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ACUTE RESPIRATORY FAILURE
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ESSENTIALS OF DIAGNOSIS & TYPICAL FEATURES
Inability to deliver oxygen or remove carbon dioxide.
PaO2 is low while PaCO2 is normal in hypoxemic respiratory failure (ventilation/perfusion [V/Q] mismatch, diffusion defects, and intrapulmonary shunt).
PaO2 is low and PaCO2 is high in hypercapnic respiratory failure (alveolar hypoventilation seen in central nervous system [CNS] dysfunction, oversedation, neuromuscular disorders).
Noninvasive mechanical ventilation can be an effective treatment for hypercapnic respiratory failure and selected patients with hypoxemic respiratory failure.
Conventional mechanical ventilation should be accomplished within a strategy of “lung-protective” ventilation.
Extracorporeal membrane oxygenation (ECMO) is a viable option for patients failing conventional mechanical ventilation.
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Acute respiratory failure, defined as the inability of the respiratory system to adequately deliver oxygen or remove carbon dioxide, is a major cause of morbidity and mortality in infants and children. Anatomic and developmental differences place infants and young children at higher risk than older children or adults for respiratory failure. An infant’s thoracic cage is more compliant, allowing a greater tendency toward alveolar collapse. The intercostal muscles are poorly developed and unable to achieve the “bucket-handle” motion characteristic of adult breathing, and the diaphragm is shorter and relatively flat with fewer type I muscle fibers, making it less effective and more easily fatigued. The infant’s airways are also smaller in caliber resulting in greater resistance to airflow and greater susceptibility to occlusion by mucus plugging and mucosal edema, particularly in the setting of respiratory infections. Alveoli in children are smaller and have less collateral ventilation than adults, again resulting in a greater tendency to collapse and develop atelectasis. Finally, young infants may have a more reactive pulmonary vascular bed, impaired immune system, or residual effects from prematurity, all of which increase the risk of respiratory failure.
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Respiratory failure can be due to inadequate oxygenation (hypoxemic respiratory failure) or inadequate ventilation (hypercapnic respiratory failure) or both. Hypoxemic respiratory failure occurs in three situations: (1) Ventilation-perfusion (V/Q) mismatch, when blood flows to inadequately ventilated lung or when ventilated areas of the lung are inadequately perfused; (2) diffusion defects, caused by thickened alveolar membranes or excessive interstitial fluid at the alveolar-capillary junction; and (3) intrapulmonary shunt, when structural anomalies in the lung allow blood to flow through the lung without participating in gas exchange. Hypercapnic respiratory failure results from impaired alveolar ventilation, due to conditions such as increased dead space ventilation, reduced respiratory drive due to CNS dysfunction or oversedation, or neuromuscular disorders (Table 14–1).
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The clinical findings in respiratory failure are the result of hypoxemia, hypercapnia, and arterial pH changes. Common features of respiratory failure are summarized in Table 14–2. These features may not be clinically obvious and many are nonspecific. As a result, a strictly clinical assessment of respiratory failure is not always reliable, and clinical findings of respiratory failure should be supplemented by laboratory data such as blood gas analysis.
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Noninvasive Monitoring & Blood Gas Analysis
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The adequacy of oxygenation and ventilation can be measured noninvasively and/or through blood gas analysis. Pulse oximetry measures arterial oxygen saturation (SaO2) continuously and noninvasively and is an important tool in the assessment and treatment of patients with potential or actual respiratory failure. However, pulse oximetry readings can be much less accurate in patients with saturations below 80%, poor skin perfusion, or significant movement. In addition, pulse oximetry can be dangerously inaccurate in certain clinical settings such as carbon monoxide poisoning or methemoglobinemia. End-tidal CO2 (ETCO2) monitoring measures exhaled carbon dioxide (CO2) noninvasively, allowing for continuous assessment of ventilation. Normally, the ETCO2 level closely approximates the alveolar CO2 level (PaCO2), which should equal arterial CO2 levels (PaCO2) because carbon dioxide diffuses freely across the alveolar-capillary barrier. While most accurate in the intubated patient, this technique can also be used in extubated patients with the proper equipment. However, the ETCO2 level may not accurately reflect the PaCO2 in patients with increased dead space ventilation or rapid, shallow breathing.
