Noninvasive Respiratory Support

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Chapter 28 Noninvasive Respiratory Support

In this chapter, supplemental oxygen therapy, humidification systems, adjunctive respiratory therapy, and noninvasive ventilation (NIV) are discussed. NIV encompasses various methods of positive pressure ventilation, including continuous positive airway pressure (CPAP), delivered without an endotracheal tube.1

OXYGEN THERAPY

Oxygen delivery to the tissues depends on arterial oxygen content, cardiac output, and individual organ perfusion. Arterial oxygen content depends on the hemoglobin concentration and arterial oxygen saturation (Sao2; see Equation 1-13). The latter is, in turn, dependent on the oxyhemoglobin dissociation curve (see Fig. 1-14) and the arterial partial pressure of oxygen (Pao2) (see Chapter 1). Supplemental oxygen therapy is indicated to maintain the Pao2 above 8 κPa (60 mmHg) or the Sao2 above 90%. Only low concentrations of supplemental oxygen are required to treat hypoxemia due to hypoventilation. In contrast, high concentrations of oxygen may be required to treat hypoxemia due to ventilation/perfusion mismatch. Oxygen is ineffective if hypoxemia is due to pure shunt. High-concentration oxygen therapy in the setting of hypoventilation may mask the development of severe hypercarbia and respiratory acidosis (see Chapter 1).

Impaired gas exchange is almost universally present following cardiac and thoracic surgery, so oxygen is indicated for the duration of a patient’s stay in the intensive care unit (ICU). It should also be continued following discharge from the ICU if a patient is receiving opioid analgesia because that predisposes the patient to nocturnal desaturation.2 Supplemental oxygen therapy during the perioperative period has also been shown to reduce the incidence of surgical wound infections.3

Excessive oxygen therapy is not without risk. High-concentration oxygen promotes absorption atelectasis and, in patients with severe chronic obstructive pulmonary disease (COPD), it may exacerbate hypercarbia (see Chapter 27). Administration of high oxygen concentrations (FIo2 >0.6) for longer than several days may potentially cause direct pulmonary toxicity and should be avoided if possible.4 However, supplemental oxygen should not be withheld in the presence of clinically significant hypoxemia (Sao2 <85% to 90%).

Oxygen Delivery Systems

Noninvasive methods of oxygen delivery can be divided into variable-performance and fixed-performance systems. In order to provide a fixed concentration of oxygen, the system must deliver gas at a flow rate that matches the patient’s peak inspiratory flow rate. This is approximately 25 to 35 l/min at rest but can rise to over 60 l/min with respiratory distress. If delivered flow is less than peak inspiratory flow, entrainment of room air dilutes the inspired gas and results in a reduced FIo2. Piped and bottled oxygen and air sources are dry and must be humidified if administered at high flow rates (see later material).

Variable-Performance Systems

Variable-performance systems have a flow rate or a reservoir size that is not sufficient to prevent entrainment of air at high-peak inspiratory flow rates.

Manual Resuscitators.

The components of manual resuscitators (such as the Laerdal and the Ambu) are illustrated in Figure 28-1. As with other variableperformance systems, FIo2 depends on the oxygen flow, tidal volume, and respiratory rate, but it can be increased by attaching an oxygen reservoir bag to the air entrainment inlet. The resuscitation bag is designed for short-term emergency use when augmentation of a patient’s respiratory effort by manual ventilation is required. Care should be taken with a patient who has respiratory distress but good respiratory drive because spontaneous breathing through a manual resuscitator increases the work of breathing, potentially worsening the respiratory distress.

HUMIDIFICATION

Humidity is a measure of the amount of water vapor in a gas. It may be expressed as a partial pressure (kPa), an absolute value (g/m3), or a relative value (%). The last is the absolute mass of water divided by the maximum mass of water that could exist in vapor form in the gas at a certain temperature.

During quiet nose breathing, inspired gas is warmed to body temperature and fully saturated with water vapor before it reaches the carina (absolute humidity 43.4 g/m3, relative humidity 100%, partial pressure 6.3 κPa at 37°C at sea level). Humidification occurs primarily in the nose, where inspired gases are exposed to a large surface area of highly vascular mucosa. Mouth breathing, particularly at high peak inspiratory flow rates, results in less humidification by the upper airway.

