Chapter 58: Inhalation Therapy & Mechanical Ventilation in the PACU & ICU

Respiratory care includes both the delivery of pulmonary therapy and performance of diagnostic tests. Respiratory therapists’ scope of practice encompasses medical gas therapy, delivery of aerosolized medications, airway management, mechanical ventilation, positive airway pressure therapy, critical care monitoring, cardiopulmonary rehabilitation, and the application of various techniques collectively termed chest physiotherapy. The latter includes administering aerosols, clearing pulmonary secretions, reexpansion of atelectatic lung, and preserving normal lung function postoperatively or during illness. Diagnostic services may include pulmonary function testing, arterial blood gas analysis, and evaluation of sleep-disordered breathing. These procedures and services are well described in clinical practice guidelines developed by the American Association for Respiratory Care.

Therapeutic medical gases include oxygen at ambient or hyperbaric pressure, helium–oxygen mixtures (heliox), and nitric oxide. Oxygen is made available in high-pressure cylinders, via pipeline systems, from oxygen concentrators, as well as in liquid form. Heliox is occasionally used to reduce the increased work of breathing caused by partial upper airway obstruction. Nitric oxide is administered as a direct, selective pulmonary vasodilator.

The primary goal of oxygen therapy is to prevent or correct hypoxemia or tissue hypoxia. Table 58–1 identifies classic categories of hypoxia. Having a patient inhale an increased concentration of oxygen alone may not correct either hypoxemia or hypoxia. Continuous positive airway pressure (CPAP) or positive end-expiratory pressure (PEEP) may be required to recruit collapsed alveoli. Patients with profound hypercapnia may require ventilatory assistance. Increased concentrations of oxygen (possibly at hyperbaric pressures) may be indicated for conditions requiring removal of entrapped gas (eg, nitrogen) from body cavities or vessels. The short-term inhalation of increased concentrations of oxygen is relatively free of complications.

Supplemental oxygen is indicated for adults, children, and infants (older than 1 month) when PaO₂ is less than 60 mm Hg (8 kPa) or SaO₂ or SpO₂ is less than 90% while breathing room air. In neonates, therapy is recommended if PaO₂ is less than 50 mm Hg (6.7 kPa) or SaO₂ is less than 88% (or capillary PO₂ is less than 40 mm Hg [5.3 kPa]). Therapy may be indicated for patients when hypoxemia or hypoxia is suspected based on a medical history and physical examination. Supplemental oxygen is given during the perioperative period because general anesthesia commonly causes a decrease in PaO₂ secondary to increased pulmonary ventilation/perfusion mismatching and decreased functional residual capacity (FRC). Supplemental oxygen should be provided before procedures such as tracheal suctioning or bronchoscopy, which commonly cause arterial desaturation. There is evidence that supplemental oxygen is effective in prolonging survival of patients with chronic obstructive pulmonary disease (COPD) whose resting PaO₂ is lower than 60 mm Hg at sea level. Supplemental oxygen therapy also appears to have a mild beneficial effect on the mean pulmonary arterial pressure and subjective indices of patients’ dyspnea.

Classifying Oxygen Therapy Equipment

Oxygen given alone or in a gas can be mixed with air as a partial supplement to patients’ tidal volume or serve as the entire source of the inspired volume. The devices or systems used for this are classified based on their maximal flow rates and a range of fractions of inspired oxygen (FiO₂). Other considerations in selecting an oxygen delivery technique include patient compliance, the presence and type of artificial airway, and the need for humidification or an aerosol delivery system.

A. Low-Flow or Variable-Performance Equipment

Oxygen (usually 100%) is supplied at a fixed flow that is only a portion of inspired gas. Such devices (eg, nasal “prongs”) are usually intended for patients with stable breathing patterns. As ventilatory demands change, variable amounts of room air will dilute the oxygen flow. Low-flow systems are adequate for patients with:

• Minute ventilation less than ∼8 to 10 L/min

• Breathing frequencies less than ∼20 breaths/min

• Tidal volumes (VT) less than ∼0.8 L

• Normal inspiratory flow (10–30 L/min)

B. High-Flow or Fixed-Performance Equipment

Inspired gas at a preset FiO₂ is supplied continuously at high flow or by providing a sufficiently large reservoir of premixed gas. Ideally, the delivered FiO₂ is not affected by variations in ventilatory level or breathing pattern. High-flow systems are indicated for patients who require:

• Consistent FiO₂

• Larger inspiratory flows of gas (>40 L/min)

1. Variable-Performance Equipment

Nasal Cannulas

The nasal cannula is available as either a single-ended soft plastic tube with an over-the-ear head-elastic or dual-flow (to both nares) with under-the-chin lariat adjustment. Sizes appropriate for adults, children, and infants are available. Cannulas are connected to flowmeters with small-bore tubing. The tubing should be adjusted to avoid pressure sores on the ears, cheeks, and nose. Patients receiving long-term oxygen therapy most commonly use a nasal cannula. The appliance is usually well tolerated, allowing unencumbered speech, eating, and drinking. Cannulas can be combined with spectacle frames for convenience or to improve cosmesis. Since oxygen flows continuously, approximately 80% of the gas is wasted during expiration.

The actual FiO₂ delivered to adults with nasal cannulas is determined by oxygen flow, nasopharyngeal volume, and the patient’s inspiratory flow (the latter depends both on VT and inspiratory time) (see Table 58–2). Oxygen from the cannula can fill the nasopharynx after exhalation, yet with inspiration, oxygen and entrained air are drawn into the trachea. The inspired percent oxygen in inspired air increases by approximately 2% (above 21%) per liter of oxygen flow with quiet breathing in adults; thus, cannulas can be expected to provide inspired oxygen concentrations up to 30% with normal breathing and oxygen flows of 4 L/min. Levels of 40% or greater can be attained with oxygen flows of 10 L/min or greater; however, flows greater than 5 L/min are poorly tolerated because of the discomfort of gas jetting into the nasal cavity and because of drying and crusting of the nasal mucosa.

Data from “normal-breathing subjects” may not be accurate for acutely ill tachypneic patients. Increasing VT and reducing inspiratory time will dilute the small flow of oxygen. Different proportions of mouth-only versus nose-only breathing and varied inspiratory flow can alter FiO₂ by up to 40%. In clinical practice, flow should be titrated according to vital signs and pulse oximetry (or arterial blood gas measurements). Some patients with COPD tend to hypoventilate with even modest oxygen flows, yet are hypoxemic on room air. They may do well with cannula flows of less than less than 2 L/min.

Special cannulas allow infants to nurse and produce less trauma of the face and nose than oxygen masks. Because of the reduced minute ventilation of infants, flow through the cannula must be proportionately reduced. This generally requires a pressure-compensated flowmeter accurate at delivering oxygen flows in the less than 3 L/min range. Hypopharyngeal oxygen sampling from infants breathing with cannulas has demonstrated mean FiO₂ of 0.35, 0.45, 0.6, and 0.68 with flows of 0.25, 0.5, 0.75, and 1.0 L/min, respectively.

Nasal Mask

The nasal mask is a hybrid of the nasal cannula and a face mask. The lower edge of the mask’s flanges rests on the upper lip, surrounding the external nose. Nasal masks provide supplemental oxygen equivalent to the nasal cannula under low-flow conditions in adult patients. Many patients find the nasal mask more comfortable than a nasal cannula. The nasal mask does not produce sores around the external nares and dry oxygen is not “jetted” into the nasal cavity. The nasal mask should be considered if it improves patient comfort and compliance.

“Simple” Oxygen Mask

The “simple” oxygen mask is a disposable lightweight plastic device that covers both nose and mouth. It has no reservoir bag. Masks are secured to the patient’s face by adjustment of an elastic headband. The seal is rarely complete: usually there is “inboard” leaking. Thus, patients receive a mixture of oxygen and secondarily entrained room air, depending on the size of the leak, oxygen flow, and breathing pattern.

The body of the mask functions as a reservoir for both oxygen and expired carbon dioxide. A minimum oxygen flow of approximately 5 L/min is applied to the mask to limit rebreathing and the resulting increased respiratory work. Wearing any mask appliance for long periods of time is uncomfortable. Speech is muffled and drinking and eating are difficult.

