CHAPTER CONTENTS Introduction 143

5
Effects of positioning and mobilization
Elizabeth Dean

Conceptual framework for clinical decision making 144 The oxygen transport pathway 144 Factors contributing to cardiopulmonary dysfunction 146 Therapeutic effects of positioning and mobilization 147 To improve oxygen transport in acute cardiopulmonary dysfunction 147 To improve oxygen transport in postacute and chronic cardiopulmonary dysfunction 154 To prevent the negative effects of restricted mobility 156 Summary and conclusion 156

INTRODUCTION
The purpose of this chapter is to provide a framework for clinical decision making in the management of patients with cardiopulmonary dysfunction with special emphasis on positioning and mobilization. Cardiopulmonary dysfunction refers to impairment of one or more steps in the oxygen transport pathway. First, the oxygen transport pathway and the factors that contribute to impairment of oxygen transport are described. Second, three clinically signicant effects of positioning and mobilization are distinguished:

to improve oxygen transport in acute cardiopulmonary dysfunction to improve oxygen transport in the post-acute and chronic stages of cardiopulmonary dysfunction to prevent the negative effects of restricted mobility, particularly those that adversely affect oxygen transport.

In addition, the physiological and scientic rationale for use of positioning and mobilization for each of the above effects is described. Conceptualizing cardiopulmonary dysfunction as impairment of the steps in the oxygen transport pathway and exploiting positioning and mobilization as primary interventions in remediating this impairment will maximize physiotherapy efcacy. Emphasis is placed on impairment of oxygen transport given that such impairment in large part determines disability and handicap (Verbrugge & Lette 1993), as dened by the World Health Organization (1980), secondary to cardiopulmonary dysfunction.
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The following terms (Ross & Dean 1989) have been adopted in this chapter. 1. Positioning refers to the application of body positioning to optimize oxygen transport, primarily by manipulating the effect of gravity on cardiopulmonary and cardiovascular function. 2. Mobilization and exercise refer to the application of progressive exercise to elicit acute cardiopulmonary and cardiovascular responses to enhance oxygen transport. In the context of cardiopulmonary physiotherapy, mobilization refers to low-intensity exercise for typically acutely ill patients or those with severely compromised functional work capacity. 3. Optimizing oxygen transport is the goal of positioning and mobilization. The adaptation or training-sensitive zone denes the upper and lower limits of the various indices of oxygen transport needed to elicit the optimal adaptation of the steps in the oxygen transport pathway. This zone is based on an analysis of the factors that contribute to cardiopulmonary dysfunction and thus is specic for each patient.

Oxygen delivery DO2 = Arterial oxygen content x Cardiac output

Oxyhaemoglobin + Dissolved oxygen

Hgb x 1.34 x SaO2

PaO2 x 0.003

Oxygen consumption VO2 = (Arterial oxygen content Venous oxygen content) x Cardiac output

Oxyhaemoglobin + Dissolved oxygen

Hgb x 1.34 x SVO2

PVO2 x 0.003

Oxygen extraction ratio Oxygen consumption Oxygen delivery VO2 DO2

OER =

CONCEPTUAL FRAMEWORK FOR CLINICAL DECISION MAKING The oxygen transport pathway
Optimal cardiopulmonary function and gas exchange reect the optimal matching of oxygen demand and supply (Dantzker 1983, Weber et al 1983). Oxygen delivery and oxygen consumption based on demand are essential components of the oxygen transport system. Figure 5.1 shows the components of oxygen delivery (DO2), namely arterial oxygen content and cardiac output (CO) and the components of oxygen consumption (VO2), namely the arteriovenous oxygen content difference and CO. In health, DO2 is approximately fourfold greater than VO2 at rest so there is considerable oxygen reserve that is drawn upon during times of increased metabolic demand such as exercise, stress, illness and repair. Because of the large reserve, VO2 is thought to be normally supply independent. This reserve capacity, however, becomes compro-

Figure 5.1 The components of oxygen delivery (DO2) and oxygen consumption (VO2).

mised secondary to acute and chronic pathological conditions. In critically ill patients in whom DO2 is severely compromised, VO2 may be supply dependent until DO2 reaches a critical threshold, i.e. the level at which metabolic demands are met (Phang & Russell 1993). Below this critical threshold, patients are increasingly dependent on anaerobic metabolism reected by increased minute ventilation, respiratory exchange ratio and serum lactate levels. The efciency with which oxygen is transported from the atmosphere along the steps of the oxygen transport pathway to the tissues determines the efciency of oxygen transport overall (Fig. 5.2). The steps in the oxygen transport pathway include ventilation of the alveoli, diffusion of oxygen across the alveolar capillary membrane, perfusion

EFFECTS OF POSITIONING AND MOBILIZATION

Figure 5.2 A scheme of the components of ventilatorycardiovascularmetabolic coupling underlying oxygen transport modified from Wasserman et al (1987). CNS, central nervous system; ANS, autonomic nervous system; DPG, diphosphoglycerate; RBC, red blood cell; Hct, haematocrit; Hb, haemoglobin.

