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Mechanical Ventilation in Critical Illness
James B. Haenel, RRT, and Jeffrey L. Johnson, MD
CHAPTER 21
MECHANICAL VENTILATION IN CRITICAL ILLNESS 1. Why might a patient require mechanical ventilation? There are three conditions for which mechanical ventilation (MV) may be required: 1. Inadequate respiratory drive 2. Inability to maintain adequate alveolar ventilation 3. Hypoxia The decision to provide MV should be based on clinical examination and assessment of gas exchange by arterial blood gas analysis. This decision must be individualized because arbitrary cutoff values for PO2, PCO2, or pH as indicators of respiratory failure may not be germane to all patients. Physiologic derangements necessitating the need for MV include primary parenchymal disorders such as pneumonia, pulmonary edema, or pulmonary contusion or systemic disease that indirectly compromises pulmonary function such as sepsis or central nervous system dysfunction. The principal goal of MV in the setting of respiratory failure is to minimize the potential for ventilator-induced injury and support gas exchange while the underlying disease process is reversed. 2. Which is the most common mode of ventilation, volume or pressure control? From a classification standpoint neither is a true mode of ventilation. To be precise, conventional modes of MV control either volume or pressure. The mode of ventilation is a function of the types of breaths delivered (e.g., either mandatory and/or spontaneous breaths) and how the timing of each breath is determined. Volume control provides breaths that are volume constant and pressure variable. Pressure control provides breaths that are pressure constant and volume variable. It is the response of the ventilator to the patient’s effort that determines the mode. 3. What are the most commonly used modes of positive-pressure ventilation? Currently there are nine modes that are based on using either volume or pressure as the control variable: n VC-CMV, volume control–continuous mandatory ventilation n VC-A-C, volume control–assist control (ventilation) n VC-IMV or VC- SIMV, volume-control intermittent or synchronized intermittent mandatory ventilation n PC-CMV, pressure control–continuous mandatory ventilation n PC-A-C, pressure control–assist control (ventilation) n PC-IMV or PC-SIMV, pressure control–intermittent mandatory ventilation or pressure control–synchronized intermittent ventilation n PSV, pressure support ventilation 4. Does PC-CMV permit the patient to interact with the ventilator? Use of a term such as PC-CMV frequently leads to confusion to the uninitiated. The term controlled MV implies that the patient is receiving a neuromuscular blocking agent and is prevented or locked out from triggering the ventilator. Therefore, when speaking of volume control or pressure control, more descriptive terms such as volume-targeted or pressuretargeted ventilation may minimize any misunderstanding.
149
150 CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 5. How does VC-A-C mode work? The VC-A-C mode delivers a set minimum number of mandatory breaths and also allows the patient to trigger (or assist) additional breaths. Each breath (mandatory or assisted) is associated with a preset flow rate to deliver a preset tidal volume (VT). AC-A-C may cause respiratory alkalosis more often and may promote auto-positive end-expiratory pressure (PEEP) because the patient receives a full set VT with every breath, even when tachypneic. 6. Do VC-A-C and VC-SIMV differ? Both modes deliver mandatory breaths at a preset frequency, a preset VT, and a preset inspiratory gas flow rate. Between machine-initiated breaths in the VC-A-C mode, the patient can trigger the ventilator and receive an assisted breath at the set VT. In the VC-SIMV mode the ventilator generates a timing window based on the set frequency of the mandatory breaths, and attempts to synchronize the delivery of the breath in concert with the patient’s spontaneous effort. In between the mandatory breaths, while in the SIMV mode, the patient is free to initiate a totally spontaneous effort and generate a VT compatible with the patient’s inspiratory muscular effort. Flow rates of gas will vary during these spontaneous breaths and will be based on the patient’s efforts and demands. 7. When initiating mechanical ventilation, how do you decide on VC-A-C over VC-SIMV? If the intent of MV is to provide full ventilator support, provision of a sufficient level of alveolar ventilation is obligatory. The preference of VC-A-C over VC-SIMV, assuming that minute ventilation demands (set frequency and set VT) are being met, is really a point of style or preference. However, once the patient has achieved cardiopulmonary stability and the goal is now to initiate partial ventilator support, the options for VC-A-C vs. VC-SIMV are very different. A patient on a set respiratory frequency of 4 breaths/min in the VC-A-C mode with a total respiratory rate of 18 breaths/min is still receiving full ventilator support. In contrast, in the VC-SIMV mode a patient with the same set frequency is considered to be in a partial mode of support and must be capable of supporting the bulk of his or her own gas exchange demands. 8. What other variables are associated with conventional modes of MV? Simplistically ventilators are classified as either a pressure, volume, or flow controller. Current intensive care unit (ICU) ventilators can mix pressure control with flow control, all within a single breath. Next there are the phase variables, events that take place during a ventilator cycle. These phase variables control how the breath is n Triggered (i.e., patient or machine) n Limited (i.e., pressure or volume) n Cycled from inspiration to exhalation (i.e., pressure, volume, flow, or time) 9. What is pressure support ventilation? PSV augments a patient’s spontaneous inspiratory effort with a clinician-selected level of positive airway pressure. Inspiration is completed when the patient’s spontaneously generated peak flow rate decreases below a minimum level or a percentage of the initial inspiratory flow, typically less than 25%. Therefore PSV is a purely patient-triggered, pressure-limited, and flow-cycled mode of ventilation. PSV allows patients to establish their own respiratory rate (RR), vary their peak flow rate based on breath–to-breath demands, and enhance delivered VT. Taken together the RR, peak flow, and VT determine the inspiratory to expiratory (I:E) ratio. It is much more physiologic and comfortable for the patient to control the I:E ratio than to impose a fixed I:E ratio that will not respond favorably to increased patient demands. 10. How does pressure control ventilation differ from pressure support ventilation? PCV, unlike PSV, is a pressure-limited, time-cycled mode of ventilation. The VT generated results from the clinician-determined inspiratory time and the applied airway pressure and are
CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 151 predominantly influenced by flow resistance and respiratory system compliance. Practically speaking, PCV is used as a mode of ventilation when full ventilatory support is necessary, whereas PSV is optimal for providing partial ventilatory support. 11. What are trigger variables? All modern ICU ventilators constantly measure one or more of the phase variables (i.e., pressure, volume, flow, or time) (Table 21-1). Inspiration occurs when one of these variables reaches a preset value. Clinically this is referred to as triggering the ventilator. The following conditions are necessary to initiate a breath under each individual variable: n Pressure triggering: requires patient-initiated effort to decrease circuit pressure below a preset value (e.g., 2 cm H2O below baseline end-expiratory pressure is common). n Flow or volume triggering: again requires patient effort that results in a drop in the flow rate or volume of gas that is continually present within the circuit. n Time triggering: does not require patient effort but occurs when the set respiratory rate on the ventilator becomes due. Two potentially hazardous forms of triggering have also been identified: n Auto-triggering: occurs when the ventilator is rapidly cycling without apparent patient effort. If the triggering system is overly sensitive (e.g., the pressure is set for 1 cm H2O) and excessive condensation is present within the circuit, water motion can result in a drop in circuit pressure, causing auto-cycling. n Ineffective triggering: occurs when the ventilator doesn’t recognize a patient’s inspiratory effort. This is commonly seen during pressure triggering in the presence of auto-PEEP that may prevent the patient from achieving the necessary drop in circuit pressure.
TABLE 21-1. B R E A T H T Y P E S F O R V O L U M E A N D P R E S S U R E M O D E S O F VENTILATOR OPERATION Mandatory
Assisted
Mode (Common Names) Trigger
Limit
Cycle
Trigger
Limit
Cycle
VC-CMV
Time
Flow
Volume or Time
—
—
—
VC-A-C
Time
Flow
Volume or
Patient
Flow
Volume
—
—
Time VC-SIMV
Time
Flow
Volume or
or Time —
Time PC-CMV
Time
Pressure Time
—
—
—
PC-A-C
Time
Pressure Time
Patient
Pressure
Time
PC-SIMV
Time
Pressure Time
—
—
—
12. What are the goals of mechanical ventilation in patients with acute respiratory failure? Most patients with acute respiratory failure require full ventilatory support. The goals are to preserve or optimize lung mechanics and gas exchange and promote patient comfort while preventing ventilator-induced lung injury. Complications may arise from elevated alveolar pressures or persistently high inspired concentrations of oxygen (FiO2).
152 CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 13. What are the initial ventilator settings in acute respiratory failure? Commonly one begins with theVC-A-C mode, which ensures delivery of a preset VT. Pressure-cycled modes are acceptable but probably offer only theoretic advantage. The FiO2 begins at 1 and is titrated downward as tolerated. High FiO2 in the face of acute lung injury results in worsening of intrapulmonary shunting, probably as a result of absorption atelectasis. VT is based on ideal body weight (IBW) and the pathophysiology of lung injury. Volumes of 6 to 10 ml/kg/IBW are acceptable as long as the plateau pressure is <30 cm H2O. However, acute respiratory distress syndrome (ARDS) decreases the volume of the lung available for ventilation. Because large pressures or volumes may exacerbate the underlying lung injury, smaller volumes in the range of 6 to 8 ml/kg/ IBW are chosen. A respiratory rate (f) is chosen, usually in the range of 10 to 20 breaths/min. Patients with high minute volume requirements or a low VT (lung protective strategy) may require an f of 32 breaths/min. Carbon dioxide elimination does not improve significantly with rates >25/min, and rates >30/min predispose to gas trapping secondary to abbreviated expiratory times. 14. What is the role of positive end-expiratory pressure? PEEP has been a cornerstone in the management of respiratory failure for over 40 years. Specifically it is applied to the exhalation circuit of the mechanical ventilator. The main goals of PEEP are to: n Increase functional residual capacity by preventing alveolar collapse and recruiting atelectatic alveoli. n Decrease intrapulmonary shunting. n Reduce the work of breathing. PEEP adjustments should be considered in response to periods of desaturations (after common causes for hypoxemia have been ruled out) such as mucous plugging and barotrauma) to assess recruitment potential. 15. How is optimal positive end-expiratory pressure identified? Although various methods for lung recruitment have been suggested, we use the following approach to identify the optimal PEEP: Patients experiencing an acute desaturation event are placed in the pressure control mode, with respiratory rate set at 10 breaths/min, I:E ratio at 1:1, and peak pressure at 20 cm H2O. The PEEP is increased to 25 to 40 cm H2O for 2 minutes. The patient is continuously monitored for adverse effects. The PEEP is then returned to the baseline value. If the patient again desaturates, the trial is repeated, but the baseline PEEP is set 5 cm H2O higher. This process is continued until the patient no longer desaturates. To enhance safety, identification of intravascular fluid deficits and optimization of the hemodynamic status should be addressed before application of high PEEP levels. 16. What is intrinsic or auto-positive end-expiratory pressure? Intrinsic PEEP (PEEPi) is unrecognized positive alveolar pressure at end exhalation during MV. Patients with high minute ventilation requirements or patients with chronic obstructive pulmonary disease (COPD) or asthma are at risk for PEEPi. In healthy lungs during MV, if the respiratory rate is too rapid or the expiratory time too short, there is insufficient time for full exhalation, resulting in stacking of breaths and generation of positive airway pressure at end exhalation. Small-diameter endotracheal tubes may also limit exhalation and contribute to PEEPi. Patients with increased airway resistance and decreased pulmonary compliance are at high risk for PEEPi. Such patients have difficulty exhaling gas because of small airway obstruction/collapse and are prone to development of PEEPi during spontaneous ventilation and MV. PEEPi has the same side effects as PEEPe, but detecting it requires more vigilance. Failure to recognize the presence of auto-PEEP can lead to inappropriate ventilator changes (Figure 21-1). The only way to detect and measure PEEPi is to occlude the expiratory port at end expiration while monitoring airway pressure. Decreasing rate or increasing inspiratory flow (to increase I:E ratio) may allow time for full exhalation. Administering a bronchodilator therapy in the setting of bronchospasm is usually beneficial.
CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 153
Figure 21-1. Failure to appreciate auto-PEEP can lead to a vicious cycle in which an increased minute ventilation (VE) in response to a rise in PaCO2 decreases exhalation time, augments gas trapping, increases dead space ventilation (VD/VT), and paradoxically decreases CO2 elimination. A further increase in VE repeats the cycle, allowing pleural pressure to increase so that the adverse effects of PEEP (e.g., decreased cardiac output) emerge.
17. What are the side effects of PEEPe and PEEPi? n Barotrauma may result from overdistention of alveoli. n Cardiac output may be decreased because of increased intrathoracic pressure, producing an increase in transmural right atrial pressure and a decrease in venous return. PEEP also increases pulmonary artery pressure, potentially decreasing right ventricular output. Dilation of the right ventricle may cause bowing of the interventricular septum into the left ventricle, thus impairing filling of the left ventricle, decreasing cardiac output, especially if the patient is hypovolemic. n Incorrect interpretation of cardiac filling pressures. Pressure transmitted from the alveolus to the pulmonary vasculature may falsely elevate the readings. n Overdistention of alveoli from excessive PEEP decreases blood flow to these areas, increasing dead space (VD / VT). n Work of breathing may be increased with PEEP because the patient is required to generate a larger negative pressure to trigger flow from the ventilator. n Increase in intracranial pressure (ICP) and fluid retention. 18. What is a ventilator bundle? The ventilator bundle is a series of interventions related to ventilator care that have been identified to significantly reduce the incidence of ventilator-associated pneumonia. The key components of the ventilator bundle are: n Elevation of the head of the bed n Daily sedation vacations and assessment for the readiness to extubate n Stress ulcer prophylaxis n Deep venous thrombosis Additional interventions likely complementary to the ventilator bundle are implementation of a hand hygiene campaign and an oral care protocol. 19. What is controlled hypoventilation with permissive hypercapnia? Controlled hypoventilation (or permissive hypercapnia) is a pressure- or volume-limiting, lung-protective strategy whereby PCO2 is allowed to rise, placing more importance on
154 CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS protecting the lung than on maintaining eucapnia. The set VT is lowered to a range of approximately 4 to 6 ml/kg/IBW in an attempt to keep the Peak airway pressure (Paw) below 35 to 40 cm H2O and the static plateau pressure below 30 cm H2O. Several studies in ARDS and status asthmaticus have shown a decrease in barotrauma, intensive care days, and mortality. The PCO2 is allowed to rise slowly to a level of up to 80 to 100 mm Hg. If pH falls below 7.20, it may be treated with a buffer. Alternatively one may wait for the normal kidney to retain bicarbonate in response to the hypercapnia. Permissive hypercapnia is usually well tolerated. Potential adverse effects include cerebral vasodilation leading to increased ICP, and intracranial hypertension is the only absolute contraindication to permissive hypercapnia. Increased sympathetic activity, pulmonary vasoconstriction, and cardiac arrhythmias may occur but are rarely significant. Depression of cardiac contractility may be a problem in patients with underlying ventricular dysfunction. 20. What is compliance? How is it determined? Compliance is a measure of distensibility and is expressed as the change in volume for a given change in pressure. Determination of compliance involves the interrelationship among pressure, volume, and resistance to airflow. The two relevant pressures that must be monitored during MV are peak and static pressures. 21. How is peak pressure measured? Peak pressure is measured during the delivery of airflow at the end of inspiration. It is influenced by the inflation volume, airway resistance, and elastic recoil of the lungs and chest wall and reflects the dynamic compliance of the total respiratory system. 22. How is static pressure measured? Static or plateau pressure is measured during an end-inspiratory pause, during a no-flow condition, and reflects the static compliance of the respiratory system, including the lung parenchyma, chest wall, and abdomen. 23. How is compliance calculated? Both dynamic and static compliance should be calculated. Dynamic compliance is calculated as VT/(Paw total PEEP), and plateau or static compliance is VT/(plateau pressure total PEEP). Normal values for both dynamic and static compliance are 60 to 100 ml/cm H2O. A decrease in dynamic compliance without a change in the static compliance suggests an acute increase in airway resistance and can be assessed further by comparing peak pressure and plateau pressure. The normal gradient is approximately 10 cm H2O. A gradient >10 cm H2O may be secondary to endotracheal tube obstruction, mucous plugging, or bronchospasm. If volume is constant, acute changes in both dynamic and static compliance suggest a decrease in respiratory system compliance that may be caused by worsening pneumonia, ARDS, atelectasis, or increasing abdominal pressures. Compliance is a global value and does not describe what is happening regionally in the lungs with ARDS, in which diseased regions are interspersed with relatively healthy regions. Compliance values of 20 to 40 cm H2O are common in advanced ARDS. Decreased lung compliance reflects the compliance of the lung that is participating in gas exchange, not the collapsed or fluid-filled alveoli. 24. Is ventilation in the prone position an option for patients who are difficult to oxygenate? Absolutely! Studies have shown that the PaO2 improves significantly in approximately two thirds of patients with ARDS when they are placed prone. The mechanisms include: n Recruitment of collapsed dorsal lung fields by redistribution of lung edema to ventral regions. n Increased diaphragm motion enhancing ventilation.
CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 155 n Elimination of the compressive effects of the heart on the inferior lower lung fields, thus
improving regional ventilation. n Maintenance of dorsal lung perfusion in the face of improved dorsal ventilation, which
leads to improved V/Q matching. 25. What are the indications for prone ventilation? Indications for prone ventilation are not clearly established. We initiate a prone trial in any patient who remains hypoxemic or requires high FiO2 concentrations after the performance of recruitment/PEEP maneuvers. The best predictor of improved outcome during prone ventilation may be a decrease in the PaCO2 and not improved oxygenation. 26. How is the patient who is fighting the ventilator approached? Initially the potential causes are separated into ventilator (machine, circuit, and airway) problems and patient-related problems. Patient-related causes include hypoxemia, secretions or mucous plugging, pneumothorax, bronchospasm, infection (pneumonia or sepsis), pulmonary embolus, myocardial ischemia, gastrointestinal bleeding, worsening PEEPi, and anxiety. The ventilator-related issues include system leak or disconnection; inadequate ventilator support or delivered FiO2; airway-related problems such as extubation, obstructed endotracheal tube, cuff herniation, or rupture; and improper triggering sensitivity or flows. Until the problem is sorted out, the patient should be ventilated manually with 100% oxygen. Breath sounds and vital signs should be checked immediately. Arterial blood gas analysis and a portable chest radiograph are valuable, but, if a tension pneumothorax is suspected, immediate decompression precedes the chest radiograph.
KEY POINTS: MECHANICAL VENTILATION IN CRITICAL ILLNESS 1. Three indications for MV are: inadequate respiratory drive, inability to maintain alveolar ventilation, and hypoxia. 2. Two indications for noninvasive positive-pressure ventilation: hypercapnic respiratory failure and comfort in terminally ill patients. 3. Risk factors for auto-PEEP: high minute ventilation, small endotracheal tube, COPD, and asthma. 4. The normal airway gradient between peak and static pressure is approximately 10 cm H2O. 5. The first step in the care of the hypoxic patient fighting the ventilator is to ventilate the patient manually with 100% oxygen.
27. Should neuromuscular blockade be used to facilitate mechanical ventilation? Neuromuscular blocking agents (NMBAs) are commonly used to facilitate MV during ARDS; but, despite wide acceptance, there are few data and as yet no consensus available for when these agents should be used. Gainnier and associates (2004) were the first to report the effects of a 48-hour NMBA infusion on gas exchange in patients with early ARDS. All patients were ventilated according to the ARDSNet protocol. Significant improvements in oxygenation and ability to lower PEEP occurred in the NMBA group and were sustained beyond the 48-hour infusion period. Although it remains to be elucidated why muscle paralysis improves oxygenation, NMBAs are thought to decrease oxygen consumption, promote patient-ventilator interface, and increase chest wall compliance. Muscle paralysis may also be of benefit in specific situations such as intracranial hypertension or unconventional modes of ventilation (e.g., inverse ratio ventilation or
156 CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS extracorporeal techniques). Drawbacks to the use of these drugs include loss of neurologic examination, abolished cough, potential for an awake paralyzed patient, numerous medication and electrolyte interactions, potential for prolonged paralysis, and death associated with inadvertent ventilator disconnects. Use of NMBAs must not be taken lightly. Adequate sedation should be attempted first; if deemed absolutely necessary, use of NMBAs should be limited to 24 to 48 hours to prevent potential complications. 28. Is split-lung ventilation ever useful? Split-lung ventilation (SLV) refers to ventilation of each lung independently, usually via a double-lumen endotracheal tube and two ventilators. Patients with severe unilateral lung disease may be candidates for SLV. SLV has been shown to improve oxygenation in patients with unilateral pneumonia, pulmonary edema, and contusion. Isolation of the lungs can save the life of patients with massive hemoptysis or lung abscess by protecting the good lung from spillage. Patients with a bronchopleural fistula also may benefit from SLV. Different modes of ventilation may be applied to each lung individually. The two ventilators need not be synchronized, and, in fact, hemodynamic stability is better maintained by using the two ventilators asynchronously.
WEBSITE Institute for Healthcare Improvement: Implement the ventilator bundle www.IHI.org
SUGGESTED READINGS 1. Alsaghir AH, Martin CM: Effects of prone positioning in patients with acute respiratory distress syndrome: a meta-analysis. Crit Care Med 36:603–609, 2008. 2. Fessler HE, Hess DR: Does high-frequency ventilation offer benefits over conventional ventilation in adult patients with acute respiratory distress syndrome? Respir Care 52:595–608, 2007. 3. Kallet RH, Branson RD: Do the NIH ARDS Clinical Trials Network PEEP/FIO2 tables provide the best evidencebased guide to balancing PEEP and FIO2 settings in adults? Respir Care 52:461–477, 2007. 4. MacIntyre NR: Is there a best way to set tidal volume for mechanical ventilatory support? Clin Chest Med 29:225–231, 2008. 5. Nichols D, Haranath S: Pressure control ventilation. Crit Care Clin 23:183–199, 2007. 6. Steinburg KP, Kacmarek RM: Should tidal volume be 6 mL/kg predicted body weight in virtually all patients with acute respiratory failure? Respir Care 52:556–567, 2007.
