The term pulmonary atelectasia is used to describe the pathological condition in which small or large areas of pulmonary parenchyma are characterized by alveolar collapse because of the lack of gas within the alveoli. Various diseases of the bronchi and alveoli can cause the development of atelectasia: intraluminal bronchial obstruction, granulomas, foreign bodies, external compression by enlarged lymph nodes or an aneurysm, external pulmonary compression by pleural fluid or gas (e.g. by a pleural effusion or pneumothorax) and surfactant deficiency.
The term anaesthesia-induced pulmonary atelectasia refers to an iatrogenic form of atelectasia caused by changes in the mechanics and physiology of the respiratory system as a result of the drugs and anaesthetic techniques used in a patient whose lungs are otherwise healthy. In humans atelectesia occurs in up to 90% of patients during general anaesthesia for elective surgery. Recent studies in dogs, cats and sheep have demonstrated that atelectasia also plays an important role in altered gas exchange in these species.
Various factors are responsible for the development of anaesthesia-induced pulmonary atelectasia, but the main mechanisms are closure of the airways and the resulting reabsorption of alveolar gas (reabsorption atelectasia), compression of the pulmonary parenchyma (compression atelectasia) and altered surfactant activity. These three mechanisms coexist, even though independently of one another and, in fact, one can predominate over the others in an individual patient.
REABSORPTION ATELECTASIA (CLOSURE OF THE AIRWAYS AND REABSORPTION OF ALVEOLAR GAS)
In order to understand this mechanism, it is essential to recall the concepts of functional residual capacity (FRC) and closing volume and the effects that general anaesthesia have on these. FRC is the volume of gas contained in the lungs at the end of a normal expiration. General anaesthesia usually causes a decrease in the FRC through various mechanisms:
- Rib cage volume reduction: different studies have shown that following the induction of general anaesthesia the dimensions of the rib cage decrease, causing a reduction of lung volume of about 200 ml in humans.
- Changes in the position and shape of the diaphragm:in the awake patient, the tone of the diaphragm separates the thoracic cavity functionally and not only physically from the abdominal cavity. During inspiration and expiration the movement of the diaphragm (the main respiratory muscle) enables expansion of the pulmonary parenchyma. Furthermore, considering the static situation at end-expiration, the contracted diaphragm prevents the weight of the abdominal organs from interfering with the function of the pulmonary parenchyma adjacent to the dome of the diaphragm, particularly when the subject is in a supine position. The muscle relaxation caused by general anaesthesia considerably reduces or eliminates (in the case of use of neuromuscular blockers) diaphragmatic tone, leading to a cranial shift in this respiratory muscle. Various studies have analysed the changes in shape and position of the diaphragm during general anaesthesia: it seems that the areas of the diaphragm most affected are the dependent ones, which are characterized by a greater cranial shift and less excursion than the non-dependent areas.
- Thoracic blood volume increase:although not universally recognized, an increase in thoracic blood volume as a result of a shift of blood from the peripheral circulation into the thorax during anaesthesia could be a co-factor in decreasing the FRC.
The closing volume is the volume of the lung at which total or partial collapse of the most distal airways occurs. In should be remembered that the bronchioles cannot guarantee their own patency autonomously since they do not have support structures (such as the cartilaginous rings present in the upper airways). The diameter of the bronchiolar lumen is, therefore, related to the condition of the surrounding pulmonary parenchyma: during expansion (inspiration) the diameter increases, while during expiration, it decreases. As the lung volume progressively decreases, a level is reached at which the bronchioles begin to collapse: this corresponds to the closing volume. The closure of the bronchioles does not happen instantaneously throughout the pulmonary parenchyma, but is a progressive condition that increases as the lung volume decreases; the closing volume is not, therefore, a fixed value but rather a range of volumes within which the phenomenon occurs.
