Ambient Oxygen Therapy Equipment
Classifying Oxygen Therapy Equipment
Oxygen given alone or in a gas can be mixed with air as a partial supplement to patients’ tidal or minute volume or serve as the entire source of the inspired volume. This approach provides the basis for classifying devices or systems according to their ability to provide adequate flow levels and a range of fraction of inspired oxygen (Fio2). Other considerations in selecting therapy include patient compliance, the presence and type of artificial airway, and the need for humidification or an aerosol delivery system.
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 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 ˜8-10 L/min
- Breathing frequencies less than ˜20 breaths/min
- Tidal volumes (VT) less than ˜0.8 L
- Normal inspiratory flow (10-30 L/min).
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. Profoundly dyspneic and hypoxemic patients may need flows of 100% oxygen in excess of 100 L/min. High-flow systems are indicated for patients who require
- Consistent Fio2
- Large inspiratory flows of gas (>40 L/min).
Variable-Performance Equipment (Table 57-2)
The nasal cannula is available as either a blind-ended soft plastic tube with an over-the-ear head-elastic or dual-flow with under-the-chin lariat adjustment. Sizes appropriate for adults, children, and infants are available. Cannulas are connected to flowmeters with small-bore tubing and can rapidly be placed on most patients. The tension of attachment should be firm yet comfortable enough 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 acceptance by improving cosmesis. Oxygen-conserving cannulas equipped with inlet reservoirs are available for patients receiving long-term oxygen. Since oxygen flows continuously, approximately 80% of the gas is wasted during expiration. There are valved reservoir devices that permit storage of incoming oxygen until inspiration occurs.
Table 57-2 Oxygen Delivery Devices and Systems. ||Download (.pdf)
Table 57-2 Oxygen Delivery Devices and Systems.
|Device/System||Oxygen Flow Rate (L/min)||Fio2 Range|
|Mask with reservoir||5||0.35-0.50|
|Partial rebreathing mask-bag||7||0.35-0.75|
|Venturi mask and jet nebulizer||4-6 (total flow = 15)||0.24|
|4-6 (total flow = 45)||0.28|
|8-10 (total flow = 45)||0.35|
|8-10 (total flow = 33)||0.40|
|8-12 (total flow = 33)||0.50|
The actual Fio2 delivered to adults with nasal cannulas is determined by oxygen flow, nasopharyngeal volume, and the patient’s inspiratory flow (which depends both on Vt and inspiratory time). 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 increases by approximately 1-2% (above 21%) per liter of oxygen flow with quiet breathing in adults. Cannulas can be expected to provide inspired oxygen concentrations up to 30-35% with normal breathing and oxygen flows of 3-4 L/min. However, levels of 40-50% can be attained with oxygen flows of greater than 10 L/min for short periods. 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, pulse oximetry, and 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 1-2 L/min.
Pediatric-sized nasal cannulas are available. Special cannulas allow babies to nurse and produce less trauma of the face and nose than oxygen masks. Because of the inherently reduced minute ventilation of infants, flow requirements to the cannula must be proportionately reduced. This generally requires a pressure-compensated flowmeter accurate at delivering oxygen flows in the less than 1-3 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.
The nasal mask is a hybrid of the nasal cannula and a face mask. It can be applied to the face by either an over-the-ear lariat or a headband strap. The lower edge of the mask’s flanges rests on the upper lip, surrounding the external nose. Nasal masks have been shown to provide supplemental oxygen equivalent to the nasal cannula under low-flow conditions for adult patients. The primary advantage of the nasal mask over nasal cannulas appears to be patient comfort. 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.
The “simple” or oxygen mask is a disposable lightweight plastic device that covers both nose and mouth. It has no reservoir bag. Masks are fastened to the patient’s face by adjustment of an elastic headband; some manufacturers provide a malleable metal nose-bridge adjustment device. The seal is rarely complete: usually there is “inboard” leaking. Thus, patients receive a mixture of oxygen and secondarily entrained room air. This varies depending on the size of the leak, oxygen flow, and breathing pattern. Some brands of the simple mask connect tubing to a standard tapered fitting; others have a small room air-entrainment hole at the connection.
