COPD Patient

[Ace844]

Hello Everyone,

For those who would like more information on this subject and would also like to read some good studies which relate I have provided you the links below, and quoted two additional studies as well.

Hope this Helps,

ACE844

http://www.emtcity.com/phpBB2/viewtopic.php?t=1027

http://www.nda.ox.ac.uk/wfsa/html/u12/u1203_03.htm

http://www.studentbmj.com/issues/01/04/education/94.php

http://en.wikipedia.org/wiki/CO2_retention

http://bmj.bmjjournals.com/cgi/content/full/317/7161/798

http://emj.bmjjournals.com/cgi/content/full/18/6/421

By “Hypoxic Drive Theory” I am referring to either the default assumption that any chronically compensated respiratory acidosis implies reliance on the hypoxic drive to maintain adequate gas exchange….or …..that chronically compensated respiratory acidosis means the central chemoreceptors are defunct or deficient.

This is more than just a theory, it’s become a clinical mindset, almost a medical urban legend. “He’s a retainer”, “that’s where he lives”, “he’s in the 50/50 club”, etc., all are like so many clinical buzzwords.

There is the existence of a hypoxic drive. It normally accounts for about 10-15% of the total drive to breathe. We all have it, unless perhaps we’ve had bilateral carotid surgery. It becomes obliterated at a PaO2 above about 170, and becomes a greater stimulus as the PaO2 drops below 70, and especially below 50.

There is a hyperoxia-associated hypercarbia, which can develop in certain patients while they are in crisis. But it has little, if anything, to do with respiratory drive.

When COPD patients are in acute respiratory failure they are usually breathing somewhere near their maximum limit. When 100% O2 is applied the CO2 can be driven up by 3 factors…

The Haldane Effect. Unsaturated hemoglobin carries CO2. A patient in crisis may arrive in the ER with an SpO2 on room air of 75%, the unmeasured mixed venous saturation may then in turn also be much lower than the 75% norm. All this unsaturated hemoglobin is then carrying an extra CO2 load. This is in the setting whereby the patient has an already elevated PaCO2, perhaps has an elevated Hgb after years of hypoxemia, and is “topped off” on their ability to ventilate. So for every rise in their SpO2 we are driving more CO2 into the plasma. If this were you or I, we would simply then ventilate this extra CO2 out via the lungs. But their lungs can’t and don’t, therefore the CO2 shows up in the “downstream” ABG.

The release of hypoxic pulmonary vasoconstriction. Imagine the worst ventilated alveoli. The local CO2 pressure there may be 100 or more. On room air the local O2 pressure will surely be less than 60 torr. At this level of local hypoxemia, the adjacent pulmonary vasculature will constrict. Blood will then be sent to the alveoli, which is ventilating more effectively. Ventilation/perfusion matching is enhanced. But if 100% O2 is given the O2 pressure will not drop below 60, the pulmonary vasculature will not constrict, and V/Q matching will not be optimized. Just as giving nitroprusside may drop the PaO2 as hypoxic pulmonary vasoconstriction is released, so giving 100% O2 may also raise the PaCO2. This also can happen to patients in an asthmatic crisis given 100% O2. It’s not that we knock out a hypoxic drive, so much as we drive in a hypercarbic potential. Then further compromise ventilation through increased V/Q mismatching.

A small amount of the CO2 retainers whom are in acute failure, and whom have their PaCO2 increased further from the two mechanisms listed above, will then reduce their minute ventilation further by about 15-20%. Usually the PaO2 will have been about 40 on room air, the PaCO2 70. Given 100% O2 the PaO2 rises well above the 170 range whereby all hypoxic drive is obliterated, and the PaCO2 rises to 90 or more. But is this a result of a central drive deficiency? Or of central wisdom? When the PaO2 is 40 the patient can’t let their PaCO2 go up to 90. If they did the PaO2 would plummet to about 20 and rapid death would ensue (per the alveolar air equation). But when the hypoxic drive “gun to the head” is removed, the patient then titrates their respiratory effort such that the ventilatory effort and work is proportioned out for the long haul. It is not a drive deficiency.

