Positive-Pressure Mechanical Ventilation in the Management of Acute Respiratory Failure

Transcription

1 PULMONARY DISEASE BOARD REVIEW MANUAL PUBLISHING STAFF PRESIDENT, GROUP PUBLISHER Bruce M. White EXECUTIVE EDITOR Debra Dreger SENIOR EDITOR Becky Krumm, ELS EDITOR Ellen M. McDonald, PhD, ELS ASSISTANT EDITOR Jennifer M. Vander Bush EDITORIAL ASSISTANT Renee Autumn Ray EXECUTIVE VICE PRESIDENT Barbara T. White, MBA PRODUCTION DIRECTOR Suzanne S. Banish PRODUCTION ASSOCIATES Tish Berchtold Klus Christie Grams Mary Beth Cunney ADVERTISING/PROJECT MANAGER Patricia Payne Castle NOTE FROM THE PUBLISHER: This publication has been developed without involvement of or review by the American Board of Internal Medicine. Endorsed by the Association for Hospital Medical Education The Association for Hospital Medical Education endorses HOSPITAL PHYSICIAN for the purpose of presenting the latest developments in medical education as they affect residency programs and clinical hospital practice. Positive-Pressure Mechanical Ventilation in the Management of Acute Respiratory Failure Series Editor and Contributing Author: Robert A. Balk, MD, FACP, FCCP, FCCM Professor of Internal Medicine, Rush Medical College, Director of Pulmonary and Critical Care Medicine, Rush-Presbyterian-St. Luke s Medical Center, Chicago, IL Contributing Author: Javier Bogarin, MD Instructor in Medicine, Rush Medical College, Chief Fellow, Section of Pulmonary and Critical Care Medicine, Rush-Presbyterian-St. Luke s Medical Center, Chicago, IL Table of Contents Introduction Indications and Modes Monitoring of Patients Complications Withdrawing Mechanical Ventilation Board Review Questions Answers References Cover Illustration by Dean Vigyikan Copyright 21, Turner White Communications, Inc., 125 Strafford Avenue, Suite 22, Wayne, PA , All rights reserved. No part of this publication may be reproduced, stored in a retrieval system, or transmitted in any form or by any means, mechanical, electronic, photocopying, recording, or otherwise, without the prior written permission of Turner White Communications, Inc. The editors are solely responsible for selecting content. Although the editors take great care to ensure accuracy, Turner White Communications, Inc., will not be liable for any errors of omission or inaccuracies in this publication. Opinions expressed are those of the authors and do not necessarily reflect those of Turner White Communications, Inc. Pulmonary Disease Volume 8, Part 3 1

2 PULMONARY DISEASE BOARD REVIEW MANUAL Positive-Pressure Mechanical Ventilation in the Management of Acute Respiratory Failure INTRODUCTION Mechanical ventilation imposes an artificial pattern of ventilation on a patient s natural breathing rhythm. In placing patients with acute respiratory failure on mechanical ventilation, physicians have an obligation to ensure that respiratory needs are met, that complications are avoided, and that the process remains as comfortable as possible. Inappropriate initial ventilator settings and failure to modify these settings based on a patient s response and changing physical condition can increase the work of breathing, worsen gas exchange, and lead to harmful sequelae. Table 1 summarizes the physiologic and clinical goals of mechanical ventilation, as determined by the 1994 American College of Chest Physicians Consensus Conference on Mechanical Ventilation. 1 In cases of acute respiratory failure, the basic goal of mechanical ventilation is to support gas exchange and/or assist the respiratory pump while minimizing adverse effects. This review will address current concepts involving positive-pressure ventilation (PPV) delivered through an endotracheal tube, specifically as they concern patients with acute respiratory failure. Current modes of mechanical ventilation, necessary steps in the monitoring of patients being mechanically ventilated, potential complications of mechanical ventilation, and methods of weaning patients from mechanical ventilation will be discussed. INDICATIONS AND MODES The respiratory and nonrespiratory indications for instituting invasive mechanical ventilation in patients with acute respiratory failure are listed in Table 2. Although these general guidelines exist, the precise timing of intubation and initiation of mechanical ventilation depends on an individual physician s assessment, as does the precise type of mechanical ventilation used. STANDARD MODES The greater complexity of today s mechanical ventilators has increased the number of variables that define a specific mode. In the case of PPV, the term mode can refer to the way of delivering tidal volume (V T ), or the degree of patient participation, or the cycling mechanism of the ventilator. Table 3 summarizes the most commonly used modes of mechanical ventilation and their different features. Way of Delivering Tidal Volume Volume-targeted modes deliver a preset V T with each breath. The inspiratory flow rate and V T are fixed, and the airway pressures are variable. In pressure-targeted modes, the ventilator applies a preset pressure level throughout inspiration. The inspiratory airway pressure is fixed, and the flow rate and V T are variable. Degree of Patient Participation In assisted modes of mechanical ventilation, patients can initiate or trigger breaths above the rate preset by the machine. In controlled modes, the machine delivers all breaths at a preset rate. Controlled modes are used in situations such as anesthesia, paralysis, or deep sedation that involve apnea. Assisted or controlled modes can be volume- or pressure-targeted. In supported modes, the patient s efforts determine the respiratory rate (RR) and V T, and the machine assists or augments each effort. Cycling Mechanism There are various ways of switching from inspiration to expiration in a ventilator. Volume-cycled modes end inspiration after a predetermined volume of gas is delivered. Time-cycled modes end inspiration after a predetermined time has elapsed (eg, in pressure-control ventilation [PCV]). Flow-cycled modes end inspiration after airflow has decreased to a predetermined level preset in the ventilator; this predetermined level is usually 25% of the peak flow achieved during inspiration, or 5 L/min (eg, in pressure-support ventilation [PSV]). ALTERNATE MODES On occasion, oxygenation or ventilation cannot be achieved without high minute volumes, high inflation pressures, or lung overdistention. Less conventional modes of mechanical ventilation can be useful in these situations. Some of these modes include inverse-ratio ventilation, high-frequency ventilation, airway pressure release ventilation, and prone ventilation. Whereas 2 Hospital Physician Board Review Manual

