PRINCIPLES OF MANAGEMENT

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1 Respiratory failure 199 admission to intensive care and high-dependency units for mechanical ventilation. CHEST WALL If a segment of chest wall becomes unstable (e.g. due to multiple rib fractures), particularly when associated with lung contusion, it may be impossible to sustain adequate ventilation (see Chapter 10). Similarly, if the thorax is deformed (e.g. due to kyphoscoliosis), lung expansion will be impaired. These patients may eventually develop ventilatory failure and are prone to recurrent chest infections. On the other hand, ventilatory failure is unusual when chest movement is restricted, but the thorax is uniform (e.g. as in ankylosing spondylitis). Rarely, patients with myopathies or myositis may develop respiratory failure. Mechanical ventilation may be required and can allow time for the diagnosis to be established (e.g. by muscle biopsy). PLEURA Pneumothorax, haemothorax, pleural effusion and empyema may all cause or exacerbate respiratory failure. LUNGS AND AIRWAYS As discussed above, diseases affecting primarily the lungs and airways initially cause hypoxaemic respiratory failure, but may later progress to the mixed type. Causes of ARF include pneumonia, asthma, left ventricular failure, acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) (see below). Examples of chronic type I respiratory failure include emphysema and fibrosing lung disease. The commonest cause of mixed respiratory failure is COPD. Upper-airway obstruction is usually well tolerated initially, but can rapidly progress to frank respiratory failure. PULMONARY CIRCULATION As well as mechanically obstructing the circulation (see Chapter 5), acute pulmonary embolism can cause V/Q inequalities, possibly via reflex mechanisms, with hypoxaemia and tachypnoea. Recurrent pulmonary emboli eventually produce chronic pulmonary hypertension and respiratory failure. PRINCIPLES OF MANAGEMENT Clearly, the specific treatment of respiratory failure will vary according to the underlying cause, but the same general principles apply in all cases: Hypoxaemia should be corrected. The load on the respiratory muscles should be reduced by improving lung mechanics and controlling fever. Ventilatory pump capacity should be optimized. Specific measures include: administration of supplemental oxygen; control of secretions; treatment of pulmonary infection; treatment of airways obstruction; measures to limit pulmonary oedema; mechanical respiratory support. The importance of chest wall stiffness and decreased abdominal compliance in increasing the respiratory load is sometimes not fully appreciated. Since it seems unlikely that overt high- or low-frequency fatigue is allowed to develop in respiratory failure, specific therapy to counteract fatigue is probably of little value (Moxham, 1990). Respiratory failure must not be considered in isolation. Not only do hypoxia and hypercarbia adversely affect cardiovascular performance, but a low cardiac output is associated with a reduction in P, exacerbating the adverse effect of a given degree of shunt on arterial oxygenation. Low cardiac output is also associated with a decrease in respiratory muscle blood flow, anaerobic metabolism in respiratory muscles (which exacerbates lactic acidosis) and respiratory muscle fatigue (Aubier et al., 1982). Many drugs that act on the cardiovascular system, such as dopamine and glyceryl trinitrate, have been shown to increase pulmonary venous admixture, probably by reversing hypoxic pulmonary vasoconstriction. Myocardial failure often causes pulmonary congestion with increased shunting, and hypotension may lead to an increased dead space, particularly during positivepressure ventilation. Finally, the increased work and metabolic cost of breathing increase the load on the myocardium and respiratory system. OXYGEN THERAPY Indications Supplemental oxygen is always indicated in patients with acute hypoxaemic or mixed respiratory failure. For reasons discussed previously, oxygen therapy is most effective when the main abnormality is V/Q mismatch, but is less efficacious in the presence of a fixed right-to-left shunt (see Chapter 3). In patients with pure ventilatory failure, the primary abnormality is retention of carbon dioxide; specific treatment is therefore directed towards lowering P a C and P A C. The administration of oxygen is, however, a useful first step since it effectively reverses the hypoxia caused by the elevated P A C. Patients with carbon monoxide poisoning will also benefit from oxygen administration. By increasing P a, the dissociation of carboxyhaemoglobin is accelerated and the increase in dissolved oxygen improves tissue oxygenation (see Chapters 3 and 19). Methods of oxygen administration In mechanically ventilated patients, the inspired oxygen concentration (F I ) is easily measured (see Chapter 3) and can be maintained at the desired level by mixing air and oxygen