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 0.3-0.6 with flows of 5-10 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 greater than cannulas provide, yet need oxygen therapy for fairly 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 with severe respiratory disease who are profoundly hypoxemic, tachypneic, or unable to protect their airway from aspiration.
Masks with Gas Reservoirs
Incorporating a gas reservoir is a logical adaptation to 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 approximately 600 mL or less of gas volume. The phrase “partial rebreather” is used because “part” of the patient’s expired VT refills the bag. Usually that gas is largely dead space that should not result in significant rebreathing of carbon dioxide.
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 influence the delivered oxygen concentration. The key factor in successful application of the masks 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 10-15 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 suspected of having significant hypoxemia, with relatively normal spontaneous minute ventilation. Such patients may include victims of trauma, myocardial infarction, or carbon monoxide exposure. Profoundly dyspneic patients with gasping respiration may be served by a fixed-performance, high-flow oxygen system.
Fixed-Performance (High-Flow) Equipment
Anesthesia Bag or Bag-Mask-Valve Systems
The basic design follows that of the nonrebreathing reservoir mask but with more “capable” components. 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 specific concentration of oxygen when this is not 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 57-3 identifies total flow at various inlet flows and FIO2.
Table 57-3 Air-Entrainment Mask Input Flow versus Total Flow at Varying FIo2.1 ||Download (.pdf)
Table 57-3 Air-Entrainment Mask Input Flow versus Total Flow at Varying FIo2.1
|Fio2||Inlet Oxygen Flow (Minimum)||Total Flow (L/min)|
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 is a serious problem in unstable patients with hypoxemia and or hypercarbia.
Direct analysis of the FIO2 during air-entrainment mask breathing is difficult to perform accurately. 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. If that occurs, then inlet oxygen flows may need to be increased or an alternate device selected.
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 at slow rates and small VT will receive 100% oxygen. This problem has been addressed by the development of high-flow, high-FIO2 nebulizers. For more common applications that use an FIO2 of 0.3-0.5, room air is entrained, reducing the FIO2 and increasing the total flow output to 40-50 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 aerosol, 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.
Another concern in clinical practice is that excess water in the tubing collects and can obstruct gas flow completely or can offer increased resistance to flow. The latter may increase the FIO2 above the desired setting. Other complications include bronchospasm or laryngospasm in some patients 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 continuous positive airway pressure (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 BIPAP for spontaneously breathing patients.
Although many of the devices previously described have pediatric-sized options, 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, and cold gas can induce an increase in oxygen consumption. 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 10-15 L/min are adequate for a majority of patients.
Helium-oxygen (heliox) mixtures have a notable, yet limited clinical role. In addition to its uses in industry and deep-sea diving, heliox has a number of 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 evidence 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 6-8 L/min with oxygen. Patients’ work of breathing can be reduced with heliox as compared to a conventional oxygen/nitrogen gas mixture.
Hyperbaric oxygen 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 include decompression sickness (the “bends”), certain forms of gas embolism, gas gangrene, carbon monoxide poisoning, and treatment of certain wounds.
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.
This complication is primarily seen in patients with COPD who have chronic CO2 retention. These patients develop an altered 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. Conversely, stable, spontaneously breathing patients with profound hypercarbia (PaCO2 > 80 mm Hg) who are being supported with supplemental oxygen should not have supplemental oxygen discontinued, even for short intervals. Oxygen therapy can be indirectly hazardous for patients being monitored with pulse oximetry while receiving opioids for pain. Hypoventilation as a consequence of opioids may fail to cause worrisome change in oxygen saturation, despite respiratory rates as infrequent as 2 per minute, delaying the diagnosis.
High concentrations of oxygen can cause pulmonary atelectasis in areas of low
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 can lead to progressive widening of the alveolar-to-arterial (A-a) gradient.
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 10-20 h is generally considered safe, concentrations greater than 50-60% are undesirable for longer periods as they may lead to pulmonary toxicity.