3 Table 1. Goals of Mechanical Ventilation Physiologic goals Increasing lung volume (eg, by increasing end-inspiratory lung inflation and functional residual capacity) Reducing the work of breathing (eg, by unloading of respiratory muscles) Supporting gas exchange (eg, alveolar ventilation [PaCO 2, ph] and arterial oxygenation [PaO 2, SaO 2,CAO 2 ]) Clinical goals Avoiding ventilator-induced lung injury and allowing the injured lung to heal Decreasing intracranial pressure Decreasing systemic or myocardial oxygen consumption Permitting sedation or neuromuscular blockade Preventing or reversing atelectasis Relieving respiratory distress Reversing acute respiratory acidosis Reversing hypoxemia Reversing ventilatory muscle fatigue Stabilizing the chest wall CAO 2 = arterial oxygen content; SaO 2 = oxygen saturation. Data from Slutsky AS. Mechanical ventilation. American College of Chest Physicians Consensus Conference [published erratum appears in Chest 1994;16:656]. Chest 1993;14: alternate modes might produce transient improvements in oxygenation or other parameters, none has shown improved outcomes over standard modes. These unconventional modes of mechanical ventilation must be applied cautiously by experienced physicians, given the potential for serious adverse effects. VENTILATOR SETTINGS Tidal Volume In volume-cycled modes, V T must be set. Initial values will depend on the underlying disease process. Patients with acute lung injury should receive an initial V T of 6 ml/kg ideal body weight. This value should be adjusted (range, 4 8 ml/kg) according to the patient s ventilatory needs, maintaining an inspiratory plateau pressure (Pplat) no greater than 3 cmh 2 O. This strategy has been associated with decreased mortality in patients with acute lung injury in a recent multicenter trial. 2 The V T is a determinant of MAP, auto positive end-expiratory pressure (auto-peep), inspiratory time expiratory time ratio (I:E), and inspiratory Pplat. Patients with acute respiratory failure resulting from neuromuscular diseases or lesions of the central nervous system usually have no Table 2. Indications for Mechanical Ventilation in Patients with Acute Respiratory Failure Respiratory Acute hypoxemia refractory to oxygen therapy Acute, progressive hypercapnia Chronic hypercapnia with acute respiratory acidosis Failure of noninvasive ventilation Inability to expectorate secretions Inadequate compensation for acute metabolic acidosis Upper airway obstruction Nonrespiratory Airway protection required (cases of seizure, coma, intoxication) Need for hyperventilation therapy Need to decrease the work of breathing in patients in shock intrinsic lung disease and might require a V T of 1 to 12 cmh 2 O to satisfy air hunger and prevent atelectasis. Respiratory Rate A baseline RR must be established in pressure- or volume-targeted assist-control modes. Usually varying from 4 to 2 breaths/min, depending on the targeted ph and/or the patient s respiratory drive, the set RR should always be 2 to 4 breaths/min below the patient s spontaneous rate to avoid inadvertent hyperventilation if minute ventilation requirements decrease. The RR is one of the determinants of I:E and auto-peep. Higher RRs decrease expiratory time and promote dynamic hyperinflation (DH). Inspiratory Flow Rate Flow refers to the volume of gas displaced per unit of time. Flow is usually measured in liters per minute in ventilators. The inspiratory flow rate usually is set between 4 and 1 L/min. Peak inspiratory flow rates are fixed (or flow limited) in volume-cycled modes and are variable in pressure- and flow-cycled modes. During flow-limited breaths (ie, during volume ventilation), additional patient efforts will only decrease airway pressures without increasing flow rate. This situation imposes an additional load on the respiratory muscles, is uncomfortable, and leads to patient-ventilator asynchrony. The higher the respiratory drive, the higher the flow rate should be, to avoid breath stacking. An inappropriately low flow rate will prolong inspiratory time, leading to increased MAP, I:E, auto-peep, and patient discomfort. Conversely, excessively high flow rates can increase peak airway pressure (PAP) and also cause discomfort. Intermediate flow rates should be selected initially and Pulmonary Disease Volume 8, Part 3 3

4 Table 3. Standard Modes of Mechanical Ventilation Mode Features Set-up Parameters Advantages Disadvantages A-C SIMV Volume targeted, volume cycled Volume targeted, volume cycled FiO 2, flow waveform, high pressure limit, inspiratory flow, PEEP, RR, trigger sensitivity, V T Same as for A-C mode; optional pressure support to assist spontaneous breaths FiO 2, inflation pressure level, inspiratory time, PEEP, RR, trigger sensitivity CPAP, FiO 2, pressure level, trigger sensitivity Guarantees V E and V T, supports every breath Same as for A-C mode; can combine with PSV and be used as a weaning tool Limits airway pressure, supports every breath Fixed flow, high PAP, hyperventilation, increased WOB (if peak flow or sensitivity is inadequate), worsened intrinsic PEEP Same as for A-C mode (for ventilator breaths); increases WOB PCV Pressure targeted, time cycled Discomfort, no ability of patient to adjust inspiratory time or V T PSV Pressure targeted, flow cycled Has use as a weaning tool, can combine with SIMV, is comfortable, usually involves less WOB Improves oxygenation, spontaneous breathing Increased WOB if pressure levels are excessive, no guarantee of RR, V E, or V T CPAP* Not applicable CPAP level, FiO 2 Same as for PSV A-C = assist-control ventilation; CPAP = continuous positive airway pressure; FiO 2 = fraction of inspired oxygen; PAP = peak airway pressure; PCV = pressure-control ventilation; PEEP = positive end-expiratory pressure; PSV = pressure support ventilation; RR = respiratory rate; SIMV = synchronized intermittent mandatory ventilation; V E = minute volume; V T = tidal volume; WOB = work of breathing. *Not a ventilatory mode per se, because it does not assist ventilation. tailored according to airway pressures, desired