Nebulizers are used by patients who gain greater relief from nebulized therapy than from in haled therapy. This may be during acute respiratory illnesses, because of disease severity, or because they are unable to use inhalers. Patients who are being considered for nebulize r therapy should be referred to a respiratory physician. If antibiotics are being nebulized , a more powerful nebulizer is required. How to use Open the ampoule containing the drug so lution and squirt the solution into the nebulizer chamber. Salbutamol and ipratropium bromi de can be taken together, but nebulized budesonide or antibiotics should be used separately . If ipratropium bromide only is being used, this should be delivered via a mouthpiece, as it can lead to glaucoma if used via a mask. Reattach the chamber to the nebulizer mask or m outhpiece. Put the mask over nose and mouth, or position mouthpiece between the lips in the mouth. Switch the nebulizer machine on. Breathe slowly in and out. Continue until all the solution is gone. Switch off the machine. Rinse the nebulizer chamber with hot soapy water after each use. If nebulization takes more than 10 min, change the neb-set (mask, chamber, tubing \200\224lasts 1 \200\2233 months). If no improvement, consider servicing the machine . If the patient is using oxygen, this can still be used during nebulization, either via na sal prongs under the nebulizer mask or by using oxygen tubing attached directly to the nebu lizer chamber to drive the nebulization; at home most cylinders do not provide suf \201 ci ent \202 ow rates to allow this. Nebulizer machines should be serviced annually. This page intentionally left blank CHAPTER 55 Inhalers and nebulizers 686 Different inhaler types and instructions for their use Table 55.1 Different inhaler types Generic name of drug (with product names) Mechanism of action Short-acting 2 agonist Duration 3 \200\2235 h Inhaler color Salbutamol (Ventolin , Asmasal , Pulvinal , Salbutamol, Salamol , Salbutamol Cyclocaps , Airomir , Asmasal Clickhaler , Salamol Easi-Breathe ) Terbutaline (Bricanyl ) Salmet erol (Serevent ) Formoterol (Foradil , Oxis , Atimos Modulite ) Ipratropium bromide (At rovent ) Ipratropium and salbutamol (Combivent ) Tiotropium (Spiriva ) Blue Long-acting 2 agonist Duration 12 h Green Green/turquoise Short-acting anticholinergic White/gray Gray Handihaler , Respimat Long-acting anticholinergic Beclometasone dipropionate (Becotide , Becloforte , Pulvinal , Beclometasone, Beclometha sone Cyclocaps , AeroBec , AerobecForte , Asmabec Clickhaler , Beclazone Easi-Breathe , Qvar ) Budesonide (Pulmicort , Budesonide Cyclocaps , Novolizer ) Fluticasone propion ate (Flixotide ) Mometasone furoate (Asmanex ) Ciclesonide (Alvesco ) Corticosteroid Brown Brown Red Red Red Salmeterol and \202 uticasone (Seretide ) Eformoterol and budesonide (Symbicort ) Sodiu m cromoglicate (Intal , Cromogen Easi-Breathe ) Neocromil sodium (Tilade ) Combination steroid and bronchodilator Purple Red and white Unknown, stabilize Yellow and white mast cells DIFFERENT INHALER TYPES AND INSTRUCTIONS FOR THEIR USE 687 Table 55.2 Instructions for use of different inhaler types Type of device Instructions for use Pressurized aerosol Remove the mouthpiece and shake the inhaler well. Hold the inhaler upri ght with the thumb on the base below the metered dose mouthpiece and the \201 rst \201 nger on the metal canister. inhaler (MDI) Aerosol Evohaler Breathe out as far as is comfo rtable then place the mouth piece between the teeth and close lips around it. Do not bite i t. As you start to breathe in through the mouth, press on the top of the inhaler to release the medication whilst still breathing in steadily and deeply. Hold your breath, take the i nhaler from your mouth, and continue holding your breath for up to 10 s if possible. Wait 3 0 s prior to taking second puff. Use with spacer device to improve drug delivery. CFC-free inhalers need washing every 2 \200\2233 weeks, as they can block. Spacer Nebuhaler Nebuchamber Volumatic Aero Chamber Able Spacer PARI Vortex Space r , Pocket Chamber OptiChamber OptiHaler Ensure spacer is compatible with patient \200\231s inhaler. Remove cap of inhaler and shake it. Insert it into end of spacer device. Place the other end of the spacer in the mouth. P ress the inhaler canister once to release one dose of the drug. Take one deep breath in and hold, or take 3 \200\2234 steady breaths in and out. Repeat as indicated. Valve should rat tle. Clean the spacer once a month with mild detergent, rinse, and air-dry. Replace after 6 \200\22312 months. Breath-actuated devices Autohaler Easi-breathe If an autohaler, remove the cap and lift the red lever. Insert device into mouth. Inhale sl owly and deeply. Continue inhaling when the device \200\230clicks \200\231. Hold breath fo r up to 10 s if possible. Slowly breathe