Pilbeam's Mechanical Ventilation (PDF): A Physiological and Clinical Guide

Effects of Positive Pressure Ventilation on the Pulmonary System CHAPTER 17 321 8. Describe clinical laboratory findings associated with metabolic 12. List the possible responses to an increase in mean airway acid-base disturbances....

Effects of Positive Pressure Ventilation on the Pulmonary System CHAPTER 17 321 8. Describe clinical laboratory findings associated with metabolic 12. List the possible responses to an increase in mean airway acid-base disturbances. pressure in a patient on mechanical ventilation. 9. Identify a patient with air trapping. 13. Describe the effects of positive pressure ventilation on 10. Provide strategies to reduce auto-PEEP. pulmonary gas distribution and pulmonary perfusion in relation 11. Suggest methods to reduce the work of breathing during to normal spontaneous breathing. mechanical ventilation. A number of inherent risks and complications are associated studied only in animal models because ventilator strategies that with the use of mechanical ventilators. These include will potentially harm the lung cannot be performed on human ventilator-associated and ventilator-induced lung injury, subjects during research investigations. the effects of positive pressure ventilation on gas distribution and VILI is a form of lung injury that resembles ARDS. It has been pulmonary blood flow, hypoventilation and hyperventilation, air studied using animal models and apparently occurs in patients trapping, oxygen (O2) toxicity, increased work of breathing receiving inappropriate mechanical ventilation. VILI is difficult to (WOB), patient-ventilator asynchrony, mechanical problems, and identify in humans because its appearance is based on radiological complications of the artificial airway. This chapter reviews the and clinical findings, which overlap with findings that occur with causes and adverse effects of these complications. the underlying pulmonary pathology such as ARDS. In fact, it is reasonable to assume that acute lung injury and ARDS may be partially the result of ventilator management rather than the LUNG INJURY WITH MECHANICAL progression of the disease.3 This supports the idea that mechanical VENTILATION ventilation saves lives and also has the potential to worsen pre- existent lung injury.1 It was not uncommon in the latter part of the 20th century for The following section defines and describes the various forms patients to receive ventilation with pressures greater than 45 cm of VALI and VILI (Key Point 17.1). H2O. Indeed, nearly 20% of patients diagnosed with acute respi- ratory distress syndrome (ARDS), at some point in their man- agement, received ventilation with pressures of 80 cm H2O or Key Point 17.1 It is the practitioner’s responsibility to do no greater and volumes in the range of 10 to 12 mL/kg.1 This is harm and to use appropriate settings when managing patients on mechanical interesting considering that it has been known for more than three ventilation. decades that using these high levels of pressure and volume can cause lung injury, referred to as barotrauma or volutrauma Barotrauma implies trauma that results from using high pressures. Volutrauma implies damage from high distending vol- Barotrauma or Extraalveolar Air umes rather than high pressures. Evidence suggests that high As mentioned, it has been known for some time that positive distending volumes result in overdistention and lung injury, pressure ventilation increases the risk for barotrauma. This type of whereas high distending pressures alone do not cause lung injury. injury involves the formation of extraalveolar gas, such as subcu- Overdistention causes the release of inflammatory mediators from taneous emphysema, pneumothorax, pneumomediastinum, the lungs that can lead to multiorgan failure. This latter response pneumoperitoneum, and pneumopericardium. has been termed biotrauma. The risk for rupture to the lung is greater for patients with lung Repeated opening and closing of lung units, also called bullae or chest wall injury. A number of conditions can predispose recruitment-derecruitment, generates shear stress, which results in a patient to barotrauma (extraalveolar air), including the direct tissue injury at the alveolar and pulmonary capillary level, following4 5: and the loss of surfactant from these unstable lung units. Shear  High peak airway pressures with low end-expiratory pressures stress injury and loss of surfactant have been termed atelectrauma.  Bullous lung disease such as may occur with emphysema or a The following section provides a summary of these various aspects history of tuberculosis of lung injury as they relate to mechanical ventilation.  High levels of positive end-expiratory pressure (PEEP) with high tidal volumes (VTs) Ventilator-Associated Lung Injury Versus  Aspiration of gastric acid Ventilator-Induced Lung Injury  Necrotizing pneumonias The terms ventilator-associated lung injury (VALI) and ventilator-  ARDS induced lung injury (VILI) have been used frequently in the liter- Barotrauma occurs when the delivery of positive pressure ature with some inconsistency regarding their meaning. The term ventilation causes alveolar rupture. Air is forced into the inter- VALI is generally used when referring to lung injury occurring in stitium of an adjacent bronchovascular (perivascular) sheath in humans that has been identified as a consequence of mechanical the area of the distal noncartilaginous airways.4 6 The “escaped” air ventilation.2 The most common forms of VALI include ventilator- moves along the sheath toward the hilum and mediastinum, associated pneumonia (VAP), air trapping, patient-ventilator causing a pneumomediastinum (Fig. 17.1).4 7 Air can then break asynchrony, and extraalveolar gas (barotrauma), such as pneu- through the pleural surface of the mediastinum into the intra- mothorax and pneumomediastinum. (See Chapter 14 for a dis- pleural space, resulting in a pneumothorax. Pneumothorax may be cussion of VAP.) unilateral or bilateral. Air in the mediastinum may also dissect VILI is lung injury that occurs at the level of the acinus. It is the along tissue planes, producing subcutaneous emphysema. Pneu- microscopic level of injury that includes biotrauma, shear stress, moperitoneum may follow pneumomediastinum and occurs when and surfactant depletion (atelectrauma). VILI can be specifically air dissects initially into the retroperitoneum. Air that is trapped 322 CHAPTER 17 Effects of Positive Pressure Ventilation on the Pulmonary System Case Study 17.1 To mediastinum Peak Pressure Alarm Activating The peak pressure alarm is activated for a patient on me- Airways chanical ventilation. Assessment of the patient reveals puffing of the skin of the patient’s neck and face, which feels crepitant to the touch. The right hemithorax is Air bubbles hyperresonant to percussion, and breath sounds are ab- sent. What would be an appropriate action for the respi- ratory therapist? Vascular sheath “Partitional alveoli” Ruptured studies have shown that the incidence of barotrauma is relatively alveolar bases low (2.9%),10 results vary across studies. Interestingly, the reduced incidence of barotrauma may be associated with use of lower VT and lower airway pressures. Pneumothorax may lead to lung collapse with mediastinal shifting occurring away from the affected side. Pneumothorax can also be detected by a resonant or hyperresonant percussion note and absence of breath sounds on the affected side, and chest ra- diographs will indicate lack of vascular markings on the affected Fig. 17.1 Artist s conception of the development of interstitial emphysema. (From side. Treatment usually requires thoracotomy and placement of a Samuelson WM, Fulkerson WJ. Barotrauma in mechanical ventilation. In: Fulkerson chest tube. Because pleural air rises to the highest (nondependent) WJ, MacIntyre NR, editors: Problems in respiratory care: complications of mechanical area of the thorax, the affected area will depend on the patient s ventilation, Philadelphia, PA, 1991, Lippincott Williams & Wilkins.) position. In the supine patient this is an area over the anterior surface of the lung. When evaluating a chest radiograph taken with the patient supine, detection of a small pneumothorax can be under the diaphragm in the peritoneum may interfere with difficult (Case Study 17.1). effective ventilation. Another way of detecting a pneumothorax in patients on me- From its location in the mediastinum, air can also dissect along chanical ventilation is to observe progressive changes in peak tissue planes near the heart and form a pneumopericardium.2 The pressure. Increases in peak pressure occurring within a short escaped air can be reabsorbed into adjacent tissues and resolve period, such as a few