A low-flow oxygen delivery system provides supplemental oxygen directly into the patient’s airway at a flow of 8 L/min or less. Because this flow is insufficient to meet the patient’s inspiratory volume requirements, it results in a variable FiO₂ as the supplemental oxygen is mixed with room air. The patient’s ventilatory pattern affects the FiO₂ of a low-flow system: as the ventilatory pattern changes, differing amounts of room air gas are mixed with the constant flow of oxygen. A nasal cannula is an example of a low-flow device.3

A reservoir system incorporates some type of device to collect and store oxygen between breaths. When the patient’s inspiratory flow exceeds the oxygen flow of the oxygen delivery system, the patient is able to draw from the reservoir of oxygen to meet his or her inspiratory volume needs. There is less mixing of the inspired oxygen with room air than in a low-flow system. A reservoir oxygen delivery system can deliver a higher FiO₂ than a low-flow system. Examples of reservoir systems are simple face masks, partial rebreathing masks, and nonrebreathing masks.3

With a high-flow system, the oxygen flows out of the device and into the patient’s airways in an amount sufficient to meet all inspiratory volume requirements. This type of system is not affected by the patient’s ventilatory pattern. An air-entrainment mask is an example of a high-flow system.3

The most detrimental effect of breathing a high concentration of oxygen is the development of oxygen toxicity. It can occur in any patient who breathes oxygen concentrations of greater than 50% for longer than 24 hours. Patients most likely to develop oxygen toxicity are those who require intubation, mechanical ventilation, and high oxygen concentrations for extended periods.3

Hyperoxia, or the administration of higher-than-normal oxygen concentrations, produces an overabundance of oxygen free radicals. These radicals are responsible for the initial damage to the alveolar-capillary membrane. Oxygen free radicals are toxic metabolites of oxygen metabolism. Normally, enzymes neutralize the radicals, preventing any damage from occurring. During the administration of high levels of oxygen, the large number of oxygen free radicals produced exhausts the supply of neutralizing enzymes. Damage to the lung parenchyma and vasculature occurs, resulting in the initiation of acute lung injury (ALI).^2,4

A number of clinical manifestations are associated with oxygen toxicity. The first symptom is substernal chest pain that is exacerbated by deep breathing. A dry cough and tracheal irritation follow. Eventually, there is definite pleuritic pain on inhalation, followed by dyspnea. Upper airway changes may include a sensation of nasal stuffiness, sore throat, and eye and ear discomforts. Chest radiographs and pulmonary function tests show no abnormalities until symptoms are severe. Complete, rapid reversal of these symptoms occurs as soon as normal oxygen concentrations are restored.⁴

In patients with severe chronic obstructive pulmonary disease (COPD), carbon dioxide (CO₂) retention may occur as a result of administration of oxygen in high concentrations. A number of theories have been proposed for this phenomenon. One states that the normal stimulus to breathe (i.e., increasing CO₂ levels) is muted in patients with COPD and that decreasing oxygen levels become the stimulus to breathe. If hypoxemia is corrected by the administration of oxygen, the stimulus to breathe is abolished; hypoventilation develops, resulting in a further increase in the arterial partial pressure of carbon dioxide (PaCO₂).2,3 Another theory is that the administration of oxygen abolishes the compensatory response of hypoxic pulmonary vasoconstriction. This results in an increase in perfusion of underventilated alveoli and the development of dead space, producing ventilation/perfusion mismatching. As alveolar dead space increases, so does the retention of CO₂.^2,3,5 One further theory states that the rise in CO₂ is related to the ratio of deoxygenated to oxygenated hemoglobin (Haldane effect). Deoxygenated hemoglobin carries more CO₂ than oxygenated hemoglobin. Administration of oxygen increases the proportion of oxygenated hemoglobin, which causes increased release of CO₂ at the lung level.⁵ Because of the risk of CO₂ accumulation, all chronically hypercapnic patients require careful low-flow oxygen administration.³

Another adverse effect of high concentrations of oxygen is absorption atelectasis. Breathing high concentrations of oxygen washes out the nitrogen that normally fills the alveoli and helps hold them open (residual volume). As oxygen replaces the nitrogen in the alveoli, the alveoli start to shrink and collapse. This occurs because oxygen is absorbed into the bloodstream faster than it can be replaced in the alveoli, particularly in areas of the lungs that are minimally ventilated.2,3