out. To take a second inhaled dose, lower the red lever and lift again. If an Easi-breathe, open the hinged cap. Insert device into mouth. In hale slowly and deeply. Continue inhaling when the device \200\230clicks \200\231. Hold br eath for up to 10 s if possible. Slowly breathe out. Close the cap and reopen for further d oses. If Easi-breathe spacer used, it will need to be removed between each inhalation so th at cap can be opened and closed. Dry powder devices Prime the device. Turbohaler: hold upright, remove the Accuhaler cap, twist the base as far as possible until the click is Turbohaler heard and then twist back again. Clickhaler: shake the Clickhaler device, remove the cap, click the top down and r elease. Twisthaler: remove the cap by twisting and the dose is Twisthaler Easyhaler then ready. Accuhaler: Open inhaler cover, mouthpiece Cyclohaler facing you and push lever dow n to pierce the blister Aerocaps Spincaps containing dose. Diskhaler: insert disc into device by Novolizer opening and pulling out mouthpiece section. To prepare dose, lift up back of lid to 90 un til the blister is pierced, then lower the lid. To use all the devices, hold them level, ex hale fully, place the mouthpiece into mouth between teeth, and inhale steadily. Hold your b reath and remove the inhaler. For a second dose, repeat the above actions. 688 CHAPTER 55 Inhalers and nebulizers Table 55.2 Instructions for use of different inhaler types \200\224(contd.) Type of device Instructions for use Handihaler Flip lid and white mouthpiece open and insert capsule. Close the mouthpiece back down until it clicks. Pierce the capsule by pressing the green button at the side. Exhale as far as i s comfortable. Place mouthpiece into mouth and breathe in slowly and deeply. Remove inhaler from your mouth and hold your breath for 10 s if possible. Slowly breathe out. Repeat if n ecessary to ensure all the powder from capsule is gone. Respimat Hold inhaler upright with cap closed. Turn the transparent base until it clicks. Open the c ap. Breathe out slowly and insert the mouthpiece and seal with lips. Point towards the back of the throat. While taking a deep breath, press the button and continue to breathe. Hold your breath for 10 s if possible and breathe out slowly. 689 Chapter 56 Intensive therapy unit (ITU): when to involve PAR (patient at risk) scoring system 691 CHAPTER 56 Intensive therapy unit (ITU) 690 Ideally communicate with ITU early, as it is much better that they know about a potentially sick patient who may need ITU input, than to \201 nd your patient (and you!) in dif \201 culty later on, with no ITU bed. Scoring systems for the early recognition of sick patients are in use in many hospitals, en abling doctors and nursing staff to readily identify and assess a deteriorating patient. An example is shown on the opposite page. The common situations in which ITU input may be req uired in rela- tion to respiratory disease are principally those relating to decisions abou t formal ventilation. Most commonly these will be: \200 Respiratory failure (either type I or type II) \200 Exacerbation of COPD (usually type II failure). Patients with COPD admitted to ITU have a h ospital mortality of 20 \200\22325%. Poor prog- nostic factors include low baseline FEV1, l ong-term oxygen use, low sodium and albumin, low BMI, poor functional status, and comorbid disease. Age does not add prognostic information Pneumonia (to maintain an adequate pO2 \200\224usually type I failure). In this situation, ITU input may not necessarily lead to i ntubation, as adequate oxygenation may be achieved by the proper use of a non- rebreathable mask or CPAP, with the additional bene \201 ts of one-to- one nursing. Altered mental sta te and dif \201 culty clearing secretions may make invasive ventilation necessary \200 \200 \200 Upper airway emergencies \211 1 organ failure (not necessarily with respiratory failure) S epsis requiring organ support Inotropic support. PAR SCORING SYSTEM 691 PAR (patient at risk) scoring system This is an example of a ward-based patient illness sev erity scoring system. It is used to assist medical and nursing staff in the early identi \201 cation of sick patients, to enable prompt and appropriate HDU/ITU liaison. Table 56.1 Scoring systems for the early recognition of sick patients Score 3 2 \211 40 1 0 1 2 3 Heart rate/min 41 \200\22350 51 \200\223100 101 \200\223110 111 \200\223130 \211 131 \211 70 71 \200\22380 80 \200\223100 101 \200\223199 \211 200 21 \200\22329 SBP \211 8 \211 30 Resp rate/min 9 \200\22314 15 \200\22320 \211 35 \211 39.5 Painful Drowsy/ confused stimuli <60 mL/2 h <40 mL/2 h 0 mL Temp/ C Conscious level Alert Unres- ponsive Urine output Calculate the PAR score by the addition of the scores in each column. Total score 1 \200 \2233: increase observations to 4-hourly. Total score 3 in one