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EDITORIAL
Low-flow oxygen: How much is your patient really getting? Key words: low flow oxygen, nasal cannulae, oxygen.
Supplemental oxygen is one of the most commonly prescribed treatments in medical care. At any given time, up to a quarter of hospitalized patients receive oxygen therapy1,2 and data from the United Kingdom suggest that 34% of all ambulance transports involve the delivery of oxygen.3 Although guidelines suggest that oxygen is not a treatment for breathlessness in the absence of hypoxaemia,4 in a Victorian Emergency Department audit, the most common reasons for oxygen administration were shortness of breath, chest pain and hypoxaemia (in that order).5 The efficacy of oxygen therapy depends on the fraction of inspired oxygen (FiO2), which in turn depends on the oxygen supply and delivery method. Low-flow oxygen delivery systems deliver oxygen at flow rates below the patient’s inspiratory flow rate, entrain room air and provide a variable FiO2. Nasal cannulae-delivering (low) flow rates of 2–4 L/min or more are provided to patients almost automatically in a range of common clinical situations, without the oxygen even necessarily being ‘prescribed’. Rule of thumb suggests that for patients with a normal rate and depth of breathing, each litre per minute increase of nasal oxygen increases the fraction of inspired oxygen (FiO2) by approximately 4%.6 However, the precise FiO2 at each flow rate is difficult to determine because of the dilution of oxygen with entrained air and the variability of the degree of dilution with variations in tidal volume, minute volume, respiratory rate, inspiratory and expiratory times and flows, anatomic dead space and the impact of an open or closed mouth. Published estimates of the FiO2 at 2 L/min have varied from 0.24 to 0.33 and at 4 L/min from 0.27–0.50.7–9 Is it important to know how much variability there is around the FiO2 delivered from nasal cannulae? Well, although oxygen has until recently been commonly provided to almost anyone seeking emergency treatment and complaining of breathlessness, clinicians are increasingly aware of the potential adverse effects of supplemental oxygen delivered in a range of acute settings and the need for minimization of hyperoxia as well as of hypoxia through closer attention to flow rates and delivery systems. Although the increasing use of continuous monitoring of oxygen saturation by pulse oximetry (SpO2) provides an assessment of the adequacy of oxygenation in the acute setting and may facilitate the titration of oxygen flows to targets, continuous SpO2 monitoring is unlikely to be readily available for routine ward care and provides little indication of the adequacy of ventilation. A reminder of the variability of FiO2 when oxygen is delivered via © 2014 Asian Pacific Society of Respirology
nasal cannulae at oxygen flow rates in 2–4 L/min as provided in the study by O’Reilly-Nugent et al.10 in this issue is timely. Their method of FiO2 measurement was novel in that they sampled the distal trachea after placement of a catheter via bronchoscopy rather than sampling more proximally in the nasopharynx. This may have eliminated some of the potential confounding factors, which may have biased the accuracy of FiO2 estimates in previous similar studies. Measurements were conducted with the subjects seated and fitted with respiratory inductive plethysmography bands to monitor ventilatory pattern. Subjects who were coached to breathe at varying predetermined rates were blinded to the treatments they received and were tested with mouth open and mouth closed. The researchers found that in a group of 20 individuals, mostly volunteers without lung disease, there was significant variability in FiO2. At lower respiratory rates (10 breaths/min), breathing 2 L/min via nasal prongs, the upper level of the range of mean FiO2 was 0.35 while the lower was 0.24. At 4 L/min, with low respiratory rates, the upper level of the range was just on 0.5. Mean FiO2 also decreased slightly with mouth open versus mouth closed, with oxygen delivery and respiratory rate constant. Although the results are similar to those of previous studies, sampling further down the airway clarifies the uncertainties of previous studies that were based upon more proximal sampling where inadequate gas mixing may have occurred. Ideally, a greater range of variation in both respiratory rate and tidal volumes as well as measurements while supine or during sleep would have provided further useful information. However, the study does provide an opportune reminder that a prescription for oxygen at 2 L/min via nasal prongs provides an inexact quantum of supplemental oxygen with FiO2 varying between 24% and 35% depending upon the many human and technical variables affecting FiO2 in lowflow oxygen delivery. A