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of the lungs, biochemical reaction of oxygen with the blood, afnity of oxygen with haemoglobin, cardiac output, integrity of the peripheral circulation and oxygen extraction at the tissue level (Johnson 1973, Wassermann et al 1987). At rest, the demand for oxygen reects basal metabolic requirements. Metabolic demand changes normally in response to gravitational (positional), exercise and psychological stressors. When one or more steps in the oxygen transport pathway is impaired secondary to cardiopulmonary dysfunction, oxygen demand at rest and in response to stressors can be increased signicantly. Impairment of one step in the pathway may be compensated by other steps, thereby maintaining normal gas exchange and arterial oxygenation. With severe impairment involving several steps, arterial oxygenation may be reduced, the work of the heart and lungs increased, tissue oxygenation impaired and, in the most extreme situation, multiorgan system failure may ensue. While the oxygen transport pathway ensures that an adequate supply of oxygen meets the demands of the working tissues, the carbon dioxide pathway ensures that carbon dioxide, a primary byproduct of metabolism, is eliminated. This pathway is basically the reverse of the oxygen transport pathway in that carbon dioxide is transported from the tissues via the circulation to the lungs for elimination. Carbon dioxide is a highly diffusible gas and is readily eliminated from the body. However, carbon dioxide retention is a hallmark of diseases in which the ventilatory muscle pump is operating inefciently or the normal elastic recoil of the lung parenchyma is lost.

Box 5.1 Factors contributing to cardiopulmonary dysfunction, i.e. factors that compromise or threaten oxygen transport (adapted from Dean 1993a, Dean & Ross 1992a and Ross & Dean 1992)

Cardiopulmonary pathophysiology Acute Chronic primary secondary Acute and chronic Bedrest/recumbency and restricted mobility Extrinsic factors Reduced arousal Surgical procedures Incisions Dressings and bindings Casts/splinting devices/traction Invasive lines/catheters Monitoring equipment Medications Intubation Mechanical ventilation Suctioning Pain Anxiety Hospital admission Intrinsic factors Age Gender Ethnicity Congenital abnormalities Smoking history Occupation Air quality Obesity Nutritional decits Deformity Fluid and electrolyte balance Conditioning level Impaired immunity Anaemia/polycythaemia Thyroid abnormalities Multisystem complications Previous medical and surgical history

Factors contributing to cardiopulmonary dysfunction

Cardiopulmonary dysfunction, in which oxygen transport is threatened or impaired, results from four principal factors: the underlying disease pathophysiology, bedrest/recumbency and restricted mobility, extrinsic factors imposed by the patients medical care and intrinsic factors relating to the patient (Box 5.1) (Dean 1993a, Dean & Ross 1992a). An analysis of

those factors that contribute to cardiopulmonary dysfunction provides the basis for assessment and prescribing the parameters of positioning and mobilization to enhance oxygen transport for a given patient. The treatment is directed at the specic underlying contributing factors. In some cases, e.g. low haemoglobin, the underlying impairment of oxygen transport cannot be affected directly by physical intervention. However, mobilization and exercise can

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improve aerobic capacity in patients with anaemia, a factor not directly modiable by non-invasive physiotherapy interventions, by increasing the efciency of other steps in the oxygen transport pathway (Williams 1995). Further, even though some factors are not directly modiable by non-invasive physio therapy interventions, they inuence treatment outcome and thus need to be considered when planning, modifying and progressing treatment. Multisystem organ dysfunction and failure may lead to or result from cardiopulmonary dysfunction; thus they are associated with signicant mortality and morbidity. In these conditions, multiple factors impair multiple steps in the oxygen transport pathway so identifying which steps are affected and amenable to physiotherapy interventions is central to optimal treatment outcome (Dean & Frownfelter 1996).

THERAPEUTIC EFFECTS OF POSITIONING AND MOBILIZATION To improve oxygen transport in acute cardiopulmonary dysfunction
Positioning and mobilization have profound acute effects on cardiovascular and cardiopulmonary function and hence on oxygen transport (Table 5.1). These effects translate into improved gas exchange overall: reduction in the fraction of inspired oxygen, pharmacological and ventilatory support (Burns & Jones 1975, Dean 1985, Svanberg 1957). Such effects need to be exploited in the management of acute cardiopulmonary dysfunction with the use of positioning and mobilization as primary treatment interventions to enhance oxygen transport and as between-treatment interventions (Dean & Ross 1992b, Ross & Dean 1992). The physiotherapists role is to prescribe these

Table 5.1 Acute effects of upright positioning and mobilization on oxygen transport (adapted from Dean & Ross (1992a) and Imle & Klemic (1989)) Systemic response Positioning (supine to upright) Cardiopulmonary Total lung capacity Tidal volume Vital capacity Functioning residual capacity Residual volume Expiratory reserve volume Forced expiratory volumes Forced expiratory ows Lung compliance Airway resistance Airway closure PaO2 AP diameter of chest Lateral diameter of rib cage and abdomen Altered pulmonary blood ow distribution Work of breathing Diaphragmatic excursion Mobilization of secretions Total blood volume Central blood volume Central venous pressure Pulmonary vascular congestion Lymphatic drainage Work of the heart Stimulus Mobilization Alveolar ventilation Tidal volume Breathing frequency AaO2 gradient Pulmonary arteriovenous shunt VA/Q matching Distension and recruitment of lung units with low ventilation and low perfusion Mobilization of secretions Pulmonary lymphatic drainage Surfactant production and distribution

Cardiovascular

Cardiac output Stroke volume and heart rate Oxygen binding in blood Oxygen dissociation and extraction at the tissue level

AP, anteroposterior; , increases; , decreases.