category: contact doctor for immediate review. Total score total \211 3: contact doctor for review within 30 min. SHO should consider senior review. Total score >6: patient needs immediate review, contact ITU outreach team if appropriate. Respiratory rate is the most sensitive marker of illness seve rity This page intentionally left blank 693 Chapter 57 Non-invasive ventilation Terminology 694 Indications 696 Contraindications 697 NIV in acute respiratory failure: pra ctical use 698 NIV in chronic respiratory failure 700 CHAPTER 57 Non-invasive ventilation 694 Terminology Ventilatory support may be invasive (via endotracheal tube or tracheos- tomy) o r non-invasive (via nose mask or face mask). Non-invasive ventila- tion may be subdivided i nto positive or negative pressure ventilation. Positive pressure ventilators (also NIV, bi- level, BiPAP (trade name)) deliver volume or pressure support; many different types are ava ilable. Bi- level pressure support devices are used extensively, and provide pressure suppo rt between inspiratory and expiratory positive airway pressures (IPAP and EPAP) that are se lected by the prescriber. They function in several modes, including patient-triggered inspi ratory support with provision of an underlying back-up rate that will cut in if the patient fails to breathe. Non- invasive positive pressure support may be provided by specialized p ortable ventilators, or by standard critical care ventilators. Negative pressure ventilator s assist inspiration by \200\230sucking out \200\231 the chest wall; expiration occurs thr ough elastic recoil of the lungs. Includes devices such as tank ventilators and chest \200 \230shell \200\231 ventilators. Other devices such as the rocking bed and \200\230pneumobe lt \200\231 displace abdominal contents to aid diaphragmatic contraction. Used extensively in the polio epidemics of the 1950s; now only rarely used to manage chronic respiratory fai lure. Continuous positive airway pressure (CPAP) supplies constant positive pressure during inspiration and expiration, and is therefore not a form of ventilation. It provides a \200\230splint \200\231 to open the upper airway and collapsed alveoli (thus improving V/Q matching). CPAP is used extensively in the community to treat obstructive sleep apnoea, but also has a role in improving oxygenation in selected patients with acute respiratory failu re, e.g. patients with cardiogenic pulmonary oedema, pneumocystis pneu- monia (p 476). Abbreviations NIV-non-invasive ventilation, also referred to as non-invasive mechanical ven tilation (NIMV). NIPPV-non-invasive positive pressure ventilation; confusingly it is also s ometimes interpreted as nasal intermittent positive pressure ventilation, and sometimes ref erred to as \200\230NIPPY \200\231, after the name of a particular type of ventilator. IPA P-inspiratory positive airways pressure. EPAP-expiratory positive airways pressure, also re ferred to as positive end-expiratory pressure (PEEP). BiPAP-bi-level positive airway pressu re (IPAP greater than EPAP), refers to a commercial product, but now used to refer to simil ar machines. CPAP-continuous positive airway pressure (IPAP equal to EPAP). Further information Mehta S, Hill NS. Noninvasive ventilation. Am J Respir Crit Care Med 20 01; 163: 540 \200\22377 This page intentionally left blank CHAPTER 57 Non-invasive ventilation 696 Indications NIV may be used in an attempt to avoid invasive ventilation and its com- plicat ions (e.g. upper airway trauma, ventilator-acquired pneumonia); alter- natively, NIV may re present the \200\230ceiling \200\231 of treatment in patients deemed unsuitable for intuba tion. NIV is not an alternative to invasive ventilation in patients who require this de \201 nitive treatment. Acute exacerbation of COPD \200 Consider NIV in patients with an acute exacerbation of COPD who have a respiratory acidosis (pH <7.30) despite initial medical treatment and controlled oxygen therapy Bene \201 ts i nclude reduced mortality and need for intubation, more rapid improvement in physiological o utcomes (respiratory rate, pH), and symptomatic relief from breathlessness, when compared w ith standard medical treatment NIV only assists ventilation; the pressures used are not eno ugh to take over ventilation due to the high airways resistance Invasive ventilation, if de emed appropriate, should be considered par- ticularly in patients with a severe respiratory acidosis (pH <7.25), as this is associated with treatment failure and increased mortality with NIV High expiratory pressures (e.g. 6 \200\2238 cmH2O, PEEP) may help reduce the work of breathing by offsetting intrinsic PEEP, but will lessen the IPAP \200\223EPAP difference , thus reducing the ventilation component. Acute cardiogenic pulmonary oedema \200 Use of CPAP via face mask is effective and should be considered in patients