Home oxygen therapy

Oxygen therapy is one of the principal non-pharmacologic treatments for severe chronic obstructive pulmonary disease (COPD) patients. Home oxygen therapy(HOT), or long-term oxygen therapy(LTOT) for 15 hours or more per day, can improve the survival rate of severe COPD patients with beneficial effects on hemodynamic state, hematological characteristic, exercise capacity, lung mechanics, and mental state. Oxygen therapy is indicated in cases of severe chronic respiratory failure with PaO2 of 55 Torr or less, or in cases with PaO2 of 60 Torr or less in whom there is remarkable hypoxia during sleep or during exercise. The induction of oxygen therapy needs evaluations of oxygen desaturation during exercise and sleep as well as hypoxia at rest. It also required to consider CO2 narcosis.     

The effect of arterial oxygen tension on antipyrine half-time in plasma.

Hospital patients with depressed arterial oxygen tensions (PaO2) from pulmonary disease were given antipyrine orally or intravenously. The half-time (t1/2) of disappearance from plasma was measured. Other patients with normal PaO2 measurements were treated similarly. Patients whose PaO2 was 55 or below had longer t1/2 times than those of patients with a PaO2 above 55. This observation parallels that made previously in rats.     

The acute haemodynamic effects of intravenous verapamil in patients with chronic obstructive airways disease

The haemodynamic effects of a single intravenous dose of verapamil have been investigated in patients with chronic obstructive airways disease both during an acute exacerbation and when in a stable clinical condition and compared with the effects of oxygen administered by nasal cannulae. In five patients studied during an episode of acute on chronic hypoxaemia (mean PaO2 = 5.4 kPa) there was a significant fall in pulmonary vascular resistance (p less than 0.03) following intravenous verapamil (10 mg) without any reduction in PaO2, cardiac index or oxygen delivery. Subsequent administration of oxygen by nasal cannulae at 2 l/min for 30 min produced similar pulmonary haemodynamic changes: pulmonary vascular resistance fell by 17 +/- 3 per cent following oxygen and by 22 +/- 4 per cent following verapamil. In a similar group of five patients in a stable clinical condition (mean PaO2 = 7.3 kPa) neither oxygen nor verapamil administered during acute exacerbations produced any significant changes in pulmonary vascular resistance, cardiac index or oxygen delivery.     

Hypoxaemia in patients with hyperventilation syndrome

We assessed 12 patients with hyperventilation syndrome (HVS) who had experienced hypoxaemia (PaO2 < 60 Torr or SaO2 < 90%) despite the lack of any other organic disease and variability in their blood gas data. Hypoxic and hypercapnic ventilatory responses were measured in nine. Eight of the 12 patients had been referred from other hospitals to our institution for hypoxaemia of unknown origin. Mean PaO2 (n = 12) at rest (non-attack stage) was 87.3 +/- 7.5 Torr (mean +/- SD). Their (n = 9) hypoxic (-0.53 +/- 0.32 l/min/%; range 0.12-0.99) and hypercapnic (2.01 +/- 0.76 l/min/Torr; range 0.69-3.17) ventilatory responses were both within the normal range in our laboratory. The patients with HVS had variable blood gas data, and some of them also exhibited hypercapnia (PaCO2 > 45 Torr). Clinicians who treat patients with HVS should be aware of the possibility of hypoxaemia, even when ventilatory responses are normal. Physicians should also consider HVS as a diagnosis when treating patients with hypoxaemia of unknown origin.      

Change in P wave height during progressive exercise in patients with chronic obstructive pulmonary disease

We examined changes in P wave height in lead II of electrocardiogram during progressive exercise in patients with chronic obstructive pulmonary disease (COPD), and obtained the slope (delta P/delta VO2, %/ml/min) of the regression line calculated from the relationship between percent change of P wave height and oxygen consumption (VO2). Four COPD patients, who had a decrease over 5 mmHg in arterial oxygen tension (PaO2) at maximal exercise (group A), had significantly greater slope (0.45 +/- 0.14%/ml/min, mean +/- S.E.) than in five COPD patients (group B, 0.14 +/- 0.05), who did not have a decrease over 5 mmHg in PaO2 at maximal exercise. The increase in P wave height during exercise was inhibited by oxygen inhalation at the given VO2 in group A. These findings suggest that increase in P wave height during exercise in COPD patients may be correlated with hypoxemia during exercise.     