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interventions judiciously to optimize gas exchange and oxygen transport overall. This role is distinct from routine positioning and mobilization often performed jointly by the physiotherapy and nursing staff. The aim of routine positioning and mobilization is primarily to reduce the adverse effects of restricted mobility including pulmonary complications, bedsores and contractures. To simulate the normal physiologic body position, the primary goal of physiotherapy is to get the patient upright and moving. Mobilization and exercise are the most physiologic and potent interventions to optimize oxygen transport and aerobic capacity and so need to be exploited with every patient. Body positioning, however, is discussed in this chapter rst because a patient cannot be in a position uninuenced by gravity. Furthermore, a patients oxygen transport status reects the body position assumed regardless of whether the position is part of a treatment regimen, a routine positioning regimen or assumed randomly by the patient. Positioning
Physiological and scientic rationale. The distribA utions of ventilation (V ), perfusion (Q) and ventilation and perfusion matching in the lungs are primarily inuenced by gravity and therefore body position (Clauss et al 1968, West 1962, 1977). The intrapleural pressure becomes less negative down the upright lung. Thus, the apices have a greater initial volume and reduced compliance than do the bases. Because the bases are more compliant in this position, they exhibit greater volume changes during ventilation. In addition to these gravity-dependent interregional differences in lung volume, ventilation is inuenced by intraregional differences which are dependent on regional mechanical differences in the compliance of the lung parenchyma and the resistance to airow in the airways. Perfusion increases down the upright lung such that the V /Q ratio in the A apices is disproportionately high compared with that in the bases. Ventilation and perfusion matching is optimal in the mid-lung region. Manipulating body position, however, alters both interregional and intraregional determinants of

ventilation and perfusion and their matching. When choosing specic positions to enhance arterial oxygenation for a given patient, one needs to consider the underlying pathophysiology impairing cardiopulmonary function, the effects of bed rest/recumbency and restricted mobility, extrinsic factors related to the patients care and intrinsic factors related to the patient. Although the negative effects of the supine position have been well documented for several decades (Dean & Ross 1992b, Dripps & Waters 1941), supine or recumbent positions are frequently assumed by patients in hospital. These positions are non-physiologic and are associated with signicant reductions in lung volumes and ow rates and increased work of breathing (Craig et al 1971, Hsu & Hickey 1976). The decrease in functional residual capacity (FRC) contributes to closure of the dependent airways and reduced arterial oxygenation (Ray et al 1974). This effect is accentuated in older persons (Leblanc et al 1970), patients with cardiopulmonary disease (Fowler 1949), patients with abdominal pathology, smokers and obese individuals. The haemodynamic consequences of the supine position are also remarkable. The gravitydependent increase in central blood volume may precipitate vascular congestion, reduced compliance and pulmonary oedema (Blomqvist & Stone 1983, Sjostrand 1951). The commensurate increase in stroke volume increases the work of the heart (Levine & Lown 1952). Within 6 hours, a compensatory diuresis can lead to a loss of circulating blood volume and orthostatic intolerance, i.e. haemodynamic intolerance to the upright position. Bed rest reconditioning has been attributed to this reduction in blood volume and the impairment of the volume-regulating mechanisms rather than physical deconditioning per se (Hahn-Winslow 1985). Thus, the upright position is essential to maximize lung volumes and ow rates and this position is the only means of optimizing uid shifts such that the circulating blood volume and the volume-regulating mechanisms are maintained. The upright position coupled with movement is necessary to promote normal uid regulation and balance (Lamb et al 1964).

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The upright position is a potent stimulus to the sympathetic nervous system. This is an important effect clinically which offsets impaired blood volume and pressure-regulating mechanisms secondary to recumbency (Hahn-Winslow 1985). Stimulation of the sympathetic nervous system has been reported to augment the effects of potent sympathomimetic pharmacological agents such that the dosages of these drugs can be reduced (Warren et al 1983). The reduction or elimination of sympathomimetic drugs is an important outcome of non-invasive physiotherapy interventions. Side-to-side positioning is frequently used in the clinical setting. If applied in response to assessment rather than routinely (Chuley et al 1982), the benets derived from such positioning can be enhanced. Adult patients with unilateral lung disease may derive greater benet when the affected lung is uppermost (Remolina et al 1981). Markedly improved gas exchange without deleterious haemodynamic effects has been reported for patients with severe hypoxaemia secondary to pneumonia (Dreyfuss et al 1992). Arterial oxygen tension is increased secondary to improved ventilation of the unaffected lung when this lung is dependent. Patients with uniformly distributed bilateral lung disease may derive greater benet when the right lung is lowermost (Zack et al 1974). In this case, arterial oxygen tension is increased secondary to improved ventilation of the right lung, which may reect the increased size of the right lung compared with the left and that, in this position, the heart and adjacent lung tissue are subjected to less compression. Improved gas exchange through non-invasive interventions can reduce or eliminate the need for supplemental oxygen which are primary treatment outcomes. Although various studies have shown benecial effects of side lying, positioning should be based on multiple considerations including the distribution of disease if optimal results are to be obtained. The prone position has long been known to have considerable physiological justication in patients with cardiopulmonary compromise (Douglas et al 1977), even those who are critically ill with acute respiratory failure (Bittner et al 1996,