It is difficult to predict delivered FiO₂ at specific oxygen flow rates. During normal breathing, it is reasonable to expect an FiO₂ of 0.3 to 0.6 with flows of 5 to 10 L/min, respectively. Oxygen levels can be increased with smaller VT or slower breathing rates. With higher flows and ideal conditions, FiO₂ may approach 0.7 or 0.8.

Masks lacking oxygen reservoirs may be best suited for patients who require concentrations of oxygen not easily attainable using cannulas, but who require oxygen therapy for short periods of time. Examples would include medical transport or therapy in the postanesthesia care unit or emergency department. It is not the device of choice for patients who are profoundly hypoxemic, tachypneic, or unable to protect their airway from aspiration.

Masks with Gas Reservoirs

Incorporating a gas reservoir expands the applicability of the simple mask. Two types of reservoir mask are commonly used: the partial rebreathing mask and the nonrebreathing mask. Both are disposable, lightweight, transparent plastic under-the-chin reservoirs. The difference between the two relates to use of valves on the mask and between the mask and the bag reservoir. Mask reservoirs commonly hold less than 600 mL of gas volume. The phrase “partial rebreather” is used because “part” of the patient’s expired VT refills the bag. Because expired gas is largely from “dead space ventilation,” significant rebreathing of carbon dioxide usually does not occur.

The nonrebreather uses the same basic system as the partial rebreather but incorporates flap-type valves between the bag and mask and on at least one of the mask’s exhalation ports. Inboard leaking is common, and room air will enter during brisk inspiratory flows, even when the bag contains gas. The lack of a complete facial seal and a relatively small reservoir limit the delivered oxygen concentration. The key factor in successful application of the mask is to use a sufficiently high flow of oxygen, so that the reservoir bag is at least partially full during inspiration. Typical minimum flows of oxygen are 10 to 15 L/min. Well-fitting partial rebreathing masks provide a range of FiO₂ from 0.35 to 0.60 with oxygen flows up to 10 L/min. With inlet flows of 15 L/min or more and ideal breathing conditions, FiO₂ may approach 1.0. Either style of mask is indicated for patients with significant hypoxemia, but relatively normal spontaneous minute ventilation.

2. Fixed-Performance (High-Flow) Equipment

Profoundly dyspneic patients with gasping respiration may be served by a fixed-performance, high-flow oxygen system.

Anesthesia Bag or Bag-Mask-Valve Systems

Self-inflating bags consist of a roughly 1.5 L bladder, usually with an oxygen inlet reservoir. Anesthesia bags are 1-, 2-, or 3-L non–self-inflating reservoirs with a tailpiece gas inlet. Masks are designed to provide a comfortable leak-free seal for manual ventilation. The inspiratory/expiratory valve systems may vary. The flow to the reservoir should be kept high so that the bags do not deflate substantially. When using an anesthesia bag, operators may frequently have to adjust the oxygen flow and exhaust valve to respond to changing breathing patterns or demands, particularly when maintaining a complete seal between the mask and face is difficult.

The most common systems for disposable and permanent self-inflating resuscitation bags use a unidirectional gas flow. Although these devices offer the potential for a constant FiO₂ greater than 0.9, tailpiece inlet valves will not open for a spontaneously breathing patient. Opening the valves requires negative-pressure bag recoil after compression. If this situation is not recognized, clinicians might be misled into thinking the patient is receiving a greater concentration of oxygen than is the case.

There are limits to the ability of each system to maintain its fixed-performance characteristics. Delivered FiO₂ can approach 1.0 with either anesthesia or self-inflating bags. Spontaneously breathing patients are allowed to breathe only the contents of the system if the mask seal is tight and the reservoir is adequately maintained.

Failure to maintain an adequate oxygen supply in the reservoir and inlet flow is a concern. The spring-loaded valve of anesthesia bags must be adjusted to prevent overdistention of the bag. Self-inflating bags look the same whether or not oxygen flow to the unit is adequate, and they will entrain room air into the bag, thus lowering the delivered FiO₂.

Air-Entraining Venturi Masks

The gas delivery approach with air-entraining masks is different than with an oxygen reservoir. The goal is to create an open system with high flow about the nose and mouth, with a fixed FiO₂. Oxygen is directed by small-bore tubing to a mixing jet; the final oxygen concentration depends on the ratio of air drawn in through entrainment ports. Manufacturers have developed both fixed and adjustable entrainment selections over an FiO₂ range. Most provide instructions for the operator to set a minimum flow of oxygen. Table 58–3 identifies total flow at various inlet flows and FiO₂.

Despite the high-flow concept, FiO₂ can vary up to 6% from the anticipated setting. The air-entraining masks are a logical choice for patients who require greater FiO₂ than can be provided by devices such as the nasal cannula. Patients with COPD who tend to hypoventilate with a moderate FiO₂ are candidates for the Venturi mask. Clinicians providing oxygen therapy with Venturi masks should be aware of the previously mentioned problems involving the mask itself. FiO₂ can increase if the air entrainment ports are obstructed by the patient’s hands, bed sheets, or water condensate. Clinicians should encourage the patient and caregivers to keep the mask on the face continuously: Interruption of oxygen delivery may be life threatening in unstable patients with hypoxemia. Accurate analysis of the delivered FiO₂ during air-entrainment mask breathing is difficult. Pulse oximetry (or arterial blood gas analysis) and the patient’s respiratory rate should guide clinicians as to whether the patient’s demands are being met by the mask’s flow.

Air-Entraining Nebulizers

Large-volume, high-output or “all-purpose” nebulizers have been used in respiratory care for many years to provide mist therapy with some control of the FiO₂. These units are commonly placed on patients following extubation for their aerosol-producing properties. Like the air-entraining masks, nebulizers use a pneumatic jet and an adjustable orifice to vary entrained air for varying FiO₂ levels. Many commercial devices have an inlet orifice diameter that maximally allows only 15 L/min when the source pressure is 50 psi. This means that on the 100% setting (no air entrainment) output flow is only 15 L/min. Only patients breathing slowly with small VT will receive 100% oxygen. This problem has been addressed by high-flow, high-FiO₂ nebulizers. For more common applications that use an FiO₂ of 0.3 to 0.5, room air is entrained, reducing the FiO₂ and increasing the total flow output to 40 to 50 L/min.

Knowledge of the air/oxygen ratio and the input flow rate of oxygen allows the total outflow to be calculated. Nebulizer systems can be applied to the patient with many different devices, including tracheostomy dome/collar, face tent, and Τ-piece adapter. These appliances can all be attached via large-bore tubing to the nebulizer. This open system freely vents inspiratory and expiratory gases around the patient’s face or out a distal port of a Τ-piece adapter. Unfortunately, the lack of any valves allows patients to secondarily entrain room air. It is common practice to use either a reservoir bag before the Τ-piece or a reservoir tube on the distal side of the Τ-piece to provide a larger volume of gas than that coming from the nebulizer. A typical concern of those applying air-entrainment aerosol therapy with controlled oxygen concentration is whether the system will provide adequate flow. Clinicians should observe the mist like a tracer to determine adequacy of flow. When a Τ-piece is used and the visible mist (exiting the distal port) disappears during inspiration, the flow is inadequate.

A common clinical problem occurs when excess water collects in the tubing, completely obstructing gas flow or increasing resistance to flow. Other complications include bronchospasm or laryngospasm as a consequence of airway irritation from sterile water droplets (condensate of the aerosol). In such circumstances, a heated (nonaerosol) humidification system should be substituted.

High-Flow Air–Oxygen Systems

Dual air–oxygen flowmeters and air–oxygen blenders are commonly used for oxygen administration as well as freestanding CPAP and “add-on” ventilator systems. These systems differ from the air-entraining nebulizers, as their total output flows do not diminish at FiO₂ greater than 0.4. With these high-flow systems, the total flow to the patient and FiO₂ can be set independently to meet patient needs. This can be done using a large reservoir bag or constant flows in the range of 50 to more than 100 L/min. Clinicians can use a variety of appliances with these systems, including aerosol masks, face tents, or well-fitted nonrebreathing system masks with air–oxygen blenders. Face-sealing mask systems can also be constructed with a reservoir bag and a safety valve to allow breathing if the blender fails. The high flows of gas require use of heated humidifiers of the type commonly used on mechanical ventilators. Humidification offers an advantage for patients with reactive airways. Because of the high flows, such systems are used to apply CPAP or bilevel positive airway pressure (BiPAP) for spontaneously breathing patients.

