In addition, force-frequency curves generated by supramaximal tetanic stimuli of the phrenic nerve were measured. Recovery times for tidal Pdi, tidal EMG, tidal shortening, low-frequency shortening, and twitch Pdi were twice as fast as for VT (40 +/- 4 min), reflecting a slower rate of recovery of accessory inspiratory muscles. High-frequency recovery was typically slower than that of VT. During tidal breathing and tetanic stimulation, costal and crural shortening recovered simultaneously. On the other hand, comparison between costal and crural by analysis of pressure-shortening relationships showed a segmental difference (crural shortened 30% more than costal at the same Pdi), which implied reduced afterload on the crural segment. However, since shortening and pressure were linearly related during paralysis and recovery, measurements of Pdi alone can accurately reflect changes in contractile mass when heterogeneity and afterload are controlled.  (+info)

Bilateral diaphragm paralysis after cardiac surgery with topical hypothermia. (74/124)

Bilateral diaphragm paralysis is a rare but important complication of open heart surgery. Two cases were found among 360 prospectively studied patients undergoing open heart surgery during one year. Both patients had insulin dependent diabetes with peripheral neuropathy and this may have contributed to their diaphragm paralysis. The patients were studied postoperatively for one year with measurements of lung function, nocturnal oximetry, diaphragmatic function, and phrenic nerve conduction. Treatment with intermittent positive airway pressure ventilation by nasal mask was effective in both patients. After nine months one patient had recovered completely with normal phrenic nerve conduction and diaphragmatic function; the other continues most of his normal daytime activities, but still requires nasal positive airway pressure ventilation for six hours at night.  (+info)

Ineffective ventilation during conscious sedation due to chest wall rigidity after intravenous midazolam and fentanyl. (75/124)

Chest wall rigidity has been reported after the administration of high-dose intravenous fentanyl. This case report supports the observation that low-dose intravenous fentanyl may also cause chest wall rigidity. The treatment of chest wall rigidity with naloxone or neuromuscular blocking agents is controversial. A discussion of the management of fentanyl-induced chest wall rigidity is presented.  (+info)

Long-term results of diaphragmatic plication in adults with unilateral diaphragm paralysis. (76/124)


Diaphragm paralysis due to pseudoaneurysm of internal mammary artery after pacemaker implantation. (77/124)


Unilateral diaphragmatic paralysis in a diabetic patient: a case of trepopnea. (78/124)


Doxorubicin causes diaphragm weakness in murine models of cancer chemotherapy. (79/124)


ERS Meeting Report. Metabolic aspects of obstructive sleep apnoea syndrome. (80/124)

Insulin resistance is often associated with obstructive sleep apnoea syndrome (OSAS) and could contribute to cardiovascular risk in OSAS. Sleep loss and intermittent hypoxia could contribute to the pathogenesis of the metabolic alterations associated with obesity, a common feature of OSAS. The biology of the adipocyte is being increasingly studied, and it has been found that hypoxia negatively affects adipocyte function. In November 2007, the European Respiratory Society and two EU COST Actions (Cardiovascular risk in OSAS (B26) and Adipose tissue and the metabolic syndrome (BM0602), held a Research Seminar in Dusseldorf, Germany, to discuss the following: 1) the effects of hypoxia on glucose metabolism and adipocyte function; 2) the role of inflammatory activation in OSAS and obesity; 3) the alarming rates of obesity and OSAS in children; 4) the harmful effects of the metabolic syndrome in OSAS; 5) the effects of OSAS treatment on metabolic variables; and 6) the relationship between daytime sleepiness and hormonal and inflammatory responses. Insulin resistance in skeletal muscle, the role of the endocannabinoid system and novel pharmacological approaches to treat insulin resistance were also discussed. As obesity and hypoxia could be the basic links between OSAS and adipocyte dysfunction, further research is needed to translate these new data into clinical practice.  (+info)