Initial Ventilator Settings
Initial ventilator settings depend on the goals of ventilation (e.g., full respiratory muscle rest versus partial exercise), the patient's respiratory system mechanics, and minute ventilation requirements. Although each critically ill patient presents myriad challenges, it is possible to identify four subsets of ventilated patients: the patient with normal lung mechanics and gas exchange, the patient with predominant airflow obstruction, the patient with acute hypoxemic respiratory failure, and the patient with restrictive lung or chest wall disease. Specific recommendations regarding ventilator settings are detailed more fully in Chaps. 38, 39, 40, and 42 but are reviewed here briefly, in addition to guidelines for ventilating patients with normal respiratory system mechanics.
In all patients, the initial FiO2 should usually be 0.5 to 1.0 to ensure adequate oxygenation, although usually it can be decreased within minutes when guided by pulse oximetry and, in the appropriate setting, applying PEEP. In the first minutes after institution of mechanical ventilation, the physician should remain alert for several common problems, most notably, airway malposition, aspiration, and hypotension. Positive-pressure ventilation may decrease venous return and, hence, cardiac output, especially in patients with a low mean systemic pressure (e.g., hypovolemia, venodilating drugs, decreased sympathetic tone from sedating drugs, or neuromuscular disease) or a very high ventilation-related pleural pressure (e.g., chest wall restriction, large amounts of PEEP, or airway obstruction causing autoPEEP). If hypotension occurs, intravascular volume should be expanded rapidly while steps are taken to decrease the pleural pressure (a smaller Vt
and less minute ventilation). Meanwhile, the FiO2 should be raised to 100%. If these steps do not rapidly restore the circulation, another complicating event (pneumothorax or myocardial ischemia) should be considered while the patient is taken off the ventilator and bagged manually to assess respiratory load and to observe the response of blood pressure to a brief suspension of positive-pressure ventilation.
The Patient with Normal Respiratory Mechanics and Gas Exchange
Patients with normal lung mechanics and gas exchange may require mechanical ventilation because of loss of the central drive to breathe (e.g., drug overdose or structural injury to the brain stem), because of neuromuscular weakness (e.g., high cervical cord injury, acute idiopathic myelitis, or myasthenia gravis), as an adjunctive therapy in the treatment of shock,40,41 or to achieve hyperventilation (e.g., in the treatment of elevated intracranial pressure after head trauma). After intubation, initial ventilator orders should be an FiO2 of 0.5 to 1.0, a Vt
of 8 to 12 mL/kg, a respiratory rate of 8 to 12 breaths/min, and a V̇ of 50 to 60 L/min (Table 36-3). Alternatively, if the patient has sufficient drive and is not profoundly weak, PSV can be used. The level of pressure support is adjusted (usually to the range of 10 to 20 cm H2O above PEEP) to bring the respiratory rate down into the low 20s, usually corresponding to a Vt
of about 500 mL. It is important to realize that PSV is mechanically supported but entirely spontaneous, with no machine “backup” unless mixed with a mode such as SIMV. Thus, hypoventilation may occur despite the use of PSV, if there is further deterioration of muscle strength or blunting of drive by disease or drugs. If gas exchange is entirely normal, the FiO2 likely can be decreased further based on pulse oximetry or arterial blood gas determinations. However, because right mainstem intubation, aspiration, and bronchospasm are relatively common complications of intubation, it is wise to initiate ventilation with the FiO2 at 0.5 or higher. Should hyperventilation be desired, the initial respiratory rate should be increased to the range of 16 to 20 breaths/min. The V̇ can be increased if the patient complains of air hunger, but 50 to 60 L/min is often sufficient.1 Even in most tachypneic patients with underlying lung disease and certainly in those individuals with normal lung mechanics, a V̇ greater than 60 L/min is rarely necessary or useful.
Table 36–3. Initial Ventilator Settings ||Download (.pdf)
Table 36–3. Initial Ventilator Settings
|Mode||FiO2||PEEP (cm H2O)||Vt (mL/kg)||RR (min21)||Flow (L/min)||Sighs|
|AHRF||ACV||1.0||15c||4–6, using IBW||24||60||No|
Soon after the initiation of ventilation, airway pressure and flow waveforms should be inspected for evidence of dyssynchrony between the patient and the ventilator or undesired patient effort (see Chap. 32). If the goal of ventilation is full rest, the patient's drive often can be suppressed by increasing the V̇, f, or Vt.42,43 The latter two changes may induce respiratory alkalemia. If such adjustments do not diminish breathing effort, despite normal blood gases, to an undetectable level, sedation may be necessary. If this does not abolish inspiratory efforts and full rest is essential (as in shock), muscle paralysis can be considered.
