Principles of Mechanical Ventilation

47 Principles of Mechanical Ventilation Jonathan E. Sevransky, MD, MHS Objectives Understand the indications for treatment with mechanical ventilation Describe ventilator strategies that will minimize complications such as ventilator-induced lung injury, ventilator-associated pneumonia and dynamic hyperinflation Key words: acute respiratory failure; mechanical ventilation; positive-pressure ventilation; ventilatorassociated pneumonia; ventilator-induced lung injury Acute respiratory failure is a frequent cause for admission to the ICU. 1 Mechanical ventilation, either through an endotracheal tube or a tight-fitting mask, serves as a supportive and often lifesaving therapy for patients with acute respiratory failure. Treatment goals of mechanical ventilation include delivering appropriate gas exchange in addition to unloading the respiratory muscles. The challenge for clinicians using mechanical ventilation is to provide adequate supportive therapy to allow diagnosis and treatment of the precipitating cause of acute respiratory failure while avoiding complications of this therapy, such as ventilator-induced lung injury (VILI) and ventilatorassociated pneumonia (VAP). This chapter focuses on the use of positive-pressure ventilation to treat patients with acute respiratory failure. Indications for Mechanical Ventilation Mechanical ventilation is most frequently initiated in the ICU to rest respiratory muscles and facilitate gas exchange in patients with acute respiratory failure. Both failure of oxygenation and failure of ventilation are indications for delivery of mechanical ventilation. Other common indications include the need to protect the airway and the need to reduce a patient s metabolic requirements. Although traditionally patients who required mechanical ventilation were treated in conjunction with endotracheal intubation, the use of mechanical ventilation through a tight-fitting mask (noninvasive mechanical ventilation, or NIV) for carefully selected patients is appropriate. An international survey 2 of mechanical ventilation noted the following primary indications for mechanical ventilation: postoperative, coma, pneumonia, sepsis, obstructive lung disease, congestive heart failure, obstructive lung disease, acute lung injury, and trauma. This chapter will include general principles for mechanical ventilation for all patients with acute respiratory failure and will discuss in further detail mechanical ventilation of patients with acute lung injury and obstructive lung disease. Initial Ventilator Settings for Treatment of Acute Respiratory Failure The physician is responsible for choosing settings that will allow the respiratory muscles to rest, provide adequate gas exchange, and maintain reasonable acid base status. Initial settings chosen by the physician include the ventilator mode, the respiratory rate, the tidal volume, and the level of positive end-expiratory pressure (PEEP). Although there is no one-size-fits-all approach, reasonable initial settings include a mode that rests the patient s respiratory muscles, a tidal volume of 8 ml/kg of ideal body weight, a high level of Fio 2 (usually 1.0), a respiratory rate of 12 to 16 breaths per minute, and a PEEP of 5 cm H 2 O. Many physicians will provide an initial inspiratory flow rate of 60 L/min, although patients with obstructive lung disease may require higher flow rates. 1 Ventilation of patients with obstructive lung disease and acute lung injury (ALI) or acute respiratory distress syndrome (ARDS) is discussed in more detail in the following sections. Ventilation Modes Most patients are treated with either a pressure-cycled or volume-cycled mode of ventilation. A volume-cycled ventilator will deliver the prescribed tidal volume. The pressure that this requires will vary according to airway resistance, including the resistance of the tubing and endotracheal tube, and the compliance of the thoracoabdominal compartment. Patients with obstructive lung disease causing high airway resistance will require high pressures to overcome the resistance and deliver the desired tidal volume. Patients with stiff, noncompliant lungs will also require high pressures to inflate the lungs and deliver the desired tidal volume. In simplified terms, a volumecycled mode will deliver a fixed volume at a variable pressure. With pressure-cycled ventilation, the clinician will set a pressure to be delivered. The tidal volume that the patient receives will vary according to airway resistance, including the resistance of the tubing and endotracheal tube, and thoracoabdominal compartment compliance. Thus, although the driving pressure will be limited, the patient may not receive the desired level of minute ventilation. In simplified terms, a pressure-cycled ventilator will deliver fixed pressures but variable volumes. Choice of ventilator modes is often driven by physician comfort and institutional practice. It important for the clinician to choose a mode in which the work of breathing is minimized. The most frequently used mode of ventilation for patients with ALI is assist control. 2 Even when a ventilator is set to a fully supportive mode such as assist control, work of breathing can be measured and is not Principles of Mechanical Ventilation 37

