Inhalational Therapy

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INHALATIONAL THERAPY:

INHALATIONAL THERAPY By Chest Department Ainshams University

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1- A small dose of drug can be used 2- There is rapid onset of action 3- There is a low incidence of systemic side effects The inhalation of aerosols for therapeutic purposes has been known from ancient times. INHALATION THERAPY Inhalation therapy has several well established advantages over the oral and intravenous (IV) routes: ( Newman and Clarke, 1983) It is a general rule that therapeutic aerosols should reach the lungs to be effective.

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Several processes account for the deposition of aerosols within the respiratory tract. Mechanisms of Deposition: Particle size: The range of sizes encountered in aerosol therapy (approx 1 to 10 µ diameter). Particles in the 1 to 5 µ range show peak deposition in the small conducting airways and alveoli. Whole particles in the 5 to 10 µ range have peak deposition in the large conducting airways. Particles < 5 µ diameter can be taken to constitute “respirable range” for therapeutic aerosols,

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The site of deposition within the respiratory tract depends on the speed of inhalation (inhaled flow rate) Inhalation Mode: Rapid inhalation increases the probability of deposition by impaction in the oropharynx and large conducting airways. Slow, steady inhalation increases the number of particles able to penetrate to the peripheral parts of the lungs. As the inhaled volume is increased, aerosol is able to penetrate more peripherally into the bronchial tree. A period of breath-holding on completion of inhalation enables those particles which penetrate to the lung periphery to settle onto the airway under gravity. ( Pavia et al., 1977)

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Includes small volume nebulizers (SVNs), metered dose inhaler (MDIs) or dry powder inhalers (DPIs). AEROSOL DELIVERY SYSTEMS: I. Metered -dose inhaler: User must first shake the inhaler, then inhale deeply while pressing the top of the inhaler to expel the drug, before holding his/her breath for the drug to have an effect. Patients who have difficulty in coordinating the operation of MDI, can use it in conjunction with a spacer device. Oropharyngeal deposition is reduced.

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Different types of spacers

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They are machines that turn a liquid medication into a mist by blowing air or oxygen through it. II. Dry powder inhalers: Multi-dose powder inhaler (Diskus/Accuhaler inhaler) containing 60 discrete and identical doses (Sufficient for one month’s therapy). Nebulizers: I. Jet Nebulizers: Continuous flow of pressurized air passes through a very narrow hole II. Ultrasonic Nebulizers: These systems produce a very dense aerosol with a larger particle size than those generated by jet nebulizer. Turbohaler Spinhaler

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SVN-Compressor / jet Advantages and Disadvantages in the use of SVN, MDI, and DPI SVN-Ultrasonic MDI MDI with accessory device DPI

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Bronchodilators are used frequently in intubated patients undergoing mechanical ventilation, and innovative therapies, including aerosolized surfactant and antibiotics, have also been administered to critically ill patients. Administration of therapeutic aerosols to mechanically ventilated patients:

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Most drugs used in the treatment of asthma and airflow obstruction are given by the inhaled route. This includes bronchodilators such as  2 -agonists, anticholinergics, and anti inflammatory medications such as corticosteroids, cromolyn sodium, and nedocromil sodium. INHALED DRUGS ASTHMA MEDICATIONS

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Short acting inhaled bronchodilators used for relief of acute symptoms. They act rapidly-(with a rapid peak effect) and locally with few side effects. The limitations of short-acting  2 -agonist are: Inhaled Beta2 Agonists: 1-Their inability to control the symptoms of nocturnal asthma Salmeterol and formoterol are potent, selective  2 -agonist which can produce bronchodilation and protection from bronchoconstriction for more than 12 hours. 2-Their short duration of protection against exercise-induced bronchospasm.

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Long acting  2 -agonist are highly effective therapeutic agents for asthmatic who experience excessive symptoms or physiologic impairment despite the regular administration of low doses of inhaled corticosteroids. Inhaled Beta2 Agonists: Regular use of long acting  2 -agonist i s recommended for any patient on low dose inhaled corticosteroids still experiencing day time symptoms once per day, night time symptoms once per week, or FEV 1 /peak flow < 80% predicted. This is better than doubling the dose of steroid Muscle tremors, tachycardia, palpitations and restlessness. Tolerance to the bronchoprotective effects of both short and long acting inhaled  2 - agonists.