Normal mucociliary function of the large airways is dependent on adequate humidification of the inspired gas. Abnormal mucociliary function results in cytologic damage and leads to the accumulation of tenacious secretions and microatelectasis. At a relative humidity of 75% (32.5 g/m3 at 37°C), mucociliary function is impaired; at 50%, it fails entirely. Changes in mucociliary function occur within minutes to a few hours if low-humidity gases are inspired. This is the rationale for providing humidification of inspiratory gas of at least 32.5 g/m3 to all patients who are receiving high flows of inspiratory gases and to those whose upper airways have been bypassed using an endotracheal tube.

Humidification Devices

ADJUNCTIVE RESPIRATORY THERAPIES

Patients unable to generate high expiratory flow rates because of respiratory muscle weakness or obstructive airway disease may be unable to cough effectively. This leads to the accumulation of excessive secretions and entry of foreign material into the lungs, with the development of atelectasis, impaired gas exchange, and pneumonia. When cough is poor, lung-expansion techniques and maintenance of normal mucociliary clearance become important.

NONINVASIVE VENTILATION

Positive-pressure ventilation increases functional residual capacity, improves oxygenation and lung mechanics, and reduces the work of breathing. In patients with auto positive end-expiratory pressure (PEEP), external PEEP (or CPAP) reduces the inspiratory threshold load (see Fig. 27-4), which reduces the work of breathing. In addition, tidal positive pressure ventilation (e.g., bilevel positive airway pressure ventilation) unloads inspiratory muscles, augments tidal volume, and reduces arterial carbon dioxide tension (Paco2). In patients with left ventricular dysfunction, cardiac performance is improved by reduction in left ventricular afterload. The rationale for NIV is to obtain these benefits without the disadvantages of endotracheal intubation, such as the need for sedation and increased risk of nosocomial pneumonia.1

Patients treated with NIV require continuous monitoring of oxygen saturation, heart rate, blood pressure, respiratory rate, respiratory pattern, ability to expectorate, and mental status. Facilities for urgent intubation and initiation of invasive ventilation must be rapidly available. In most cases, an intraarterial catheter for monitoring blood pressure and arterial blood gases is indicated. Inappropriate persistence with NIV in the face of clinical deterioration of a patient may lead to serious adverse events and worse outcome. Patients in whom NIV is most likely to be successful have a low volume of respiratory secretions, intact dentition, and minimal nonrespiratory organ dysfunction.

Indications and Contraindications

NIV is well established for treating acute exacerbations of COPD.68 However, of greater relevance to the cardiothoracic ICU is the use of NIV in treating cardiogenic pulmonary edema, postoperative respiratory failure, and thoracic trauma. Patient refusal or failure to cooperate precludes the use of NIV. Other contraindications to NIV are listed in Table 28-1.

Table 28-1 Contraindications to Noninvasive Ventilation

Neurologic Impaired level of consciousness, confusion, or inability to protect airway
Anatomic Trauma or recent surgery to the upper airway, face, or esophagus
  Upper airway obstruction
Respiratory Severe hypoxemia
  Moderate or large quantity of sputum
  Weak cough
  Undrained pneumothorax
Cardiovascular Marked hemodynamic instability
Abdominal Abdominal distension or vomiting

Cardiogenic Pulmonary Edema

In patients with acute cardiogenic pulmonary edema, the addition of face-mask CPAP to standard medical therapy leads to a more rapid improvement in respiratory rate, heart rate, Paco2, and oxygenation than does standard medical therapy (oxygen, morphine, diuretics, and nitrates) alone.9,10 In addition, CPAP reduces the need for endotracheal intubation and may decrease mortality rates.11 Similar physiologic benefits have been demonstrated with bilevel positive airway pressure ventilation.12,13 In a head-to-head comparison of bilevel positive airway pressure and CPAP, an increased rate of myocardial infarction was reported in the former group.14 However, because a greater proportion of patients had chest pain at entry into the bilevel support group, it is possible that this outcome was not related to the mode of ventilation. Until more data are available, CPAP is the preferred mode of NIV.