We may view this as patient permissive hypercapnea, may apply non-invasive ventilation, may simply realize that hypoxemia kills and hypercapnea does not, or may intubate them. Or hypoxemia may be used as a respiratory stimulant. But if this is the tactic chosen, it should be viewed as akin to giving epinephrine to an already compromised myocardium in order to maintain adequate perfusion pressure. Just as if we were to see this same patient arrive in stable condition for a clinic condition later we wouldn’t insist they needed an epi drip to maintain a sufficient cardiac output, so too should we not insist that a CO2 retainer not in crisis needs hypoxemia in order to stimulate adequate respiratory drive.

In the May 98 issue of Clinical Pulmonary Medicine is an article titled Acute Respiratory Failure in Chronic Obstructive Pulmonary Disease” by Schiavi. In it the author concludes that “.... the traditional idea that oxygen induces hypoventilation by suppressing hypoxic ventilatory drive at the level of peripheral chemoreceptors is no longer tenable.”

During my talk I read almost all of an editorial that appeared in the Sept. 97 issue of Critical Care Medicine, “Debunking Myths of Chronic Obstructive Lung Disease”, by Dr. John Hoyt.

“There are examples of mythology that float about in the atmosphere of medical information that desperately need to be debunked because they influence the care of patients. One sample of medical mythology is the commonly told story that the administration of oxygen to a patient with chronic obstructive lung disease will shut down the patient’s hypoxic respiratory drive and lead to apnea, cardiorespiratory arrest, and the subsequent death of the patient.

“It is not clear where this fallacious information comes from, but it seems to enter the medical information database at an early age, almost like a computer virus corrupting the appropriate function of the equipment. In addition, this myth becomes very difficult to extinguish during the career of the physician, even with clear factual information of long standing. The danger here is that this medical mythology will inappropriately influence treatment decisions in patients.

The basic issue in this story is oxygen. The human body, particularly key organs such as the heart and brain, are not all that forgiving of insufficient supplies of oxygen. Thus, medical decision-making based on the mythology that oxygen causes apnea and cardiorespiratory arrest in patients with chronic obstructive pulmonary disease by turning off the oxygen respiratory drive might take the path of withholding or delivering inadequate doses of oxygen to meet the metabolic needs of the patient in respiratory failure. This mistake is generally fatal for the patient, and a treatment tragedy for the misinformed physician.”…(the author goes on to describe the study…to be described later JW)

“Most mythological stories are based on some observation, which may be a correct observation, but an incorrect interpretation of the facts It is true that the administration of oxygen to a patient with an exacerbated chronic obstructive lung disease and acute respiratory failure may lead to an increased CO2. It is true that the hypercarbia may become severe and be associated with cardiorespiratory arrest. The problem is with interpreting the cause of the events…

One should not fear apnea and cardiorespiratory arrest when giving oxygen to a patient with an exacerbated chronic obstructive lung disease and respiratory failure. Instead, one should be prepared to help the patient eliminate CO2 when deadspace increases. Providing assistance with the elimination of CO2 has been around since the beginning of critical care medicine. It is called mechanical ventilation.”

Focusing on one of the real causes of oxygen induced hypercarbia, enhanced V/Q mismatch, may also allow us to recognize that a rising CO2 level in a patient with status asthmaticus (on 100% O2) may not be so much an indication of advancing respiratory failure but, rather, of a worsening V/Q mismatch arising from the release of regional hypoxic pulmonary vasoconstriction.

Furthermore, it may not be so benign to have COPD, even real CO2 retainer, patients chronically hovering the boundary of an acceptable PaO2 or SpO2 value.

There is growing evidence that the pathogenesis of Cor Pulmonale, nutritional status (lack of weight gain despite adequate nutritional consumption), cardiac modulation, post-operative wound healing, and recovery from acute respiratory distress, all are adversely affected by the default acceptance or goal of an SpO2 of 88-90% in these patients.

-----------------------------------------------------------

To the tune of Bob Dylan's song “ Positively 4th Street”..

You had a lot of nerve

To turn up his O2

Just because he was dying

And really turning blue

I don't know the reason

why you won't accept the show

When it comes to the oxygen drug

You just have to "Say No"

You had a lot of nerve, to turn up his O2

Just because he was distressed and turning blue

I don't know the reason you worry about his hypoxic distress

If he were hiking Everest, it would be even less

Below is a list of references on this topic. I would most enthusiastically recommend in particular reading the studies and discussion occurring in references #11 and # 17, both from the European Journal of Respiratory Disease.