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Stepwise pharmacologic management of COPD Adapted from: Chest 113(4), 1998 Supp. Intermittent symptoms Beta-agonists pm Mild persistent symptoms Ipratropium + Beta-agonists pm Severe persi-stent symptoms Ipratropium + Beta-agonists + Theophylline Monitor levels) Ipratropium + Beta-agonists + Trial of Steroids Crisis Inhaled Beta2 Agonists in COPD therapy:

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Anticholinergic agent which blocks muscarinic receptors on airway smooth muscle, decreases vagal tone; inhibits smooth muscle contraction and decreases mucous secretion. It is the drug of choice in COPD patients. Ipratropium bromide: Inhaled steroid therapy: It was major advance in the treatment of asthma. Glucocorticoids are the only approved therapy that reduces inflammation in the airways of patients who have asthma.

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Side effects of inhaled corticosteroids: Local side effects: These are caused by deposition of glucocorticoids in the upper airway. Rinsing the mouth may reduce the local deposition associated with dry-powder inhalers. Dysphonia in more than 50% of the patients. The multiple-dose, dry powder delivery system (Turbuhaler) reduces laryngeal symptoms.

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Disodium cromoglycate: Disodium cromoglycate (DSCG. Cromolyn sodium): DSCG have a stabilizing effect on mast cell membranes, so that the release of various chemical mediators of asthma is inhibited. Nedocromil sodium: Nedocromil sodium (NS) is the disodium salt of pyranoquinoline dicarboxylic acid. Similar potency to DSCG

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AEROSOLIZED ANTIBIOTICS e.g. cystic fibrosis and bronchiectasis Antibiotics commonly used include amikacin, gentamicin, and tobramycin. The direct delivery of aminoglycosides to the lower airway by aerosol administration produces high concentrations of antibiotic at the site of infection. ( O’Donohue, 1996)

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AEROSOLIZED PENTAMIDINE: Aerosolized pentamidine have been studied for the treatment and prophylaxis of pneumocystis carinii pneumonia (PCP) ( Corkery et al., 1988) Aerosolized pentamidine may have a role in the treatment of mild PCP after a period of clinical and radiographic improvement achieved with standard parenteral therapy or oral trimethoprim-sulfa methoxazole. AEROSOLIZED RIBAVIRIN Ribavirin is a synthetic nucleoside analogue which has antiviral agent in both oral and aerosolized forms.

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MUCOLYTIC AGENTS The aerosolized delivery of mucolytic agents such as N-acetyl cysteine, that modify secretions through their actions on mucus glycoproteins, has met with limited clinical success. ( Wanner and Rao, 1980) In patients with bronchospastic diseases, it shuold be delivered in conjunction with a  2 -agonist. ( O’Donohue, 1996)

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INHALED NITRIC OXIDE Cystic fibrosis transmembrane conductance regulator (CFTR) gene. Inhaled nitric oxide (NO) vasodilate pulmonary vessels in various hypertensive lung disease such as hypoxic pulmonary vasoconstriction, persistent pulmonary hypertension in the neonate, congenital heart diseases, cardiac surgery, the adult respiratory distress syndrome and chronic obstructive pulmonary diseases. ( Adnot et al., 1993) GENE THERAPY IN CYSTIC FIBROSIS Considerable efforts is being invested in gene therapy to replace the faulty gene directly and thus to correct all the downstream consequences that arise from CFTR dysfunction.

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Anne et al., (1999), evaluated the efficacy of oral prednisolone, followed by inhaled budesonide in patients with newly diagnosed (<3months) stage I and stage II pulmonary sarcoidosis. MISCELLANEOUS AGENTS They concluded that an initial treatment with prednisolone followed by long term inhalation of budesonide is more effective than placebo in patients with stage II sarcoidosis. Ahmed et al., (1993), found that a large dose (1000u/kg) of nebulized heparin was more effective than cromoglycate in preventing exercise-induced broncho-constriction . Heparin inhibits histamine release from mast cells, and could form a basis for new asthma treatment.

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Oxygen therapy is used to correct arterial hypoxemia and to improve oxygen delivery to the tissues. OXYGEN THERAPY Guidelines for the institution of acute oxygen therapy Acute hypoxemia (P a O 2 <60mmHg, SaO 2 <90%) Acute exacerbation of COPD Cardiac and respiratory arrest Hypotension (systolic blood pressure < 100 mmHg) Low cardiac output and metabolic acidosis (bicarbonate < 18 mmol/L) Respiratory distress (respiratory rate > 24 /min)

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1. Tissue hypoxia associated with arterial hypoxemia: Arterial hypoxemia. Ventilation perfusion mismatch is the most common pathophysiological cause of arterial hypoxemia. Hypoxemia secondary to right to left shunting is less responsive to O 2 administration. A P a O 2 of 60 mmHg is a reasonable goal in the initial treatment of arterial hypoxemia. 2. Acute myocardial infarction (MI) The P a O 2 should be used to guide therapy. 3. When Hb is abnormal or tissue O2 delivery is inadequate: a- Carboxyhemoglobinemia produces tissue hypoxia. b- Methemoglobinemia produces tissue hypoxia. c- Sickle cell crisis.