minutes to a few hours, may signal the itself. If it is not reabsorbed by the body, evacuation by a drainage presence of pneumothorax of either rapid onset or one caused by a system may be required. Failure to remove this extraalveolar air slow, insidious leak. Physical examination and a chest radiograph can lead to life-threatening problems, such as tension pneumo- should be used to confirm the diagnosis. thorax or pneumopericardium. Because a simple pneumothorax can develop into a tension pneumothorax, careful monitoring is essential. Administering Subcutaneous Emphysema excessive amounts of positive pressure may aggravate the presence Subcutaneous emphysema can be easily detected during physical of air in the pleural space, so manual ventilation with a resusci- examination. It may be visible as a puffing of the skin in the pa- tation bag on 100% O2 may be advisable until the problem can be tient s neck, face, or chest and may even be present in distal areas treated.7 However, it is important for the clinician to avoid using such as the feet and abdomen. The skin feels crepitant to the touch. excessive pressure with manual compression of a resuscitation Subcutaneous emphysema typically occurs without complication bag.11 and tends to clear without treatment as mean airway pressures are A tension pneumothorax is a life-threatening situation that reduced. However, if it is present with dyspnea, cyanosis, and must be treated immediately. It occurs when air enters the pleural increased peak pressures, it may be accompanied by a space and becomes trapped. Pressure gradually builds, collapsing pneumothorax. the affected lung. Mediastinal structures will shift in the thorax, away from the area of tension, and put pressure on the heart and Pneumomediastinum the unaffected lung. Tracheal deviation and neck vein distention Pneumomediastinum can lead to compression of the esophagus, are possible signs. Breath sounds will be absent and the percussion great vessels, and heart. It can usually be easily identified on chest note tympanic. A chest radiograph on a patient with a tension radiographs. Treatment depends on the severity of the problem pneumothorax is not advisable because it might delay lifesaving and its effect on adjacent structures. In severe cases, pneumo- treatment. In a chest radiograph of a tension pneumothorax, one mediastinum can cause cardiac tamponade. If the air is not diaphragm will be more depressed than the other and may display removed, cardiac tamponade can ultimately lead to cardiopul- a deep sulcus sign, with air appearing adjacent to the depressed monary arrest. diaphragm. Treatment for tension pneumothorax involves inserting a 14- Pneumothorax gauge needle, or similar device, into the anterior second to third Early clinical studies suggested that the most common clinical intercostal space on the affected side in the midclavicular line over manifestation of extraalveolar air was pneumothorax.8 9 Although the top of the rib with the patient in upright position. This  Effects of Positive Pressure Ventilation on the Pulmonary System CHAPTER 17 323 maneuver can be lifesaving. While waiting for trained personnel to be summoned to perform this procedure, the respiratory therapist BOX 17.2 Chest Wall Compliance and Protection should decrease mean airway pressures as much as possible while From Overdistention using manual ventilation with a high fraction of inspired O2 (FIO2). The term chest wall pressure as used in the clinical setting in- cludes forces or pressures from the overlying ribs and muscles, Pneumoperitoneum pressure from the diaphragm, and abdominal pressure. As Pneumoperitoneum generally follows pneumomediastinum. It abdominal pressure increases (>20 cm H2O is high), an occurs when air dissects into the retroperitoneal space. The peri- increased amount of pressure is placed on the diaphragm and toneum can rupture, resulting in air moving into the peritoneal the vena cava. This added abdominal pressure augments cavity. As you might expect, this can be painful. If a significant venous return to the thorax as blood shifts into the thorax amount of air is present, it can interfere with the movement of the from the abdominal area. If the lung is injured and leaking, diaphragm and reduce effective ventilation. lung fluid is increased. Thus as abdominal pressure increases, more lung collapses. For example, in an obese patient with Barotrauma or Volutrauma peritonitis, an airway pressure of 30 cm H 2O may not be adequate to ventilate the patient sufficiently. In early studies, researchers tried to determine whether the cause of lung injury during mechanical ventilation was the result of the delivery of high pressures (barotrauma) or high volumes (volu- trauma). Dreyfuss and colleagues coined the term volutrauma to describe the injurious effects of mechanical ventilation they not occur under these conditions. In the clinical setting, restriction observed in laboratory studies using an animal model.12 They to chest wall movement is present when patients are in the prone found that it was not high pressure but the relatively large regional position, in severely obese patients, or when heavy dressings are volumes that overstretched compliant areas of the lung that used to manage surgical sites of chest or chest wall injuries resulted in alveolar stretch and edema formation in these (Box 17.2).15 areas.12 13 To understand the importance of pressure in this setting and its It is now generally accepted that using inordinately high VT can distribution, several circumstances that affect lung pressures must lead to lung overdistention and iatrogenic lung injury. Over- be examined. Pressure at the upper airway is not equal to alveolar distention occurs in those areas of the lungs where high distending pressure (Palv) except when flow is zero and the airway is open. pressuresdin other words, high transpulmonary pressures (alve- (This is usually termed plateau pressure [Pplat].) To interpret Palv, olar pressure pleural pressure [Palv Ppl])dare present. Indeed, or Pplat, the circumstances in which it is measured should be pressures as low as 30 to 35 cm H2O have been shown to cause known. The following are seven of these circumstances15: lung injury in animals.4 12 1. The lungs are normal, but the chest wall is stiff but relaxed, Because regional differences in lung compliance and trans- resulting in high pleural pressures (e.g., 60 cm H2O). pulmonary pressures (PL) occur in most pulmonary disorders, 2. The lungs and chest wall are normal, but the pressure around positive pressure applied to the lung tends to produce larger vol- the chest is high (e.g., pressure on the chest or in the abdomen, umes in more compliant lung areas (Box 17.1). The resulting such as with obesity). overdistention to these areas causes acute alveolar injury and the 3. The lungs and chest wall are normal, but the expiratory mus- formation of pulmonary edema by both increased permeability cles are actively contracting (e.g., the patient performs a Val- and filtration mechanisms (e.g., VTs of 10 12 mL/kg can cause salva maneuver, which causes the pleural pressure to be overdistention of these areas of greater compliance). positive). Additional animal studies found that when the chest wall 4. The lungs are normal, but the abdomen is turgidly overdis- movement was restricted by binding the thorax and pressure was tended (similar to the first circumstance). applied to the lungs, less lung injury occurred.12-14 Thoracic 5. The lungs are stiff, leaving pleural pressure near normal binding prevented severe transpulmonary (alveolar distending) (e.g., 5 cm H2O). pressure. Furthermore, alveolar stretch and edema formation did 6. The lungs are normal, but an incorrectly positioned endotra- cheal tube (ET) expands only one lung to a dangerous degree (e.g., right mainstem intubation with large VTs). 7. Both lungs are dangerously overdistended inside a normal BOX 17.1 Chest Wall and Transpulmonary Pressures chest wall. In the first four examples, structures around the lung (e.g., chest wall and abdomen) oppose most of the alveolar pres- Transpulmonary pressure (PL), as defined in Chapter 1, is the difference between the pressure inside the alveolus and the sure; the pleural pressure is high, but the distending pressure is pressure immediately outside, or the intrapleural pressure. 