I:E, and patient comfort. Flow profiles (eg, decelerating, sine, or square waveform) can be selected in volume-targeted modes. Flow profiles affect the PAP and the speed of delivery of V T. Square waves keep a constant level of flow throughout inspiration, thereby decreasing inspiratory time at the expense of higher PAP. Fraction of Inspired Oxygen As a general rule, a fraction of inspired oxygen (FiO 2 ) value of 1. should be used immediately after intubation until the patient s condition stabilizes. Thereafter, the minimal levels of FiO 2 needed for acceptable oxygenation (to maintain a PaO 2 > 55 6 mm Hg or an oxygen saturation > 9%) should be used. After patient stabilization, FiO 2 values above.6 raise concerns about worsening lung injury resulting from oxygen toxicity. However, the precise amount or duration of hyperoxia required to cause harm to injured lungs is not known. The FiO 2 requirements can be minimized by optimizing PEEP and MAP and by decreasing peripheral oxygen utilization (eg, by inducing deep sedation). Inspiratory Time Inspiratory time is set in time-cycled modes (eg, PCV). As mentioned earlier, the normal I:E in spontaneous breathing varies between 1:1.5 and 1:2. Lengthening inspiratory time increases MAP, a vital determinant of oxygenation, and can improve ventilation of lung units with high time constants (ie, product of compliance and resistance). Lung units with higher time constants require more time to fill and empty, thus increasing the risk of nonhomogeneous ventilation and DH. In volume ventilation, inspiratory time varies, depending on the flow rate and V T chosen. In flowcycled modes, the patient determines inspiratory time. Trigger Sensitivity The trigger sensitivity is set in assisted modes of ventilation. Triggering allows the ventilator to detect an inspiratory effort and initiate breath delivery. The trigger sensitivity should be set at the most sensitive level that will prevent autocycling. When trigger sensitivity is set by pressure triggering, a decrease in airway pressure (usually.5 to 2. cmh 2 O below end-expiratory pressure) is required to initiate a ventilator breath. Conversely, when flow triggering is used, gas flows continuously (usually at 3 to 1 L/min) through the inspiratory and expiratory circuits of the ventilator; with an inspiratory effort, flow in the ventilator s expiratory circuit will decrease, thereby initiating a ventilator breath. Low trigger sensitivities (ie, higher set pressure values) increase inspiratory effort and work of breathing (WOB). Flow triggering requires less effort than does pressure triggering, but the clinical implications of this distinction are unknown. 4 Hospital Physician Board Review Manual

5 Positive End-Expiratory Pressure PEEP is applied primarily to improve oxygenation, to prevent alveolar recruitment-derecruitment (the socalled open-lung strategy), or to decrease the triggering effort caused by auto-peep. The overall effects of PEEP are summarized in Table 4. The ideal amount of PEEP for a specific patient is difficult to estimate, and the question of how to determine it has sparked much debate. The construction of pressurevolume curves for the determination of lower and upper inflection points has been suggested as a possible solution, with the ideal PEEP set 2 cmh 2 O above the lower inflection point. However, this technique is cumbersome, requires paralysis, and is poorly reproducible. Moreover, the inflection points can vary with time, mandating serial measurements for accurate adjustments. The Acute Respiratory Distress Syndrome Network trial 2 sought a stepwise increase in PEEP/FiO 2, employing a protocol based on PaO 2 and inspiratory Pplat. Another approach is based on finding the lowest PEEP needed to achieve a PaO 2 of 6 mm Hg or more, with FiO 2 levels of.5 or less. Beneficial effects of PEEP on oxygenation should be balanced with potentially negative effects on cardiac output and oxygen transport to tissues. Continuous Positive Airway Pressure Superatmospheric pressures are applied to the airways continuously in spontaneously breathing patients. The effect is the same as that achieved by PEEP. Strictly speaking, continuous positive airway pressure (CPAP) is not a ventilatory mode, because it does not assist ventilation. A preset CPAP level can be used alone or in combination with PSV. Excessively high CPAP pressure can increase the effort involved in breathing (by inducing expiratory muscle contraction to overcome hyperinflation) and also can produce hemodynamic alterations. Pressure Levels In pressure-targeted modes of ventilation (PCV, PSV), an inflation pressure level is set and kept constant by the ventilator throughout inspiration. The sum of the set inflation pressure and PEEP determines the PAP. V T can vary with changes in compliance and resistance of the respiratory system and with PEEP. Careful monitoring of minute ventilation is essential in pressure-targeted modes. In volume-targeted modes, an upper pressure limit (referred to as the pop-off pressure) is established to prevent excessive airway pressures and lung rupture. The machine automatically cycles to exhalation when this limit is reached. The pressure limit usually is set at a level slightly above the PAP observed during regular cycling (but usually not higher than 5 55 cmh 2 O). Table 4. Effects of Positive End-Expiratory Pressure Beneficial effects Decreases shunt fraction Increases end-expiratory lung volume Increases mean airway pressure and oxygenation Prevents recurrent alveolar collapse Recruits atelectatic aveoli RV = right ventricular; V D = dead space. Automatic Tube Compensation Some ventilators have an automatic tube compensation function that automatically compensates for resistance of the endotracheal tube. Changes in inspiratory and expiratory flow dependent pressures are measured. Based on the results, the machine applies a given positive pressure during inspiration and negative pressure during exhalation. Although PSV also can compensate for increased resistances imposed by the endotracheal tube, the level of pressure support needed varies widely and is not easy to determine. The exact role of automatic tube compensation in mechanical ventilation and/or weaning remains to be determined. MONITORING OF PATIENTS Adverse effects Can cause volutrauma or barotrauma Decreases venous return and cardiac output