An improvement in vital signs should be seen within 30 minutes, and many patients can be successfully weaned within a few hours. A patient who requires intubation because of deterioration despite CPAP therapy has a very poor prognosis unless the underlying cause of the cardiogenic pulmonary edema responds to a specific intervention (e.g., thrombolysis, percutaneous coronary intervention, or cardiac surgery).

Postoperative Respiratory Failure

NIV may be used to treat (rescue therapy) or prevent (prophylaxis) postoperative respiratory failure. Prophylaxis refers to the application of NIV immediately following extubation so as to prevent respiratory failure. As rescue therapy, NIV has been shown to reduce the incidence of reintubation and other complications in patients who develop respiratory distress following thoracic surgery15 and solid-organ (liver, kidney, lung) transplantation.16 It has also been shown to be beneficial as rescue therapy following major abdominal surgery.17

In patients deemed at high risk for postextubation respiratory failure, prophylactic NIV has been shown to reduce the need for reintubation,18,19 with a possible survival advantage in hypercarbic patients19; however, in both trials, postoperative patients constituted only a minority of study subjects. Neither rescue nor prophylactic NIV has been specifically studied following cardiac surgery.

CPAP is a highly efficacious treatment for obstructive sleep apnea and, although there are few trial data, prophylactic use during the postoperative period is strongly recommended in patients with this condition who were being treated with NIV preoperatively.20

No clear advantage of either CPAP or bilevel positive airways pressure can be identified from the literature for treating postoperative patients. As a simple rule of thumb, CPAP may be used to treat isolated hypoxemia, and bilevel positive airways pressure can be used to treat hypoxemia associated with hypercarbia.

Delivery systems and settings

Continuous Positive Airway Pressure Systems

Continuous Fresh-Gas-Flow Systems.

Continuous fresh-gas-flow systems consist of a humidified fixedperformance gas delivery system, an interface (tightfitting mask), and a spring-loaded valve (CPAP valve) that provides constant pressure against expiratory flow (Fig. 28-2). Gas delivery is usually provided by a high-flow system, but gas flow can be reduced and system-imposed work of breathing reduced if a weighted, high-compliance reservoir bag is incorporated into the inspiratory limb of the system.22 High fresh-gas-flow rates are generated by a pressurized gas supply, a gas turbine, or a jet Venturi mechanism. The addition of a pressure-relief valve in the inspiratory limb of the circuit provides safety against barotrauma in the event that the CPAP valve becomes obstructed.

Bilevel Positive Airway Pressure Ventilation

Theoretically, any mode of ventilation can be used for NIV. Intensive care ventilators provide a wide choice of modes, but they are designed for invasive ventilation and may be unable to compensate for interface leaks, potentially resulting in inadequate tidal ventilation (see subsequent material). Modern noninvasive ventilators are leak tolerant, can provide high inspiratory flow rates and high FIo2, and have appropriate monitors and alarms. In general, pressure-limited modes are better tolerated than volume-limited modes and are less prone to inadequate tidal breath delivery in the presence of a significant leak. Therefore, the majority of NIV is performed with CPAP plus pressure support or bilevel positive airway pressure modes, both of which are pressure-limited modes.

The pressure-support mode is either pressure-triggered or flow-triggered and is flow-cycled (see Chapter 29). The bilevel positive airway pressure mode is also pressure- or flow-triggered and is flow-cycled but has a facility for time triggering at a set respiratory rate (spontaneous/timed mode). Bilevel positive airway pressure has two pressure settings—the expiratory positive airway pressure (EPAP) and the inspiratory positive airway pressure (IPAP). The level of IPAP is inclusive of EPAP. (In contrast, the level of pressure support is in addition to CPAP.) Standard initial settings are an EPAP of 4 to 8 cm H2O and an IPAP of 8 to 12 cm H2O, with an FIo2 sufficient to maintain the SPo2 above 90%. These pressures can subsequently be increased according to the patient’s response and tolerance, but IPAP values over 20 cm H2O are likely to cause unacceptable leak or patient discomfort. Because bilevel positive airway pressure is primarily a spontaneous mode of ventilation, the breath rate is set to a lower rate than the patient’s expected breath rate. A rate of 8 to 12 is appropriate. Bilevel positive airway pressure (BiPAP), which is available in the Vision noninvasive ventilator (Respironics, Murrysville, PA; Fig. 28-3) is an example of a commercially available bilevel positive airway pressure NIV mode.

