required minute volume with the least amount of energy expenditure. The total WOB (necessary tocreate pressure gradients to move air) is divided into 2 parts. The 1st part is to overcome the lungand chest wall elastance, and is referred to as elastic work (Welast). The 2nd part is to overcomeairway and tissue resistance, and is referred to as resistive work (Wresist). Welast is directlyproportional to tidal volume, whereas Wresist is determined by the rate of airflow and, therefore, therespiratory rate. The total WOB is lowest at a rate of 35-40/min for neonates and 14-16/min for older children and adults. Welastis disproportionately increased in diseases with decreased complianceand Wresist is increased in airway obstruction. Respirations are therefore shallow (low VT) and rapidin diseases of low compliance and deep and relatively slow (low flow rate) in diseases of increasedresistance. Compared to older children, young infants have disproportionately greater Welastbecause the negative intrapleural pressure during inspiration causes the retractile (more compliant)chest wall to collapse and pose an impediment to air entry. Young infants increase their respiratoryrate with any mechanical abnormality. Other examples of compliant chest wall being a disadvantageinclude flail chest resulting from rib fractures, thoracotomy, and neuromuscular weakness. One of the salutary effects of continuous positive airway pressure in such situations is the stabilization of thechest wall.Time constant, measured in seconds, is a product of compliance and resistance. It is a reflection of the amount of time required for proximal airway pressure (and, therefore, volume) to equilibrate withalveolar pressure. It takes 3 time constants for 95%, and 5 time constants for 99% of pressureequilibration to occur. Since airways expand during inspiration and narrow during expiration,expiratory time constant is longer than inspiratory time constant. Diseases characterized bydecreased compliance (pneumonia, pulmonary edema, atelectasis) are associated with a shorter time constant and therefore require less time for alveolar inflation and deflation. Diseases associatedwith increased resistance (asthma, bronchiolitis, aspiration syndromes) have prolonged timeconstant, and therefore require more time for alveolar inflation and deflation. Pathologic alterations intime constants have practical significance during mechanical ventilation. Patients with shorter timeconstants are best ventilated with relatively smaller tidal volumes and faster rates to minimize peakinflation pressure. In patients with increased airway resistance, a fast respiratory rate (and,therefore, less time) does not allow enough pressure equilibration to occur between the proximalairway and the alveoli. Inadequate inspiratory time results in lower tidal volume, whereas insufficientexhalation time results in inadvertent PEEP, often referred to as auto-PEEP or intrinsic PEEP. Suchpatients are therefore best ventilated with relatively slower rates and larger tidal volumes.
370.4Â Airway Dynamics In Health And Disease
The trachea and airways of an infant are much more compliant than those of older children andadults, thus changes in intrapleural pressure result in much greater changes in airway diameter. Theairway can be divided into 3 anatomic parts: the extrathoracic airway extends from the nose to thethoracic inlet; the intrathoracic-extrapulmonary airway extends from the thoracic inlet to the mainstem bronchi; and the intrapulmonary airway is within the lung parenchyma. During normalrespirations, intrathoracic airways expand in inspiration as intrapleural pressure becomes morenegative and narrow in expiration as they return to their baseline at FRC. The changes in diameter are of little significance in normal respiration. In diseases characterized by airway obstruction, muchgreater changes in intrapleural pressure are required to generate adequate airflow, resulting ingreater changes in airway lumen. The changes in the size of airway during respiration areaccentuated in young infants with their softer, more compliant airways.In extrathoracic airway obstruction (choanal atresia [ 373 ], retropharyngeal abscess,laryngotracheobronchitis [ 382 ]), the high negative intrapleural pressure during inspiration istransmitted up to the site of obstruction, after which there is a rapid dissipation of pressure.Therefore, the extrathoracic airway below the site of obstruction has markedly increased negativepressure inside, resulting in its collapse, which makes the obstruction worse 6A ). This producesinspiratory difficulty, prolongation of inspiration, and inspiratory stridor. Also, the increased negativeintrapleural pressure results in chest wall retractions. During expiration, the increased positiveintrapleural pressure is again transmitted up the airways to the site of