Diverts blood from normal lung units in unilateral lung disease Increases V D ventilation Increases RV afterload The changeable condition of critically ill patients mandates periodic reassessment of several criteria to ensure that the goals of mechanical ventilation are being met (Table 1). The following paragraphs discuss some of the most critical assessments. PHYSICAL EXAMINATION Frequent physical examinations will help identify patients who require further adjustments in their ventilatory support. Acceptable values on arterial blood gas analysis do not guarantee adequate inflation pressures or patient comfort. Unexplained tachycardia, tachypnea, diaphoresis, agitation, or patient-ventilator dyssynchrony indicate the need to reassess the ventilatory parameters. Careful observation might reveal inspiratory efforts that do not trigger the ventilator, suggesting inadequate trigger sensitivity, auto-peep, or muscle weakness. Expiratory muscle contractions might be caused by a high respiratory drive, DH, airway obstruction, or excessively high preset levels of tidal volume, CPAP, or pressure support. Pulmonary Disease Volume 8, Part 3 5

6 Dyspnea (ie, fighting the ventilator ) can be caused by faulty ventilator settings (eg, inadequate RR, tidal volume, I:E, inspiratory flow rate), pain, discomfort, auto-peep, anxiety, need for airway suctioning, or complications (eg, pneumothorax). Unilaterally decreased breath sounds might indicate selective intubation of a mainstem bronchus, the presence of a pneumothorax or pleural effusion, or airway obstruction by mucus plugs. CHEST RADIOGRAPHY Controversy exists regarding the need for routine daily chest radiographs in mechanically ventilated patients with translaryngeal endotracheal intubation in the absence of changes in respiratory parameters. However, routine chest radiographs of endotracheally intubated ventilated patients can disclose unsuspected complications (eg, endotracheal tube migration, atelectasis, barotrauma) before they become clinically evident. Therefore, despite the lack of evidenced-based data from multicenter, prospective, randomized, controlled clinical trials, obtaining chest radiographs of patients who are critically ill and being treated with endotracheal intubation and mechanical ventilation is generally accepted as standard practice and the current state of the art. GAS EXCHANGE Ensuring adequate tissue oxygenation is one of the major goals of ventilatory support. A target PaO 2 of at least 55 to 6 mm Hg or an arterial oxygen saturation of 88% to 92% is optimal. Oxygen delivery to tissues (DO 2 ) is a function of cardiac output (Q T ), hemoglobin (Hgb), and oxygen saturation (SaO 2 ) and is determined by the following equation: DO 2 = [(1.39 Hgb SaO 2 ) + (.3 PaO 2 )] Q T. Mechanical ventilation affects two of the main determinants of oxygen transport, namely oxygen saturation and cardiac output. Maneuvers aimed at increasing oxygen saturation (eg, PEEP) can decrease cardiac output and cause a net decrease in tissue oxygen supplies. When patients have severe disease or when uncertainty exists about the adequacy of tissue oxygenation, a balloon flotation pulmonary artery catheter should be used to monitor cardiovascular function more closely. An acceptable arterial ph (ie, > 7.35) rather than a normal PaCO 2 should be sought to guarantee a compensated state, regardless of underlying acid-base status (eg, chronic hypercapnia, metabolic acidosis). The PaCO 2 is directly proportional to carbon dioxide production and inversely proportional to alveolar ventilation. Thus, a high minute volume requirement might indicate increased dead space (V D ) ventilation or increased carbon dioxide production. In normal subjects, the V D to V T ratio (V D :V T ) seldom exceeds.3. In ventilated patients, V D :V T can reach.7 to.8, significantly increasing the minute volume required for carbon dioxide elimination. Higher V T s can cause a paradoxical increase in V D :V T in ventilated patients by inducing overinflation and increasing physiologic V D. Permissive hypercapnia implies that respiratory acidosis is tolerated when excessive minute volumes and/or airway pressures are needed to maintain normocapnia. When therapeutic hyperventilation is used to treat intracranial hypertension, a PaCO 2 of 25 to 3 mm Hg is targeted to induce cerebral vasoconstriction and acutely lower intracranial pressure. Because this desired outcome is transient, lasting only 12 to 24 hours, inducing therapeutic hyperventilation is at best a temporizing measure until other more definitive treatments are instituted. Moreover, controlled studies on the effectiveness of this practice (in terms of outcomes) are not available. There is no evidence to support the use of prophylactic hyperventilation in patients with head trauma. AIRWAY PRESSURES Proximal Airway Pressure The proximal airway pressure (P AW ) needed to inflate a relaxed respiratory system can be predicted from the following equation (known as the Equation of the Motion of the Lung), in which C RS represents respiratory system compliance, R RS resistance of the respiratory system, and V inspiratory flow rate: P AW = V T /C RS + (R RS V) + PEEP + auto-peep. In other words, a higher P AW is required when V T, resistance, flow rate, or PEEP are increased, and a lower P AW is needed with increased respiratory system compliance. Mean Airway Pressure MAP is the average system pressure over the entire respiratory cycle; it usually underestimates mean alveolar pressure because of dissipation of pressure with expiratory resistance. The absolute value of MAP is the major determinant of oxygenation, hemodynamic effects, and barotrauma related to PPV. MAP can be increased by increasing respiratory minute volume, PEEP, or inspiratory time or by adding an inspiratory pause. Plateau Pressure Alveolar overdistention is associated with barotrauma, activation of inflammatory mediators, and ventilatorassociated lung injury. Alveolar pressure and volume in mechanically ventilated patients are estimated by measuring end-inspiratory Pplat, which roughly reflects transpulmonary pressure at end-inspiration (ie, alveolar pressure minus pleural pressure). Pplat is measured after 6 Hospital Physician Board Review Manual