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Given the limitations of these noninvasive techniques, arterial blood gas (ABG) analysis remains the gold standard for assessment of acute respiratory failure. ABGs provide measurements of the patient’s acid-base status (with a measured pH and calculated bicarbonate level) as well as PaO2 and PaCO2 levels. Capillary or venous blood gases may provide some reassurance regarding the adequacy of ventilation and can be useful for following trends; however, they yield virtually no useful information regarding oxygenation and may generate highly misleading information about the ventilatory status of patients who have poor perfusion or who had difficult blood draws. As a result, ABG analysis is important for all patients with suspected respiratory failure, particularly those with abnormal venous or capillary gases.
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Knowing the ABG values and the inspired oxygen concentration also enables one to calculate the alveolar-arterial oxygen difference (A–aDO2, or A–a gradient). The A–a gradient is less than 15 mm Hg under normal conditions, widening with diffusion impairment, shunts, and V/Q mismatch. The degree of widening has prognostic value in severe hypoxemic respiratory failure, with A–a gradients over 400 mm Hg being strongly associated with mortality. Assessment of intrapulmonary shunting (the percentage of pulmonary blood flow that passes through nonventilated areas of the lung) may also be helpful. Normal individuals have less than a 5% physiologic shunt from bronchial, coronary, and thebesian (cardiac intramural) circulations. Shunt fractions greater than 15% usually indicate the need for aggressive respiratory support. However, calculation of the shunt fraction requires a pulmonary arterial catheter, the use of which has decline significantly over the past decade.
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Modes of Respiratory Support
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Patients with severe hypoxemia, hypoventilation, or apnea require immediate assistance with bag and mask ventilation. Although assisted ventilation can generally be maintained for some time with a properly sized mask, gastric distention, emesis leading to aspiration of gastric contents, and inadequate tidal volumes leading to atelectasis are possible complications. In patients not requiring immediate intubation, several modalities can be used to provide respiratory support, including supplemental oxygen, heated high-flow nasal cannula (HHFNC), and noninvasive ventilation (NIV).
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Supplemental oxygen with a nasal cannula or oxygen mask may be adequate to treat patients with mild respiratory insufficiency (Table 14–3). Patients with hypoventilation and diffusion defects respond better to supplemental oxygen than patients with significant shunts or V/Q mismatch. For patients requiring more support, HHFNC can be considered. HHFNC devices deliver heated and humidified oxygen mixtures via nasal cannula at flow rates higher than possible with cooler dry air. Depending on the flow rate and size of patient, HHFNC can also generate some amount of positive pressure and potentially improve work of breathing without further escalation of support. Generally, flow rates of 1–2 L/kg/min are considered high flow in infants and children (up to a maximum of 25 L/min) although some studies have utilized up to 60 L/min in adults. HHFNC use has been studied in children with bronchiolitis and appears to be well tolerated, potentially decreasing the need for noninvasive ventilation or intubation. However, if the patient is not improving on HHFNC after 30–60 minutes, additional escalation of care may be warranted, including initiation of noninvasive ventilation that can deliver positive pressure more consistently.
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Noninvasive ventilation (NIV) refers to the administration of positive pressure breathing through various interfaces (mouthpiece or nasal, face, or helmet mask) rather than an invasive artificial airway (endotracheal tube [ETT] or tracheostomy tube). NIV has become an integral tool in the management of both acute and chronic respiratory failure, reducing need for intubation in milder cases of respiratory failure or as a bridge after extubation in patients with marginal lung function and respiratory mechanics. Various modes of support can be used with NIV, such as continuous positive airway pressure (CPAP), bilevel positive airway pressure (BiPAP), or average volume-assured pressure support (AVAPS).