Jeff Whitnack RRT/RPFT

References…

1. The Control of Breathing in Clinical Practice, Caruana-Montaldo, et al, Chest 117/1 Jan., 2000, pages 205-225

2. Debunking Myths of Chronic Obstructive Pulmonary Disease (Editorial) Hoyt, Crit Care Med 1997 Vol. 25, Number 9, pgs. 1450-51

3. Respiratory Failure, Campbell and Arnott, et al, Lancet 1960, ii 12, 1-7

4. 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

5. (Hypothesis) Hypercapnea During Oxygen Therapy in Acute Exacerbation of Chronic Respiratory Failure, Rudolf, et al Lancet Sept. 3, 1977, pages 483-486

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. (Editorial) Hypercapnea during oxygen therapy in airways obstruction: a reappraisal. Stradling, Thorax 1986 41:897-902

8. Correspondence (Aubier and Stradling regarding study cited in # 6 above, Am Rev Resp Dis. Oct. 16th, 1986

9. Central Respiratory Drive in Acute Respiratory Failure of Patients with Chronic Obstructive Pulmonary Disease, Aubier, et al, Am Rev Resp Dis Volume 122, pages 191-199, 1980

10. Hyperoxic-induced Hypercapnea in Stable Chronic Obstructive Pulmonary Disease, Sassoon, et al, Am Rev. Resp. Dis. 1987 135:pgs. 907-911

11. 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

12. Oxygen-induced Hypercarbia in Obstructive Pulmonary Disease, Dunn, et al, Am Rev Resp Dis 1991, 144:526-530

13. 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

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. 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

16. 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

17. Carbon dioxide responsiveness in COPD patients with and without chronic hypercapnia Scano, et al, Eur. Resp. J. 1995 8:78-85

18. May 98 issue of Clinical Pulmonary Medicine is an article titled Acute Respiratory Failure in Chronic Obstructive Pulmonary Disease” by Schiavi

19. Supplemental Perioperative Oxygen to Reduce the Incidence of Surgical-Wound Infection, Robert Greif et al, The New England Journal of Medicine January 20, 2000 -- Vol. 342, No. 3

20. Tissue oxygenation, anemia, and perfusion in relation to wound healing in surgical patients by Jonsson K, et al, Ann Surg 1991 Nov;214(5):605-13

21. Oxygen and wound healing by LaVan FB; Hunt TK, Clin Plast Surg 1990 Jul;17(3):463-72

22. Oxygen Supplementation and Cardiac-Autonomic Modulation in COPD* Matthew N. Bartels, MD, MPH; John M. Gonzalez, BS; Woojin Kim, BS and Ronald E. De Meersman, PhD Chest. 2000;118:691-696

23. The Relationsip between Chronic Hypoxemia and Activation of the Tumor Necrosis Factor-x system in Patients with Chronic Obstructive Pulmonary Disease, by Noriaki, et al, Am Jr. Resp Crit Care Med Volume 161 Number 4 April 2000, 1179-1184

24. Elevated O2 cost of ventilation contributes to tissue wasting in COPD. Mannix ET; Manfredi F; Farber MO, Chest 1999 Mar;115(3):708-13

25. November 97 issue of Clinical Pulmonary Medicine, MacNee and Skwarski article titled “The Pathogenesis of Peripheral Edema in Chronic Obstructive Pulmonary Disease”

26. Oxygen Pressue Field Theory for Perfusionists, Nov. 1999, by Gary Grist BS, RN, CCP, Chief Perfusionist The Childrens Mercy Hospital, Kansas City, MO

27. Long term domiciliary oxygen therapy in chronic hypoxic cor pulmonale complicating chronic bronchitis and emphysema, Report of the Medical Research Council Working Party, Lancet 1981; 1(8222):681-686

28. Incidence of Nocturnal Desaturation While Breathing Oxygen in COPD Patients Undergoing Long-term Oxygen Therapy by Robert Plywaczewski, MD, et al, Chest. 2000;117:679-683.)