7 applying a.5- to 2-second end-inspiratory pause, which eliminates airflow and the influence of airway resistance. Pplat is a valid measurement of alveolar volume only during passive inflation of the lungs and only with normal chest wall and abdominal compliance. In normal subjects, a negative pleural pressure near 35 cmh 2 O is needed to maintain lung inflation at total lung capacity. Therefore, assuming normal respiratory system compliance, a Pplat higher than 35 cmh 2 O can lead to alveolar overdistention and lung injury. Although decreased respiratory system compliance caused by pleural, chest wall, or abdominal conditions will increase the Pplat, this increase does not reflect increased transpulmonary (alveolar) pressure or alveolar overdistention; consequently, this type of higher Pplat value is tolerated. Changes in esophageal pressure reflect changes in pleural pressure. Transpulmonary pressure can be estimated by calculating the Pplat and subtracting the esophageal pressure. Pplat values are lowered by decreasing V T, PEEP, or DH. Peak Airway Pressure PAP is the maximum pressure measured during active gas delivery and is therefore influenced by both the resistance and the compliance of the respiratory system; it is not an accurate measurement of alveolar distention. The difference between PAP and Pplat can be used in certain situations to calculate inspiratory airway resistance during mechanical ventilation. OTHER MEASUREMENTS Resistance Airway resistance can be calculated by the change in airway pressures divided by the flow rate. Total airway resistance in mechanically ventilated patients is the sum of the resistance of the endotracheal tube and of the patient s airways; the endotracheal tube accounts for most of the resistance. Inspiratory resistance (R) can be calculated as follows: R = (PAP Pplat)/flow rate; during volume ventilation, if a flow rate of 6 L/min (or 1 L/s) is used, then inspiratory resistance is determined by subtracting the Pplat from the PAP. Airway resistance always should be less than 1 cmh 2 O/L per second. Expiratory resistance is always higher than inspiratory resistance and is calculated by subtracting PEEP from Pplat. Respiratory System Compliance Compliance is the change in volume per unit change in pressure. Respiratory system compliance (C RS ) can be determined as follows: C RS = V T /(Pplat PEEP). Respiratory system compliance involves the lungs, pleura, chest wall, and abdomen and varies between 5 and 1 ml/cmh 2 O in ventilated patients. Lung Compliance Lung compliance is calculated with the aid of an esophageal balloon and uses transpulmonary pressure instead of Pplat. Transpulmonary pressure is the difference between alveolar pressure (measured as Pplat) and pleural (or esophageal) pressure. A normal value for lung compliance is 2 ml/cmh 2 O. Work of Breathing Work is defined as the product of force times distance of motion in the direction of force. In the case of the respiratory system, work is the product of pressure times volume change and is calculated as the area within a volumepressure loop. By definition, if there is no motion (or change in volume), there is no work. Thus, measuring WOB in the mechanically ventilated patient underestimates the effort or energy cost of breathing, because isometric contractions and flow-resistance are not taken into account. The tension-time index of the diaphragm is more closely related to respiratory muscle oxygen consumption than is WOB. Measurement of the WOB requires special equipment and the insertion of an esophageal balloon; consequently, such measurements have been relegated largely to the research arena. Commercial systems that allow bedside measurements of WOB are now available. However, the role of WOB measurements in the routine management of mechanically ventilated patients currently is not established. GRAPHICS ANALYSIS Analysis of graphics during PPV provides information that can assist in optimizing mechanical ventilation and increasing patient comfort. Flow-Time Graphics Flow waveforms can be used to detect auto-peep. If flow does not return to baseline (zero) during expiration, there is still positive pressure in the chest at endexpiration, an occurrence referred to as auto-peep (Figure 1). The presence of positive pressure, however, does not confirm DH in the actively breathing patient and could instead reflect expiratory muscle contraction. By the same token, a return to zero flow at end-expiration does not rule out the presence of auto-peep with premature airway closure (ie, air trapping). Dips in the expiratory flow wave might indicate missed trigger efforts and prompt ventilator adjustments (Figure 1). The area within the flow-time curve represents V T. During PCV, failure to reach zero flow during inspiration indicates that V T might be augmented by increasing inspiratory time. On the other hand, if a flow wave reaches zero (ie, a no-flow state), PAP is equal to Pplat Pulmonary Disease Volume 8, Part 3 7

8 Flow Inhalation Spontaneous breathing 1 E CPAP Inspiratory effort 1 E Assist-control ventilation with PEEP Auto-PEEP 1 E PEEP Exhalation SIMV with PEEP Figure 1. Flow-time waveform with auto-peep and missed trigger effort. PEEP = positive end-expiratory pressure. (Adapted with permission from Hess DR, Medoff BD, Fessler MB. Pulmonary mechanics and graphics during positive pressure ventilation. Int Anesthesiol Clin 1999;37:24.) Assisted Spontaneous Pressure-support ventilation with PEEP 1 E Pressure-control ventilation with PEEP (analogous to an end-expiratory pause), and further increases in inspiratory time will not increase V T. 1 E Pressure-control, inverse-ratio ventilation Pressure-Time Graphics Figure 2 illustrates pressure-time waveforms for different modes of mechanical ventilation. Pressure waveforms can display graphically the difference between PAP and Pplat (ie, airway resistance). During volume ventilation, active inspiratory efforts by the patient can be estimated by the degree of scooping of the pressure-time waveform (Figure 3). This scooping can indicate a high respiratory drive and the need to increase inspiratory flow. Trigger failures are represented by small drops in airway pressures that do not initiate a breath. Excessive inflation pressure during PSV will produce an end-inspiratory pressure spike as the patient terminates the inspiratory phase by actively exhaling. This spike commonly is seen in patients with increased time constants (eg, patients with chronic obstructive pulmonary disease [COPD], asthma). Volume-Time Graphics Leaks in the system can be detected by comparing the symmetry of a volume-time graphic during inspiration and expiration. Flow-Volume Graphics Expiratory airflow obstruction produces a convexity toward the volume axis. A sawtooth pattern on both inspiratory and expiratory flow volume graphics indicates airway secretions and the need for suctioning. This graphic evidence has been shown to be more reliable than is physical examination. 