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CPAP refers to the constant application of airway pressure, usually in the range of 5–10 cm H2O. BiPAP cycles between a higher inspiratory positive airway pressure (IPAP) and a lower expiratory positive airway pressure (EPAP). The additional inspiratory support in this mode improves tidal volume and ventilation in patients who are breathing shallowly and can improve oxygenation by providing a higher mean airway pressure (MAP). Common initial settings would place the IPAP at 12–14 cm H2O and the EPAP at 6–8 cm H2O. The IPAP can then be titrated upward to achieve adequate tidal volumes, usually in the range of 5–7 mL/kg, and based on the patient’s work of breathing and respiratory rate. EPAP and delivered oxygen concentration can be adjusted upward to achieve adequate oxygenation. AVAPS targets a tidal volume within an allowable inspiratory pressure range. Usually, a tidal volume of approximately 8 mL/kg is set with an IPAP max of 20–30 cm H2O. EPAP is approached in a similar manner as BiPAP. With any mode of NIV, close respiratory monitoring is essential for assessing response to NIV therapy and guiding further adjustments.
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Although NIV is generally well tolerated, successful application of NIV requires careful patient selection and close respiratory monitoring. The best candidates are patients with moderate lung disease, in the recovery phases of their illness, or those with primarily hypercapnic respiratory failure, such as patients with muscular dystrophies or other forms of neuromuscular weakness. These patients should be closely monitored, however, as NIV may mask symptoms of underlying disease progression, making eventual intubation more precarious. Patients suffering from coma, impaired respiratory drive, an inability to protect their airway, or cardiac or respiratory arrest are not candidates for NIV. In patients with severe respiratory failure or those who are not improving with NIV, endotracheal intubation should not be delayed.
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For patients with acute respiratory failure, endotracheal intubation and the initiation of mechanical ventilation can be life-saving. Safe placement of an ETT in infants and children requires experienced personnel and appropriate equipment at the bedside, including a correctly sized mask, Ambu bag, oral airways, ETTs, and appropriate suction catheters. The patient should first be positioned properly to facilitate air exchange while supplemental oxygen is provided. The sniffing position is used in infants. Head extension with jaw thrust is used in older children without neck injuries. If obstructed by secretions or vomitus, the airway must be cleared by suction. When not obstructed and properly positioned, the airway should be patent and easily visualized, allowing the placement of an oral or nasopharyngeal ETT of the correct size. Patients with normal airway anatomy may be intubated under intravenous (IV) anesthesia by experienced personnel (Table 14–4). Endotracheal intubation of high-risk patients, such as those with significant upper airway obstruction (eg, patients with croup, epiglottitis, foreign bodies, or subglottic stenosis), mediastinal masses, or suspected or known difficult airways should be approached with extreme caution; minimal sedation should be used and paralytic agents should be strictly avoided unless trained airway specialists decide otherwise.
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Appropriately sizing the ETT is important for reducing complications and providing adequate respiratory support. An inappropriately large ETT is a risk factor for subglottic pressure necrosis, potentially leading to scarring and stenosis requiring surgical repair. An inappropriately small ETT can result in excessive air leak around the ETT, making adequate ventilation and oxygenation difficult, or inability to clear secretions effectively. Two useful methods for calculating the correct size of ETT for a child are (1) measuring the child’s height with a Broselow tape and then reading the corresponding ETT size on the tape, or (2) in children older than 2 years, choosing a tube size using the formula ETT size = (16 + age in years) ÷ 4. Either cuffed or uncuffed tubes may be used, although a cuffed tube can ensure more effective provision of mechanical ventilation. Assessment of air leakage around the ETT is an important measure of appropriate ETT sizing. An audible leak (with the cuff deflated) noted at pressures of 15–20 cm H2O generally indicates acceptable ETT size. If there is insufficient leak, the decision to change the ETT needs to be carefully considered, especially in those with severe lung disease. Approximate proper insertion depth (in cm) as measured at the teeth can be estimated by tripling the size of the ETT. Correct placement of the ETT should be confirmed by auscultation for equal bilateral breath sounds and by detecting carbon dioxide using either a colorimetric filter or quantitative capnography. A chest radiograph is necessary for final assessment of ETT placement. A correctly positioned ETT will terminate in the mid-trachea between the thoracic inlet and the carina, at approximately the level of the second thoracic vertebra.