Diagnostic value of gas exchange tests in patients with clinical suspicion of pulmonary embolism

OBJECTIVE: To assess the value of parameters derived from arterial blood gas tests in the diagnosis of pulmonary embolism. METHOD: We measured alveolar-arterial partial pressure of oxygen [P(A-a)O2] gradient, PaO2 and arterial partial pressure of carbon diaxide (PaCO2) in 773 consecutive patients with suspected pulmonary embolism who were enrolled in the Prospective Investigative Study of Acute Pulmonary Embolism. DIAGNOSIS: The study design required pulmonary angiography in all patients with abnormal perfusion scans. RESULTS: Of 773 scans, 270 were classified as normal/near-normal and 503 as abnormal. Pulmonary embolism was diagnosed by pulmonary angiography in 312 of 503 patients with abnormal scans. Of 312 patients with pulmonary embolism, 12, 14 and 35% had normal P(A-a)O2, PaO2 and PaCO2, respectively. Of 191 patients with abnormal scans and negative angiograms, 11, 13 and 55% had normal P(A-a)O2, PaO2 and PaCO2, respectively. The proportions of patients with normal/near-normal scans who had normal P(A-a)O2, PaO2 and PaCO2 were 20, 25 and 37%, respectively. No differences were observed in the mean values of arterial blood gas data between patients with pulmonary embolism and those who had abnormal scans and negative angiograms. Among the 773 patients with suspected pulmonary embolism, 364 (47%) had prior cardiopulmonary disease. Pulmonary embolism was diagnosed in 151 (41%) of 364 patients with prior cardiopulmonary disease, and in 161 (39%) of 409 patients without prior cardiopulmonary disease. Among patients with pulmonary embolism, there was no difference in arterial blood gas data between patients with and those without prior CPD. CONCLUSION: These data indicate that arterial blood gas tests are of limited value in the diagnostic work-up of pulmonary embolism if they are not interpreted in conjunction with clinical and other laboratory tests.     

Nitric oxide contamination of hospital compressed air improves gas exchange in patients with acute lung injury

OBJECTIVE: We tested the hypothesis that NO contamination of hospital compressed air also improves PaO(2) in patients with acute lung injury (ALI) and following lung transplant (LTx). DESIGN: Prospective clinical study. SETTING: Cardiothoracic intensive care unit. PATIENTS: Subjects following cardiac surgery (CABG, n=7); with ALI (n=7), and following LTx (n=5). INTERVENTIONS: Four sequential 15-min steps at a constant FiO(2) were used: hospital compressed air-O(2) (H1), N(2)-O(2) (A1), repeat compressed air-O(2) (H2), and repeat N(2)-O(2) (A2). MEASUREMENTS AND RESULTS: NO levels were measured from the endotracheal tube. Cardiorespiratory values included PaO(2) were measured at the end of each step. FiO(2) was 0.46+/-0.05, 0.53+/-0.15, and 0.47+/-0.06 (mean+/-SD) for three groups, respectively. Inhaled NO levels during H1 varied among subjects (30-550 ppb, 27-300 ppb, and 5-220 ppb, respectively). Exhaled NO levels were not detected in 4/7 of CABG (0-300 ppb), 3/6 of ALI (0-140 ppb), and 3/5 of LTx (0-59 ppb) patients during H1, whereas during A1 all but one patient in ALI and three CABG patients had measurable exhaled NO levels (P<0.05). Small but significant decreases in PaO(2) occurred for all groups from H1 to A1 and H2 to A2 (132-99 Torr and 128-120 Torr, P <0.01, respectively). There was no correlation between inhaled NO during H1 and exhaled NO during A1 or the change in PaO(2) from H1 to A1. CONCLUSIONS: Low-level NO contamination improves PaO(2) in patients with ALI and following LTx.     

Health, economic, psychological and social impact of educating carers of patients with advanced pulmonary disease (protocol)

People with advanced pulmonary disease (APD), such as those with chronic obstructive pulmonary disease, have markedly impaired quality of life. Home Oxygen Therapy (HOT) itself is burdensome, although it often improves survival duration and quality of life in these patients. The exact burdens on informal caregivers of these patients are unknown. The central purpose of the pragmatic randomized controlled study described in this protocol is to determine the effectiveness of improving the skills and knowledge of carers of patients with APD who use HOT. Specifically we aimed to estimate the incremental impact of this carer intervention above usual care on health, economic, psychological and social domains for patient and carer dyads relative to the level of current burden. Eligible patients and their carers were recruited through three major hospitals, and randomized to an intervention or control group. The carers in the intervention group received two home-delivered education sessions based on the principles of academic detailing. Participants are currently being followed over 12 months. The primary outcome will be the proportion of patients surviving without a chronic obstructive pulmonary disease-related readmission / residential (non respite) care over 12 months. Carer secondary outcomes include perceived caregiver burden, level of expected and received social support, perceived level of mastery, self esteem, health related quality of life and disability, and ability to conduct domestic chores and household maintenance, social activities and provide service to others, and fatigue. Secondary patient outcomes include health related quality of life and disability, and current respiratory health status.     

