During respiration, the movement of air into and out of the lungs requires that:

Effects of Inhaled Anesthetics on Bronchomotor Tone in Humans and the Work of Breathing

Sevoflurane (1 MAC) reduced respiratory system resistance by 15% in patients undergoing elective surgery, whereas desflurane had no effect.30 Rooke and associates37 compared the bronchodilating effects of halothane, isoflurane, sevoflurane, desflurane, and thiopental–nitrous oxide in healthy patients undergoing induction of anesthesia and tracheal intubation. In contrast to thiopental–nitrous oxide, all volatile agents with the exception of desflurane significantly reduced respiratory resistance (Fig. 21.3).

The work of breathing is defined as pressure or force multiplied by the tidal volume during inspiration. Respiratory work is further divided into elastic work (required to overcome the recoil of the lung) and resistive work (requiredto overcome airway flow resistance and viscoelastic resistance of pulmonary tissues). The work of breathing is usually derived from transpulmonary pressure volume curves. Volatile anesthetics increase the work of breathing in adults and children. In rats, sevoflurane reduced pulmonary compliance at the lung periphery rather than at the airway level, thereby increasing viscoelastic and elastic pressures in the lung.38 In addition, in a murine model of chronic asthma, sevoflurane significantly decreased resistance in central and distal airways and also lowered resistance in the lung periphery. These data suggest that sevoflurane exerts a beneficial effect in the presence of chronic airway obstruction and indicate that sevoflurane might reduce the work of breathing in comparison to other drugs (Fig. 21.4).39

Studies in humans demonstrate a ceiling effect where low concentrations of volatile anesthetics significantly reduceupper airway resistance, reflecting changes in airway smooth muscle tone in the major airways. In contrast, distal airways and lung parenchyma lack a smooth muscle component (withlower airway and alveolar resistance being more a measure of viscoelastic changes in the lung). Increasing concentrations of inhalational agents have diminished effect on these more distal pulmonary components and thus do not further reduce total lung resistance (Fig. 21.5).40

Expiration is passively affected by the recoil characteristics of the lung during normal breathing. In anesthetized patients, the ventilatory response to expiratory resistance is reduced to a greater extent than the response to inspiratory resistance. Conscious and anesthetized humans exhibit decreases in respiratory rate when expiratory resistive loads are applied, but only anesthetized subjects develop rib cage–abdominal wall motion dyssynchrony that causes less effective ventilation and reduction in minute alveolar ventilation. This concept may be particularly important in spontaneously breathing anesthetized patients who demonstrate expiratory obstruction, such as in cases of asthma, COPD, airway secretions, or during hypopharyngeal obstruction or partial breathing circuit occlusion.

Work of Breathing

The work of breathing (WOB) is a reflection of the amount of energy required to overcome the elastic and resistive elements of the respiratory system and move gas into and out of the lung during spontaneous breathing. WOB is defined as the cumulative product of distending pressure and the given volume displaced during inhalation or exhalation (Fig. 44.4):

WOB=∫PdV,

where P is pleural pressure (in time) above resting pleural pressure and V is the volume (in time) relative to the resting thoracic volume (see Fig. 44.4).

The WOB required to ventilate the lungs of normal newborns is approximately 10% of that required in adults (McIlroy and Tomlinson, 1955). However, infants have been shown to have a higher oxygen cost and lower mechanical efficiency associated with the WOB than adults (Thibeault et al., 1966). In healthy infants, most of the WOB is done by the diaphragm during inhalation. Approximately one-third of the total inspiratory WOB is related to overcoming the resistance to gas flow in the airways (Mortala et al., 1982). Exhalation is usually passive because of the potential energy stored in the lung and the chest wall at the end of inhalation but may become active as expiratory resistance increases or lung volumes decrease below FRC.

Work of Breathing.

Work of breathing is defined as the energy necessary to perform tidal ventilation over a set unit of time. The work of breathing is determined by the pressure-volume characteristics (compliance and resistance) of the respiratory system (Fig. 14.6). During breathing, work must be done to overcome the tendency of the lungs to collapse and the chest wall to spring out (see Fig. 14.6, area ADC) and the frictional resistance to gas flow that occurs in the airways (see Fig. 14.6, area ABC). Work of breathing (see Fig. 14.6, area ABCD) is increased by conditions that increase resistance or decrease compliance or when respiratory frequency increases.