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4. Hypoxemia is likely to occur and supplemental O 2 is indicated: 1- Postoperative: General anesthesia, by reducing functional residual capacity (FRC) and increasing V/Q mismatch, may lead to transient hypoxemia in the immediate postoperative setting. Treatment consists of low-flow O 2 therapy combined with lung expansion maneuvers and early ambulation. 2- Endoscopic procedures can result in hypoxemia because of sedative-related hypoventilation. 3- large or symptomatic pneumothorax, administration of supplemental 100% O 2 .

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Chronic, outpatient, home (domiciliary) O 2 therapy: A- long-term O 2 therapy should only be ordered for patients who have been on maximal medical therapy for at least 30 days prior to ordering O 2 . O 2 never be prescribed on an as-needed (prm) basis. 1- Medical Research Council (MRC) (1981) trial clearly demonstrated that continuous O 2 therapy has the best therapeutic effect in patients with COPD, with survival increasing in proportion to the number of hours per day that O 2 was administered. Continuous O 2 therapy is superior to nocturnal therapy, while both are better than no therapy. 2- An O 2 prescription must specify the O 2 flow rate and number of hours per day O 2 will be given. The majority of patients will require  4 L/min to maintain a PaO 2  55 mmHg. LONG TERM O 2 THERAPY ( O’Donohue, 1992)

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B- The overwhelming majority of patients requiring long-term home O 2 (>30 days) have COPD (chronic bronchitis, emphysema), LONG TERM O 2 THERAPY Lone term oxygen therapy will reverse: Secondary polycythemia Decrease pulmonary vascular pressure Alleviate right heart failure due to cor pulmonale Strengthen cardiac function Enhance neuropsychological function Improve exercise performance and activities of daily ( Tarpy and Celli, 1995) Long term oxygen therapy in hypoxemic patients with COPD improves survival and decreased hospitalization, (Fletcher et al., 1987)

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OXYGEN DELIVERY SYSTEMS Oxygen in the home is often delivered by nasal cannula at low flow rates of 2-4 L/minute. There are three delivery systems currently available for use in the home: compressed-oxygen cylinders, liquid oxygen systems and oxygen concentrators. Compressed oxygen is provided in high-pressure cylinders. Liquid oxygen system offer several advantages over compressed oxygen cylinders

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OXYGEN DELIVERY SYSTEMS Compressed concentrators separates oxygen from the air for delivery to the patient and returns nitrogen to the atmosphere. This device can deliver more than 90% oxygen as flows of up to 4 L/minutes. They are used as stationary sources of oxygen in the home. Portable liquid systems can be easily refilled from the larger stationary systems; they weigh less and will last four times longer than compressed oxygen cylinders at a given flow rate. The major disadvantage of liquid oxygen systems is their high cost.

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The advantages and disadvantages of the different modes of Long Term Oxygen Therapy Tarpy and Celli 1995

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A) Low-flow delivery systems i- Nasal cannulas: OXYGEN DELIVERY DEVICES Are the least expensive, most convenient, and most commonly used means of delivering O 2 . Nasal cannulas are comfortable and allow the patient to talk and eat. O 2 is delivered by polyethylene or plastic prongs at a rate of 1-6 L/min (controlled by a flow regulator and displayed on the flow meter), achieving a F i O 2 of 22% to 40%. ii- Simple face masks: With flow rates of 6-8 L/min are able to deliver a F i O 2 as 60%. In contrast to nasal cannulas,the mask must be removed for eating, drinking expectoration, and effective communication. iii- Partial rebreathing and nonrebreathing (reservoir) masks.

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OXYGEN DELIVERY DEVICES and F i O 2 CAPABILITIES

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a,b: Simple masks c: nasal cannula

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B) High-flow delivery systems i- Venturi masks: OXYGEN DELIVERY DEVICES The F I O 2 is regulated by adjusting the O 2 flow rate (3-15 L/min) and the size of ports in the mask (Ventimask) F I O 2 levels of 24% 26%, 28% 30%, 35%, 40% and 50% can be accurately produced. These masks deliver reliable levels of F I O 2 and are particularly useful when hyperoxia must be avoided. The principal use for the Venturi mask is in hypercapnic COPD, in which hyperoxia can be complicated by worsening hypercapnia and precise levels of F I O 2 must be delivered