flow rate of 4 L/min may provide a FiO2 as high as 50%. These results were from subjects without lung disease, predominantly, with the variations in breathing parameters regulated by the researchers. In an unwell individual with an altered breathing pattern, and possibly many changes in other physiological variables, the true FiO2 may be even more difficult to judge. Are these results of clinical relevance? In patients with chronic obstructive pulmonary disease (COPD), high concentrations of oxygen delivered via low-flow mask systems have been associated with increased mortality compared with lower concentrations delivered via nasal cannulae titrated to SpO2.11 Whether adverse outcomes are associated with the use of oxygen Respirology (2014) 19, 469–470 doi: 10.1111/resp.12290
470 delivered via nasal cannulae in inpatient COPD management is unclear. Other areas of potential concern may be the asthmatic with a high ventilatory rate, whose FiO2 may be as low as 22% at a flow rate of 2 L/min; or the postoperative patient, prescribed low-flow oxygen, perhaps requiring ongoing pain relief, who despite satisfactory oxygen ‘sats’ may be at risk for worsening hypoventilation. Commonly used oxygen concentrations are known to cause hypoventilation, elevations of arterialized venous partial pressure of carbon dioxide and acidaemia in people with stable obesity hypoventilation syndrome.12 Sixty percent of our Australian population are now overweight or obese. Such individuals may also be at risk of hypercapnia if low-flow supplemental oxygen with FiO2s of 2–4 L/min (perhaps providing up to 50% FiO2) is provided acutely for ‘breathlessness’ or for treatment of ‘low sats’ without careful monitoring. The risk may not be recognized as the SpO2 may remain in an apparently satisfactory range because of hyperoxia- and the hypercapnia may not be reliably evident on the venous blood gas measurement, which is commonly the investigation of first choice in many emergency departments. A variety of potential clinical questions come to mind, which the technique described by these authors has the potential to answer. In the meantime, this paper provides us with a salutary reminder about the variability of the inspired oxygen fraction delivered via low-flow oxygen therapy and alerts us to be judicious in our choice of oxygen flow rates, to monitor their effectiveness closely and to carefully consider the potential for worsening hypoxaemia or hypercapnia in those at potential risk. Christine F. McDonald, MBBS (Hons), FRACP, PhD Department of Respiratory and Sleep Medicine, Austin Hospital, Institute for Breathing and Sleep, Melbourne, Australia
Respirology (2014) 19, 469–470
Editorial
REFERENCES 1 O’Driscoll BR, Howard LS, Bucknall LS, Welham SA, Davison AG. British Thoracic Society emergency oxygen audits. Thorax 2011; 66: 734–5. 2 Eastwood GM, Peck L, Young H, Prowle J, Jones D, Bellomo R. Oxygen administration and monitoring for ward adult patients in a teaching hospital. Intern. Med. J. 2011; 41: 784–8. 3 Hale KE, Gavin C, O’Driscoll BR. Audit of oxygen use in emergency ambulances and in a hospital emergency department. Emerg. Med. J. 2008; 265: 773–6. 4 O’Driscoll BR, Howard LS, Davison AG, on behalf of the British Thoracic Society. BTS guidelines for emergency oxygen use in adult patients. Thorax 2008; 63 (Suppl 6): vi1–68. 5 Considine J, Botti M, Thomas S. Descriptive analysis of oxygen use in Australian emergency departments. Eur. J. Emerg. Med. 2012; 19: 48–52. 6 Wilkins RL, Stoller JK, Kacmarek RM (eds). Egan’s Fundamentals of Respiratory Care, 9th edn. Shelledy DC, Kester L (consulting eds). Mosby Elsevier, St. Louis, MO, 2009. 7 Schachter EN, Littner MR, Luddy P, Beck GJ. Monitoring of oxygen delivery systems in clinical practice. Crit. Care Med. 1980; 8: 405–9. 8 Waldau T, Larsen VH, Bonde J. Evaluation of five oxygen delivery devices in spontaneously breathing subjects by oxygraphy. Anaesthesia 1998; 53: 256–63. 9 Wettstein RB, Shelledy DC, Peters JI. Delivered oxygen concentrations using low-flow and high-flow nasal cannulas. Respir. Care 2005; 50: 604–9. 10 O’Reilly-Nugent A, Kelly P, Stanton J, Swanney M, Graham B, Beckert L. The oxygen concentration delivered via nasal cannulae as measured by tracheal sampling. Respirology 2014; 19: 538– 43. 11 Austin MA, Wills KE, Blizzard L, Walters EH, Wood-Baker R. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. BMJ 2010; 341: c5462. 12 Hollier CA, Harmer AR, Maxwell LJ, Menadue C, Wilson GN, Unger G, Flunt D, Black DA, Piper AJ. Moderate concentrations of supplemental oxygen worsen hypercapnia in obesity hypoventilation syndrome: a randomised crossover study. Thorax 2014; 69: 346–53.
© 2014 Asian Pacific Society of Respirology
EDITORIAL
Low-flow oxygen: How much is your patient really getting? Key words: low flow oxygen, nasal cannulae, oxygen.