An oropharyngeal airway is made of plastic and is available in various sizes. The proper size is selected by holding the airway against the side of the patient’s face and ensuring that it extends from the corner of the mouth to the angle of the jaw. If the airway is improperly sized, it will occlude the airway.6,7 An oral airway is placed by inserting a tongue depressor into the patient’s mouth to displace the tongue downward and then passing the airway into the patient’s mouth, slipping it over the patient’s tongue.⁷ When properly placed, the tip of the airway lies above the epiglottis at the base of the tongue. It should be used only in an unconscious patient who has an absent or diminished gag reflex.^6,7

A nasopharyngeal airway is usually made of plastic or rubber and is available in various sizes. The proper size is selected by holding the airway against the side of the patient’s face and ensuring that it extends from the tip of the nose to the earlobe.6,7 A nasal airway is placed by lubricating the tube and inserting it midline along the floor of the naris into the posterior pharynx.⁷ When properly placed, the tip of the airway lies above the epiglottis at the base of the tongue.^6,7

Before intubation, the necessary equipment is gathered and organized to facilitate the procedure. Readily available equipment should include a suction system with catheters and tonsil suction, an MRB with a mask connected to 100% oxygen, a laryngoscope handle with assorted blades, a variety of sizes of ETTs, and a stylet. Before the procedure is initiated, all equipment is inspected to ensure that it is in working order. The patient should be prepared for the procedure, if possible, with an intravenous catheter in place, and should be monitored with a pulse oximeter. The patient is sedated before the procedure (as clinical condition allows), and a topical anesthetic is applied to facilitate placement of the tube. In some cases, a paralytic agent may be necessary if the patient is extremely agitated.9,11,14

The procedure is initiated by positioning the patient with the neck flexed and head slightly extended in the “sniff” position. The oral cavity and pharynx are suctioned, and any dental devices are removed. The patient is preoxygenated and ventilated using the MRB and mask with 100% oxygen. Each intubation attempt is limited to 30 seconds. After the ETT is inserted, the patient is assessed for bilateral breath sounds and chest movement. Absence of breath sounds is indicative of an esophageal intubation, whereas breath sounds heard over only one side is indicative of a main stem intubation. A disposable end-tidal CO₂ detector is used to initially verify correct airway placement, after which the cuff of the tube is inflated and the tube is secured. Finally, a chest radiograph is obtained to confirm placement.^9–11 The tip of the ETT should be approximately 3 to 4 cm above the carina when the patient’s head is in the neutral position.¹⁰ After final adjustment of the position is complete, the level of insertion (marked in centimeters on the side of the tube) at the teeth is noted.^9,10,14

A number of complications can occur during the intubation procedure, including nasal and oral trauma, pharyngeal and hypopharyngeal trauma, vomiting with aspiration, and cardiac arrest.¹⁴ Hypoxemia and hypercapnia can also occur, resulting in bradycardia, tachycardia, dysrhythmias, hypertension, and hypotension.^8,12,14

Several complications can occur while the ETT is in place, including nasal and oral inflammation and ulceration, sinusitis and otitis, laryngeal and tracheal injuries, and tube obstruction and displacement. Other complications can occur days to weeks after the ETT is removed, including laryngeal and tracheal stenosis and a cricoid abscess (Table 16-3). Delayed complications usually require some form of surgical intervention.¹⁵

A tracheostomy tube is inserted by an open procedure or a percutaneous procedure. An open procedure is usually performed in the operating room, whereas a percutaneous procedure can be done at the patient’s bedside.18

A number of complications can occur during the tracheostomy procedure, including misplacement of the tracheal tube, hemorrhage, laryngeal nerve injury, pneumothorax, pneumomediastinum, and cardiac arrest.^15,18

Several complications can occur while the tracheostomy tube is in place, including stomal infection, hemorrhage, tracheomalacia, tracheoesophageal fistula, tracheoinnominate artery fistula, and tube obstruction and displacement.18

A number of complications can occur days to weeks after the tracheostomy tube is removed, including tracheal stenosis and tracheocutaneous fistula (Table 16-4). Delayed complications usually require some form of surgical intervention.¹⁸

Humidification of air normally is performed by the mucosal layer of the upper respiratory tract. When this area is bypassed, as occurs with ETT and tracheostomy tubes, or when supplemental oxygen is used, humidification by external means is necessary. Various humidification devices add water to inhaled gas to prevent drying and irritation of the respiratory tract, to prevent undue loss of body water, and to facilitate secretion removal.19,20 The humidification device should provide inspired gas conditioned (heated) to body temperature and saturated with water vapor.²¹

