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RESPIRATORY FUNCTION IN THE ELDERLY
GERIATRIC ANESTHESIA
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RESPIRATORY FUNCTION IN THE ELDERLY Michael Zaugg, MD, and Eliana Lucchinetti, MS
Respiratory complications after surgery account for approximately 40% of the perioperative deaths in patients over 65 years of age.16,47, 61 Although pulmonary dysfunction is more frequent in elderly patients after anesthesia and surgery, age itself is considered to be only a minor risk factor for perioperative pulmonary dysfunction until the ages of natural death >re reached.z9,46 Nonetheless, with advancing age a significant decrement in the functional capacity of the respiratory system occurs.7z Longitudinal data show that even in older athletes, physiologic respiratory capacities progressively deteriorate with age despite continued vigorous endurance exercise (approximately 10% per decade).M,54 Accordingly, the ability to deliver more oxygen to tissues than they require ("reserve capacity") decreases by a factor of four from the age of 20 to 64 the age of 70 years in apparently healthy Inadequacy of respiratory function becomes particularly relevant in the supine position during anesthesia, as well as po~toperatively.'~, 14, 24 A variety of coexisting factors, prevalent in the elderly surgical patient, further predispose to pulmonary complications. These factors include smoking, obesity, and pre-existing pulmonary pathology. Chronic obstructive pulmonary disease (COPD-chronic bronchitis and emphysema), principally a geriatric disorder, is considered to be one of the major risk factors for post-coronary artery bypass graft (CABG) morbidity and mortality.29Prolonged operations (longer than 6 hours) and thoracic or upper abdominal surgery significantly increase the risk for perioperative respiratory complications. Nonetheless, the number of elderly patients with pulmonary disease undergoing surgery, including hgh-risk procedures, is rapidly 76 A better understanding of the altered physiology in the aged respiratory system may help to improve patient care and outcome. The purpose of this article is to sketch a panorama of the major age-related changes in the respiratory system. The following topics are addressed and their anesthetic implications discussed: From the Department of Anesthesiology, University Hospital Zurich (MZ); and the Laboratory for Biomechanics, Swiss Federal Institute of Technology (EL), Zurich, Switzerland
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a) structural alterations in the upper and lower airways; b) changes in respiratory mechanics and lung volumes; c) impaired efficiency of gas exchange; and d) alterations in ventilatory drive and control.
STRUCTURAL ALTERATIONS IN THE UPPER AND LOWER A1RWAYS With advancing age, structural changes occur both in the upper and lower airways including the adjacent tissues. Loss of muscular pharyngeal support predisposes the elderly to upper airway obstruction?, In addition, loss of protective reflexes of coughing and swallowing-presumably owing to an agerelated peripheral deafferentation together with a decreased central nervous reflex activity-increases the risk of a~piration.~; More profound morphologic changes occur in the lung tissue itself. A decline in the volume of the pulmonary capillary bed results in a marked increase of the mean pulmonary artery pressure by 30%, and an increase of the pulmonary vascular resistance by up to 80%.15 Also, the increased total tension in the alveolar sheet of the aged lung increases pulmonary vascular resistance (see next section). A progressive concomitant loss of alveolar surface area by at least 30% occurs from the age of 20 to the age of 70 mainly owing to intra-alveolar fene~tration.~~ This process, in contrast to alterations typically observed in the emphysematic lung, is non-inflammatory, without septa1 destruction and is related to the enlargement of the pores of Kohn.62,70 An additional typical microscopic finding in the aged lung is ductectasia. It represents the dilatation of the respiratory bronchioles and alveolar d ~ c t s . 5From ~ a functional point of view, ductectasia shifts the intrapulmonary gas content away from the alveolar surface, increasing the anatomical dead space. Many important structural alterations are based on molecular changes in protein structures. Accordingly, increased proteolysis of elastin resulting in a lower degree of ~ross-linking,~' and changes in the composition and amount of lung surfactant,* are responsible for the marked decrease in intrinsic elastic recoil, typically observed in the aged lung. The absolute elastin content in the lung tissue does not appear to decline with aging; however, its proportion in relation to collagen decreases. Microscopically, young lungs show small collagen fibers that radiate from the posts, whereas in older lungs, more and enlarged fiber bundles are seen around the The increased interstitial collagen content may also contribute to the observed decrease in oxygen diffusing capacity.52The age-related structural changes and their functional correlates for both lung and thorax are summarized in Table 1. Cumulative oxidative damage by industrial and environmental factorsnamely reactive oxygen species, including the superoxide anion, hydrogen peroxide, and hydroxyl radical-is thought to be responsible for the structural deterioration and functional decline of the lung in aging. Oxidative stress either directly affects the extracellular matrix proteins or mitochondria1 DNA which is not protected by histones and DNA-binding proteins ("genome instability").', 32. '' The direct toxicity of oxidants to key lung structures is also known to foster the development of chronic obstructive pulmonary disease.58Interestingly, increased antioxidant consumption (e.g., vitamins C and E) is able to markedly improve lung function in the elderly.20For every extra milligram increase in vitamin E in the daily diet, forced expiratory volume in 1 second (FEV,) increases by 42 mL and forced vital capacity (FVC) by 54 mL, on average.
