Asthma—clinical and physiological assessment

Asthma—clinical and physiological assessment

PAEDIATRIC RESPIRATORY REVIEWS (2004) 5(Suppl A), S89–S92 Asthma – clinical and physiological assessment Allan L. Coates Division of Respiratory Medi...

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PAEDIATRIC RESPIRATORY REVIEWS (2004) 5(Suppl A), S89–S92

Asthma – clinical and physiological assessment Allan L. Coates Division of Respiratory Medicine, University of Toronto, Hospital for Sick Children, Toronto, Canada M5G 1X8 While the vast majority of patients with asthma have relatively mild disease, there are some with life threatening episodes. Some key factors in life threatening asthma1,2 are the presence of significant airway obstruction despite a maximal therapeutic plan which has the adherence of the patient, history of extreme liability, patients who do not demonstrate the usual dyspnea and respiratory distress despite impending respiratory failure and previous severe episodes of asthma with very poor adherence to the therapeutic plan. In each of these four scenarios, the approach and management is different. In the acute situation, from the physiological perspective, there are two main factors that must govern clinical decisions. One is the rate of change and the other is the degree of cardiac compromise that accompanies the respiratory distress. With regard to the rate of change, absolute laboratory values, be they spirometric values or blood levels of carbon dioxide, unless extreme, are less useful in guiding the therapeutic approach than the trend. For example, irritant receptors in the lung interstitium usually heighten the drive to breathe in an asthmatic attack and, for mild to moderate attacks, result in a PCO2 in the blood that is lower than normal.3 As the situation deteriorates, the PCO2 will rise. If the rise is slow, while still indicating impending respiratory failure, the time available to act will be longer than if it is rising precipitously. The same can be said about the forced expiratory volume in 1 second (FEV1 ). To fully understand the respiratory physiology of an asthma attack, it is necessary to go * Correspondence to: Allan L. Coates, MD. Tel.: +1-(416)-813-6167; Fax: +1-(416)-813-6246; E-mail: [email protected] Correspondence address: Hospital for Sick Children, 555 University Avenue, Toronto, Ontario, Canada M5G 1X8 1526-0542/$ – see front matter

% VC 80 4

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Fig. 1. The pressure volume relationship of both the relaxed chest wall (W) and the lung (L). The combination of the two is the respiratory system compliance (rs). The point where the outward recoil of the chest wall is exactly balanced by the inward recoil of the lung is the resting end expiratory volume, the functional residual capacity (FRC). At high lung volumes (4) the respiratory muscles must over come the inward recoil of both the chest wall and the lung.

back to the normal respiratory physiology and see how the asthmatic differs. During normal quiet breathing, relatively small efforts by the respiratory muscles result in changes in pleural pressure in the order of −0.5 to −1 kPa. Starting from the volume, the functional residual capacity (FRC), where the outward elastic recoil of the chest is exactly balanced by the inward recoil of the lung (Figure 1), the lung inflates for a size appropriate tidal volume (Figure 2). The change in pleural pressure is brought about by the combination of the diaphragm and the intercostal muscles, the latter serving to stiffen the chest as well as cause changes in pleural pressure.4 The inspiration takes place relatively effortlessly, following the pressure volume curve of the lung (Figure 2) and results in no intercostal or subcostal indrawing or supra sternal retractions. Around FRC, the slope of the pressure volume curve is high, e.g., a high compliance so small changes in pressure give rise to large changes in volume. The airways are interconnected with the © 2004 Elsevier Science Ltd. All rights reserved.

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A.L. COATES LUNG COMPLIANCE IN HYPERINFLATION

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Fig. 2. The effect of hyperinflation on the pressure volume relationship of the lung. Starting at FRC, a small change in pleural pressure does not cause retractions but does result in a sufficiently high inspiratory volume that the respiratory rate is normal. In contrast, at high lung volumes, on the flat part of the pressure volume curve, greater inspiratory effort is needed which results in retractions but such a small tidal volume that tachypnea is necessary to maintain normal ventilation.