who fail to imp rove with medical management alone Bi-level NIV has not been shown to be superior to CPAP a nd there is a suggestion of increased myocardial infarction rates following its use. It may , however, have a role in patients who do not respond to CPAP. Decompensated obstructive sleep apnoea NIV is effective in the treatment of obstructive sle ep apnoea and the overlap syndrome (i.e. raised PaCO2, typically with associated obesity hy poventilation or COPD, p 582 ) when CPAP alone fails to reverse the CO2 retention. NIV is g enerally recommended as the \201 rst choice over CPAP when an acute respiratory acidosis is present, but conversion to CPAP later may be possible. Respiratory failure from neuromus cular weakness \200 NIV is the treatment of choice for ventilatory failure resulting from neuromuscular weaknes s or chest wall deformity The pressures used may be adequate to fully take over ventilation , because the chest and lung compliance are often little impaired CONTRAINDICATIONS 697 Immunocompromised patients \200 Immunocompromised patients who develop acute respiratory failure have an extremely high mor tality following endotracheal intubation and ventilation In immunocompromised patients with pulmonary in \201 ltrates, fever, and hypoxaemic acute respiratory failure, intermittent NIV results in lower intu- bation rates and hospital mortality when compared with standard treatment CPAP is effective in the treatment of pneumocystis pneumonia. Community-acquired pneumonia \200 Use of NIV may result in a reduction in need for intubation compared with standard medical treatment, although no signi \201 cant differences in hospital mortality or length of hosp italization have been shown CPAP may have a role in improving oxygenation in severe pneumon ia In patients who would potentially be candidates for intubation, use of NIV or CPAP shoul d not inappropriately delay invasive ventilation, and so should only be attempted in an ITU setting. \200 Other conditions \200 \200 There is no evidence to support the use of NIV in acute severe asthma There is no strong ev idence to support the use of NIV in exacerbations of bronchiectasis and cystic \201 brosi s, although NIV may be useful as a \200\230ceiling \200\231 of treatment in patients with severe underlying disease who would not be considered suitable candidates for invasive vent ilation Bi-level NIV or CPAP may have a role in improving gas exchange following trauma or surgery. Contraindications Relative contraindications to the use of NIV are listed below. They shoul d be considered in the context of individual patients; for example, severe hypoxaemia may n ot be considered a contraindication for NIV in a patient who is unsuitable for invasive ven tilation. Contraindications to NIV \200 Cardiac or respiratory arrest \200 Impaired consciousness or confusion \200 Severe hypoxaemia \200 Copious respiratory secretions \200 Haemody namic instability \200 Facial surgery, trauma, burns, or deformity \200 Upper airway ob struction \200 Tracheal injury \200 Undrained pneumothorax \200 Inability to cooperat e or to protect the airway \200 Vomiting, bowel obstruction, recent upper gastrointestina l tract surgery, oesophageal injury. Further information BTS guidelines on non-invasive ventilation in acute respiratory failure . Thorax 2002; 57: 192 \200\223211 Plant et al. Early use of non-invasive ventilation for a cute exacerbations of chronic obstructive pulmonary disease on general respiratory wards: a multicentre randomized controlled trial. Lancet 2000; 355: 1931 \200\2235 CHAPTER 57 Non-invasive ventilation 698 NIV in acute respiratory failure: practical use The decision to start NIV should follow a p eriod of initial standard medical treatment including appropriate supplementary and control led oxygen therapy; a proportion of patients will improve and will no longer require ventil ation. Prior to commencing NIV a senior doctor should make a deci- sion with the patient an d their family regarding suitability for invasive ven- tilation should NIV fail and documen t this clearly in the medical notes. If the patient is a candidate for invasive ventilation , care must be taken to avoid inappropriate delays in intubation through the use of NIV or CPAP. Liaise with ITU staff early. Setting up NIV 1. Select an appropriate mask type and size for the patient. Masks may be na sal or oronasal (full face). Nasal masks require clear nasal pas- sages and may allow mouth leaks, particularly in the acutely breathless patient, but they are more comfortable. Full -face masks avoid mouth leakage and are generally favored for initial use in acute respirat ory failure. 2. Allow the patient to hold the mask to their face prior to attaching the head straps \200 \224this may increase con \201 dence and compliance. Mask adjustments are often necessary to minimize air leaks, although some leakage may have to be accepted. Avoid excessive strap tension; 1 or 2 \201 ngers should be able to \201 t under the strap. 