Oxygen Hoods

Many infants and neonates will not tolerate facial appliances. Oxygen hoods cover only the head, allowing access to the child’s lower body while still permitting use of a standard incubator or radiant warmer. The hood is ideal for relatively short-term oxygen therapy for newborns and inactive infants. However, for mobile infants requiring longer term therapy, the nasal cannula, face mask, or full-bed enclosure allow for greater mobility.

Normally, oxygen and air are premixed by an air–oxygen blender and passed through a heated humidifier. Nebulizers should be avoided. Most pneumatic jet-type nebulizers create noise levels (>65 dB) that may cause newborn hearing loss. Hoods come in different sizes. Some are simple Plexiglas boxes; others have elaborate systems for sealing the neck opening. There is no attempt to completely seal the system, as a constant flow of gas is needed to remove carbon dioxide (minimum flow >7 L/min). Hood inlet flows of 10 to 15 L/min are adequate for a majority of patients.

Helium–Oxygen Therapy

Helium–oxygen (heliox) mixtures have notable medical applications. Helium is premixed with oxygen in several standard blends. The most popular mixture is 79%/21% helium–oxygen, which has a density that is 40% that of pure oxygen. Helium–oxygen mixtures are available in large-sized compressed gas cylinders.

In anesthetic practice, pressures needed to ventilate patients with small-diameter tracheal tubes can be substantially reduced when the 79%/21% mixture is used. Heliox can provide patients with upper airway–obstructing lesions (eg, subglottic edema, foreign bodies, and tracheal tumors) with relief from acute distress until more definitive care can be delivered. The benefit is less convincing in treating lower airway obstruction from COPD or acute asthma. Helium mixtures may also be used as the driving gas for small-volume nebulizers in bronchodilator therapy for asthma. However, with heliox, the nebulizer flow needs to be increased to 11 L/min versus the usual 6 to 8 L/min with oxygen. Patients’ work of breathing can be reduced with heliox as compared to a conventional oxygen/nitrogen gas mixture.

Hyperbaric Oxygen

Hyperbaric oxygen therapy uses a pressurized chamber to expose the patient to oxygen tensions exceeding ambient barometric pressure (at sea level the ambient pressure is 760 mm Hg). With a one-person hyperbaric chamber, 100% oxygen is usually used to pressurize the chamber. Larger chambers allow for the simultaneous treatment of multiple patients and for the presence of medical personnel in the chamber with patients. Multiplace chambers use air to pressurize the chamber, whereas patients receive 100% oxygen by mask, hood, or tracheal tube. Common indications for hyperbaric oxygen where outcome benefits have been shown include decompression sickness (the “bends”), certain forms of gas embolism, gas gangrene, anaerobic bacterial infections, carbon monoxide poisoning, and treatment of certain wounds.

3. Hazards of Oxygen Therapy

Oxygen therapy can result in both respiratory and nonrespiratory toxicity. Important factors include patient susceptibility, the FiO₂, and duration of therapy.

Hypoventilation

This complication is often seen in patients with COPD who have chronic CO₂ retention or in patients receiving opioids. Patients who retain CO₂ have a respiratory drive that becomes at least partly dependent on the maintenance of relative hypoxemia. Elevation of arterial oxygen tension to “normal” can therefore cause severe hypoventilation in these patients. Oxygen therapy can be indirectly hazardous for patients being monitored with pulse oximetry while receiving opioids for pain. Opioid-induced hypoventilation may not cause arterial oxygen desaturation, despite markedly reduced respiratory rates. Thus, supplemental oxygen renders pulse oximetry a poor monitor for opioid-induced respiratory depression.

Absorption Atelectasis

High concentrations of oxygen can cause pulmonary atelectasis in areas of low V̇/Q̇ ratios. As nitrogen is “washed out” of the lungs, the lowered gas tension in pulmonary capillary blood results in increased uptake of alveolar gas and absorption atelectasis. If the area remains perfused but nonventilated, the resulting intrapulmonary shunt with increasing “venous admixture” can lead to progressive widening of the alveolar-to-arterial (A–a) gradient.

Pulmonary Toxicity

Prolonged high concentrations of oxygen may damage the lungs. Toxicity is dependent both on the partial pressure of oxygen in the inspired gas and the duration of exposure. Alveolar rather than arterial oxygen tension is most important in the development of oxygen toxicity. Although 100% oxygen for up to 10 to 20 h is generally considered safe, concentrations greater than 50% to 60% are undesirable for longer periods as they may lead to pulmonary toxicity.

Oxygen toxicity is thought to be due to intracellular generation of highly reactive O₂ metabolites (free radicals) such as superoxide and activated hydroxyl ions, singlet O₂, and hydrogen peroxide. A high concentration of O₂ increases the likelihood of generating toxic species. These metabolites are cytotoxic because they readily react with DNA, proteins, and lipids. Two cellular enzymes, superoxide dismutase and catalase, protect against toxicity by sequentially converting superoxide first to hydrogen peroxide and then to water. Additional protection may be provided by antioxidants and free radical scavengers; however, there is no good clinical evidence that these agents prevent pulmonary toxicity. Oxygen toxicity may present as tracheobronchitis initially in some patients. Pulmonary O₂ toxicity in newborn infants is manifested as bronchopulmonary dysplasia. In experimental animals oxygen-mediated injury of the alveolar–capillary membrane produces a condition that is indistinguishable from acute respiratory distress syndrome (ARDS).

Retinopathy of Prematurity

Retinopathy of prematurity (ROP), formerly termed retrolental fibroplasia, is a neovascular retinal disorder that develops in the great majority of premature survivors born at less than 28 weeks’ gestation. ROP may include disorganized vascular proliferation and fibrosis and may lead to retinal detachment and blindness. ROP resolves in approximately 80% of these cases without visual loss from retinal detachments or scars. ROP was very common in the 1940s–1950s when unmonitored high (>0.5 FiO₂) oxygen was often administered to premature infants. However, it is now known that hyperoxia and hypoxia are risk factors for but not the primary causes of ROP. Neonates’ risk of ROP increases with low birth weight and complexity of comorbidities (eg, sepsis). In contrast to pulmonary toxicity, ROP correlates better with arterial than with alveolar O₂ tension. The recommended arterial concentrations for premature infants receiving oxygen are 50 to 80 mm Hg (6.6–10.6 kPa). If an infant requires arterial O₂ saturations of 96% to 99% for cardiopulmonary reasons, fear about causing or worsening ROP is not a reason to withhold the oxygen.

Hyperbaric Oxygen Toxicity

The increased inspired O₂ tensions associated with hyperbaric O₂ therapy greatly accelerate O₂ toxicity. The risk and expected degree of toxicity are directly related to the pressures used as well as the duration of exposure. Prolonged exposure to O₂ partial pressures in excess of 0.5 atmosphere can cause pulmonary O₂ toxicity. This may present initially with retrosternal burning, cough, and chest tightness. There will be progressive impairment of pulmonary function with continued exposure. Patients exposed to O₂ at 2 atmospheres or greater are also at risk for central nervous system toxicity that may be expressed as behavior changes, nausea, vertigo, muscular twitching, or convulsions.

Fire Hazard

Oxygen vigorously supports combustion. The potential for uncontained oxygen enriched gas mixtures to promote fires and explosions is discussed in Chapter 2.

Patients with critical illness often require mechanical ventilation. Mechanical ventilation can replace or supplement normal spontaneous ventilation. In some instances, the problem is primarily that of impaired CO₂ elimination (ventilatory failure). In other instances, mechanical ventilation may be used as an adjunct (usually to positive-pressure therapy, as discussed next) in the treatment of hypoxemia. The decision to initiate mechanical ventilation is made on clinical grounds, but certain parameters have been suggested as guidelines (Table 58–4).