Chatte et al 1997, Mure et al 1997) and patients with trauma-induced adult respiratory distress syndrome (Friedrich et al 1996). The benecial effects of the prone position on arterial oxygenation may reect improved lung compliance secondary to stabilization of the anterior chest wall, tidal ventilation, diaphragmatic excursion, FRC and reduced airway closure (Dean 1985, Pelosi et al 1998). In a dog model of acute lung injury, however, improved PaO2 in prone has been attributed to a reduced shunt fraction (Albert et al 1987). A variant of the prone position, prone abdomen free, has shown additional benets over prone abdomen restricted. In the prone abdomenfree position, the patient is positioned such that the movement of the abdomen is unencumbered by the bed. This can be achieved either by raising the patients body in relation to the bed so that the abdomen falls free or by using a bed with a hole cut out at the level of the abdomen. Despite compelling evidence to support the prone position, it may be poorly tolerated in some patients or may be contraindicated in haemodynamically unstable patients. In these situations, intermediate positions approximating prone may produce many of the benecial effects and minimize any potential hazard. Positioning for drainage of pulmonary secretions may be indicated in some patients (Kirilloff et al 1985). Historically, these positions have been based on the anatomical arrangement of the bronchopulmonary segments to facilitate drainage of a particular segment. The bronchiole to the segment of interest is positioned perpendicular to facilitate drainage with the use of gravity. The efcacy of postural drainage compared with deep breathing and coughing induced with mobilization/exercise and repositioning of the patient has not been established. However, the fact that mobilization impacts on more steps in the oxygen transport pathway including the airways, to effect secretion clearance, supports the exploitation of mobilization coupled with deep breathing manoeuvres and coughing as a primary treatment intervention. Physiotherapists need to consider two aspects of body positioning when the goal is to optimize oxygen transport. One is to select and apply

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specic body positions based on the patients presentation, laboratory test results and radiographic imaging. The other is to elicit physiologic stir-up (Dean 1996a, Dripps & Waters 1941). The purpose is to effect the normal gravitational stress on cardiopulmonary and cardiovascular function that is experienced in health. This is best simulated if patients are changed from one extreme position to another, e.g. supine to prone or upright, rather than from half to full side lying which is associated with a lesser stir-up effect. Haemodynamically unstable patients, however, require greater monitoring during extreme position changes and may not tolerate some position changes well. Thus, based on assessment and patient response, frequent extreme position changes may be preferable to minimal shifts in body position in order to optimize cardiovascular, pulmonary and haemodynamic function. Assessment and treatment planning. Body positioning, i.e. the specic positions selected, the duration of time spent in each position and the frequency with which the position is assumed, is based on a consideration of the factors that contribute to cardiopulmonary dysfunction, and treatment response. Understanding of the physi-

ology of cardiopulmonary and cardiovascular function and the effects of disease highlights certain positions that are theoretically ideal. However, these positions need to be modied or may be contraindicated for a given patient, based on other considerations (see Box 5.1). For example, if extreme positional changes are contraindicated, small degrees of positional rotation performed frequently can have signicant benet on gas exchange and arterial oxygenation. A three-quarters prone position may produce favourable results when the full prone position is contraindicated or is not feasible. This modication may simulate the prone abdomenfree position which has been shown to augment the effect of the traditional prone abdomenrestricted position (Douglas et al 1977). Furthermore, a three-quarters prone position may be particularly benecial in patients with obese or swollen abdomens who may not tolerate other variations of the prone position. With attention to the patients condition, invasive lines and leads and appropriate monitoring, a patient can be aggressively positioned (Fig. 5.3). The time which a patient spends in a position and the frequency with which that position is assumed over a period of time are based on the

Figure 5.3 Positioning a critically ill patient may require several people and continual monitoring of the patients response. Even though a position (particularly an upright position) may only be tolerated for a short period of time, the physiological benets are considerable.