1 E Airway pressure release ventilation High-frequency ventilation Figure 2. Airway pressure profiles. Pressure-time waveforms for different mechanical ventilation modes are shown. CPAP = continuous positive airway pressure; E = expiration; I = inspiration; PEEP = positive end-expiratory pressure; SIMV = synchronized intermittent mandatory ventilation. (Adapted with permission from Lapinski SE, Slutsky AS. Principles of mechanical ventilation and weaning. In: Dantzker DR, Scharf SM, editors. Cardiopulmonary critical care. 3rd ed. Philadelphia: WB Saunders; 1998:253.) COMPLICATIONS Table 5 lists common complications of intubation and PPV. Some, but not all, of these complications can be prevented or minimized by careful monitoring of patients and using state-of-the-art techniques. RESPIRATORY COMPLICATIONS As previously stated, auto-peep (also referred to as intrinsic- and occult-peep) implies the persistence of PAP at end-expiration. DH refers to a failure of lung 8 Hospital Physician Board Review Manual

9 volumes to return to passive functional residual capacity before the onset of the next inspiration. Mechanism Auto-PEEP can occur without DH in actively breathing patients with expiratory muscle effort. In this situation, end-expiratory volumes can be at or below functional residual capacity, and so the negative consequences of auto- PEEP are not seen. Auto-PEEP with DH occurs in patients with expiratory airflow obstruction (eg, in patients with COPD or with an endotracheal tube that is too small) or in the absence of obstruction when the expiratory time is too short for the required minute ventilation (eg, in patients with acute respiratory distress syndrome). Measurement Unlike extrinsic or applied PEEP, auto-peep is not registered on the ventilator pressure manometer, because the latter is open to atmospheric pressure. As already described, the persistence of expiratory airflow at the onset of the next inspiration in the passively ventilated patient implies that a positive end-expiratory airway pressure persists. Various methods can quantify auto-peep. The endexpiratory occlusion technique measures static auto- PEEP by occluding the expiratory valve of the ventilator just before the next inspiration. This step allows for equalization of pressures in the system; the magnitude of auto- PEEP is displayed on the manometer. For this measurement to be accurate, active respiratory efforts must be absent. Dynamic auto-peep is measured in actively breathing patients with an esophageal balloon in place. The amount of esophageal pressure deflection needed to start inspiratory airflow equals the auto-peep. Other techniques include noting the change in airway pressure before the onset of mechanical inflation, the difference in expiratory lung volumes after a prolonged expiration, and the level of extrinsic or applied PEEP at which endexpiratory lung volume starts to increase. Each of these techniques has its limitations. Adverse Effects Auto-PEEP with DH has several harmful effects, including predisposing patients to alveolar overdistention and barotrauma and increasing the effort involved in breathing by increasing the amount of pressure the patient must overcome to trigger the ventilator (auto- PEEP plus sensitivity setting) and to inflate the lungs. This situation can lead to patient-ventilator dyssynchrony and weaning failures. Failure to consider auto- PEEP in the calculation of lung compliance will result Airway pressure, cm H 2 O A Airway pressure, cm H 2 O B Time (sec) 1. Time (sec) Figure 3. Pressure-time waveforms as a measure of inspiratory muscle contraction and inadequate ventilator settings. The waveform of a passively ventilated patient is shown in A, and waveform scooping caused by inspiratory efforts (that possibly indicate inadequate inspiratory flow settings) is shown in B. (Adapted with permission from Tobin MJ, Van de Graaf WB. Monitoring of lung mechanics and work of breathing. In: Tobin MJ, editor. Principles and practice of mechanical ventilation. New York: McGraw-Hill; 1994:988.) in an underestimation. Auto-PEEP also can contribute to deleterious cardiovascular effects. Treatment Once recognized, auto-peep can be decreased by reducing minute volume (ie, by decreasing V T and/or RR), by increasing the expiratory time (eg, using higher inspiratory flow rates, a square flow waveform, sedation), by treating expiratory airflow obstruction (eg, with bronchodilators), and by avoiding endotracheal tubes with small diameters. Setting the ventilator PEEP level approximately 8% below measured auto-peep will decrease the effort needed to trigger the machine. Adding extrinsic PEEP does not worsen hyperinflation unless the amount added is equal to or higher than intrinsic-peep. The type of triggering method used (eg, flow versus pressure) does not influence the extra work imposed by auto-peep. Pulmonary Disease Volume 8, Part 3 9

10 Table 5. Complications of Mechanical Ventilation Complications related to the artificial airway Bypass of the normal protective upper airway mechanisms Misplacement/migration of endotracheal tubes Tracheal ulcers/stenosis Tube malfunction/obstruction Upper airway trauma, including vocal cords Complications related to the ventilator Bacterial contamination of tubing or water reservoirs Inadequate humidification Machine malfunction Overheating of inspiratory gases Respiratory complications Acute lung injury Aspiration of gastric contents Bronchopulmonary dysplasia Hypoventilation/hyperventilation Oxygen toxicity Ventilator-associated pneumonia Volutrauma/barotrauma ADH = antidiuretic hormone. Cardiovascular complications Decreased cardiac output Hypotension (related to decreased venous return) Gastrointestinal complications Erosive gastritis and stressrelated gastrointestinal bleeding Gastric distention Nausea/vomiting Renal complications Prerenal azotemia Water retention (associated with increased