Confusion in terminology can arise because BIPAP (with a capital I) refers to biphasic positive airway pressure mode, which is similar to pressure-control ventilation, with the ventilator switching between inspiratory and expiratory pressure levels at set time intervals (i.e., time cycled). It differs from true (invasive) pressure-control ventilation in that additional spontaneous breathing is allowed at both pressure levels because of the presence of an open (active) expiratory valve. In contrast, the invasive pressure-control ventilation mode has a closed (or inactive) expiratory valve during inspiration.

Patient-ventilator dysynchrony

Even with minimal interface leak, patient-ventilator dysynchrony is common with bilevel modes and may be the principal determinant of success or failure of NIV.24 Graphic monitoring of pressure-time and flow-time signals can help to detect specific patterns of dysynchrony.

Inspiratory Dysynchrony

Inspiratory dysynchrony usually occurs during the trigger phase (the signal that initiates the change to the inspiratory pressure level). It manifests as ineffective respiratory efforts, with either failure to trigger or, at the other extreme, autotriggering. Failure to trigger is likely in patients with dynamic lung hyperinflation and auto-PEEP that is much higher than the set EPAP level. Autotriggering occurs with sensitive trigger settings and either a variable leak or water in the tubing. Flow triggering reduces the inspiratory effort and the trigger delay more than pressure triggering does, but all ventilators have unavoidable, intrinsic trigger-activation delays, usually greater than 120 ms.25,26 The theoretic advantage of flow triggering may be less significant in modern ventilators that have pressure sensors closer to the patient, thus reducing trigger delay.

The flow waveform method of triggering (BiPAP Vision, Respironics) results in a transition from expiration to inspiration by means of volume triggering or by the shape signal method (Fig. 28-4). The flow waveform method results in fewer episodes of trigger failure but more frequent autotriggering than standard flow triggering, although this has been studied only in intubated patients.25,27

Inspiratory dysynchrony may also result from an inappropriate rate of pressure rise to the set inspiratory pressure level (rise time; see Fig. 28-4). A rapid rise time reduces inspiratory effort but increases air leak and worsens patient tolerance.28

Interfaces

Appropriate selection and application of the patient interface is essential for the successful management of NIV.

REFERENCES

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2 Stone JG, Cozine KA, Wald A. Nocturnal oxygenation during patient-controlled analgesia. Anesth Analg. 1999;89:104-110.

3 Greif R, Akca O, Horn EP, et al. Supplemental perioperative oxygen to reduce the incidence of surgical-wound infection. Outcomes Research Group. N Engl J Med. 2000;342:161-167.

4 Jenkinson SG. Oxygen toxicity. New Horiz. 1993;1:504-511.

5 Dhand R, Tobin MJ. Inhaled bronchodilator therapy in mechanically ventilated patients. Am J Respir Crit Care Med. 1997;156:3-10.

6 Brochard L, Mancebo J, Wysocki M, et al. Noninvasive ventilation for acute exacerbations of chronic obstructive pulmonary disease. N Engl J Med. 1995;333:817-822.

7 Plant PK, Owen JL, Elliott MW. Early use of non-invasive ventilation for acute exacerbations of chronic obstructive pulmonary disease on general respiratory wards: a multicentre randomised controlled trial. Lancet. 2000;355:1931-1935.

8 Ram FS, Picot J, Lightowler J, et al. Non-invasive positive pressure ventilation for treatment of respiratory failure due to exacerbations of chronic obstructive pulmonary disease. Cochrane Database of Systematic Reviews. 2004:CD 004104.