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CONVENTIONAL MECHANICAL VENTILATION
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The principal indication for institution of mechanical ventilation is respiratory failure caused either by illness, injury, or treatment with sedating medications. The goals of mechanical ventilation are to facilitate the movement of gas into and out of the lungs (ventilation) and to improve oxygen uptake into the bloodstream (oxygenation). While lifesaving in many situations, positive pressure ventilation can also be harmful. As a result, mechanical ventilation strategies must be adapted to achieve these goals in a way that minimizes further injury to the lung. The overriding principles of this “lung-protective ventilation strategy” are to safely recruit underinflated lung, sustain lung volume, minimize phasic overdistention, and decrease lung inflammation. This strategy requires adjustment of ventilator settings with an understanding of the difference between the gas exchange that is permissible and that which is normal.
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Modes of Mechanical Ventilation
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The parameters used to control the delivery of mechanical ventilation breaths are known as the trigger, cycle, control, and limit variables. The trigger variable describes how breaths are initiated, either by the patient or by the ventilator. The most common triggers are patient effort, sensed as a drop in return pressure or gas flow to the ventilator, and time. A newer trigger method, neurally adjusted ventilatory assist (NAVA), measures the electrical activity of the diaphragm via an esophageal catheter in order to adjust the ventilator breaths to meet the patient’s neural activity. While NAVA holds promise for improving patient-ventilator synchrony and facilitating ventilator weaning, its ideal role in clinical practice remains to be determined. The cycle variable describes how the inspiratory phase is terminated, either by the patient or by the ventilator. Most ventilator modes cycle according to a set inspiratory time (I-time) although flow-cycled modes can be used in spontaneously breathing patients. The control variable determines whether the ventilator delivers a specific tidal volume (volume-controlled modes) or a specific pressure (pressure-controlled modes). Limit variables are parameters whose magnitude is constrained during inspiration in order to prevent excessive pressure or volume from being delivered by the ventilator.
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Breathing during mechanical ventilation can be classified as spontaneous or mandatory. The patient controls the timing and size of spontaneous breaths. The ventilator controls the timing and/or size of mandatory breaths, independent of patient activity. In addition, the breathing pattern provided by the ventilator can be set to one of three configurations. In continuous mandatory ventilation (CMV), the ventilator determines the size and duration of all breaths. In intermittent mandatory ventilation (IMV), the ventilator delivers mandatory breaths, but additional spontaneous breaths between and during mandatory breaths are allowed. In continuous spontaneous ventilation (CSV), the patient initiates and controls all breaths, but the ventilator can assist those efforts.
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A ventilator mode consists of a specific control variable (pressure or volume), a specific pattern of breathing (CMV, IMV, or CSV), and a specific set of phase variables (trigger, limit, and cycle). Initiation of breaths and the length of exhalation are controlled by setting the respiratory rate. In time-cycled modes of ventilation, the inspiratory time (I-time) determines the length of inspiration and when to allow exhalation. Most modern ventilators can deliver either a pressure-targeted or a volume-targeted breath in several manners. In synchronized IMV (SIMV), the ventilator delivers breaths in an IMV pattern, but the machine breaths are synchronized with the patient’s efforts. If the patient does not make adequate respiratory efforts to trigger the ventilator, the machine delivers a mandatory breath at a preset time interval. In pressure-support ventilation, the patient’s own efforts are assisted by the delivery of gas flow to achieve a targeted peak airway pressure. Pressure support ventilation allows the patient to determine the rate and pattern of breaths (CSV breathing pattern), thus improving patient comfort and decreasing the work of breathing. The most commonly used mode of ventilation in many PICUs is synchronized IMV with pressure support (SIMV + PS), a mixed mode allowing pressure-supported breaths between the synchronized machine breaths.
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In pressure-controlled ventilation, air flow begins at the start of the inspiratory cycle and continues until a preset airway pressure is reached. That airway pressure is then maintained until the end of the set I-time, when the exhalation valve on the ventilator opens and gas exits into the machine. With this mode of ventilation, changes in the compliance of the respiratory system will lead to fluctuations in the actual tidal volume delivered to the patient. The advantage of pressure-targeted ventilation lies primarily in the avoidance of high airway pressures that might cause barotrauma or worsen lung injury. The main disadvantage of pressure-controlled ventilation is the possibility of delivering either inadequate or excessive tidal volumes during periods of changing lung compliance. In volume-controlled ventilation, the machine delivers a set tidal volume to the patient. Changes in lung compliance will lead to fluctuations in the peak airway pressure generated by the breath. The main advantage of volume ventilation is more reliable delivery of the desired tidal volume and thus better control of ventilation. More reliable tidal volume delivery may also help prevent atelectasis due to hypoventilation. Disadvantages of volume ventilation include the risk of barotrauma from excessive airway pressures and difficulties overcoming leaks in the ventilator circuit. In either pressure- or volume-controlled modes, alarm limits can be set in order to restrict changes in either tidal volume or airway pressure with changing lung compliance; interpreting those alarms and adjusting the ventilator require the ICU clinician to understand the ventilator mode in use.