Supplemental oxygen is one of the most commonly prescribed treatments in medical care. At any given time, up to a quarter of hospitalized patients receive oxygen therapy1,2 and data from the United Kingdom suggest that 34% of all ambulance transports involve the delivery of oxygen.3 Although guidelines suggest that oxygen is not a treatment for breathlessness in the absence of hypoxaemia,4 in a Victorian Emergency Department audit, the most common reasons for oxygen administration were shortness of breath, chest pain and hypoxaemia (in that order).5 The efficacy of oxygen therapy depends on the fraction of inspired oxygen (FiO2), which in turn depends on the oxygen supply and delivery method. Low-flow oxygen delivery systems deliver oxygen at flow rates below the patient’s inspiratory flow rate, entrain room air and provide a variable FiO2. Nasal cannulae-delivering (low) flow rates of 2–4 L/min or more are provided to patients almost automatically in a range of common clinical situations, without the oxygen even necessarily being ‘prescribed’. Rule of thumb suggests that for patients with a normal rate and depth of breathing, each litre per minute increase of nasal oxygen increases the fraction of inspired oxygen (FiO2) by approximately 4%.6 However, the precise FiO2 at each flow rate is difficult to determine because of the dilution of oxygen with entrained air and the variability of the degree of dilution with variations in tidal volume, minute volume, respiratory rate, inspiratory and expiratory times and flows, anatomic dead space and the impact of an open or closed mouth. Published estimates of the FiO2 at 2 L/min have varied from 0.24 to 0.33 and at 4 L/min from 0.27–0.50.7–9 Is it important to know how much variability there is around the FiO2 delivered from nasal cannulae? Well, although oxygen has until recently been commonly provided to almost anyone seeking emergency treatment and complaining of breathlessness, clinicians are increasingly aware of the potential adverse effects of supplemental oxygen delivered in a range of acute settings and the need for minimization of hyperoxia as well as of hypoxia through closer attention to flow rates and delivery systems. Although the increasing use of continuous monitoring of oxygen saturation by pulse oximetry (SpO2) provides an assessment of the adequacy of oxygenation in the acute setting and may facilitate the titration of oxygen flows to targets, continuous SpO2 monitoring is unlikely to be readily available for routine ward care and provides little indication of the adequacy of ventilation. A reminder of the variability of FiO2 when oxygen is delivered via © 2014 Asian Pacific Society of Respirology
nasal cannulae at oxygen flow rates in 2–4 L/min as provided in the study by O’Reilly-Nugent et al.10 in this issue is timely. Their method of FiO2 measurement was novel in that they sampled the distal trachea after placement of a catheter via bronchoscopy rather than sampling more proximally in the nasopharynx. This may have eliminated some of the potential confounding factors, which may have biased the accuracy of FiO2 estimates in previous similar studies. Measurements were conducted with the subjects seated and fitted with respiratory inductive plethysmography bands to monitor ventilatory pattern. Subjects who were coached to breathe at varying predetermined rates were blinded to the treatments they received and were tested with mouth open and mouth closed. The researchers found that in a group of 20 individuals, mostly volunteers without lung disease, there was significant variability in FiO2. At lower respiratory rates (10 breaths/min), breathing 2 L/min via nasal prongs, the upper level of the range of mean FiO2 was 0.35 while the lower was 0.24. At 4 L/min, with low respiratory rates, the upper level of the range was just on 0.5. Mean FiO2 also decreased slightly with mouth open versus mouth closed, with oxygen delivery and respiratory rate constant. Although the results are similar to those of previous studies, sampling further down the airway clarifies the uncertainties of previous studies that were based upon more proximal sampling where inadequate gas mixing may have occurred. Ideally, a greater range of variation in both respiratory rate and tidal volumes as well as measurements while supine or during sleep would have provided further useful information. However, the study does provide an opportune reminder that a prescription for oxygen at 2 L/min via nasal prongs provides an inexact quantum of supplemental oxygen with FiO2 varying between 24% and 35% depending upon the many human and technical variables affecting FiO2 in lowflow oxygen delivery. A flow rate of 4 L/min may provide a FiO2 as high as 50%. These results