Why do they decompensate? PE, Pneumonia, URI, CHF/Ischemia/Dysrhythmia, Med changes or noncompliance, or Pneumothorax
PE-bronchitics are predisposed
Do not sedate COPDers, may cause resp. depression
NIPPV should be first line therapy in all exacerbations with respiratory failure (Cochrane Review BMJ. 2003; 326 (7382) 185-189)
Elastase breaks down lung parenchyma. Compensate c tachypnea. Marks above the knees from tripoding.
Hypertrophy of submucosal glands and goblet cells. Polycythemia means they can become cyanotic very easily and yet still be comfortable.
Note: Retrocardiac space can be eliminated by cor pulmonale giving enlarged right ventricle.
P Pulmonale-increased ps in II, III, AVF
Adrenergic state of acute attack leads to white cell demarginalization (epi given to a pt does same thing)
Assoc c Multifocal A. Tach
Load aminophylline 5 mg/kg over 0 minutes, then .5 mg/kg/hr
Methylxanthines Offer No Benefit in Acute COPD Exacerbations (BMJ 2003 Sep 20)
Make sure patient has received s. pneumo and influenza vaccines.
Get chest x-ray (prompts change in short-term 21%)
Aim for sats 90-92%
use combined bronchodilator therpay
bactrim, doxy, or amox for purulent sputum or acute exac. (N Engl J 2002, 347 supports treatment of acute exac but doesnt say which ABX)
Statistically significant benefit to antibiotics in acute exacerbations. (Chest 2001;119:1190-209. and JAMA 1995;273:957-60.)
Also send ’em home with steroids (NEJM Volume 348:2618-2625 June 26, 2003
Prednisone 8 day taper starting at 40 and decreasing by 10 each day
Stoller Acute Exacerbations of Chronic Obstructive Pulmonary Disease NEJM 2002; 346
prednisone 40mg PO daily for ten days upon discharge from the ED. It should be noted that patients who had taken steroids within the preceding 30 days were excluded from the study. (Aaron SD, Vandemheen KL, Hebert P, et al. Outpatient oral prednisone after emergency treatment of chronic obstructive pulmonary disease. N Engl J Med 2003;348:2618-2625.
Give Mg in severe exac. (Emerg Med J 2004; 21:203)
Re:Hypoxia and hypercapnia in COPD…. There was a good theoretical article in CCM in 1996 I think which took a mathematical approach to the problem. Crit Care Med. 1996 Jan;24(1):23-8. Causes of hypercarbia with oxygen therapy in patients with chronic obstructive pulmonary disease. Hanson CW 3rd, Marshall BE, Frasch HF, Marshall C. Department of Anesthesia, Hospital of the University of Pennsylvania, Philadelphia 19104, USA. OBJECTIVES: To compare data derived from a computer model of the pulmonary circulation with data from a case series of patients with chronic obstructive pulmonary disease (COPD). To evaluate the specific factors contributing to CO2 retention due to oxygen therapy in patients with acute exacerbations of COPD. DESIGN: Data from a computer model of the pulmonary circulation were compared with a previous case series. PATIENTS: Patient data were derived from previous case series. INTERVENTIONS: Simulated application of oxygen therapy. MEASUREMENTS AND MAIN RESULTS: The computer model of the pulmonary circulation generates data comparable with those data from a series of patients with COPD treated with supplemental oxygen and permits identification of the causes for hypercarbia. Therapy with supplemental oxygen alters hypoxic pulmonary vasoconstriction and modulates the Haldane effect, resulting in changes in physiologic deadspace. CONCLUSION: Changes in physiologic deadspace are ! sufficient to account for the hypercarbia developed by patients with acute exacerbations of COPD when treated with supplemental oxygen. I enjoyed this article my interpretation is as follows… Hypercapnia can be explained in terms of increased physiological dead space due to: 1 Haldane effect CO2 is less soluble in red (arterialised) blood therefore as venous oxygen tension increases with excessive administered O2, less CO2 is transported back to lungs. 