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Finally, in any mode of ventilation, the minimum distending pressure applied to the lung during the respiratory cycle is determined by setting the positive end-expiratory pressure (PEEP). PEEP helps prevent the end-expiratory collapse of open lung units, thus preventing atelectasis and shunting. In disease states such as pulmonary edema, pneumonia, or acute respiratory distress syndrome (ARDS), a higher PEEP (10–15 cm H2O) may increase the patient’s functional residual capacity (FRC), helping to keep open previously collapsed alveoli and improve oxygenation. However, high levels of PEEP may also cause complications such as gas trapping and CO2 retention, barotrauma with resultant air leaks, and decreased central venous return leading to reduced cardiac output or increased intracranial pressure (ICP).
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Setting & Adjusting the Ventilator
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When initiating either volume-controlled or pressure-controlled modes of ventilation, the ICU clinician sets a respiratory rate, an inspiratory time (I-time), and a level of PEEP. The respiratory rate will depend on multiple factors, including patient comfort and blood gas measurements. However, many patients will initially require full support with respiratory rates between 20-30 breaths/min. The minimum PEEP is usually 5 cm H2O but can be titrated up to maintain adequate oxygenation at acceptable inspired oxygen concentrations (< 60%–65%), while monitoring for adverse effects of increased intrathoracic pressure. In volume-controlled ventilation, a reasonable initial tidal volume is 8 mL/kg, as long as that volume does not cause excessive airway pressures (> 30 cm H2O) (see below for open-lung strategies in ARDS). In pressure-controlled ventilation, the amount of peak inspiratory pressure required will depend on the overall respiratory compliance. Patients without lung disease require peak inspiratory pressures of 15–20 cm H2O, while patients with respiratory illnesses may require 20–30 cm H2O pressure to provide adequate ventilation. Adequacy of the inspiratory pressure is assessed by observing the patient’s chest rise and by measuring the delivered tidal volume and gas exchange.
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Ventilated patients require careful monitoring for the efficacy of mechanical ventilation, including respiratory rate and activity, chest wall movement, and quality of breath sounds. Gas exchange (oxygenation and ventilation) should be monitored using either noninvasive or invasive methods as described above. Frequent or continuous systemic blood pressure monitoring is also necessary for patients ventilated with high PEEP levels, given the risk of adverse hemodynamic effects.
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Ventilator settings can be adjusted to optimize both ventilation (PaCO2) and oxygenation (PaO2). Ventilation is most closely associated with the delivered minute volume, or the tidal volume multiplied by the respiratory rate. As a result, abnormal PaCO2 values can be most effectively addressed by changes in the respiratory rate or the tidal volume. Increased respiratory rate or tidal volume should increase minute volume and thus decrease PaCO2 levels; decreases in respiratory rate or tidal volume should act in the opposite fashion. In some circumstances, additional adjustments may also be necessary. For example, for patients with disease characterized by extensive alveolar collapse, increasing PEEP may improve ventilation by helping to keep open previously collapsed lung units. Also, for patients with disease characterized by significant airway obstruction, decreases in respiratory rate may allow more time for exhalation and improve ventilation despite an apparent decrease in the minute volume provided.