were from subjects without lung disease, predominantly, with the variations in breathing parameters regulated by the researchers. In an unwell individual with an altered breathing pattern, and possibly many changes in other physiological variables, the true FiO2 may be even more difficult to judge. Are these results of clinical relevance? In patients with chronic obstructive pulmonary disease (COPD), high concentrations of oxygen delivered via low-flow mask systems have been associated with increased mortality compared with lower concentrations delivered via nasal cannulae titrated to SpO2.11 Whether adverse outcomes are associated with the use of oxygen Respirology (2014) 19, 469–470 doi: 10.1111/resp.12290
470 delivered via nasal cannulae in inpatient COPD management is unclear. Other areas of potential concern may be the asthmatic with a high ventilatory rate, whose FiO2 may be as low as 22% at a flow rate of 2 L/min; or the postoperative patient, prescribed low-flow oxygen, perhaps requiring ongoing pain relief, who despite satisfactory oxygen ‘sats’ may be at risk for worsening hypoventilation. Commonly used oxygen concentrations are known to cause hypoventilation, elevations of arterialized venous partial pressure of carbon dioxide and acidaemia in people with stable obesity hypoventilation syndrome.12 Sixty percent of our Australian population are now overweight or obese. Such individuals may also be at risk of hypercapnia if low-flow supplemental oxygen with FiO2s of 2–4 L/min (perhaps providing up to 50% FiO2) is provided acutely for ‘breathlessness’ or for treatment of ‘low sats’ without careful monitoring. The risk may not be recognized as the SpO2 may remain in an apparently satisfactory range because of hyperoxia- and the hypercapnia may not be reliably evident on the venous blood gas measurement, which is commonly the investigation of first choice in many emergency departments. A variety of potential clinical questions come to mind, which the technique described by these authors has the potential to answer. In the meantime, this paper provides us with a salutary reminder about the variability of the inspired oxygen fraction delivered via low-flow oxygen therapy and alerts us to be judicious in our choice of oxygen flow rates, to monitor their effectiveness closely and to carefully consider the potential for worsening hypoxaemia or hypercapnia in those at potential risk. Christine F. McDonald, MBBS (Hons), FRACP, PhD Department of Respiratory and Sleep Medicine, Austin Hospital, Institute for Breathing and Sleep, Melbourne, Australia
Respirology (2014) 19, 469–470
Editorial
REFERENCES 1 O’Driscoll BR, Howard LS, Bucknall LS, Welham SA, Davison AG. British Thoracic Society emergency oxygen audits. Thorax 2011; 66: 734–5. 2 Eastwood GM, Peck L, Young H, Prowle J, Jones D, Bellomo R. Oxygen administration and monitoring for ward adult patients in a teaching hospital. Intern. Med. J. 2011; 41: 784–8. 3 Hale KE, Gavin C, O’Driscoll BR. Audit of oxygen use in emergency ambulances and in a hospital emergency department. Emerg. Med. J. 2008; 265: 773–6. 4 O’Driscoll BR, Howard LS, Davison AG, on behalf of the British Thoracic Society. BTS guidelines for emergency oxygen use in adult patients. Thorax 2008; 63 (Suppl 6): vi1–68. 5 Considine J, Botti M, Thomas S. Descriptive analysis of oxygen use in Australian emergency departments. Eur. J. Emerg. Med. 2012; 19: 48–52. 6 Wilkins RL, Stoller JK, Kacmarek RM (eds). Egan’s Fundamentals of Respiratory Care, 9th edn. Shelledy DC, Kester L (consulting eds). Mosby Elsevier, St. Louis, MO, 2009. 7 Schachter EN, Littner MR, Luddy P, Beck GJ. Monitoring of oxygen delivery systems in clinical practice. Crit. Care Med. 1980; 8: 405–9. 8 Waldau T, Larsen VH, Bonde J. Evaluation of five oxygen delivery devices in spontaneously breathing subjects by oxygraphy. Anaesthesia 1998; 53: 256–63. 9 Wettstein RB, Shelledy DC, Peters JI. Delivered oxygen concentrations using low-flow and high-flow nasal cannulas. Respir. Care 2005; 50: 604–9. 10 O’Reilly-Nugent A, Kelly P, Stanton J, Swanney M, Graham B, Beckert L. The oxygen concentration delivered via nasal cannulae as measured by tracheal sampling. Respirology 2014; 19: 538– 43. 11 Austin MA, Wills KE, Blizzard L, Walters EH, Wood-Baker R. Effect of high flow oxygen on mortality in chronic obstructive pulmonary disease patients in prehospital setting: randomised controlled trial. BMJ 2010; 341: c5462. 12 Hollier CA, Harmer AR, Maxwell LJ, Menadue C, Wilson GN, Unger G, Flunt D, Black DA, Piper AJ. Moderate concentrations of supplemental oxygen worsen hypercapnia in obesity hypoventilation syndrome: a randomised crossover study. Thorax 2014; 69: 346–53.
© 2014 Asian Pacific Society of Respirology