Measures to prevent atelectasis should include sighs (6 to 12 per hour at 1.5 to 2 times the Vt
) or small amounts of PEEP (5 to 7.5 cm H2O). This is particularly important in patients with neuromuscular diseases during protracted ventilation because atelectasis is common. In these patients, we use the upper limit of Vt
(12 mL/kg). Three-point turning and chest physiotherapy are desirable in all patients unless other conditions preclude their use. Rotating beds may be effective in some patients for preventing atelectasis and pneumonia.44
Patients with Dominant Airflow Obstruction
Two general types of patients require mechanical ventilation for significant airflow obstruction; those with status asthmaticus (see Chap. 40) and those with exacerbations of chronic airflow obstruction (see Chap. 39). Rare alternative causes are inhalation injury or central airway lesions, such as tumor or foreign body, not bypassed with the endotracheal tube. In isolated upper airway injuries, assessment of the extent of damage is often possible by bronchoscopy shortly before or at the time of intubation. Bronchoscopy should not be performed routinely in patients with asthma.
Because the gas exchange abnormalities of airflow obstruction are largely limited to ventilation-perfusion mismatch, an FiO2 of 0.5 suffices in the vast majority of patients.45 Requirements for a higher FiO2 should prompt a search for an alveolar filling process or for lobar atelectasis. We have had success ventilating these patients with PSV by setting Pi
at 25 to 30 cm H2O. Because these patients are typically anxious, we often give large doses of narcotics to suppress drive, an approach that, when combined with high-level PSV, often leads to an unusual but stable pattern of breathing, with a Vt
larger than 900 mL and an f of 3 to 7. This approach appears to minimize autoPEEP by allowing such a long Te. Alternatively, ventilation can be initiated using the ACV mode with a normal Vt (5 to 7 mL/kg) and respiratory rate of 12 to 15 breaths/min (see Table 36-3). A peak flow of 60 L/min is recommended, and higher flow rates do little to increase Te. For example, if the Vt is 500 mL, the respiratory rate is 15 breaths/min, and the V̇ 60 L/min, the Te is 3.5 seconds. Raising V̇ (dramatically) to 120 L/min increases the Te to only 3.75 seconds, a trivial improvement. In contrast, a small reduction in respiratory rate to 14 breaths/min increases the Te to 3.8 seconds. This example emphasizes not only the relative lack of benefit of raising the flow rate but also the importance of minimizing minute ventilation when the goal is to reduce autoPEEP. If the patient is triggering the ventilator, it is essential that some PEEP be added to reduce the work of triggering. This does not generally worsen the hyperinflation as long as PEEP is not higher than about 85% of the autoPEEP.16,46–48 Ventilatory goals are to minimize alveolar overdistention (keep Pplat <30) and to minimize dynamic hyperinflation (keep autoPEEP <10 cm H2O or end-inspiratory lung volume <20 mL/kg), a strategy that largely prevents barotrauma.49 Reducing minute ventilation to achieve these goals generally causes the partial pressure of CO2 to rise above 40 mm Hg, often to 70 mm Hg or higher. Although this requires sedation, such permissive hypercapnia is quite well tolerated except in patients with increased intracranial pressure and perhaps in those with ventricular dysfunction or pulmonary hypertension.
Patients with status asthmaticus requiring mechanical ventilation are usually extremely anxious and distressed, especially when ventilated using a volume-preset mode. Deep sedation is usually necessary and supplemented in rare patients by therapeutic paralysis. The frequent occurrence of postparalytic myopathy in patients with asthma50–52 has led us to greatly decrease our use of paralytics, an approach facilitated by the use of high-level PSV.
Sighs are undesirable because they may lead to lung rupture. Because peak proximal airway pressure is so high in this patient group, upper-limit alarms of 75 cm H2O (and sometimes higher) are often required. Careful attention should be paid to the V̇ and flow profile. Changes in flow that have little effect in the patient without airflow obstruction can have a dramatic impact in obstructed patients. Specifically, reducing the inspiratory flow or changing to a decelerating flow profile reduces the airway pressures and the amount of ventilator alarming but, by prolonging inspiration, actually worsens autoPEEP. Although the ventilator looks “better,” the patient is worse, but this is only recognized if autoPEEP is regularly sought or if the expiratory flow profile is examined (see Fig. 36-3). Aggressive chest physiotherapy is advised because many patients mobilize mucous plugs during their recovery phase; often these plugs are so large and tenacious that they compromise endotracheal tube patency.
Acute‐on-Chronic Respiratory Failure
Acute-on-chronic respiratory failure is a term used to describe exacerbations of chronic ventilatory failure usually occurring in patients with COPD53 (see Chap. 39). Many of these patients are successfully (and preferably) ventilated noninvasively (see Chap. 33). When intubated, they are found to have relatively smaller increases in inspiratory resistance (compared with asthma), with their expiratory flow limitation arising largely from loss of elastic recoil.54 As a consequence, in the patient with COPD, peak airway pressures tend to be only modestly elevated (e.g., 30 cm H2O), but autoPEEP and its consequences are common.55 At the time of intubation, hypoperfusion is common, as manifested by tachycardia and relative hypotension, and typically responds to briefly ceasing ventilation combined with fluid loading.