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The variables most closely associated with oxygenation are the inspired oxygen concentration and the MAP during the respiratory cycle. Increases in inspired oxygen concentration will generally increase arterial oxygenation, unless right-to-left intracardiac or intrapulmonary shunting is a significant component of the patient’s illness. Concentrations of inspired oxygen above 60%–65%, however, may lead to hyperoxic lung injury. For patients requiring those levels of oxygen or higher to maintain adequate arterial saturations, increases in MAP should be considered as a means to recruit underinflated lung units. MAP is affected by PEEP, peak inspiratory pressure, and I-time. Increases in any one of those factors will increase MAP and should improve arterial oxygenation. Importantly, increases in MAP may also lead to decreases in cardiac output, primarily by decreasing venous return to the heart. In this circumstance, raising MAP may increase arterial oxygenation but actually compromise oxygen delivery to the tissues. For patients with severe hypoxemic respiratory failure, these tradeoffs highlight the need for careful monitoring by experienced personnel.
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Supportive Care of the Mechanically Ventilated Patient
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Patients undergoing mechanical ventilation require meticulous supportive care. Mechanical ventilation is often frightening and uncomfortable for critically ill children. In order to reduce dyssynchrony with the ventilator and impaired gas exchange, careful attention must be directed toward optimizing patient comfort and decreasing anxiety. Sedative anxiolytics are typically provided as intermittent doses or continuous infusions. Since oversedation of the ventilated patient may lead to longer durations of ventilation and difficulty weaning from the ventilator, standardized assessments of sedation level and targeting treatment to the minimum sedation level necessary to maintain patient comfort and adequate gas exchange are important.
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For patients with severe respiratory illness, even small physical movements can compromise gas exchange. In such cases, muscle paralysis may facilitate oxygenation and ventilation. Nondepolarizing neuromuscular blocking agents are most commonly used for this purpose, given as intermittent doses or as continuous infusions. When muscle relaxants are given, extra care must be taken to ensure that levels of sedation are adequate, as these medications will mask many of the usual signs of patient discomfort. In addition, ventilator support may need to be increased to compensate for the elimination of patient respiratory effort.
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Mechanically ventilated patients can usually be fed enterally with the use of temporary or existing feeding tubes. In patients where reflux or emesis is a major concern, transpyloric feeding or parenteral nutrition should be considered. Ventilator-associated pneumonia (VAP) is a significant complication of mechanical ventilation, leading to longer ICU stays and increased hospital costs. As a result, many local and national quality improvement initiatives have focused on minimizing the risks of VAP. These preventative measures include proper hand washing, elevation of the head of the bed to 30 degrees to prevent reflux, frequent turning of the patient, proper oral care, the use of closed suction circuits on all ventilated patients and avoidance of breaking the closed suction system, sedation protocols to minimize sedation administration, and daily assessment of extubation readiness.
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Mechanical ventilation should be weaned and discontinued as soon as safely possible. Extubation failure rates in mechanically ventilated children have been estimated between 4% and 20%. Considerable effort has been devoted to identifying predictors of extubation readiness and there is literature describing tests used to predict extubation success utilizing trials of spontaneous breathing on pressure support mode. Successful extubation requires adequate gas exchange, adequate respiratory muscle strength, and the ability to protect the airway. To assess extubation readiness, most intensivists will perform a trial of spontaneous breathing in which the patient, while remaining intubated, breathes either without assistance (through a T-piece) or with a low level of pressure support (through the ventilator) for a defined period of time, usually 1–2 hours. The patient is observed carefully for signs of rapid shallow breathing or worsened gas exchange during this trial, and if neither is observed, the patient can generally be safely extubated.
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Troubleshooting a sudden deterioration in the mechanically ventilated patient should begin with examining the patient. Determine whether the ETT is patent and in the correct position by auscultating for bilateral breath sounds, attempting to pass a suction catheter, assessing for detectable ETCO2, and direct laryngoscopy, if necessary. A chest x-ray may also be helpful for ensuring appropriate ETT positioning. If the ETT is patent and correctly positioned, the next step is to determine whether any changes in the physical examination—such as poor or unequal chest rise, or absent or unequal breath sounds—suggest atelectasis, bronchospasm, pneumothorax, or pneumonia. Next, determine whether hemodynamic deterioration could be underlying acute respiratory compromise (shock or sepsis). If the problem cannot be readily identified, take the patient off the ventilator and begin manual ventilation by hand-bagging. Hand-bagging can support the patient while the ventilator is checked for malfunction as well as assess for changes in compliance, informing necessary ventilator adjustments.