48 negligible. 3 5 It is important to avoid patient ventilator dyssynchrony because it can worsen gas exchange and increase the work of breathing. However, some low-level work of breathing may be necessary to prevent diaphragmatic muscle atrophy. 6 When a patient cannot tolerate one mode of mechanical ventilation because of patient ventilator dyssynchrony, the clinician can try an alternate mode. However, before switching modes, the clinician must ensure that no other medical condition (eg, pneumothorax, delirium, early sepsis) is triggering the dyssynchrony. Additional ventilator modes allow time cycling or flow cycling of ventilation. With time-cycled ventilation, the ventilator may alternate between two different pressures, as with airway pressure-release ventilation (APRV). With a flow-cycled mode, such as pressure support, the ventilator will deliver a preset pressure until the airflow reaches a predetermined level. Although there are theoretic reasons to consider using an alternate mode of ventilation such as APRV or high-frequency oscillation ventilation, there are little outcome data to support the primary use of the modes. 7 9 Thus, APRV and high-frequency oscillation ventilation are most commonly used as rescue modes when initial therapy with a conventional volume or pressure mode fails. Monitoring the Respiratory System During Mechanical Ventilation Monitoring the respiratory system may provide useful diagnostic information for clinicians caring for patients with respiratory failure. During positive-pressure ventilation, pressure is directed from the ventilator, through the circuit, and to the patient interface; the effect of the positive pressure on airway resistance (including the ventilator tubing, the endotracheal tube, and the airways) as well as on thoracoabdominal-compartment compliance (lung, chest, and abdominal wall) will determine the degree of gas exchange and change in lung volumes. 10 12 The relative components of these two parts of the system can be measured while a patient is receiving a volumecycled breath. The peak pressure, also referred to as the peak airway pressure or peak inspiratory pressure, is the total pressure required to overcome the resistance of the airways and well as the compliance of the thoracoabdominal compartment. 10 Placing an inspiratory hold at the end of a passive inspiration will provide information on the amount of pressure required to distend the lung to the volume present at end-inspiration. 1 The pressure obtained is commonly referred to as the plateau pressure. It is possible to estimate the plateau pressure by measuring the pressure in the lower third of the esophagus, but this is done more frequently in a research setting than in a clinical setting. 13 High plateau pressures may be caused by stiff, noncompliant lungs; by problems associated with chest wall rigidity due to medications or burns; or by abdominal factors such as obesity, cirrhosis, pancreatitis, or surgery. Whether it is reasonable to tolerate higher levels of plateau pressures in patients with elevated intraabdominal pressure remains controversial. 10 The difference between the peak airway pressure and the plateau pressure will provide information about the amount of airway resistance. Airway resistance with a ventilator is predominantly a function of the large airways and is influenced by bronchospasm, the presence of secretions, and the endotracheal tube. 11,12 Large gradients between the peak and plateau pressure may indicate narrowing of the airways and high airway resistance as seen in patients with obstructive lung disease. Patients with increased airway resistance are at increased risk for developing expiratory airflow limitation and inability to reach functional residual capacity (FRC) at endexpiration. Failure to reach FRC at end-expiration will lead to dynamic hyperinflation and pressures that are higher than atmospheric. Pressures above atmospheric pressure (or the extrinsic PEEP) at end-expiration are designated as auto-peep, or intrinsic PEEP. Auto-PEEP may be diagnosed by measurement of pressures at end-expiration in a passively exhaling patient; this pressure should be 0, or the level of extrinsic PEEP set on the ventilator. The presence of persistent flow at the end of expiration may also suggest the presence of auto-peep. Mechanical Ventilation in Selected Patient Populations Parenchymal Lung Disease A primary goal in ventilating patients with parenchymal lung injury is to ensure adequate gas exchange without exacerbating the initial lung injury. Patients with ALI or ARDS are often cited as paradigmatic of patients with parenchymal lung injury. However, in addition to ALI and ARDS, other forms of acute processes, such as pneumonia and aspiration, may cause unilateral parenchymal lung injury and acute respiratory failure. Additional causes of parenchymal lung injury include diseases that may have a subacute time course such as interstitial pneumonia, pulmonary fibrosis, and other restrictive lung diseases. Most approaches to ventilate patients with parenchymal lung disease center around attempts to limit tidal volumes and distending pressures. The goal of lung-protective ventilation is to minimize mechanical and inflammatory injury of lung parenchyma, thereby minimizing local and systemic effects of ventilation. Most of the outcome data supporting the use of lungprotective ventilation of patients with parenchymal lung injury is derived from studies of patients with ALI or ARDS. The use of a ventilator protocol based on a tidal volume of 6 ml/kg of ideal body weight coupled with a plateau pressure <30 cm H 2 O was shown to have a mortality benefit in patients with ALI compared with larger tidal volumes with a higher plateau pressure. 14 Some evidence suggests that lower tidal volumes may be useful in preventing the development of ALI in patients at risk. 15,16 Ventilation of patients with other forms of parenchymal lung injury may be challenging. Patients with unilateral lung injury may have differential responses to positive pressure between the relatively normal lung and the affected lung. For example, a tidal volume that is appropri- 38 Adult Multiprofessional Critical Care Review