29. Uncontrolled Oxygen Administration and Respiratory Failure in Acute Asthma, Chien, et al, Chest 117/3/March 2000 pgs. ;728-733

30. 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

31. (Case Report) Extreme Obesity Associated with Alveolar Hypoventilation—A Pickwickian Syndrome, Burnell, et al, Am. J. Med 1956 21:811-818

(

Emerg Med J 2001; 18:421-423

© 2001 the Emergency Medicine Journal

Review

Emergency oxygen therapy for the breathless patient. Guidelines prepared by North West Oxygen Group

R Murphy1 @ K Mackway-Jones1, I Sammy2, P Driscoll2, A Gray3, R O'Driscoll4, J O'Reilly5, R Niven6, A Bentley7, G Brear8 and R Kishen9

1 Department of Emergency Medicine, Manchester Royal Infirmary

2 Department of Emergency Medicine, Hope Hospital, Salford

3 Department of Emergency Medicine, Stepping Hill Hospital, Stockport

4 Department of Chest Medicine, Hope Hospital, Salford

5 Department of Chest Medicine, Victoria Hospital, Blackpool

6 Department of Chest Medicine, Wythenshawe Hospital, Manchester

7 Department of Intensive Care Medicine, North Manchester General Hospital

8 Department of Intensive Care Medicine, Wythenshawe Hospital, Manchester

9 Department of Intensive Care Medicine, Hope Hospital, Salford

Correspondence to: Dr O'Driscoll (rodriscoll@hope.srht.nwest.nhs.uk )

Accepted for publication

June 11, 2001)

Introduction

TOP Introduction Introduction Problems faced by ambulance... Problems faced by hospital... Emergency oxygen therapy for...

Based on a systematic review of the scientific literature, the North West Oxygen Group have developed guidelines for oxygen therapy for patients who present with acute breathlessness. The above emergency medicine physicians, chest physicians and intensive care physicians have gained approval from their regional societies to have this document accepted as the agreed regional guidelines for the use of oxygen in the immediate care of breathless patients in the North West of England. Flow charts are also currently being developed, based on these guidelines, for use by ambulance and emergency department staff in the area.

It is recognised that the present use of oxygen across these specialties is inconsistent. This protocol will help us to deliver standardised oxygen therapy to breathless patients by paramedics, doctors and nurses. This will also improve the consistency of medical training across these disciplines in the North West.

Introduction

TOP Introduction Introduction Problems faced by ambulance... Problems faced by hospital... Emergency oxygen therapy for...

It is crucial to provide optimal oxygen therapy while the acutely breathless patient is being transferred to hospital, assessed in the emergency department and treated for their disease. For most such patients, the main concern is to give sufficient oxygen to support their needs. The major risk is giving too little oxygen (hypoxia). Insufficient oxygen therapy can lead to cardiac arrhythmias, tissue damage, renal damage and, ultimately, cerebral damage. However, excessive oxygen therapy can be dangerous for some patients with respiratory failure.

Problems faced by ambulance staff

TOP Introduction Introduction Problems faced by ambulance... Problems faced by hospital... Emergency oxygen therapy for...

Patients who present acutely with breathlessness will have varying requirements for oxygen therapy depending on the underlying cause of their symptoms. Most acutely breathless patients will have conditions such as asthma, heart failure, pneumonia, pleural effusions, pulmonary embolism or pneumothorax and some may be victims of major trauma. These patients require high concentration oxygen therapy. For most of these patients, 40%–60% oxygen will be sufficient to maintain satisfactory oxygenation (for example, 4–10 l/min from a medium concentration mask depending on the brand—check mask packaging for details) but some patients will require 100% oxygen from a non-rebreathing reservoir mask. The oxygen delivery system should be adjusted to maintain a saturation greater than 90%.

A proportion of breathless patients will have chronic bronchitis and emphysema. In a survey of 11 000 emergency medical admissions to Hope Hospital, Salford between August 1998 and July 1999 it was established that 25%–30% had conditions such as COPD (6.2%), asthma (5.5%), pneumonia (2.9%), heart failure (3.8%) or other respiratory or cardiac diseases that were likely to have presented with acute breathlessness. Based on these figures it is likely e that about a quarter of patients with acute breathlessness will have COPD as their main diagnosis (Dr Ronan O'Driscoll, unpublished observation). Many of these patients will require controlled oxygen therapy because they are at risk of carbon dioxide retention or respiratory acidosis. Data from the study by Plant et al, referred to in the previous article, indicate that 47% of COPD patients admitted to their hospital had a PaCO2 above 6.0 kPa, 20% had a respiratory acidosis (pH <7.35), 4.6% had a severe acidosis (pH <7.25) and that acidosis was commoner if the blood oxygen was above 10 kPa.

