SUMMARY OF APPROACH The approach to surgery in the patient with COPD is summa-rized below. Surgery Definitely indicated Lung resection. Pulmonary function studies should be performedbefore lung resection. Simple spirometry has the greatest utilityin documenting physiologic operability. FEV, > 2 L in an adultman or > 60% of predicted is acceptable for pneumonectomy.Values below this suggest that further studies, such as split func-tion assessment by quantitative lung scintigraphy and exercisetesting, are warranted.FEV, predicted after lung resection to be less than 40 to 50%of normal for the patient’s sex, age, and height suggests highermorbidity and mortality. An exercise 90, of less than 10 to 15ml/min per kg of body weight is associated with higher mor-bidity and mortality after lung resection.All elective surgery Prophylaxis against deep venous throm-bosis should be given before most procedures that will requirepostoperative bed rest or significantly reduce mobility. Heparinin low doses seems well accepted for most procedures. Externalpneumatic compression of the lower legs can be used when anti-coagulants are contraindicated.

/pdf/standards-for-the-diagnosis-and-care-of-patients-with-13vz6fyao0.pdf

Standards for the Diagnosis and Care of Patients with Chronic Obstructive Pulmonary Disease

Chronic obstructive pulmonary disease (COPD) is a major cause of morbidity and mortality. In the European Union, COPD and asthma, together with pneumonia, are the third most common cause of death. In North America, COPD is the fourth leading cause of death, and mortality rates and prevalence are increasing. The major characteristic of COPD is the presence of chronic airflow limitation that progresses slowly over a period of years and is, by definition, largely irreversible. Most patients with COPD are, or were, cigarette smokers. Prevention by reducing the prevalence of smoking remains a priority. Although much of the damage is irreversible at the time of clinical presentation, treatments are available to improve the quality of life, the life expectancy, and perhaps the functional ability of patients with COPD. Several national and international consensus statements on optimal assessment and management of asthma have been published in recent years. These consensus statements have led to international standardization of diagnosis and management and to better care. They also form a basis for clinical audits and suggest areas of future research. However, there have been few attempts to develop consensus guidelines on management of COPD [1, 2]. The European Respiratory Society (ERS) has taken the initiative of producing a consensus statement on COPD. A Task Force of scientists and clinicians was invited to provide this European consensus. The guidelines are intended for use by physicians involved in the care of patients with COPD, and their main goals are to inform health professionals and to reverse a widespread nihilistic approach to the management of these patients. This Task Force firmly believes that treatment can significantly improve the quality and length of life of patients suffering from this chronic, progressive condition. Subcommittees of the Task Force focused on the five main sections of this project: Pathology/Pathophysiology, Epidemiology, Assessment, Treatment, and Management. Experts produced papers within each section, and these papers were brought together by the subcommittee heads. At a plenary meeting held in Wiesbaden, Germany on November 11–13, 1993, all contributions were extensively discussed, and additional working group meetings were arranged. Flowcharts for management in common clinical situations were produced. However, at all stages, members of the Task Force found themselves confronted by unresolved questions and regional differences in management across Europe. A practical approach was adopted, combining established scientific evidence and a consensus view when current data were inadequate. This approach identified more clearly those areas where further research is needed. Comments on drafts of the consensus statement were invited from participants of the original meeting, which included colleagues from North America. The edited document was sent to independent experts for external review. All members had an opportunity to comment on the document at the ERS meeting in Nice on October 2, 1994. As chairmen of the Task Force, we hope that the final document will promote better management of COPD in Europe. We would like to thank all who contributed to it. On behalf of the ERS, we also gratefully acknowledge a generous educational grant from Boehringer Ingelheim and the organizational assistance provided by M.T. Lopez-Vidriero.

https://erj.ersjournals.com/content/erj/8/8/1398.full.pdf

Optimal assessment and management of chronic obstructive pulmonary disease (COPD). The European Respiratory Society Task Force

Though exercise training is part of most pulmonary rehabilitation programs, whether there is a physiologic basis for increased exercise tolerance is unclear. We sought to determine whether patients with chronic obstructive pulmonary disease (COPD) are capable of obtaining a physiologic training effect, as manifested by a reduction in blood lactate and ventilation (VE) at a given level of exercise. We also sought to determine whether training work rate determines the size of the training effect. Nineteen participants with COPD of predominantly moderate severity in an inpatient rehabilitation program performed two cycle ergometer exercise tests at a low and a high work rate for 15 min or to tolerance and also an incremental exercise test to tolerance. Arterial blood was sampled for blood gas and lactate analyses. Identical tests were performed before and after 5-day-per-week cycle ergometer training for 8 wk either for 45 min/day at a high work rate (average, 71 W) or for a proportionally longer time at a low work rate (average, 30 W). Average FEV1 was 56 +/- 12% predicted and did not change with training. Peak exercise lactate (average, 6.5 mEq/L) was not correlated with FEV1. For the high work rate training group, identical work rates engendered less lactate (4.5 versus 7.2 mEq/L) and less VE (48 versus 55 L/min) after training; the low work rate training group had significantly less lactate and VE decrease (p less than 0.01). Further, endurance time for the high constant work rate increased 73% in the high work rate training group but only 9% in the low work rate training group. At identical work rates, VE decrease average 2.5 L/min per mEq/L decrease in lactate (r = 0.75). We conclude that most COPD subjects studied increased blood lactate at low work rates. Many of these patients were able to achieve a physiologic training effect. Though total work was the same, training at a high work rate was more effective than was training at a low work rate. The lower VE requirement to perform exercise was in proportion to the lower lactate level, but the VE decrease for a given decrease in lactate was smaller than that seen in normal subjects (7.2 L/min/mEq/L), apparently because patients with COPD fall to hyperventilate in response to lactic acidosis (PaCO2 does not drop). These findings provide a physiologic rationale for exercise training of patients with COPD.

