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Division of Critical Care Medicine, Hofstra North Shore-LIJ School of Medicine, Cohen Children's Medical Center of New York, North Shore Long Island Jewish Health System, 269-01 76th Avenue, New Hyde Park, NY 11040, USA
Division of Critical Care Medicine, Hofstra North Shore-LIJ School of Medicine, Cohen Children's Medical Center of New York, North Shore Long Island Jewish Health System, 269-01 76th Avenue, New Hyde Park, NY 11040, USA
Acute respiratory failure is common in critically ill children.
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Monitoring for respiratory failure includes commonly used invasive tests, such as blood gas analysis, but noninvasive monitoring has recently grown in importance and proven reliable.
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Recent advancements in therapeutic options for respiratory failure have improved the overall outcome of critically ill children, but much more rigorous investigation is still needed.
Introduction
Acute respiratory failure is a common dilemma faced by pediatric critical care practitioners. As many as two-thirds of pediatric intensive care unit (PICU) patients will be admitted with a diagnosis of respiratory failure,
which represents a common end point to multiple pathologic processes, categorized as hypoxemic, hypercapnic, or mixed. Common causes are listed in Table 1. In 2012, primary infections of the lung were responsible for 2% of all mortalities in children younger than 5 years in the United States and 18% worldwide.
Developmental variations contribute to the diverse etiologies and higher incidence of acute respiratory failure in children compared with adults. Infants have more compliant chest walls than adults, making it more difficult to generate the negative intrathoracic pressure required to inspire sufficient tidal volumes in conditions of decreased lung compliance (ie, pneumonia, hyaline membrane disease). The infant chest wall also has less elastic recoil. Further, collateral ventilation through pores of Kohn or Lambert are not well developed in early life. These characteristics make young children more susceptible to alveolar collapse. Childhood airways lack the more rigid cartilaginous supports that strengthen into adulthood, making them more susceptible to dynamic compression and subsequent airway obstruction in disease states associated with increased airway resistance (ie, bronchiolitis, asthma). Last, the pediatric airways are naturally smaller in diameter than in adults. Because the resistance to airflow is inversely proportional to the fourth power of the radius (R = 8NL/πr4), any narrowing of the pediatric airway will have a much greater impact on the resistance. This will lead to a more profound decrease in airflow, as laminar flow transitions to turbulent flow, as described by Reynolds number (Re = 2 rVρ/N, where r is the radius of the airway, V is the velocity of the gas flow, ρ is the density of the gas, and N is the viscosity of the gas). In the adult, the peripheral airways contribute about 20% of the total airway resistance. In infants and young children, they contribute about 50%, explaining why diseases affecting the peripheral airways (ie, bronchiolitis) have such a profound clinical impact. It is clear that the management of acute respiratory failure in children requires a thorough understanding of these physiologic differences, reminding the clinician that children are, in fact, not little adults.
Table 1Etiologies of acute respiratory failure in children
Adapted from Ghuman AK, Newth CJ, Khemani RG. Respiratory support in children. Paediatr Child Health 2011;21(4):163–9; with permission.
Acute respiratory failure occurs when embarrassment of the respiratory system results in the inability to properly transfer oxygen (O2) from the atmosphere to the blood or remove carbon dioxide (CO2) from the blood and eliminate it to the atmosphere. Hypoxic respiratory failure is defined by a partial pressure of arterial O2 (PaO2) that is less than 60 mm Hg on room air at sea level, and hypercapnic respiratory failure occurs when the partial pressure of CO2 (PaCO2) is greater than 50 mm Hg (with a concomitant respiratory acidosis) under the same conditions. To better understand these, it is first important to examine the mechanisms of oxygenation and ventilation.
Oxygenation
Ideally, oxygen that is contained within the alveolus at inspiration will equilibrate with arterial blood, as described by the alveolar gas equation:
Pao2 = Pio2 – (Paco2/R),
then Pao2 = Fio2 (PB – PH2O) – Paco2/R,
where Pao2 = partial pressure of alveolar oxygen; Pio2 = partial pressure of inspired oxygen; Paco2 = partial pressure of alveolar CO2 (substituted by arterial [PaCO2] due to the highly efficient manner that CO2 crosses cell membranes); R = respiratory quotient: ratio of CO2 production (VCO2) to O2 consumption (Vo2) (R = VCO2/Vo2), averages 0.8 on a normal, mixed adult diet; PB = barometric pressure; and PH2O = water vapor pressure.