In healthy, awake subjects the closing volume is less than the FRC, which means that the airways close only during forced expiration and not at the normal tidal volume. Unlike the FRC, the closing volume is not influenced by anaesthesia so that after induction of general anaesthesia, the FRC is lowered to values below the closing volume and total or partial closure of the distal airways occurs at a normal tidal volume. The alveoli distal to the closed airways are no longer ventilated but are still perfused and the gas within them is, therefore, gradually reabsorbed into the capillaries causing progressive collapse of the alveoli. This is the mechanism of formation of reabsorption atelectasia. The rate of reabsorption of alveolar gas depends on the composition of the gas and, in particular, on the diffusing capacity of the gases contained within the alveoli. Oxygen is a highly diffusible gas and for this reason the rate of reabsorption increases as the fraction of inspired oxygen (FiO2) increases. The time to collapse in the case of ventilation with a FiO2 of 0.21 (room air) is more than 12 hours, whereas when the FiO2 is 1 (pure oxygen), the alveoli collapse within 5 minutes.
It should also be considered that there are not only closed bronchioles and open bronchioles, but a midway state with only partial reduction of bronchiolar lumen, described as partial closure of the airways. From a functional point of view, these alveoli are hypoventilated but with unaltered perfusion, that is, they form areas with a low ventilation/perfusion ratio (low V/Q). In these areas there is a delicate balance between the arrival of fresh gas from the upper airways and the removal of gas by the capillary bed. If one of the two components gradually increases (removal) or decreases (arrival), a V/Q ratio is reached beyond which the alveoli collapse. This is called the critical V/Q. High concentrations of inspired oxygen increase capillary absorption (removal of gas from the alveolus), so the critical V/Q is reached more easily and alveolar collapse is, therefore, facilitated. Thus, if a high FiO2 is used, an area of hypoventilated lung parenchyma passes to a state in which there is a total lack of ventilation (atelectasia, V/Q = 0).
The foregoing is the basis of another important concept: the FiO2 directly influences the formation of atelectasia by affecting areas of the lung in which there is total or partial closure of the airways. For this reason, for some time now, high levels of FiO2 have been avoided in human medicine – compatibly with the patient’s clinical need for adequate oxygenation. The standard of care is to ventilate healthy patients with an FiO2 between 30% and 40%. The role that the FiO2 plays in the development of atelectasia during general anaesthesia has also been studied recently in the dog and cat, with the findings generally confirming the data from humans.
COMPRESSION ATELECTASIA
Compression of pulmonary parenchyma is another factor that contributes to alveolar collapse: when an external pressure is applied to the alveolus which exceeds the pressure within the alveolus, the alveolus collapses. During anaesthesia, the muscle tone of the diaphragm is reduced or absent (when neuromuscular blocking agents are used) with a whole series of already described consequences for lung function; furthermore, in this circumstance the weight of the abdominal viscera bears directly on the pulmonary parenchyma adjacent to the diaphragm, exerting a pressure that can cause alveolar collapse. Numerous factors can influence the development of compression atelectasia: the position of the patient during surgery (lateral, dorsal, sternal), the constitution of the patient (obese vs lean), type of surgery, etc. Confirming the importance of diaphragmatic tone in the development of atelectasia, various studies have demonstrated that all those conditions in which some diaphragmatic tone is preserved (e.g. assisted ventilation) reduce the formation of atelectasia.
ALTERED SURFACTANT ACTIVITY
An alteration in surfactant function caused by mechanical ventilation can play in role in the development of atelectasia in mechanically ventilated patients. Surfactant has a fast turnover and so alterations of its activity are of little importance in causing atelectasia during anaesthesia, but are definitely more important during long-term ventilation in intensive care.
The phenomena described above are found during general anaesthesia with all drugs except ketamine [1]. The explanation for this different behaviour of ketamine is essentially that this drug, unlike the others, increases the tone of striated muscles so that all changes related to muscle relaxation are considerably reduced. This, however, applies to situations in which ketamine is the only anaesthetic agent used (a now obsolete practice); when combined with an adequate muscle relaxant (e.g., a benzodiazepine), this ‘positive’ effect of ketamine is lost.