Because most of these patients are ventilated after days to weeks of progressive deterioration, the goal is to rest the patient (and respiratory muscles) completely for 36 to 48 hours, although excessive rest and ventilatory support may contribute to atrophy and weakness of the diaphragm.56 Also, because the patient typically has an underlying compensated respiratory acidosis, excessive ventilation risks severe respiratory alkalosis and, over time, bicarbonate wasting by the kidney. The goals of rest and appropriate hypoventilation usually can be achieved with initial ventilator settings of a Vt
of 5 to 7 mL/kg and a respiratory rate of 16 to 24 breaths/min, with an ACV mode set on minimal sensitivity (see Table 36-3). Because gas exchange abnormalities are primarily those of ventilation-perfusion mismatch, supplemental oxygen in the range of an FiO2 of 0.4 should achieve better than 90% saturation of arterial hemoglobin. Gas exchange abnormalities requiring an FiO2 greater than 0.5 should prompt a search for complicating alveolar filling processes, such as left ventricular failure with pulmonary edema, pneumonia, or lobar collapse. V̇ may be adjusted for patient comfort but usually is in the range of 50 to 60 L/min. Measures to prevent atelectasis and its complications (e.g., three-point turning, chest physiotherapy, or sighs) are necessary. PEEP should be used in this phase when the patient is triggering the ventilator because autoPEEP is universally present.
Most patients with COPD appear exhausted at the time when mechanical support is instituted and will sleep with minimal sedation. To the extent that muscle fatigue has played a role in a patient's functional decline, rest and sleep are desirable. Two days of such rest presumably will restore biochemical and functional changes associated with muscle fatigue, but 24 hours is probably not sufficient.57 Small numbers of patients are difficult to rest on the ventilator and they continue to demonstrate effortful breathing. Examination of airway pressure and flow waveforms can be very helpful in identifying this extra work and in suggesting strategies for improving the ventilator settings (Fig. 36-6). In many patients, this is the result of autoPEEP-induced triggering difficulty, as discussed in Chap. 32 and shown in Fig. 36-4.58 Frequently, adding extrinsic PEEP to nearly counterbalance the autoPEEP dramatically improves the patient's comfort.59 An alternative approach is to increase minute ventilation to drive down the partial pressure of CO2, but this will worsen autoPEEP and waste bicarbonate. This can be a difficult management problem. We advise a careful search for processes that might drive the patient to a respiratory rate higher than is desirable (e.g., hypoperfusion, pleural effusion or pain). If the patient continues to make significant inspiratory efforts—especially if these efforts are ineffective in actually triggering a machine breath or generating a Vt —judicious sedation is in order.
Signs of patient effort during volume-preset ventilation (assist-control ventilation [ACV] or intermittent mandatory ventilation [IMV] breaths). In these two breaths of equal tidal volume, the left tracing represents a muscle-relaxed patient, and the right tracing indicates a patient making inspiratory effort. The change in esophageal pressure (Peso) is shown in the bottom tracings. Signs of patient effort in the tracing of the pressure-airway opening (Pao) include a decrease in Pao just before the ACV or synchronized IMV breath (triggering; a), a concave upward rise in Pao during inspiration (b), and a peak airway pressure that is less than it would be if the patient made no effort (c). d. During the triggered breath, Peso (as an indicator of the pleural pressure) remains more negative than baseline throughout the breath and even after end inspiration (arrow).
Once the patient improves and the respiratory muscles are rested, the patient should assume some of the work of breathing and be evaluated for liberation. During this phase, some extrinsic PEEP is typically useful to reduce the work of triggering.59
Patients with Acute Hypoxemic Respiratory Failure
Acute hypoxemic respiratory failure is caused by alveolar filling with blood, pus, or edema, the end results of which are impaired lung mechanics and gas exchange (see Chap. 31). The gas exchange impairment results from intrapulmonary shunt that is largely refractory to oxygen therapy. In ARDS (see Chap. 38), the significantly reduced FRC due to alveolar flooding and collapse leaves many fewer alveoli to accept the Vt
, making the lung appear stiff and dramatically increasing the work of breathing. The ARDS lung should be viewed as a small lung rather than as a stiff lung. In line with this current conception of ARDS, it is clearly established that excessive distention of the ARDS lung compounds lung injury and may induce systemic inflammation.8,60 Ventilatory strategies have evolved markedly in the past decade and have changed clinical practice and generated tremendous excitement.