Of the two available techniques, positive-pressure ventilation and negative-pressure ventilation (iron lung), the former has much wider applications and is almost universally used. Although negative-pressure ventilation does not require tracheal intubation, it cannot overcome substantial increases in airway resistance or decreases in pulmonary compliance, and it also limits access to the patient.

During positive-pressure ventilation, lung inflation is achieved by periodically applying positive pressure to the upper airway through a tight-fitting mask (noninvasive mechanical ventilation) or through a tracheal or tracheostomy tube. Increased airway resistance and decreased lung compliance can be overcome by manipulating inspiratory gas flow and pressure. The major disadvantages of positive-pressure ventilation are altered ventilation-to-perfusion relationships, potentially adverse circulatory effects, and risk of pulmonary barotrauma and volutrauma. Positive-pressure ventilation increases physiological dead space because gas flow is preferentially directed to the more compliant, nondependent areas of the lungs, whereas blood flow (influenced by gravity) favors dependent areas. Reductions in cardiac output are primarily due to impaired venous return to the heart from increased intrathoracic pressure. Barotrauma is closely related to repetitive high peak inflation pressures and underlying lung disease, whereas volutrauma is related to the repetitive collapse and reexpansion of alveoli.

1. Positive-Pressure Ventilators

Positive-pressure ventilators periodically create a pressure gradient between the machine circuit and alveoli that results in inspiratory gas flow. Exhalation occurs passively. Ventilators and their control mechanisms can be powered pneumatically (by a pressurized gas source), electrically, or by both mechanisms. Gas flow is either derived directly from the pressurized gas source or produced by the action of a rotary or linear piston. This gas flow then either goes directly to the patient (single-circuit system) or, as commonly occurs with operating room ventilators, compresses a reservoir bag or bellows that is part of the patient circuit (double-circuit system).

All ventilators have four phases: inspiration, the changeover from inspiration to expiration (cycling), expiration, and the changeover from expiration to inspiration (trigger) (see Chapter 4). These phases are defined by VT, ventilatory rate, inspiratory time, inspiratory gas flow, and expiratory time.

Classification of Ventilators

Modern ventilators are complicated and defy simple classification. Incorporation of microprocessors into ventilators has further complicated this task. Complexity of ventilator nomenclature combined with proprietary naming schema for similar ventilator functionality has led to calls for uniform taxonomy for ventilator modes. Chatburn provides one such nomenclature, and its salient points are used to frame the following discussion on ventilator modes.

Phase Variables

The breathing period can be divided into four phases: (1) change from expiration to inspiration (trigger), (2) inspiration (target), (3) change from inspiration to expiration (cycle), and (4) expiration. The trigger variable starts inspiration when it (pressure, volume, flow, or time) reaches a preset value. When time is the trigger, breaths are initiated on a defined frequency regardless of patient effort (see Figure 58–1). Alternatively, pressure, flow, or volume triggers initiate a breath when the ventilator detects a change in pressure, flow, or volume, respectively caused by patient effort.

The target variable (pressure, volume, or flow) must reach a specified level before inspiration ends. This used to be called “limit” but nomenclatures have changed. The target variable does not define the end of inspiration, but only the upper boundary for each breath. When the cycle variable is reached, inspiration ends. Options include pressure, volume, flow, or time.

Pressure-cycled ventilators cycle into the expiratory phase when airway pressure reaches a predetermined level. VT and inspiratory time vary, being related to airway resistance and pulmonary and circuit compliance. A significant leak in the patient circuit can prevent the necessary rise in circuit pressure and machine cycling. Conversely, an acute increase in airway resistance, or decrease in pulmonary compliance, or circuit compliance (eg, a kinked tube) causes premature cycling and decreases the delivered VT. Pressure-cycled ventilators have been most often used for short-term indications (eg, transport).

Volume-cycled ventilators terminate inspiration when a preselected volume is delivered. Many adult ventilators are volume cycled but also have secondary limits on inspiratory pressure to guard against pulmonary barotrauma. If inspiratory pressure exceeds the pressure limit, the machine cycles into expiration even if the selected volume has not been delivered.

Properly functioning volume-cycled ventilators do not deliver the set VT to the patient. A percentage of the set VT is always lost due to expansion of the breathing circuit during inspiration. Circuit compliance is usually about 3 to 5 mL/cm H₂O; thus, if a pressure of 30 cm H₂O is generated during inspiration, 90 to 150 mL of the set VT is lost to the circuit. Loss of VT from expansion of the breathing circuit is therefore inversely related to lung compliance. For accurate measurement of the exhaled VT, the spirometer must be placed at the tracheal tube rather than the exhalation valve of the ventilator.

Flow-cycled ventilators have pressure and flow sensors that allow the ventilator to monitor inspiratory flow at a preselected fixed inspiratory pressure; when this flow reaches a predetermined level (usually 25% of the initial peak mechanical inspiratory flow rate), the ventilator cycles from inspiration into expiration (see the later sections on pressure support and pressure-controlled ventilation).

Time-cycled ventilators cycle to the expiratory phase once a predetermined interval elapses from the start of inspiration. VT is the product of the set inspiratory time and inspiratory flow rate. Time-cycled ventilators are commonly used for neonates and in the operating room.

Ventilator Modes

A ventilator mode is a combination of control variable, breath sequence, and target scheme. Additionally, to understand ventilator mechanics one must consider the phase variables (introduced earlier).

Control Variables

The control variable is the independent variable in the ventilator mode (see Figure 58–2). Choice are pressure, volume, and flow. In pressure-controlled ventilation (PCV), pressure is independent variable, and pressure waveform is specified (eg, rectangular waveform). In volume-controlled ventilation (VCV), similarly a volume waveform is defined. In common terminology, flow-controlled ventilation is not commonly used because flow is derivative of volume. When one directly controls volume, one indirectly controls flow.

Targeting Scheme

Targeting scheme is a feedback control design to deliver a specific pattern. A type of targeting scheme called set point targeting is the most basic. One sets a value, and ventilator seeks to deliver it. For VCV, set points would be VT and flow. For PCV, commonly it would be inspiratory pressure and inspiratory time.

Breath Sequence

Breath sequence is the pattern of mandatory or spontaneous breaths in a ventilator mode, or both (see Figure 58–3). A spontaneous breath is defined as a breath in which a patient determines both timing and size of the breath. It is patient triggered and patient cycled. A mandatory breath is any breath that is not spontaneous. An assisted breath is a breath in which the ventilator does some of the work for a patient-initiated breath.

There are three possible breath sequences. Continuous spontaneous ventilation (CSV) is a sequence in which all breaths are spontaneous. Intermittently mandatory ventilation (IMV) is a sequence in which spontaneous breaths are permitted in between mandatory breaths. If a mandatory breath is triggered by the patient, it a “synchronized” mandatory breath. In continuous mandatory ventilation (CMV), all breaths (including those by patient effort) are mandatory.

Combining the two types of control variables (pressure control [PC] and volume control [VC]) with three breath sequences gives us five breathing patterns: VC-CMV, VC-IMV, PC-CMV, PC-IMV, and PC-CSV. The sixth, VC-CSV, would mean that patient would specify time and size of breath; however, in VC mode, a patient could not specify the size of breath.

A. IMV Breath Sequences

IMV permits spontaneous ventilation while the patient is on the ventilator. A selected number of mechanical breaths (with fixed VT) are given to supplement spontaneous breathing. At high mandatory rates (10–12 breaths/min), IMV essentially provides all of the patient’s ventilation; at low rates (1–2 breaths/min), it provides minimal mechanical ventilation and allows the patient to breathe relatively independently. The frequency and VT of spontaneous breaths are determined by the patient’s ventilatory drive and muscle strength. The IMV rate can be adjusted to maintain a desired minute ventilation. IMV has found greatest use as a weaning technique.

Synchronized intermittent mandatory ventilation (SIMV) times the mechanical breath, whenever possible, to coincide with the beginning of a spontaneous effort. Proper synchronization prevents superimposing (stacking) a mechanical breath in the middle of a spontaneous breath, which might otherwise result in a very large VT. As with CMV and assist-control (AC) ventilation (discussed next), settings to limit inspiratory pressure guard against pulmonary barotrauma. The great advantage of SIMV over IMV is that it provides for increased patient comfort. When IMV or SIMV are used for weaning, the machine breaths provide a backup if the patient becomes fatigued. However, if the rate is set too low (4 breaths/min), the backup may be insufficient, particularly for weak patients who may not be able to overcome the added work of breathing during spontaneous breaths.