From the foregoing explanation of the mechanisms of formation of atelectasia it is logical that the lung districts most involved are the dependent areas and those close to the diaphragm. An alveolus that collapses and is, therefore, no longer ventilated but is still perfused creates a shunt, while a hypoventilated alveolus has a low V/Q. This situation obviously has an effect on gas exchange at the alveolar-capillary barrier, with consequent reduction of the partial pressure of oxygen in the arterial blood (PaO2). Another important clinical consequence of atelectasia is a reduction in pulmonary compliance. These conditions can constitute a problem not only during anaesthesia for an operation, but also during recovery of consciousness after the general anaesthesia. It has been shown in humans that anaesthesia-induced atelectasia persists during the post-operative period and takes 2-3 days to resolve completely. The presence of areas of atelectasia in the immediate post-operative period can be the cause of hypoxia of varying severity since the patient is frequently no longer intubated and is breathing spontaneously, often room air (FiO2 0.21). Furthermore, areas of atelectasia can be important foci of pulmonary infections in the post-operative period. It is, therefore, essential that the anaesthetist is able to prevent, recognize and, if necessary, treat atelectasia induced by general anaesthesia.
Among all the above described mechanisms of formation of atelectasia, the one that is definitely most susceptible to manipulation in order to prevent this change in pulmonary parenchyma is alveolar reabsorption. The use of low FiO2 (0.3 – 0.5) from the start of general anaesthesia can reduce pulmonary atelectasia substantially, while guaranteeing that the patient is well oxygenated.
The term “alveolar recruitment” is used to describe the re-opening of an area of atelectatic lung when positive pressure is applied. Simple positive pressure mechanical ventilation does not prevent the formation of atelectasia and indeed, if incorrectly used, can actually worsen it, as clearly demonstrated in humans. Ventilated patients are usually given neuromuscular blocking agents which completely eliminate diaphragmatic muscle contraction (with its role in the development of atelectasia), or, in any case, are in a deep level of anaesthesia with profound depression of diaphragmatic tone. Collapse of the airways and consequent reabsorption of alveolar gas in the more distal parts of the lung also occurs during positive pressure ventilation. The use of high tidal volumes, which instinctively may seem the best approach for resolving the problem, could actually re-open these areas during inspiration but they would collapse again during expiration (referred to as tidal recruitment). Cyclical opening and closing of the alveoli would, therefore, be established. It has recently been clearly demonstrated that this phenomenon is a notable stress to the alveolar epithelium, which suffers considerable damage. Furthermore, the use of high tidal volumes also generates high pressures that can be responsible for cardiovascular complications (a decrease in cardiac output) and respiratory system damage (barotrauma, volutrauma).
In order to avoid collapse of the alveoli and airways at end-expiration, positive pressure can be applied at this moment, thus preventing the lungs from returning to the basal condition. This is the concept of positive end-expiratory pressure (PEEP). PEEP prevents alveolar collapse at the end of expiration and is often associated with a corresponding increase in the PaO2. However, the other side of the coin is that this strategy inevitably increases intrathoracic pressure, thus favouring the development of complications in the systemic and pulmonary circulation, which are usually clinically relevant in patients with already compromised haemodynamics (hypotension, hypovolaemia) but respond well to fluid therapy [2]and the possible administration of sympathomimetic agents (e.g. dopamine, dobutamine). In patients with a good cardiocirculatory state, any adverse effects of the application of PEEP can be treated by the administration of fluids. Pressures of up to ten times higher than those normally necessary to distend non-atelectatic alveoli are required to re-open an area of atelectatic lung, but once re-opened, these areas can be ventilated with normal pressures. This is the concept of recruitment manoeuvres: the atelectatic lung is ventilated at high pressures for a limited period of time in order to re-open all the atelectatic areas and then, immediately afterwards, ventilated with a normal volume and PEEP in order to prevent the alveoli from collapsing again. The most commonly used recruitment manoeuvre in general anaesthesia is lung insufflation at an airway pressure of 40 cmH2O for 10 – 15 seconds (in humans data on up to 40 seconds have been reported) in order to re-open all the lung and then application of PEEP, restoring the tidal volume to normal values. The application of PEEP prevents the re-closure of recruited areas (derecruitment).