Adequate gas exchange also requires that the inspired alveolar gas matches blood distribution in the pulmonary capillaries. There is a normal gradient between alveolar and arterial Po2, known as the A-a gradient, which is less than 10 mm Hg. The alveolar gas equation also helps to understand some of the mechanisms behind hypoxemia (Box 1).
Nonpulmonary causes, such as decreased cardiac output, increased extraction of O2, and abnormal hemoglobin, can also contribute to abnormal gas exchange.
The most common etiology for hypoxemia in critically ill children is inequality in the relationship between ventilation and perfusion (V/Q). Regional differences in ventilation and blood flow, owing to regional differences in intrapleural pressures and gravitational forces, cause ventilation and perfusion to decrease from the base to the apex of the lung, although perfusion does so much more rapidly. This leads to an abnormally high V/Q ratio at the apex of the lung (in an upright position) and a much lower one at the base.
Atelectasis from various pathologic states (ie, pneumonia, mucous plug) exaggerates the mismatching of V/Q, causing well-oxygenated blood from high V/Q regions to mix with poorly oxygenated blood from low V/Q regions, leading to worsening hypoxia with an increased A-a gradient. Pulmonary edema (ie, cardiac failure, systemic inflammatory response syndrome, acute respiratory distress syndrome [ARDS]) will lead to worsening V/Q mismatching, compromised diffusion, and atelectasis. Hypoxemia caused by V/Q inequality can be corrected by inspiring a higher concentration of oxygen, as well as the provision of positive pressure ventilation, which may recruit consolidated or collapsed lung units and improve V/Q matching.
When alveolar ventilation is decreased, insufficiently replenishing alveolar oxygen, the alveolar Po2 falls as the Pco2 rises, not altering the normal A-a gradient. Elevation of PaCO2 that occurs with airway obstruction will not result in hypoxemia until severe obstruction is present, with forced expiratory volume in 1 second less than approximately 15% predicted.
The hypoxia that results from CO2 retention is easily overcome with the addition of increased inspired oxygen.
Shunting describes the direct mixing of deoxygenated venous blood that has not undergone gas exchange in the lungs with arterial blood. Normal anatomic shunting occurs as venous blood from the bronchial veins and Thebesian veins collects in the left-sided circulation. Pathologically, patients may have abnormal vascular connections (ie, arterial-venous fistula) or intracardiac communications allowing blood to traverse the heart from the right to the left without undergoing gas exchange at the level of the lungs. Intrapulmonary shunting most commonly occurs as blood perfuses regions of the lung that are not well ventilated. The addition of mixed venous blood (with depressed Po2) to oxygenated capillary blood results in decreased PaO2, increasing the A-a gradient. The amount of shunted blood that would need to be mixed with arterial blood to account for the A-a gradient can be calculated by the shunt equation:
QS/QT = (CcO2 – CaO2)/(CcO2 – CvO2),
where QS is shunt flow to unventilated lung units; QT is total pulmonary blood flow; and CaO2, CcO2, and CvO2 is the content of oxygen in arterial, end-capillary, and mixed venous blood, respectively.
The addition of supplemental oxygen, increasing the Pao2, has minimal effect on improving the hypoxemia, as the shunted blood is not exposed to the high alveolar Po2.
Diffusion of oxygen between the alveolus and capillary blood can be altered by thickening of the alveolar-capillary barrier, by decreased alveolar capillary volume, or increased oxygen extraction. Further, decreasing the Pao2 at high altitude decreases the alveolar-capillary Po2 pressure gradient, limiting diffusion. Diffusion impairment is a rare primary cause of hypoxemia in children, although it can contribute to the hypoxemia associated with shunt and V/Q mismatching. More than 50% of the diffusion capacity of the lung must be compromised to develop hypoxemia from primary diffusion limitation. Supplemental oxygen can rapidly overcome hypoxemia associated with diffusion limitations.