IMV circuits provide a continuous flow of gas for spontaneous ventilation between mechanical breaths. Modern ventilators incorporate SIMV into their design, but older models required modification with a parallel circuit, a continuous flow system, or a demand flow valve. Regardless of the system, proper functioning of one-way valves and sufficient gas flow are necessary to prevent an increase in the patient’s work of breathing, particularly when PEEP is also used.

Thus far the discussion of IMV has assumed this to be a volume-limited format; however, IMV can also be provided in pressure-limited format if desired (as described next).

B. Pressure-Controlled Breath Sequences (PC-CMV, PC-IMV, and PC-CSV)

PC breath sequences may be used in both the AC and IMV modes. In AC mode, all breaths (either machine initiated or patient initiated) are time cycled and pressure limited. In IMV, machine-initiated breaths are time cycled and pressure limited. The patient may breathe spontaneously between the set rate, and the VT of the spontaneous breaths is determined by the patient. The advantage of PCV is that by limiting inspiratory pressure, the risks of barotrauma and volutrauma may be decreased. Also, by extending inspiratory time, better mixing and recruitment of collapsed or flooded alveoli may be achieved, when used with adequate levels of PEEP levels. The disadvantage of conventional PCV is that VT is not guaranteed (although there are modes in which the consistent delivered pressure of PCV can be combined with a predefined volume delivery). Changes in compliance or resistance will affect the delivered VT. This is a major issue in patients with acute lung injury because if the compliance decreases and the pressure limit is not increased, adequate VT may not be attained. PCV has been used for patients with acute lung injury or ARDS, often with a prolonged inspiratory time or inverse inspiratory/expiratory (I:E) ratio ventilation (IRV) (see later discussion) in an effort to recruit collapsed and flooded alveoli. The disadvantage of using IRV with PCV is that patients will require deep sedation, perhaps with paralysis to tolerate this ventilatory mode.

With PCV, pressure and inspiratory time are preset, whereas flow and volume are variable and dependent on the patient’s resistance and compliance. With volume ventilation, on the other hand, inspiratory time is also preset but flow and VT are also preset, and with increased resistance or reduced compliance the inspiratory pressure can be greatly increased.

PCV is similar to pressure support ventilation (PSV) in that peak airway pressure is controlled but is different in that a mandatory rate and inspiratory time are selected. As with pressure support, gas flow ceases when the pressure level is reached; however, the ventilator does not cycle to expiration until the preset inspiration time has elapsed.

Mode Examples

A. Continuous Mandatory Ventilation (Example of VC-CMV Breathing Pattern)

In this mode, the ventilator cycles from expiration to inspiration after a fixed time interval. The interval determines the ventilatory rate. Typical settings on this mode provide a fixed VT and fixed rate (and, therefore, minute ventilation) regardless of patient effort, because the patient cannot breathe spontaneously. Settings to limit inspiratory pressure guard against pulmonary barotrauma, and indeed CMV can be provided in a pressure-limited (rather than volume-limited) way. Controlled ventilation is best reserved for patients capable of little or no ventilatory effort. Awake patients with active ventilatory effort require sedation, possibly with muscle paralysis, to safely receive CMV.

B. Assist-Control Ventilation (Example of VC-CMV Breathing Pattern, or Can Be Set as PC-CMV)

Incorporation of a pressure sensor in the breathing circuit of AC ventilators permits the patient’s inspiratory effort to be used to trigger inspiration. A sensitivity control allows selection of the inspiratory effort required. The ventilator can be set for a fixed ventilatory rate, but each patient effort of sufficient magnitude will trigger the set Vt. If spontaneous inspiratory efforts are not detected, the machine functions as if in the control mode. Most often, AC ventilation is used in a volume-limited format, but it can also be provided in a pressure-limited way (as discussed later).

C. Pressure Support Ventilation (Example of PC-CSV Breathing Pattern)

PSV was designed to augment the VT of spontaneously breathing patients and overcome any increased inspiratory resistance from the tracheal tube, breathing circuit (tubing, connectors, and humidifier), and ventilator (pneumatic circuitry and valves). Microprocessor-controlled machines have this mode, which delivers sufficient gas flow with every inspiratory effort to maintain a predetermined positive pressure throughout inspiration. When inspiratory flow decreases to a predetermined level, the ventilator’s feedback (servo) loop cycles the machine into the expiratory phase, and airway pressure returns to baseline (Figure 58–4). The only setting in this mode is inspiratory pressure. The patient determines the respiratory rate and VT varies according to inspiratory gas flow, lung mechanics, and the patient’s own inspiratory effort. Low levels of PSV (5–10 cm H₂O) are usually sufficient to overcome any added resistance imposed by the breathing apparatus. Higher levels (10–40 cm H₂O) can function as a standalone ventilatory mode if the patient has sufficient spontaneous ventilatory drive and stable lung mechanics. The principal advantages of PSV are its ability to augment spontaneous VT, decrease the work of breathing, and increase patient comfort. However, if the patient fatigues or lung mechanics change, VT may be inadequate, and there is no backup rate if the patient’s intrinsic respiratory rate decreases (eg, after opioid dosing). Note that one can add “pressure support” to IMV breathing breath sequences (Figure 58–5). The IMV machine mandatory breaths provide backup, and a low level of pressure support is used to offset the increased work of breathing resulting from the breathing circuit and machine during the spontaneous breaths.

D. Inverse I:E Ratio Ventilation Modes, Including Airway Pressure Release Ventilation (Usually Examples of PC-IMV Breathing Pattern)

IRV reverses the normal I:E time ratio of 1:3 or greater to a ratio of greater than 1:1 (eg, 1.5:1). This may be achieved by adding an end-inspiratory pause, by decreasing peak inspiratory flow during volume-controlled ventilation (CMV), or by setting an inspiratory time such that inspiration is longer than expiration during PCV (PC-IRV). Intrinsic PEEP may be produced during IRV and is caused by air trapping or incomplete emptying of the lung to the baseline pressure prior to the initiation of the next breath. This air trapping increases FRC until a new equilibrium is reached. This mode does not allow spontaneous breathing and requires heavy sedation or neuromuscular blockade. IRV with PEEP is effective for improving oxygenation in patients with decreased FRC.

E. Airway Pressure Release Ventilation

Airway pressure release ventilation (APRV), or bilevel ventilation, is a mode in which a relatively high PEEP is used, despite the patient being allowed to breathe spontaneously. Intermittently, the PEEP level decreases to help augment the elimination of CO₂ (Figure 58–6). The inspiratory and expiratory times, high and low PEEP levels, and spontaneous respiratory activity determine minute ventilation. Initial settings include a minimum PEEP of 10 to 12 cm H₂O and a release level of 5 to 10 cm H₂O. Commonly, 10 to 12 releases are chosen as a starting point, along with a time at low PEEP to allow only 50% to 70% of expiratory flow (to provide “autoPEEP”). Advantages of APRV appear to be less circulatory depression and pulmonary barotrauma as well as less need for sedation. This technique appears to be an attractive alternative to PC-IRV for overcoming problems with high peak inspiratory pressures in patients with reduced lung compliance.

Basic Mechanics of Ventilators

Most modern ventilators behave like flow generators. Constant flow generators deliver a constant inspiratory gas flow regardless of airway circuit pressure. Constant flow is produced by the use of either a solenoid (on–off) valve with a high-pressure gas source (5–50 psi) or via a gas injector (Venturi) with a lower-pressure source. Machines with high-pressure gas sources allow inspiratory gas flow to remain constant despite large changes in airway resistance or pulmonary compliance. Ventilator performance varies with airway pressure for gas injectors. Nonconstant flow generators consistently vary inspiratory flow with each inspiratory cycle (such as by a rotary piston); a sine wave pattern of flow is typical.

Constant-pressure generators maintain airway pressure constant throughout inspiration and irrespective of inspiratory gas flow. Gas flow ceases when airway pressure equals the set inspiratory pressure. Pressure generators typically operate at low gas pressures (just above peak inspiratory pressure).