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Table 1. STRUCTURAL CHANGES AND THEIR FUNCTIONAL CORRELATES IN THE AGED LUNGS AND THORAX System
Lung
Thorax
MorphologyIStructure
Function
alveolar surface 1 (intraalveolar fenestration = pores of Kohn t ) interstitial connective tissue T ductectasia (enlarged respiratory bronchioles and alveolar ducts) proteolysis of elastin t (crosslinking 1), altered location and orientation of elastic fibers elastin/collagen ratio 1 surfactant 1 ( + altered composition) stiffness 1' (calcification of ribs and vertebral joints) loss of respiratory muscle mass
diffusing capacity dead space f
1, physiologic
anatomic dead space T tracheo-bronchial instability with early closure of small airways, increased compliance (barrel-shaped chest wall, flat diaphragm), changes in lung volumes, ventilation/ perfusion mismatch with progressive impairment of arterial oxygenation 3
*
tidal volume 1,respiratory frequency f maximum^voluntary respiratory
pressure
1
CHANGES IN RESPIRATORY MECHANICS AND LUNG VOLUMES The elastic properties of the lung tissue and thoracic wall gradually change by aging. The lung parenchyma loses elastic recoil and becomes more compliant, while the chest wall becomes stiffer (calcification of the ribs and vertebral joints).45,68 The volume-pressure curve of the lung itself shows a shift to the left, whereas the volume-pressure curve of the thorax itself shifts to the right. The volume-pressure curve of the aged total system (lung and thorax) is flatter and shows less compliance. In their 1972 published biomechanical model, Fung and Sobin= found that the compliance of the alveolar sheet-the sum of two alveolar-capillary membranes connected by a system of densely spaced posts-is linked to the total tension (vectorial sum of the opposing surface tension and elastic recoil tension) by an inverse relationship. Accordingly, an increase in total tension by inflation will lead to a decrease in the compliance of the alveolar sheet, which will decrease its thickness, increase pulmonary vascular resistance (by a power of 4), and finally cause a decrease in blood flow in both the juvenile and the aged lung (Fig. 1A). However, because the change in volume for a specific increase in pressure is more pronounced in the aged lung, a greater drop in compliance occurs (Fig. 1B). Therefore, the loss of elastic recoil in the aged lung leads to an increased overall tissue tension and, consequently, contributes to an increased pulmonary vascular resistance. The tidal volume slightly decreases, while the respiratory frequency slightly increases. Also, the abdominal contribution to tidal breathing increases. Although the divergent changes of chest wall and lungs do not considerably affect total lung capacity, when corrected for the age-related decrease in height, this leads to a barrel-like appearance of the chest and a flattened diaphragm. Related
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Figure 1. A, The volume-pressure relationship of the lung becomes steeper and shifts to the left with increasing age. For each given volume V, the elastic recoil po,. in the aged lung is smaller than the elastic recoil pojin the juvenile lung. Consequently, the compliance C.(V,) of the aged lung is increased compared with the compliance Ci(V,) of the juvenile lung. B, The dependence of the compliance on the lung volume and, consequently, on the tension of the lung tissue is illustrated. An increase in the volume by inflation (from V, to V,) increases the overall tension in the tissue. As a consequence, the compliance
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changes in the respiratory mechanics are schematically shown in Figure 2. The new equilibrium of the opposing thoracic and pulmonary forces increases the intrapleural pressure by 2 to 4 cm H20, and has a significant impact on static and dynamic lung volumes, as well as on the respiratory mechanics. Figure 3 schematically indicates the changes of the different lung volumes with age. Forced expiratory volume in 1 second annually decreases by approximately 30 mL” 29; and closing capacity (CC), the volume at which the elastic recoil of the lungs becomes insufficient to support small bronchioles without cartilaginous support (< 1 mm), reaches functional residual capacity (FRC) in the erect 60year-old. In the supine position, CC reaches FRC even earlier at about 44 years of Smoking disproportionately accelerates these alteration^.^^ Although some investigators report a small increase of FRC at about 1%per decade of life: this increase is largely counteracted by the immediate and profound decrease of FRC during anesthesia (supine position with cephalad displacement of the diaphragm).18Because vital capacity (VC) is significantly decreased and FRC is slightly increased, preoxygenation by only four maximal breaths prior to induction of anesthesia may not be sufficient in the elderly.69 Based on the Laplace equation (p = 2 y/r; p = transdiaphragmatic pressure, y = diaphragm tension, r = diaphragm radius), a tenfold increase in diaphragm radius (r) leads to a tenfold reduction in maximum transdiaphragmatic pressure (p). The resulting increased amount of energy needed for the same amount of respiratory work predisposes to muscle fatigue and difficulties in weaning. It is notable that a maximum inspiratory pressure greater than 30 cm H,O may not guarantee easy weaning from mechanical ventilation in the elderly. A maximum inspiratory pressure during voluntary breathing of less than 40% of the peak inspiratory pressure appears to be a more reliable indicator
curvature
W normal elastic recoil
A
+
t.
decreased elastic recoil
B
Figure 2. Decreased elastic recoil leads to enlargement of the thorax (barrel-shaped appearance) and flattening of the diaphragm. The flatter diaphragm requires more muscle power and, consequently, more energy to develop the same transdiaphragmatic pressure (increasedwork of breathing). During increased loads on the diaphragm, such as postoperative abdominal distension or increased airway resistance by mucus formation, the flatter diaphragm tends to fatigue and decompensate earlier. Also, airway patency, particularly during forced voluntary breathing, is less well maintained in the aged lung. A, Juvenile lung. B, Aged lung.
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100
80 h
.-E 60
0 0 0 C
340
-
A
Q
e
c
20
0
20
60
40
80
100
Age (Y) Figure 3. Changes in lung volumes with aging (erect position). Residual volume (RV) (+5%-10%per decade) and functional residual capacity (FRC = ERV + RV) ( + 1%-3% per decade) gradually increase by aging, while expiratory and inspiratory reserve volumes (ERV, IRV) and thus vital capacity (VC = ERV IRV) decrease. Specific (height-adapted) total lung capacity (TLC) does not change with aging. The small reported increase in FRC is controversial in the literature and is clinically not relevant because it is overcome by the 20% reduction in FRC following induction of anesthesia. Forced expiratory volume in 1 second (FEV1) can be significantly reduced in old people (-6%-8%) per decade), and FEVl/FVC may be as low as 65%-55%. The loss of elastic recoil results in a narrowing of small aitways with a diameter less than 1 mm and increases the closing volume (CV). The closing capacity (RV CV) may even be larger than FRC, thus closing the small airways during normal tidal breathing (star). This may significantly impair pulmonary gas exchange.