The goals of ventilation are to reduce shunt, avoid toxic concentrations of oxygen, and choose ventilator settings that do not amplify lung damage. The initial FiO2 should be 1.0 in view of the typically extreme hypoxemia (see Table 36-3). PEEP is indicated in patients with diffuse lung lesions but may not be helpful in patients with focal infiltrates, such as lobar pneumonia. In patients with ARDS, PEEP should be instituted immediately, beginning with 15 cm H2O, and then rapidly adjusted to the least PEEP necessary to produce an arterial saturation of 88% on an FiO2 no higher than 0.6 (the “least PEEP approach”). An alternative approach (the “open-lung approach”61) sets the PEEP at a value 2 cm H2O higher than the lower inflection point of the inflation pressure-volume curve (see Chap. 32), but this has not been shown to confer benefit. The Vt should be 6 mL/kg IBW on ACV because a higher Vt is associated with a higher mortality rate.8 Some have speculated that unstudied Vt values, such as 9 or 3 mL/kg IBW, might be even more beneficial than 6 mL/kg. It seems likely that there is a dose-response relation, with lower Vt values being superior, and this explains the resurgence in interest in HFV in which Vt can be very small. Nevertheless, because 6 mL/kg IBW has been conclusively shown to be safe and effective, this represents the standard of care to which other (potentially better, potentially worse) ventilator strategies should be compared. There is little doubt that lung protection can be achieved with pressure-preset ventilation, but safe settings are unknown. Some have extrapolated from the 30 cm H2O plateau pressure limit in the ARDS Network study that a Pi of 30 cm H2O ought to be safe; however, because the mean Pplat in those ventilated with 6 mL/kg IBW was only 26 cm H2O, 30 cm H2O may be too high. Whatever the mode, the respiratory rate should be set at 24 to 36 breaths/min as long as there is no autoPEEP. An occasional consequence of lung protective ventilation is hypercapnia. This approach of preferring hypercapnia to alveolar overdistention (“permissive hypercapnia”) is discussed further in Chaps. 37 and 40.61–63 Alternative modes of ventilation for ARDS, such as IRV, HFV, and tracheal gas insufflation, may have a role as salvage therapies but are of unproven benefit.
Once specimens have been collected from the airway for microbiologic and other studies, PEEP generally should not be disconnected to suction patients or to measure hemodynamic values because alveoli readily re-flood, provoking extreme hypoxemia. This supports multiple observations that PEEP does not reduce lung water but rather redistributes it into the lung interstitium to improve gas exchange.26 Several modified suction adapters are available to provide a route to the airway and maintain PEEP, although most tend to leak at PEEP levels above 15 cm H2O.
Sighs and other measures to prevent atelectasis are not necessary during the acute phases of acute hypoxemic respiratory failure, when PEEP levels are typically in excess of 10 cm H2O. It should be remembered that these patients are at risk of atelectasis as they improve and PEEP levels are lowered. This is probably due in part to surfactant deficiency during the recovery from diffuse alveolar damage and certainly will be aggravated by the use of small Vt.
The Patient with Restriction of the Lungs or Chest Wall
Several restrictive diseases of the lungs or chest wall can lead to respiratory failure, especially when there is a superimposed ventilatory challenge (e.g., pneumonia). These conditions are fully discussed in Chaps. 42 and 66 and include lung disease (e.g., advanced pulmonary fibrosis or late-stage ARDS), abdominal disease (e.g., massive ascites), and other chest wall abnormalities (e.g., kyphoscoliosis). We describe ventilator management.
Small Vt (5 to 7 mL/kg) and rapid rates (18 to 24 breaths/min) are especially important to minimize the hemodynamic consequences of positive-pressure ventilation and to reduce the likelihood of barotrauma (see Table 36-3). The FiO2 is usually determined by the degree of alveolar filling or collapse, if any. Rarely, we have encountered patients with enormous restrictive loads from intraabdominal catastrophes (e.g., massive intraperitoneal bleeding) who have a large intrapulmonary shunt but lack signs of alveolar flooding on the chest radiograph. We speculate that, in such patients, large numbers of alveolar units may be subserved by airways forced below their closing volume throughout tidal ventilation, so that these nonventilated alveoli comprise a large intrapulmonary shunt (see Chap. 42). Reversible contributors to restriction (e.g., circumferential burn eschar or tense ascites) should be identified and treated. Sitting the patient up in bed or on a chair may reduce the abdominal pressure, thereby easing the work of breathing.
The high Pa values typically generated in these patients may lead to increased physiologic dead space (when Pa exceeds the pulmonary artery pressure), especially when large Vt values are used. When the restrictive abnormality involves the chest wall (including the abdomen), the large ventilation-induced rise in pleural pressure has the potential to compromise cardiac output. This in turn will lower the mixed venous partial pressure of O2 and, in the setting of ventilation-perfusion mismatch or shunt, the arterial partial pressure of O2. If the physician responds to this decreasing arterial partial pressure of O2 by augmenting PEEP or increasing the minute ventilation, further circulatory compromise ensues. A potentially catastrophic cycle of worsening gas exchange, increasing ventilator settings, and progressive shock is begun. This circumstance must be recognized because treatment is to reduce dead space (e.g., by lowering minute ventilation or correcting hypovolemia).