ADH level) Complication related to sedation/paralysis Disorientation Hypotension Ileus Neuropathy Psychological complications Anxiety/mental distress Fear Impaired sleep Inability to communicate Data from Slutsky AS. Mechanical ventilation. American College of Chest Physicians Consensus Conference [published erratum appears in Chest 1994;16:656.] Chest 1993;14: (3) aggravation of right ventricular ischemia; and (4) decreased left ventricular filling caused by a leftward shift of the interventricular septum. Hypovolemia and auto- PEEP enhance these effects and usually lead to hypotension with initiation of PPV. Other causes of hypotension immediately after institution of mechanical ventilation include vagal reflexes related to intubation, use of sedatives, barotrauma, and decreased sympathetic drive. During withdrawal of mechanical ventilation, an abrupt discontinuation of positive pressure in the chest has been associated with increased venous return, pulmonary congestion and/or edema, and weaning failure. Myocardial ischemia detected by electrocardiography and scintigraphy has been shown to occur in up to 47% of patients during weaning. Cardiac ischemia during weaning was an independent risk factor for weaning failure. On the other hand, mechanical ventilation can have beneficial effects in the setting of heart failure and volume overload. Cardiac function can be augmented by decreased venous return (a nitrate-like effect), decreased transmural cardiac pressure (intracardiac pressure minus pleural pressure), decreased myocardial oxygen consumption, and decreased left ventricular afterload (through acceleration of aortic blood flow). INCREASED WORK OF BREATHING Mechanical ventilation can actually increase the breathing workload through several mechanisms. For example, increased resistance can be imposed by the endotracheal tube or ventilator tubing. Moreover, inadequate trigger sensitivity, malfunctioning demand valves, inadequate flow settings, insufficient flow capacity, excessive pressure support or CPAP (inducing expiratory muscle activation), ventilator-response delays before initiation of breath delivery, and inadequately set tidal volumes all can increase the work of breathing, as can the presence of auto-peep with DH. Finally, anxiety and discomfort leading to increased minute ventilation has a similar effect. CARDIOVASCULAR COMPLICATIONS Positive pressure applied to the lungs is transmitted to the heart and intrathoracic vessels, potentially causing adverse cardiovascular effects: the more compliant the lungs, the larger the pressure transmitted. Oxygen transport to tissues can decrease, even with an increased PaO 2, if cardiac output decreases owing to mechanical ventilation. Four factors particularly can lead to decreased cardiac output and hypotension: (1) increased right atrial pressure with decreased venous return (ie, decreased right ventricular filling); (2) increased pulmonary artery outflow pressure (ie, decreased right ventricular output); WITHDRAWING MECHANICAL VENTILATION Discontinuation of mechanical ventilation implies transferring the workload associated with breathing from the mechanical ventilator back to the patient. When the condition that prompted the initiation of mechanical ventilation resolves, termination of mechanical ventilation is fast and straightforward in more than 7% of patients. In patients with underlying lung disease (eg, acute respiratory failure), a slowly resolving illness, or a chronic debilitating disease, longer periods of weaning from mechanical ventilation that 1 Hospital Physician Board Review Manual

11 require close monitoring might be needed. Three basic criteria must be met before mechanical ventilation is discontinued: (1) resolution or significant improvement of the disease process that led to mechanical ventilation; (2) absence of findings (such as lifethreatening arrhythmias, hemodynamic instability, recurrent seizures, fluid overload) that indicate clinical instability; and (3) certainty that the patient is awake and able to clear secretions and protect the upper airways. The ability to predict success or failure of extubation attempts varies greatly according to the patient population studied, the duration of mechanical ventilation, and the cause of respiratory failure; likewise, the ability to predict the clinical outcome in particular patients after extubation is quite limited. Clinical signs such as dyspnea, tachycardia, tachypnea, cardiac arrhythmias, and arterial desaturation (measured by pulse oximetry) indicate weaning failure. BASIC WEANING METHODS There are 3 basic weaning methods: (1) trials of spontaneous breathing (T-piece weaning), (2) synchronized intermittent mandatory ventilation (SIMV) weaning, and (3) PSV weaning. With T-piece weaning, the patient is removed from the ventilator and allowed to breathe spontaneously through the endotracheal tube while humidified oxygen is provided. When signs of fatigue or respiratory distress develop, the patient is connected back to the ventilator. T-piece weaning trials can be attempted once or more daily. When the patient is able to breathe for 3 to 12 minutes with no signs of distress, extubation can occur; 3-minute trials of spontaneous ventilation have been shown to be as effective as 12-minute trials in predicting successful extubation. With SIMV weaning, the machine s RR is progressively decreased (usually by 2 4 breaths/min every 1 3 hours). Patients can be extubated when they tolerate machine rates of 5 breaths/min (or fewer) with no signs of distress. SIMV weaning, however, has been associated with increased WOB. Inspiratory muscle activation is similar in machine breaths and spontaneous breaths. With PSV weaning, the pressure-support level is progressively decreased. The patient can be safely extubated after tolerating a pressure-support level of to 7 cmh 2 O for 3 to 12 minutes. An alternative to spontaneous breathing trials that uses low PSV (ie, pressure-support levels set at 6 7 cmh 2 O) to overcome imposed circuit and endotracheal tube resistance has had similar results to those of using a conventional T-piece weaning. 