+
+
for a successful ~ e a n i n g . 3The ~ diaphragmatic efficiency in the elderly is also impaired by a significant loss of muscle mass. A reduction of electromyogram activity by as much as 50% normally occurs in skeletal muscles of the 70-yearold individual, mainly owing to the loss of fast-twitch muscle fibers (type II)?8 The reduction in diaphragm strength may be smaller (10%-20%).53Nonetheless, maximum pressures generated by full inhalation and expiration are significantly decreased, and with increasing age the FEVl/FVC ratio may be as low as 65%:55% in apparently healthy individuals2l The rule of thumb that 70% represents the lower limit of the normal range for the FEVl /FVC ratio is not applicable in the elderly. Although age itself does not relevantly increase airway resistance at rest, the work of breathing may be elevated by 30% during exercise.68 IMPAIRED EFFICIENCY OF GAS EXCHANGE
Arterial oxygenation is progressively impeded with increasing age," The impaired whereas carbon dioxide elimination is unaffected by
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oxygenation is reflected by the progressively increasing alveolar-arterial oxygen gradient and the decreasing arterial oxygen tension (approximately 5 mm Hg per decade from the age of 20 years). A more recent study showed that the decrease in arterial oxygen tension is most significant from 40 to 75 years of age. Thereafter, arterial oxygen tension remains relatively stable at about 83 mm Hg." Impaired oxygenation is primarily owing to an increased ventilation/ perfusion mismatch with shunt- and dead-space-like effects, rather than to a decrease in diffusing ~apacity.~, l9 Uneven distribution of inspired gas is the most probable explanation for the increasing age-related deterioration in ventilation/ perfusion match and results from early airway closure in small bronchioles owing to the uneven loss of elastic recoil in the aged lung. A close relationship between preoperative closing capacity, air trapping, and alveolar-arterial oxygen tension during anesthesia has been Attenuation of the hypoxic pulmonary vasoconstriction and hypocapnic bronchoconstriction response owing to the stiffening of the vasculature and airways ("fine tuning of ventilation/perfusion ratio") additionally contributes to the observed ventilation/ perfusion maldistribution in the elderly and may become particularly evident during onelung ventilation." Age itself is not predictive of adequacy of pulmonary gas exchange during thoracic surgery.63Following induction of anesthesia, the shunting is often markedly increased by atelectasis formation. Shunt owing to atelectasis is the most important factor for gas exchange impairment during anesthesia in individuals at ages less than 50 years, whereas ventilation/ perfusion maldistribution becomes progressively important in elderly patients. Atelectasis formation during general anesthesia does not appear to be increased in the e l d e r l ~ ?Notably, ~ patients with COPD tend to show, at least initially following induction of anesthesia, less atelectasis formation and less shunting owing to their chronic hyperinflation?* From a practical point of view, ventilation of the lungs with a few "near vital capacity inflations" is more effective in reopening atelectatic tissue and improving oxygenation than the administration of positive endexpiratory pressure. Ventilation/ perfusion mismatch and the loss of functional alveolar surface significantly decrease the diffusing capacity with agings1 Men appear to be more affected than women (0.24 mL oxygen/mm Hg/year versus 0.16 mL oxygen/mm Hg/year). Women 25 to 46 years of age have the smallest decrease in diffusing capacity, suggesting a protective effect of ALTERATIONS IN VENTILATORY DRIVE AND CONTROL
Ventilatory control depends on peripheral mechanoreceptors in the chest wall, lungs, and joints, and upon peripheral and central chemoreceptors. Respiratory response to hypoxemia and hypercapnia is roughly decreased by 50% in the 70-year-old healthy i n d i ~ i d u a l This . ~ ~ decreased responsiveness to hypoxemia and hypercapnia mainly reflects the reduced central nervous activity and the reduced neuronal output to respiratory muscles (ventilatory drive)." Sudden increases in airflow resistance by mechanical loading are significantly less well compensated in older individual^.^ Opioids, benzodiazepines, and, in particular, small residual amounts of inhalational anesthetics further reduce the respiratory response to chemical (hypoxemia, hypercapnia) and mechanical stress (increased airway resistance), and increase the incidence of pathologic breathing patterns and apnea.5, yl The control of breathing is also profoundly affected by the arousal state of an individual. In healthy adults, arousal from isocapnic hypoxemia during rapid eye movement (REM) sleep does not occur
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until desaturation below 70Y0.'~In the elderly, the response to hypoxemia during REM sleep is even more profoundly impaired. Also, severe and prolonged postoperative hypoxemic episodes with subsequent myocardial ischemia can be less well compensated by the aged cardiovascular system (decreased left ventricular ejection fraction, lower maximum heart rate, decreased myocardial contraction, decreased response to P-adrenergic stimulation). Supplementation of oxygen, not only for the immediate postoperative period, but also for several days following surgery is crucial.39,57 CLINICAL AND ANESTHETIC IMPLICATIONS