Facilitating Patient Comfort and Communication
Ideally, the mechanically ventilated patient should be alert, comfortable, and capable of communicating with the health care team. These desirable goals must be weighed against the need to heavily sedate and even therapeutically paralyze some patients with cardiovascular instability, severely compromised oxygen delivery to peripheral tissues, or severely deranged respiratory system mechanics.64
Much excessive sedation can be avoided by frequent communication, reassurance, and identification of sources of pain, anxiety, and agitation. Often, ventilator adjustment is more effective than drug therapy for calming the patient (see Table 36-1). Patients should be maximally alert during the day, with sedation limited to the evening, if possible. Short-acting benzodiazepines or haloperidol may facilitate sleep, thereby ensuring that the patient is maximally rested for efforts at spontaneous breathing during the day. Many patients must be deeply sedated to ensure comfort or to stabilize them hemodynamically during acute illness. A daily “wake up” during which sedatives are withheld until the patient awakens and is able to follow commands (or becomes agitated) is safe and effective in shortening time on the ventilator and in the ICU.65 We advocate such a wake up in essentially all patients, even those who are hemodynamically unstable and unlikely to be breathing spontaneously for days.
Whenever neuromuscular blockers are used, the agent should be withdrawn on a daily basis until neuromuscular function returns to prevent excessive drug accumulation.63 It also may be useful to monitor the degree of neuromuscular blockade with a nerve stimulator (aiming for a train-of-two out of four), although this has not been shown to decrease the incidence of postparalytic myopathy. In patients with impaired renal and hepatic function, continuous infusion of cis-atracurium is preferred because pancuronium may accumulate and lead to protracted paralysis. During muscle paralysis, careful assessment of the level of sedation is essential because individuals differ widely in their response to sedatives and narcotics.
When the patient is optimally alert, it is important that the caretakers provide brief, clear explanations of all interventions proposed, especially changes in ventilator settings, to evaluate the patient's perception of beneficial effect. This allows the patient to be a part of the decision making concerning the optimal ventilator settings.
The initial ventilator settings should be reassessed promptly to assess their appropriateness for the individual patient. Such fine tuning of the ventilator often means the difference between a patient who rests on the ventilator or who continues to perform fatiguing efforts, who is calm yet awake, or who requires deep sedation or therapeutic paralysis. Assessing the patient-ventilator interaction requires substantial skill and experience. In part, the adequacy of ventilator settings is judged by the appearance of the patient (comfortable and resting versus diaphoretic and fighting) and arterial blood gas analysis. Tremendously valuable additional information comes from examination of waveforms, as elaborated in Chap. 32.
The intensivist should ensure that the patient and ventilator are synchronized, that is, that each attempt by the patient to trigger the ventilator generates a breath. The most common situation in which the patient fails to trigger breaths occurs in severe obstruction when autoPEEP is present (see Fig. 36-4). This is recognized at the bedside when the patient makes obvious efforts that fail to produce a breath. Using waveforms, these ineffective efforts cause a temporary slowing of expiratory flow, sometimes halting it completely (Fig. 36-7).
Ventilation of an obstructed patient with assist-control or intermittent mandatory ventilation. A failed attempt to trigger can be detected in the expiratory flow waveform, where the expiratory flow briefly ceases (due to the patient's inspiratory effort) but the effort is insufficient to initiate a breath. Often the patient can be seen to make obvious inspiratory efforts between ventilator breaths.V̇, flow.
As an example, a patient was newly ventilated for septic shock and ARDS. His physicians found very high Pplat (38 cm H2O) on the following settings: ACV mode, Vt of 480 mL, an f of 28/min, and V̇ of 60 L/min. By reducing the V̇ to 30 L/min, Pplat was newly measured at 28 cm H2O, which the physicians interpreted as an improvement (Fig. 36-8). However, the airway pressure decreased only at the cost of greatly increased efforts on the patient's part, efforts that can consume a remarkable fraction of the cardiac output (>30% in animal models40,66,67). Moreover, the transpulmonary pressure remained excessive because the Vt was not reduced.
Ventilated patient with acute respiratory distress syndrome and sepsis. The first breath, at an inspiratory flow rate of 60 L/min, shows no signs of patient effort in the pressure-airway opening (Pao) waveform or the esophageal pressure (Peso) tracing. After the inspiratory flow is reduced to 30 L/min, the Pao decreases, but at the cost of greater patient effort, as reflected in the Pao waveform and the Peso. V̇, flow.
Response to “Crises” in the Ventilated Patient
A vast array of sudden and potentially catastrophic changes in clinical condition can occur in the course of mechanical ventilation (Table 36-4). We focus on high- and low-pressure alarms, worsened oxygenation, and hypercapnia. Whenever the function of the ventilator or the position and patency of the airway are in question, the patient should be removed from the ventilator and hand bagged with 100% oxygen. This point is extremely important because this maneuver immediately circumvents the ventilator (and any malfunction of it), provides the clinician with a direct assessment of respiratory system mechanics, and focuses attention on the patient and not on the machine.
