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