Because pulmonary morbidity is prevalent in elderly patients undergoing major surgery, preoperative optimization of the respiratory function is of utmost importance. Smoking cessation is known to be associated with a lower perioperative risk.73Preoperative evaluation of the respiratory system should include a thorough history taking and physical examination with auscultation of both lungs and examination of the mouth and upper airways (neck and jaw mobility, dentures, loose teeth). A good dental state has been shown to be a reliable marker of a good respiratory function in the elderly.49Measurement of exercise capacity by supine bicycle ergometry appears to be of clinical value for preoperative risk stratification for both pulmonary and cardiac complications prior to major elective abdominal and noncardiac surgery in the elderly patient.25Although most studies do not show additional benefits for the patient care from an "unindicated" preoperative chest radiograph, screening chest radiographs are helpful in elderly patients with suspected cardiac or pulmonary disease.'l Rigorous preoperative evaluation including ventilation/perfusion scanning is required in patients undergoing pulmonary surgery. Predicted postoperative FEV, should exceed 800 mL (> 40% of predicted). Whenever cognitive function is impaired, respiratory impedance measurement seems a more useful tool than spirometry for assessing lung function in the elderly.I0Postoperative pulmonary dysfunction is the clinical picture of a restrictive lung disease with a maximally reduced FRC and VC, typically seen during days 2 and 3 after surgery. Postoperative respiratory care of elderly patients should always include early respiratory therapy and mobilization, as well as the liberal use of the seated position that significantly improves respiratory mechanics and oxygenation. Careful examination for postoperative myocardial infarction, congestive heart failure, thromboembolism, and pneumonia are essential. Minimal invasive surgical approaches, combined with regional anesthetic techniques, may be advantageous for the elderly, particularly for patients with 60, 76 Recently, perioperative P-adrenergic blockobstructive pulmonary ade has been reported to significantly decrease cardiovascular morbidity and mortality in elderly cardiac high-risk patients undergoing noncardiac surgery.41 Perioperative P-adrenergic blockade is usually well tolerated, even in patients with mild COPD, and should be liberally used. Table 2 gives an overview of the key features in the perioperative respiratory management of elderly patients. CONCLUSION
As for other organ systems, the progressive loss of function in the respiratory system by aging is extremely variable between individuals of the same chronologic age. However, loss of alveolar surface area and intrinsic elastic recoil
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Table 2. KEY FEATURES IN THE PERIOPERATIVE MANAGEMENT OF THE AGED RESPIRATORY SYSTEM Evaluation of pre-existing (pulmonary) diseases
Choice of the proper anesthetic technique Prevention of perioperative hypoxemic episodes
Prevention of tracheobronchial aspiration (silent regurgitation-silent aspiration-pneumonia with depressed or absent clinical signs)
Blunting of the increased sympathetic response to tracheal intubation: risk for myocardial damage
J risk stratification for perioperative pulmonary complications: the coexisting disease and not the chronologic age is the major criterion for assessing perioperative risk J optimization of the preoperative respiratory function J consider regional anesthesia (spinal and epidural) particularly for orthopedic and vascular surgery of the lower extremities J 3-minute period of normal breathing at 100% oxygen prior to induction of general anesthsia J generous supplementation of inspired oxygen (up to 5 days postoperatively) J early postoperative respiratory therapy (incentive spirometry) J adequate hydration to allow mobilization of secretions J avoid deep sedation (dementia further minimizes the ability to protect airways) J gentle ventilation and proper airway management (coexisting restrictive and obstructive pulmonary disease force use of higher airway pressure for sufficient ventilation) J consider laryngeal mask or regional anesthesia J generous use of local anesthetics, padrenergic blockers, a,-agonists
represent the major age-related changes in the respiratory system and render the elderly patient more susceptible to perioperative respiratory stress. Generous supplementation of oxygen and optimized pain management decrease the risk for pulmonary complications in elderly surgical patients. References 1. Agarwal S, Sohal RS: Differential oxidative damage to mitochondria1 proteins during aging. Mech Ageing Dev 85:55-63, 1995 2. Allen SJ: Respiratory considerations in the elderly surgical patient. Clin Anesthesiol 4~899-930, 1986 3. Allen SR, Seiler WO, Stahelin HB, et al: Seventy-two hour polygraphic and behavioral recording of wakefulness and sleep in a hospital geriatric unit: Comparison between demented and nondemented patients. Sleep 10:143-159, 1987 4. Altose MD, Leitner J, Cherniack NS: Effects of age and respiratory efforts on the perception of resistive ventilatory loads. J Gerontol 40:147-153, 1985 5. Arunasalam K, Davenport HT, Painter S, et al: Ventilatory response to morphine in young and old subjects. Anaesthesia 38:529-533, 1983 6. Berry DT, Phillips BA, Cook YR, et al: Sleep disordered breathing in healthy aged persons: Possible daytime sequelae. J Gerontol42:620-626, 1987
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7. Buist AS: Early detection of airway obstruction by the closing volume technique. Chest 64495-499, 1973 8. Campbell EJ, Lefrak SS Physiologic processes of aging in the respiratory system. In Krechel SW (ed): Anesthesia and the Geriatric Patient. Orlando, Grune & Stratton, 1984, pp 23-43 9. Cardus J, Burgos F, Diaz 0, et al: Increase in pulmonary ventilation-perfusion inequality with age in healthy individuals. Am J Respir Crit Care Med 156:648-653, 1997 10. Carvalhaes-Net0 N, Lorino H, Gallinari C, et al: Cognitive function and assessment of lung function in the elderly. Am J Respir Crit Care Med 152:1611-1615, 1995 11. Cerveri I, Zoia MC, Fanfulla F, et al: Reference values of arterial oxygen tension in the middle-aged and elderly. Am J Respir Crit Care Med 152:936941, 1995 12. Clark FJ, von Euler C: On the regulation of depth and rate of breathing. J Physiol (Lond) 222267-295, 1972 13. Craig DB, Wahba WM, Don HF, et al: "Closing volume" and its relationship to gas exchange in seated and supine positions. J Appl Physiol31:717-721, 1971 14. Craig DB: Postoperative recovery of pulmonary function. Anesth Analg 60:46-52, 1981 15. Davidson WR Jr, Fee EC: Influence of aging on pulmonary hemodynamics in a population free of coronary artery disease. Am J Cardiol 6514561458, 1990 16. Djokovic JL, Hedley-Whyte J: Prediction of outcome of surgery and anesthesia in patients over 80.JAMA 242:2301-2306, 1979 17. Dodds C: Cardiopulmonary physiology in the elderly. In Dodds C (ed): Anaesthesia and the Geriatric Patient. (Clinical Anaesthesiology, International Practice and Research, vol 7.1) London, Bailliere Tindall, 1993, pp 39-64 18. Don HF, Wahba M, Cuadrado L, et al: The effects of anesthesia and 100 per cent oxygen on the functional capacity of the lungs. Anesthesiology 32521-529, 1970 19. Donevan RE, Palmer WH, Varvis CJ, et al: Influence of age on pulmonary diffusing capacity. J Appl Physiol 14483-492, 1959 20. Dow L, Tracey M, Villar A, et al: Does dietary intake of vitamins C and E influence Iung function in older people? Am J Respir Crit Care Med 1543401-1404, 1996 21. Enright PL, Kronmal RA, Higgins M, et al: Spirometry reference values for women and men 65 to 85 years of age. Cardiovascular Health Study. Am Rev Respir Dis 147125-133, 1993 22. Ferris BG, Anderson DO, Zickmantel R Prediction values for screening tests of pulmonary function. Am Rev Respir Dis 91:252-261,1965 23. Fung YC, Sobin SS: Elasticity of the pulmonary alveolar sheet. Circ Res 30:451469, 1972 24. Germain MG, Wahba WM, Gillies DM: Ventilation following induction of general anaesthesia with thiopentone. Can Anaesth Soc J 2910&104, 1982 25. Gerson MC, Hurst JM, Hertzberg VS, et al: Prediction of cardiac and pulmonary complications related to elective abdominal and noncardiac thoracic surgery in geriatric patients. Am J Med 88:lOl-107, 1990 26. Gerstenblith G, Lakatta E, Weisfeld M. Age change in myocardial function and exercise response. Prog Cardiovasc Dis 19:l-21, 1976 27. Gunnarsson L, Tokics L, Gustavsson, et al: Influence of age on atelectasis formation and gas exchange impairment during general anesthesia. Br J Anaesth 66:423432,1991 28. Gunnarsson L, Tokics L, Lundquist H, et al: Chronic obstructive pulmonary disease and anesthesia: Formation of atelectasis and gas exchange impairment. Eur Respir J 4:1106-1116, 1991 29. Hankinson JL, Odencrantz JR, Fedan KB: Spirometric reference values from a sample of the general U.S. population. Am J Respir Crit Care Med 159:179-187, 1999 30. Higgins TL, Estafanous FG, Loop FD, et al: Stratification of morbidity and mortality outcome by preoperative risk factors in coronary artery bypass patients. A clinical severity score. JAMA 2672344-2348, 1992 31. John R, Thomas J: Chemical compositions of elastins isolated from aortas and pulmonary tissues of humans of different ages. Biochem J 127261-269, 1972 32. Johnson FB, Sinclair DA, Guarente L: Molecular biology of aging. Cell 96:291-302,1999 33. Jones JG: The aged pulmonary system. In Davenport HT (ed): Anaesthesia and the Aged Patient. Oxford, Blackwell Scientific Publications, 1988, pp 47-69
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Address reprint requests to Michael Zaugg, MD Department of Anesthesiology University Hospital Zurich Ramistrasse 100 CH-8091 Zurich Switzerland e-mail: [email protected]
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RESPIRATORY FUNCTION IN THE ELDERLY Michael Zaugg, MD, and Eliana Lucchinetti, MS
Respiratory complications after surgery account for approximately 40% of the perioperative deaths in patients over 65 years of age.16,47, 61 Although pulmonary dysfunction is more frequent in elderly patients after anesthesia and surgery, age itself is considered to be only a minor risk factor for perioperative pulmonary dysfunction until the ages of natural death >re reached.z9,46 Nonetheless, with advancing age a significant decrement in the functional capacity of the respiratory system occurs.7z Longitudinal data show that even in older athletes, physiologic respiratory capacities progressively deteriorate with age despite continued vigorous endurance exercise (approximately 10% per decade).M,54 Accordingly, the ability to deliver more oxygen to tissues than they require ("reserve capacity") decreases by a factor of four from the age of 20 to 64 the age of 70 years in apparently healthy Inadequacy of respiratory function becomes particularly relevant in the supine position during anesthesia, as well as po~toperatively.'~, 14, 24 A variety of coexisting factors, prevalent in the elderly surgical patient, further predispose to pulmonary complications. These factors include smoking, obesity, and pre-existing pulmonary pathology. Chronic obstructive pulmonary disease (COPD-chronic bronchitis and emphysema), principally a geriatric disorder, is considered to be one of the major risk factors for post-coronary artery bypass graft (CABG) morbidity and mortality.29Prolonged operations (longer than 6 hours) and thoracic or upper abdominal surgery significantly increase the risk for perioperative respiratory complications. Nonetheless, the number of elderly patients with pulmonary disease undergoing surgery, including hgh-risk procedures, is rapidly 76 A better understanding of the altered physiology in the aged respiratory system may help to improve patient care and outcome. The purpose of this article is to sketch a panorama of the major age-related changes in the respiratory system. The following topics are addressed and their anesthetic implications discussed: From the Department of Anesthesiology, University Hospital Zurich (MZ); and the Laboratory for Biomechanics, Swiss Federal Institute of Technology (EL), Zurich, Switzerland
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a) structural alterations in the upper and lower airways; b) changes in respiratory mechanics and lung volumes; c) impaired efficiency of gas exchange; and d) alterations in ventilatory drive and control.