Reductions in Exercise Lactic Acidosis and Ventilation as a Result of Exercise Training in Patients with Obstructive Lung Disease

The goals of therapy for chronic obstructive pulmonary disease include relieving symptoms, improving abnormal physiology, and limiting complications, including abnormal gas exchange and exacerbations of the disease. This review summarizes current guidelines and provides recommendations for management, including assessment of lung function, preventive measures, stepwise medical therapy, and pulmonary rehabilitation and surgical therapy. By the time this disease becomes symptomatic, the forced vital capacity of most patients has already declined by about 50 percent.

https://internal.medicine.ufl.edu/files/2012/07/5.18.08.02.-COPD-review.pdf

Management of chronic obstructive pulmonary disease.

Mild-to-moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. Pulmonary hypertension usually worsens during exercise, sleep and exacerbation. Pulmonary vascular remodelling in COPD is the main cause of increase in pulmonary artery pressure and is thought to result from the combined effects of hypoxia, inflammation and loss of capillaries in severe emphysema. A small proportion of COPD patients may present with "out-of-proportion" pulmonary hypertension, defined by a mean pulmonary artery pressure >35-40 mmHg (normal is no more than 20 mmHg) and a relatively preserved lung function (with low to normal arterial carbon dioxide tension) that cannot explain prominent dyspnoea and fatigue. The prevalence of out-of-proportion pulmonary hypertension in COPD is estimated to be very close to the prevalence of idiopathic pulmonary arterial hypertension. Cor pulmonale, defined as right ventricular hypertrophy and dilatation secondary to pulmonary hypertension caused by respiratory disorders, is common. More studies are needed to define the contribution of cor pulmonale to decreased exercise capacity in COPD. These studies should include improved imaging techniques and biomarkers, such as the B-type natriuretic peptide and exercise testing protocols with gas exchange measurements. The effects of drugs used in pulmonary arterial hypertension should be tested in chronic obstructive pulmonary disease patients with severe pulmonary hypertension. In the meantime, the treatment of cor pulmonale in chronic obstructive pulmonary disease continues to rest on supplemental oxygen and a variety of measures aimed at the relief of airway obstruction.

https://erj.ersjournals.com/content/erj/32/5/1371.full.pdf

Pulmonary hypertension in COPD

Nocturnal Oxyhemoglobin Desaturation in COPD Patients with Arterial Oxygen Tensions Above 60 mm Hg

Pulmonary vascular hemodynamics in chronic lung disease patients with and without oxyhemoglobin desaturation during sleep.

The Rate of Fall of Arterial Oxyhemoglobin Saturation in Obstructive Sleep Apnea

Nocturnal oxyhemoglobin desaturation (NOD) has been reported in patients with disease of the pulmonary parenchyma and/or chest wall. The resulting hypoxemia could play a role in the development of pulmonary hypertension. We have previously demonstrated a small but statistically significant difference in resting pulmonary artery pressure (Ppa) and pulmonary vascular resistance (PVR) between two groups of patients with COPD of similar age, symptomatology, and degree of pulmonary dysfunction. These two groups were selected only on the basis of the presence or absence of NOD, and all had a mean daytime PaO2 at or above 60 mm Hg. The present study uses exercise to stress the pulmonary circulation of two groups of patients similar to the above. The purpose was to see if exercise can amplify underlying cardiopulmonary hemodynamic differences between NOD and non-NOD subjects. In addition, we attempted to confirm or refute previous studies which claimed that exercise desaturation correlates with NOD. Resting supine, resting upright, and upright exercise cardiopulmonary hemodynamics were measured using an indwelling right heart catheter, and arterial blood and expiratory gases were collected to assess metabolic and other gas exchange parameters. Although both groups showed increase in Ppa during exercise, the increases in systolic Ppa, mean Ppa, and driving pressure were disparately higher in subjects with NOD. Exercise desaturation was not predictive of NOD. The presence of NOD was predictive of a resting PVR greater than 120 dyne.s.cm-5, whereas mean sleep SaO2 and daytime PaO2 were unable to discriminate patients with COPD above or below this level.(ABSTRACT TRUNCATED AT 250 WORDS)

Trey Miller

Papers

Nocturnal Oxyhemoglobin Desaturation in COPD Patients with Arterial Oxygen Tensions Above 60 mm Hg

Pulmonary vascular hemodynamics in chronic lung disease patients with and without oxyhemoglobin desaturation during sleep.

The Rate of Fall of Arterial Oxyhemoglobin Saturation in Obstructive Sleep Apnea

Exercise Hemodynamics and Gas Exchange in Patients with Chronic Obstruction Pulmonary Disease, Sleep Desaturation, and a Daytime PaO2 above 60 mm Hg