If minute volume is constant, the “compliance” component of work is increased when tidal ventilation is large and respiratory rate slow. The “resistance” component of work is increased when the respiratory rate is rapid and tidal ventilation decreased. When the two components are summated and the total work plotted against the respiratory frequency, an optimal respiratory frequency that minimizes the total work of breathing can be obtained (Fig. 14.7). In children with restrictive lung disease (EELV < FRC, low compliance) and short time constants, the optimal respiratory frequency is increased, whereas children with obstructive lung diseases (EELV > FRC, high resistance) with long time constants have a lower optimal respiratory frequency.

Work of Breathing

Work of breathing (WOB) may be defined as the product of pressure and volume. It may be analyzed by plotting transpulmonary pressure against tidal volume. The WOB per kilogram body weight is similar in infants and adults. However, the oxygen consumption of a full-term neonate (5–7 mL/kg per minute) is several times that of an adult (2-3 mL/kg per minute).60 This greater oxygen consumption (and greater carbon dioxide production) in infants accounts in part for their increased respiratory frequency compared with older children. In preterm infants, the oxygen consumption related to breathing is three times that in adults.61

The location of airway resistance within the tracheobronchial tree differs between infants and adults. The nasal passages account for 25% of the total resistance to airflow in a neonate, compared with 60% in an adult.33,62 In infants, most resistance to airflow occurs in the bronchi and small airways. This results from the relatively smaller diameter of the airways and the greater compliance of the supporting structures of the trachea and bronchi.32,63,64 In particular, the soft cartilaginous chest wall of a neonate is very compliant; the ribs provide less support to maintain negative intrathoracic pressure. This lack of negative intrathoracic pressure combined with the increased compliance of the bronchi can lead to functional airway closure with every breath.65–67 In infants and children, therefore, small-airway resistance accounts for most of the WOB, whereas in adults, the nasal passages provide the major proportion of flow resistance.33,65,66,68–73

In the presence of increased airway resistance or decreased lung compliance, an increased transpulmonary pressure is required to produce a given tidal volume, and therefore the WOB is increased. Any change in the airway that increases the WOB may lead to respiratory failure. Recall that the WOB (resistance to air flow) is inversely proportional to the fourth power of the radius of the lumen during laminar flow (beyond the fifth bronchial division) and to the fifth power of the radius during turbulent flow (upper airway to the fifth bronchial division). Because the diameter of the airways in infants is smaller than in adults, pathologic narrowing of the airways in infants exerts a greater adverse effect on the WOB. Increase in the WOB may also occur with a long ETT of small diameter, an obstructed ETT, or a narrowed airway. All of these situations increase oxygen consumption, which in turn increases oxygen demand.74 The increased oxygen demand is initially addressed by an increase in respiratory rate, but the increased WOB may not be sustainable. The end result may be exhaustion, which leads to respiratory failure (CO2 retention and hypoxemia) (Fig. 4.9).

The difference in histology of the diaphragm and intercostal muscles of preterm and full-term infants compared with older children contributes to increased susceptibility of infants to respiratory fatigue or failure. Type I muscle fibers permit prolonged repetitive movement; for example, long-distance runners through repeated exercise increase the proportion of type I muscle fibers in their legs. The percentage of type I muscle fibers in the diaphragm and intercostal muscles increases with age (preterm infants < full-term infants < 2-year-old children) (Fig. 14.11). Any condition that increases the WOB in preterm and full-term neonates may fatigue the respiratory muscles and precipitate respiratory failure more readily than in an adult.75–77

Work of Breathing

Work of breathing may be defined as the product of pressure and volume. It may be analyzed by plotting transpulmonary pressure against tidal volume. The work of breathing per kilogram body weight is similar in infants and adults. However, the oxygen consumption of a full-term neonate (4 to 6 mL/kg/min) is twice that of an adult (2 to 3 mL/kg/min).49 This greater oxygen consumption in infants accounts in part for the increased respiratory frequency compared with older children. In preterm infants, the oxygen consumption related to breathing is three times that in adults.50