STRUCTURAL ALTERATIONS IN THE UPPER AND LOWER A1RWAYS With advancing age, structural changes occur both in the upper and lower airways including the adjacent tissues. Loss of muscular pharyngeal support predisposes the elderly to upper airway obstruction?, In addition, loss of protective reflexes of coughing and swallowing-presumably owing to an agerelated peripheral deafferentation together with a decreased central nervous reflex activity-increases the risk of a~piration.~; More profound morphologic changes occur in the lung tissue itself. A decline in the volume of the pulmonary capillary bed results in a marked increase of the mean pulmonary artery pressure by 30%, and an increase of the pulmonary vascular resistance by up to 80%.15 Also, the increased total tension in the alveolar sheet of the aged lung increases pulmonary vascular resistance (see next section). A progressive concomitant loss of alveolar surface area by at least 30% occurs from the age of 20 to the age of 70 mainly owing to intra-alveolar fene~tration.~~ This process, in contrast to alterations typically observed in the emphysematic lung, is non-inflammatory, without septa1 destruction and is related to the enlargement of the pores of Kohn.62,70 An additional typical microscopic finding in the aged lung is ductectasia. It represents the dilatation of the respiratory bronchioles and alveolar d ~ c t s . 5From ~ a functional point of view, ductectasia shifts the intrapulmonary gas content away from the alveolar surface, increasing the anatomical dead space. Many important structural alterations are based on molecular changes in protein structures. Accordingly, increased proteolysis of elastin resulting in a lower degree of ~ross-linking,~' and changes in the composition and amount of lung surfactant,* are responsible for the marked decrease in intrinsic elastic recoil, typically observed in the aged lung. The absolute elastin content in the lung tissue does not appear to decline with aging; however, its proportion in relation to collagen decreases. Microscopically, young lungs show small collagen fibers that radiate from the posts, whereas in older lungs, more and enlarged fiber bundles are seen around the The increased interstitial collagen content may also contribute to the observed decrease in oxygen diffusing capacity.52The age-related structural changes and their functional correlates for both lung and thorax are summarized in Table 1. Cumulative oxidative damage by industrial and environmental factorsnamely reactive oxygen species, including the superoxide anion, hydrogen peroxide, and hydroxyl radical-is thought to be responsible for the structural deterioration and functional decline of the lung in aging. Oxidative stress either directly affects the extracellular matrix proteins or mitochondria1 DNA which is not protected by histones and DNA-binding proteins ("genome instability").', 32. '' The direct toxicity of oxidants to key lung structures is also known to foster the development of chronic obstructive pulmonary disease.58Interestingly, increased antioxidant consumption (e.g., vitamins C and E) is able to markedly improve lung function in the elderly.20For every extra milligram increase in vitamin E in the daily diet, forced expiratory volume in 1 second (FEV,) increases by 42 mL and forced vital capacity (FVC) by 54 mL, on average.
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Table 1. STRUCTURAL CHANGES AND THEIR FUNCTIONAL CORRELATES IN THE AGED LUNGS AND THORAX System
Lung
Thorax
MorphologyIStructure
Function
alveolar surface 1 (intraalveolar fenestration = pores of Kohn t ) interstitial connective tissue T ductectasia (enlarged respiratory bronchioles and alveolar ducts) proteolysis of elastin t (crosslinking 1), altered location and orientation of elastic fibers elastin/collagen ratio 1 surfactant 1 ( + altered composition) stiffness 1' (calcification of ribs and vertebral joints) loss of respiratory muscle mass
diffusing capacity dead space f
1, physiologic
anatomic dead space T tracheo-bronchial instability with early closure of small airways, increased compliance (barrel-shaped chest wall, flat diaphragm), changes in lung volumes, ventilation/ perfusion mismatch with progressive impairment of arterial oxygenation 3
*
tidal volume 1,respiratory frequency f maximum^voluntary respiratory
pressure
1
CHANGES IN RESPIRATORY MECHANICS AND LUNG VOLUMES The elastic properties of the lung tissue and thoracic wall gradually change by aging. The lung parenchyma loses elastic recoil and becomes more compliant, while the chest wall becomes stiffer (calcification of the ribs and vertebral joints).45,68 The volume-pressure curve of the lung itself shows a shift to the left, whereas the volume-pressure curve of the thorax itself shifts to the right. The volume-pressure curve of the aged total system (lung and thorax) is flatter and shows less compliance. In their 1972 published biomechanical model, Fung and Sobin= found that the compliance of the alveolar sheet-the sum of two alveolar-capillary membranes connected by a system of densely spaced posts-is linked to the total tension (vectorial sum of the opposing surface tension and elastic recoil tension) by an inverse relationship. Accordingly, an increase in total tension by inflation will lead to a decrease in the compliance of the alveolar sheet, which will decrease its thickness, increase pulmonary vascular resistance (by a power of 4), and finally cause a decrease in blood flow in both the juvenile and the aged lung (Fig. 1A). However, because the change in volume for a specific increase in pressure is more pronounced in the aged lung, a greater drop in compliance occurs (Fig. 1B). Therefore, the loss of elastic recoil in the aged lung leads to an increased overall tissue tension and, consequently, contributes to an increased pulmonary vascular resistance. The tidal volume slightly decreases, while the respiratory frequency slightly increases. Also, the abdominal contribution to tidal breathing increases. Although the divergent changes of chest wall and lungs do not considerably affect total lung capacity, when corrected for the age-related decrease in height, this leads to a barrel-like appearance of the chest and a flattened diaphragm. Related
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Figure 1. A, The volume-pressure relationship of the lung becomes steeper and shifts to the left with increasing age. For each given volume V, the elastic recoil po,. in the aged lung is smaller than the elastic recoil pojin the juvenile lung. Consequently, the compliance C.(V,) of the aged lung is increased compared with the compliance Ci(V,) of the juvenile lung. B, The dependence of the compliance on the lung volume and, consequently, on the tension of the lung tissue is illustrated. An increase in the volume by inflation (from V, to V,) increases the overall tension in the tissue. As a consequence, the compliance
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changes in the respiratory mechanics are schematically shown in Figure 2. The new equilibrium of the opposing thoracic and pulmonary forces increases the intrapleural pressure by 2 to 4 cm H20, and has a significant impact on static and dynamic lung volumes, as well as on the respiratory mechanics. Figure 3 schematically indicates the changes of the different lung volumes with age. Forced expiratory volume in 1 second annually decreases by approximately 30 mL” 29; and closing capacity (CC), the volume at which the elastic recoil of the lungs becomes insufficient to support small bronchioles without cartilaginous support (< 1 mm), reaches functional residual capacity (FRC) in the erect 60year-old. In the supine position, CC reaches FRC even earlier at about 44 years of Smoking disproportionately accelerates these alteration^.^^ Although some investigators report a small increase of FRC at about 1%per decade of life: this increase is largely counteracted by the immediate and profound decrease of FRC during anesthesia (supine position with cephalad displacement of the diaphragm).18Because vital capacity (VC) is significantly decreased and FRC is slightly increased, preoxygenation by only four maximal breaths prior to induction of anesthesia may not be sufficient in the elderly.69 Based on the Laplace equation (p = 2 y/r; p = transdiaphragmatic pressure, y = diaphragm tension, r = diaphragm radius), a tenfold increase in diaphragm radius (r) leads to a tenfold reduction in maximum transdiaphragmatic pressure (p). The resulting increased amount of energy needed for the same amount of respiratory work predisposes to muscle fatigue and difficulties in weaning. It is notable that a maximum inspiratory pressure greater than 30 cm H,O may not guarantee easy weaning from mechanical ventilation in the elderly. A maximum inspiratory pressure during voluntary breathing of less than 40% of the peak inspiratory pressure appears to be a more reliable indicator
curvature
W normal elastic recoil
A
+
t.