As most ambulance journeys in urban areas in England and Wales will be less than 15 minutes, this risk of hypercapnia, developing or becoming worse as a result of oxygen therapy, should be minimal for most patients if the oxygen saturation is maintained at 90%–92%. Rural ambulance journeys may be much longer and hypercapnia may be a risk for some COPD patients. In these circumstances, patients with previous episodes of hypercapnia should be identified and treated with either low flow oxygen from a medium concentration mask (2–4 l/min equivalent to approximately 28%-40% oxygen) or preferably with controlled oxygen (24% or 28%) from a Venturi device to maintain an oxygen concentration of 90%–92% during the ambulance journey. It may be appropriate to use "Alert Bracelets" for this group of patients suggesting optimal therapy based on previous blood gas measurements.

Problems faced by hospital staff

TOP Introduction Introduction Problems faced by ambulance... Problems faced by hospital... Emergency oxygen therapy for...

Once transferred to hospital, breathless patients need to be assessed immediately to identify the cause of their breathlessness. For the majority of patients, the main issue is the avoidance of hypoxia but about 12% of breathless medical patients are at risk of hypercapnic (type II) respiratory failure according to the above figures. In these special circumstances, high concentration oxygen therapy may be harmful. Most such patients have COPD (chronic bronchitis and emphysema) with reduced respiratory drive. However, there are some other circumstances in which type II respiratory failure may occur. Emergency medical teams should consider the following possibilities in patients with a raised PaCO2 level with or without hypoxia:

CAUSES OF TYPE II RESPIRATORY FAILURE (MANAGEMENT DIFFERS FOR EACH GROUP)

· COPD (especially "blue bloaters" with additional heart failure).

· Cystic fibrosis with severe airway obstruction

· Very severe asthma (needs high dose oxygen and management in ICU, not low dose oxygen therapy)

· Excessive use or overdose of narcotics/sedatives (These patients will not feel breathless and they require naloxone with high dose oxygen, not low dose oxygen therapy)

· Severe kyphoscoliosis

· Neuromuscular disease affecting respiratory muscles (may require ventilatory support)

· Gross obesity (body mass index above 40 kg/m. Type II failure common during sleep)

· Extensive previous chest disease (for example, extensive post-tuberculous scarring or lung resection)

To identify such patients, it is important to have a high index of suspicion and to perform arterial blood gas measurements at the earliest opportunity. Reliance on oxygen saturation alone in these patients may be misleading. Each of these patient groups may require very different medical management.

OTHER PRINCIPLES OF OXYGEN THERAPY

· Oxygen therapy should continue during other treatments such as nebulised therapy.

· Some patients, especially those with high respiratory rates, can be made more comfortable (less breathless) by increasing the flow of oxygen without increasing the concentration. This applies especially to low concentration Venturi masks where the gas flow available to the patient at the lowest recommended oxygen flow rate may be much lower than the patient's inspiratory flow rate. These masks provide a fixed oxygen concentration whatever the flow rate provided.

· For breathless patients requiring high concentration oxygen, a well fitted non-rebreathing reservoir mask will increase the amount of oxygen available during inspiration.

· Emergency oxygen treatment is best given by face masks. Nasal prongs are best suited to the treatment of patients who are stable where the flow rate can be titrated to the desired response (based on blood gas analysis). The only role for nasal prongs in emergency treatment is to give supplementary low flow oxygen therapy to patients with known hypercapnic COPD during bronchodilator treatment with air driven nebuliser systems.

· The use of a structured oxygen prescription document has been shown to improve oxygen prescribing and administration in hospitals.

Emergency oxygen therapy for the breathless patient. Guidelines prepared by North West Oxygen Group

TOP Introduction Introduction Problems faced by ambulance... Problems faced by hospital... Emergency oxygen therapy for...

The guidelines are divided into three stages:

1. Pre-hospital stage;

2. Emergency department assessment stage;

3. Pre-admission stage.

(1) PRE-HOSPITAL STAGE (ACUTELY BREATHLESS PATIENTS)

· In this situation the diagnosis is often unclear and the risk of hypoxia is much greater than the risk of hypercapnia for most patients.