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OTHER MODES OF RESPIRATORY SUPPORT
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High-Frequency Oscillatory Ventilation
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High-frequency oscillatory ventilation (HFOV) is an alternative mode of mechanical ventilation in which the ventilator provides very small, very rapid tidal volumes at high rates around a higher MAP. Respiratory rates used during oscillatory ventilation typically range from 5 to 10 Hz (rates of 300–600 breaths/min) in most PICU patients. This mode of ventilation has been used successfully in neonates, older pediatric patients, and adults, although recent work has suggested that HFOV use may be associated with worse outcomes in adults with ARDS. HFOV is most widely used in severe, diffuse lung diseases, such as ARDS, which require high MAP to maintain lung expansion and oxygenation. Diseases characterized by significant heterogeneity or extensive gas trapping often respond too poorly to HFOV, although reports do exist of successful HFOV use in asthma. The advantage of HFOV is that high levels of MAP can be achieved without high peak inspiratory pressures or large tidal volumes, thus theoretically protecting the lung from ventilator-induced lung injury. Disadvantages of HFOV include poor tolerance by patients who are not heavily sedated or paralyzed, the risk of cardiovascular compromise due to high MAP, and the risk of gas-trapping and barotrauma in patients with highly heterogeneous lung disease. Although HFOV can be useful as a rescue mode for selected patients, recent literature suggests that HFOV has a limited role in ARDS compared with carefully managed conventional modes of ventilation.
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Extracorporeal Membrane Oxygenation
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Extracorporeal membrane oxygenation (ECMO) has been used as a rescue therapy to support pediatric patients with severe respiratory failure who have not improved with mechanical ventilation. ECMO circuits generally consist of a membrane oxygenator, a heater, and a pump. Central venous blood from the patient is directed out of the body, oxygenated, warmed and returned back to the patient. ECMO can be provided in two major modes: venoarterial (VA) and venovenous (VV). VA ECMO bypasses the lungs and the heart, thus supporting both the cardiovascular and respiratory systems, and requires cannulation of a large central artery and vein. VV ECMO utilizes central venous cannulation to provide extracorporeal oxygenation and carbon dioxide removal, thus augmenting the function of the patient’s lungs, but the patient’s own cardiac output is required to provide systemic oxygen delivery. VV ECMO use has increased over the past 15 years and provides the advantage of a reduced risk of systemic and, particularly, cerebral emboli when compared to VA ECMO. Patients with moderate hemodynamic compromise prior to ECMO initiation can also experience improvements in circulatory status on VV ECMO, likely due to the improvements in acid base status, oxygenation, and decreased intrathoracic pressures achieved with ECMO. ECMO is indicated for patients with reversible cardiovascular and/or respiratory failure and is not recommended in patients with severe neurologic compromise or who is in the terminal stages of a lethal condition. Despite an increase in the complexity of patients placed on ECMO, survival has remained acceptable over the past two decades. According to recent registry data, 57% of pediatric respiratory failure patients who are supported with ECMO survive, and survival rates are even better for ECMO patients with a diagnosis of viral pneumonia (especially due to respiratory syncytial virus) and without significant co-morbidities. Of note, in both neonatal and adult randomized controlled trials, patients with severe respiratory failure who were referred to an ECMO center for consideration of ECMO had improved survival, even though not all patients were actually placed on ECMO. These results emphasize the importance of early referral to experienced centers if ECMO is to be considered.
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Determining the optimal time to consider ECMO initiation is one of the most challenging aspects of using this technology. Survival appears equally good for most indications with mechanical ventilation for up to 14 days prior to ECMO initiation. Patients placed on ECMO later in the course of their illness or with prolonged ECMO runs (> 14 days) may have worse outcomes. Protocols to improve secretion clearance and lung recruitment have been described and should be considered to hasten lung recovery and shorten the ECMO course, although the optimal mechanical ventilation strategy has yet to be elucidated.
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While ECMO remains a viable therapy for selected patients with severe respiratory failure, serious complications such as CNS injury, hemorrhage, renal insufficiency, infection, and complications of immobility do occur, and each patient should be carefully evaluated by experienced personnel in order to choose the optimal timing and mode of ECMO support.
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