Cycling (Changeover from Inspiration to Expiration)

Time-cycled ventilators cycle to the expiratory phase once a predetermined interval elapses from the start of inspiration. VT is the product of the set inspiratory time and inspiratory flow rate. Time-cycled ventilators are commonly used for neonates and in the operating room.

Volume-cycled ventilators terminate inspiration when a preselected volume is delivered. Many adult ventilators are volume cycled but also have secondary limits on inspiratory pressure to guard against pulmonary barotrauma. If inspiratory pressure exceeds the pressure limit, the machine cycles into expiration even if the selected volume has not been delivered.

Pressure-cycled ventilators cycle into the expiratory phase when airway pressure reaches a predetermined level. VT and inspiratory time vary, being related to airway resistance and pulmonary and circuit compliance. A significant leak in the patient circuit can prevent the necessary rise in circuit pressure and machine cycling. Conversely, an acute increase in airway resistance, or decrease in pulmonary compliance, or circuit compliance (kink) causes premature cycling and decreases the delivered VT. Pressure-cycled ventilators have been most often used for short-term indications (transport).

Flow-cycled ventilators have pressure and flow sensors that allow the ventilator to monitor inspiratory flow at a preselected fixed inspiratory pressure; when this flow reaches a predetermined level (usually 25% of the initial peak mechanical inspiratory flow rate), the ventilator cycles from inspiration into expiration (see the earlier sections on pressure support and pressure-controlled ventilation).

Microprocessor-Controlled Ventilators

These versatile machines can be set to function in any one of a variety of inspiratory flow and cycling patterns. Microprocessor-controlled ventilators are the norm in modern critical care units and on newer anesthesia machines.

High-Frequency Ventilation

High-frequency ventilation is sufficiently different from conventional modes of mechanical ventilation that its mechanics require separate mention. Three forms of high-frequency ventilation (HFV) are available. High-frequency positive-pressure ventilation involves delivering a small “conventional” VT at a rate of 60 to 120 breaths/min. High-frequency jet ventilation (HFJV) utilizes a small cannula at or in the airway through which a pulsed jet of high-pressure gas is delivered at a set frequency of 120 to 600 times/min (2–10 Hz). The jet of gas may entrain air (Bernoulli effect), which may augment VT. High-frequency oscillation employs a driver (usually a piston) that creates to-and-fro gas movement in the airway at rates of 180 to 3000 times/min (3–50 Hz).

These forms of ventilation all produce VT at or below anatomic dead space. The exact mechanism of gas exchange is unclear but is probably a combination of effects. Jet ventilation has found widest use in the operating room. It may be used for laryngeal, tracheal, and bronchial procedures and can be lifesaving in emergency airway management when tracheal intubation and conventional positive-pressure ventilation are unsuccessful (see Chapter 19). In the intensive care unit (ICU), HFJV may be useful in managing some patients with bronchopleural and tracheoesophageal fistulas when conventional ventilation has failed. Occasionally, HFJV or high-frequency oscillation is used in patients with ARDS to try to improve oxygenation. Inadequate heating and humidification of inspired gases during prolonged HFV, however, can be a problem. Initial settings for HFJV are typically a rate of 120 to 240 breaths/min, an inspiratory time of 33%, and a drive pressure of 15 to 30 psi. Mean airway pressure should be measured in the trachea at least 5 cm below the injector to avoid an artifactual error from gas entrainment. Carbon dioxide elimination is generally increased by increasing the drive pressure, whereas adequacy of oxygenation relates to the mean airway pressure. An intrinsic PEEP effect is seen during HFJV at high drive pressures and inspiratory times greater than 40%.

Differential Lung Ventilation

This technique, also referred to as independent lung ventilation, may be used in patients with severe unilateral lung disease or those with bronchopleural fistulae. Use of conventional positive-pressure ventilation and PEEP in such instances can aggravate ventilation/perfusion mismatching or, in patients with fistula, result in inadequate ventilation of the unaffected lung. In patients with restrictive disease of one lung, overdistention of the normal lung can lead to worsening hypoxemia or barotrauma. After separation of the lungs with a double-lumen tube, positive-pressure ventilation can be applied to each lung independently using two ventilators. When two ventilators are used, the timing of mechanical breaths is often synchronized, with one ventilator, the “master,” setting the rate for the “slave” ventilator.

2. Care of Patients Requiring Mechanical Ventilation

Tracheal Intubation

Tracheal intubation is most commonly undertaken in ICU patients to manage pulmonary failure with mechanical ventilation. Both nasotracheal and orotracheal intubation appear to be relatively safe for at least 2 to 3 weeks. When compared with orotracheal intubation, nasotracheal intubation may be more comfortable for the patient and more secure (fewer instances of accidental extubation). Nasal intubation, however, has its own set of associated adverse events, including nasal bleeding, transient bacteremia, submucosal dissection of the nasopharynx or oropharynx, and sinusitis or otitis media (from obstruction of sinus outflow or of the auditory tubes). Nasal intubations will also generally incorporate a smaller diameter tube than orotracheal intubations, and this can make it more difficult to clear secretions and can force the clinician to use smaller fiberoptic bronchoscopes.

Intubation often can be carried out without the use of sedation or muscle paralysis in agonal or unconscious patients. However, topical anesthesia of the airway and sedation are helpful in patients who still have active airway reflexes. More vigorous and uncooperative patients require varying degrees of sedation. Small doses of relatively short-acting agents are generally used; popular agents include midazolam, etomidate, dexmedetomidine, and propofol. If necessary, a neuromuscular blocker can be used for paralysis after a hypnotic is given.

The time of tracheal intubation and initiation of mechanical ventilation can be a period of great hemodynamic instability. Hypertension or hypotension and bradycardia or tachycardia may be encountered. Responsible factors include activation of autonomic reflexes from stimulation of the airway, myocardial depression and vasodilation from sedative-hypnotic agents, straining by the patient, withdrawal of intense sympathetic activity, and reduced venous return due to positive pressure in the airways. Careful monitoring is required during and immediately following intubation of patients with critical illness.

When left in place for more than 2 to 3 weeks, both orotracheal and nasotracheal tubes predispose patients to subglottic stenosis. If longer periods of mechanical ventilation are necessary, the tracheal tube should be replaced by a cuffed tracheostomy tube. If it is clear that a tracheal tube will be required for more than 2 weeks, a tracheostomy may be performed soon after intubation. While earlier tracheostomy does not reduce mortality, it may reduce the incidence of pneumonia, the duration of mechanical ventilation, and the length of stay.

Initial Ventilator Settings

Depending on the type of pulmonary failure, mechanical ventilation is used to provide either partial or full ventilatory support. For full ventilatory support, CMV, AC, or PCV is generally employed with a respiratory rate of 10 to 14 breaths/min, a VT of 6 mL/kg, and PEEP of 5 to 10 cm H₂O. These settings reduce the likelihood of high peak inflation pressures (greater than 35 to 40 cm H₂O), barotrauma, and volutrauma. High airway pressures that overdistend alveoli (transalveolar pressure >35 cm H₂O) promote experimental lung injury. Likewise, compared with a VT of 12 mL/kg, a VT of 6 mL/kg and plateau pressure (P_plt) less than 30 cm H₂O have been associated with reduced mortality in patients with ARDS. Partial ventilatory support is usually provided by lower SIMV settings (<8 breaths/min), either with or without pressure support. Lower P_plt (<20–30 cm H₂O) is recommended to better preserve cardiac output, and lessen adverse effects on ventilation/perfusion relationships.

Patients breathing spontaneously on SIMV must overcome the additional resistances of the tracheal tube, demand valves, and breathing circuit of the ventilator. These imposed resistances increase the work of breathing. Smaller tubes (<7.0 mm internal diameter in adults) increase resistance and should be avoided if possible. The simultaneous use of pressure support of 5 to 15 cm H₂O during SIMV can compensate for tube and circuit resistance.

The addition of 5 to 8 cm H₂O of PEEP during positive-pressure ventilation preserves FRC and gas exchange. This “physiological” PEEP is purported to compensate for the loss of a similar amount of intrinsic PEEP (and decrease in FRC) in patients following tracheal intubation. Periodic sigh breaths (large VT) are not necessary when a PEEP of 5 to 8 cm H₂O accompanies VT of appropriate volumes.

