Weaning from mechanical ventilation: an update.

Many patients admitted to the intensive care unit have respiratory failure and thus require mechanical ventilation. Weaning patients from mechanical ventilation after their primary disease process has been treated can be difficult in approximately 30% of patients. Inadequacies in pulmonary gas exchange and in the performance of the respiratory muscle pump are the most common causes for failure to wean. Assessing whether a patient can be weaned from mechanical ventilation involves two major factors: (1) examining the patient for evidence of an increase in the work of breathing, and (2) measuring spontaneous breathing variables. Although different modalities have been used in weaning patients from mechanical ventilation, none has been shown to be more successful than repeated trials of spontaneous breathing.

Circadian rhythm sleep disorders.

"Night owls" and "morning larks" are descriptive terms used to characterize individuals who go to sleep or awaken differently than most individuals. Many of these individuals have a primary circadian sleep dysrhythmia. Identification and proper treatment of a specific condition can markedly improve their quality of life. Secondary circadian dysrhythmias are very common. Nearly everyone at some time in his or her life experiences jet lag or shift work sleep disorder, two conditions in which we ignore our biologic rhythms. The impact of these conditions on performance and judgment can be tempered by certain pharmacologic and nonpharmacologic strategies. A better understanding of both primary and secondary circadian rhythm sleep disorders will be valuable to the primary care physician, leading to earlier diagnosis and improved treatment of patients with these conditions.

Comparison of oxygen therapy with nasal continuous positive airway pressure on Cheyne-Stokes respiration during sleep in congestive heart failure.

STUDY OBJECTIVES: Both oxygen therapy and nasal continuous positive airway pressure (CPAP) therapy have independently been shown to be effective in the treatment of Cheyne-Stokes respiration (CSR) in patients with congestive heart failure (CHF). The purpose of this study was to compare the short-term effects of oxygen therapy and nasal CPAP therapy on CSR in a group of stable patients with severe CHF. DESIGN: Prospective, randomized, controlled trial. SETTING: University hospital. PATIENTS: Twenty-five stable patients (mean [+/- SD] age, 56 +/- 9) with CHF and a mean left ventricular ejection fraction (LVEF) of 17 +/- 0.8%. INTERVENTIONS AND MEASUREMENTS: All patients had a right heart catheterization prior to the study and an echocardiogram performed to measure LVEF. In addition, all patients had an initial sleep study to identify the presence of CSR. Sleep studies included continuous recordings of breathing pattern, pulse oximetry, and EEG. Those patients identified as having CSR were randomized to a night on oxygen therapy (2 L/min by nasal cannula) and another night on nasal CPAP therapy (9 +/- 0.3 cm H(2)O). RESULTS: Fourteen of the 25 patients (56%) studied had CSR (apnea hypopnea index [AHI], 36 +/- 7 events per hour) during their initial sleep study. Nine of the 14 patients with CSR completed the study. When compared with baseline measurements, both oxygen therapy and nasal CPAP therapy significantly decreased the AHI (from 44 +/- 9 to 18 +/- 5 and 15 +/- 8 events per hour, respectively; p < 0.05), with no significant difference between the two modalities. The mean oxygen saturation increased significantly and to a similar extent with oxygen therapy and nasal CPAP therapy (from 93 +/- 0.7% to 96 +/- 0.8% and 95 +/- 0. 7%, respectively; p < 0.05), as did the lowest oxygen saturation during the night (from 80 +/- 2% to 85 +/- 3% and 88 +/- 2%, respectively; p < 0.05). In addition, the mean percent time the oxygen saturation was < 90% also improved with both interventions (from a baseline of 17 +/- 5 to 6 +/- 3% with oxygen therapy and 5 +/- 2% with nasal CPAP therapy; p < 0.05). When compared with baseline measurements, the apnea-hypopnea length, cycle length, circulation time, and heart rate did not significantly change with either oxygen therapy or nasal CPAP therapy. Total sleep time and sleep efficiency decreased only with nasal CPAP therapy (from 324 +/- 20 to 257 +/- 14 min, and from 82 +/- 3 to 72 +/- 2%, respectively; p < 0.05). The arousal index, when compared with baseline, remained unchanged with both oxygen therapy and nasal CPAP therapy. CONCLUSION: CSR occurs frequently in stable patients with severe CHF. In addition, oxygen therapy and nasal CPAP therapy are equally effective in decreasing the AHI in those CHF patients with CSR.