9 Bersten AD, Holt AW, Vedig AE, et al. Treatment of severe cardiogenic pulmonary edema with continuous positive airway pressure delivered by face mask. N Engl J Med. 1991;325:1825-1830.

10 Rasanen J, Heikkila J, Downs J, et al. Continuous positive airway pressure by face mask in acute cardiogenic pulmonary edema. Am J Cardiol. 1985;55:296-300.

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13 Park M, Sangean MC, Volpe Mde S, et al. Randomized, prospective trial of oxygen, continuous positive airway pressure, and bilevel positive airway pressure by face mask in acute cardiogenic pulmonary edema. Crit Care Med. 2004;32:2407-2415.

14 Mehta S, Jay GD, Woolard RH, et al. Randomized, prospective trial of bilevel versus continuous positive airway pressure in acute pulmonary edema. Crit Care Med. 1997;25:620-628.

15 Auriant I, Jallot A, Herve P, et al. Noninvasive ventilation reduces mortality in acute respiratory failure following lung resection. Am J Respir Crit Care Med. 2001;164:1231-1235.

16 Antonelli M, Conti G, Bufi M, et al. Noninvasive ventilation for treatment of acute respiratory failure in patients undergoing solid organ transplantation: a randomized trial. JAMA. 2000;283:235-241.

17 Squadrone V, Coha M, Cerutti E, et al. Continuous positive airway pressure for treatment of postoperative hypoxemia: a randomized controlled trial. JAMA. 2005;293:589-595.

18 Nava S, Gregoretti C, Fanfulla F, et al. Noninvasive ventilation to prevent respiratory failure after extubation in high-risk patients. Crit Care Med. 2005;33:2465-2470.

19 Ferrer M, Valencia M, Nicolas JM, et al. Early noninvasive ventilation averts extubation failure in patients at risk: a randomized trial. Am J Respir Crit Care Med. 2006;173:164-170.

20 Gross JB, Bachenberg KL, Benumof JL, et al. Practice guidelines for the perioperative management of patients with obstructive sleep apnea: a report by the American Society of Anesthesiologists Task Force on Perioperative Management of patients with obstructive sleep apnea. Anesthesiology. 2006;104:1081-1093. quiz 1117-1118

21 Gunduz M, Unlugenc H, Ozalevli M, et al. A comparative study of continuous positive airway pressure (CPAP) and intermittent positive pressure ventilation (IPPV) in patients with flail chest. Emerg Med J. 2005;22:325-329.

22 Bersten AD, Rutten AJ, Vedig AE. Optimizing fresh gas flow and circuit design for the delivery of continuous positive airway pressure. Crit Care Med. 1991;19:266-270.

23 Takeuchi M, Williams P, Hess D, et al. Continuous positive airway pressure in new-generation mechanical ventilators: a lung model study. Anesthesiology. 2002;96:162-172.

24 Nava S, Ceriana P. Patient-ventilator interaction during noninvasive positive pressure ventilation. Respir Care Clin North Am. 2005;11:281-293.

25 Nava S, Ambrosino N, Bruschi C, et al. Physiological effects of flow and pressure triggering during non-invasive mechanical ventilation in patients with chronic obstructive pulmonary disease. Thorax. 1997;52:249-254.

26 Stell IM, Paul G, Lee KC, et al. Noninvasive ventilator triggering in chronic obstructive pulmonary disease: a test lung comparison. Am J Respir Crit Care Med. 2001;164:2092-2097.

27 Prinianakis G, Kondili E, Georgopoulos D. Effects of the flow waveform method of triggering and cycling on patient-ventilator interaction during pressure support. Intens Care Med. 2003;29:1950-1959.

28 Prinianakis G, Delmastro M, Carlucci A, et al. Effect of varying the pressurisation rate during noninvasive pressure support ventilation. Eur Respir J. 2004;23:314-320.

29 Calderini E, Confalonieri M, Puccio PG, et al. Patient-ventilator asynchrony during noninvasive ventilation: the role of expiratory trigger. Intens Care Med. 1999;25:662-667.