decreased elastic recoil
B
Figure 2. Decreased elastic recoil leads to enlargement of the thorax (barrel-shaped appearance) and flattening of the diaphragm. The flatter diaphragm requires more muscle power and, consequently, more energy to develop the same transdiaphragmatic pressure (increasedwork of breathing). During increased loads on the diaphragm, such as postoperative abdominal distension or increased airway resistance by mucus formation, the flatter diaphragm tends to fatigue and decompensate earlier. Also, airway patency, particularly during forced voluntary breathing, is less well maintained in the aged lung. A, Juvenile lung. B, Aged lung.
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ZAUGG & LUCCHINETTI
100
80 h
.-E 60
0 0 0 C
340
-
A
Q
e
c
20
0
20
60
40
80
100
Age (Y) Figure 3. Changes in lung volumes with aging (erect position). Residual volume (RV) (+5%-10%per decade) and functional residual capacity (FRC = ERV + RV) ( + 1%-3% per decade) gradually increase by aging, while expiratory and inspiratory reserve volumes (ERV, IRV) and thus vital capacity (VC = ERV IRV) decrease. Specific (height-adapted) total lung capacity (TLC) does not change with aging. The small reported increase in FRC is controversial in the literature and is clinically not relevant because it is overcome by the 20% reduction in FRC following induction of anesthesia. Forced expiratory volume in 1 second (FEV1) can be significantly reduced in old people (-6%-8%) per decade), and FEVl/FVC may be as low as 65%-55%. The loss of elastic recoil results in a narrowing of small aitways with a diameter less than 1 mm and increases the closing volume (CV). The closing capacity (RV CV) may even be larger than FRC, thus closing the small airways during normal tidal breathing (star). This may significantly impair pulmonary gas exchange.
+
+
for a successful ~ e a n i n g . 3The ~ diaphragmatic efficiency in the elderly is also impaired by a significant loss of muscle mass. A reduction of electromyogram activity by as much as 50% normally occurs in skeletal muscles of the 70-yearold individual, mainly owing to the loss of fast-twitch muscle fibers (type II)?8 The reduction in diaphragm strength may be smaller (10%-20%).53Nonetheless, maximum pressures generated by full inhalation and expiration are significantly decreased, and with increasing age the FEVl/FVC ratio may be as low as 65%:55% in apparently healthy individuals2l The rule of thumb that 70% represents the lower limit of the normal range for the FEVl /FVC ratio is not applicable in the elderly. Although age itself does not relevantly increase airway resistance at rest, the work of breathing may be elevated by 30% during exercise.68 IMPAIRED EFFICIENCY OF GAS EXCHANGE
Arterial oxygenation is progressively impeded with increasing age," The impaired whereas carbon dioxide elimination is unaffected by
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oxygenation is reflected by the progressively increasing alveolar-arterial oxygen gradient and the decreasing arterial oxygen tension (approximately 5 mm Hg per decade from the age of 20 years). A more recent study showed that the decrease in arterial oxygen tension is most significant from 40 to 75 years of age. Thereafter, arterial oxygen tension remains relatively stable at about 83 mm Hg." Impaired oxygenation is primarily owing to an increased ventilation/ perfusion mismatch with shunt- and dead-space-like effects, rather than to a decrease in diffusing ~apacity.~, l9 Uneven distribution of inspired gas is the most probable explanation for the increasing age-related deterioration in ventilation/ perfusion match and results from early airway closure in small bronchioles owing to the uneven loss of elastic recoil in the aged lung. A close relationship between preoperative closing capacity, air trapping, and alveolar-arterial oxygen tension during anesthesia has been Attenuation of the hypoxic pulmonary vasoconstriction and hypocapnic bronchoconstriction response owing to the stiffening of the vasculature and airways ("fine tuning of ventilation/perfusion ratio") additionally contributes to the observed ventilation/ perfusion maldistribution in the elderly and may become particularly evident during onelung ventilation." Age itself is not predictive of adequacy of pulmonary gas exchange during thoracic surgery.63Following induction of anesthesia, the shunting is often markedly increased by atelectasis formation. Shunt owing to atelectasis is the most important factor for gas exchange impairment during anesthesia in individuals at ages less than 50 years, whereas ventilation/ perfusion maldistribution becomes progressively important in elderly patients. Atelectasis formation during general anesthesia does not appear to be increased in the e l d e r l ~ ?Notably, ~ patients with COPD tend to show, at least initially following induction of anesthesia, less atelectasis formation and less shunting owing to their chronic hyperinflation?* From a practical point of view, ventilation of the lungs with a few "near vital capacity inflations" is more effective in reopening atelectatic tissue and improving oxygenation than the administration of positive endexpiratory pressure. Ventilation/ perfusion mismatch and the loss of functional alveolar surface significantly decrease the diffusing capacity with agings1 Men appear to be more affected than women (0.24 mL oxygen/mm Hg/year versus 0.16 mL oxygen/mm Hg/year). Women 25 to 46 years of age have the smallest decrease in diffusing capacity, suggesting a protective effect of ALTERATIONS IN VENTILATORY DRIVE AND CONTROL
Ventilatory control depends on peripheral mechanoreceptors in the chest wall, lungs, and joints, and upon peripheral and central chemoreceptors. Respiratory response to hypoxemia and hypercapnia is roughly decreased by 50% in the 70-year-old healthy i n d i ~ i d u a l This . ~ ~ decreased responsiveness to hypoxemia and hypercapnia mainly reflects the reduced central nervous activity and the reduced neuronal output to respiratory muscles (ventilatory drive)." Sudden increases in airflow resistance by mechanical loading are significantly less well compensated in older individual^.^ Opioids, benzodiazepines, and, in particular, small residual amounts of inhalational anesthetics further reduce the respiratory response to chemical (hypoxemia, hypercapnia) and mechanical stress (increased airway resistance), and increase the incidence of pathologic breathing patterns and apnea.5, yl The control of breathing is also profoundly affected by the arousal state of an individual. In healthy adults, arousal from isocapnic hypoxemia during rapid eye movement (REM) sleep does not occur
