Obesity has long been recognized as having significant effects on respiratory function. The topic has been studied for at least the last half century, and some clear patterns have emerged. Obese patients tend to have higher respiratory rates and lower tidal volumes. Total respiratory system compliance is reduced for a variety of reasons, which will be discussed. Lung volumes tend to be decreased, especially expiratory reserve volume. Spirometry, gas exchange and airway resistance all tend to be relatively well preserved when adjusted for lung volumes. Patients may be mildly hypoxaemic, possibly due to ventilation-perfusion mismatching at the base of the lungs, where microatelectasis is likely to occur. Weight loss leads to a reversal of these changes. For all of these changes, the distribution of fat, that is, upper versus lower body, may be more important than body mass index.

In obese patients without cardiopulmonary disease, oxygen levels decrease as BMI increases. This effect is associated with the obesity-related reduction in ERV and is independent of hypoventilation.

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During a T-tube trial following disconnection of mechanical ventilation, patients failing the trial do not develop contractile diaphragmatic fatigue despite increases in inspiratory pressure output. Studies in volunteers, patients, and animals raise the possibility of spinal and supraspinal reflex mechanisms that inhibit central-neural output under loaded conditions. We hypothesized that diaphragmatic recruitment is submaximal at the end of a failed weaning trial despite concurrent respiratory distress. Tidal transdiaphragmatic pressure (ΔPdi) and electrical activity (ΔEAdi) were recorded with esophago-gastric catheters during a T-tube trial in 20 critically ill patients. During the T-tube trial, ∆EAdi was greater in failure patients than in success patients (p=0.049). Despite increases in ΔPdi, from 18.1±2.5 to 25.9±3.7 cm H2O (p<0.001), rate of transdiaphragmatic-pressure development (from 22.6±3.1 to 37.8±6.7 cm H2O/sec; p<0.0004), and concurrent respiratory distress, ∆EAdi at the end of a failed T-tube trial was half of maximum, signifying inhibition of central neural output to the diaphragm. The increase in ΔPdi in the failure group, while ∆EAdi remained constant, indicates unexpected improvement in diaphragmatic neuromuscular coupling (from 46.7±6.5 to 57.8±8.4 cm H2O∙%-1; p=0.006). Redistribution of neural output to the respiratory muscles characterized by a progressive increase in rib-cage and accessory muscle contribution to tidal breathing and expiratory muscle recruitment contributed to enhanced coupling. In conclusion, diaphragmatic recruitment is submaximal at the end of a failed weaning trial despite concurrent respiratory distress. This finding suggests that reflex inhibition of central neural output to the diaphragm contributes to weaning failure.

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BackgroundPolysomnograms are not always feasible when sleep disordered breathing (SDB) is suspected in hospitalized patients. Portable monitoring is a practical alternative; however, it has not been recommended in patients with comorbidities.ObjectiveWe evaluated the accuracy of portable monitoring in hospitalized patients suspected of having SDB.DesignProspective observational study.SettingLarge, public, urban, teaching hospital in the United States.ParticipantsHospitalized patients suspected of having SDB.MethodsPatients underwent portable monitoring combined with actigraphy during the hospitalization and then polysomnography after discharge. We determined the accuracy of portable monitoring in predicting moderate to severe SDB and the agreement between the apnea hypopnea index measured by portable monitor (AHIPM) and by polysomnogram (AHIPSG).ResultsSeventy-one symptomatic patients completed both tests. The median time between the two tests was 97 days (IQR 25–75: 24–109). Forty-five percent were hospitalized for cardiovascular disease. Mean age was 52±10 years, 41% were women, and the majority had symptoms of SDB. Based on AHIPSG, SDB was moderate in 9 patients and severe in 39. The area under the receiver operator characteristics curve for AHIPM was 0.8, and increased to 0.86 in patients without central sleep apnea; it was 0.88 in the 31 patients with hypercapnia. For predicting moderate to severe SDB, an AHIPM of 14 had a sensitivity of 90%, and an AHIPM of 36 had a specificity of 87%. The mean±SD difference between AHIPM and AHIPSG was 2±29 event/hr.ConclusionIn hospitalized, symptomatic patients, portable monitoring is reasonably accurate in detecting moderate to severe SDB.