2 It within safe limits. Only the last three examples are situations in is not uncommon to read scientific journal articles in which PL which lung distending pressure (i.e., the transpulmonary pressure is defined as the difference between the static airway pressure [Palv Ppl]) is abnormally high and thus can cause lung injury. measured during a plateau maneuver and the average intra- Palv can be high by itself without causing lung damage, but if pleural pressure, which is estimated by using an esophageal Palv Ppl is high, lung damage is more likely to occur. balloon.13 Do not be confused by this subtle difference. Both Lung injury from overdistention is more subtle than air leaks definitions imply alveolar pressure (airway pressure during a described in the preceding section on barotrauma. Overdistention plateau) minus intrapleural pressure. lung injury causes excessive stretching of alveolar cells, the for- mation of edema, and the release of inflammatory mediators, also 324 CHAPTER 17 Effects of Positive Pressure Ventilation on the Pulmonary System Normal Low regional CL VT Volume (mL) Overdistention Positive pressure breath PEEP PIP Pressure (cm H2O) Fig. 17.2 A pressure-volume curve in a patient with acute overdistention of the lung during positive pressure ventilation. Notice the duck-billed appearance of the top right portion of the curve (overdistention). PEEP, Positive end-expiratory pressure; PIP, peak inspiratory pressure; VT, tidal volume. Fig. 17.3 The volume from a positive pressure breath distributes homogeneously throughout a lung with normal compliance (CL) (left). In a lung with instability, the volume from a positive pressure breath distributes preferentially to the regions with called chemical mediators. As mentioned earlier, the release of more normal CL (right). Thus a tidal volume (VT) of normal size in a lung with regions these chemical mediators is termed biotrauma. of low CL can overdistend the healthier regions. This creates shearing between Fig. 17.2 shows a pressure-volume curve that indicates the adjacent lung units. (Redrawn from MacIntyre NR: Minimizing alveolar stretch injury presence of overdistention. The shape of this curve is sometimes during mechanical ventilation. Respir Care 41:318 326, 1996.) said to have a “duck-bill” appearance. Most clinicians now think this portion of the curve occurs with overdistention of more compliant areas of the lung, resulting in volutrauma. For the sake space between the two, force is exerted as these two units move of simplicity, the term barotrauma will be used in this text to imply or slide against each other. There is a potential zone of risk at the leaking of air into body tissues (extraalveolar air leak) and the the interface of open and closed lung units. This is similar to term volutrauma to describe damage from overdistention that what occurs when a paper clip is repeatedly twisted; eventually occurs at the alveolar level and involves alveolar and interstitial the paper clip breaks. In the lung, the stress pulls normal tissues edema formation, alveolar stretch, and biotrauma. apart, resulting in physical damage to the alveolar cells, particularly epithelial and endothelial cells (pulmonary micro- Atelectrauma vasculature). The term shear stress has been applied to this type The term atelectrauma is used to describe the injuries to the lungs of situation. The amount of stress across the entire lung can be that occur because of repeated opening and closing of lung units at estimated by using transpulmonary pressure (Fig. 17.3 and lower lung volumes. Atelectrauma can occur in the management Key Point 17.2).5 27 of ARDS when low VTs are used and inadequate levels of PEEP are applied (see Chapter 13). Under these circumstances, alveoli tend to open on inspiration and close on expiration. (This occurs most Key Point 17.2 Shear stress causes intense strain and rupture of often in the dependent areas of the lung. In supine patients this lung tissue, which may lead to an inflammatory response and edema formation. would be the dorsal area near the spine.) The repeated opening and closing of lung units in ARDS produces three primary types of lung injury: shear stress, alteration and washout of surfactant, and The importance of shear stress has been known for a number of microvascular injury.16-18 years. In fact, more than 30 years ago, Mead and colleagues28 Research studies involving animal models showed that venti- calculated from a model that a transpulmonary pressure of only lating pressures of 30 to 80 cm H2O produce atelectrauma with 30 cm H2O could result in a stress of 140 cm H2O being exerted resulting reduced compliance and severe hypoxemia. Atelectrauma between two adjacent alveoli as one expands and the other unstable may be described as alveolar rupture, interstitial emphysema, or unit remains collapsed. Not surprisingly, this force acting on the perivascular and alveolar hemorrhage, which can eventually lead to delicate tissues of the acinus can result in tearing of alveolar death.12 19-26 Death occurred in experimental animal models in epithelium and capillary endothelium along with other structural some cases within an hour. injury. Shear Stress Surfactant Alteration Shear stress occurs when an alveolus that is normally expanded A second consequence of the repeated opening and closing of is adjacent to one that is collapsed (atelectasis) and unstable. As alveoli involves reorientation of the surfactant molecules lining the airway pressure increases during inspiration, the normal alve- alveolar surface. In the alveolus, surfactant forms a molecular layer olus inflates but the collapsed unit does not. In the interstitial between the air and the liquid alveolar surface. During alveolar  Effects of Positive Pressure Ventilation on the Pulmonary System CHAPTER 17 325 collapse, as the surface area of the alveolus decreases, the surfactant the inflammatory mediators are released, the lung begins to molecules can form together until some actually pop out or get resemble a lung with ARDS. Indeed, the damage that can be caused squeezed out at low lung volumes. These “used” lipids do not by ventilator mismanagement may actually be indistinguishable rapidly spread as the alveolus reopens.2 Rather, it is theorized that from the underlying disease process of ARDS.3 newly secreted surfactant replaces surfactant that is lost from the affected area. Reduction in surface area that occurs during exha- Multiple Organ Dysfunction Syndrome lation (i.e., lower alveolar volumes) causes a greater number of Chemical mediators produced in the lung can leak into the pul- surfactant molecules to migrate from the affected area. Thus a monary blood vessels. The circulation then carries these substances greater amount of new surfactant is required to stabilize the lung to other areas of the body and sets up an inflammatory reaction in unit.29 How quickly and for what length of time the alveolar cells other organs, such as the kidneys, gut, and liver.31 36 The release of can continue to produce an adequate amount of surfactant are mediators may therefore lead to multiple organ failure, also called uncertain. It is thought that eventually not enough surfactant will multisystem organ failure and multiple organ dysfunction be present and the alveolus will become unstable. Besides the ef- syndrome 2 37 38 fects of opening and closing of alveoli on surfactant production, it Treating patients with ARDS with lung-protective strategies, such has been suggested that overdistention also reduces surface tension as low VT and therapeutic PEEP, can significantly reduce morbidity and is believed to alter surfactant function.5 and mortality rates in these patients (see Chapter 13).35 39-41 It has also been suggested that hypercapnia may be beneficial in patients Biotrauma with ARDS (who are difficult to ventilate) because it has an anti- Mechanical stress disrupts normal cell function, strains normal cell oxidant effect and may actually reduce inflammation. Therapeutic configuration, and can also lead to an inflammatory response in hypercapnia may be a more appropriate name, but additional studies the lungs.13 Current theory suggests that pulmonary cells, partic- are needed (see Chapter 13).13 42-44 ularly epithelial cells, become distorted during mechanical venti- lation when they are overstretched (overdistention). This Vascular Endothelial Injury overdistention causes the release of chemical mediators (i.e., cy- A third problem that can occur with repeated alveolar collapse and tokines). In addition to epithelial cells, the alveolar macrophages reopening involves the pulmonary microvasculature. Recall that are another important source of inflammatory mediators, which during a positive-pressure breath, alveolar capillaries flatten but are produced in response to a stretching strain and result in a corner alveolar vessels open wider (see Fig. 13.12). The interstitial potential molecular and cellular basis for VILI (Box 17.3).30-35 areas adjacent to the corner vessels develop negative pressure It is important to understand that ARDS does not have to be relative to the inside of the vessels. This negative-pressure gradient present for this inflammatory response to occur. However, when tends to