2 Reduction in hypoxic pulmonary constriction. As O2 levels increase there is less hypoxic vasoconstriction, therefore increased shunt, therefore increased difficulty in eliminating CO2. Both these effects are small, but synergise and will with a fixed maximal minute ventilation will cause CO2 to rise. Aubier did a study on COPD patients in the early 80’s and found that hypercapnia could be explained by increased VQ mismatch See below: Am Rev Respir Dis. 1980 Nov;122(5):747-54. Effects of the administration of O2 on ventilation and blood gases in patients with chronic obstructive pulmonary disease during acute respiratory failure. Aubier M, Murciano D, Milic-Emili J, Touaty E, Daghfous J, Pariente R, Derenne JP. The effects of the administration of 100% oxygen on minute ventilation (VE) and arterial blood gases were studied in patients with chronic obstructive pulmonary disease during acute respiratory failure. The administration of O2 resulted in an early decrease in VE, which averaged 18% +/- 2 SE of the control VE, and was due to a decrease in both tidal volume (VT) and respiratory frequency (f). This was followed by a slow increase in VE, such that after 15 min of breathing O2, VE rose to 93 +/- 6% of the control room air value, with both VT and f similar to control values. Despite the small difference between VE while breathing room air and that at the fifteenth minute of O2 inhalation, PaCO2 increased by 23 +/- 5 mmHg, and no significant correlation was found between the changes in VE and PaCO2. By the fifteenth minute of O2 inhalation the PaO2 averaged 225 +/- 23 mmHg, and it was concluded that despite the removal of the hypoxic stimulus of O2 inhalation, the activity of the ! respiratory muscles remained great enough to maintain VE at nearly the same degree as that while breathing room air. Consequently, the changes in PaCO2 after the administration of O2 were mainly due to increased inhomogeneity of VA/Q distribution within the lungs. Another study in paralysed ventilated patients in CCM in did not find the expected rise in CO2: Crit Care Med. 1997 Sep;25(9):1522-6. Comment in: Crit Care Med. 1997 Sep;25(9):1450-1. Influence of inspired oxygen concentration on deadspace, respiratory drive, and PaCO2 in intubated patients with chronic obstructive pulmonary disease. Crossley DJ, McGuire GP, Barrow PM, Houston PL. Department of Anaesthesia, Toronto Hospital, ON, Canada. OBJECTIVES: To investigate the response of CO2-retaining chronic obstructive pulmonary disease (COPD) patients to an increase in FIO2 following a period of mechanical ventilation with PaO2 in the normal range. The administration of a high FIO2 to chronic obstructive pulmonary disease (COPD) patients may result in hypercapnia. Recent evidence indicates that the hypercapnia may be due to reversal of preexisting regional hypoxic pulmonary vasoconstriction resulting in a greater deadspace. This effect would be more pronounced in patients whose initial PaO2 was < 60 torr (< 7.9 kPa). DESIGN: Single blinded, prospective study. SETTING: A medical surgical intensive care until in a tertiary care, teaching hospital. PATIENTS: COPD CO2-retaining patients. INTERVENTIONS: FIO2 increased to 0.7. MEASUREMENTS AND MAIN RESULTS: Twelve intubated COPD patients weaned from mechanical ventilation were studied both at their baseline FIO2 (0.3 to 0.4), and following a 20-min period of exposure t! o an FIO2 of 0.7. Mean baseline values were: PaO2 of 85 torr (11.3 kPa), PCO2 of 56 torr (7.5 kPa), deadspace of 73%, and respiratory drive normal, as measured by P0.1. Statistical analysis using the paired Student’s t-test showed that the PaO2 increased significantly when the FIO2 was increased to 0.7, but there was no