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B) High-flow delivery systems ii- Continuous positive air way pressure (CPAP) masks: The most widely used therapy for obstructive sleep apnea syndrome (OSAS) is nasal CPAP,. A constant pressure is applied to the nasal inlet through out the respiratory cycle via a nasal mask or nasal prong. The most common used is bilevel positive airway pressure, in which a higher pressure is applied during inspiration than during expiration. Artificial airway into the trachea allow accurate O2 delivery with concentrations up to 100% iii- Intubation and mechanical ventilation: OXYGEN DELIVERY DEVICES

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Oxygen Tent: Their main application is in childhood; children do not tolerate masks well. Insertion of a catheter percutaneously between the second and third tracheal interspaces. Oxygen enters the trachea via this catheter. TTO is invasive and requires special training by the physician. Relative contraindications include high-dose steroids (>30mg/d) and conditions that predispose to delayed healing, e.g., diabetes mellitus, connective tissue disease, or severe obesity. Transtracheal oxygen (TTO): Not all patients are suitable candidates for TTO. The ideal candidate for TTO has a strong desire to remain active.

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1- measurement of arterial blood gases (ABG) means of assessing gas exchange status. Blood gas measurement errors: sample site (vein), inadequate blood handling techniques (too much heparin remains in the syringe and mixes with the sample (falsely PaO 2 ), the sample is not promptly placed on ice (falsely PaO 2 ) and instrumentation error. Oximetry is not considered sufficiently accurate to replace ABG-in an initial assessment and can not be used to determine acid base status. MONITORING OF OXYGEN THERAPY 2- Pulse oximetry, provides a non invasive and continuous method for assessing SaO 2 in certain settings (e.g. operating rooms, intensive care units, transporting critically ill patients, invasive diagnostic procedures). 3- transcutaneous PO 2 measures local oxygen level across the dermal surface.

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Hyperbaric oxygen therapy is the intermittent administration of 100% oxygen at pressure greater than sea level. HYPERBARIC O 2 THERAPY Hyperbaric O 2 therapy mechanically compresses gas so that more can be dissolved in the blood. Gas Embolism, carbon monoxide poisoning, crush injury, acute traumatic ischemia, decompression sickness, gas gangrene, clostridial myonecrosis, necrotizinganaerobic infections, refractory osteomyelitis, radiation tissue damage, thermal burns and compromised wounds or skin grafts Hyperbaric oxygen therapy may be implemented in a chamber, filled with compressed air in which the patient breaths 100% oxygen through a mask, head tent, or endotracheal tube. The arterial partial pressure of oxygen will approach 1500 mmHg at a pressure equivalent of 33 feet of sea level. (Epstein, 1997)

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O2 toxicity occurs more frequently when O2 is delivered under hyperbaric condition. Complications: Barotrauma. Pneumothorax.

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Depression of hypoxic ventilatory drive PULMONARY OXYGEN TOXICITY Oxygen in high concentrations is cytotoxic Pulmonary vasodilatation and absorption Lung injury These events interrupt normal cellular function, and if severe enough, lead to cellular death. Alveolar macrophage function is altered following hyperoxic exposure.

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Sequence of pulmonary changes during hyperoxic exposure in humans Adopted from Beers (1998)

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Diagnosing Oxygen Toxicity: The diagnosis is generally based on a high index of suspicion in the patient who demonstrates progressive respiratory deterioration after prolonged exposure to high oxygen mixtures. In neonates, the administration of 50% to 100% O2 can produce a serious form of retinopathy (retrolental fibroplasia due to hyperoxic vasoconstriction of the retinal vessels. Other complications of O2 therapy: Central nervous system toxicity.

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INHALATION OF HELIOX: Helium-oxygen (heliox) mixtures in the treatment of acute severe asthma been rediscovered. To lower airway pressures in intubated patients. Also rapidly decrease airway resistance and dyspnea in nonintubated patients with severe asthma. Heliox causes both a rapid improvement in peak flow and a decrease in dyspnea in adult patients with acute severe asthma that is maintained for at least 8 h. Helium alter flow from turbulent to laminar in the large airways, there by effectively lowering airway resistance.

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PEFR may be simply measured using equipment such as the Wright peak expiratory flow meter. Peak expiratory flow rate: The machines are cheap and portable and serve a variety of functions. Variability in PEFR of greater than 15-20% in a single day or from day to day is very suggestive of asthma. Most normal subjects demonstrate less than 10% variation in PEFR over a 24-h period. PEFR may be used as an index of response to treatment in asthma. PEFR is the most convenient measurement for use in the diagnosis of exercise-induced asthma, where a fall in PEFR of greater than 15% following exercise is considered diagnostic.