49 ate for a normal lung region may be inappropriate for a damaged lung region. Whether patients with other forms of parenchymal lung disease have similar responses to lungprotective ventilation is not clear. Acute respiratory failure in patients with chronic parenchymal lung disease often carries a poor prognosis. 17 Ventilator-Induced Lung Injury Webb and Tierney 18 first reported the potential injurious effect of positive-pressure ventilation on healthy lungs. These harmful effects are commonly referred to as VILI. Both overdistention of alveoli, as well as cyclic recruitment and derecruitment of alveoli have been suggested as potential causes of VILI. In addition to local damage of lung tissue, VILI has been shown to cause systemic inflammation and organ failure. 19 21 Although chest radiographs of patients with ALI or ARDS may suggest homogenous lung injury, chest computed tomography scans often demonstrate regions of healthy and abnormal lung, with the dependent lung areas having a higher concentration of abnormal lung tissue. 22 A differential response to positive-pressure ventilation between healthy and damaged regions of the lung may contribute to VILI. 23 Methods of limiting VILI focus on limiting tidal volume and plateau pressure, especially in patients with ALI or ARDS. The use of a lung-protective strategy with a tidal volume of 6 ml/kg of ideal body weight coupled with a plateau pressure 30 cm H 2 O was shown to improve mortality rates in patients with ALI compared with a higher tidal volume of 12 ml/kg. Plateau pressure may be a surrogate for the severity of lung injury. 24 Thus, some have advocated limiting plateau pressures rather than tidal volumes as a method to prevent VILI. 25 A 2005 analysis 26 suggested that there is benefit to lowering tidal volumes even when patients plateau pressures are not high; it is not known whether there are safe limits of plateau pressure in patients with ALI or ARDS. Limitation of tidal volumes often leads to reduction in minute ventilation. To compensate, the clinician may increase the respiratory rate to increase minute ventilation. However, this increase may not be sufficient to deliver a normal Pco 2, and the patient may develop an elevated Pco 2, a clinical approach known as permissive hypercapnia. Potential consequences of permissive hypercapnia include increased pulse, cardiac output, and cerebral blood flow. Myocardial ischemia and elevated intracranial pressure are relative contraindications to the use of permissive hypercapnia. Normally functioning kidneys may be able to buffer the respiratory acidosis associated with permissive hypercapnia; one therapeutic option for patients with a ph <7.3 is treatment with sodium bicarbonate or other buffers. 14,27 Renal failure or lactic acidosis may limit the ability of a clinician attempting to use permissive hypercapnia and its associated respiratory acidosis. Ventilation of Patients with Obstructive Lung Disease Both chronic obstructive pulmonary disease (COPD) and asthma are prevalent diseases, and COPD exacerbations and status asthmaticus are common causes of acute respiratory failure requiring treatment with mechanical ventilation. 2 Patients may present with hypercarbic respiratory failure, hypoxemic respiratory failure, or both. Several factors lead to inadequate ventilation in this population. First, increased airway resistance and decreased expiratory time may lead to inadequate emptying of the lung, or inability to return to FRC. This leads to dynamic hyperinflation and intrinsic or auto-peep. Intrinsic PEEP may lead to increased work of breathing, further exacerbating alveolar hypoventilation. 28 In addition, regional airway hyperinflation may lead to increased dead space. Ventilation of the patient with obstructive lung disease requires attention to providing adequate oxygenation while minimizing dynamic hyperinflation. Maintenance of a minute ventilation sufficient to ensure normal acid base status may lead to inadequate emptying time, which will lead to breath stacking and dynamic hyperinflation. 29 Methods to minimize dynamic hyperinflation include decreasing tidal volumes and respiratory rates, as well as increasing flow rates and sedation. The use of neuromuscular blockers is best avoided if possible, given the risk of critical illness weakness. All of these treatments for dynamic hyperinflation may lead to permissive hypercapnia; however, for most patients with obstructive lung disease, the risks of dynamic hyperinflation outweigh the risks of hypercapnea. 29 Several other techniques may allow for decreased work of breathing in a patient with dynamic hyperinflation. It is possible to switch modes to one that improves patient ventilator synchrony; this is usually done at the bedside by doing short trials of alternate modes. Some researchers also suggest adding extrinsic PEEP to decrease the amount of work required to trigger a breath, although this should be done with caution in patients at risk for consequences of increased PEEP, such as pneumothorax. Ventilation of Patients with Other Conditions Other possible causes of respiratory failure and subsequent ICU admission include surgery, medications, neuromuscular weakness, and trauma. 