2 200 INTENSIVE CARE a b c d Expired gas Fig. 8.2 Methods of administering supplemental oxygen to an unintubated patient. (a) Simple facemask; (b) nasal cannulae: both (a) and (b) are variable-performance devices; (c) Venturi mask (d) mask with rebreathing bag: both (c) and (d) are fixed performance devices. in appropriate proportions. This also applies to spontaneously breathing patients with an endotracheal tube or a tracheostomy in place connected to either a T-piece or a continuous positive airway pressure (CPAP) circuit (see Chapter 7). In the non-intubated spontaneously breathing patient, measuring F I is not usually a practical proposition. Fortunately, in the majority of patients, the precise concentration of oxygen delivered is not crucial and a variableperformance device, such as a simple facemask or nasal cannulae (Fig. 8.2) will suffice. With these devices, the patient entrains a variable amount of air to supplement the flow of oxygen during inspiration, and it is not possible to predict with any degree of accuracy the concentration of oxygen being delivered to the patient s lungs. Furthermore, the F I is dependent on the oxygen flow rate, as well as the patient s V T and respiratory rate and therefore varies during the respiratory cycle (Goldstein et al., 1982). Since the peak inspiratory flow rate may be as much as 30 L/min, considerable volumes of air may be entrained at this point in the respiratory cycle. On the other hand, if the patient hypoventilates, the inspired oxygen concentration may be higher than expected. With these devices, the F I probably varies from about 0.35 to 0.55% with oxygen flows of 6 10 L/min. Higher concentrations of oxygen can be delivered by using a mask with a reservoir bag attached (Fig. 8.2). Nasal cannulae are often preferred to facemasks because they are less claustrophobic and do not interfere with sleep, feeding or speaking. They may, however, cause ulceration of the nasal or pharyngeal mucosa, and in some cases are associated with abdominal distension caused by swallowing oxygen. Although oxygen flow rates of L/min can be used through nasal cannulae, high flow rates (more than 2 4 L/min) are very uncomfortable; it may then be preferable to administer additional oxygen via a facemask. This has the added advantage that if the mask is removed (e.g. to perform mouth care), the patient continues to receive some supplemental oxygen via the nasal cannulae. If more accurate administration of oxygen is required, a fixed-performance device should be used. There are three ways of delivering a known, constant F I. Firstly, a gas mixture of the required oxygen concentration can be delivered to the patient via a tight-fitting facemask and a circuit containing a reservoir bag and a one-way valve. The reservoir bag partially collapses during inspiration and supplements the fresh gas flow; during expiration, the bag is refilled. Because there is no entrainment of air, the F I is known and remains constant throughout the respiratory cycle. As with the use of tight-fitting facemasks for the application of CPAP, these masks are often poorly tolerated and can produce pressure necrosis of the facial skin. The second method involves the application of the Venturi principle (Fig. 8.2), producing high airflow with oxygen enrichment (HAFOE) (Campbell, 1960a, b). If oxygen is delivered through an injector at a given flow rate, a fixed amount of air will be entrained and the F I can be accurately predicted. Relatively low flows of oxygen entrain large volumes of air and the high flows, combined with the large volume of the mask, ensure that the patient s requirements for fresh gas are satisfied even at peak inspiration. Masks are available that will deliver 24%, 28%, 34% or 60% oxygen. For example, a 24% Ventimask uses an oxygen flow rate of only 2 L/min, but produces a total fresh gas flow of 50 L/min downstream of the injector. The design of the mask is crucial, particularly with regard to its volume, and some commercially available devices are unsatisfactory (Campbell, 1982). Finally, oxygen tents can be used as fixed-performance devices and have proved to be particularly useful in children. They require a high fresh gas flow with a preset F I. Rebreathing is prevented by allowing gas to escape around the lower unsealed edges of the tent. Physiological effects of oxygen therapy In normal subjects, breathing oxygen causes a reduction in minute ventilation of approximately 10%, probably due to a