significant change in PaCO2, deadspace, or respiratory drive. CONCLUSION: These results show that following a period of mechanical ventilation with an FIO2 sufficient to maintain a normal PaO2, a further increase in FIO2 does not result in an increased PaCO2 in this group of CO2-retaining COPD patients. Not sure how to reconcile this….perhaps there is a difference wrt to CO2 elimination and physiological dead space issues in paralysed ventilated patients vs spont breathing?? Perhaps differences in cardiac outputs paralysed vs spont breathing. Don’t know…and even if someone tried to explain this to me I probably wouldn’t understand. That’s my N.Z. 2 peso’s worth. I asked the question some time ago. Jeff Whitnack was so kind as to send me these references on the subject. Try numbers 20 and 21, and you might find the origin of this urban legend. Nick
1. Debunking Myths of Chronic Obstructive Pulmonary Disease (Editorial) Hoyt, Crit Care Med 1997 Vol. 25, Number 9, pgs. 1450-51 2. Respiratory Failure, Campbell, Arnott, et al, Lancet 1960 ii:12 pages 1-7 3. The J. Burns Amberson Lecture-The Management of Acute Respiratory Failure in Chronic Bronchitis and Emphyzema by E.J.M. Campbell, Am Rev. Resp. Dis. 1967 Oct. 96(4): 626=39 4. Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia Scano, et al, Eur. Resp. J. 1995 8:78-85 5. The Role of Hypoventilation and Ventilation-Perfusion Redistribution in Oxygen-induced Hypercapnea during Acute Excacerbation of Chronic Obstructive Pulmonary Disease, Robinson, et al, Am. J. Resp. Crit. Care Med Vol. 161, pgs. 1524-1529 2000 6. Effects of the Administration of O2 on Ventilation and Blood Gases in Patients with Chronic Obstructive Pulmonary Disease During Acute Respiratory Failure, Aubier, et al, Am. Rev. Resp. Dis. Vol. 122 pages 747-754 1980 7. Causes of Hypercapnia with Oxygen Therapy in Patients with Chronic Obstructive Pulmonary Disease by Hanson, et al, Crit. Care Med 1996 Vol. 24 pgs. 23-28 8. Hyperoxic-induced Hypercapnea in Stable Chronic Obstructive Pulmonary Disease, Sassoon, et al, Am Rev. Resp. Dis. 1987 135:pgs. 907-911 9. Uncontrolled Oxygen Administration and Respiratory Failure in Acute Asthma, Chien, et al, Chest 117/3/March 2000 pgs. ;728-733 10. The Control of Breathing in Clinical Practice, Caruana-Montaldo, et al, Chest 117/1 Jan., 2000, pages 205-225 11. Oxygen-induced Hypercarbia in Obstructive Pulmonary Disease, Dunn, et al, Am Rev Resp Dis 1991, 144:526-530 12. (Hypothesis) Hypercapnea During Oxygen Therapy in Acute Exacerbation of Chronic Respiratory Failure, Rudolf, et al Lancet Sept. 3, 1977, pages 483-486 13. (Editorial) Hypercapnea during oxygen therapy in airways obstruction: a reappraisal. Stradling, Thorax 1986 41:897-902 14. Influence of Inspired oxygen concentration on deadspace, respiratory drive, and PaCO2 in intubated patients with chronic obstructive pulmonary disease, Crossley, et al, Crit Care Med 1997 Vol. 25, Number 9, pages 1522-1526 15. Correspondence (Aubier and Stradling regarding study cited in # 6 above, Am Rev Resp Dis. Oct. 16th, 1986****(get exact issue) 16. One year prevalence study of respiratory acidosis in acute exacerbations of COPD: implications for the provision of non-invasive ventilation and O2 administration, Plantt, et al, Thorax 2000, 55:550-554 17. Respiratory Arrest in Near-Fatal Asthma, Molfino, et al, N. Eng. J. Med 1991 324:285-288…see also editorial same issue, page 409-411 by McFadden 18. (Case Report) Extreme Obesity Associated with Alveolar Hypoventilation-A Pickwidkian Syndrome, Burnell, et al, Am. J. Med 1956 21:811-818 19. Ventilation-perfusion inequality in chronic obstructive pulmonary disease, Wagner, et al, The Journal of Clinical Investigations, Vol. 59, Feb. 1977, pages 203-216 20. The J. Burns Amberson Lecture—The Management of Acute