pleura and tend to be pulled open during inspiration (Figure 3). The tidal volume achieved is sufficient to meet the metabolic needs of the body and there is no tachypnea. Expiration is passive, brought about by the elastic recoil of the lung with the chest wall elastic recoil being relatively neutral, given its position in its own pressure volume curve. Since, by definition, gas must flow down a pressure gradient; the pressure in the alveoli next to the airway must be greater than the pressure in the airway (Figure 3), thereby favoring collapse of the airway.5 If, in the periphery of the lung, the resistance to airflow is low and the differences in pressure are small, the interdependence of the airway and the lung pleura will be sufficient to maintain bronchiolar patency. In the larger cartilaginous airways, the stiffness of the airway itself helps to maintain patency. In the absence of tachypnea, expiratory time is sufficient to allow the lung to go back to the resting FRC. In asthma, there are a number of factors that cause disruption of this normal pattern. Chronic lung inflammation, a hallmark of asthma, results in edema and narrowing of the airways. In this case, resistance of the airways may not be so small and the pressure drop between the surrounding alveoli and the small airways are sufficient to cause collapse of the small airways trapping gas behind them during expiration.6 This means that expiration will not result in reaching the “relaxed” FRC. Hence, the next breath will take place from a higher tidal volume. As long as the volume is not much higher than the “relaxed” FRC, small changes in pleural pressure will still result in adequate changes in volume and the absence of tachypnea or retractions but the normal mechanics have been disrupted. While this may not

Fig. 3. A schematic of the interaction between the chest wall and the lung. The diaphragm, represented by the piston descend and generates a negative pleural pressure (Ppl) on inspiration. Part of this is transmitted across the lung (Plt) to the alveolus (Palv). Gas flows down the pressure gradient from the airway opening (Pao). The springs represent the tethering of the airways to the pleural by the interstitium of the lung which act to pull the airway open during inspiration. During expiration, positive alveolar pressure is generated by elastic recoil and since this must be greater than that at the Pao, pressure around the airway (Pbr) favors collapse. In the large airways this is resisted by cartilage but may lead to gas trapping in the distal small airways if Pbr is large.

be sufficient to cause changes in spirometry, lung volumes measured by plethysmography will show an elevated residual volume to total lung capacity ratio (RV/TLC), signs that despite being asymptomatic with normal spirometry, there is ongoing pathology in the lung that should be addressed with antiinflammatory treatment. If the pathology worsens, the amount of gas trapping increases. The new FRC is now much higher than the “resting” FRC and has moved from the steep part of the pressure volume curve to the flatter part (Figure 2). Now, increased respiratory effort is required for inspiration, to inflate both the chest wall and the lungs (Figure 1) and yet smaller tidal volumes are achieved. If PCO2 is to be maintained as normal, respiratory rate must increase resulting in tachypnea. The increased respiratory effort may result in retractions and indrawing. Fortunately, the increased lung volume augments the stability of the narrowed small airways and the increased elastic recoil7 at the high lung volumes provides additional force for expiration. However, over time, the over-stretching of the lung interstitium results in a loss of elastic recoil that has been attributed to chronic “remodelling” of the airways so that even maximal treatment will not result in reversibility of the airflow obstruction. As the situation progresses, bronchospasm, increased edema, increased mucus production and airway plugging all give rise to increased gas trapping and airflow limitation to the point where even maximal and not sustainable respiratory efforts do not result in adequate ventilation and PCO2 begins to rise and heralds the onset of respiratory failure. From the respiratory physiologist’s perspective,