3 Respiratory failure 201 decrease in chemoreceptor drive. The consequent rise in P a C is exacerbated by a reduction in the buffering capacity of oxygenated haemoglobin. V D may be increased by redistribution of pulmonary blood flow, and absorption collapse can increase venous admixture (see below). In some cases, reversal of hypoxic pulmonary vasoconstriction may be associated with a fall in pulmonary vascular resistance, while cardiac output may decrease in association with a rise in peripheral resistance. Occasionally, administration of oxygen to those with ARF leads to a transient deterioration in conscious level. This is thought to be due to an acute reduction in cerebral blood flow when the reversal of hypoxia leaves the cerebral vasoconstrictor effect of hypocarbia unopposed. There is also increasing evidence to suggest that hyperoxia, which may occur when oxygen is administered unnecessarily or in inappropriately high concentrations, can promote reflex vasoconstriction in arteriolar smooth muscle via local regulatory mechanisms and may be harmful. For example, hyperoxia may reduce coronary blood flow, especially to ischaemic areas, and can reduce cardiac output and increase systemic vascular resistance in patients with myocardial infarction or congestive heart failure (Thomson et al., 2002). Oxygen toxicity (Jackson, 1990) Although oxygen is present in the air we breathe, and is essential to life, the possibility that prolonged administration of high concentrations of this gas may have toxic effects has been recognized for many years. As long ago as 1775, Joseph Priestley introduced the concept of oxygen toxicity, and a century later hyperbaric oxygen was shown to cause convulsions in birds. In 1899, Lorrain-Smith demonstrated that mice and other small animals developed pulmonary complications when exposed to high P. It was not until the 1920s, however, that the therapeutic use of oxygen became common practice and the possibility of oxygen toxicity began to concern clinicians. Even now, the relevance of oxygen-induced lung damage to clinical practice remains controversial. Experimental work has shown that continuous exposure to high concentrations of oxygen can damage mammalian lungs, but the evidence that high concentrations of oxygen cause lung injury in humans is less conclusive. Volunteers exposed to high concentrations of oxygen for more than 24 hours develop tracheobronchitis (manifested as substernal pain), with a reduction in vital capacity (VC), lung compliance and pulmonary diffusing capacity (Caldwell et al., 1966; Comroe et al., 1945). Also mucociliary clearance and macrophage function are impaired within a few hours of breathing 100% oxygen. It is more difficult to prove that oxygen damages the lungs of patients who receive high concentrations to correct hypoxaemia since clearly such patients already have underlying lung disease, the histological appearances of which are often non-specific. In addition, there are no pathognomonic chest radiographic or pathological appearances of oxygen-induced lung damage. Finally, there are obvious difficulties in devising a study with a suitable control group. Despite these problems, two prospective controlled studies have been performed. In one (Singer et al., 1970), postcardiac surgery patients were ventilated with either 100% oxygen or less than 50% oxygen for approximately 24 hours. There were no differences in intrapulmonary shunt, effective compliance, V D /V T ratio or clinical course between the two groups. The other study (Barber and Hamilton, 1970), performed in patients with irreversible brain damage, showed that after hours, P a was lower, while intrapulmonary shunt and the V D /V T ratio were greater in those ventilated with 100% oxygen than in the control group. Radiographic appearances and measurement of total lung weight supported these findings, although there were no noteworthy histological differences between the two groups. These investigations suggest that 100% oxygen can cause some deterioration in lung function, but this is probably only significant when exposure is for more than 24 hours. Pulmonary oedema is thought to develop after hours of exposure to high concentrations of oxygen and lung fibrosis after about 96 hours. The mechanisms by which oxygen damages the lungs are unclear, although it seems probable that, as with ARDS, the formation of reactive oxygen species is an important cause of direct cellular damage (Deneke and Fanburg, 1982) (see Chapter 5). A number of drugs, including paraquat and bleomycin, may exacerbate oxygen-induced lung