Pulmonary Pathophysiology and Lung Mechanics in Anesthesiology

Tracheobronchial Structure

The trachea extends from the cricoid cartilage at the level of C6 to the carina at approximately the level of T4/5, at which point it branches into the right and left mainstem bronchi. The trachea is approximately 12 cm in women and 14 cm in men, and ranges from a mean of 19 ± 1.5 mm in diameter in women to 22 ± 1.5 mm in men. The right mainstem bronchus is shorter, wider, and more vertical than the left mainstem bronchus. Its length is approximately 1.4 to 1.8 cm compared with 4.4 to 4.9 cm on the left; thus the right lung is generally more susceptible to aspiration.

There are three right-sided lobes: the upper, middle, and lower lobes. On the left, there are two lobes, the upper and lower lobes, with the lingula being a “tongue-like” extension of the left upper lobe. The lobes are covered with visceral pleura and are separated by folds of pleura known as the horizontal and oblique fissures on the right, and by the oblique fissure on the left. Each lobe has a lobar, or secondary bronchus, as well as lobar blood supply. The lobes are further divided into bronchopulmonary segments, which again have dedicated named bronchi and blood supply. The right and left lungs each have 10 segments, although nomenclature for these segments may vary slightly in the literature ( Fig. 5.1 ). ^,

The primary, or mainstem, bronchi branch from the trachea at the carina, then further branch into the lobar bronchi, and the segmental bronchi. These airways contain rings of cartilage that help keep them open. Once the airways branch into bronchioles, the walls are made of smooth muscle, and at the level of the respiratory bronchioles, the walls are made of only epithelium. This marks the transition from the conducting airways, encompassing the oropharynx and nasopharynx through bronchioles, to the respiratory airways, which participate in gas exchange and include the respiratory bronchioles and the alveoli. On average, the lungs have 23 generations of dichotomous branching, as shown in Fig. 5.2 .

Respiratory Airways

The respiratory bronchioles end in the acinus, which is the functional unit of the lung, and consists of the alveolar ducts and alveolar sacs. The acinus appears as a cluster of grapes, each of which may contain up to 2000 alveoli. In total, the human lung consists of approximately 300 million alveoli creating a surface area for gas exchange of 40 to 80 m. ^, The alveoli contain alveolar type I cells, alveolar type II cells, and alveolar macrophages. Type I cells are squamous cells, comprising the very thin alveolar walls to facilitate gas exchange, and they cover up to 95% of the surface area of the alveoli. Type II cells are cuboidal and contain lamellar bodies, which secrete pulmonary surfactant, a film of phospholipids which reduces alveolar surface tension to facilitate lung expansion. Alveolar macrophages are scavengers that engulf foreign particles throughout the lungs, playing a key immunologic role. ^,

Nomenclature

Lung volume at any given point in time depends upon lung and chest wall mechanics, the activity of the diaphragm and accessory muscles of respiration, and the size of the individual, as well as the ambient conditions (temperature, pressure, humidity) in which such volumes are measured. The standard lung volumes and capacities measured by spirometry are expressed at body temperature, atmospheric pressure, saturated with water vapor (BTPS), and are compared with volumes predicted by the individual’s age, sex, and body size. Measures of lung volume are denoted as either “volumes” or “capacities,” where volumes are not subdivided, whereas capacities are the sum of two or more standard lung volumes. Of note, lung volumes correlate better with impairment of patient functional capabilities than respiratory function measurements related to airflow.

Tidal Volume

The tidal volume (V _T ) is the volume of gas inhaled and exhaled with each breath. With quiet breathing at rest, it is approximately 500 mL per breath for a 70-kg adult, that is, 5 to 7 mL/kg of predicted body weight. The V _T may be augmented considerably in several conditions (e.g., during exercise) and is achieved by increased work of the diaphragm and the accessory muscles of respiration.

Residual Volume

The amount of gas left in the lungs following a forced maximal exhalation is known as the residual volume (RV). It is determined by the balance between the outward expansion of the chest wall opposing the inward recoil of the lungs with the force generated by the muscles of expiration. Normal RV for a 70-kg adult is around 1.5 L, but because of dynamic airway collapse with forced expiratory effort, gas may become trapped in the alveoli. Thus the RV can become much larger in emphysema, where the lungs’ inward recoil is diminished and amount of gas trapping increases.