pull fluid and blood products out of the vessels and into the space. Thus the alveoli and perivascular areas become edematous. If the vascular pressure of the lung is further increased, at a BOX 17.3 Chemical Mediators, Cytokines, and certain point the vessel can rupture and release red blood cells and Chemokines other blood components into the alveoli and interstitial space (Fig. 17.4). In Mead s model, a stress of 140 cm H2O was proposed The production of cytokines and chemokines (i.e., chemotactic as occurring between two alveoli as one expanded and the other cytokines) is increased by harmful ventilator strategies. Pul- monary epithelial and alveolar macrophages are, in part, responsible for the production of these substances, which can occur within 1 to 3 hours of the initiation of an inappropriate ventilatory strategy. Inflammatory mediators, such as platelet- activating factor (PAF), thromboxane-B2, tumor necrosis fac- tor-a (TNF-a), and interleukin-1B, have been found isolated from the lungs when low end-expiratory volumes are used. As already discussed, release of these inflammatory mediators is thought to be associated with tidal alveolar reopening and collapse. Neutrophils that migrate into the lung after injury or infection can also release inflammatory mediators. A number of strategies have been proposed to reduce the adverse effects associated with the production of inflamma- tory mediators in the lungs. Protective ventilation strategies discussed in Chapter 13 can be used to avoid overinflation and the repeated opening and closing of alveoli and thus reduce the cytokine response. Instilling antiinflammatory antibodies into the trachea, such as anti TNF-a, also has been shown to improve oxygenation and lung compliance. Infiltration of leukocytes into the lungs is also reduced. Furthermore, the pathological changes seen in an experimental animal model ventilated with inappropriate settings were reduced when Fig. 17.4 An electron micrograph of the lung showing a red blood cell rupturing antibodies were administered. through the wall of the pulmonary microvasculature. (Courtesy John J. Marini, M.D., Minneapolis, Minn.) 326 CHAPTER 17 Effects of Positive Pressure Ventilation on the Pulmonary System Case Study 17.2 Patient CasedAcute Pancreatitis Two days after admission to the hospital, a 50-year-old man with acute pancreatitis requires mechanical ventila- tion. Although his minute ventilation is maintained with the ventilator, oxygenation becomes a concern. The PaO2 is 70 mm Hg on an F O2 of 0.75. The patient is receiving pressure-controlled continuous mandatory ventilation (PC- CMV) with a set pressure of 20 cm H2O and a current PEEP setting of 5 cm H2O. Auscultation reveals bibasilar crackles and scattered crackles in the posterior basal segments. What is the source of the problem based on auscultation and blood gas findings? What change in therapy might be appropriate? Fig. 17.5 Macroscopic aspect of rat lungs after mechanical ventilation at 45 cm H2O peak airway pressure. Left, Normal lungs; middle, after 5 minutes of high airway pressure mechanical ventilation (notice the focal zones of atelectasis, particularly at the left lung apex); right, after 20 minutes. (From Dreyfus D, Saumon G: Ventilator- establishing an optimum PEEP level is not an exact science and induced lung injury: lessons from experimental studies, Am J Respir Crit Care Med can be challenging in critically ill patients. (Case Study 17.2; see 157:294 323, 1998.) Chapter 13 for additional information on setting PEEP.) To summarize, lung injury may occur as a result of either overdistention of the lungs or repeated opening and closing of unit remained collapsed.28 This pressure could also be transmitted lung units throughout the respiratory cycle during mechanical to the pulmonary vessels, which could represent a second cause of ventilation.45 These two phenomena can result in shear stress and vessel rupture. The increased fluid leaking into the lung would alveolar injury, edema formation, surfactant washout or alteration, create a dramatic increase in lung weight, which may be one of the microvascular injury, stretch injury, and biotrauma. Stretch injury mechanisms associated with the hemorrhagic appearance of lungs and the associated biotrauma produce inflammatory mediators by on autopsy in animal models subjected to low VT ventilation lung tissue and leaking of these mediators into the circulation, without PEEP (Fig. 17.5).45 Studies using a canine model have where they have the potential to affect distal organs and ultimately shown that it takes 90 to 100 mm Hg to produce this phenomenon. cause multiple organ dysfunction syndrome.37 Research findings Perhaps leaving areas of the lung collapsed or at least providing strongly support the concept of maintaining Pplat at less than ventilation at low pressures might not damage the lung or 30 cm H2O, setting low VT, and using enough PEEP to adequately vasculature. Whether resting parts of the lung is better than trying maintain open alveoli in patients with ARDS to avoid lung injury to recruit the majority of the lung will require additional studies. from mechanical ventilation.46 Historic Webb and Tierney Study Ventilator-Induced Respiratory Muscle Seminal studies conducted by Webb and Tierney22 in the early Weakness 1970s showed that using inspiratory pressures of 45 cm of H2O It is clear that delivering high airway pressures and volumes during without PEEP resulted in the rapid death of normal rats. Their study mechanical ventilation can lead to damage to the lung paren- is frequently cited as evidence of the benefits of using protective chyma. Recent studies have shown that mechanical ventilation ventilatory strategies. Interestingly, their discovery took nearly two may also cause damage to the respiratory muscles.47 Specifically, decades to be recognized. In a 2003 editorial, Tierney wrote, “We imposing too little stress on the diaphragm during mechanical could hardly believe the results. It was as if we violated a thermo- ventilation by lowering the demands on a patient s respiratory dynamic law and got more out of it than we put into it. Within muscles can induce respiratory muscle weakness.47 minutes the rats were cyanotic and appeared moribund. It took a Laboratory studies using animal models have shown that decade or two for others to conclude that human lungs could be prolonged controlled mechanical ventilation in which complete injured by such ventilation. Our final paragraph 30 years ago sug- diaphragmatic inactivity occurs (i.e., no respiratory efforts are gested management... using protective ventilation and low VTs.”29 made and the mechanical ventilator performs all of the WOB) can lead to a significant decrease in the cross-sectional area of dia- Role of PEEP in Lung Protection phragmatic fibers.47 Studies by Levine and colleagues involving In acute lung injury, PEEP appears to provide some protection from human subjects support these findings.48 In their studies, Levine tissue damage when high pressures are used. This is especially true if and colleagues obtained diaphragmatic muscle biopsies from PEEP levels are greater than the opening pressure for recruitable mechanically ventilated patients who exhibited complete dia- alveoli. PEEP helps restore functional residual capacity (FRC) by phragmatic inactivity for 18 to 69 hours. Histological measure- recruiting previously collapsed alveoli. Adequate levels of PEEP ments of these muscle samples from the costal diaphragm revealed prevent repeated collapse and reopening of alveoli and help main- marked diaphragmatic atrophy. Biochemical analysis of the muscle tain lung recruitment.14 27 However, if PEEP overinflates already samples suggested that the atrophy occurred as a result of patent alveoli, increasing PEEP for a given VT may maximally increased oxidative stress and activation of protein-degradation stretch alveoli. This situation may also reduce cardiac output. Safely pathways.48  Effects of Positive Pressure Ventilation on the Pulmonary System CHAPTER 17 327 The implications of these findings on clinical management of the diaphragm is most displaced in the nondependent regions of mechanically ventilated patients are unclear at this time. Addi- the lung (see Fig. 17.6C). The diaphragm becomes less compliant tional clinical studies will be required to identify more completely than the chest wall adjacent to the anterior part of the lungs in the  the presence of ventilator-induced respiratory muscle weakness supine patient. This alters the V Q ratios by directing the greatest and its effect on weaning and ventilator discontinuation. Although amount of gas flow to the nondependent lung regions, taking the respiratory muscle weakness can result from ventilator injury, it is path of least