CHAPTER 21
MECHANICAL VENTILATION IN CRITICAL ILLNESS 1. Why might a patient require mechanical ventilation? There are three conditions for which mechanical ventilation (MV) may be required: 1. Inadequate respiratory drive 2. Inability to maintain adequate alveolar ventilation 3. Hypoxia The decision to provide MV should be based on clinical examination and assessment of gas exchange by arterial blood gas analysis. This decision must be individualized because arbitrary cutoff values for PO2, PCO2, or pH as indicators of respiratory failure may not be germane to all patients. Physiologic derangements necessitating the need for MV include primary parenchymal disorders such as pneumonia, pulmonary edema, or pulmonary contusion or systemic disease that indirectly compromises pulmonary function such as sepsis or central nervous system dysfunction. The principal goal of MV in the setting of respiratory failure is to minimize the potential for ventilator-induced injury and support gas exchange while the underlying disease process is reversed. 2. Which is the most common mode of ventilation, volume or pressure control? From a classification standpoint neither is a true mode of ventilation. To be precise, conventional modes of MV control either volume or pressure. The mode of ventilation is a function of the types of breaths delivered (e.g., either mandatory and/or spontaneous breaths) and how the timing of each breath is determined. Volume control provides breaths that are volume constant and pressure variable. Pressure control provides breaths that are pressure constant and volume variable. It is the response of the ventilator to the patient’s effort that determines the mode. 3. What are the most commonly used modes of positive-pressure ventilation? Currently there are nine modes that are based on using either volume or pressure as the control variable: n VC-CMV, volume control–continuous mandatory ventilation n VC-A-C, volume control–assist control (ventilation) n VC-IMV or VC- SIMV, volume-control intermittent or synchronized intermittent mandatory ventilation n PC-CMV, pressure control–continuous mandatory ventilation n PC-A-C, pressure control–assist control (ventilation) n PC-IMV or PC-SIMV, pressure control–intermittent mandatory ventilation or pressure control–synchronized intermittent ventilation n PSV, pressure support ventilation 4. Does PC-CMV permit the patient to interact with the ventilator? Use of a term such as PC-CMV frequently leads to confusion to the uninitiated. The term controlled MV implies that the patient is receiving a neuromuscular blocking agent and is prevented or locked out from triggering the ventilator. Therefore, when speaking of volume control or pressure control, more descriptive terms such as volume-targeted or pressuretargeted ventilation may minimize any misunderstanding.
149
150 CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 5. How does VC-A-C mode work? The VC-A-C mode delivers a set minimum number of mandatory breaths and also allows the patient to trigger (or assist) additional breaths. Each breath (mandatory or assisted) is associated with a preset flow rate to deliver a preset tidal volume (VT). AC-A-C may cause respiratory alkalosis more often and may promote auto-positive end-expiratory pressure (PEEP) because the patient receives a full set VT with every breath, even when tachypneic. 6. Do VC-A-C and VC-SIMV differ? Both modes deliver mandatory breaths at a preset frequency, a preset VT, and a preset inspiratory gas flow rate. Between machine-initiated breaths in the VC-A-C mode, the patient can trigger the ventilator and receive an assisted breath at the set VT. In the VC-SIMV mode the ventilator generates a timing window based on the set frequency of the mandatory breaths, and attempts to synchronize the delivery of the breath in concert with the patient’s spontaneous effort. In between the mandatory breaths, while in the SIMV mode, the patient is free to initiate a totally spontaneous effort and generate a VT compatible with the patient’s inspiratory muscular effort. Flow rates of gas will vary during these spontaneous breaths and will be based on the patient’s efforts and demands. 7. When initiating mechanical ventilation, how do you decide on VC-A-C over VC-SIMV? If the intent of MV is to provide full ventilator support, provision of a sufficient level of alveolar ventilation is obligatory. The preference of VC-A-C over VC-SIMV, assuming that minute ventilation demands (set frequency and set VT) are being met, is really a point of style or preference. However, once the patient has achieved cardiopulmonary stability and the goal is now to initiate partial ventilator support, the options for VC-A-C vs. VC-SIMV are very different. A patient on a set respiratory frequency of 4 breaths/min in the VC-A-C mode with a total respiratory rate of 18 breaths/min is still receiving full ventilator support. In contrast, in the VC-SIMV mode a patient with the same set frequency is considered to be in a partial mode of support and must be capable of supporting the bulk of his or her own gas exchange demands. 8. What other variables are associated with conventional modes of MV? Simplistically ventilators are classified as either a pressure, volume, or flow controller. Current intensive care unit (ICU) ventilators can mix pressure control with flow control, all within a single breath. Next there are the phase variables, events that take place during a ventilator cycle. These phase variables control how the breath is n Triggered (i.e., patient or machine) n Limited (i.e., pressure or volume) n Cycled from inspiration to exhalation (i.e., pressure, volume, flow, or time) 9. What is pressure support ventilation? PSV augments a patient’s spontaneous inspiratory effort with a clinician-selected level of positive airway pressure. Inspiration is completed when the patient’s spontaneously generated peak flow rate decreases below a minimum level or a percentage of the initial inspiratory flow, typically less than 25%. Therefore PSV is a purely patient-triggered, pressure-limited, and flow-cycled mode of ventilation. PSV allows patients to establish their own respiratory rate (RR), vary their peak flow rate based on breath–to-breath demands, and enhance delivered VT. Taken together the RR, peak flow, and VT determine the inspiratory to expiratory (I:E) ratio. It is much more physiologic and comfortable for the patient to control the I:E ratio than to impose a fixed I:E ratio that will not respond favorably to increased patient demands. 10. How does pressure control ventilation differ from pressure support ventilation? PCV, unlike PSV, is a pressure-limited, time-cycled mode of ventilation. The VT generated results from the clinician-determined inspiratory time and the applied airway pressure and are
CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 151 predominantly influenced by flow resistance and respiratory system compliance. Practically speaking, PCV is used as a mode of ventilation when full ventilatory support is necessary, whereas PSV is optimal for providing partial ventilatory support. 11. What are trigger variables? All modern ICU ventilators constantly measure one or more of the phase variables (i.e., pressure, volume, flow, or time) (Table 21-1). Inspiration occurs when one of these variables reaches a preset value. Clinically this is referred to as triggering the ventilator. The following conditions are necessary to initiate a breath under each individual variable: n Pressure triggering: requires patient-initiated effort to decrease circuit pressure below a preset value (e.g., 2 cm H2O below baseline end-expiratory pressure is common). n Flow or volume triggering: again requires patient effort that results in a drop in the flow rate or volume of gas that is continually present within the circuit. n Time triggering: does not require patient effort but occurs when the set respiratory rate on the ventilator becomes due. Two potentially hazardous forms of triggering have also been identified: n Auto-triggering: occurs when the ventilator is rapidly cycling without apparent patient effort. If the triggering system is overly sensitive (e.g., the pressure is set for 1 cm H2O) and excessive condensation is present within the circuit, water motion can result in a drop in circuit pressure, causing auto-cycling. n Ineffective triggering: occurs when the ventilator doesn’t recognize a patient’s inspiratory effort. This is commonly seen during pressure triggering in the presence of auto-PEEP that may prevent the patient from achieving the necessary drop in circuit pressure.