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indications for the position and treatment outcome. Objective measures of the various steps that are compromised in the oxygen transport pathway as well as indices of oxygen transport overall are used in making these decisions. Subjective evaluation based on clinical judgement also has a role. A specic position can be justied, provided there is objective and subjective evidence of improvement. Signs and symptoms of deterioration need to be monitored so that deleterious positions can be avoided and deterioration secondary to excessive time in any one position can be detected. Prolonged duration in any single position will inevitably lead to compromise of the function of dependent lung zones and impaired gas exchange. The ratio of treatment to between-treatment time is low. Typically, between-treatment time consists of some combination of positioning and mobilization. Positioning and mobilizing patients between treatments may be incorporated as an extension of treatment. Patients require monitoring and observation during these periods, as well as treatments. Between-treatment time may incorporate the use of maximally restful positions that do not compromise oxygen transport. Lastly, patients are positioned and mobilized between treatments to prevent the negative effects of restricted mobility and recumbency. Special consideration (e.g. with respect to specic positioning and the use of supports) needs to be given to positioning patients who are comatose or paralysed because their joints and muscles are relatively unprotected and prone to trauma. Positions need to be selected that avoid injury to unprotected head, neck and limbs. Progression. Progression of positioning involves new positions or modication of previous positions and modication of the duration spent in each position and the frequency with which each position is assumed over a period of time. These clinical decisions are based on the factors that contribute to cardiopulmonary dysfunction and objective and subjective indices of change in the patients cardiopulmonary status. With improvement in cardiopulmonary status, the patient spends more time in erect positions and is mobilized more frequently and independently.

Mobilization
Physiological and scientic rationale. Compared with long-term exercise, the mechanisms underlying adaptation of the oxygen transport system to acute exercise, i.e. from session to session and day to day, are less well understood. However, although these mechanisms have yet to be elucidated, the responses to acute exercise are well documented. The acute response to mobilization/ exercise reects a commensurate increase in oxygen transport to provide oxygen to the working muscles and other organs. The increase is dependent on the intensity of the mobilization/ exercise stimulus. The demand for oxygen and oxygen consumption (VO2) increases as exercise continues, with commensurate increases in minute ventilation (VE), i.e. the amount of air inhaled per minute, cardiac output and oxygen extraction at the tissue level. Relatively low intensities of mobilization can have a direct and profound effect on oxygen transport in patients with acute cardiopulmonary dysfunction (Dean & Ross 1992a, Dull & Dull 1983, Lewis 1980) and need to be instituted early after the initial pathological insult (Orlava 1959, Wenger 1982). The resulting exercise hyperpnoea, i.e. the increase in VE, is effected by an increase in tidal volume and breathing frequency. In addition, ventilation and perfusion matching is augmented by the distension and recruitment of lung zones with low ventilation and low perfusion. Spontaneous exercise-induced deep breaths are associated with improved ow rates and mobilization of pulmonary secretions (Wolff et al 1977). In clinical populations, these effects elicit spontaneous coughing. When mobilization is performed in the upright position, the anteroposterior diameter of the chest wall assumes a normal conguration compared with the recumbent position in which the anteroposterior diameter is reduced and the transverse diameter is increased. In addition, diaphragmatic excursion is favoured, ow rates augmented and coughing is mechanically facilitated. The work of breathing may be reduced with caudal displacement of the diaphragm and the work of the heart is minimized by the displacement of uid away from the central circulation to the legs. Thus,

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despite increased metabolic demands of mobilization and exercise, the goal is to ensure that this increased demand is not wasteful and the demand can be met by the supply. With respect to cardiovascular effects, acute mobilization/exercise increases CO by increasing stroke volume and heart rate. This is associated with increased blood pressure and increased coronary and peripheral muscle perfusion. Passive movement of the limbs may stimulate deep breaths and heart function (West 1995). There is little scientic evidence, however, to support any additional benet from various facilitation techniques (Bethune 1975). Thus, time allocated to the use of passive manoeuvres may compete with time for positioning and mobilization, i.e. interventions with demonstrated clinical efcacy. Although passive movements have a relatively small effect on cardiopulmonary function, they have several important benets for neuromuscular and musculoskeletal function which support their use provided they do not replace active movement. Assessment and treatment planning. For practical and ethical considerations, the mobilization plan for the patient with acute cardiopulmonary dysfunction cannot be based on a standardized exercise test, as is the case for patients with chronic conditions. However, response to a mobilization/exercise stimulus can be assessed during a mobilization challenge test, i.e. during the patients routine activities such as turning or moving in bed, activities of daily living or responding to routine nursing and medical procedures (Dean 1996b). Comparable to prescribing exercise for the patient with chronic cardiopulmonary dysfunction, the parameters are specically dened so that the stimulus is optimally therapeutic. The optimal stimulus is that which stresses the oxygen transport capacity of the patient and effects the greatest adaptation without deterioration or distress. To promote adaptation of the steps in the oxygen transport pathway to the stimulation of acute mobilization, the stimulus is administered in a comparable manner to that in an exercise programme prescribed for chronic cardiopulmonary dysfunction. The components include a pre-exer-