injury by their effects on lung antioxidant defences and/or by increasing the rate of production of reactive oxygen species. Other factors, such as a deficiency of vitamins E and C, old age, hypermetabolic states, hyperthyroidism and catecholamines, may predispose to oxygen toxicity, while enzymes such as superoxide dismutase are generally protective (see Chapter 5). High inspired concentrations of oxygen will also displace nitrogen from the lungs, and this may be associated with absorption collapse of underventilated lung units. The contribution of reduced surfactant production to atelectasis and lung damage in this situation is uncertain. Finally, inadequate humidification of oxygen will exacerbate pulmonary abnormalities by drying both the bronchial mucosa, which impairs the mucociliary transport mechanism, and the bronchial secretions. Other adverse effects of high concentrations of oxygen include retrolental fibroplasia and exacerbation of barotrauma-induced bronchopulmonary dysplasia in neonates, while hyperbaric oxygen can precipitate convulsions. Although it is clear that retrolental fibroplasia is caused by excessively high P a, it seems that lung damage is related more to P A than to the P a. It is also worth noting that it is the normal areas of lung that are exposed to the highest P and that it is therefore these areas that may be most damaged by the use of a high F I. In conclusion, it seems reasonable to assume that administration of oxygen can damage the lungs and that the extent of the injury depends on the duration of exposure and the

4 202 INTENSIVE CARE concentration of oxygen. It is therefore important to use the lowest F I compatible with adequate arterial oxygenation. Conventionally, the aim is to achieve at least 90%, and preferably 95%, saturation of haemoglobin with oxygen. It must be remembered, however, that at levels of S a approaching 90%, the patient is close to the steep segment of the oxyhaemoglobin dissociation curve where small falls in P a cause potentially dangerous reductions in oxygen content. Although there is only limited information on safe levels for oxygen therapy, long-term administration of an F I 0.5 or of 100% oxygen for less than 24 hours is traditionally considered to be acceptable. Dangerous hypoxia should never be tolerated through a fear of oxygen toxicity. Finally, although experimental evidence suggests that treatment with antioxidants or administration of exogenous surfactant may ameliorate oxygen toxicity, the value of such measures in clinical practice is unclear. Monitoring the effects of oxygen therapy In view of the risks of pulmonary oxygen toxicity and the potential dangers of hyperoxia it is important to ensure that oxygen therapy is prescribed, administered and monitored with care (Thomson et al., 2002). Some clinical improvement may be obvious following the administration of oxygen (e.g. reversal of cyanosis, slowing of the respiratory rate and a reduction in respiratory distress). Arterial blood gas analysis is, however, essential for proper assessment of the effects of treatment; ideally a baseline sample should be obtained first with the patient breathing air. In most cases, the aim is to achieve a P a within normal limits and more than 95% saturation of haemoglobin with oxygen. It is pointless to administer oxygen in concentrations that produce a higher than normal P a since, because of the shape of the dissociation curve, oxygen content is not significantly increased. If potentially toxic concentrations of oxygen are required to achieve a normal P a, lower values may be accepted provided that oxygen content, and by implication oxygen delivery (D ), remains acceptable. In particular, more than 90% saturation of haemoglobin with oxygen can sometimes be considered adequate, and this may be achieved at P a values as low as 8 kpa (60 mmhg). Compensatory mechanisms such as polycythaemia, a shift of the dissociation curve, an increase in cardiac output and a redistribution of blood flow may preserve cellular oxygenation despite severe arterial hypoxaemia. Clinical assessment of cellular oxygenation is difficult, although a reduction in P v or mixed venous oxygen saturation (S v ) is thought to be a reasonable indication that tissue oxygenation is impaired (see Chapters 3 6). Other indices such as the development of lactic acidosis are too insensitive to be of value in assessing oxygen therapy. It is also worth re-emphasizing that when P is low, the patient is operating on the steep segment of the oxyhaemoglobin dissociation curve and small increases in P will produce clinically useful improvements in oxygen content. This fact is utilized when administering