Because the cuff of the ETT or tracheostomy tube is a major source of the complications associated with artificial airways, proper cuff management is essential. To prevent the complications associated with cuff design, only low-pressure, high-volume cuffed tubes are used in clinical practice.13,22 Even with these tubes, cuff pressures can be generated that are high enough to lead to tracheal ischemia and injury. Proper cuff inflation techniques and cuff pressure monitoring are critical components of the care of the patient with an artificial airway.^10,22

Suctioning is often required to maintain a patent airway in the patient with an ETT or tracheostomy tube. Suctioning is a sterile procedure that is performed only when the patient needs it and not on a routine schedule.10,24 Indications for suctioning include coughing, secretions in the airway, respiratory distress, presence of rhonchi on auscultation, increased peak airway pressures on the ventilator, and decreasing oxygenation saturation.¹¹ Complications associated with suctioning include hypoxemia, atelectasis, bronchospasms, dysrhythmias, increased intracranial pressure, and airway trauma.^11,24

Closed Tracheal Suction System

One device to facilitate the suctioning of a patient on a ventilator is the closed tracheal suction system (CTSS) (Figure 16-3). This device consists of a suction catheter in a plastic sleeve that attaches directly to the ventilator tubing. It allows the patient to be suctioned while remaining on the ventilator. Advantages of the CTSS include maintenance of oxygenation and PEEP during suctioning, reduction of hypoxemia-related complications, and protection of staff members from the patient’s secretions. The CTSS is convenient to use, requiring only one person to perform the procedure.

Concerns related to the CTSS include autocontamination, inadequate removal of secretions, and increased risk of unintentional extubation resulting from the extra weight of the system on the ventilator tubing. Autocontamination has been shown not to be an issue if the catheter is cleaned properly after every use. Inadequate removal of secretions may or may not be a problem, and further investigation is required to settle this issue.¹¹ Although recommendations for changing the catheter vary, one study indicated that the catheter could be changed on an as-needed basis without increasing the incidence of HAP.³¹

One of the major stressors for the patient with an artificial airway is impaired communication. This is related to the inability to speak, insufficient explanations from staff members, inadequate understanding, fear of being unable to communicate, and difficulty with communication methods.32 A number of interventions can facilitate communication in the patient with an ETT or tracheostomy tube. These include performing a complete assessment of the patient’s ability to communicate, teaching the patient how to communicate, using a variety of methods to communicate, and facilitating the patient’s ability to communicate by providing the patient with his or her eyeglasses or hearing aid.³³

Methods to facilitate communication in this patient population include the use of verbal and nonverbal language and a variety of devices to assist the patient on short-term and long-term ventilator assistance. Nonverbal communication may include the use of sign language, gestures, lip-reading, pointing, facial expressions, or eye blinking. Simple devices available include pencil and paper; Magic Slates; magnetic boards with plastic letters; picture, alphabet, or symbol boards; and flash cards. More sophisticated devices include typewriters, computers, talking ETT and tracheostomy tubes, and external handheld vibrators. Regardless of the method selected, the patient must be taught how to use the device.^10,33

Passy-Muir Valve

One device used to assist the mechanically ventilated patient with a tracheostomy to speak is the Passy-Muir valve. This one-way valve opens on inhalation, allowing air to enter the lungs through the tracheostomy tube, and closes on exhalation, forcing air over the vocal cords and out the mouth, permitting the patient to speak (Figure 16-4). Before the valve can be placed on a tracheostomy tube, the cuff must be deflated to allow air to pass around the tube, and the tidal volume of the ventilator must be increased to compensate for the air leak. In addition to aiding communication, the Passy-Muir valve can assist the ventilator-dependent patient with relearning normal breathing patterns. The valve is contraindicated in patients with laryngeal or pharyngeal dysfunction, excessive secretions, or poor lung compliance.³⁴

Patients with artificial airways are extremely susceptible to developing HAP due to microaspiration of subglottic secretions. Subglottic secretions are fluids from the oropharyngeal area that pool above the inflated cuff of the ETT or tracheostomy tube. These secretions are full of microorganisms from the patient’s mouth. Because the cuff of the artificial airway does not create a tight seal in the patient’s airway, these secretions seep around the cuff and into the patient’s lungs, promoting the development of HAP.35 Although bacteria are normally present in a patient’s mouth, in the critically ill patient there are increased amounts of bacteria and more resistant bacteria. Decreased salivary flow, poor mucosal status, and dental plaque all contribute to this problem.³⁶