ASTHMA – CLINICAL AND PHYSIOLOGICAL ASSESSMENT the thoracic compartment is frequently represented by a cylinder containing the lungs and with a piston changing the volume (Figure 3). With this model, changes in pleural pressure are used to predict the event outlined above. What is frequently overlooked is that the heart shares the thorax with the lungs and is subjected to changes in intrathoracic pressure. In general, during normal breathing, these changes are small, usually less than 5% of the systolic blood pressure. The small changes in pleural pressure during inspiration have little effect on the high pressure left ventricle and serve only to augment venous return that slightly increases stroke volume and results in a slight increase in blood pressure during inspiration. However, during an acute asthma attack, pleural pressure8 swings may be as much as a third of the systemic systolic blood pressure. The job of the left ventricle is to deliver blood outside the thorax at a physiological systolic pressure (Figure 4). This requires tension of the ventricular wall proportional to the difference in systolic blood pressure and the pleural pressure. If the pleural pressure is (negative) one-third systolic blood pressure, the tension on the ventricular wall required to deliver blood outside the thorax may not be achievable. The stroke volume falls, and the blood pressure during inspiration is less than during expiration when the ventricle is not so loaded. The clinically observed effect is pulsus paradoxus.9 A significant pulsus paradoxus (1.5–2 kPa or more) occurs in the context of greatly increased respiratory work, which may lead to respiratory failure with increasing PCO2 . With the stroke volume falling during inspiration, cardiac output may be compromised as the ability to compensate by increased cardiac output during expiration may not be possible as the very overinflated lungs reduce diastolic filling. The combination of cardiopulmonary failure is manifested by a rising metabolic and respiratory acidosis, which may give rise to a profound metabolic acidemia. This type of situation requires an immediate therapeutic response to deal with a life-threatening situation. Unlike cardiovascular collapse where the manifestations of low cardiac output are immediately apparent on the skin, the clinical appreciation of respiratory failure is largely by observing what the patient is doing to maintain gas exchange despite a worsening pathophysiological situation. With no involvement of the pulmonary vascular bed, cyanosis tends to be a relatively late manifestation and most patients undergoing emergency assessment are given oxygen as a routine. Because of the alveolar gas equation: PalvO2 = (Pbar − PH2 O ) × FiO2 − PaCO2 /0.8, (where PalvO2 is the alveolar partial pressure of O2 ,

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Fig. 4. Diagrammatic representation of the effects changing pleural pressure on right-ventricular inflow and left-ventricular outflow. a. Normal: The heart and lung are shown as a single pump oxygenator filled from a venous reservoir at a pressure of 2 mm Hg via collapsible tubes. The pump oxygenator expels blood into the systemic arteries to achieve a pressure head equivalent to 100 mm Hg. b. Muller ¨ Maneuver: Reducing intrathoracic pressure to −30 mm Hg is comparable to lowering the pressure within the heart–lung pump by an equivalent amount relative to that in the systemic and arterial reservoirs. The left ventricle must develop more force to “raise” the pressure of blood to the previous arterial pressure. Filling of the right ventricle is potentiated by the favorable venous-return gradient. c. Valsalva Maneuver: Elevation of intrathoracic pressure to 30 mm Hg has the opposite effect. The heart–lung pump is “raised” relative to the systemic reservoirs. Systolic ejection is facilitated since less energy is required to raise aortic blood to the level of the previous arterial pressure. Venous return to the right heart is impeded by the adverse gradient.

(Pbar − PH2 O ) is the barometic pressure minus water vapor pressure, FiO2 is the fractional concentration of O2 and PaCO2 is the partial pressure of arterial CO2 ). Arterial PO2 is very responsive to increased O2 and, with added ambient O2 , hypoxia will not occur even in the advent of a very high PCO2 . Until cardiopulmonary failure is imminent, most of the signs of impending respiratory failure are the results of the patient struggling to overcome the worsening pulmonary mechanics. This gives rise to indrawing and retractions, tachypnea and the look of anxiety. The presence of audible wheezing may actually be reassuring in that it indicates that the patient is able to exchange gas. There is a very wide range of normal in terms of a ventilatory response to rising blood levels of CO2 .10 Perhaps for this reason or perhaps for other reasons, some patients do not “defend” their PCO2 ’s with the usual obvious increased respiratory effort and tachypnea. The lack of wheezing, the “silent chest” may be mistaken for a good sign when it in fact means a lack of gas exchange. Levels of PCO2 may rise to very surprising heights until the change in pH brings about an obvious noticeable change in clinical condition. By this time it may be too late. Analogous to central alveolar hypoventilation syndrome, examining the