Influence of tidal volume and pulmonary artery occlusion on arterial oxygenation during endobronchial anesthesia.

Arterial blood gases, intrapulmonary right-to-left shunt, airway pressures, and systemic and pulmonary arterial pressures were studied in 20 patients ventilated through a double lumen endobronchial tube during thoracotomy. Inspired oxygen concentration was 98% to 100%. Blood samples for measurement of blood gases and oxygen content were obtained during ventilation of both lungs (VT 15 ml/kg), one lung (VT 15 ml/kg and 8 ml/kg), and after occlusion of the opposite pulmonary artery. Mean oxygen tensions fell significantly, from 310 mm Hg during two-lung ventilation to 155 during one-lung ventilation, and rose again to 280 after pulmonary artery occlusion. Corresponding mean shunt values rose from 25% to 34% of cardiac output and fell again to 25%. When VT was reduced, patients who had had low oxygen tensions (less than 150 mm Hg) at the higher volume showed an increase in PaO2, and conversely. Shunts changed accordingly. Even with this high FIO2, some patients had oxygen tensions of less than 80 mm Hg during lung collapse. PaO2 values during one-lung ventilation were significantly related to patients' preoperative oxygen tensions, as well as to those during two-lung ventilation. In view of the low arterial oxygen tensions found in some patients and the lack of absolute correlation of the PaO2 with tidal volume, an FIO2 of close to 1.0 is recommended during one-lung ventilation, along with frequent or continuous monitoring of the arterial PaO2.     

The degree of exercise hypoxemia reflects pulmonary artery pressure during early exercise in chronic obstructive pulmonary disease patients

The causes of both exertional pulmonary hypertension and pulmonary hypertension in general in chronic obstructive pulmonary disease (COPD) remain to be elucidated. To further understand the pathophysiology in COPD patients, it may be important to recognize the existence of exertional pulmonary hypertension and to determine the severity of exertional hypoxemia. However, little is known about their relationship. To investigate whether the severity of exertional hypoxemia, as evaluated by the Deltaartery oxygen tension/Deltaoxygen consumption (PaO(2)-slope) correlates with the mean pulmonary artery pressure (Ppa), cardiopulmonary exercise testing with haemodynamics was done in 10 patients with moderate to very severe COPD. The PaO(2)-slope was significantly correlated with the mean Ppa from 25% to 40% of the maximum Watts (Wmax), and was most significant at 30% Wmax (r = -0.904, P<0.0001). In this phase, all parameters, except for the mean Ppa and the mixed venous oxygen tension, were not markedly changed from resting levels. At 30% Wmax, the mean Ppa (mean, 27 mmHg) with no or mild hypoxemia was also significantly correlated with the Deltaartery oxygen saturation/Deltaoxygen consumption (SpO(2)-slope) (r = -0.789, P = 0.004). On stepwise multiple regression analysis, the PaO(2)-slope was the most significant predictor of mean Ppa at 30% Wmax. In conclusion, the PaO(2)-slope and the SpO(2)-slope reflect Ppa during the early exercise phase. Thus, assessment of these parameters could be useful to evaluate the cardiopulmonary haemodynamic pathophysiology of COPD patients.     

