Failure Rates for Endotracheal Tube Placement Using Videolaryngoscopy in Patients with a Difficult Airway.

Airway management has undergone dramatic transformation since the development of videolaryngoscopy (VL). VL improves glottic views when compared to direct laryngoscopy (DL). The image obtained is from a camera at the tip of the curved blade, and the view is not direct line of sight. Placement of the endotracheal tube (ETT) may therefore require the ETT to be manipulated in multiple planes to match the curvature of the VL blade. This placement of the ETT "around the corner" may be difficult without additional airway aids. The aim of this retrospective observational study was to determine whether endotracheal placement during VL in patients with a difficult airway required the use of an additional airway aid (bougie or fiberoptic scope). Difficult airway was defined as a Cormack and Lehane (C&L) grade 3 or 4 view obtained using DL prior to VL use. Data from 165 patients was included in the study. Simple ETT placement without an additional airway device was achieved in only 20.6% of cases (n = 34). The remaining 131 patients required a bougie or fiberscope to assist intubation. ETT placement was not possible with the bougie in 33 patients. These 33 patients were successfully intubated using a fiberscope-assisted VL (FAV) technique. VL improved C&L grade 3 views by at least one grade in 99.1% of cases, and grade 4 view to a grade 1 or 2 in 96.3% of cases. VL improves glottic view in patients with a difficult airway; but in nearly 80% of patients, a bougie or fiberscope is required to properly place the ETT. Practitioners should be aware that improved glottic views with VL may not translate into simple ETT placement, and additional airway aids need to be readily available.

Vastus lateralis Na(+)-K(+)-ATPase activity, protein, and isoform distribution in chronic obstructive pulmonary disease.

In this study we investigate the hypothesis that protein abundance, isoform distribution, and maximal catalytic activity of sodium-potassium-adenosine triphosphatase (Na(+)-K(+)-ATPase) would be altered in muscle of patients with moderate to severe chronic obstructive pulmonary disease (COPD). Tissue samples were obtained from the vastus lateralis of 10 patients with COPD (mean +/- SE: age = 67 +/- 2.9 years; FEV1 = 39 +/- 5.5%) and 10 healthy, matched controls (CON: age = 68 +/- 2 years; FEV1 = 114 +/- 4.2%). The samples were assessed for maximal catalytic activity (Vmax) of the enzyme using the K(+)-stimulated 3-O-methylfluorescein-phosphatase (3-O-MFPase) assay, enzyme abundance using the [3H]-ouabain assay, and isoform content of both alpha (alpha1, alpha2, alpha3) and beta (beta1, beta2, beta3) using Western blot techniques. A 19.4% lower (P < 0.05) Vmax was observed in COPD compared with CON (90.7 +/- 6.7 vs. 73.1 +/- 4.7 nmol x mg protein(-1) h(-1)). No differences between groups were observed for pump concentration (259 +/- 15 vs. 243 +/- 17 pmol x g wet weight). For the isoforms, alpha1 was decreased by 28% (P < 0.05), and alpha2 was increased by 12% (P < 0.05) in COPD compared with CON. No differences between groups were observed for alpha3 or for the beta isoforms. We conclude that moderate COPD compromises Vmax, which occurs in the absence of changes in pump abundance. The reduction in Vmax could be due to a shift in isoform expression (alpha1, alpha2), alterations in intrinsic regulation, or to structural changes in the enzyme. The changes observed in the catalytic activity of the pump could have major effects on membrane excitability and fatigability, which are typically compromised in COPD.

McArdle's disease presenting as unexplained dyspnea in a young woman.

McArdle's disease is a rare, inherited deficiency of myophosphorylase, an enzyme required for the utilization of glycogen. Patients with myophosphorylase deficiency classically present with exercise intolerance, leg pain and muscle fatigue. The case of a young woman with exertional dyspnea and leg cramps is described. Exercise testing confirmed the presence of exercise intolerance and demonstrated an accelerated heart rate response, despite the absence of an anaerobic threshold and a respiratory exchange ratio of less than 1.0. Subsequent ischemic forearm testing and muscle biopsy confirmed the diagnosis of myophosphorylase deficiency. Evaluation of lung mechanics with esophageal pressure measurements demonstrated the presence of respiratory muscle weakness and early fatiguability, suggesting that the patient's dyspnea might have been attributable to an increased respiratory effort. Dyspnea is not a classic symptom associated with myophosphorylase deficiency, although subclinical respiratory muscle impairment may be present. No previous studies have evaluated respiratory muscle function during exercise in patients with myophosphorylase deficiency.