cise period, a warm-up period, a steady-state period, a cool-down period and a recovery period (Blair et al 1988). These components optimize the response to exercise by preparing the cardiopulmonary and cardiovascular systems for steadystate exercise and by permitting these systems to reestablish resting conditions following exercise. The cool-down period, in conjunction with the recovery period, ensures that exercise does not stop abruptly and allows for biochemical degradation and removal of the byproducts of metabolism. Mobilization consists of discrete warm-up, steady-state and cool-down periods; the components need to be identied, even in the patient with a very low functional capacity, i.e. a critically ill patient who may be only able to sit up over the edge of the bed. In such cases, preparing to sit up constitutes a warm-up period for the patient; the stimulus of sitting unsupported for several minutes while being aroused and encouraged to talk or be interactive non-verbally, if mechanically ventilated, constitutes a steady-state period; returning to bed constitutes the cool-down period. In the recovery period, observation of the patient continues to ensure that mobilization is tolerated well and that the indices of oxygen transport return to resting levels. This information is then used as the basis for mobilization in the next treatment. Valid and reliable monitoring practices provide the basis for dening the parameters of mobilization, assessing the need for progression and dening the adaptation or training-sensitive zone. Monitoring is also essential given that subjecting patients to mobilization/exercise stimulation is inherently risky, particularly for patients with cardiopulmonary dysfunction. Indices of overall oxygen transport in addition to indices of the function of the individual steps in the oxygen transport pathway provide a detailed prole of the patients cardiopulmonary status. In critical care settings, the physiotherapist has access to a wide range of measures to assess the adequacy of gas exchange. Minimally, in the general ward setting, measures of breathing frequency, arterial blood gases, arterial saturation, heart rate, blood pressure and clinical observation provide the basis for ongoing assessment, mobilization/exercise

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and progression. With appropriate attention to the patients condition, invasive lines and leads and appropriate monitoring, a patient can be aggressively mobilized and ambulated (Fig. 5.4). A fundamental requirement in dening the parameters for mobilization is that the patients oxygen transport system is capable of increasing the oxygen supply to meet an increasing metabolic demand. If not, mobilization is absolutely contraindicated and the treatment of choice to optimize oxygen transport is body positioning. However, in the case of a patient being severely haemodynamically unstable, even the stress of positioning may be excessive. Thus, although critically ill patients may be treated aggressively, every patient has to be considered individually, otherwise the patient may deteriorate or be seriously endangered. Progression. Progression and modication of the mobilization stimulus occur more rapidly in the management of the patient with acute cardiopulmonary dysfunction compared with the progression of the exercise stimulus for the patient with chronic illness. The status of acutely ill

patients can vary considerably within minutes or hours. Whether the mobilization stimulus is increased or decreased in intensity depends on the patients status and altered responses to mobilization. The mobilization stimulus is adjusted such that it remains optimal despite the patients changing metabolic needs. Capitalizing on narrow windows of opportunity for therapeutic intervention must be exploited 24 hours a day with respect to the type of mobilization stimulus, its intensity, duration and frequency, particularly in the critically ill patient. The immovable patient. Given the welldocumented negative effects of restricted mobility, the immovable patient deserves special consideration. Although bed rest or activity restriction is ordered for patients frequently without reservation, the risks need to be weighed against the benets. Restricted mobility coupled with recumbency constitutes a death knell for many severely compromised patients. Thus, an order for bed rest needs to be evaluated and challenged to ensure that this order is physiologically justied.

Figure 5.4 Example of mobilizing a patient to a self-supported upright sitting position. Mobilizing a critically ill patient needs to be a priority wherever possible. Short frequent sessions to the erect position (sitting or standing if possible) with continual monitoring of the patients response should be the goal. As the patient progresses, sessions increase in intensity and duration and reduce in frequency.

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Kinetic beds and chairs. Advances in furniture technology to facilitate positioning and mobilizing patients have lagged behind advances in clinical medicine, particularly in the critical care area. Conventional hospital beds are designed to be stationary and their widths and heights are often non-adjustable, making it difcult for the patient to get in and out of bed. Kinetic beds and chairs have become increasingly available over the past decade but they are not widely used clinically. These devices were originally designed to facilitate positioning and moving heavy and comatose patients. Some beds are designed to rotate on their long axis from side to side over several minutes. Other beds simulate a side-toside movement with ination and deation of the two sides of an air-lled mattress. Although these beds have potential cardiopulmonary benet (Glavis et al 1985, Kyle et al 1992), they do not replace active positioning and movement. Mechanically adjustable bedside chairs constitute an important advance. These chairs adjust to a at horizontal surface that can be matched to bed height and positioned beneath the patient lying on the bed. The device with the patient on top is then wheeled parallel to the bed where it can be adjusted back into a chair and thus the patient assumes a seated position. The degree of recline can be altered to meet the patients needs and for comfort. This chair also facilitates returning the patient to bed. Comparable to these chairs are beds which can be converted into a chair while the patient is lying down. These avoid the negative effects of using tilt tables where the uid shifts caudally are extreme and more risky by comparison. The disadvantages of kinetic beds and chairs include the expense and the potential for overreliance on them. Without these devices, a heavy patient may require several people and several minutes to position in a chair which may be only tolerated for a few minutes. However, the cardiopulmonary benets of the stimulation of preparing to be moved, the reex attempts of the patient to assist and adjust to changing position, as well as actually sitting upright in a chair are not reproduced by bed positioning alone or by a kinetic bed. Research is needed to determine the

indications and potential benets of kinetic beds and chairs so that they can be used judiciously in the clinical setting as an integral therapeutic intervention.