BACKGROUND:The ability to rapidly and precisely evaluate patients in respiratory distress is essential. Due to limited opportunities for formal instruction during training, textbooks are the main educational source to teach junior physicians how to interpret the signs of respiratory distress. The quality of the textbook content relevant to respiratory distress is unknown. OBJECTIVE: To examine the content on the evaluation of a patient in respiratory distress in a representative sample of textbooks and Internet resources. METHODS: Two physicians individually reviewed the most recent edition of 21 standard textbooks from a variety of specialties. Smartphone applications, UptoDate, and MD Consult were examined. Each physician reviewed the source for 14 different signs. For each sign, the reviewers determined 3 parameters: a mention of the sign, its pathophysiology, and its detection. The reviews were compared for discrepancies, and a third reviewer resolved them. RESULTS: The normal respiratory rate was mentioned in 10 (48%) of textbooks, and ranged between 10 and 22 breaths/min. Each sign was mentioned by a mean of 45 ؎ 26% of the textbooks. The pathophysiology of the signs was described by a mean of 33 ؎ 30% of the textbooks. The most and least commonly mentioned inspection signs were cyanosis and retraction of suprasternal notch, respectively. They were mentioned in 20 (95%) and 4 (19%) textbooks, respectively. The most and least commonly mentioned palpation signs were thoracoabdominal asynchrony or paradox and tracheal tug, respectively. They were mentioned in 17 (81%) and 4 (19%) textbooks, and their pathophysiology was described in 15 (71%) and 4 (19%) textbooks, respectively. The reviewers also found inconsistency in the descriptions of the meaning of scalene muscle contraction and thoracoabdominal asynchrony and paradox. CONCLUSIONS: The content of the reviewed textbooks on the evaluation of respiratory distress is inconsistent and deficient.

Embarrassment is a powerful teacher. I was barely 3 months into my internship, on night float at my residency's Veterans Affairs hospital, when I received a page from a concerned ward nurse. A patient was unresponsive. He was admitted for a severe COPD exacerbation. I examined him, and he only groaned with a vigorous sternal rub. Suspecting hypercapnic narcosis, I drew an arterial blood gas. The results confirmed my suspicion. The patient was suffering from acute respiratory acidosis. In a panic, I paged the resident taking ICU admissions. The patient needed to go to the ICU and be intubated. The resident said he would see the patient. He wordlessly slipped into the room and went straight to the oxygen flow meter. He turned the flow down several liters and waited. He did not have to wait long: it was as if the patient had received a naloxone injection. Within 90 seconds, he woke suddenly and looked around the room, puzzled. "What is everyone doing in here?" he asked. The resident, again wordlessly, slipped out of the room.I learned my lesson, and I will never forget it. I take minor consolation in Tobin and Jubran's 1 grievance, "This perennial problem apparently must be rediscovered by each new rotation of house-staff personnel." I have heard anecdotal reports of internal medicine and emergency department attending physicians doubting the existence of this phenomenon: hyperoxia-induced hypercapnia in patients with COPD. Why are we so recalcitrant? Part of the reason may be that the pathophysiologic mechanism behind it defies a simple explanation. In this issue of RESPI-RATORY CARE, Rialp et al 2 address the complicated mechanisms behind this phenomenon.Campbell 3 first hypothesized about the mechanism in 1960. His hypothesis was attractive in its simplicity: chronically hypercapnic COPD patients are dependent solely on their hypoxic respiratory drive, as the chronic hypercapnia blunts their hypercapnic respiratory drive. Unfortunately, this hypothesis was too simple. When it was tested, Aubier et al 4 found that the reduction in minute ventilation (V E ) was transient and inadequate to explain the degree of hypercapnia.In another study, Aubier et al 5 found no correlation between the degree of hypercapnia and the decrease in V E . Instead, they hypothesized that the excess hypercapnia was caused by 2 factors. The first was the Haldane effect (ie, the release of CO 2 when deoxyhemoglobin converts to SEE THE ORIGINAL STUDY ON PAGE 328 oxyhemoglobin). This mechanism was later confirmed by Luft et al. 6 The second was a decrease in pulmonary ventilation/perfusion matching due to the release of hypoxic pulmonary arterial vasoconstriction. This leads to a subsequent increase in functional dead space. This hypothesis was supported in a later study by Robinson et al. 7 Others found that hyperoxia also lessens the hyperventilation that follows acute hypercapnia in subjects with COPD. 8 Still others found the increase in P aCO 2 from hyperoxia to be a function of both increased functional dead space and decreased ventil...