· The main issue for paramedics is to maintain oxygenation.

· These patients should be given high concentration oxygen to maintain an oxygen saturation above 90% until arrival at an emergency department. This can be achieved in most cases by the use of approximately 40%–60% oxygen via a medium concentration mask. (Oxygen flow of 4–10 l/min depending on brand of mask). Use a reservoir (non-rebreathing) mask if the patient is severely hypoxic and in all major trauma cases.

· For patients with known COPD, it is not desirable to exceed an oxygen saturation of 93%. In these cases, oxygen therapy should be started at approximately 40% (4–6 l/min for most brands of medium concentration mask) and titrated upwards if the oxygen saturation decreases below 90% and downwards if the patient becomes drowsy and the saturation exceeds 93–94%.

· For the vast majority of patients in urban areas in the United Kingdom, the journey to hospital will take less than 15 minutes and the risks of hypercapnia are minimal during this short journey. Patients with known type II respiratory failure need special care, especially if they require a prolonged rural ambulance journey (see introductory notes).

(2) EMERGENCY DEPARTMENT ASSESSMENT STAGE

(Management of acutely breathless patients before blood gas results become available)

· On arrival at the emergency department, breathless patients with a significant likelihood of severe COPD should be triaged as very urgent (Orange Status). These patients should be seen by a doctor within 10 minutes of arrival in the department.

· Continuous oximetry should be initiated and blood gases should be measured. The inspired oxygen concentration at the time of blood gas sampling should be noted and recorded. Blood gas measurements need to be repeated after changes in oxygen therapy.

· Although history taking and clinical examination may clarify the diagnosis, oxygen at 40%–60% should be continued until blood gas results are available unless the patient is drowsy or is known to have had previous episodes of hypercapnic respiratory failure. In these circumstances, a lower FiO2 may be required such as 2–4 l/min via a medium concentration mask (equivalent to approximately 28%–40% oxygen) or preferably by the use of controlled oxygen at 24% or 28% via a Venturi mask titrated upwards or downwards to maintain an oxygen saturation of 90%–92% pending the results of blood gas estimations.

· Oxygen treatment should be given continuously and concurrently with nebulised bronchodilators, if these are indicated, by running the nebuliser on high concentration oxygen (prior to availability of blood gas results).

3 (A) PRE-ADMISSION STAGE AND EARLY ADMISSION STAGE (NON-COPD PATIENTS)

· Patients with asthma, left ventricular failure, pneumonia, pneumothorax, trauma, etc, should be treated appropriately for their condition using 40%–60% oxygen via a medium concentration mask (4–10 l/min) for milder cases or a reservoir mask for hypoxic patients and for all major trauma cases.

3 ( PRE-ADMISSION STAGE AND EARLY ADMISSION STAGE (COPD PATIENTS)

· In the normocapnic COPD patient,, oxygen should be adjusted (by downward titration) to the lowest concentration required to maintain an oxygen saturation of 90%–92%. There is no known value in maintaining an oxygen saturation above 93% in patients with COPD but this may cause respiratory acidosis or worsen pre-existing acidosis.

· If the PaCO2 is raised the history, examination and relevant investigations should be reviewed to confirm that this patient is suffering from an acute exacerbation of COPD (see introductory notes for a list of other causes of type 2 respiratory failure). If a diagnosis of an exacerbation of COPD is confirmed, standard COPD therapy should be given as recommended in the British Thoracic Society COPD Guidelines. Controlled oxygen therapy is best given via a fixed performance Venturi mask at the lowest oxygen concentration required to maintain an oxygen saturation of 90%–92% and satisfactory blood gas levels and pH level.

· When nebulised bronchodilators are given to hypercapnic acidotic patients, they should be driven by compressed air and, if necessary, supplementary oxygen should be given concurrently by nasal prongs at 1–4 litres per minute to maintain an oxygen saturation of 90%–92%. Once the nebulised treatment is completed, controlled oxygen therapy with a Venturi mask should be re-instituted. The PaCO2 and pH should be monitored every hour or more frequently if there is a clinical deterioration. If the pH does not decrease below 7.26 and the PaCO2 does not rise above 80 mm Hg (10.6 kPa), and if the patient's condition is considered satisfactory, oxygen therapy at this concentration can be continued. If the pH falls below 7.26 or the PaCO2 rises above 80 mm Hg (10.6 kPa), or if the patient becomes drowsy or fatigued, non-invasive ventilation should be initiated if available. Local guidelines for earlier institution of non-invasive ventilation may apply—recent research has shown benefit from non-invasive ventilation at a pH from 7.25 to 7.35. Senior advice should be sought and a decision should be made about the appropriateness of invasive ventilation. Doxapram may be considered if non-invasive ventilation is unavailable.