Table 36–4. Ventilator Crises ||Download (.pdf)
Table 36–4. Ventilator Crises
|Increased peak airway pressure|
| Endotracheal tube obstruction, kink, malposition|
| Airway obstruction (e.g., bronchospasm, mucous plug)|
| Reduced lung compliance (e.g., pulmonary edema)|
| Reduced chest wall/abdomen compliance (e.g., pneumothorax,|
| Patient effort, agitation (e.g., coughing, biting, fighting)|
|Reduced oxygen saturation|
| Ventilator/mixer malfunction|
| Endotracheal tube malposition, leak|
| New lung derangement (e.g., atelectasis, aspiration, edema)|
| New cardiovascular derangement (e.g., shock, pulmonary embolism,|
|fall in hemoglobin concentration)|
| Increased oxygen consumption|
| Change in body position, increasing shunt|
|Rising partial pressure of CO2|
| Ventilator malfunction|
| Endotracheal tube malfunction, leak|
| New patient mechanical derangement (e.g., bronchospasm, edema)|
| Increased dead space|
| Increased CO2 production|
| Pain, discomfort unrelated to the ventilator or respiratory system|
|(e.g., myocardial ischemia)|
| Endotracheal tube malposition|
| Rising work of breathing|
| Rising partial pressure of CO2 (see above)|
| Oxyhemoglobin desaturation (see above)|
| Shock, pulmonary embolism|
| Inadequate sedation|
| Alcohol or other drug, withdrawl|
Aside from alarm or gauge malfunction, increased airway pressure indicates obstruction of the airway, obstruction to gas flow through the ventilator circuit, patient effort against the ventilator, or a change in the mechanics of the respiratory system. If manual bag ventilation is difficult, a suction catheter should be passed immediately through the endotracheal tube. If the catheter cannot be advanced 25 cm or farther, obstruction of the airway is likely. If repositioning of the head does not relieve kinking, and if the patient is not biting the airway, reintubation is necessary. If the patient is biting an endotracheal tube, a bite block should be placed; if this cannot be done, a short-acting neuromuscular blocking drug should be administered.
If the airway is patent but manual ventilation is difficult and the patient is struggling, a sedative should be given. If the patient can be easily ventilated (implicating vigorous respiratory muscle activity), the cause of the patient's distress should be sought. Possibilities include hypoxemia, hypercapnia, shock, or a new central nervous system process.
If ventilation remains difficult after deep sedation or muscle paralysis of a patient with a patent endotracheal tube, a new lower airway, pleural, lung, or chest wall process should be sought. Auscultation, palpation, and percussion often identify pneumothorax, collapse, or consolidation. Early portable chest radiography confirms these diagnoses or identifies an alternative cause of the crisis. Placing the patient back on the ventilator and measuring peak and plateau pressures and autoPEEP will further delineate the problem, as described above.
Low-pressure alarms signal machine malfunction, a leak, or inspiratory effort by the patient (usually obvious). Large persistent leaks can occur within the ventilator itself, in the inspiratory limb, at the connection to the Y adaptor and endotracheal tube, around the endotracheal tube cuff, or through a bronchopleural fistula. If normal resistance to ventilation is noted during manual ventilation, the problem lies with the ventilator or tubing. If hand bagging shows minimal resistance, an endotracheal tube cuff leak is likely. This can be confirmed by listening over the neck or by placing a hand over the mouth. A large bronchopleural fistula can be identified by inspection of the chest tube and pleural drainage system.
When a patient develops hypoxemia, sufficient oxygen should be given immediately to return the saturation to 88%. However, this must be followed by a search for the cause of deterioration. Progression of the primary cause of respiratory failure (ARDS, pneumonia, or lung hemorrhage) will impair gas exchange, but this should not be assumed to be the case. Also possible is a new lesion (e.g., nosocomial pneumonia) that may be identified by physical examination or chest radiograph. However, a systematic approach is useful to identify the myriad (including nonpulmonary) causes of hypoxemia.
From a pathophysiologic perspective, new hypoxemia implies a reduced FiO2 (including ventilator malfunction), hypoventilation, ventilation-perfusion mismatching, shunt, or a decrease in the mixed venous oxygen saturation. Hypoventilation is usually obvious, being signaled by hypercapnia. Ventilation-perfusion mismatch typically causes mild hypoxemia that is easily corrected with supplemental oxygen. Bronchospasm, airway secretions, and airway plugging are common contributors in intubated patients. Inhaled bronchodilators may acutely worsen ventilation-perfusion relations,68 as will vasodilators.45 The combination of worsened ventilation-perfusion matching and an increase in dead space should prompt consideration of pulmonary embolism. Most often, when new hypoxemia develops in a mechanically ventilated patient, shunt or a decrease in mixed venous oxygenation can be found. A new shunt (e.g., pulmonary edema, pneumonia, or atelectasis) typically can be found on the chest radiograph, whereas mixed venous desaturation is detected by analyzing a venous blood sample or performing venous oximetry. The causes of venous desaturation include reduced cardiac output or hemoglobin concentration or increased systemic oxygen consumption. These nonpulmonary causes of hypoxemia are particularly common in patients with severe shunt lung disease and may herald life-threatening crises (e.g., pneumothorax).