Molecular oxygen (O2) is unusual in that each atom has unpaired electrons. This gives the molecule the paramagnetic property that allows precise measurements of oxygen concentration. Notably, internal rearrangement of these electrons or their interaction with other atoms (iron) or molecules (xanthine) can produce potentially toxic chemical species. 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 cellular DNA, sulfhydryl 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, clinical evidence supporting the use of these agents in preventing pulmonary toxicity is lacking.
In experimental animals oxygen-mediated injury of the alveolar-capillary membrane produces a syndrome that is pathologically and clinically indistinguishable from ARDS. Tracheobronchitis may also be present initially in some patients. Pulmonary O2 toxicity in newborn infants is manifested as bronchopulmonary dysplasia.
Retinopathy of Prematurity
Retinopathy of prematurity (ROP), formerly termed retrolental fibroplasia, is a neovascular retinal disorder that develops in 84% 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, 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 50-80 mm Hg (6.6-10.6 kPa). If an infant requires arterial O2
saturations of 96%-99% for cardiopulmonary reasons, fear about causing or worsening ROP is not a reason to withhold the oxygen
Hyperbaric Oxygen Toxicity
The high 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 atmospheres can cause pulmonary O2 toxicity. This may present initially with retrosternal burning, cough, and chest tightness and will result in 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.
Oxygen vigorously supports combustion. The potential for oxygen enriched gas mixtures to promote fires and explosions is discussed in Chapter 2.
Despite early intervention and appropriate respiratory care, patients with critical illness will often require mechanical ventilation. Mechanical ventilation can replace or supplement normal spontaneous ventilation. In most 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; see below) 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 57-4).
Table 57-4 Indicators of the Need for Mechanical Ventilation. ||Download (.pdf)
Table 57-4 Indicators of the Need for Mechanical Ventilation.
Arterial oxygen tension
Arterial CO2 tension
<50 mm Hg on room air
>50 mm Hg in the absence of metabolic alkalosis
|Pao2/Fio2 ratio||<300 mm Hg|
|PA-ao2 gradient||>350 mm Hg|
|Respiratory rate||>35 breaths/min|
|Tidal volume||<5 mL/kg|
|Vital capacity||<15 mL/kg|
|Maximum inspiratory force||> −25 cm H2O (eg, -15 cm H2O)|
Of the two available techniques, positive-pressure ventilation and negative-pressure ventilation, 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.
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, expiration, and the changeover from expiration to inspiration (see Chapter 4). These phases are defined by VT, ventilatory rate, inspiratory time, inspiratory gas flow, and expiratory time.
Classification of Ventilators
The complexity of modern ventilators defies simple classification. Incorporation of microprocessor technology into the newest generation of ventilators has further complicated this task. Nonetheless, ventilators are most commonly classified according to their inspiratory phase characteristics and their method of cycling from inspiration to expiration.
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. The performance of ventilators with gas injectors varies more with airway pressure. 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.
Properly functioning volume-cycled ventilators do not deliver the set volume 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 3-5 mL/cm H2O; thus, if a pressure of 30 cm H2O is generated during inspiration, 90-150 mL of the set VT is lost to the circuit. Loss of VT to 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.
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 sections on Pressure Support and Pressure Control Ventilation).
These versatile machines can be set to function in any one of a variety of inspiratory flow and cycling patterns. The microprocessor allows closed-loop control over the ventilator’s performance characteristics. Microprocessor-controlled ventilators are the norm in modern critical care units and on newer anesthesia machines.
Ventilatory mode is defined by the method by which the ventilator cycles from expiration to inspiration as well as whether the patient is able to breathe spontaneously (Table 57-5 and Figure 57-1). Most modern ventilators are capable of multiple ventilatory modes, and some (microprocessor-controlled ventilators) can combine modes simultaneously. Typical ventilatory modes are regulated to deliver a defined VT or a defined maximal inspiratory pressure. Modern ventilators can provide for breaths that are volume-controlled (machine-initiated inspiration stops when the set volume is delivered), volume-assisted (patient-initiated inspiration stops when the set volume is delivered), pressure-controlled (machine-initiated inspiration at a mandatory inspiratory pressure stops after a defined time has elapsed), pressure-assisted (patient-initiated inspiration at a mandatory inspiratory pressure stops after a defined time has elapsed), or pressure-supported (patient-initiated inspiration continues at a mandatory inspiratory pressure until the inspiratory flow declines to a defined value).