"Near miss" death in obstructive sleep apnea: a critical care syndrome

OBJECTIVE: The objective of this study was to alert critical care physicians to the syndrome of obstructive sleep apnea with respiratory failure ("near miss" death) and to elucidate characteristics that might allow earlier recognition and treatment of such patients. DESIGN: We examined clinical and laboratory characteristics of eight patients with obstructive sleep apnea presenting to the ICU with respiratory failure. These characteristics were compared with those of eight stable apnea patients of similar severity but without a history of presentation with respiratory failure. SETTING: Medical ICU and pulmonary outpatient clinic at the Houston Veterans Administration Medical Center, a teaching hospital affiliated with Baylor College of Medicine. PATIENTS: Eight patients with obstructive sleep apnea who presented in, or developed, acute respiratory failure requiring tracheal intubation and mechanical ventilation were matched to eight stable obstructive sleep apnea outpatients from the chest clinic. MEASUREMENTS AND MAIN RESULTS: The records of these 16 patients were reviewed and multiple characteristics that might predict these obstructive sleep apnea patients prone to respiratory failure and death (called the "near miss" death group; n = 8) were examined. The mean age of the near miss group was 57 yrs. All eight patients presented with respiratory acidosis (mean pH 7.22), hypercarbia (mean PaCO2 82 torr [10.9 kPa]), and hypoxemia (mean PaO2 45 torr [6.0 kPa]). Six of the eight patients had concomitant chronic obstructive pulmonary disease as determined by clinical characteristics and spirometry. Predisposing factors included facial trauma, lower respiratory tract infections or bronchospasm, and use of pain medication. All but one of the near miss subjects had awake hypercarbia (mean PaCO2 49 torr [6.5 kPa]) and hypoxemia (mean PaO2 58 torr [7.7 kPa]) during periods of clinical stability while only two controls had concomitant chronic obstructive pulmonary disease and none had hypercarbia. The prevalence of a history of wheezing and prior hospitalization for "respiratory problems" were greater in the near miss group. Once cured of apnea, no patient presented with recurrence of respiratory failure in follow-up ranging from 6 to 80 months, and cor pulmonale recurred in only one patient during subsequent onset of central apneas. CONCLUSION: Patients with obstructive sleep apnea who have concomitant chronic obstructive pulmonary disease or hypercarbia and hypoxemia are more prone to develop severe respiratory failure and probable death than those patients with apnea alone. The current study shows that recurrent respiratory failure and presumably mortality from this acute complication can be reversed with effective treatment of the obstructive apnea.     

Effects of long-term oxygen therapy on mortality and morbidity

In general, based on the above studies of the effects of supplemental oxygen on reducing mortality and improving sleep and exercise function in certain patient groups, patients whose disease is stable on a full medical regimen with PaO2 < or = 55 mm Hg (SaO2 < or = 88%) should be considered for LTOT. Patients with PaO2 of 55-59 mm Hg with signs of tissue hypoxemia (i.e., cor pulmonale, polycythemia, impaired cognition) should also be considered for LTOT. Oxygen therapy should also be considered for those who desaturate during sleep or exercise. These guidelines have been adopted by Medicare as reimbursement criteria and have also been endorsed by the American Thoracic Society. Indications for LTOT endorsed by the American Thoracic Society and published in the "Standards for the Diagnosis and Care of Patients with COPD" are shown in Table 6. More research is required to investigate the use of supplemental oxygen in patients who suffer nocturnal desaturation but do not have signs of end organ dysfunction, those who have an improvement in dyspnea with supplemental oxygen, and in normoxemic patients with impaired exercise performance who improve while inspiring supplemental oxygen.     

慢性阻塞性肺病呼吸衰竭的机械通气治疗：附32例分析

对３２例慢性阻塞性肺病（ＣＯＰＤ）引起的呼吸衰竭肺性脑病患者进行机械通气治疗。所有患者均全程监测血氧饱和度，上机及撤机前后共４次进行动脉血气分析，２９例应用压力支持通气（ＰＳＶ）模式。结果：３０例治疗获得成功，患者存活出院，抢救成功率９３．８％（３０／３２）。动脉血气分析提示机械通气治疗可显著提高动脉血氧分压及降低二氧化碳分压     

新型口鼻面罩用于慢性阻塞性肺病病人氧疗效果观察

为观察新型口鼻面罩（Ventrui面罩）和双侧鼻导管氧疗效果,对30例慢性阻塞性肺病急性加重期病人吸氧前后动脉血pH值、PaCO2及PaO2进行观察。结果显示：Ventrui面罩吸氧组病人的PaO2上升幅度较大,且迅速,能尽快改善病人的缺氧症状,而不加重二氧化碳潴留,与鼻导管组相比差异有统计学意义（P＜0．01）。建议对慢性阻塞性肺病急性加重期病人使用Ventrui面罩持续吸氧,可迅速改善病人的缺氧症状。     

A nationwide system of long-term oxygen therapy: the Polish experience

Poland's Institute of Tuberculosis and Lung Diseases oversees 49 provincial clinics, which provide and monitor LTOT for patients with COPD, interstitial pulmonary fibrosis, and other pulmonary conditions. Because of limited resources, eligibility for LTOT is fairly strictly defined, and LTOT equipment is distributed to and retained only by nonsmoking patients who continue to demonstrate need of the equipment (i.e., those who have ongoing hypoxemia that can benefit from LTOT). This national LTOT system provides a large, nonselected population suitable for LTOT research, and recent studies have produced important data regarding survival, pulmonary hemodynamics, and the effect of withdrawing LTOT from patients whose oxygenation has recovered to above the LTOT qualification level of PaO2 < or = 55 mm Hg.     