Ventilation
Exchange of CO2 follows similar physiologic principles to O2. Because of differences in the solubility, dissociation curves of CO2 and O2, as well as the way each gas effects central ventilatory control, CO2 exchange (and invariably PaCO2) is ultimately determined by alveolar minute ventilation and the degree of dead space present. PaCO2 is related to the balance between the production of CO2 (VCO2), which is a function of the metabolic conditions of the patient, and the alveolar minute ventilation (VA), as described by the equation:
Paco2 = VCO2 * K/VA
Minute ventilation is determined by the product of the respiratory frequency (f) and the tidal volume (Vt). Dead space gas, both anatomic (in the conducting airways) and physiologic (areas of ventilation lung units that are poorly perfused; V>Q), does not participate in CO2 elimination. Therefore, total alveolar ventilation is determined by the difference between total minute ventilation (VE) and the degree of dead space ventilation (VD):
VA = VE – VD
As a result, elevations in PaCO2 will result from conditions of decreased tidal volume or increased physiologic dead space (Table 2). Ventilatory muscles generally can maintain adequate tidal volumes with only 50% of normal strength.
Hyperinflation further compromises respiratory muscle function. Diseases associated with airway obstruction increase the end expiratory lung volume greater than functional residual capacity (FRC), decreasing muscle fiber length below what is optimal. Muscle fibers generate less force at these shorter lengths.
V/Q mismatching generally does not cause a direct increase in Pco2 because elevated CO2 from low V/Q units is a potent stimulator of the central respiratory centers, increasing alveolar minute ventilation.
As a common end point to multiple clinical conditions, the incidence of respiratory failure in the pediatric population is difficult to ascertain. In one study, 17.1% of patients admitted to a PICU at several large children’s hospitals required mechanical ventilation, with acute respiratory conditions as the culprit in 62.4% of these patients. In this cohort of patients, bronchiolitis (26.7%) and pneumonia (15.8%) were the leading etiologies for respiratory failure.
; 10% of intubated children admitted to a European PICU had ALI, with a mortality rate of 27%. Of the patients with ALI, 54% had ARDS at presentation and 80% progressed to ARDS at some point during their hospitalization.
Bronchiolitis, both respiratory syncytial virus (RSV) and non-RSV, accounts for up to 16% of all hospital admissions, with RSV bearing responsibility for 1 of every 334 hospitalizations.
From 7.4% to 28.0% of children with bronchiolitis require mechanical ventilation. The burden of RSV is more severe at younger age and in patients with chronic disease. Of all RSV admissions, for both bronchiolitis and pneumonia, 4% require intubation and mechanical ventilation.
Respiratory failure in asthmatic individuals has declined over time, as novel therapies have emerged. Current intubation rates vary widely for asthmatic patients, from 5% to 17% based on presentation to a community hospital or tertiary care center, with a higher rate for those presenting to community hospitals.
Monitoring respiratory function appropriately will help identify the development of respiratory failure as well as guide therapy based on response, and can predict outcome.
The fundamental and most important assessment of respiratory function is the clinical examination. Respiratory rate and pattern are indicative of the physiologic status of the respiratory system. Tachypnea is often the first sign of respiratory compromise.
Infants and young children may present with grunting in an attempt to increase their positive end-expiratory pressure and maintain functional residual capacity, indicating the presence of restrictive lung disease.
Cyanosis is evident when greater than 3 to 5 g/dL of deoxygenated hemoglobin is present in arterial blood. This correlates with an arterial saturation of 80% in healthy individuals, but is unreliable in conditions of anemia, or in the presence of abnormal forms of hemoglobin, such as methemoglobin or carboxyhemoglobin.
Traditionally, adequacy of gas exchange has been monitored by invasive means, in particular blood gas analysis. The arterial blood gas (ABG) is the gold standard for Po2 determination, as it reliably measures Po2 directly. The percent oxyhemoglobin saturation from a blood gas is highly unreliable, as it is a calculated value based on temperature, PaCO2, pH, and PaO2. Free-flowing capillary blood can accurately assess pH and PaCO2.
and should be avoided for clinical decisions regarding ventilation.
Since the 1980s, noninvasive monitoring of oxygenation has been available in the form of pulse oximetry (SpO2). Pulse oximeters are accurate when oxyhemoglobin concentrations are greater than 60%, but may not be reliable in conditions of poor perfusion (ie, septic shock), peripheral vasoconstriction (ie, norepinephrine), hypothermia, peripheral edema, significant extremity movement, or in the presence of methemoglobin or carboxyhemoglobin. Other important clinical data can be interpreted by the pulse oximeter as well, such as heart rate, rhythm, and peripheral perfusion.