Proper oral hygiene has the potential to decrease the incidence of HAP.³⁷ However, recent studies have shown that routine oral care is not a priority intervention for many nurses.³⁸ Currently there is no evidence-based protocol for oral care. Research studies are lacking, particularly with regard to frequency and effectiveness of different procedures.³⁹ Most experts agree, however, that oral care should consist of brushing the patient’s teeth with a soft toothbrush to reduce plaque, brushing the patient’s tongue and gums with a foam swab to stimulate the tissue, and performing deep oropharyngeal suctioning to remove any secretions that have pooled above the patient’s cuff.^37–39 One intervention that has evidence supporting its use is rinsing the patient’s mouth with chlorhexidine (15 mL of 0.12% oropharyngeal rinse applied twice daily for 30 seconds). This procedure has been shown to reduce oral colonization of bacteria and to decrease the incidence of ventilator-associated pneumonia, particularly in cardiac surgery patients.⁴⁰

After the airway is no longer needed, it is removed. Extubation is the process of removing an ETT. It is a simple procedure that can be accomplished at the bedside.10,11 Before the cuff of an ETT or tracheostomy tube is deflated in preparation for removal, it is very important to ensure that secretions are cleared from above the tube cuff. Complications of extubation include sore throat, stridor, hoarseness, odynophagia, vocal cord immobility, pulmonary aspiration, and cough.¹⁵ Decannulation is the process of removing a tracheostomy tube. It is also a simple process that can be performed at the bedside. After removal of the tracheostomy tube, the stoma is usually covered with a dry dressing, with the expectation that it will close within several days.^10,11 Difficulty removing the tracheostomy tube because of a tight stoma is usually the only complication associated with decannulation.¹⁵

The two main types of ventilators currently available are positive-pressure ventilators and negative-pressure ventilators. Negative-pressure ventilators are applied externally to the patient and decrease the atmospheric pressure surrounding the thorax to initiate inspiration. They generally are not used in the critical care environment. Positive-pressure ventilators use a mechanical drive mechanism to force air into the patient’s lungs through an ETT or tracheostomy tube.42

The ventilator must complete four phases of ventilation to properly ventilate the patient: (1) change from exhalation to inspiration; (2) inspiration; (3) change from inspiration to exhalation; and (4) exhalation. The ventilator uses four different variables to begin, sustain, and terminate each of these phases. These variables are described in terms of volume, pressure, flow, and time.7,43,44

The term ventilator mode refers to how the machine ventilates the patient. Selection of a particular mode of ventilation determines how much the patient will participate in his or her own ventilatory pattern. The choice depends on the patient’s situation and the goals of treatment. The mode is determined by the combination of phase variables selected. Many modes are available (Table 16-5),^7,42–44 and some may be used in conjunction with others. Because brands of ventilators vary in their ability to perform certain functions, not all modes are available on all ventilators.⁴³

Settings on the ventilator allow the ventilator parameters to be individualized to the patient and also allow selection of the desired ventilation mode (Table 16-6). Each ventilator has a patient-monitoring system that allows all aspects of the patient’s ventilatory pattern to be assessed, monitored, and displayed.^42–45

Mechanical ventilation can cause two different types of injury to the lungs: air leaks and biotrauma.44,46 Air leaks related to mechanical ventilation are the result of excessive pressure in the alveoli (barotrauma), excessive volume in the alveoli (volutrauma), or shearing due to repeated opening and closing of the alveoli (atelectrauma).^44,47 Barotrauma, volutrauma, and atelectrauma can lead to excessive alveolar wall stress and damage to the alveolar-capillary membrane, resulting in air leakage into the surrounding spaces. The air then travels out through the hilum and into the mediastinum (pneumomediastinum), pleural space (pneumothorax), subcutaneous tissues (subcutaneous emphysema), pericardium (pneumopericardium), peritoneum (pneumoperitoneum), and retroperitoneum (pneumoretroperitoneum). The resultant disorders vary from the fairly benign to the potentially lethal—the most lethal of which is a pneumothorax or pneumopericardium resulting in cardiac tamponade.^44,48

Barotrauma, volutrauma, and atelectrauma can also cause the release of cellular mediators and initiation of the inflammatory-immune response. This type of ventilator-induced injury is known as biotrauma.^44,49 Biotrauma can result in the development of ALI.⁵⁰ To limit ventilator-induced lung injury, the plateau pressure (pressure needed to inflate the alveoli) should be kept at less than 32 cm H₂O, PEEP should be used to avoid end-expiratory collapse and reopening, and the tidal volume should be set at 6 to 10 mL/kg.^46,49