Respiratory Failure in Chronic Bronchitis and Emphyzema by E.J.M. Campbell, Am Rev Resp Dis 1967, Oct. 96(4):626-639 21. Respiratory Failure, Campbell and Arnott, et al, Lancet 1960, ii 12, 1-7 22. O2-induced changes in Ventilation and Ventilatory Drive in COPD. Dick, et all, Am J Resp Crit Care Med vol 115, pages 609-614, 1997 23. Inter-individual Variability of the Response to Oxygen Administration in Hypercapneic Patients, Gasparini, et al, Eur J of Resp Dis., 1986; 69(suppl 146) 427-443 24. May 98 issue of Clinical Pulmonary Medicine is an article titled Acute Respiratory Failure in Chronic Obstructive Pulmonary Disease” by Schiavi 25. Plant PK, Owen JL, Elliott MW. One year period prevalence study of respiratory acidosis in acute exacerbations of COPD: implications for the provision of noninvasive ventilation and oxygen administration. Thorax 2000; 55: 550-54 26. Critical Care Medicine Jan. 2002, Oxygen therapy for hypercapnic patients with chronic obstructive pulmonary disease and acute respiratory failure: A randomized, controlled pilot study Charles D. Gomersall, MBBS, FFICANZCA; Gavin M. Joynt, MBBCh, FFA (SA)(Crit Care); Ross C. Freebairn, MBBCh, FFICANZCA; Christopher K. W. Lai, DM, FRCP; Teik E. Oh, MD, FFICANZCA 27. Editorial, same issue P. 258 Oxygen-induced acute hypercapnia in chronic obstructive pulmonary disease: What’s the problem? [NL]Steven Q. Simpson, MD 28. What say others on this issue?
(Chest. 2005;128:48-54.) © 2005 American College of Chest PhysiciansBack to top
A Randomized Controlled Trial To Assess the Optimal Dose and Effect of Nebulized Albuterol in Acute Exacerbations of COPD*
No difference between 2.5 and 5 for COPD
COPD Exacerbation in the ED – When to Consider the Diagnosis of Pulmonary Embolism The diagnosis of acute PE is difficult in patients with COPD; PE resembles COPD exacerbation so closely that these 2 entities are often impossible to distinguish clinically (2). The reported incidence of PE in studies done postmortem of patients with COPD ranges from 28% – 51% (1). Several studies have indicated that the frequency of PE in patients with COPD with a severe exacerbation (i.e. one requiring hospitalization) of unknown origin is approximately 25% (1-3). Clinical symptoms such as change in dyspnea, pleuritic pain, hemoptysis, tachycardia (pulse rate >100 beats/min), and edema of the lower limbs, were not associated with PE. A just-released study (1) found that only 3 factors predicted PE in patients with COPD requiring hospital admission for severe exacerbation of unknown origin: history of thromboembolism, malignant disease, and a decrease in PaCO2 of at least 5 mm Hg relative to baseline. Therefore, when a severe exacerbation of COPD occurs (i.e., one requiring hospitalization) of unknown origin (e.g. without purulence of sputum, history of a cold or sore throat, or pneumothorax), the Emergency Physician should consider pursuing the diagnosis of PE with appropriate studies (e.g. venous lower-limb ultrasonography, spiral CT scan, etc.). References: (1) Tillie-Leblond I, et al. Pulmonary embolism in patients with unexplained exacerbation of chronic obstructive pulmonary disease: prevalence and risk factors Ann Intern Med 2006;144:390-6. (2) Lesser BA, et al. The diagnosis of acute pulmonary embolism in patients with chronic obstructive pulmonary disease Chest 1992;102:17-22. (3) Hartmann IJ, et al. Diagnosing acute pulmonary embolism: effect of chronic obstructive pulmonary disease on the performance of D-dimer testing, ventilation/perfusion scintigraphy, spiral computed tomographic angiography, and conventional angiography. ANTELOPE Study Group. Advances in New Technologies Evaluating the Localization of Pulmonary Embolism Am J Respir Crit Care Med 2000;162: 2232-7.
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