Airway pressure waveforms of ventilatory modes.
Table 57-5 Ventilatory Modes.1 ||Download (.pdf)
Table 57-5 Ventilatory Modes.1
|I to E Cycling||E to I Cycling|
|Mode||Volume||Time||Pressure||Flow||Time||Pressure||Allows Spontaneous Ventilation||Weaning Mode|
Continuous Mandatory Ventilation (CMV)
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.
Assist-Control (AC) Ventilation
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 (see below).
Intermittent Mandatory Ventilation (IMV)
IMV allows spontaneous ventilation while the patient is on the ventilator. A selected number of mechanical breaths (with fixed VT) is 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 VT and frequency 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, resulting in a very large VT. As with CMV and AC, settings to limit inspiratory pressure guard against pulmonary barotrauma. The advantages of SIMV include patient comfort, and if used for weaning, the machine breaths provide a backup if the patient becomes fatigued. However, if the rate is too low (4 breaths/min), the backup may be too low, particularly for weak patients who may not be able to overcome the added work of breathing during spontaneous breaths.
IMV circuits provide a continuous supply of gas flow for spontaneous ventilation between mechanical breaths. Modern ventilators incorporate SIMV into their design, but older models must be modified by 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.
The IMV discussion has considered this to be a volume-limited format; however, it can also be provided in pressure-limited format if desired (see below).
Mandatory Minute Ventilation (MMV)
With MMV, the patient is able to breathe spontaneously (with pressure support) and also receive SIMV mechanical breaths, while the machine monitors the exhaled minute ventilation. In this mode, the machine continuously adjusts the number of SIMV mechanical breaths so that the sum total of spontaneous and mechanical ventilation equals the desired set minute ventilation. The role of this mode in weaning remains to be defined.
Pressure Support Ventilation (PSV)
Pressure support ventilation 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 57-2). 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 or the patient becomes apneic. Pressure support is often used in conjunction with IMV (Figure 57-3). The IMV machine 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.
Pressure support ventilation. The patient initiates a breath; the machine is set to deliver 15 cm H2O pressure (above 5 cm H2O of continuous positive airway pressure [CPAP]). When flow ceases, the machine cycles into the expiratory mode.
Intermittent mechanical ventilation with pressure support. M = machine breath → set tidal volume (Vt) delivered. S = spontaneous breath, 15 cm of pressure support over 5 cm of PEEP. Vt depends on patient effort and lung mechanics. V, flow; Paw, partial airway pressure; PEEP, positive end-expiratory pressure.
Pressure Control Ventilation (PCV)
Pressure control ventilation is similar to 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. PCV
may be used in both the AC
and IMV modes. In AC
, 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’s pulmonary muscle strength. 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, provided adequate PEEP levels are used.
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). Any change 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 I:E ratio ventilation (IRV) (see below) in an effort to recruit collapsed and flooded alveoli. The disadvantage of using IRV with PCV
is that the patient needs to be heavily sedated and often paralyzed to tolerate this particular ventilatory mode.
With PCV, pressure and inspiratory time are preset, whereas airflow 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 in this circumstance the inspiratory pressure can be very high.
Inverse I:E Ratio Ventilation (IRV)
IRV reverses the normal inspiratory:expiratory time ratio of 1:3 or greater to a ratio of greater than 1:1. This may be achieved by adding an end-inspiratory pause, by decreasing peak inspiratory flow during volume-cycled 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.
Airway Pressure Release Ventilation (APRV)
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 57-4). The inspiratory and expiratory times, high and low PEEP levels, and spontaneous respiratory activity determine minute ventilation. Initial settings include a minimum PEEP of 10-12 cm H2O and a release level of 5-10 cm H2O. 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.
Airway pressure release ventilation.