Positive-pressure ventilation increases intrathoracic pressure, which decreases venous return to the right side of the heart. Impaired venous return decreases preload, which results in a decrease in cardiac output. As a secondary consequence, hepatic and renal dysfunction may occur. Positive-pressure ventilation impairs cerebral venous return. In patients with impaired autoregulation, positive-pressure ventilation can result in increased intracranial pressure.44,51

Gastrointestinal disturbances can occur as a result of positive-pressure ventilation. Gastric distention occurs when air leaks around the ETT or tracheostomy tube cuff and overcomes the resistance of the lower esophageal sphincter.7 Vomiting can occur as a result of pharyngeal stimulation from the artificial airway.¹⁵ These problems can be prevented by inserting a nasogastric tube and ensuring appropriate cuff inflation. Hypomotility and constipation may occur as a result of immobility and the administration of paralytic agents, analgesics, and sedatives.⁷

Because the ventilatory pattern is normally initiated by the establishment of negative pressure within the chest, the application of positive pressure can lead to patient difficulties in breathing while on the ventilator. To achieve optimal ventilatory assistance, the patient should breathe in synchrony with the machine. The selected mode of ventilation, the settings, and the type of ventilatory circuitry used can increase the work of breathing and lead to breathing out of synchrony with the ventilator. Patient-ventilatory dyssynchrony can result in decreased effectiveness of mechanical ventilation, the development of auto-PEEP, and psychological distress. Patients who are not breathing in synchrony with the ventilator appear to be fighting or “bucking” the ventilator. To minimize this problem, the ventilator is adjusted to accommodate the patient’s spontaneous breathing pattern and to work with the patient. If this is not possible, the patient may need to be sedated or pharmacologically paralyzed.43,52

Ventilator-associated pneumonia (VAP) is a subgroup of HAP that refers to the development of pneumonia 48 to 72 hours after endotracheal intubation.53 There is great potential for the development of pneumonia after placement of an artificial airway, because the tube bypasses or impairs many of the lung’s normal defense mechanisms. After an artificial airway has been placed, contamination of the lower airways follows within 24 hours. This results from a number of factors that directly and indirectly promote airway colonization. The use of respiratory therapy devices (e.g., ventilators, nebulizers, intermittent positive-pressure breathing machines) also can increase the risk of pneumonia. The severity of the patient’s illness and the presence of ALI or malnutrition significantly increase the likelihood that an infection will ensue. Therapeutic measures such as nasogastric tubes and gastric alkalinization with enteral feedings or medications facilitate the development of pneumonia. Nasogastric tubes promote aspiration by acting as a wick for stomach contents, whereas enteral feedings, antacids, histamine inhibitors, and proton-pump inhibitors increase the pH level of the stomach, promoting the growth of bacteria that can then be aspirated.⁵³ Additional information on managing the patient with pneumonia is provided in Chapter 15.

Prevention of VAP is critical. Several strategies may assist with prevention, including semirecumbent positioning, continuous aspiration of subglottic secretions (CASS), meticulous oral hygiene with antiseptics such as chlorhexidine (discussed earlier), and proper hand hygiene (Evidence-Based Practice box on Hand Hygiene Guidelines in Chapter 15).^53–55

Patients should be screened every day for their readiness to wean. The screen should include an evaluation of the patient’s level of consciousness, physiological and hemodynamic stability, adequacy of oxygenation and ventilation, spontaneous breathing capability, and respiratory rate and pattern. The rapid, shallow breathing index (RSBI) can predict weaning success. To calculate an RSBI, the patient’s respiratory rate and minute ventilation are measured for 1 minute during spontaneous breathing. The measured respiratory rate is then divided by the tidal volume (expressed in liters). An RSBI of less than 105 is considered predictive of weaning success. If the patient is receiving sedation, the medication should be discontinued at least 1 hour before the RSBI is measured. If the patient meets criteria for weaning readiness and has an RSBI of less than 105, a spontaneous breathing trial can be performed.61 One study showed that implementation of a weaning program that incorporated daily spontaneous-breathing trials had a positive impact on extubation rates and no effect on reintubation rates.⁶²

After readiness to wean has been established, the patient is prepared for the weaning trial. The patient is positioned upright to facilitate breathing and suctioned to ensure airway patency. The process is explained to the patient, and the patient is offered reassurance and diversional activities. The patient is assessed immediately before the start of the trial and frequently during the weaning period for signs of weaning intolerance (Box 16-1).^60,61,63,64