obstruction, leading to adistension of the extrathoracic airway and amelioration of obstruction 6 B).Because of the increased positive intrapleural pressure, the chest wall tends to bulge out, whichproduces the classical paradoxical respiration, in which the chest retracts during inspiration andbulges out during expiration. The younger the child, the softer is the chest wall and the more markedis the paradoxical respiration of extrathoracic airway obstruction. A pattern of seesaw respirationmay also be evident in newborns and young infants as the compliant chest wall is sucked in and theabdomen bulges out during inspiration, with the converse happening during expiration.In obstruction of intrathoracic-extrapulmonary airway (vascular ring [ 383 ], mediastinal tumors) andintrapulmonary airway (asthma, bronchiolitis), the increased negative intrapleural pressure results ina distention of intrathoracic airways during inspiration, thus providing some relief from obstruction .During expiration, the increased positive intrathoracic pressure is transmitted up to the site of obstruction, after which it dissipates rapidly. The intrathoracic airway above the site of obstruction istherefore subjected to much greater intrapleural pressure from outside, which cannot be adequatelybalanced by enough positive pressure inside, resulting in collapse above the site of obstruction.The site at which pressures inside and outside the airway during exhalation are equal is referred toas the equal pressure point (EPP). With intrathoracic airway obstruction, the EPP is shifted distallytoward the alveolus, causing airway collapse above. Marked inspiratory/expiratory changes in ayoung infant's airway lumen above the EPP is often termed collapsible trachea. Tracheal collapse isoften a sign of airway obstruction, and even contributes to its severity, but is rarely the primaryabnormality. With intrapulmonary airway obstruction, an even wider portion of intrathoracic airway issubjected to pressure swings during inspiration and expiration.Both intrathoracic-extrapulmonary and intrapulmonary airway obstruction result in increasingdifficulty during expiration, prolongation of expiration, and expiratory wheezing. Any airwayobstruction within the thorax results in expiratory wheezing.
370.5Â interpretation of clinical signs to localize the site of pathology
Appropriate interpretation of clinical findings is the 1st step in establishing the diagnosis of respiratory disease. Respiratory distress can occur without respiratory disease, and severerespiratory failure can be present without significant respiratory distress. Diseases characterized byCNS excitation, such as encephalitis, and neureoexcitatory drugs are associated with centralneurogenic hyperventilation. Similarly, diseases that produce metabolic acidosis, such as diabeticketoacidosis, salicylism, and shock, result in hyperventilation as a compensatory response. Patientsin either group could be considered clinically to have respiratory distress; they are distinguished frompatients with respiratory disease by their increased tidal volume as well as the respiratory rate. Their blood gas values reflect a low PaCO2 and a normal Pao2. Patients with neuromuscular diseases,such as Guillain-BarrÃ© syndrome or myasthenia gravis, and those with an abnormal respiratorydrive may develop severe respiratory failure but are not able to mount sufficient effort to appear inrespiratory distress. In these patients, respirations are ineffective or may even appear normal in thepresence of respiratory acidosis and hypoxemia.The rate and depth of respiration and the presence of retractions, stridor, wheezing, and grunting arevaluable signs in localizing the site of respiratory pathology. Rapid and shallow respirations(tachypnea) are characteristic of parenchymal pathology, in which the elastic work of breathing isincreased disproportionately to the resistive work of breathing. Chest wall, intercostal, andsuprasternal retractions are most striking, with increased negative intrathoracic pressure duringinspiration. This occurs in extrathoracic airway obstruction as well as diseases of decreasedcompliance. Inspiratory stridor is a hallmark of extrathoracic airway obstruction. Expiratory wheezingis characteristic of intrathoracic airway obstruction, either extrapulmonary or intrapulmonary.Grunting is produced by expiration against a partially closed glottis and is an attempt to maintainpositive airway pressure during expiration for as long as possible. Such prolongation of positivepressure is most beneficial in alveolar diseases that produce widespread loss of FRC, such as inpulmonary edema, hyaline membrane disease, and pneumonia. Grunting is also effective in smallairway obstruction (bronchiolitis) to maintain a higher positive pressure in the airway duringexpiration, decreasing the airway collapse.