A rising PaCO2 often elicits a change in the ventilator orders (increased frequency or Vt). However, a pathophysiologic approach is useful in this situation. From the equation for PaCO2:
where VCO2 is CO2 production, k is a constant, and Vd is the dead space, it can be seen that, in addition to a decrease in minute ventilation, rising CO2 production (e.g., fever, shivering, or agitation) or increasing dead space (e.g., hypovolemia, pulmonary embolism, PEEP) may account for new hypercapnia. Responding to hypercapnia by simply raising the minute ventilation is dangerous because causes of increased CO2 production and dead space may be important to diagnose in their own right. In addition, augmenting minute ventilation has the potential to (paradoxically) decrease alveolar ventilation if the increase in Vt
or f worsens dead space (such as when autoPEEP is present). In this setting, the PaCO2 may rise when minute ventilation is increased and fall when minute ventilation is reduced. These issues are further discussed in Chap. 40.
Liberation of the Patient from Mechanical Ventilation
We refer to the discontinuation of mechanical ventilation not as weaning (which implies the withdrawal of a nurturing life-support system) but as liberation (connoting freedom from a confining, noxious, and dangerous circumstance69). Because liberation from the ventilator is fully discussed in Chap. 44, we make only a few points relevant to all ventilated patients. Patients recover the ability to breathe spontaneously because central drive is regained, neuromuscular competence is restored, and respiratory system load is reduced. Once these are achieved, the ventilator is no longer needed. Gradual adjustments of IMV rates or pressure-support levels that are too slow for the patient's needs simply serve to prolong the duration of mechanical ventilation, as shown in large trials of weaning strategies,10,11 and do not facilitate the recognition of evolving ventilatory failure.70 However, if drive, strength, and load are not repaired, no amount of ventilator technology will allow the patient to breathe on his or her own. Most often, when physicians believe they are “weaning” the patient, they are simply allowing time for their other therapies to treat the respiratory failure; ventilator changes are prescribed coincidentally but are irrelevant. Accordingly, effective liberation of each patient begins with intubation and stabilization on the ventilator, with the measurement of respiratory mechanics to assist in evaluating the reversible features of the patient's abnormally increased load; as soon as is clinically relevant, the respiratory muscle strength is evaluated for reversible causes of weakness.
Before an acceptable balance between neuromuscular competence and load is attained, different methods for exercising the patient may be useful because disuse causes muscles to weaken56 (see Table 36-3). These include T-piece sprints with which the patient is allowed to breathe without ventilatory assistance for progressively longer periods as ventilatory function improves. Alternatively, the pressure-support mode can be adjusted to allow a reasonably spontaneous Vt
(e.g., 300 to 500 mL H2O) and respiratory rate (<30 breaths/min) but at a level that demands some work from the patient. The physician should be familiar with a number of different modes because patient preference can then dictate which is used in a particular circumstance. SIMV appears to prolong the period of ventilator dependency and should no longer be used for weaning. Aside from this, the method of exercise chosen is not clearly important and certainly secondary to the main goals of restoring drive, improving neuromuscular competence, and reducing load.
Of overriding importance is an approach that asks on a daily basis, “Can this patient breathe on his or her own?” In several studies of methods of weaning, 75% of patients assessed at entry into the trial were extubated successfully.10,11 The use of interdisciplinary weaning teams or respiratory therapist–driven protocols may expedite successful liberation by actively addressing this question each day.71,72
Conversion to a Tracheostomy
A tracheostomy provides easier tracheobronchial toilet, enhances communication, and is more comfortable for the patient than translaryngeal intubation (TLI). In contrast, endotracheal intubation is less invasive and, in the short run, less likely to cause complications. The timing of tracheostomy involves balancing its complications73 against the (typically) more delayed complications of TLI. The major complication of TLI is laryngeal damage with resulting postextubation upper airway obstruction or dysphonia.74 Injuries likely arise from abrasion and compression of laryngeal structures, with sequelae including posterior commissural stenosis, posterior cordal synechiae, arytenoid fixation, and subglottic stenosis. The precise contributions of insertion trauma, duration of TLI, and movement during ICU management to these injuries is not clear, but all are likely important. Some clinicians have suggested that women and patients with diabetes mellitus, rheumatoid arthritis, and ankylosing spondylitis are at increased risk of laryngeal injury during TLI. The incidence of cuff-induced injury to the trachea itself is probably similar between tracheostomy and TLI, at least in the critical care environment.75
Our own approach is to begin with TLI in most critically ill patients. Those with an immediate indication for tracheostomy, such as upper airway obstruction or severe sleep apnea, are scheduled for this procedure at the earliest opportunity. Patients who are extremely restless, have copious pulmonary secretions, or are likely to require more than 2 weeks of mechanical ventilation are also considered for early tracheostomy. All other patients are reassessed on a daily basis for these indications for tracheostomy. If extubation seems likely within the first 2 to 3 weeks, TLI is maintained. Occasionally, this approach provides TLI for 3 weeks or longer; however, even with soft cuffs and careful monitoring, the complications of this prolonged TLI begin to outweigh its advantages, and tracheostomy becomes indicated for its greater comfort and potential for enhanced communication. Percutaneous tracheostomy has several advantages in the critically ill patient. Performance of tracheostomy in the ICU provides a safely monitored environment for the procedure and obviates the risks of transporting the patient.