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Result of exposure to normobaric hyperoxia: 1- Acute tracheobronchitis 2- Absorption atelectasis 3- An acute alveolar lung injury (adult respiratory distress syndrome (ARDS) 4- Bronchopulmonary dysplasia.

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PEFR in acute severe asthma Peak expiratory flow chart recorded 6-hourly over 4 days in an asthmatic patient. A marked diurnal variation is seen with the lowest values recorded in the early morning. “The morning dipper” pattern.

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Advantages and Disadvantages in the use of SVN, MDI and DPI Adapted from Resp. Care 1991; 36: 960

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Advantages and Disadvantages in the use of SVN, MDI and DPI

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Adnot S, Kouyoumdjian C, Defouillory C, Andrivet P (1993): Hemodynamic and gas exchange responses to infusion of acetylcholine and inhalation of nitric oxide in patients with chronic obstructive lung disease and pulmonary hypertension. Am. Rev. Resp. Dis. 148: 310-316. REFERENCES Ahmed T et al., (1993): Preventing bronchoconstriction in exerecise-induced asthma with inhaled heparin. NEGM, 329:90-5. Beers F, (1998): Oxygen therapy and pulmonary oxygen toxicity in Fishman AP et al. Fishman’s pulmonary diseases and disorders. McGraw-Hill, 3rd edition, Volume 4, page 2627. Corkery K, Luce J, Montgomery A (1988): Aerosolized pentamidine for treatment and prophylaxis of pneumocystic carnii pneumonia. An. Update. Resp. Care, 33:676-585. Epstein S, (1997): Oxygen therapy in Goldstein RH, O’connell J, Karlnsky J. A practical approach to pulmonary medicine, Lippincott-Raven Page 543-560. Anne P., Haahtela T, Person T., Selroos O. (1999): Oral prednisolone followed by inhalled budsonide in newly diagnosed pulmonary sarcoidosis, Chest, 116:424-431.

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REFERENCES Fletcher EC, Miller J, Divine GW, Miller T. (1987): Nocturnal Oxyhemoglobin desaturation in COPD patients with arterial oxygen tensions above 60 mmHg. Chest, 92: 604-608. Wanner A and Rao A (1980): Clinical indications for and effects of bland, mucolytic and antimicrobial aerosols. Am. Rev. Resp. Dis. 112:79-87. O’Donohue W (1996): Guidelines for the use of nebulizers in the home and at domicilliary sites. Chest, 109; 814-20. O’Donohue W.J. (1992): Prescribing home oxygen therapy. What the primary care physician needs to know. Arch. Intern. Med., 152: 746-748. Tarpy SP, Celli BR, (1995): Long term oxygen therapy. N. Engl. J. Med, 333: 710-714.

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Making the Best Use of a Deprtment of Clinical Radiology: Guideliners for Doctors, 3rd edn. London: Royal College of Radiologists, 1995. REFERENCES Biello ER, Matter AG, Mcknight RC, Siegel BA. Ventilation-perfusion studies in suspected pulmonary embolism. Am J Radiol 1979; 133: 1033. Bowen A. Quantitative roentgen diagnosis of pleural effusions. Radiology 1931; 17: 520. Kaunitz J. Landmarks in simple pleural effusions J AMA 1939; 113: 1312.

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Jaakkola MS, Jaakkola JJK, Ernst P. Becklake MP: Respiratory symptoms should not be overlooked. Am Rev Respir Dis 147: 359-366, 1993. REFERENCES Johnston H, Reisz G: Changing spectrum of hemoptysis. Arch intern Med 149: 1666-1668, 1989. Kamin SS (ed): Lung sounds. Semin Respir Med 6: 157-242, 1985. Lemansk RF, Busse WW: Asthma. JAMA 278:1855-1873, 1997. Sharms OP: Symptoms and signs in pulmonary medicine: Old observations and new interpretations. Dis Mon 41: 577-638, 1995.

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ATS Statement: Standardization of spirometry-1994 update. Am J Resir Crit Care Med 152:1107-1136, 1995. REFERENCES Britton J, Pavord I, Richards K, et al: Factors influencing the occurrence of airway hyperreactivity in the general population: The importane of atopoy and airway calibre. Eur Respir J 7:881-887, 1994. Glindmeyer HW, Lefante JJ, McColloster C, et al: Blue-collar normative spirometric values for Caucasian and African-American men and women aged 18 to 65. Am J Respir Crit Care Med 151: 412-422, 1995. Johnson, BD, Beck KC, Zeballos RJ, Weisman IM: Advances in pulmonry laboratory testing, Chest 116: 1377-1387, 1999.

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