resistance. Unfortunately, this is also the area with the important for clinicians to recognize that it can be associated with least blood flow. other medical conditions and interventions, such as sepsis and During positive pressure ventilation, alveolar collapse is sus- pharmacological therapy (e.g., antibiotics, corticosteroids, seda- pected to most likely occur in the dependent areas with absence of tives, neuromuscular blocking agents).49 spontaneous diaphragmatic movement. These are also the areas that receive the most blood flow, resulting in increased mis-  matching of V Q and increased dead space ventilation.50 EFFECTS OF MECHANICAL VENTILATION ON GAS DISTRIBUTION AND PULMONARY BLOOD FLOW Ventilation-to-Lung Periphery Experimental studies have shown that during spontaneous ventila- Ventilation to Nondependent Lung tion, the distribution of gas favors the dependent lung areas and also Early studies of the effects of positive pressure breathing on gas appears to favor the periphery of the lung closest to the moving distribution in normal lungs were conducted by Froese and pleural surfaces. The peripheral areas receive more ventilation than Bryan.49 In their studies, these investigators evaluated the move- the central areas.51 52 However, during a positive pressure breath ment of the diaphragm in spontaneously breathing, anesthetized with passive inflation of the lung (paralysis), the central, upper adult volunteers. During spontaneous ventilation in the supine airway, or peribronchial portions of the lung are preferentially filled position, the greatest displacement of the diaphragm occurs in the with air.51 This may be another mechanism by which mismatching dependent region, near the back (Fig. 17.6A).49 The dependent occurs during positive pressure ventilation. If spontaneous breath-  lung areas receive a higher portion of ventilation and perfusion ing can be preserved when possible, these changes in V Q associ-  (i.e., V Q is best matched). When anesthesia is administered but ated with mechanical ventilation may be reduced. Thus ventilator spontaneous ventilation is still present, the diaphragm shifts its modes that preserve spontaneous breathing may be beneficial movement cephalad (toward the head). The effect of this shift is (e.g., pressure support ventilation [PSV]). most pronounced in the dependent (dorsal) regions of the lung, the reverse of normal (see Fig. 17.6B). With anesthesia and the administration of paralytic agents, the contraction of the dia- Increase in Dead Space phragm is blocked. When positive pressure ventilation is provided, Positive pressure ventilation increases the size of the conductive airways, which in turn increases the amount of dead space venti- lation. Additionally, if normal alveoli are overexpanded during positive pressure ventilation and compression of pulmonary ves- sels results, alveolar dead space will also increase. On the other hand, if an increased VT is delivered and positive pressure venti- lation improves ventilation distribution with respect to perfusion, A positive pressure ventilation will decrease the amount of dead space ventilation. Redistribution of Pulmonary Blood Flow Normal pulmonary blood flow favors the gravity-dependent areas and the central, or core, areas of the lungs. However, during B positive pressure ventilation, particularly when PEEP is adminis- tered, cardiac output may decrease and pulmonary perfusion re- distributes to the lung periphery rather than to the center area (i.e., as if the lung had been exposed to a centrifugal force).46 53 The  clinical significance of this is unknown, but it may influence V Q matching. The increased volume during a positive pressure breath and C PEEP squeezes the blood out of nondependent zones, particularly  Fig. 17.6 The solid line in each figure represents the normal position of the dia- in areas of normal lung. This further contributes to V Q mis- phragm. The dotted lines represent the position of the diaphragm as it is altered matching and physiological dead space by sending more blood during anesthesia and positive pressure ventilation. (A) Normal spontaneous breathing into dependent areas, where ventilation is now lower, or into in a supine patient with diaphragm movement primarily in the dependent area of the disease-affected areas of the lung, where lung volumes are not lungs. (B) During anesthesia with spontaneous ventilation maintained, the diaphragm substantially increased. This can lead to increased shunting and shifts cephalad. The shift is most pronounced in the dependent regions. (C) Anesthesia decreased PaO2 54  is sufficient to block spontaneous breaths (paralysis). Positive pressure ventilation Conversely, improvement in V Q matching occurs when PEEP displaces the diaphragm to the nondependent regions of the lung. is applied to patients who have refractory hypoxemia resulting 328 CHAPTER 17 Effects of Positive Pressure Ventilation on the Pulmonary System hypoventilation and hyperventilation. Patients may additionally Normal alveolar demonstrate metabolic acid-base imbalances that can seriously Normal filling affect their ventilatory management. vessel size Hypoventilation Acute hypoventilation can occur in patients receiving ventilatory support if adequate alveolar ventilation is not achieved. Hypo- ventilation will result in an elevated PaCO2 (i.e., hypercapnia) and an acidotic pH. Evaluation of clinical signs and symptoms, as well as an ABG analysis, will lead to recognition of the problem. Acidosis causes a right shift in the oxyhemoglobin dissociation Overdistention curve and reduces the ability of hemoglobin to bind and carry O2 of alveolus in the lung. Additionally, in the absence of supplemental O2 de- livery, an increase in PaCO2 will lead to proportionate decreases in Thinning of pulmonary capillary PaO2 and contribute to hypoxemia. If the patient already had hypoxemia, these factors may further reduce oxygenation. On the Fig. 17.7 The shaded area represents a normal alveolar volume. Overfilling of an other hand, a right shift of the curve facilitates unloading of O2 at alveolus results in thinning and compression of the pulmonary capillary. Pulmonary the tissue level. vascular resistance is increased. Rapidly rising PaCO2 levels and falling pH values can lead to serious problems, including coma. Elevated plasma hydrogen ion from a decreased FRC and increased shunting (i.e., ARDS). PEEP levels can contribute to high plasma potassium levels (hyper- reduces intrapulmonary shunting, resulting in an increase in PaO2 kalemia), which can affect cardiac function and lead to cardiac  dysrhythmias (Box 17.4). Hypercapnia also increases cerebral This increase in PaO2 implies improvement in V Q matching.2 6 55 perfusion and can lead to increased intracranial pressure (ICP), A classic and predictable response of gas distribution and pul- which can be detrimental to patients with cerebral trauma, cerebral monary perfusion during positive pressure ventilation apparently hemorrhage, or similar disorders. does not exist. On the other hand, in patients with ARDS, ventilation may be difficult to maintain without causing VILI. In these situations, Effects of Positive Pressure on Pulmonary permissive hypercapnia may be appropriate. In addition, hyper- Vascular Resistance capnia may reduce the release of inflammatory mediators (see As described previously, pulmonary perfusion may be compro- Chapter 13).42-44 Ultimately the decision to allow respiratory mised during positive pressure ventilation, especially when high acidosis to persist must be carefully evaluated on the basis of the levels of PEEP are also applied. Increased airway and alveolar patient s condition. pressures can lead to thinning and compression of pulmonary The kidneys can normally compensate for respiratory acidosis capillaries, decreased perfusion, and increased pulmonary vascular within 18 to 36 hours. Obviously, it is desirable for the problem to resistance (PVR) (Fig. 17.7). Fortunately, if expiration is prolonged be corrected by increasing alveolar ventilation rather than waiting and unimpeded (i.e., PEEP is not applied), the decreased pulmo- for renal compensation. Increasing ventilation can be accom- nary perfusion may be offset by normal flow back into the thorax plished by increasing the VT or mandatory rate. during expiration with no net effect on PVR. In most patients, severe hypoxia leads to increased PVR. This is caused by constriction of the pulmonary vessels and subsequent pulmonary hypertension. When mechanical ventilation improves BOX 17.4 Clinical and Electrocardiographic (ECG) oxygenation by opening these capillary beds, pulmonary perfusion Changes Associated With Respiratory and PVR may actually improve. Acidosis, Hypoxia, and Hyperkalemia At low lung volumes in which FRC is decreased, the addition of PEEP can potentially open collapsed alveoli, recruiting intra- Clinical Signs and Symptoms   Hypertension (mild to moderate acidosis) parenchymal (e.g., corner) vessels. This improves the V Q re- lations of the lungs. Thus positive pressure ventilation has no clear  Hypotension (severe acidosis)  Anxiety effect with or without PEEP on PVR. Sometimes positive pressure  Agitation reduces PVR, whereas at other times it increases PVR.  “Fighting the ventilator” (ventilator asynchrony)  Dyspnea  Attempts to increase minute ventilation RESPIRATORY AND METABOLIC ACID-BASE  Headaches STATUS IN MECHANICAL VENTILATION  Hot, moist skin (associated with increased PaCO2) The primary goal of mechanical ventilation is to maintain ECG Changes Associated With Hyperkalemia acceptable arterial blood gas (ABG) values in patients with  Elevated and peaked T waves compromised ventilatory function. Failure to achieve this goal  ST-segment depression occurs when the ventilator is not optimally adjusted or when  Widened QRS complex adverse effects occur. As previously noted, ventilatory problems  Long P-R interval associated with positive pressure ventilation can result in  Effects of Positive Pressure Ventilation on the Pulmonary System CHAPTER 17 329 When respiratory acidosis is present, patients receiving controlled mechanical ventilation may try to override the venti- Case Study 17.3 lator and take in a breath. They may not be able to trigger the Appropriate Ventilator Changes machine or receive adequate flow and will appear to be fighting the A 60-kg female patient has been maintained on mechan- ventilator. Increasing the sensitivity or flow will allow the patient ical ventilation for 7 days. The patient’s normal baseline to trigger the ventilator and receive an adequate breath. (See the ABG values on room air are pH of 7.38, PaCO2 of 51 mm Hg, discussion of ventilator asynchrony in this chapter.) PaO2 of 58 mm Hg, and HCO3 of 29 mEq/L. Current ABGs on volume-controlled intermittent mandatory ventilation Hyperventilation (VC-IMV) at a mandatory rate of 8 breaths/min, VT of Hyperventilation results in a lower than normal PaCO2 and a rise 600 mL, and F O2 of 0.25 at a pH of 7.41, PaCO2 of 40 mm in pH. Patient-induced hyperventilation is often associated with Hg, PaO2 of 67 mm Hg, and HCO3 of 24 mEq/L. The patient hypoxemia, pain and anxiety syndromes, circulatory failure, and is not breathing spontaneously. The VC-IMV mandatory airway inflammation. Ventilator-induced hyperventilation is rate is reduced to 4 breaths/min. The patient’s sponta- generally caused by inappropriate ventilator settings. Alkalosis neous rate increases to 28 breaths/min, with a sponta- causes a left shift in the O2 dissociation curve, which enhances the neous VT of 250 mL; SpO2 drops from 95% to 91%. The ability of hemoglobin to pick up O2 in the lungs but makes it less patient appears anxious. What could be the source of this available at the tissue level (i.e., the Haldane effect). Reduced patient’s problem? hydrogen ion concentrations in the blood (i.e., arterial pH) are often accompanied by hypokalemia (low potassium levels), which can lead to cardiac arrhythmias (Box 17.5). Sustained severe hypocapnia can lead to tetany and also reduces cerebral perfusion, which may contribute to increased cerebral apnea will remain until the PaO2 drops low enough to stimulate hypoxia. In patients with increased ICP and cerebral edema, the peripheral chemoreceptors. however, this reduced perfusion may be beneficial in reducing If chronic hyperventilation and respiratory alkalosis are sus- acute abnormally high ICPs that cannot be controlled by other tained for an extended period (e.g., typically 18 36 hours), renal methods (see Chapter 7). compensation will occur. The kidneys remove bicarbonate from Hyperventilation in mechanically ventilated patients reduces the plasma, and it is excreted in the urine. Simultaneously, bi- the drive to breathe and leads to apnea. This has the advantage of carbonate is actively transported out of the CSF so that CSF bal- preventing the patient from trying to “fight” the ventilator or ances with the plasma bicarbonate. The pH is restored to normal experiencing feelings of dyspnea. The disadvantage is that weaning in both the plasma and CSF. The bicarbonate and PCO2 levels will becomes more difficult if the respiratory alkalosis persists for a be lower than normal. prolonged period. With extended periods of hyperventilation, It is important to note that weaning becomes more difficult when respiratory muscle activity is absent, respiratory muscle at- when a patient has experienced prolonged hyperventilation. As the rophy can occur. In addition, the central chemoreceptors, which respiratory rate of the ventilator is reduced, the blood PCO2 in- respond to changes in PCO2 and pH, will have an altered function. creases and pH falls. The patient tries to maintain a high alveolar When respiratory alkalosis occurs, carbon dioxide (CO2) diffuses ventilation to keep the PCO2 at the level at which it has been out of the cerebrospinal fluid (CSF) because of the low blood CO2 equilibrated. The patient may become fatigued and unable to level. The hydrogen ion concentration in the CSF decreases, and maintain the high levels of alveolar ventilation. Consequently, the respirations are not stimulated. As long as this condition persists, PaCO2 continues to rise. The CO2 diffuses into the CSF, where the pH will fall. This stimulates the central receptors to increase ventilation, but the patient may not be able to increase ventilation. Thus weaning is difficult until the patient s normal bicarbonate BOX 17.5 Clinical and Electrocardiographic (ECG) and PaCO2 levels are reestablished and the pH level returns to the Changes Associated With Respiratory patient s normal value (Case Study 17.3). Alkalosis and Hypokalemia Metabolic Acid-Base Imbalances and Clinical Signs and Symptoms Mechanical Ventilation  Cool skin (decreased PaCO2) When a patient receives adequate alveolar ventilation, PaCO2 and  Twitching pH levels can be expected to be near that patient s normal (i.e.,  Tetany eucapnic breathing). If the PaCO2 is near the patient s normal but the pH is not, the cause is probably a metabolic abnormality that ECG Changes Associated With Hypokalemia should be corrected. Severe metabolic acidosis may require the  Prolonged Q-T interval administration of bicarbonate, although its use is controversial.  Low, rounded T waves Intravenous administration of bicarbonate is indicated in the  Depressed ST segment presence of life-threatening hyperkalemia either caused by or  Inverted T waves associated with metabolic acidosis.56 It is also indicated in cases of  Inverted P waves  Atrioventricular block salicylate toxicity.56 When administered, bicarbonate is given  Premature ventricular contractions slowly and not by bolus. An estimate of the bicarbonate replace-  Paroxysmal tachycardia ment required can be determined by multiplying one third of the  Atrial flutter patient s body weight in kilograms by the base excess (BE). Generally, only half of the deficit should be corrected initially (this 330 CHAPTER 17 Effects of Positive Pressure Ventilation on the Pulmonary System TABLE 17.1 Blood Chemistry in Metabolic Acidosis and Alkalosis Serum Sodium Serum Chloride Serum Potassium Arterial Blood pH P aCO2 Alkalosis / or Y Y / or Y [ / or [ Acidosis / or [ [ / or [ Y Y [, Increase; Y, decrease; /, no change. Normal values: sodium, 135 145 mEq/L; chloride, 98 106 mEq/L; potassium, 3.5 5.0 mEq/L; pH, 7.35 7.45; PaCO2, 35 45 mm Hg. allows for the patient s compensatory mechanisms to contribute to Normal FRC the correction), so the product is divided by two: ð1=3Kg  BEÞ HCO3 required ¼ 2 Extrinsic PEEP If a patient is not receiving ventilation or cannot increase spontaneous ventilation, the additional bicarbonate will combine Auto-PEEP with plasma hydrogen ions and increase CO2 production. If the CO2 is retained, the acidosis may increase. Metabolic alkalosis is most often associated with loss of acid from the gastrointestinal tract (e.g., vomiting) or through the kidneys (e.g., diuretic administration). It may also result from excess base that is gained by either oral or parenteral bicarbonate Fig. 17.8 Alveolar filling. The smallest circle represents resting functional residual administration or administration of lactate, acetate, or citrate. capacity (FRC) under normal conditions. The second circle represents the addition of Normally the body will correct a mild to moderate metabolic extrinsic positive end-expiratory pressure (PEEP). The largest circle shows the resting alkalosis if the cause is removed. On the other hand, if the alkalosis lung volume with auto-PEEP also present. is severe, prompt action is necessary. Administration