For patients with a rising PaCO2 and a falling pH in whom mechanical ventilation is not considered appropriate by the consultant physician or emergency department consultant or ICU consultant, the concentration of inspired oxygen could be decreased further as long as the PaO2 does not decrease below 50 mm Hg (6.6 kPa) (approximately 80% oxygen saturation). This may result in a decrease in PaCO2 and a rise in pH. It is recognised that some of these patients may have resting oxygen saturations below 90% when stable. Again, the patient must be monitored regularly (oximetry and consciousness level) and have regular arterial blood gas analysis until stable.

Acknowledgments

Contributors

Ross Murphy, Peter Driscoll, Alistair Gray and Ronan O'Driscoll initiated the project. All authors, particularly Ronan O'Driscoll, contributed to the development and implementation of the guidelines. Ronan O'Driscoll acts as guarantor for the paper.

Footnotes

Funding: we are grateful to Boehringer Ingelheim for an educational grant to support a guidelines development meeting and printing costs to assist with the implementation of the guidelines in the North West.

Conflicts of interest: none.

[Ace844]

(American Journal of Respiratory and Critical Care Medicine Vol 173. pp. 1309-1315 @ (2006)

© 2006 American Thoracic Society

doi: 10.1164/rccm.200601-037OC

--------------------------------------------------------------------------------

Original Article

Airflow Limitation and Airway Dimensions in Chronic Obstructive Pulmonary Disease

Masaru Hasegawa, Yasuyuki Nasuhara, Yuya Onodera, Hironi Makita, Katsura Nagai, Satoshi Fuke, Yoko Ito, Tomoko Betsuyaku and Masaharu Nishimura

First Department of Medicine and Department of Radiology, Hokkaido University School of Medicine, Sapporo, Japan

Correspondence and requests for reprints should be addressed to Masaharu Nishimura, M.D., First Department of Medicine, Hokkaido University School of Medicine, N-15 W-7 Kita-ku, Sapporo 060-8638, Japan. E-mail: ma-nishi@med.hokudai.ac.jp)

Rationale: Chronic obstructive pulmonary disease (COPD) is characterized by airflow limitation caused by emphysema and/or airway narrowing. Computed tomography has been widely used to assess emphysema severity, but less attention has been paid to the assessment of airway disease using computed tomography.

Objectives: To obtain longitudinal images and accurately analyze short axis images of airways with an inner diameter 2 mm located anywhere in the lung with new software for measuring airway dimensions using curved multiplanar reconstruction.

Methods: In 52 patients with clinically stable COPD (stage I, 14; stage II, 22; stage III, 14; stage IV, 2), we used the software to analyze the relationship of the airflow limitation index (FEV1, % predicted) with the airway dimensions from the third to the sixth generations of the apical bronchus (B1) of the right upper lobe and the anterior basal bronchus (B8) of the right lower lobe.

Measurements and Main Results: Airway luminal area (Ai) and wall area percent (WA%) were significantly correlated with FEV1 (% predicted). More importantly, the correlation coefficients ® improved as the airways became smaller in size from the third (segmental) to sixth generations in both bronchi (Ai: r = 0.26, 0.37, 0.58, and 0.64 for B1; r = 0.60, 0.65, 0.63, and 0.73 for B8).

Conclusions: We are the first to use three-dimensional computed tomography to demonstrate that airflow limitation in COPD is more closely related to the dimensions of the distal (small) airways than proximal (large) airways.

(Chest. 2006;129:1516-1522.)

© 2006 American College of Chest Physicians

Use of Peak Oxygen Consumption in Predicting Physical Function and Quality of Life in COPD Patients*

Michael J. Berry @ PhD; Norman E. Adair, MD and W. Jack Rejeski, PhD

* From the Department of Health and Exercise Science, and Section on Pulmonary and Critical Care Medicine, Department of Medicine, Wake Forest University, Winston-Salem, NC.