Effects of noninvasive positive pressure ventilation on gas exchange and sleep in COPD patients.

STUDY OBJECTIVE: The role of nocturnal noninvasive positive pressure ventilation (NPPV) in the treatment of patients with hypercapnic COPD remains controversial. Beneficial effects reported after prolonged use have included an improvement in gas exchange. The purpose of this study was to examine the short-term effects of NPPV on gas exchange and sleep characteristics in patients with hypercapnic COPD and to determine if similar acute changes in gas exchange are associated with improved sleep quality. DESIGN: Prospective, randomized, controlled trial. SETTING: Sleep laboratory of a university hospital. PATIENTS: Six patients with severe but stable hypercapnic COPD (PaCO2=58+/-4 [SE] mm Hg). Mean age was 63+/-6 (SD) with an FEV1=0.58+/-0.09 L. INTERVENTIONS AND MEASUREMENTS: Patients were studied in the sleep laboratory for a total of three nights. On nights 2 and 3, arterial catheters were placed prior to the study. Following an acquaintance night, patients were randomized to either a control-sham night on 5 cm H2O nasal continuous positive airway pressure (CPAP) or an NPPV night using a ventilatory support system (BiPAP; Respironics Inc; Murrysville, Pa) at previously determined optimal settings. The third night consisted of the opposite for each patient, either a control-sham or an NPPV night. On the second and third nights, three arterial blood gas readings were obtained: (1) baseline wakefulness; (2) non-rapid eye movement (NREM) sleep; and (3) rapid eye movement (REM) sleep. RESULTS: During NREM sleep, NPPV in comparison to the control-sham night on low level CPAP caused no significant change in PaCO2 (60+/-4 to 59+/-3 mm Hg [p=0.6]) and a decrease in PaO2 (96+/-9 to 72+/-5 mm Hg [p=0.04]). During REM sleep, NPPV in comparison to the control-sham night on low level CPAP caused no significant change in either PaCO2 (63+/-7 to 57+/-2 mm Hg [p=0.46]) or PaO2 (67+/-7 to 75+/-8 mm Hg [p=0.51]). Sleep efficiency and total sleep time (TST) increased significantly with NPPV in comparison to the control-sham night on low level CPAP: from 63+/-7% to 81+/-4% (p<0.05) and from 205+/-32 to 262+/-28 min (p<0.05), respectively. Sleep architecture, expressed as a percentage of TST, was unchanged on the NPPV night compared to the control-sham night on low level CPAP. The number of arousals during the night was also unchanged with NPPV in comparison to the control-sham night on low level CPAP (45+/-11 to 42+/-9 [p=not significant]). CONCLUSIONS: NPPV acutely improved sleep efficiency and TST in patients with hypercapnic COPD without significantly improving gas exchange. Other sleep parameters, including sleep architecture and the number of arousals during the night, remained unchanged during NPPV. These data suggest that the beneficial effects of NPPV in patients with hypercapnic respiratory failure are not solely due to an improvement in gas exchange but may be more complex with other factors potentially having contributing roles.

Cheyne-Stokes respiration during sleep in congestive heart failure.

Cheyne-Stokes respiration (CSR) is a form of sleep-disordered breathing seen in approximately 40% of congestive heart failure patients with a left ventricular ejection fraction of < 40%. It is characterized by a crescendo-decrescendo alteration in tidal volume separated by periods of apnea or hypopnea. Sleep is generally disrupted, often with frequent nocturnal arousals. Clinical features include excessive daytime sleepiness, paroxysmal nocturnal dyspnea, insomnia, and snoring. Proposed mechanisms include the following: (1) an increased CNS sensitivity to changes in arterial PCO2 and PO2 (increased central controller gain); (2) a decrease in total body stores of CO2 and O2 with resulting instability in arterial blood gas tensions in response to changes in ventilation (underdamping); and (3) an increased circulatory time. In addition, hyperventilation induced hypocapnia seems to be an important determinant for the development of CSR. Mortality appears to be increased in patients with CSR compared to control subjects with a similar degree of left ventricular dysfunction. Therapeutic options include medically maximizing cardiac function, nocturnal oxygen therapy, and nasal continuous positive airway pressure. The role that other therapeutic modalities, such as inhaled CO2 and acetazolamide, might have in the treatment of CSR associated with congestive heart failure has yet to be determined.

Obstructive sleep apnea: a multisystemic disorder.