Sedation & Paralysis

Sedation and paralysis may be necessary in patients who become agitated and “fight” the ventilator. Repetitive coughing (“bucking”) and straining can have adverse hemodynamic effects, can interfere with gas exchange, and may predispose to pulmonary barotrauma and self-inflicted injury. Sedation with or without paralysis may also be desirable when patients continue to be tachypneic despite high mechanical respiratory rates (>16–18 breaths/min).

Commonly used sedatives include opioids (morphine or fentanyl), benzodiazepines (usually midazolam), propofol, and dexmedetomidine. These agents may be used alone or in combination and are often administered by continuous infusion. Propofol is uncommonly used for prolonged sedation due to concerns about propofol infusion syndrome (see Chapter 9). Nondepolarizing paralytic agents are used in combination with sedation when ventilation cannot otherwise be accomplished.

Monitoring

Critically ill patients receiving mechanical ventilation should be cared for a head-up position to reduce the risk of ventilator-associated pneumonia. Such patients require continuous monitoring for adverse hemodynamic and pulmonary effects arising from positive pressure in the airways. Continuous electrocardiography, pulse oximetry, and capnometry are useful. Direct intraarterial pressure monitoring is often employed for sampling of arterial blood for respiratory gas analysis. Accurate recording of fluid intake and output is necessary to assess fluid balance. An indwelling urinary catheter will lead to an increased risk of urinary tract infections and should be avoided when possible, but it is helpful for monitoring urinary output. Chest radiographs are commonly obtained to confirm tracheal tube and central venous catheter positions, evaluate for evidence of pulmonary barotrauma or pulmonary disease, and determine whether there are signs of pulmonary edema.

Airway pressures (baseline, peak, plateau, and mean), inhaled and exhaled VT (mechanical and spontaneous), and fractional concentration of oxygen should be closely monitored. Monitoring these parameters not only allows optimal adjustment of ventilator settings but helps detect problems with the tracheal tube, breathing circuit, and ventilator. For example, an increasing P_plt for a set VT can indicate worsening compliance. A declining blood pressure and increasing P_plt from dynamic hyperinflation (autoPEEP) can be quickly diagnosed (and treated) by disconnecting the patient from the ventilator. Inadequate suctioning of airway secretions and the presence of large mucus plugs are often manifested as increasing peak inflation pressures (a sign of increased resistance to gas flow) and decreasing exhaled VT. An abrupt increase in peak inflation pressure together with sudden hypotension strongly suggests a pneumothorax.

3. Discontinuing Mechanical Ventilation

There are two phases to discontinuing mechanical ventilation. In the first, “readiness testing,” so-called weaning parameters and other subjective and objective assessments are used to determine whether the patient can sustain progressive withdrawal of mechanical ventilator support. The second phase, “weaning” or “liberation,” describes the way in which mechanical support is removed.

Readiness testing should include determining whether the process that necessitated mechanical ventilation has been reversed or controlled. Complicating factors such as bronchospasm, heart failure, infection, malnutrition, increased CO₂ production due to increased carbohydrate loads, acid–base derangements, anemia, altered mental status, and sleep deprivation should be adequately treated. Chronic lung disease, respiratory muscle wasting from prolonged disuse, and heart failure may lead to complicated (or failed) weaning.

Weaning from mechanical ventilation should be considered when patients no longer meet criteria for mechanical ventilation (see Table 58–4). In general, this occurs when patients have a pH greater than 7.25, show adequate arterial oxygen saturation while receiving FiO₂ less than 0.5, are able to spontaneously breathe, are hemodynamically stable, and have no current signs of myocardial ischemia. Additional mechanical indices have also been suggested (Table 58–5). Useful weaning parameters include arterial blood gas tensions, respiratory rate, and rapid shallow breathing index (RSBI). Intact airway reflexes are mandatory and a cooperative patient is helpful for successful weaning and extubation, unless the patient will retain a cuffed tracheostomy tube. Similarly, adequate oxygenation (arterial oxygen saturation >90% on 40–50% O₂ with <5 cm H₂O of PEEP) is mandatory prior to extubation. When the patient is weaned from mechanical ventilation and extubation is planned, the RSBI is frequently used to help predict who can be successfully weaned from mechanical ventilation and extubated. With the patient breathing spontaneously on a Τ-piece, the VT (in liters) and respiratory rate (f) are measured:

Most patients with an RSBI less than 105 can be successfully extubated. Those with an RSBI greater than 120 should retain some degree of mechanical ventilator support.

The common techniques to wean a patient from the ventilator include SIMV, pressure support, or periods of spontaneous breathing alone on a Τ-piece or on low levels of CPAP. Many institutions use “automated tube compensation” to provide just enough pressure support to compensate for the resistance of breathing through an endotracheal tube. Newer mechanical ventilators have a setting that will automatically adjust gas flows to make this adjustment. In practice in adults breathing through conventionally sized tubes (7.5–8.5), the adjustment will typically amount to pressure support of 5 cm H₂O and PEEP of 5 cm H₂O.

Weaning with SIMV

With SIMV the number of mechanical breaths is progressively decreased (by 1–2 breaths/min) as long as the arterial CO₂ tension and respiratory rate remain acceptable (generally <45–50 mm Hg and <30 breaths/min, respectively). If pressure support is concomitantly used, it should generally be reduced to 5 to 8 cm H₂O. In patients with acid–base disturbances or chronic CO₂ retention, arterial blood pH (>7.35) is more useful than CO₂ tension. Blood gas measurements can be checked after a minimum of 15 to 30 min at each setting. When an IMV of 2 to 4 breaths is reached, mechanical ventilation is discontinued if arterial oxygenation remains acceptable.

Weaning with PSV

Weaning with PSV alone is accomplished by gradually decreasing the pressure support level by 2 to 3 cm H₂O while VT, arterial blood gas tensions, and respiratory rate are monitored (using the same criteria as for IMV). The goal is to try to ensure a VT of 4 to 6 mL/kg and an f of less than 30 with acceptable PaO₂ and PaCO₂. When a pressure support level of 5 to 8 cm H₂O is reached, the patient is considered weaned.

Weaning with a T-Piece or CPAP

Τ-piece trials allow observation while the patient breathes spontaneously without any mechanical breaths. The Τ-piece attaches directly to the tracheal tube or tracheostomy tube and has corrugated tubing on the other two limbs. A humidified oxygen–air mixture flows into the proximal limb and exits from the distal limb. Sufficient gas flow must be given in the proximal limb to prevent the mist from being completely drawn back at the distal limb during inspiration; this ensures that the patient is receiving the desired oxygen concentration. The patient is observed closely during this period; obvious new signs of fatigue, chest retractions, tachypnea, tachycardia, arrhythmias, or hypertension or hypotension should terminate the trial. If the patient appears to tolerate the trial period and the RSBI is less than 100, mechanical ventilation can be discontinued permanently. If the patient can also protect and clear the airway, the tracheal tube can be removed.

If the patient has been intubated for a prolonged period or has severe underlying lung disease, sequential Τ-piece trials may be necessary. Periodic trials of 10 to 30 min are initiated and progressively increased, typically by 5 to 10 min per trial as long as the patient appears comfortable, maintains acceptable arterial saturation, and does not become hypercarbic.

Many patients develop progressive atelectasis during prolonged Τ-piece trials. This may reflect the absence of a normal “physiological” PEEP when the larynx is bypassed by a tracheal tube. If this is a concern, spontaneous breathing trials on low levels (5 cm H₂O) of CPAP can be tried. The CPAP helps maintain FRC and prevent atelectasis.

Positive airway pressure therapy can be used in patients who are breathing spontaneously as well as those who are mechanically ventilated. The principal indication for positive airway pressure therapy is a decrease in FRC resulting in absolute or relative hypoxemia. By increasing transpulmonary distending pressure, positive airway pressure therapy can increase FRC, improve (increase) lung compliance, and reverse ventilation/perfusion mismatching. Improvement in the latter parameter will show as a decrease in venous admixture and an improvement in arterial O₂ tension.