3. Set up the ventilator. Typical initial pressures for ventilating a patient with hypercap nic respiratory failure due to an exacerbation of chronic obstructive pulmonary disease (CO PD) would be EPAP 4 cmH2O and IPAP 12 cmH2O, with a back-up rate of 15/min and inspiratory: expira- tory ratio of 1:3 in spontaneous/timed mode. Increase the IPAP in incre- ments of 2 cmH2O to a maximum of 20, as tolerated by the patient. Similar settings can be used for p atients with hypercapnic respiratory failure resulting from neuromuscular weakness. Conside r increasing the EPAP (e.g. to 8 or 10 cm) in obese patients with an \200\230overlap \200 \231 syndrome of COPD and obstructive sleep apnoea. Pressure support ventilators can also be set to provide CPAP by equalizing the IPAP and EPA P; typical pressures range from 5 to 12.5 cmH2O. CPAP may improve oxygenation in selected p atients with car- diogenic pulmonary oedema or pneumonia. 4. Supplementary oxygen concentration (FiO2) should be guided by the underlying disease pro cess and by oximetry monitoring. For many hypercapnic patients with COPD, maintenance of ox ygen saturations between 88% and 92% effectively balances the risks of hypoxia and hypercap nic respiratory acidosis. 5. Patient monitoring should involve assessment of comfort, respiratory rate, synchrony wit h the ventilator, mask leaks, pulse rate, blood pres- sure, and oxygen saturations. 6. Arterial or capillary blood gas analysis should be performed after 1 h and again after 4 h if there has been no improvement. Improvement in acidosis, and decline in respiratory ra te after 1 and 4 h of treatment are NIV IN ACUTE RESPIRATORY FAILURE: PRACTICAL USE 699 associated with a better outcome. Repeat the blood gas analysis if the clinical condition c hanges. 7. Lack of response may be indicated by a worsening acidosis or persist- ently abnormal art erial blood gasses, or by a reduced conscious level and clinical deterioration. Consider in vasive ventilation, if appropriate. The decision to halt NIV depends on the circumstances o f the individual patient, and should be made by a senior doctor. 8. Subsequent management depends on the patient \200\231s response. Optimal duration of NIV is unclear, but it is typically administered for up to 3 days in acute respiratory failure . NIV does not need to be continuous, and the patient may have breaks for meals and nebuliz ers. Table 57.1 Troubleshooting Problem Possible solution Clinical deterioration or worsening respiratory failure Ensure optimal medical therapy Consider complications, e.g. pneumothorax, aspiration, sputu m retention Does the patient require intubation, if appropriate? pCO2 remains high (persistent respiratory acidosis) Exclude inappropriately high FiO2 Check mask and circuit for leaks Check for patient \200 \223ventilator asynchrony Check expiration valve is patent. Consider increasing IPAP pO2 remains low (<7 kPa) Consider increasing FiO2 Consider increasing EPAP Irritation or ulceration of nasal bridge Adjust strap tension Try cushion dressing Change mask type Dry nose or mouth Consider humidi \201 er Check for leaks Dry sore eyes Check mask \201 t Nasal congestion Decongestants Hypotension Reduce IPAP (or EPAP if high) CHAPTER 57 Non-invasive ventilation 700 NIV in chronic respiratory failure Chest wall deformity and neuromuscular weakness (p 582) \200 NIV has a well-established role in the management of chronic respira- tory failure due to c hest wall deformity or neuromuscular weakness, and has been shown to improve symptoms, gas exchange, and mortality Common underlying diagnoses include chest wall deformity and kypho- scoliosis, post-polio syndrome, motor neuron disease, spinal cord injury, neuropathies, my opathies, and muscular dystrophies. The nature of the underlying disease must in \202 uenc e the appropriateness of initi- ating ventilation: progressive conditions such as motor neu ron disease often result in increasing dependence on the ventilator, and the patient and th eir care-givers should be made aware of this NIV is administered at home overnight and this improves daytime gas exchange. The mechanism for this is unclear: it probably resets the c entral respiratory drive, although respiratory muscle rest and improved chest wall and lung compliance may also play a part Small portable positive pressure ventilators with either f ace or nasal masks are used in the majority of cases; negative pressure or abdominal ventil ators may rarely have a role in patients who are intolerant of masks, although their use ma y be limited by upper airways obstruction The decision to introduce overnight NIV is dif \201 cult, and is based on both symptoms (morning headaches, hypersomnolence, fatigue, poor