The presence of pulsus paradoxus, indicated by respiratory variability in the pulse oximeter plethysmography tracing, correlates with important upper airway obstruction (eg, croup), as well as degree of lower airway obstruction (eg, asthma), and offers a continuous and accurate evaluation of response to therapy (Fig. 1).
Pediatric intensivists frequently substitute pulse oximetry for arterial catheters while caring for critically ill children with respiratory failure, with management decisions and outcomes remaining equal.
Fig. 1Pulse oximeter waveforms. Solid line: normal. Broken line: evidence of pulsus paradoxus. Arrow indicates inspiration and concordant decrease in peak of plethysmography tracing, indicating cardiovascular consequence of increased work of breathing, generating a more negative intrapleural pressure. This can be seen in upper airway obstruction (ie, infectious croup, postextubation) or lower airway obstruction (ie, asthma) and improves with appropriate therapy.
Similarly, ventilation can be monitored continuously and noninvasively. Capnography monitors detect CO2 levels, determined by its unique infrared light absorption characteristics. Capnography can be used at the end of the endotracheal tube in intubated patients or in nonintubated patients by nasal cannula during procedural sedation to assess the quality of ventilation.
The value of end-tidal CO2 monitoring when comparing three methods of conscious sedation for children undergoing painful procedures in the emergency department.
Table 3 lists the many clinical uses of capnography waveforms (Fig. 2). Generally, end-tidal CO2 (ETCO2) is about 1 to 3 mm Hg lower than PaCO2 in healthy individuals owing to physiologic dead space ventilation. In fact, the difference between the ETCO2 and PaCO2 directly correlates with the degree of dead space present, and can be used to estimate dead space ventilation according to the Bohr equation:
VD/VT = (Paco2 – PECO2)/Paco2
Table 3Clinical conditions determined by use of capnography
Increase in ETCO2
Decrease in ETCO2
Hypoventilation
Unplanned extubation
Administration of sodium bicarbonate
Endotracheal tube obstruction
Increase in cardiac output
Ventilator disconnection
Increased dead space
Pulmonary embolism
Decreased cardiac output
Continuous capnography also allows for accurate evaluation of respiratory rate, rhythm, and patient-ventilator asynchrony.
Fig. 2Capnograph (time-based). Solid line: normal. Phase I: dead space (anatomic) gas exhaled from conducing airways; CO2 content near zero. Phase II: mixing of alveolar gas, which contains CO2. Phase III: plateau phase corresponds to pure alveolar gas. Phase IV: rapid fall due to inspiration, with negligible CO2. x and x': ETCO2. Dotted line: obstructed airway disease. Phase III slopes upward because of delay in emptying of alveolar gas from different lung units owing to increased airway resistance. The upsloping directly correlates with degree of obstruction, and improves with response to bronchodilator therapy.
(Data from Krauss B, Deykin A, Lam A, et al. Capnogram shape in obstructive lung disease. Anesth Analg 2005;100(3):884–8; and Yaron M, Padyk P, Hutsinpiller M, et al. Utility of the expiratory capnogram in the assessment of bronchospasm. Ann Emerg Med 1996;28(4):403–7.)
Therefore, continuous capnography can be used to detect alterations in dead space ventilation and response to therapeutic interventions.
Severe respiratory illness, such as ALI or ARDS, has traditionally been monitored and defined based on the severity of hypoxemia according to invasive measurements of PaO2.
Report of the American-European Consensus conference on acute respiratory distress syndrome: definitions, mechanisms, relevant outcomes, and clinical trial coordination.
See Box 2 for diagnostic criteria for ALI/ARDS. The severity of hypoxemia has been determined by the ratio of PaO2 to the fraction of inspired oxygen (PaO2/Fio2). The oxygenation index (OI) is commonly used as a superior indication of oxygenation impairment, as it takes into account the level of ventilatory support provided ([OI = Fio2 * mean airway pressure]/PaO2). Unlike in adults, the degree of hypoxemia in children is associated with mortality,
A significant proportion of children with acute hypoxemic respiratory failure are managed without arterial lines, and therefore cannot be classified as ALI/ARDS.
Noninvasive correlates of severity of hypoxemia have now been established, as the definition of ALI/ARDS is being reconsidered. The SpO2/Fio2 ratio (substituting SpO2 for PaO2), as well as the OSI (oxygen saturation index, substituting SpO2 for PaO2) are gaining specific attention as validated measures of hypoxemia.