Extubation after prolonged (>5 days) intubation should be approached cautiously. In addition to demonstrating freedom from mechanical ventilatory support, as discussed in Chap. 44, the patient must be capable of maintaining airway patency, have sufficient airway reflexes to avoid aspiration, and have adequate cough to mobilize secretions. Laryngeal injury causing postextubation upper airway obstruction should be anticipated.
The most common cause of postextubation stridor is posterior commissure edema, arising from direct mechanical injury to these soft tissues, and impaired vocal cord abduction. Before extubation, the degree of upper airway edema may be assessed by direct laryngoscopy or by deflating the tube cuff, obstructing its lumen, and measuring the amount of airflow around it. Alternatively, the airway can be inspected by fiberoptic laryngoscopy immediately after extubation. Despite these precautions, progressive airway edema with stridor will be encountered in 1% to 5% of patients after prolonged TLI. The initial management should include bag-mask ventilation synchronized to augment the patient's efforts. Noninvasive positive-pressure ventilation is generally considered to be useful, although one clinical trial showed no benefit,76 and another trial has called into use its general application for respiratory failure emerging shortly after extubation.76a Racemic epinephrine by inhalation and intravenous corticosteroids are usually recommended but have not been rigorously studied. A helium-oxygen gas mixture (heliox) also can be useful in this setting.77 Administration of this low-density gas mixture reduces the large pressure drop associated with turbulent flow across the obstruction, thus reducing the work of breathing. Heliox (21% oxygen and 79% helium) can be delivered by a mask connected to an H tank, supplemented by nasal cannula oxygen, to maintain an arterial hemoglobin saturation of 90%. Heliox and noninvasive positive-pressure ventilation should be used only to temporize while awaiting more definitive therapy of the critical airway narrowing.
If stridor fails to respond to initial measures or reemerges while on therapy, reintubation is usually necessary. The usual approach is to use a small endotracheal tube (6.0 or 6.5 mm) through the nasal route to minimize further injury to the posterior commissure. The managing team should be prepared to perform cricothyrotomy or tracheostomy, if necessary. After reintubation, edema resolves in most patients over 48 to 72 hours. During this time, corticosteroid therapy should be continued (e.g., dexamethasone 4 mg every 6 hours), and the airway should be viewed directly to confirm resolution of edema.
Extubation failure is a marker for prolonged ventilation and ICU stay, increased hospital costs and mortality rate, and greater likelihood of tracheostomy.78 Risk factors include age, longer duration of ventilation, continuous sedative infusion, and anemia.
Airway during Split-Lung Ventilation
The lungs may be separated for purposes of differential ventilation by two major means: blocking the bronchus of a lobe or whole lung while ventilating with a standard endotracheal tube or passing a double-lumen tube. Different devices have been used to obstruct a bronchus, but experience is greatest with the Fogarty embolectomy catheter. Double-lumen tubes carry the advantages of allowing each lung to be ventilated, collapsed, reexpanded, or inspected independently.
Split-lung ventilation is only rarely useful in the critical care unit, but occasionally its benefits are dramatic. Large bronchopleural fistulas severely compromise ventilation and may not respond to HFV.79 A double-lumen tube will maintain ventilation of the healthy lung and facilitate closure of the bronchopleural fistula.80 During massive hemoptysis, lung separation may be lifesaving by minimizing blood aspiration, maintaining airway patency, and tamponading the bleeding site while awaiting definitive therapy.81 Patients with focal causes of acute hypoxemic respiratory failure, such as lobar pneumonia or acute total atelectasis, may benefit from differential ventilation and application of PEEP.82
Complications with these devices are common because they are difficult to maintain in ideal position during a protracted period of respiratory failure and tend to directly injure the trachea and main bronchi. A clear protocol for airway assessment and repositioning should exist, and routine input from senior anesthesiology staff is required.