sleep quality) and evidence of ventilatory failure (daytime hypercapnia (pCO2 >6.0 kPa) an d/or nocturnal hypoventilation with O2 saturations <88% on overnight oximetry). Daytime ven tilatory failure, however, is often a late feature, and is typically preceded by hypercapni c hypoventi- lation during sleep. A recent study in patients with myopathies demonstrated s upine inspiratory vital capacity to be an accurate predictor of respiratory reserve: supine IVC <40% of predicted was signi \201 cantly associated with hypercapnic hypoventilation a nd such patients should be considered for treatment with NIV. Supine IVC <20% was typically associated with daytime respiratory failure, whereas supine IVC >60% indicated a minimal r isk of respiratory complications. Other factors include signs of cor pulmonale or hospital admission with respiratory failure Patients with excessive secretions may not be suitable f or non-invasive ventilation, although face mask ventilation is possible even in the setting of bulbar weakness Regular follow-up of patients on overnight ventilation is important. As k about symptoms and compliance, and repeat arterial or capillary blood gas analysis. Lack of improvement in gas exchange may re \202 ect non-compliance, excessive air leakage, inad equate pressure support, or progression of underlying disease; consider repeating nocturnal oxim- etry monitoring. Patients with persisting severe hypoxia may bene \201 t from long- term supplementary oxygen, although this may worsen CO2 retention. NIV IN CHRONIC RESPIRATORY FAILURE 701 Sleep apnoea (p 574) Overnight NIV may have a role in patients with central hypoventilation , Cheyne \200\223Stokes respiration, obesity hypoventilation, overlap syndromes of obstruct ive sleep apnoea with coexisting COPD or obesity. Cystic \201 brosis (p 218) Overnight NIV may have a useful role as a \200\230bridge \200 \231 to transplantation in patients with cystic \201 brosis and chronic respiratory failu re. COPD (p 179) Use of NIV in the management of chronic stable COPD is controversial. Trials h ave shown con \202 icting results, although some possible bene \201 t in a subgroup of pa tients with severe hypercapnia, extra nocturnal hypoventi- lation, and recurrent admissions for worsening ventilatory failure. Further information Clinical indications for noninvasive positive pressure ventilation in c hronic respiratory failure due to restrictive lung disease, COPD, and nocturnal hypoventila tion \200\224a consensus conference report. Chest 1999; 116: 5 21 \200\22334 Ragette R et a l. Patterns and predictors of sleep disordered breathing in primary myopathies. Thorax 2002 ; 57: 724 \200\2238 This page intentionally left blank 703 Chapter 58 Oxygen therapy Acute oxygen therapy 704 Home oxygen therapy 706 Practical issues 710 CHAPTER 58 Oxygen therapy 704 Acute oxygen therapy Acute oxygen therapy is either \200\230controlled \200\231 or \200 \230uncontrolled \200\231. \200 Uncontrolled Use when extra O2 is required to raise the SaO2 above 92%, to ensure adequate O2 delivery to the tissues and where there are no concerns that high PaO2 values will depre ss ventilatory drive to the point that PaCO2 will rise, and pH fall, dangerously, e.g. pneu monia, pneumothorax, pulmonary emboli, asthma, LVF, etc. Controlled Use when extra O2 is re quired, but ventilation critically depends on hypoxic drive, e.g. exacerbations of COPD (pa rticularly when there has been a chronically raised PaCO2, as evidenced by a signi \201 ca nt base excess), chronic ventilatory failure due to scoliosis, neuromuscular disease, and a ny other cause of \200\230pump \200\231 failure. With stable type II ventilatory failure, ventilation still seems to be domi- nantly driven by PaCO2/pH, but in exacerbations (when P aO2 usually falls), peripheral chemoreceptor drive from low PaO2 becomes domi- nant. Thus, O2 therapy must not raise PaO2 above 8 kPa ( 92% SaO2) as this will \200\230turn off \200 \231 ventilatory drive, allowing hypoventilation, hyper- capnia, acidosis, and potentially death. There is some evidence that high alveolar PO2 also \200\230turns off \200\231 pulmo nary hypoxic vasoconstriction. This allows an increase in pulmonary blood \202 ow to poor ly ventilated areas and reducing CO2 excretion (accounts for \211\210 20% of the PaCO2 ris e fol- lowing excessive FiO2 in COPD exacerbations). Delivering uncontrolled oxygen This can be done in many ways, essentially by blowing O2 ove r the face, whilst limiting inhalation of surrounding air or exhaled CO2. \200 Standard O2 masks (sometimes called high- \202 ow masks). Set the O2 regulator to at least 4 L/min, much more if very breathless, to prevent dilution by air drawn into mask by high inspiratory \202 ows via exit holes. Can deliver about 50 \200\22360% O2. Nasal cannulae/ prongs/catheters are uncontrolled