Obstructive sleep apnea is a multisystemic disorder with pathologic sequelae that become apparent after a number of years. Patients with obstructive sleep apnea generally present with hypersomnolence, and diagnosis is eventually established through observation of the patient during sleep. Patients with obstructive sleep apnea snore loudly and experience nocturnal oxygen desaturation and repetitive disruptions from sleep that eventually lead to daytime hypersomnolence. Numerous complex interactive pathophysiologic events occur during each obstructive episode, and it is important for the clinician to be aware of the cardiopulmonary, neurologic, and anatomic abnormalities associated with this condition. The anatomic configuration of the pharynx and the physiologic response to occlusion of the upper airway have a major role in the pathogenesis of this disorder. Alveolar ventilation during an apneic episode is immediately reduced to zero, and the metabolic demands for oxygen must be met by oxygen stores within the body. With repetitive episodes of obstruction, the oxygen stores within the lungs are diminished and the rate of arterial oxyhemoglobin desaturation increases. During apneic episodes, the systemic blood pressure increases while heart rate and cardiac output decrease. Bradydysrhythmias have been noted with the obstructive apneic episodes, and ventricular dysrhythmias are associated with episodes of severe oxyhemoglobin desaturation. Coexisting cardiopulmonary or neuromuscular disease in patients with obstructive sleep apnea contributes to the development of hypoventilation, serious gas exchange derangement, and general cardiovascular instability.

Sleep in the intensive care unit.

The most critically ill patients in the hospital are located in the ICU. Due to intensive individualized care and monitoring, these patients often suffer from severe sleep deprivation. The amount and continuity of sleep as well as normal sleep architecture are all affected. Moreover, by impairing protein synthesis, cell division, and cellular immunity, sleep deprivation can affect the healing process and thus contribute to an increased morbidity and mortality. Reasons for sleep deprivation appear to be multifactorial and include the following: the patient's chronic underlying illness, an acute superimposed illness or surgical procedure, medications used in treatment of the primary illness, and the ICU environment itself. Therapeutic interventions need to address each of these potential causes, with an emphasis placed on providing an environment that is both diurnal and focused on the importance of uninterrupted sleep.

Effects of dobutamine on oxygen transport and consumption in the adult respiratory distress syndrome.

OBJECTIVE: To determine if oxygen consumption (VO2) in patients with adult respiratory distress syndrome (ARDS) is dependent on, and thus limited by, oxygen transport (TO2) rather than O2 demand. DESIGN: Prospective study. SETTING: Intensive care unit of a tertiary referral center. PATIENTS: 12 patients with ARDS and sepsis syndrome. INTERVENTIONS: Routine intensive care unit monitoring including pulmonary and radial artery catheters. MEASUREMENTS: Dobutamine was used to increase cardiac output, thereby directly varying TO2 under conditions of constant O2 demand. After baseline measurements of TO2 and VO2, dobutamine was infused intravenously at progressively increasing doses of 5, 10, 15 and 20 micrograms/kg/min and measurements of TO2 and VO2 were repeated after 30 min at each dose. RESULTS: Dobutamine increased TO2 in 8 of the 12 patients, by 29% at 5 micrograms/kg/min and by 45% (net) at 10 micrograms/kg/min, but not at higher doses. In these 8 patients dobutamine also increased VO2 by 15% at 5 micrograms/kg/min, but did not further increase VO2 at higher doses. There was no correlation between baseline blood lactate concentration and the response of either TO2 or VO2 to dobutamine. CONCLUSIONS: In some but not all patients with ARDS and sepsis syndrome, short-term infusion of low-dose dobutamine can increase both TO2 and VO2. Achievement of a TO2-independent level of VO2 could not be convincingly demonstrated in any individual patient. The response of TO2 and VO2 to dobutamine could not be predicted from baseline blood lactate concentration. Determination of the impact on patient outcome of a more prolonged infusion of dobutamine requires further study.

Diagnosis and management of asthma: a brief review of two asthma expert panel reports.

During the past decade, asthma morbidity and mortality have increased noticeably. Although the reasons for the increase are not clear, the prevalence of asthma has been reported to be increasing not only in the United States but also in other countries throughout the world, including the United Kingdom, New Zealand, and Australia. Asthma mortality rates and morbidity trends are increasing despite what appears to be major scientific advances in our understanding of asthma and in the face of a multitude of new therapeutic modalities. This article presents a brief overview of the pathogenesis and diagnosis of asthma, and highlights the major management recommendations of two expert panel reports.