of carbonic anhydrase inhibitors, acid infusion (ammonium chloride or po- tassium chloride), or low-sodium dialysis may be necessary.57 (Fig. 17.8). Auto-PEEP is also referred to as occult PEEP, inad- Table 17.1 provides a summary of abnormalities in blood chem- vertent PEEP, breath stacking, and intrinsic PEEP. istry that are associated with metabolic acidosis and alkalosis. Because air trapping is not typically measured or detectable, its occurrence is an even greater threat. When air trapping occurs in spontaneously breathing, intubated patients, the inspiratory WOB AIR TRAPPING (AUTO-PEEP) increases, making it more difficult for them to inhale. Auto-PEEP can lead to barotrauma by trapping large volumes of air in the lung When airway resistance is increased in spontaneously breathing at the end of exhalation.59 60 Alveolar overinflation can be life individuals, both inspiratory and expiratory flows are impeded. threatening in patients with acute, severe asthma who are receiving Severe airflow obstruction increases the time needed for exhala- ventilatory support. The risk for tension pneumothorax and cir- tion. This can occur in patients with severe chronic obstructive culatory depression is increased in this group of patients. pulmonary disease (COPD), status asthmaticus, or similar prob- lems. The loss of structural quality of the conductive airways re- How Auto-PEEP Occurs sults in small or medium airways closing off or collapsing during An expiratory time (TE) of at least three to four time constants is exhalation, increasing FRC. Increased airway resistance reduces required for the lungs to empty 98% of the inspired volume. When the patient s ability to exhale in a normal amount of time TE is decreased, complete emptying of the lungs to their normal (increased time constants).58 resting lung volume (FRC) is prevented. For example, suppose TE When air trapping occurs, particularly with positive pressure is shortened on a ventilated patient so that exhalation is incom- ventilation, the increased alveolar pressure is transmitted to the plete. For a few breaths, pressure builds and exhaled volume is intrapleural space, creating an undesired PEEP effect. This reduces lower than delivered volume. As a progressively higher FRC is venous return and cardiac output. Artificially high intravascular produced, tissue recoil increases, so the force (pressure) pushing pressures result, such as an increase in pulmonary artery occlusion air out of the lungs increases. This higher pressure helps splint the pressure, which normally reflects left heart function.58 When this airways open (diameter increases). The airway resistance to occurs during positive pressure ventilation, it is commonly exhaled flow decreases. Within a few breaths the lung volumes referred to as auto-PEEP. stabilize at an elevated FRC. At this point the ventilator VT Auto-PEEP is defined as an unintentional PEEP that occurs delivered can also be exhaled (Fig. 17.9).58 The result, however, is a during mechanical ventilation when a new inspiratory breath be- higher FRC than normal and higher alveolar pressures at end gins before expiratory flow has ended. It is an insidious compli- expiration (auto-PEEP without lung distention). cation that may not be apparent unless the practitioner is looking for it. Auto-PEEP differs from operator-set PEEP (applied or Physiological Factors That Lead to Auto-PEEP extrinsic PEEP [PEEPE]), which is a selected value at the end of Auto-PEEP occurs in the following three distinct forms: expiration. Total PEEP is the sum of auto-PEEP and PEEPE and is 1. Auto-PEEP can occur because the expiratory muscles are a measure of the total pressure in the lungs at end exhalation actively contracting during exhalation. This raises alveolar  Effects of Positive Pressure Ventilation on the Pulmonary System CHAPTER 17 331 Inspiration Normal VT Patient Volume Flow (L/min) Trapped Time (s) volume } FRC Air trapping Auto-PEEP Time Expiration Fig. 17.9 Volume of trapped air above the functional residual capacity (FRC) as a result of auto positive end-expiratory pressure (PEEP). The gradual rise in volume shows the progressive trapping of air in the lungs. (Redrawn from Tuxen Fig. 17.10 Flow-time waveform showing a normal expiratory flow pattern during DV: Detrimental effects of positive end-expiratory pressure during controlled exhalation (dotted line) compared with a patient with air trapping (auto-PEEP) where mechanical ventilation of patients with severe airflow obstruction, Am Rev Respir flow does not return to zero during exhalation (solid line). PEEP, Positive end- Dis 140:145, 1989.) expiratory pressure. (From Dhand R: Ventilator graphics and respiratory mechanics in the patient with obstructive lung disease [conference proceedings], Respir Care 50:246 261, 2005.) pressures at end exhalation without increasing the volume at end exhalation (auto-PEEP without lung distention). breath sounds and an increase in resonance on percussion of the 2. Auto-PEEP can occur in patients who do not have airway chest wall. Chest radiographs may show increased radiolucency. obstruction. In patients with normal airway resistance, air The amount of auto-PEEP present in the patient s lungs at end trapping can occur with the presence of high minute ventila- exhalation is normally not registered on the ventilator manometer. tion, short expiratory times, and mechanical devices that in- During exhalation, the expiratory valve is usually open to atmo- crease expiratory resistance (e.g., small ETs, high-resistance sphere, assuming no extrinsic PEEP is being used (Fig. 17.11). expiratory valves, certain PEEP devices). Total expiratory Pressure in the circuit is zero because the manometer measures resistance across the lungs, ET, and exhalation line and valve atmospheric pressure, but air may still be actively flowing out of is normally less than 4 cm H2O/L/s. the patient s lungs. When inspiration triggers, some of this volume 3. Auto-PEEP also occurs in patients with airflow obstruction remains in the patient s lungs. This adds to normal FRC. However, who tend to have airway collapse during exhalation and flow this pressure remains undetected. limitation during normal tidal breathing. In these individuals, Many intensive care unit (ICU) ventilators have end-expiratory an increased expiratory effort only increases the alveolar pres- pause buttons for measuring auto-PEEP. There has been some sure and does not improve expiratory flow. debate regarding the accuracy of this method of measuring auto- The last two result in dynamic hyperinflation, or the failure of PEEP.68 69 This technique can provide a reference for the pres- lung volume to return to passive FRC during exhalation by the ence of auto-PEEP. time inspiration again begins. The level of auto-PEEP cannot be Another method for measuring auto-PEEP uses a Braschi valve accurately predicted. The following factors increase the risk for (Fig. 17.12). The Braschi valve, which is a T-piece, or Briggs, auto-PEEP58 61-66: adapter, is positioned inline on the inspiratory side of the patient  Chronic obstructive airway disease circuit. A manometer is placed near the patient to measure airway  High minute ventilation (more than 10 20 L/min) in patients pressure. Part of the T-piece has an opening that is normally on ventilation capped but is uncapped during auto-PEEP measurement. A one-  Age older than 60 years way valve is another part of the T-piece and allows flow to go  Increased airway resistance (e.g., small ET size, bronchospasm, from the ventilator to the patient during normal ventilation. increased secretions, mucosal edema) To measure auto-PEEP, the cap is removed during exhalation.  