and deliver unpredict- able levels of O2 (depending on \202 ow rate, minute ventilation, and oral vs. nasal breathing route). Titrate using an oxy gen saturation monitor. Non-rebreathe reservoir masks can deliver FiO2 values over 60% by m eans of a soft plastic bag between the end of the tubing and mask, plus one-way valves betw een the bag and mask and on the mask exit ports. This mechanism ensures that most of the in spired air is pure O2. The ability of the reservoir to empty on inspiration brie \202 y al lows higher inspiratory \202 ows than the actual O2 regulator setting, and the bag valve prevents inhalation of very much exhaled CO2; the mask exit valves close, preventing air in halation. The usual problem is kinking of the junction between the mask and bag when the he ad tilts forward, reducing the effectiveness of the reservoir. Very high FiO2 requires a ti ght seal, and is generally delivered with CPAP masks (using pressures of about 5 \200\2237 cmH2O). This ensures no air is entrained through blow off vents or leaks, as well as improv ing V/Q matching by recruiting collapsed alveoli. Delivering controlled oxygen therapy This requires the ability to reliably control the FiO2 in order to keep the patient \200\231s SaO2 less than 92% (some suggest 90%), but high eno ugh to prevent anaerobic metabolism. This lower ACUTE OXYGEN THERAPY 705 acceptable level is debatable: 88% is generous, 85% is likely to be adequate, and 80% may b e acceptable if cardiac output is adequate. \200 FiO2 is controlled through Venturi masks \200\224O2 is directed through a narrow nozzle and exits at speed, lowering the air pressure at this point. This draws in surrounding air, di luting the O2 A proper Venturi mask mixes O2 and air in the same proportion, regardless of the oxygen \202 ow The minimum \202 ow setting of the regulator, written on the nozzle, ensures adequate overall \202 ow to prevent air being drawn through the exit holes durin g inhalation, e.g. a 28% Ventimask has a 1:10 entrainment ratio, 1 L/min O2 entrains 10 L/m in air (total \202 ow 11 L/min), 2 L/min O2 entrains 20 L/min (total \202 ow 22 L/min) Nasal cannulae are de \201 nitely not controlled O2 therapy and are in fact the opposite. If nasal cannulae do deliver too high an FiO2, and ventila- tion decreases as a consequence , the proportion of the minute ventila- tion containing the \201 xed \202 ow nasal oxyg en will rise, increasing the FiO2 and hence PaO2 still further \200\224a vicious cycle Cont rolled and very low \202 ow oxygen is also needed sometimes with NIV when the patient is still required to trigger inspiration. Added O2 should be avoided if possible and rarely re quires more than 1 L/min to be entrained; again it should be titrated using the SaO2. When adding too much oxygen, it is easy to be lulled into a false sense of security by an SaO2 o ver 92%, while the PaCO2 gradually rises undetected. Oxygen alert card should be given to all patients with a previous episode of hypercapnic re spiratory failure. This alerts ambulance crews and medical staff to the potential risk of h ypercapnia with high- \202 ow oxygen and documents usual resting baseline SaO2. However, t he ambulance staff protocols are suf \201 ciently rigid that they are not allowed to overr ide them. In some areas, letters from the patient \200\231s consultant and head of the ambu - lance service must be with the patient. Patient details Carry the card with you at all times Sticky label If you need to call the ambulance service or attend the hospital accident and emergency dep artment, show this card to the GP, paramedics, doctor or emergency department staff looking after you, as it provides them with essential information regarding your personal oxygen n eeds. Introduction If you have a sudden worsening of your lung disease (usually due to a chest in fection) it is essential that you do not receive too much or too little oxygen, either can be dangerous. Too much oxygen can cause a rise in the level of carbon dioxide in your blood and this can make you drowsy and slow your breathing. Too little oxygen can also be danger ous. Latest blood gas recordings: Date: ____/____/_______ On: Air, or % oxygen ____% pH:____ pCO 2_____pO2_____ Oxygen saturation: _______ % Purpose of this card The purpose of this oxygen alert card is to make sure that the doctors or ambulance staff involved in your care are made aware of your special needs regarding ox ygen therapy. The card recommends the appropriate amount of oxygen therapy for you based on your previous blood gas tests. You should receive enough Oxygen to achieve a %O2 saturation of no higher than 92%, but hig her than 86%, if possible. This is usually done with either a 24% or 28% venturi mask. Sign ed Name Designation Fig. 58.1 Oxygen alert card. CHAPTER 58 Oxygen therapy 706 Home oxygen therapy Home oxygen is