TABLE 21-1. B R E A T H T Y P E S F O R V O L U M E A N D P R E S S U R E M O D E S O F VENTILATOR OPERATION Mandatory
Assisted
Mode (Common Names) Trigger
Limit
Cycle
Trigger
Limit
Cycle
VC-CMV
Time
Flow
Volume or Time
—
—
—
VC-A-C
Time
Flow
Volume or
Patient
Flow
Volume
—
—
Time VC-SIMV
Time
Flow
Volume or
or Time —
Time PC-CMV
Time
Pressure Time
—
—
—
PC-A-C
Time
Pressure Time
Patient
Pressure
Time
PC-SIMV
Time
Pressure Time
—
—
—
12. What are the goals of mechanical ventilation in patients with acute respiratory failure? Most patients with acute respiratory failure require full ventilatory support. The goals are to preserve or optimize lung mechanics and gas exchange and promote patient comfort while preventing ventilator-induced lung injury. Complications may arise from elevated alveolar pressures or persistently high inspired concentrations of oxygen (FiO2).
152 CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 13. What are the initial ventilator settings in acute respiratory failure? Commonly one begins with theVC-A-C mode, which ensures delivery of a preset VT. Pressure-cycled modes are acceptable but probably offer only theoretic advantage. The FiO2 begins at 1 and is titrated downward as tolerated. High FiO2 in the face of acute lung injury results in worsening of intrapulmonary shunting, probably as a result of absorption atelectasis. VT is based on ideal body weight (IBW) and the pathophysiology of lung injury. Volumes of 6 to 10 ml/kg/IBW are acceptable as long as the plateau pressure is <30 cm H2O. However, acute respiratory distress syndrome (ARDS) decreases the volume of the lung available for ventilation. Because large pressures or volumes may exacerbate the underlying lung injury, smaller volumes in the range of 6 to 8 ml/kg/ IBW are chosen. A respiratory rate (f) is chosen, usually in the range of 10 to 20 breaths/min. Patients with high minute volume requirements or a low VT (lung protective strategy) may require an f of 32 breaths/min. Carbon dioxide elimination does not improve significantly with rates >25/min, and rates >30/min predispose to gas trapping secondary to abbreviated expiratory times. 14. What is the role of positive end-expiratory pressure? PEEP has been a cornerstone in the management of respiratory failure for over 40 years. Specifically it is applied to the exhalation circuit of the mechanical ventilator. The main goals of PEEP are to: n Increase functional residual capacity by preventing alveolar collapse and recruiting atelectatic alveoli. n Decrease intrapulmonary shunting. n Reduce the work of breathing. PEEP adjustments should be considered in response to periods of desaturations (after common causes for hypoxemia have been ruled out) such as mucous plugging and barotrauma) to assess recruitment potential. 15. How is optimal positive end-expiratory pressure identified? Although various methods for lung recruitment have been suggested, we use the following approach to identify the optimal PEEP: Patients experiencing an acute desaturation event are placed in the pressure control mode, with respiratory rate set at 10 breaths/min, I:E ratio at 1:1, and peak pressure at 20 cm H2O. The PEEP is increased to 25 to 40 cm H2O for 2 minutes. The patient is continuously monitored for adverse effects. The PEEP is then returned to the baseline value. If the patient again desaturates, the trial is repeated, but the baseline PEEP is set 5 cm H2O higher. This process is continued until the patient no longer desaturates. To enhance safety, identification of intravascular fluid deficits and optimization of the hemodynamic status should be addressed before application of high PEEP levels. 16. What is intrinsic or auto-positive end-expiratory pressure? Intrinsic PEEP (PEEPi) is unrecognized positive alveolar pressure at end exhalation during MV. Patients with high minute ventilation requirements or patients with chronic obstructive pulmonary disease (COPD) or asthma are at risk for PEEPi. In healthy lungs during MV, if the respiratory rate is too rapid or the expiratory time too short, there is insufficient time for full exhalation, resulting in stacking of breaths and generation of positive airway pressure at end exhalation. Small-diameter endotracheal tubes may also limit exhalation and contribute to PEEPi. Patients with increased airway resistance and decreased pulmonary compliance are at high risk for PEEPi. Such patients have difficulty exhaling gas because of small airway obstruction/collapse and are prone to development of PEEPi during spontaneous ventilation and MV. PEEPi has the same side effects as PEEPe, but detecting it requires more vigilance. Failure to recognize the presence of auto-PEEP can lead to inappropriate ventilator changes (Figure 21-1). The only way to detect and measure PEEPi is to occlude the expiratory port at end expiration while monitoring airway pressure. Decreasing rate or increasing inspiratory flow (to increase I:E ratio) may allow time for full exhalation. Administering a bronchodilator therapy in the setting of bronchospasm is usually beneficial.
CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 153
Figure 21-1. Failure to appreciate auto-PEEP can lead to a vicious cycle in which an increased minute ventilation (VE) in response to a rise in PaCO2 decreases exhalation time, augments gas trapping, increases dead space ventilation (VD/VT), and paradoxically decreases CO2 elimination. A further increase in VE repeats the cycle, allowing pleural pressure to increase so that the adverse effects of PEEP (e.g., decreased cardiac output) emerge.
17. What are the side effects of PEEPe and PEEPi? n Barotrauma may result from overdistention of alveoli. n Cardiac output may be decreased because of increased intrathoracic pressure, producing an increase in transmural right atrial pressure and a decrease in venous return. PEEP also increases pulmonary artery pressure, potentially decreasing right ventricular output. Dilation of the right ventricle may cause bowing of the interventricular septum into the left ventricle, thus impairing filling of the left ventricle, decreasing cardiac output, especially if the patient is hypovolemic. n Incorrect interpretation of cardiac filling pressures. Pressure transmitted from the alveolus to the pulmonary vasculature may falsely elevate the readings. n Overdistention of alveoli from excessive PEEP decreases blood flow to these areas, increasing dead space (VD / VT). n Work of breathing may be increased with PEEP because the patient is required to generate a larger negative pressure to trigger flow from the ventilator. n Increase in intracranial pressure (ICP) and fluid retention. 18. What is a ventilator bundle? The ventilator bundle is a series of interventions related to ventilator care that have been identified to significantly reduce the incidence of ventilator-associated pneumonia. The key components of the ventilator bundle are: n Elevation of the head of the bed n Daily sedation vacations and assessment for the readiness to extubate n Stress ulcer prophylaxis n Deep venous thrombosis Additional interventions likely complementary to the ventilator bundle are implementation of a hand hygiene campaign and an oral care protocol. 19. What is controlled hypoventilation with permissive hypercapnia? Controlled hypoventilation (or permissive hypercapnia) is a pressure- or volume-limiting, lung-protective strategy whereby PCO2 is allowed to rise, placing more importance on
154 CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS protecting the lung than on maintaining eucapnia. The set VT is lowered to a range of approximately 4 to 6 ml/kg/IBW in an attempt to keep the Peak airway pressure (Paw) below 35 to 40 cm H2O and the static plateau pressure below 30 cm H2O. Several studies in ARDS and status asthmaticus have shown a decrease in barotrauma, intensive care days, and mortality. The PCO2 is allowed to rise slowly to a level of up to 80 to 100 mm Hg. If pH falls below 7.20, it may be treated with a buffer. Alternatively one may wait for the normal kidney to retain bicarbonate in response to the hypercapnia. Permissive hypercapnia is usually well tolerated. Potential adverse effects include cerebral vasodilation leading to increased ICP, and intracranial hypertension is the only absolute contraindication to permissive hypercapnia. Increased sympathetic activity, pulmonary vasoconstriction, and cardiac arrhythmias may occur but are rarely significant. Depression of cardiac contractility may be a problem in patients with underlying ventricular dysfunction. 20. What is compliance? How is it determined? Compliance is a measure of distensibility and is expressed as the change in volume for a given change in pressure. Determination of compliance involves the interrelationship among pressure, volume, and resistance to airflow. The two relevant pressures that must be monitored during MV are peak and static pressures. 21. How is peak pressure measured? Peak pressure is measured during the delivery of airflow at the end of inspiration. It is influenced by the inflation volume, airway resistance, and elastic recoil of the lungs and chest wall and reflects the dynamic compliance of the total respiratory system. 22. How is static pressure measured? Static or plateau pressure is measured during an end-inspiratory pause, during a no-flow condition, and reflects the static compliance of the respiratory system, including the lung parenchyma, chest wall, and abdomen. 23. How is compliance calculated? Both dynamic and static compliance should be calculated. Dynamic compliance is calculated as VT/(Paw total PEEP), and plateau or static compliance is VT/(plateau pressure total PEEP). Normal values for both dynamic and static compliance are 60 to 100 ml/cm H2O. A decrease in dynamic compliance without a change in the static compliance suggests an acute increase in airway resistance and can be assessed further by comparing peak pressure and plateau pressure. The normal gradient is approximately 10 cm H2O. A gradient >10 cm H2O may be secondary to endotracheal tube obstruction, mucous plugging, or bronchospasm. If volume is constant, acute changes in both dynamic and static compliance suggest a decrease in respiratory system compliance that may be caused by worsening pneumonia, ARDS, atelectasis, or increasing abdominal pressures. Compliance is a global value and does not describe what is happening regionally in the lungs with ARDS, in which diseased regions are interspersed with relatively healthy regions. Compliance values of 20 to 40 cm H2O are common in advanced ARDS. Decreased lung compliance reflects the compliance of the lung that is participating in gas exchange, not the collapsed or fluid-filled alveoli. 24. Is ventilation in the prone position an option for patients who are difficult to oxygenate? Absolutely! Studies have shown that the PaO2 improves significantly in approximately two thirds of patients with ARDS when they are placed prone. The mechanisms include: n Recruitment of collapsed dorsal lung fields by redistribution of lung edema to ventral regions. n Increased diaphragm motion enhancing ventilation.
CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS 155 n Elimination of the compressive effects of the heart on the inferior lower lung fields, thus
improving regional ventilation. n Maintenance of dorsal lung perfusion in the face of improved dorsal ventilation, which
leads to improved V/Q matching. 25. What are the indications for prone ventilation? Indications for prone ventilation are not clearly established. We initiate a prone trial in any patient who remains hypoxemic or requires high FiO2 concentrations after the performance of recruitment/PEEP maneuvers. The best predictor of improved outcome during prone ventilation may be a decrease in the PaCO2 and not improved oxygenation. 26. How is the patient who is fighting the ventilator approached? Initially the potential causes are separated into ventilator (machine, circuit, and airway) problems and patient-related problems. Patient-related causes include hypoxemia, secretions or mucous plugging, pneumothorax, bronchospasm, infection (pneumonia or sepsis), pulmonary embolus, myocardial ischemia, gastrointestinal bleeding, worsening PEEPi, and anxiety. The ventilator-related issues include system leak or disconnection; inadequate ventilator support or delivered FiO2; airway-related problems such as extubation, obstructed endotracheal tube, cuff herniation, or rupture; and improper triggering sensitivity or flows. Until the problem is sorted out, the patient should be ventilated manually with 100% oxygen. Breath sounds and vital signs should be checked immediately. Arterial blood gas analysis and a portable chest radiograph are valuable, but, if a tension pneumothorax is suspected, immediate decompression precedes the chest radiograph.
KEY POINTS: MECHANICAL VENTILATION IN CRITICAL ILLNESS 1. Three indications for MV are: inadequate respiratory drive, inability to maintain alveolar ventilation, and hypoxia. 2. Two indications for noninvasive positive-pressure ventilation: hypercapnic respiratory failure and comfort in terminally ill patients. 3. Risk factors for auto-PEEP: high minute ventilation, small endotracheal tube, COPD, and asthma. 4. The normal airway gradient between peak and static pressure is approximately 10 cm H2O. 5. The first step in the care of the hypoxic patient fighting the ventilator is to ventilate the patient manually with 100% oxygen.
27. Should neuromuscular blockade be used to facilitate mechanical ventilation? Neuromuscular blocking agents (NMBAs) are commonly used to facilitate MV during ARDS; but, despite wide acceptance, there are few data and as yet no consensus available for when these agents should be used. Gainnier and associates (2004) were the first to report the effects of a 48-hour NMBA infusion on gas exchange in patients with early ARDS. All patients were ventilated according to the ARDSNet protocol. Significant improvements in oxygenation and ability to lower PEEP occurred in the NMBA group and were sustained beyond the 48-hour infusion period. Although it remains to be elucidated why muscle paralysis improves oxygenation, NMBAs are thought to decrease oxygen consumption, promote patient-ventilator interface, and increase chest wall compliance. Muscle paralysis may also be of benefit in specific situations such as intracranial hypertension or unconventional modes of ventilation (e.g., inverse ratio ventilation or
156 CHAPTER 21 MECHANICAL VENTILATION IN CRITICAL ILLNESS extracorporeal techniques). Drawbacks to the use of these drugs include loss of neurologic examination, abolished cough, potential for an awake paralyzed patient, numerous medication and electrolyte interactions, potential for prolonged paralysis, and death associated with inadvertent ventilator disconnects. Use of NMBAs must not be taken lightly. Adequate sedation should be attempted first; if deemed absolutely necessary, use of NMBAs should be limited to 24 to 48 hours to prevent potential complications. 28. Is split-lung ventilation ever useful? Split-lung ventilation (SLV) refers to ventilation of each lung independently, usually via a double-lumen endotracheal tube and two ventilators. Patients with severe unilateral lung disease may be candidates for SLV. SLV has been shown to improve oxygenation in patients with unilateral pneumonia, pulmonary edema, and contusion. Isolation of the lungs can save the life of patients with massive hemoptysis or lung abscess by protecting the good lung from spillage. Patients with a bronchopleural fistula also may benefit from SLV. Different modes of ventilation may be applied to each lung individually. The two ventilators need not be synchronized, and, in fact, hemodynamic stability is better maintained by using the two ventilators asynchronously.
WEBSITE Institute for Healthcare Improvement: Implement the ventilator bundle www.IHI.org
SUGGESTED READINGS 1. Alsaghir AH, Martin CM: Effects of prone positioning in patients with acute respiratory distress syndrome: a meta-analysis. Crit Care Med 36:603–609, 2008. 2. Fessler HE, Hess DR: Does high-frequency ventilation offer benefits over conventional ventilation in adult patients with acute respiratory distress syndrome? Respir Care 52:595–608, 2007. 3. Kallet RH, Branson RD: Do the NIH ARDS Clinical Trials Network PEEP/FIO2 tables provide the best evidencebased guide to balancing PEEP and FIO2 settings in adults? Respir Care 52:461–477, 2007. 4. MacIntyre NR: Is there a best way to set tidal volume for mechanical ventilatory support? Clin Chest Med 29:225–231, 2008. 5. Nichols D, Haranath S: Pressure control ventilation. Crit Care Clin 23:183–199, 2007. 6. Steinburg KP, Kacmarek RM: Should tidal volume be 6 mL/kg predicted body weight in virtually all patients with acute respiratory failure? Respir Care 52:556–567, 2007.