2 For patients who require mechanical ventilation for <24 hours, the choice of ventilator mode is not likely to influence outcome. For patients with progressive neuromuscular weakness, it may be reasonable to attempt NIV first. 30 Patients who have ingested toxins and those who have diseases that limit the body s ability to protect the airway should be treated with invasive mechanical ventilation. Noninvasive Ventilation Positive pressure delivered through a tight-fitting mask has several advantages over invasive mechanical ventilation. It avoids the need for intubation in many patients and thus may limit or avoid the use of sedative and analgesic agents. It also allows the patient to intermittently take off the mask for brief periods of time to allow communication. Clinical trials show both a decreased need for endotracheal intubation and a reduction in mortality with the use of NIV Principles of Mechanical Ventilation 39

50 compared with conventional therapy (without mechanical ventilation) in patients with hypercarbic respiratory failure due to COPD exacerbation. 31,32 There are also data supporting the use of NIV in patients with congestive heart failure 33 and in immunosuppressed patients with bilateral infiltrates and hypoxemic respiratory failure. 34 It is important to recognize that NIV is not appropriate for many patients with acute respiratory failure. Patients with unstable hemodynamics, with frequent purulent sections, with hemoptysis, with intractable agitation, and those unable to protect their airway (Glasgow coma scale score of <8) are not good candidates for the use of NIV. In addition, a subset of patients treated with NIV will require conversion to invasive mechanical ventilation, and patients should be treated in an area where failure of NIV will be rapidly noticed. 31 It is also important not to excessively delay institution of invasive mechanical ventilation in patients whose condition does not respond to NIV. Complications of NIV include facial trauma, eye irritation, agitation, patient ventilator dyssynchrony, and aspiration. Several but not all studies have suggested that NIV may exacerbate cardiac ischemia. 33 Finally, the use of NIV as rescue therapy for patients in whom extubation fails has no clear benefit but has the potential for harm. 35,36 Positive End-Expiratory Pressure A constant positive pressure throughout the respiratory cycle, commonly and confusingly known as PEEP, may recruit atelectatic lung regions and prevent the cyclic opening and closing of the airways. 37 In doing so, PEEP may facilitate delivery of adequate oxygenation with lower levels of inspired Fio 2 and thus minimize the intermittent recruitment and derecruitment of lung regions, known as atelectrauma. 38 Potential complications of PEEP include overdistention of normal alveoli, increasing plateau pressure, and decreasing venous return and cardiac output. 39 In addition, although many patients with ALI or ARDS will show radiographic and clinical evidence of a response to PEEP, there are subsets of patients whose condition will not respond to increasing levels of PEEP. 40 PEEP is most commonly used for patients with ALI or ARDS and for patients with heart failure. 33,37 In clinical trials, the use of higher levels of PEEP, the so-called openlung approach, have not shown mortality benefits in patients with ALI or ARDS, although measures of oxygenation were improved and time on the ventilator decreased in some of the trials. 41 Many clinicians will attempt trials of higher PEEP in patients who are difficult to oxygenate at higher levels of Fio 2, while monitoring effects on oxygenation and plateau pressure. 37 Hemodynamic Effects of Positive-Pressure Ventilation Increasing airway pressure may lead to hemodynamic embarrassment. The degree of transfer of positive pressure through the airway to the pleural space and the thoracic great blood vessels depends on lung compliance. In patients with stiff, noncompliant lungs, there is less transfer of pressure than in patients with higher lung compliance, such as patients with COPD. Some of the airway pressure increase caused by PEEP may have affects on venous return to the heart and may lead to reduced cardiac output. 42 Although the reduction in venous return may have beneficial effects on patients with congestive heart failure, 33 it may lead to hypotension in other patients, including those who have just been intubated and have just received medications that may lead to lower blood pressure and decreased systemic catecholamines. Ventilator-Associated Pneumonia The incidence of VAP, defined as pneumonia that develops after 48 hours of invasive mechanical ventilation, is associated with the duration of mechanical ventilation. 43 Factors that have been shown to minimize VAP in patients with acute respiratory failure include limiting patient sedation, 44 avoiding the supine position when feeding patients, 45 delivering oral care, 46 and using NIV in appropriate patients. Other techniques to minimize VAP such as the use of subglottic suctioning 47 and coated endotracheal tubes 48 have not attained widespread clinical use. Summary Mechanical ventilation is a supportive therapy used for the treatment of acute respiratory failure. Although this therapy may be lifesaving for patients, special care must be paid to ensure that the therapy does not lead to complications. Avoidance of nosocomial complications such as VILI, VAP, and dynamic hyperinflation remain important goals of treatment. References 1. Tobin MJ. 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