Positive End-Expiratory Pressure

Application of positive pressure during expiration as an adjunct to a mechanically delivered breath is referred to as PEEP. The ventilator’s PEEP valve provides a pressure threshold that allows expiratory flow to occur only when airway pressure exceeds the selected PEEP level.

Continuous Positive Airway Pressure

Application of a positive-pressure threshold during both inspiration and expiration with spontaneous breathing is referred to as CPAP. Constant levels of pressure can be attained only if a high-flow (inspiratory) gas source is provided. When the patient does not have an artificial airway, tightly fitting full-face masks, nasal masks, or nasal “pillows” can be used. Because of the risks of gastric distention and regurgitation, CPAP masks should be used only on patients with intact airway reflexes and with CPAP levels less than 15 cm H₂O (less than lower esophageal sphincter pressure in normal persons). Expiratory pressures greater than 15 cm H₂O should only be administered by tracheal or tracheostomy tube.

CPAP versus PEEP

The distinction between PEEP and CPAP is often blurred in the clinical setting because patients may breathe with a combination of mechanical and spontaneous breaths. Therefore, the two terms are often used interchangeably. In the strictest sense, “pure” PEEP is provided as a ventilator-cycled breath. In contrast, a “pure” CPAP system provides only sufficient continuous or “on-demand” gas flows (60–90 L/min) to prevent inspiratory airway pressure from falling perceptibly below the expiratory level during spontaneous breaths (Figure 58–7). Some ventilators with demand valve–based CPAP systems may not be adequately responsive and result in increased inspiratory work of breathing. This situation can be corrected by adding low levels of (inspiratory) PSV if in a volume-targeted mode or changing to a pressure-targeted mode. In clinical practice, controlled ventilation, PSV, and CPAP/PEEP support can be delivered by most modern ICU ventilators. Manufacturers have also developed specific devices to deliver bilevel inspiratory positive airway pressure (IPAP) with expiratory positive airway pressure (EPAP) in either a spontaneous or time-cycled fashion. The term bilevel positive airway pressure (BiPAP) has become a commonly used phrase, adding to the confusion of airway pressure terminology.

Pulmonary Effects of PEEP & CPAP

The major effect of PEEP and CPAP on the lungs is to increase FRC. In patients with decreased lung volume, appropriate levels of either PEEP or CPAP will increase FRC and tidal ventilation above closing capacity, will improve lung compliance, and will correct ventilation/perfusion abnormalities. The resulting decrease in intrapulmonary shunting improves arterial oxygenation. The principal mechanism of action for both PEEP and CPAP appears to be expansion of partially collapsed alveoli. Recruitment (reexpansion) of collapsed alveoli occurs at PEEP or CPAP levels above the inflection point, defined as the pressure level on a pressure–volume curve at which collapsed alveoli are recruited (open); with small changes in pressure there are large changes in volume (Figure 58–8). Although neither PEEP nor CPAP decreases total extravascular lung water, studies suggest that they do redistribute extravascular lung water from the interstitial space between alveoli and endothelial cells toward peribronchial and perihilar areas. Both effects can potentially improve arterial oxygenation.

Excessive PEEP or CPAP, however, can overdistend alveoli (and bronchi), increasing dead space ventilation and reducing lung compliance; both effects can significantly increase the work of breathing. By compressing alveolar capillaries, overdistention of normal alveoli can also increase pulmonary vascular resistance and right ventricular afterload.

A higher incidence of pulmonary barotrauma is observed with PEEP or CPAP at levels greater than 20 cm H₂O. Disruption of alveoli allows air to track interstitially along bronchi into the mediastinum (pneumomediastinum). From the mediastinum, air can then rupture into the pleural space (pneumothorax) or the pericardium (pneumopericardium) or can dissect along tissue planes subcutaneously (subcutaneous emphysema) or into the abdomen (pneumoperitoneum or pneumoretroperitoneum). A bronchopleural fistula results when an air leak fails to seal (close). Although barotrauma must be considered in any discussion of CPAP and PEEP, in fact, it may be more clearly associated with higher peak inspiratory pressures that result with increasing level of PEEP or CPAP. Other factors that may increase the risk of barotrauma include underlying lung disease (asthma, interstitial lung disease, COPD), dynamic hyperinflation (too frequent breaths or too short expiratory times leading to intrinsic [or auto] PEEP), and excessive VT (>10–15 mL/kg).

Adverse Nonpulmonary Effects of PEEP & CPAP

Nonpulmonary adverse effects are primarily circulatory and the result of transmission of the elevated airway pressure to the contents of the chest. Transmission is directly related to lung compliance; thus, patients with decreased lung compliance (most patients requiring PEEP) are least affected.

Progressive reductions in cardiac output may be seen as mean airway pressure and mean intrathoracic pressure rise. The principal mechanism appears to be inhibition of return of venous blood to the heart from increased intrathoracic pressure. Other mechanisms may include reduced left ventricular filling from leftward displacement of the interventricular septum (when overdistention of alveoli and increased pulmonary vascular resistance lead to increased right ventricular volume). When this occurs, left ventricular compliance may be reduced, necessitating a higher filling pressure to achieve the same cardiac output. An increase in intravascular volume will usually at least partially offset the effects of CPAP and PEEP on cardiac output. Circulatory depression is most often associated with end-expiratory pressures greater than 15 cm H₂O.

PEEP-induced elevations in intrathoracic pressure and reductions in cardiac output decrease both renal and hepatic blood flow. Urinary output, glomerular filtration, and free water clearance decrease.

Increased end-expiratory pressures impede blood return from the brain to the heart and may increase intracranial pressure in patients whose intracranial compliance is decreased. Therefore, with evidence of increased intracranial pressure, the level of PEEP must be carefully chosen to balance oxygenation requirements against potential adverse effects on intracranial pressure.

Optimum Use of PEEP & CPAP

The goal of positive-pressure therapy is to increase oxygen delivery to tissues, while avoiding the adverse sequelae of excessively increased (>0.5) FiO₂. The need for excessive FiO₂ is most easily avoided with an adequate cardiac output and hemoglobin concentration. Ideally, mixed venous oxygen tensions should be followed. As we have repeatedly emphasized, the salutary effect of PEEP (or CPAP) on arterial oxygen tension must be balanced against any detrimental effect on cardiac output. Volume infusion or inotropic support may be necessary.

At optimal PEEP the benefits of PEEP exceed any risks. Practically, PEEP is usually added in increments of 2 to 5 cm H₂O until the desired therapeutic endpoint is reached. The most commonly suggested endpoint is an arterial oxygen saturation of hemoglobin of greater than 88% to 90% on a nontoxic inspired oxygen concentration (≤50%). Many clinicians favor reducing the inspired oxygen concentration to 50% or less because of the potentially adverse effect of greater oxygen concentrations on the lung. Alternatively, PEEP may be titrated to the mixed venous artery oxygen saturation (Sv̄₂ >50–60%).

Other respiratory care techniques, including administration of aerosolized water or bronchodilators and clearing of pulmonary secretions, preserve or improve pulmonary function.

An aerosol mist is a gas or gas mixture containing a suspension of liquid particles. Aerosolized water may be administered to loosen inspissated secretions and facilitate their removal from the tracheobronchial tree. Aerosol mists are also used to administer bronchodilators, mucolytic agents, or vasoconstrictors (metered-dose inhalers are preferred for administration of bronchodilators). A normal cough requires an adequate inspiratory capacity, an intact glottis, and adequate muscle strength (abdominal muscles and diaphragm). Aerosol mists with or without bronchodilators may induce cough as well as loosen secretions. Instillation of hypertonic saline has been used as a mucolytic and to induce cough. Additional effective measures include chest percussion or vibration therapy and postural drainage of the various lung lobes.

Maneuvers that produce sustained maximum lung inflation, such as the use of an incentive spirometer, can be helpful in inducing cough as well as preventing atelectasis and preserving normal lung volume. Patients should be instructed to inhale maximally and to hold their breath for 2 to 3 s before exhalation.

When thick, copious secretions are associated with atelectasis and hypoxemia, more aggressive measures may be indicated. These include suctioning the patient with a catheter or fiberoptic bronchoscope. When there is atelectasis without retention of secretions, a brief period of CPAP by mask or positive-pressure ventilation through a tracheal tube is often effective.