Expiratory and Inspiratory Reserve Volumes

The expiratory reserve volume (ERV) is the difference between the functional residual capacity (FRC) and the RV, or the amount of gas that can be forcibly exhaled at the end of a normal tidal exhalation. Similarly, the inspiratory reserve volume (IRV) is the volume of gas that can be forcibly inhaled starting at the end of a normal tidal inhalation. The ERV is approximately 1.5 L, while the IRV is approximately 2.5 L in a healthy 70-kg adult.

Functional Residual Capacity

FRC is the volume of gas remaining in the lungs at the end of a normal tidal exhalation; therefore it is the sum of the RV and the ERV. It is determined by the balance of the inward recoil of the lungs and the outward expansion of the chest wall, as well as the level of tone of the respiratory muscles. The FRC is approximately 3 L in a healthy 70-kg adult. The point at which the inward recoil is exactly balanced by the outward expansion is known as the relaxation volume (V _r ). FRC may be equal to, greater than, or less than the V _r , depending on the circumstances. For instance, in obstructive lung disease, relaxed exhalation can be incomplete as the next inspiratory effort starts resulting in FRC greater than V _r .

Lung hyperinflation results in increased RV and FRC. Static hyperinflation is produced by the reduction in lung elasticity because of emphysema. It can also be caused by excessive positive end-expiratory pressure (PEEP). Dynamic hyperinflation results from air trapping from incomplete exhalation of inhaled gas. Interestingly, during mechanical ventilation, while PEEP adds to the risk of hyperinflation in chronic obstructive pulmonary disease (COPD) patients, it can also result in reduced hyperinflation in a subset of COPD patients because of airways being “stented open” by its application.

Total Lung Capacity

The total lung capacity (TLC) is the maximal volume of gas in the lungs after a maximal inhalation; thus it is the sum of the RV, ERV, V _T , and IRV. TLC is approximately 6 L for a healthy 70-kg adult. The vital capacity (VC) is the maximal volume of gas exhaled during a forced exhalation after a forced inhalation. Thus VC is the sum of the V _T , IRV, and ERV. The VC is approximately 4.5 L in a healthy 70-kg adult.

Fig. 5.3 shows a summary of how the standard lung volumes and capacities relate, along with average values for a 70-kg adult.

Closing Capacity and Closing Volume

Closing capacity (CC) is the lung volume at which small airway closure begins to occur. CC is the sum of the closing volume (CV) and RV. Usually, the CC is smaller than FRC, so airways do not close with normal tidal breathing. However, age, supine positioning, pregnancy, and obesity, among other conditions, all increase CC. Airway closure at a larger CC increases the likelihood of hypoxemia. CV is measured using the nitrogen washout test, as illustrated in Fig. 5.4 . In this method, the subject takes a breath of 100% oxygen and exhales through a one-way valve measuring nitrogen content and volume of the gas exhaled. The initial portion of the curve where the nitrogen content is zero is the dead space, where no gas exchange has occurred. The nitrogen content increases as the patient breathes a VC breath to RV. The CV is the volume between the terminal point of slope change and the RV. CC is the sum of the CV measured and the RV. As CC increases with age, CC exceeds FRC, resulting in small airway closure during normal tidal breathing. This transition occurs at a younger age in the supine patient (approximately 44 years) compared with the upright patient (approximately 66 years), whereas FRC does not change with age ( Fig. 5.5 ).

Effects of Anesthesia

It is well accepted that supine positioning and subsequent induction of general anesthesia with neuromuscular blockade reduces FRC, with reports of as much as a 9% decrease. This reduction of FRC occurs consistently following induction, and progresses at a slower rate throughout the duration of anesthesia; it is further accentuated in obese patients. The sitting position, as compared with supine, invariably increases FRC, even in patients under general anesthesia, as it favors the caudad displacement of the diaphragm.