oxygen to patients who are dependent on a hypoxic drive to respiration in whom too great an increase in P a may cause dangerous carbon dioxide retention (see below). CONTROL OF SECRETIONS Many patients with respiratory failure produce large quantities of bronchial secretions, which are often infected. In order to prevent sputum retention, with its attendant dangers of pulmonary collapse and perpetuation of infection, these secretions must be cleared. Hydration Patients with severe respiratory failure are often unable to drink and lose large quantities of fluid due to pyrexia, hyperventilation and the excessive work of breathing. Dehydration is therefore frequent, and as a result secretions may become more tenacious. This can be avoided by humidifying inspired gases (see Chapter 7) and, more importantly, by achieving adequate systemic hydration with intravenous crystalloid solutions. On the other hand, lung water is frequently increased in patients with respiratory failure, particularly in ALI/ARDS, and some patients with COPD are unable to handle a salt or water load, perhaps at least in part due to autonomic dysfunction (Stewart et al., 1995). In such patients some degree of fluid restriction is usually indicated. Mucolytic agents A number of mucolytic agents have been developed that can reduce sputum viscosity in vitro. For example, various cysteine analogues have been described that reduce the number of cross-linking disulphide bridges in polymeric mucous glycoproteins to produce less viscid thiomonomers. Chest physiotherapy (Selsby and Jones, 1990) Chest physiotherapy, which may be preventive or curative, conventionally uses postural drainage, percussion and vibration (PDPV) in an attempt to mobilize secretions and expand collapsed lung segments. In those with copious sputum production these techniques, usually in combination with directed coughing in those who are conscious and cooperative, may be associated with an enhanced clearance of secretions and improved lung function. Patients with acute exacerbations of COPD, but without excessive secretions, do not, however, benefit from PDPV and chest physiotherapy may even be associated with worsening airways obstruction, although this can usually be prevented by prior administration of a bronchodilator. Moreover PDPV is of no value, and may even be detrimental, in patients with acute primary pneumonia. Percussion is effective when the proximal airways are obstructed. The forced expiratory technique (FET), which involves expiring forcefully from mid to low lung volumes while maintaining an open glottis (puffing exercises) may be superior to both directed coughing and PV in enhancing sputum clearance; it may be most effective when combined with postural drainage. Incentive spirometry (also known as sustained maximal inspiration) uses an indicator (usually visual) to inform the patient whether or not he or she has produced sufficient flow or insufflatory volume

5 References pp Barber RE, Hamilton WK (1970) Oxygen toxicity in man. A prospective study in patients with irreversible brain damage. New England Journal of Medicine 283: Caldwell PR, Lee WL Jr, Schildkraut HS, et al. (1966) Changes in lung volume, diffusing capacity, and blood gases in men breathing oxygen. Journal of Applied Physiology 21: Campbell EJ (1960b) Respiratory failure. The relation between oxygen concentrations of inspired air and arterial blood. Lancet 2: Campbell EJ (1982) How to use the Venturi mask. Lancet 2: Comroe JH Jr, Dripps RD, Dumke PR, et al. (1945) Oxygen toxicity. The effect of inhalation of high concentrations of oxygen for twenty-four hours on normal men at sea level and at a simulated altitude of 18,000 feet. Journal of the American Medical Association 128: Deneke SM, Fanburg BL (1982) Oxygen toxicity of the lung: an update. British Journal of Anaesthesia 54: Goldstein RS, Young J, Rebuck AS (1982) Effect of breathing pattern on oxygen concentration received from standard facemasks. Lancet 2: Jackson RM (1990) Molecular, pharmacologic, and clinical aspects of oxygen-induced lung injury. Clinics in Chest Medicine 11: Singer MM, Wright F, Stanley LK, et al. (1970) Oxygen toxicity in man. A prospective study in patients after open-heart surgery. New England Journal of Medicine 283: Thomson AJ, Webb DJ, Maxwell SR, et al. (2002) Oxygen therapy in acute medical care. British Medical Journal 324: Extracts 2008 Elsevier Limited. All rights reserved.

Rodney Shandukani 14/03/2012

Rodney Shandukani 14/03/2012 OXYGEN THERAPY Aerobic metabolism accounts for 90% of Oxygen consumption by tissues. generates ATP by oxidative phosphorylation. Oxygen cascade: Oxygen exerts a partial pressure,