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until desaturation below 70Y0.'~In the elderly, the response to hypoxemia during REM sleep is even more profoundly impaired. Also, severe and prolonged postoperative hypoxemic episodes with subsequent myocardial ischemia can be less well compensated by the aged cardiovascular system (decreased left ventricular ejection fraction, lower maximum heart rate, decreased myocardial contraction, decreased response to P-adrenergic stimulation). Supplementation of oxygen, not only for the immediate postoperative period, but also for several days following surgery is crucial.39,57 CLINICAL AND ANESTHETIC IMPLICATIONS
Because pulmonary morbidity is prevalent in elderly patients undergoing major surgery, preoperative optimization of the respiratory function is of utmost importance. Smoking cessation is known to be associated with a lower perioperative risk.73Preoperative evaluation of the respiratory system should include a thorough history taking and physical examination with auscultation of both lungs and examination of the mouth and upper airways (neck and jaw mobility, dentures, loose teeth). A good dental state has been shown to be a reliable marker of a good respiratory function in the elderly.49Measurement of exercise capacity by supine bicycle ergometry appears to be of clinical value for preoperative risk stratification for both pulmonary and cardiac complications prior to major elective abdominal and noncardiac surgery in the elderly patient.25Although most studies do not show additional benefits for the patient care from an "unindicated" preoperative chest radiograph, screening chest radiographs are helpful in elderly patients with suspected cardiac or pulmonary disease.'l Rigorous preoperative evaluation including ventilation/perfusion scanning is required in patients undergoing pulmonary surgery. Predicted postoperative FEV, should exceed 800 mL (> 40% of predicted). Whenever cognitive function is impaired, respiratory impedance measurement seems a more useful tool than spirometry for assessing lung function in the elderly.I0Postoperative pulmonary dysfunction is the clinical picture of a restrictive lung disease with a maximally reduced FRC and VC, typically seen during days 2 and 3 after surgery. Postoperative respiratory care of elderly patients should always include early respiratory therapy and mobilization, as well as the liberal use of the seated position that significantly improves respiratory mechanics and oxygenation. Careful examination for postoperative myocardial infarction, congestive heart failure, thromboembolism, and pneumonia are essential. Minimal invasive surgical approaches, combined with regional anesthetic techniques, may be advantageous for the elderly, particularly for patients with 60, 76 Recently, perioperative P-adrenergic blockobstructive pulmonary ade has been reported to significantly decrease cardiovascular morbidity and mortality in elderly cardiac high-risk patients undergoing noncardiac surgery.41 Perioperative P-adrenergic blockade is usually well tolerated, even in patients with mild COPD, and should be liberally used. Table 2 gives an overview of the key features in the perioperative respiratory management of elderly patients. CONCLUSION
As for other organ systems, the progressive loss of function in the respiratory system by aging is extremely variable between individuals of the same chronologic age. However, loss of alveolar surface area and intrinsic elastic recoil
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Table 2. KEY FEATURES IN THE PERIOPERATIVE MANAGEMENT OF THE AGED RESPIRATORY SYSTEM Evaluation of pre-existing (pulmonary) diseases
Choice of the proper anesthetic technique Prevention of perioperative hypoxemic episodes
Prevention of tracheobronchial aspiration (silent regurgitation-silent aspiration-pneumonia with depressed or absent clinical signs)
Blunting of the increased sympathetic response to tracheal intubation: risk for myocardial damage
J risk stratification for perioperative pulmonary complications: the coexisting disease and not the chronologic age is the major criterion for assessing perioperative risk J optimization of the preoperative respiratory function J consider regional anesthesia (spinal and epidural) particularly for orthopedic and vascular surgery of the lower extremities J 3-minute period of normal breathing at 100% oxygen prior to induction of general anesthsia J generous supplementation of inspired oxygen (up to 5 days postoperatively) J early postoperative respiratory therapy (incentive spirometry) J adequate hydration to allow mobilization of secretions J avoid deep sedation (dementia further minimizes the ability to protect airways) J gentle ventilation and proper airway management (coexisting restrictive and obstructive pulmonary disease force use of higher airway pressure for sufficient ventilation) J consider laryngeal mask or regional anesthesia J generous use of local anesthetics, padrenergic blockers, a,-agonists
represent the major age-related changes in the respiratory system and render the elderly patient more susceptible to perioperative respiratory stress. Generous supplementation of oxygen and optimized pain management decrease the risk for pulmonary complications in elderly surgical patients. References 1. Agarwal S, Sohal RS: Differential oxidative damage to mitochondria1 proteins during aging. Mech Ageing Dev 85:55-63, 1995 2. Allen SJ: Respiratory considerations in the elderly surgical patient. Clin Anesthesiol 4~899-930, 1986 3. Allen SR, Seiler WO, Stahelin HB, et al: Seventy-two hour polygraphic and behavioral recording of wakefulness and sleep in a hospital geriatric unit: Comparison between demented and nondemented patients. Sleep 10:143-159, 1987 4. Altose MD, Leitner J, Cherniack NS: Effects of age and respiratory efforts on the perception of resistive ventilatory loads. J Gerontol 40:147-153, 1985 5. Arunasalam K, Davenport HT, Painter S, et al: Ventilatory response to morphine in young and old subjects. Anaesthesia 38:529-533, 1983 6. Berry DT, Phillips BA, Cook YR, et al: Sleep disordered breathing in healthy aged persons: Possible daytime sequelae. J Gerontol42:620-626, 1987
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Address reprint requests to Michael Zaugg, MD Department of Anesthesiology University Hospital Zurich Ramistrasse 100 CH-8091 Zurich Switzerland e-mail: [email protected]