Increased lung compliance (longer time constants) When the next breath begins, inspiratory flow from the ventilator  High respiratory frequency is diverted out the uncapped hole and to the room. The expiratory  High inspiratory-to-expiratory ratios, that is short TE (e.g., 1:1 valve is closed during inspiration (normal function of the venti- and 2:1); low inspiratory flow lator during inspiration). The patient continues to exhale, but the  Increased VT, particularly with airflow obstruction expiratory valve is closed. As a result, the pressure equilibrates between the patient s lungs and the ventilator circuit. The pressure Identifying and Measuring Auto-PEEP can then be read on the manometer. This procedure may be more As discussed in Chapter 9, the easiest way to detect air trapping accurate than occluding the exhalation valve because pressure is is to evaluate the flow-time curve on the ventilator s graphic measured closer to the patient. One disadvantage is that the display. If the expiratory flow does not return to zero before the measurement is made only during the length of inspiration. If the next inspiration begins, auto-PEEP is present (Fig. 17.10).67 Air pressure does not have enough time to equilibrate, the pressure trapping can also be detected by using flow-volume loops. reading may be underestimated. Air trapping can be identified during volume ventilation by Detecting auto-PEEP by measuring end-expiratory pressure observing changes in pressure and volume. Peak and plateau requires a quiet, relaxed patient on controlled ventilation. The pressures will increase, and a transient reduction in exhaled vol- patient cannot be assisting or breathing spontaneously because an umes will occur. Physical examination reveals a reduction in actively breathing patient may forcibly inhale or exhale during 332 CHAPTER 17 Effects of Positive Pressure Ventilation on the Pulmonary System Exhalation valve open to room air Pressure manometer Pressure No flow cm H2O P0 Cap Main inspiratory line Pressure manometer connects to inspiratory side of circuit One-way A valve 0 Expiratory valve Main expiratory line Patient connector P  15 Fig. 17.12 Braschi valve used to measure auto positive end-expiratory pressure. Continuous expiratory flow (See text for explanation.) Case Study 17.4 Manometer still shows zero B Difficulty Triggering in a Patient With Chronic Obstructive Pulmonary Disease (COPD) Exhalation valve closed at A patient with COPD is receiving volume-controlled beginning of inspiration continuous mandatory ventilation (VC-CMV) mode. The set tidal volume (VT) is increased from 500 to 700 mL, and 15 the rate is increased from 10 to 18 breaths/min. The res- piratory therapist notices a progressive rise in peak pres- P  15 sures; VTs transiently are less than 650 mL after the change. Inspiratory flow Eventually the exhaled VT reads 650 mL. Baseline pressure prevented remains at zero. The patient appears unable to trigger a breath and is using accessory muscles to trigger the Condition of no flow breath. What is the most likely cause of this problem? C 1.5 Fig. 17.11 A mechanical ventilator connected to a lung under normal conditions and until mouth pressure exceeds this value.70 The presence of auto- also when auto-PEEP is present. (A) Ventilator system during normal exhalation, with PEEP will also make it more difficult for spontaneously breath- no air trapping and no auto-PEEP. The manometer reading is zero. (B) During ing patients to trigger a ventilator breath even when sensitivity exhalation with auto-PEEP present, the manometer still reads zero (ambient) because settings are appropriate (Case Study 17.4). (See Chapter 7 for a the exhalation valve is open to room air. (C) When the exhalation valve is closed and detailed discussion of how to adjust ventilator settings to minimize inspiratory flow stopped at end exhalation and before the next breath, a manometer the effects of auto-PEEP.) will be able to read the approximate auto-PEEP level in the lungs and circuit. PEEP, Positive end-expiratory pressure. (Redrawn from Pepe PE, Marini JJ: Occult positive Measuring Static Compliance With Auto-PEEP end-expiratory pressure in mechanically ventilated patients with airflow obstruction, Static compliance values are normally calculated as VT/(Pplat Am Rev Respir Dis 126:166, 1982.) PEEP). For this calculation to be accurate, the PEEP value must include the set (applied) PEEP and any auto-PEEP present.71 measurement and alter the results. Whether the patient should be Methods of Reducing Auto-PEEP sedated or paralyzed to measure auto-PEEP depends on the pa- To reduce auto-PEEP, higher inspiratory gas flows should be used tient s pulmonary pathophysiology and the physician s assessment to shorten inspiratory time and allow a longer time for exhalation of the patient s condition. In addition, there should be no circuit (TE). Longer TE can also be accomplished by using smaller VTs leaks when making the auto-PEEP measurement. and decreased respiratory rates. Use of low-resistance exhalation valves, changing partially obstructed expiratory filters, and using Effect on Ventilator Function large ETs may also reduce air trapping. The presence of auto-PEEP will actually slow the beginning of gas Sometimes severe airway obstruction or high minute ventila- flow during inspiration. If alveolar pressure is higher than ambient tion demands make reduction of auto-PEEP impossible. Some at the end of exhalation (auto-PEEP), flow delivery will not start clinicians recommend hypoventilation (permissive hypercapnia)  Effects of Positive Pressure Ventilation on the Pulmonary System CHAPTER 17 333 under these circumstances (see Chapter 12). This may actually be Absorption Atelectasis preferable to the complications that occur with auto-PEEP. High O2 concentrations (>70% O2) lead to rapid absorption atel- Another alternative is to use methods of ventilation that allow as ectasis, particularly in hypoventilated lung units.77-80 In one study, much spontaneous ventilation to occur as the patient can tolerate. 40% O2 or 100% O2 was administered after a recruitment maneuver Intermittent mandatory ventilation (IMV), pressure support, had been performed on patients undergoing general anesthesia. In continuous positive airway pressure, and airway pressure release lungs receiving ventilation with 40% O2, lung expansion was sus- ventilation may be beneficial in these situations. tained. In patients on ventilation with 100% O2, lung collapse reappeared within minutes.79 Furthermore, absorption atelectasis HAZARDS OF OXYGEN THERAPY WITH has been shown to increase the level of intrapulmonary shunting. In patients on mechanical ventilation, this is always a concern when MECHANICAL VENTILATION providing ventilation for patients with low VTs. Oxygen Toxicity and the Lower Limits of Hypoxemia Depression of Ventilation It is generally agreed that breathing enriched O2 mixtures for an In patients with chronic CO2 retention (e.g., COPD), breathing extended period increases the risk for pulmonary complications. high O2 levels can increase PaCO2. This is partly caused by the Indeed, adults breathing a gas mixture containing an FIO2 of more Haldane effect, which increases the unloading of CO2 from the than 0.6 for prolonged periods (>48 hours), or maintaining a PaO2 hemoglobin. It is also caused by an improvement in blood flow to of more than 80 mm Hg in a newborn or premature infant, can lung units that are not well ventilated. As increased O2 reduces lead to pulmonary O2 toxicity.24 Adults can generally breathe an pulmonary vasoconstriction to these units, CO2 may increase. Less FIO2 of up to 0.5 for extended periods without significant lung likely but still possible is a suppression of the hypoxic drive to damage.72 73 breathe. However, in mechanically ventilated COPD patients, this The use of 100% O2 can induce pulmonary changes in humans should not be a problem if adequate alveolar ventilation is in as little as 6 hours. Pulmonary changes associated with high O2 maintained. concentrations are listed in Box 17.6 24 74 75 Exposures for more than 72 hours can result in the development of a pattern that is similar to ARDS.75 However, resistance to O2 toxicity varies. In INCREASED WORK OF BREATHING fact, studies suggest normal lung tissues may be more susceptible to O2 damage than diseased tissue.74 Increased WOB is another common complication associated with The chest radiographs of most patients with acute respiratory artificial airways and mechanical ventilation systems. Fatigue can failure are abnormal because of their underlying lung pathology. result from increased WOB, which can be both intrinsic and As a result, assessment of the onset of O2 toxicity is often difficult. extrinsic.81-86 If an FIO2 of greater than 0.6 is required, other techniques such as PEEP should be instituted (see Chapter 13). The improvement in System-Imposed Work of Breathing oxygenation that occurs when PEEP is initiated often allows the Until IMV became a popular mode of ventilation in the 1970s, FIO2 to be reduced. Prone positioning may also be of value (see WOB was not a major concern for clinicians. Most clinicians Chapter 13). assumed that the ventilator performed most, if not all, of the WOB The lower limits of permissive hypoxemia remain controver- when a patient was receiving continuous mandatory ventilation sial. In general, most clinicians agree that a target PaO2 of 60 mm (CMV). It is now recognized that WOB during volume-controlled Hg and an SpO2 of 90% are acceptable lower limits.74 76 77 IMV (VC-IMV) can be greater than that required for other modes.84 87 During VC-IMV with PSV, when the patient s effort is reduced (e.g., sedation, sleep, high level of assist), the time interval between BOX 17.6 Pulmonary Changes Associated With the onset of the patient s effort and the final ventilator triggering of Oxygen Toxicity inspiration increases. In