Consensus criteria for definition of acute lung injury or acute respiratory distress syndrome
Acute onset
Bilateral infiltrates on chest radiograph
Severe hypoxemia resistant to oxygen therapy
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PaO2/Fio2 ratio ≤200 torr (≤26.6 kPa) for ARDS
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PaO2/Fio2 ratio ≤300 torr (≤40 kPa) for ALI
No evidence of left atrial hypertension
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Pulmonary artery occlusion pressure <18
Therapy
Specific aspects of the therapy for respiratory failure vary depending on the underlying cause. In all cases, however, the goal of therapy is to supplement the patient’s gas exchange. Initial measures should include steps to ensure airway patency and clearance. Supplemental oxygen may be administered via facemask or nasal cannula.
The use of noninvasive positive pressure ventilation (NPPV), in the form of continuous positive airway pressure (CPAP) or bilevel positive airway pressure (BiPAP), has gained widespread acceptance as a therapy for respiratory failure from a variety of etiologies.
NPPV may supplement respiratory mechanics by unloading the respiratory musculature, stabilizing the chest wall, and improving minute ventilation. The recruitment of atelectatic alveolar units and improved clearance of intra-alveolar fluid augment end expiratory lung volume, approaching FRC, and decrease the A-a gradient.
A number of disadvantages are intrinsic to NPPV that limit its utility. The risk of aspiration is significant; therefore, enteral feeding is generally avoided, and gastric decompression may be considered prophylactically. Patients, particularly those with developmental or cognitive impairments, may experience substantial anxiety with the placement of the BiPAP mask, risking proper positioning and function. Although small doses of anxiolytics may be administered, caution must be taken when providing respiratory depressants to patients with a native airway and impaired pulmonary function.
The mainstay of therapy in the most severe forms of acute hypoxemic respiratory failure is intubation and mechanical ventilation. The goal of mechanical ventilation in this group of patients is to provide adequate gas exchange while avoiding ventilator-associated secondary lung injury (VILI). Ventilation with high volumes and pressures, cyclic opening and closing of alveoli, and delivery of high Fio2 result in a proinflammatory cascade causing lung injury and pulmonary edema.
By using a “lung-protective” strategy using low tidal volumes of 6 to 8 mL/kg and limiting plateau pressure to 30 or less, secondary lung injury may be curtailed. This approach necessitates decrease in minute ventilation, with a concomitant respiratory acidosis. Usual targets include a pH of 7.25 or higher, with a Pco2 of 60 to 80 torr, and oxygen saturation goals of 88% or greater. Adult data have demonstrated significant improvement in mortality with this approach.
Another approach to “lung protective ventilation,” or “‘open lung strategy,” is high-frequency oscillatory ventilation (HFOV). HFOV allows for increased mean airway pressure with decreased peak airway pressure, facilitating recruitment of atelectatic lung segments, while avoiding the cyclic shearing open and subsequent alveolar collapse, decreasing the risk of VILI. Over the past 20 years, HFOV has been used extensively in the pediatric population; however, definitive data demonstrating clear clinical benefit versus low tidal volume conventional ventilation are lacking.
Prone positioning has been suggested as an adjunctive therapy to ventilator management. The prone position improves recruitment and clearance of alveolar debris in dependent lung segments. Studies have documented an improvement in oxygenation in the prone position, but have failed to demonstrate improvements in ventilator-free days or survival.
A recent meta-analysis found that prone positioning may reduce the relative risk of mortality in patients with PaO2/Fio2 ratios of less than 100 mm Hg by 16%, although it was associated with increased risk of pressure ulcers, endotracheal tube obstruction, and chest tube dislodgement.
As such, prone positioning may be considered in those patients with the most severe ARDS, although careful consideration of the risks and benefits must be taken.
Another adjunctive therapy used in ARDS is inhaled nitric oxide (iNO). A potent, locally acting pulmonary vasodilator, the aim of therapy is to overcome regional hypoxic vasoconstriction and improve V/Q matching and oxygenation. Studies have demonstrated an initial, albeit transient, improvement in oxygenation; however, no improvement in clinically relevant outcomes, such as ventilator-free days or survival,
Qualitative and quantitative surfactant deficiencies occur in ARDS because of intra-alveolar edema and inflammatory mediators, as well as impaired production, resulting in impaired pulmonary compliance.