Serum phospholipase A2 and pulmonary changes in acute fulminant pancreatitis

Twenty-three patients with acute fulminant pancreatitis were studied. The diagnosis was confirmed at laparotomy in every case. Blood samples for the assay of phospholipase A2 were collected for 14 days, and the pulmonary status of the patients was followed by monitoring the blood gases and the inspired oxygen fraction and studying a derived variable, the alveolar to arterial oxygen tension difference--the arterial oxygen tension ratio (A--aDo2/PaO2). The serum phospholipase A2 activities correlated with the changes in pulmonary function and with the outcome of the disease. Eight patients succumbed and they showed higher phospholipase A2 activities and A--aDo2/PaO2 ratios than the five patients who survived after major complications and the ten patients who survived without major complications. The results suggest that in acute fulminant pancreatitis serum phospholipase A2 activity correlates with the severity of the pulmonary changes. Furthermore, it seems to reflect the prognosis.     

Long-term oxygen therapy: physiologic and economic considerations.

Long-term oxygen therapy appears to be a safe means of treating hypoxemia. It can provide many physiologic improvements and prolongs life in persons with severe chronic arterial hypoxemia at rest. Recent studies suggest that arterial hypoxia is common during exercise and sleep, and it is likely that some patients with intermittent desaturation would benefit physiologically from supplemental oxygen. Oxygen is an expensive drug, and we do not know whether its benefits are greater than its costs in patients who are not hypoxic at rest. I believe that low-flow oxygen administered as continuously as possible should be strongly considered for all patients whose PaO2 is 55 mm Hg or less at rest, regardless of whether they have cor pulmonale, and for all patients with cor pulmonale, regardless of their PaO2.     

Time required for partial pressure of arterial oxygen equilibration during mechanical ventilation after a step change in fractional inspired oxygen concentration

OBJECTIVE: To determine the time required for the partial pressure of arterial oxygen (PaO2) to reach equilibrium after a 0.20 increment or decrement in fractional inspired oxygen concentration (FIO2) during mechanical ventilation. SETTING: A multi-disciplinary ICU in a university hospital. PATIENTS AND METHODS: Twenty-five adult, non-COPD patients with stable blood gas values (PaO2/FIO2 > or = 180 on the day of the study) on pressure-controlled ventilation (PCV). Following a baseline PaO2 (PaO2b) measurement at FIO2 = 0.35, the FIO2 was increased to 0.55 for 30 min and then decreased to 0.35 without any other change in ventilatory parameters. Sequential blood gas measurements were performed at 3, 5, 7, 9, 11, 15, 20, 25 and 30 min in both periods. The PaO2 values measured at the 30th min after a step change in FIO2 (FIO2 = 0.55, PaO2[55] and FIO2 = 0.35, PaO2[35]) were accepted as representative of the equilibrium values for PaO2. Each patient's rise and fall in PaO2 over time, PaO2(t), were fitted to the following respective exponential equations: PaO2b + (PaO2[55]-PaO2b)(1-e-kt) and PaO2[55] + (PaO2[35]-PaO2[55])(e-kt) where "t" refers to time, PaO2[55] and PaO2[35] are the final PaO2 values obtained at a new FIO2 of 0.55 and 0.35, after a 0.20 increment and decrement in FIO2, respectively. Time constant "k" was determined by a non-linear fitting curve and 90% oxygenation times were defined as the time required to reach 90% of the final equilibrated PaO2 calculated by using the non-linear fitting curves. RESULTS: Time constant values for the rise and fall periods were 1.01 +/- 0.71 min-1, 0.69 +/- 0.42 min-1, respectively, and 90% oxygenation times for rises and falls in PaO2 periods were 4.2 +/- 4.1 min-1 and 5.5 +/- 4.8 min-1, respectively. There was no significant difference between the rise and fall periods for the two parameters (p > 0.05). CONCLUSION: We conclude that in stable patients ventilated with PCV, after a step change in FIO2 of 0.20, 5-10 min will be adequate for obtaining a blood gas sample to measure a PaO2 that will be representative of the equilibrium PaO2 value.