delivered with essentially three different aims. First, to reduce the long-term complications of chronic hypoxia such as cor pulmo- nale, usually c alled long-term oxygen therapy or LTOT. This requires \211 15 h a day to be successful. Ho me oxygen can also be supplied for the relief of breathlessness, usually called \200\230sh ort \200\231 burst oxygen therapy or SBOT. If SBOT is used for many hours a day, it is some times incorrectly called LTOT, particularly by the oxygen supply companies. Oxygen can also be supplied to ambulant patients so that they can leave the house and travel (ambulatory o xygen). Long-term oxygen therapy (LTOT) Background and indications Two landmark trials of LTOT in t he 1980s: the British MRC Working Party trial and the American Nocturnal Oxygen Therapy Tri al (NOTT). The MRC trial compared COPD patients receiving oxygen for 15 h/day with controls receiving no oxygen. The NOTT trial compared continuous daily oxygen (average 17.7 h/day) with overni ght oxygen (average 12 h). The patients in the MRC trial were on average hypercapnic (mean PaCO2 7.3 kPa), whereas those in the NOTT trial were on average normocapnic (mean PaCO2 5.7 kPa). The main outcome in both trials was improved survival in those patients receiving ox ygen for at least 15 h/day, though this improved survival was not seen in the MRC trial unt il after a year of oxygen therapy. The NOTT trial showed a reduced exercise pulmonary artery pressure (PAP) after 6 months of continuous or nocturnal oxygen therapy. The 8-year survival was related to the fall in mean PAP during the \201 rst 6 months of continuous oxygen use. The MRC trial failed to show a fall in mean PAP with LTOT, but the mean annual increase in PAP (3 mmHg) in patients in the control arm was not seen in the oxygen treated group. The reason for the improved survival with LTOT is not clear, and is unlikely to relate to the small changes in pulmonary haemodynamics seen. COPD is the disease for which LTOT is most commonly prescribed, and the disease in which th e original studies were completed. Subsequent oxygen studies have shown improved exercise e ndurance in COPD patients breathing supplemental oxygen, with improved walking distance and ability to perform daily activities. FEV1 is the strongest predictor of survival in COPD; LTOT does not in \202 uence the decline in FEV1. Additional bene \201 ts of LTOT include: \200 \200 \200 Reduction of secondary polycythaemia Improved sleep quality, by reducing hypoxia-associated brain arousals Reduced cardiac arrthymias, and potentially reducing the risk of noc- turna l sudden death Reduced sympathetic out \202 ow leading to improved renal function, with in creased salt and water excretion, and reduced peripheral oedema HOME OXYGEN THERAPY 707 Indications for LTOT in COPD patients Criteria for prescription of LTOT in the UK are based on the clinical parameters of patients showing improved survival in the two LTOT trials. \200 PaO2 <7.3 kPa (55 mmHg) breathing air (i.e. a saturation on air \211 88%), in a stab le clinical state. Borderline results may need reassessment after 3 months, particularly if oximetry SaO2 <92% PaO2 7.3 \200\2238 kPa (56 \200\22359 mmHg, SaO2 89 \200\22390%) if pul monary hyperten- sion (i.e. symptoms and signs of cor pulmonale), polycythaemia, or addi- t ional nocturnal hypoxaemia (SaO2 \211 90% for at least 30% of the night). There is no evid ence that treating solely nocturnal hypoxaemia leads to improved survival Clinical stabilit y is the absence of an exacerbation for the previous 4 weeks. This is usually assessed twic e, several weeks apart, to ensure stability and ideally at least 6 weeks following an exace rbation LTOT is usually prescribed for those with FEV1 <1.5 L or <40% pre- dicted. If the F EV1 is higher in the presence of hypoxia/hypercapnia, it suggests an additional cause for t he ventilatory failure, such as addi- tional obstructive sleep apnoea; further investigatio ns may be indicated Medical management of the disease must be optimized prior to the prescr iption of LTOT PaCO2 does not in \202 uence the prescription of LTOT for COPD. There is a small risk of precipitating worsening hypercapnia with LTOT in those who are already hyperc apnic, particularly if the patient has OSA or is experiencing an exacerbation Blood gasses should be checked on LTOT to ensure the absence of worsening hypercapnia, if symptoms such as headache and confusion suggest that this has occurred, and to ensure a satisfactory incr ease in PaO2. Aim for PaO2 values of 8 \200\2239 kPa (60 \200\22365 mmHg, SaO2 90 \200\2239 2%) Patients should have stopped smoking: the bene \201 t of LTOT in continued smokers is limited, and there is an increased risk of \201 re. However, most studies suggest that ar ound 18% of patients on LTOT continue to smoke; they should be warned of the risks.