Importantly, recruitment breaths and increased V _T may temporarily recruit consolidated lung volume under anesthesia, but they are insufficient to keep an atelectatic lung open. This concept has been demonstrated both experimentally and in humans. In a study of pigs undergoing one lung ventilation, the ventilated lung experienced substantial V./Q. mismatch, hyperperfusion, and alveolar damage on histologic examination. Further, tidal recruitment with a V _T of 10 mL/kg increased the volume of the ventilated lung that was normally aerated (versus consolidated), but applied cyclic recruitment was associated with the initiation of an injurious immune response. ^, Similarly, in a rabbit model, one lung ventilation with high V _T s and zero PEEP resulted in higher mean pulmonary artery pressure (MPAP), greater lung weight, and higher levels of thromboxane B ₂ , all suggestive of acute lung injury (ALI). In morbidly obese patients, the effect of increased PEEP alone, a recruitment maneuver alone, and a recruitment maneuver followed by increased PEEP were compared using computed tomography (CT) scans and arterial partial pressure of oxygen (PaO ₂ )/inspired oxygen fraction (FiO ₂ ) ratios. Similar to animal studies, the recruitment maneuver only transiently improved respiratory function, and PEEP by itself could not recruit the lungs, whereas the combination of the recruitment maneuver with the increased PEEP improved PaO ₂ /FiO ₂ ratios and reduced atelectasis on CT.

Transpulmonary Pressure

The transpulmonary pressure , P _L , represents the distending pressure across the lungs, which is the difference between the airway pressure and the pleural pressure. It is an essential concept because it represents the pressure that effectively promotes air flow and distends the lungs. At end-inspiration, if respiratory flow equals zero and there is a clear plateau of the airway pressure, end-inspiratory P _L = P _plateau – end-inspiratory P _pleural represents the pressure acting across the alveolar units. At end exhalation, that pressure would be represented, in the absence of auto-PEEP, by end-expiratory P _L = PEEP – end-expiratory P _pleural . The importance of the concept of P _L becomes clear as the inspiratory P _L is the pressure which provides tidal ventilation at the same time that could produce stretch lung injury; and the end-expiratory P _L is that required to prevent lung collapse at end-exhalation by being kept positive.

Unfortunately, the assessment of P _L is not usual in clinical practice because measurement of pleural pressure is not simple, in contrast to measurement of airway pressure. Yet, pleural pressure may be estimated using an esophageal balloon, which is either standalone or attached to an esophagogastric tube and positioned in the lowest third of the esophagus ( Fig. 5.6 ). These esophagogastric tubes are generally 100 cm long, and the average depth for a correctly positioned balloon is approximately 35 to 45 cm. The catheter is connected to a pressure transducer via a three-way stopcock, and the balloon is inflated to a standard volume depending on the device, which is necessary to prevent artifact because of passive recoil of the balloon walls. Further, the balloon should be long enough to avoid regional variability, providing an average measurement of esophageal pressure to estimate pleural pressure. Although use of an esophageal balloon represents an improvement in the accuracy of pulmonary pressure monitoring, it is not without its limitations. Artifact may arise from mediastinal weight, gravitational gradients in pleural pressure, and airway closure at end exhalation. Furthermore, there is considerable controversy in the literature on whether the esophageal pressure measurements should be directly taken as absolute estimates of pleural pressures for PEEP adjustments, or whether changes in esophageal pressures should be used to compute chest wall and lung elastances, which are then used to set the level of the administered PEEP. Although a ventilator strategy guided by the transpulmonary pressure measured with esophageal balloons improved oxygenation and compliance in a small group of acute respiratory distress syndrome (ARDS) patients, a subsequent large trial on patients with moderate to severe ARDS resulted in no significant difference in death and days free from mechanical ventilation between patients receiving an esophageal balloon-guided PEEP and those receiving empirical high PEEP-FiO ₂ settings. Those findings did not support esophageal balloon-guided PEEP titration in ARDS. In critically ill patients with class 3 obesity (body mass index [BMI] ≥40 kg/m ² ) and ARDS, a retrospective analysis compared a standard protocol of ventilator settings determined by the ARDS net table for lower PEEP/higher FiO ₂ with a “lung rescue” management strategy with settings determined by an individualized protocol based on lung recruitment maneuvers, esophageal manometry, and hemodynamic monitoring. Patients receiving the standard protocol had almost double the 28-day mortality compared with the lung rescue cohort (31% vs. 16%, P = .012; hazard ratio [HR], 0.32; 95% confidence interval [CI] 95%, 0.13–0.78).

In robotic-assisted laparoscopic surgery, esophageal manometry can help delineate the portion of increased driving pressure, which is applied to the lungs versus that applied to the chest wall; the increase in elastance associated with pneumoperitoneum is substantially greater for the chest wall (E _CW ) than for the lungs (E _LS ). This may improve the ability to maintain open lung by appropriately titrating PEEP in this and other perioperative conditions with high susceptibility to lung derecruitment.