High-Frequency Ventilation (HFV)
Three forms of HFV are available. High-frequency positive-pressure ventilation involves delivering a small “conventional” VT at a rate of 60-120 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 120-600 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 180-3000 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 (including convective ventilation, asymmetrical velocity profiles, Taylor dispersion, pendelluft, molecular diffusion, and cardiogenic mixing). 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 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 in the operating room are typically a rate of 120-240 breaths/min, an inspiratory time of 33%, and a drive pressure of 15-30 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.
Care of Patients Requiring Mechanical Ventilation
Tracheal intubation for mechanical ventilation is most commonly undertaken in ICU patients to manage pulmonary failure. Both nasotracheal and orotracheal intubation appear to be relatively safe for at least 2-3 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 significant adverse events associated with its use, 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 intubation will also generally necessitate use of a smaller diameter tube than orotracheal intubation, and this can make it more difficult to clear secretions and can limit fiberoptic bronchoscopy to use of smaller devices.
Intubation usually can be carried out without the use of sedation or muscle paralysis in agonal and 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; administration of a paralytic agent also greatly facilitates orotracheal intubation. Small doses of relatively short-acting agents are generally used; popular agents include midazolam, etomidate, dexmedetomidine, and propofol. Succinylcholine or a nondepolarizing 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.
When left in place for more than 2-3 weeks, both orotracheal and nasotracheal tubes predispose patients to subglottic stenosis. If longer periods of mechanical ventilation are necessary, the tracheal tube should generally be replaced by a cuffed tracheostomy tube. If it is anticipated that a tracheal tube will be required for more than 2 weeks, a tracheostomy may be performed soon after intubation. There is a trend to earlier tracheostomy in victims of trauma, particularly those with major head injuries. While earlier tracheostomy does not reduce mortality, it does tend to 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 10-12 breaths/min and a VT of 8-10 mL/kg; lower VT (6-8 mL/kg) may be necessary to avoid high peak inflation pressures (>35-40 cm H2O) and pulmonary barotrauma and volutrauma. High airway pressures that overdistend alveoli (transalveolar pressure >35 cm H2O) have been shown experimentally to promote lung injury. Likewise, compared with a VT of 12 mL/kg, a VT of 6 mL/kg and plateau pressure (Pplt) less than 30 cm H2O have been associated with reduced mortality in patients with ARDS. Partial ventilatory support is usually provided by low SIMV settings (<8 breaths/ min), either with or without pressure support. Lower Pplt (<20-30 cm H2O) can help preserve cardiac output, may be less likely to alter normal ventilation/perfusion relationships, and is the current recommendation.
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 i.d. in adults) increase resistance and should be avoided whenever possible. The simultaneous use of pressure support of 5-15 cm H2O during SIMV can compensate for tube and circuit resistance.
The addition of 5-8 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 5-8 cm H2O accompanies VT of appropriate volumes.
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. Nondepolarizing paralytic agents are used in combination with sedation when sedation alone and all other means to ventilate the patient have failed.
Patients on mechanical ventilation require continuous monitoring for adverse hemodynamic and pulmonary effects from positive pressure in the airways. Continuous electrocardiography and pulse oximetry are useful. Direct intraarterial pressure monitoring also allows frequent sampling of arterial blood for respiratory gas analysis (both a convenience and a disadvantage, given the large number of unnecessary laboratory tests that are often performed on patients with critical illness). 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. Central venous (and rarely pulmonary artery) pressure monitoring are used in hemodynamically unstable patients. Frequent 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 Pplt for a set VT can indicate worsening compliance. A declining blood pressure and increasing Pplt from dynamic hyperinflation (autoPEEP) can be quickly diagnosed 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.
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, metabolic acidosis or alkalosis, anemia, increased CO2 production due to increased carbohydrate loads, altered mental status, and sleep deprivation should be adequately treated. Underlying lung disease and respiratory muscle wasting from prolonged disuse often complicate weaning. Patients who fail to wean despite apparent readiness often have COPD or chronic heart failure.