The location of airway resistance differs between infants and adults. The nasal passages account for 25% of the total resistance to airflow in a neonate, compared with 60% in an adult.22,51 In infants, most resistance to airflow occurs in the bronchial and small airways. This results from the relatively smaller diameter of the airways and the greater compliance of the supporting structures of the trachea and bronchi.21,52,53 In particular, the chest wall of a neonate is very compliant; the ribs provide less support to maintain negative intrathoracic pressure. This lack of negative intrathoracic pressure combined with the high compliance of the bronchi can lead to functional airway closure with every breath.54–56 In infants and children, therefore, small-airway resistance accounts for most of the work of breathing, whereas in adults, the nasal passages provide the major proportion of flow resistance.22,54,55,57–62 In the presence of increased airway resistance or decreased lung compliance, an increased transpulmonary pressure is required to produce a given tidal volume and, thus, the work of breathing is increased. Any change in the airway that increases the work of breathing may lead to respiratory failure. Recall that the resistance component of respiratory work is inversely proportional to the radius of the lumen increased by the power of 4 during laminar flow and to the power of 5 during turbulent flow (a crying child). Because the diameter of the airways in infants is smaller than those in adults, pathologic narrowing of the airways in infants exerts a greater adverse effect on the work of breathing. Increase in the work of breathing may also occur with a long ETT of small diameter, an obstructed ETT, or a narrowed airway. These situations all result in increased oxygen consumption, which in turn increases oxygen demand.63 The increased oxygen demand is initially met by an increase in respiratory rate, but the increased work of breathing may not be sustainable. The end result may be exhaustion, which leads to respiratory failure (carbon dioxide [CO2] retention and hypoxemia).

The difference in histology of the diaphragm and intercostal muscles of preterm and full-term infants compared with older children also contributes to increased susceptibility of infants to respiratory fatigue or failure. Type I muscle fibers permit prolonged repetitive movement; for example, long-distance runners through repeated exercise increase the proportion of type I muscle fibers in their legs. The percent of type I muscle fibers in the diaphragm and intercostal muscles change with age (preterm infants < full-term infants < 2-year-old children) (Fig. 12-11). Thus, any condition that increases the work of breathing in neonates and infants may fatigue the respiratory muscles and precipitate respiratory failure.64–66

The opposing forces to ventilation

The work of breathing derives from the two resistive forces of the lungs and chest wall, i.e. the elastic (see Figure 7.3) and frictional forces. Forces within the respiratory system that oppose inflation of the lung and therefore ventilation can be grouped into two categories:

the elastic opposition to expansion of the lungs;

the frictional opposition or resistance to air movement.

The pressure change that is generated on inspiration must be sufficient to overcome such forces. The effort required and the resulting volume change is termed the ‘work of breathing’. Normally, the work of breathing is minimal (healthy lungs). A pressure gradient of 2–5 cmH2O is typically needed to move the average tidal volume.

The elastic forces are encountered as a result of both the lungs and chest wall being ‘elastic’ structures, i.e. they resist changes in shape. When they have been inflated or deflated, they tend to return to the same resting/starting position of equilibrium once the driving force has been removed. The lungs naturally want to collapse and the chest wall naturally to expand. Thus, each exerts a pull on the other. In the absence of other forces (e.g. muscles) a position is reached in which the opposing forces are balanced.

Owing to these opposing forces (of lung and chest wall), the intrathoracic pressure is negative (sub-atmospheric). To inflate the lungs an extra force must be applied (by the muscles) and intrathoracic pressure falls lower.

Expiration is mostly passive as a result of the elastic forces returning the lungs and chest wall to a balanced position (Figure 7.4). It can, however, be active, for example forced breathing and coughing, where the expiratory muscles assist the elastic forces (resulting in a more rapid expiratory rate of flow and faster lung deflation).

The inspiratory muscles perform mechanical work through upsetting the balance of the elastic forces. Hence, the harder and faster the respiratory effort is, the more ‘elastic’ work is required. A certain amount of pressure is required to stretch the lungs to a certain volume. The normal value for elastance is around 10 cmH2O/L. However, in disease states, the lungs become stiffer and the same pressure change may result in a smaller volume change, i.e. the elastance of the lung is higher. Pneumonia, acute respiratory distress syndrome (ARDS) and pulmonary oedema are common lung conditions affecting elastance. Others include fibrotic lung disease, pleural effusion, kyphoscoliosis and obesity.

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