Correspondence to: Michael J. Berry, PhD, Department of Health and Exercise Science, PO Box 7868, Wake Forest University, Winston-Salem, NC 27109-7868; e-mail: berry@wfu.edu)

Abstract

Objective: To determine whether peak oxygen consumption (O2peak) adds to the power of FEV1 in predicting physical function and quality of life in COPD patients.

Design: Single-center cross-sectional study.

Methods: Subjects included 291 COPD patients who completed pulmonary function testing, a graded exercise test, a 6-min walk, and stair climb test to assess physical function; a questionnaire assessing self-reported physical function; and a disease-specific, health-related quality-of-life questionnaire. Hierarchical multiple regression analysis was used to determine the contribution of O2peak in predicting physical function and quality of life after accounting for FEV1.

Results: After accounting for FEV1, O2peak added significantly to the prediction of 6-min walk distance (R2 increased by 0.395 [p < 0.005]); stair climb time (R2 increased by 0.262 [p < 0.005]); self-reported function (R2 increased by 0.109 [p < 0.005]); and health-related quality-of-life domain of mastery (R2 increased by 0.044 [p < 0.005]). Only O2peak was found to significantly predict the health-related quality-of-life domain of fatigue (R2 = 0.094 [p < 0.005]).

Conclusion: After controlling for FEV1, O2peak adds significantly to the prediction of physical function and health-related quality-of-life domain of mastery in COPD patients. These results provide additional support for the use of O2peak in the multidimensional assessment of COPD patients.

[briguy222]

Once again, thank you everyone for your comments and input. It really helped and solved a lot of arguments. Keep 'em coming if you want, the more thoughts and ideas the better.

[EMTBgirl]

In my EMT-B class we were taught to never withhold oxygen from a patient that needs it and we were also taught that as a general rule every patient gets oxygen. You did the right thing. I would have done the same thing in that situation.

[stretcher monkey]

Here in the UK the latest guidlines are to do whatever is needed to ensure perpheral oxy saturations of between 92-95%. I have yet to see or hear of a case where pre-hospital oxygenation of a COPD patient has caused them to lose respiratory drive, and even if it did happen we can all use a bag&mask.

Oxygenation management of acute execerbation of COPD here will often include:

Nebulised brocho-dilators (with 02 a the drive gas)

High flow 02 via NRB

Targeted insipried 02 levels with a venturi mask (between 24-60% inspired 02)

[1EMT-P]

Based on what you have told us so far it sounds like you did the right thing!

[iMac]

Good post. If you don't give your patient O2 because he has COPD he isn't getting what he needs. If you give him O2 he is getting what he needs but even if his/her hypoxic drive were to kick in which from what you guys are saying would take hours anyways, we can still treat the pt when he/she quits breathing and loses consciousness. Am I missing a bigger picture?

[TechMedic05]

Good post. If you don't give your patient O2 because he has COPD he isn't getting what he needs. If you give him O2 he is getting what he needs but even if his/her hypoxic drive were to kick in which from what you guys are saying would take hours anyways, we can still treat the pt when he/she quits breathing and loses consciousness. Am I missing a bigger picture?

Pretty much right on the ball...Simplified, but on the ball for Prehospital scenarios. Except for the COPD part. They can get mostly everything they need, they just can't get rid of what they don't.

[Paramagic14]

Good job putting the Patient on high flow oxygen.

I am gonna get a little off track, its sill the whole "do i put the patient on high flow oxgen or not"....what is your opinion about putting high flow oxygen on hyperventilating patients?

[VentMedic]

Why are they "hyperventilating"?

Hyperventilation can only be confirmed by blood gas analysis to see if the CO2 is low or lower than their norm.

Pt with rapid respiratory rates can have an acidosis; respiratory or metabolic as in sepsis or DKA.

Pulmonary emboli, pneumonia, bronchitis and head trauma (not always visible) may also present with tachypnea.

Now, what would you do with any of the above mentioned situations?

Emotional hysteria; you might be able to do something even if it is just oxygen in attempts to calm until more definitive treatment/needs can be met.

You can always take oxygen off, but you can not put oxygen starved cells back.