Weaning (or liberation) from mechanical ventilation should be considered when patients no longer meet general criteria for mechanical ventilation (see Table 57-4). 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 57-6). Useful weaning parameters include arterial blood gas tensions, respiratory rate, and rapid shallow breathing index (RSBI, see below). Intact airway reflexes and a cooperative patient are also mandatory prior to completion of the 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 imperative 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:
Table 57-6 Mechanical Criteria for Weaning/Extubation. ||Download (.pdf)
Table 57-6 Mechanical Criteria for Weaning/Extubation.
|Inspiratory pressure||<−25 cm H2O|
|Tidal volume||>5 mL/kg|
|Vital capacity||>10 mL/kg|
|Minute ventilation||<10 mL|
|Rapid shallow breathing index||<100|
Patients with an RSBI less than 100 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. Mandatory minute ventilation has also been suggested as an ideal weaning technique, but experience with it is limited. Finally, 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.
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 5-8 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 15-30 min at each setting. When an IMV of 2-4 breaths is reached, mechanical ventilation is discontinued if arterial oxygenation remains acceptable.
Weaning with PSV alone is accomplished by gradually decreasing the pressure support level by 2-3 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 4-6 mL/kg and an f of less than 30 with acceptable PaO2 and PaCO2. When a pressure support level of 5-8 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 10-30 min are initiated and progressively increased by 5-10 min or longer per trial as long as the patient appears comfortable and maintains acceptable arterial blood gas measurements.
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
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, nasal “pillows” (ADAM circuit), or nasal prongs (neonatal) 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 above 15 cm H2O require an artificial airway.
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 57-5). 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.
Airway pressure during positive end-expiratory pressure (PEEP) and continuous positive airway pressure (CPAP). Note that by increasing inspiratory gas flows, PEEP progressively becomes CPAP.
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 57-6). 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.
Pressure-volume curve for pulmonary system (eg, lung, thoracic). Inflection point (IP) above which the majority of alveoli are recruited. E, result of excessive pressure when alveoli are overdistended and pulmonary compliance decreases.
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 excessive PEEP or CPAP, particularly at levels greater than 20 cm H2
O. 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 is the result of failure of an air leak 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, stacking of breaths (from too frequent breaths or too short expiratory times) so that intrinsic PEEP (dynamic hyperinflation or autoPEEP) develops, large VT
(>10-15 mL/kg), and younger age.
Adverse Nonpulmonary Effects of PEEP & CPAP
Nonpulmonary adverse effects are primarily circulatory and are related to transmission of the elevated airway pressure to the contents of the chest. Fortunately, 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 are often seen as mean airway pressure and, secondarily, mean intrathoracic pressure rise. The principal mechanism appears to be intrathoracic pressure-related inhibition of return of venous blood to the heart. Other mechanisms may include leftward displacement of the interventricular septum (interfering with left ventricular filling) because of the increase in pulmonary vascular resistance (increased right ventricular afterload) from overdistention of alveoli, leading to an increase in right ventricular volume. Left ventricular compliance may therefore be reduced; when this occurs, to achieve the same cardiac output may require a higher filling pressure. 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 central venous pressure and reductions in cardiac output decrease both renal and hepatic blood flow. Circulating levels of antidiuretic hormone and angiotensin are usually elevated. Urinary output, glomerular filtration, and free water clearance decrease.
Increased end-expiratory pressures, because they impede blood drainage from the brain and blood return to the heart, may increase intracranial pressure in patients whose ventricular compliance is decreased. Therefore, in patients on mechanical ventilation for acute lung injury and who have 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 latter is best accomplished with an adequate cardiac output and hemoglobin concentration. Ideally, mixed venous oxygen tensions or the arteriovenous oxygen content difference should be followed. 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 and should be guided by hemodynamic measurements.
At optimal PEEP the beneficial effects of PEEP exceed any detrimental risks. Practically, PEEP is usually added in increments of 3-5 cm H2O until the desired therapeutic end point is reached. The most commonly suggested end point is an arterial oxygen saturation of hemoglobin of greater than 88-90% 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 (
> 50-60%). Monitoring lung compliance and dead space has also been suggested.