To improve oxygen transport in post-acute and chronic cardiopulmonary dysfunction

In post-acute and chronic cardiopulmonary dysfunction, a primary consequence of impaired oxygen transport is reduced functional work capacity (Belman & Wasserman 1981, Wasserman & Whipp 1975). Work capacity can be improved with long-term exercise which improves the efciency of the steps in the oxygen transport pathway and promotes compensation within the pathway as well as by other mechanisms. To optimize the patients response, exercise can be carried out in judicious body positions in which oxygen transport is favoured. Exercise is the treatment of choice for patients whose impaired oxygen transport has resulted from chronic cardiopulmonary dysfunction. Body positioning, however, may have some role in severe patients in optimizing oxygen transport at rest. Barach & Beck (1954), for example, reported that emphysematous patients were less breathless, had reduced accessory muscle activity and had a signicant reduction in ventilation when positioned in a 16 head-down position. Some patients exhibited greater symptomatic improvement than in the upright position with supplemental oxygen. Classic relaxation positions, e.g. leaning forward with the forearms supported, can also be supported physiologically. Coupling such physiologically justiable positions with mobilization/exercise will augment the benets of exercise. Physiological and scientic rationale. Although the physiological responses to long-term exercise in patients with chronic cardiopulmonary disease may differ from those in healthy persons, patients can signicantly improve their functional work capacity (Table 5.2). In healthy persons, an improvement in aerobic capacity reects improved efciency of the steps in the oxygen transport pathway to adapt to increased

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oxygen demands imposed by exercise stress. This adaptation is effected by both central (cardiopulmonary) and peripheral (at the tissue level) changes (Dean & Ross 1992a, Wasserman & Whipp 1975). Such aerobic conditioning is characterized by a training-induced bradycardia secondary to an increased stroke volume and increased oxygen extraction capacity of the working muscle. These adaptation or training responses result in an increased maximal oxygen uptake and maximal voluntary ventilation and reduced submaximal VE, cardiac output, heart rate, blood pressure and perceived exertion. Patients with chronic lung disease, however, are often unable to exercise at the intensity required to elicit an aerobic training response. Their functional work capacity is improved by other mechanisms, e.g. desensitization to breathlessness, improved motivation, improved biomechanical efciency, increased ventilatory muscle strength and endurance or some combination (Belman & Wasserman 1981, Loke et al 1984). Patients with chronic heart disease, such as those with infarcted left ventricles, may be able to train aerobically; however, training adaptation primarily results from peripheral rather than central factors
Table 5.2 Chronic effects of mobilization/exercise on oxygen transport Systemic response Cardiopulmonary Effect Capacity for gas exchange Cardiopulmonary efciency Submaximal minute ventilation Work of breathing Exercise-induced bradycardia Maximum V O2 Submaximal heart rate, blood pressure, myocardial oxygen demand, stroke volume, cardiac output Work of the heart Perceived exertion Plasma volume Cardiac hypertrophy Vascularity of the myocardium Vascularity of working muscle Myoglobin content and oxidative enzymes in muscle Oxygen extraction capacity

Cardiovascular

Tissue level

, increases; , decreases.

(Bydgman & Wahren 1974, Hossack 1987, Ward et al 1987). Planning an exercise programme. The exercise programme is based on the principle that oxygen delivery and uptake are enhanced in response to an exercise stimulus which is precisely dened for an individual in terms of the type of exercise, its intensity, duration, frequency and the course of the training programme. These parameters are based on an exercise test in conjunction with assessment ndings. Exercise tests are performed on a cycle ergometer or treadmill or with a walk test. The general procedures and protocols are standardized to maximize the validity and reliability of the results (Dean et al 1989, Blair et al 1988). The principles of and guidelines for exercise testing and training patients with chronic lung and heart disease have been well documented (Dean 1993b). The training-sensitive zone is dened by objective and subjective measures of oxygen transport determined from the exercise test. The components of each exercise training session include baseline, warm-up, steady-state portion, cool-down and recovery period (Blair et al 1988, Dean 1993b). The cardiopulmonary and cardiovascular systems are gradually primed for sustaining a given level of exercise stress, whilst in addition the musculoskeletal system adapts correspondingly. Following the steady-state portion of the training session, the cool-down period permits a return to the resting physiological state. Cool-down and recovery periods are essential for the biochemical degradation and elimination of the metabolic byproducts of exercise. Progression. Progression of the exercise programme is based on a repeated exercise test. This is indicated when the exercise prescription no longer elicits the desired physiological responses specically, when the steady-state work rate consistently elicits responses at the low end or below the lower limit of the training-sensitive zone for the given indices of oxygen transport. This reects that maximal adaptation of the steps in the oxygen transport pathway to the given exercise stimulus has occurred. The degree of conditioning achieved is precisely matched to the demands of the exercise stimulus imposed.