A number of methods can be used to wean a patient from the ventilator. The method selected depends on the patient, his or her pulmonary status, and length of time on the ventilator. The three main methods for weaning are (1) T-tube (T-piece) trials, (2) synchronized intermittent mandatory ventilation (SIMV), and (3) pressure support ventilation (PSV).60,63,65

In the postoperative period, acute respiratory failure may result from atelectasis or pneumonia. Atelectasis can occur as a result of anesthesia, the surgical procedure, immobilization, and pain. Treatment should be aimed at correcting the underlying problems and supporting gas exchange. Supplemental oxygen and mechanical ventilation with PEEP may be necessary.83

Development of a postoperative bronchopleural fistula is a major cause of mortality after a lung resection. A bronchopleural fistula develops when the suture line fails to secure occlusion of the bronchial stump and an opening develops into the pleural space. This can result from an imperfect stump closure, perforation of the stump (e.g., with a suction catheter), high pressure within the airways (e.g., caused by mechanical ventilation),84 or infection.⁸⁵ During surgery, careful attention is given to isolating and closing the bronchus in an attempt to secure a lasting seal with subsequent stump healing.⁸¹ In addition, early extubation is encouraged to eliminate the possibility of perforation of the stump and high airway pressures.⁸⁴ Clinical manifestations of a bronchopleural fistula include shortness of breath and coughing up serosanguineous sputum. Immediate surgery is usually necessary to close the stump and prevent flooding of the remaining lung with fluid from the residual space.⁸⁵ If this occurs, the patient should be placed with the operative side down (remaining lung up) and a chest tube should be inserted to drain the residual space.⁸¹

Hemorrhage is an early, life-threatening complication that can occur after a lung resection. It can result from bronchial or intercostal artery bleeding or disruption of a suture or clip around a pulmonary vessel.84 Excessive chest tube drainage can signal excessive bleeding. During the immediate postoperative period, chest tube drainage should be measured every 15 minutes; this frequency should be decreased as the patient stabilizes. If chest tube loss is greater than 100 ml/hour, fresh blood is noted, or a sudden increase in drainage occurs, hemorrhage should be suspected.

Cardiovascular complications after thoracic surgery include dysrhythmias and pulmonary edema. Resections of a large lung area or a pneumonectomy may be followed by a rise in central venous pressure. With the loss of one lung, the right ventricle must empty its stroke volume into a vascular bed that has been reduced by 50%. This means a higher pressure system is created, which increases right ventricular workload and precipitates right ventricular failure. Depending on previous heart function, acute decompensation of both ventricles can result. Measures are aimed at supporting cardiac function and avoiding intravascular volume excess. These measures include optimizing preload, afterload, and contractility with vasoactive agents.84

Chest tubes are placed after most thoracic surgery procedures to remove air and fluid. The drainage will initially appear bloody, becoming serosanguineous and then serous over the first 2 to 3 days postoperatively. Approximately 100 to 300 mL of drainage will occur during the first 2 hours postoperatively, which will decrease to less than 50 mL/hour over the next several hours. Routine stripping of chest tubes is not recommended because excessive negative pressure can be generated in the chest. If blood clots are present in the drainage tubing or an obstruction is present, the chest tubes may be carefully milked. The chest tube may be placed to suction or water seal.88

During auscultation of the lungs, air leaks should be evaluated. In the early phase, an air leak is commonly heard over the affected area, because the pleura have not yet tightly sealed. As healing occurs, this leak should disappear. An increase in an air leak or the appearance of a new air leak should prompt investigation of the chest drainage system to discover whether air is leaking into the system from outside or whether the leak is originating from the incision. Increased air leaks not related to the thoracic drainage system may indicate disruption of sutures.⁸⁴

Within a few days after surgery, range-of-motion exercises for the shoulder on the operative side should be performed. The patient frequently splints the operative side and avoids shoulder movement because of pain. If immobility is allowed, stiffening of the shoulder joint can result. This is referred to as frozen shoulder and may require physical therapy and rehabilitation to regain satisfactory range of motion of the shoulder joint.85

Usually on the day after surgery, the patient is able to sit in a chair. Activity should be systematically increased, with attention to the patient’s activity tolerance. With adequate pulmonary function before surgery and a surgical approach designed to preserve respiratory function, full return to previous activity levels is possible. This may take as long as 6 months to 1 year, depending on the tissue resected and the patient’s general condition.⁸¹