S92 child is not a guide to a rising PCO2 and respiratory failure. Fortunately, there are a number of physiological evaluations that can guide one as to the severity of asthma. In terms of cardiopulmonary dysfunction, the magnitude of the pulsus paradoxus is easily measured without upsetting the child and is an excellent guide to the degree of distress as evidenced by the magnitude of pulmonary pressure changes. In the end, the bottom line is the level of CO2 in the blood. While the gold standard for assessment of PCO2 is and always has been an arterial blood gas, there are a number of reasons why a warmed capillary sample may be preferable. Prior to non-invasive oximetry, arterial blood gases were the only way to measure hypoxia and most emergency room physicians were particularly adept at drawing them. This is not always the case today and in the absence of prior infiltration with a local anesthetic, touching the arterial wall frequently results in spasm of the artery. Prodding and poking can cause significant distress of the child which can lead to false values. If the PCO2 in venous blood is normal, there can be reassurances that the arterial PCO2 is less than that but in the face of an elevated venous PCO2 , the cause could be hypoventilation but prolonged tourniquet application is the much more common reason. While not ideal, free flowing capillary blood from a previously warmed source can often offer the easiest and most reliable way to assess ventilation. Oxygenation is easily assessed using non-invasive oxygen saturation monitors. Spirometry can offer objective evidence of both the degree of airflow obstruction and the response to therapy. It can usually be done reliably by children over five years of age who are in mild to moderate degrees of distress. In the ambulatory setting, there are a number of physiological parameters that can be used to guide therapy. While normal spirometry can offer reassurance that the degree of impairment is relatively mild, it does not mean that there is no impairment at all. Inflammation of the small airways can result in considerable obstruction that can be reversed with anti-inflammatory medication in the presence of normal spirometry. Properly done plethysmographic measurements11 of RV/TLC can often indicate gas trapping in the distal airways and be of use in guiding therapy. For those children whose pulmonary function tests remain abnormal despite aggressive ambulatory therapy, it is clear that they have already compromised their respiratory reserve without having an exacerbation. In such situations, an exacerbation is much more likely to

A.L. COATES lead to early respiratory failure and a rising PCO2 than in a child with prior normal lung function. Lung function testing can also be an indication of the failure to comply with recommended therapy in children who are asymptomatic but still at risk for severe disease because of their past history. Unfortunately, for those children who do not sense dyspnea, there are few tests to guide us other than past history. If the past history is worrisome, they should be regarded at special risk, in large part because care givers are frequently misled by their lack of overt signs of respiratory distress. In summary, understanding the pathophysiology of both the acute and chronic manifestations of asthma can be of great assistance in developing a therapeutic plan. The pulmonary function laboratory offers us a number of techniques for monitoring treatment and the severity of illness. Symptoms of asthma can clearly fail to tell the whole picture. In that one would never run an hypertensive clinic based solely on symptoms and not bothering to measure blood pressure, one should not run an airway disease clinic without making objective physiological measurements of airway function and health.

REFERENCES 1. Benatar SR. Fatal asthma. N Engl J Med 1986; 314: 423−429. 2. Larson GL. Asthma in children. N Engl J Med 1992; 326: 1540−1545. 3. Manning HL, Schwartzstein RM. Pathophysiology of dyspnea. N Engl J Med 1995; 333: 1547−1553. 4. Papastanekis C, Panitch HB, England SJ, Allen JL. Developmental changes in chest wall compliance in infancy and early childhood. J Appl Physiol 1995; 78: 179−184. 5. Desmond KJ, Demizio DL, Allen PD, MacDonald NE, Coates AL. The effect of salbutamol on gas compression in cystic fibrosis and asthma. Am J Respir Crit Care Med 1994; 149: 673−677. 6. Desmond KJ, Coates AL, Martin J, Beaudry PH. Trapped gas and the severity of airflow limitation in children with cystic fibrosis and asthma. Pediatr Pulmonol 1986; 2: 128−134. 7. Zapletal A, Desmond KJ, Demizio DL, Coates AL. Lung recoil and the determination of airflow limitation in cystic fibrosis and asthma. Pediatr Pulmonol 1993; 15: 13−18. 8. Stalcup SA, Mellins RB. Mechanical forces producing pulmonary edema in acute asthma. N Engl J Med 1977; 297: 593−595. 9. Martin JG, Jardim J, Sampson M, Engels LE. Factors influencing pulsus paradoxus in asthma. Chest 1981; 80: 543−549. 10. Pianosi P, Grondin D, Desmond KJ, Aranda JV, Coates AL. Effect of caffeine on the ventilatory response to inhaled carbon dioxide. Respir Physiol 1994; 95: 311−320. 11. Coates AL, Peslin R, Rodenstein DO, Stocks J. Measurement of lung volumes by plethysmography. Eur Respir J 1997; 10: 1415−1427.