3 This technique is widely used and might be preferred because the patient remains connected to the ventilator, thus enabling the added safety features of more sophisticated monitoring and availability of apneic ventilation should the patient develop problems. PSV also is often used to augment spontaneous breaths during SIMV weaning. However, the advantage of this alternative technique is not proved, and the technique complicates the weaning process. COMPARISON OF BASIC WEANING METHODS No single weaning method can be considered superior, based on the current literature. The success of a weaning method can be assessed by the number of patients successfully weaned and by the time it takes to wean them. Comparisons between modes have yielded conflicting results. Brochard and colleagues 4 compared T-piece weaning, SIMV weaning, and PSV weaning in 19 patients who could not sustain a 2-hour selfbreathing trial. PSV weaning produced the lowest weaning failure rate and the shortest mean time to wean. In a similar study, Esteban and colleagues 5 compared SIMV weaning, PSV weaning, and once (or more) daily trials of T-piece weaning in 13 patients who failed a 2-hour selfbreathing trial. In this study, T-piece weaning was better (ie, greater success rate, shorter time to wean) than was SIMV weaning or PSV weaning. These conflicting findings result partly from different application of the same weaning mode across studies (eg, different rates of SIMV, decreases in pressure-support level), different criteria for weaning success and extubation, and different patient populations. PROTOCOL-DIRECTED WEANING The way a weaning method is applied and the early identification of patients who are ready to be weaned might be more important than is the weaning method itself. Only approximately 4% of patients who selfextubate (ie, cases of unplanned extubation) need to be reintubated, suggesting that patients generally are kept intubated longer than necessary. Published data increasingly support the concept that a structured, organized approach to weaning makes the process more efficient. Ely and colleagues 6 showed that the institution of a weaning protocol that systematically identifies patients capable of spontaneous breathing reduced the duration, complication rate, and costs of mechanical ventilation. Kollef and colleagues 7 found that protocol-directed weaning involving nurses and respiratory therapists shortened the duration of weaning. Similar results were reported by Cohen and colleagues 8 with the use of a ventilation management team. However, protocol-directed weaning has not been shown to affect mortality rates. Pulmonary Disease Volume 8, Part 3 11

12 EXTUBATION The evaluation of airway-protective reflexes before extubation is as critical as completing a spontaneous breathing trial. The presence of efficient cough and gag reflexes should be assessed before proceeding with extubation. The cuff-leak test is performed on occasion to rule out tracheal narrowing before extubation. However, the results of this test have never been validated, and its positive and negative predictive values have been questioned. Similarly, the administration of systemic corticosteroids for prophylaxis of stridor in intubated patients has not been shown to be beneficial in adults. Noninvasive positive-pressure ventilation (NPPV) can aid the weaning and extubation process. A randomized trial 9 has documented the effectiveness of NPPV in patients with COPD who were extubated before standard extubation criteria were met. Patients with exacerbations of COPD, acute pulmonary edema, or increased upper airway resistance resulting from glottic swelling might benefit from this intervention. More controlled trials are needed, however, to confirm these findings. BOARD REVIEW QUESTIONS Choose the single best answer for each question. 1. Flow-time graphics are NOT useful for which of the following steps in patient monitoring? A) Adjusting tidal volume in pressure-control ventilation B) Determining whether peak airway pressure is equal to plateau pressure during pressurecontrol ventilation C) Identifying auto positive end-expiratory pressure in paralyzed patients D) Identifying dynamic hyperinflation in an actively breathing patient E) Identifying missed trigger efforts 2. Which of the following is NOT decreased by protocol-directed weaning from a ventilator? A) Complications of mechanical ventilation B) Costs related to mechanical ventilation C) Duration of mechanical ventilation D) Duration of the weaning process E) Mortality related to mechanical ventilation 3. Which of the following will NOT increase the work of breathing in patients on mechanical ventilation? A) Auto positive end-expiratory pressure with dynamic hyperinflation B) Excessive pressure support or continuous positive airway pressure C) Inadequate inspiratory flow rate settings in volume-targeted modes D) Low trigger sensitivity E) Use of flow triggering ANSWERS 1. D 2. E 3. E REFERENCES 1. Slutsky AS. Mechanical ventilation. American College of Chest Physicians Consensus Conference [published erratum appears in Chest 1994;16:656]. Chest 1993;14: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. The Acute Respiratory Distress Syndrome Network. N Engl J Med 2; 342: Esteban A, Alia I, Gordon F, et al. Extubation outcomes after spontaneous breathing trials with T-tube or pressure support ventilation. Am J Respir Crit Care Med 1997; 156: Brochard L, Rauss A, Benito S, et al. Comparison of three methods of gradual withdrawal from ventilatory support during weaning from mechanical ventilation. Am J Respir Crit Care Med 1994;15: Esteban A, Frutos F, Tobin MJ, et al. A comparison of four methods of weaning patients from mechanical ventilation. N Engl J Med 1995;332: Ely EW, Baker AM, Dunagan DP, et al. Effect on the duration of mechanical ventilation of identifying patients capable of breathing spontaneously. N Engl J Med 1996;335: Kollef MH, Shapiro SD, Silver P, et al. A randomized, controlled trial of protocol-directed versus physiciandirected weaning from mechanical ventilation. Crit Care Med 1997;25: Cohen IL, Bari N, Strosberg MA, et al. Reduction of duration and cost of mechanical ventilation in an intensive care unit by use of a ventilatory management team. Crit Care Med 1991;19: Girault C, Daudenthun I, Chevron V, et al. Noninvasive ventilation as a systematic extubation and weaning technique in acute-on-chronic respiratory failure: a prospective, randomized controlled study. Am J Respir Crit Care Med 1999;16: Copyright 21 by Turner White Communications Inc., Wayne, PA. All rights reserved. 12 Hospital Physician Board Review Manual