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To prevent the negative effects of restricted mobility

Although physiologically distinct, the effects of immobility are frequently confounded by the effects of recumbency in the hospitalized patient. Restricted mobility and the concomitant reduction in exercise stress affect virtually every organ system in the body with profound effects on the cardiovascular and neuromuscular systems. Recumbency and the elimination of the vertical gravitational stress exert their effects primarily on the cardiovascular and cardiopulmonary systems (Blomqvist & Stone 1983, Dock 1944, Harrison 1944). The most serious consequences of restricted mobility and recumbency are those resulting from the effects on the cardiopulmonary and cardiovascular systems and hence on oxygen transport. Although other consequences of restricted mobility, e.g. increased risk of infection, skin breakdown and deformity, may not constitute the same immediate threat to oxygen transport and tissue oxygenation, they can have signicant implications with respect to morbidity and mortality (Rubin 1988). Thus, restricted mobility and recumbency need to be

minimized and mobility and the upright position maximized to avert the negative consequences of restricted mobility, the risk of morbidity associated with these effects and the direct and indirect cardiopulmonary and cardiovascular effects. These negative consequences are preventable with frequent repositioning and mobilizing of the patient (Table 5.3). The prevention of these effects is a primary goal of positioning and mobilizing patients between treatments.

SUMMARY AND CONCLUSION

Cardiopulmonary dysfunction refers to impairment of one or more steps in the oxygen transport pathway which can impair oxygen transport overall. Thus, a conceptual framework for clinical problem solving in the management of patients with cardiopulmonary dysfunction, based on oxygen transport, can facilitate the identication of decits and the directing of treatment to each specic decit. Factors that can impair the transport of oxygen from the atmosphere to the tissues include cardiopulmonary pathology, bedrest, recumbency and restricted mobility, extrinsic factors related to the patients medical care,

Table 5.3

Effects of positioning and mobilization that prevent the negative effects of restricted mobility and recumbency* Effect Alveolar ventilation Airway closure Alters the distributions of ventilation, perfusion and ventilation and perfusion matching Alters pulmonary blood volume Alters distending forces on uppermost lung elds Secretion pooling Secretion mobilization and redistribution Alters chest wall conguration and pulmonary mechanics Varies work of breathing Alters cardiac compression (positioning), wall tensions, lling pressures Alters preload, afterload and myocardial contraction Alters lymphatic drainage Varies work of the heart Promotes uid shifts Stimulates pressure- and volume-regulating mechanisms of the circulation Stimulates vasomotor activity Maintains normal uid balance and distribution Alters hydrostatic pressure and tissue perfusion Maintains oxygen extraction capacity (mobilization)

Systemic response Cardiopulmonary

Cardiovascular

Tissue level

*Some of the preventive effects of body positioning and mobilization are comparable; however, the magnitude of these effects in response to mobilization tends to be greater than with body positioning.

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intrinsic factors related to the patient or a combination of these. Positioning and mobilization are two interventions that have potent and direct effects on several of the steps in the oxygen transport pathway. These interventions have a primary role in improving oxygen transport in acute and chronic cardiopulmonary dysfunction and in averting the negative effects of restricted mobility and recumbency, particularly those related to cardiopulmonary and cardiovascular function. The principal goal of physiotherapy in the management of cardiopulmonary dysfunction is to optimize oxygen transport. A systematic approach to achieving this goal consists of: 1. Distinguishing the specic steps in the oxygen transport pathway which are impaired or threatened. 2. Establishing which factors contribute to this impairment 3. Distinguishing which factors are (a) amenable to positioning and mobilization and (b) not directly amenable to positioning and mobilization, as these factors will modify treatment 4. Specifying the parameters for positioning and mobilization so that they directly address the factors responsible for the cardiopulmonary

dysfunction wherever possible, i.e. to elicit the acute effects of these interventions to enhance oxygen transport or to elicit the longterm effects on oxygen transport, i.e. training responses and improved functional work capacity 5. Avoiding the multisystem consequences of restricted mobility and recumbency, particularly those that impair or threaten oxygen transport 6. Recognizing when positioning or mobilizing a patient needs to be modied to avoid a deleterious outcome. Conceptualizing cardiopulmonary dysfunction as decits in the steps in the oxygen transport pathway and identifying the factors responsible for each impaired step provides a systematic, evidence-based approach to clinical decision making in cardiopulmonary physiotherapy. Positioning and mobilization can then be specically directed at the mechanisms underlying cardiopulmonary dysfunction wherever possible. Such an approach will maximize the efcacy of positioning and mobilizing patients with cardiopulmonary dysfunction and enhance the outcome of medical management overall.

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FURTHER READING American College of Sports Medicine 1991 Guidelines for exercise testing and prescription, 4th edn. Lea and Febiger, Philadelphia Bates DV 1989 Normal pulmonary function. Respiratory function in disease, 3rd edn. WB Saunders, Toronto Convertino VA 1987 Aerobic tness, endurance training and orthostatic intolerance. Exercise and Sports Sciences Review 15: 223259 Dantzker DR 1991 Cardiopulmonary critical care, 2nd edn. WB Saunders, Philadelphia McArdle WD, Katch FI, Katch VL 1996 Exercise physiology. Energy, nutrition and human performance, 4th edn. Lea and Febiger, Philadelphia Pollack ML, Wilmore JH 1990 Exercise in health and disease, 2nd edn. WB Saunders, Philadelphia Reinhart K, Eyrich K (eds) 1989 Clinical aspects of oxygen transport and tissue oxygenation. Springer-Verlag, London West JB 1990 Ventilation, blood ow and gas exchange, 5th edn. Blackwell Science, Oxford West JB 1995 Respiratory physiology: the essentials, 5th edn. Williams and Wilkins, Baltimore