Replacement of surfactant in neonates with meconium aspiration syndrome is well documented to result in improved pulmonary mechanics and survival, and serves as the rational basis for studies in pediatrics.
although power was lacking to make definitive recommendations for its use. Ongoing clinical trials are further exploring the utility of this therapy.
Corticosteroids have been used for ARDS in an attempt to attenuate the inflammatory process responsible for the syndrome. Although some studies have documented an improvement in survival, others have failed to show benefit, with the indication that steroids started after 14 days of the disease process may worsen survival.
The use of paralytic agents in patients with ARDS has recently shown promise. The judicious use of neuromuscular blockade has been used to improve patient-ventilator synchrony, although concerns about prolonged muscle weakness have persisted. In an adult study, the use of cisatricurium within 48 hours of ARDS onset was demonstrated to improve adjusted 90-day mortality and time off the ventilator, without an increased incidence of muscle weakness.
No pediatric data currently exist to guide the use of neuromuscular blocking agents in respiratory failure.
Asthma
The mechanics of respiratory failure due to asthma and other obstructive pulmonary processes are different than those related to ARDS and pneumonia, and require different management strategies. As previously described, obstructive lung disease results in air trapping and an increase in end expiratory lung volume over FRC, resulting in increased intrinsic pulmonary pressure at end expiration, termed auto-PEEP. This places the respiratory system at a mechanical disadvantage, in the face of increased work of breathing required to initiate inspiration (to overcome the auto-PEEP) as well as to overcome the resistance to airflow.
The act of intubation and initiation of positive pressure ventilation in a patient with high levels of auto-PEEP bears additional risks, such as barotrauma and resultant air leak syndrome. Adding positive pressure can further impair venous return to the heart, which can result in compromised cardiac output and cardiac arrest. Significant efforts are therefore made to prevent intubation of asthmatic patients. These include anti-inflammatory therapy with steroids, and bronchodilation with inhaled or intravenous β-agonists. Other acute asthma adjuncts include magnesium, anticholinergics, and methylxanthines. In-depth discussion on these therapies is beyond the scope of this article.
The use of BiPAP has been advocated as a safe and effective way to realize some of the benefits of positive pressure ventilation on the sick asthmatic patient without some of the risks inherent in endotracheal intubation.
By providing assistance to inspiratory flow, BiPAP can help unload the respiratory muscles and decrease work of breathing. Perhaps more importantly, the PEEP maintained at end exhalation stents the small airways open, reducing airway collapse due to elevated intrathoracic pressures and dynamic compression, and relieves hyperinflation. Further, PEEP decreases the amount of negative intrathoracic pressure required to initiate a breath, reducing the work of breathing.
Helium-oxygen (heliox) gas mixture may be considered for severe asthma. Helium is less dense than air, reducing the Reynolds number, improves laminar flow to and from obstructed airways, and may help in delivery of aerosolized particles to the distal airways.
Heliox is available in concentrations ranging from 80%: 20% to 60%: 40% helium: oxygen, with the highest benefit derived from the highest helium concentration. Heliox has been used to drive albuterol nebulization, and can be blended into BiPAP and ventilator circuits. Limited studies have failed to show consistent benefit with the use of heliox, with the suggestion of benefit in the most severe patients.
More rigorous study is indicated before heliox can be routinely recommended for asthmatic individuals with respiratory failure.
Intubation and mechanical ventilation may be required in patients who fail noninvasive therapy. The general approach most frequently advocated is a prolonged exhalatory phase, targeted to allow complete exhalation and reversal of the dynamic hyperinflation. Monitoring should ensure that a complete exhalation has taken place before the next ventilator breath is delivered, preventing worsening dynamic hyperinflation, compromising gas exchange and cardiac function further. This requires low respiratory rates with limitation of minute ventilation and accepting a concomitant respiratory acidosis. A pH above 7.20 and PaCO2 below 90 are generally accepted goals.
Volume control modes of ventilation offer a fixed tidal volume in patients with dynamic changes in airway resistance, whose delivered volumes in pressure control modes may vary significantly from breath to breath.
The role of PEEP for mechanically ventilated asthmatic individuals is controversial. The use of PEEP may help overcome increased respiratory effort needed to overcome auto-PEEP in the spontaneously breathing patient. In addition, PEEP may assist in stenting open distal airways during exhalation, preventing dynamic collapse during exhalation; however, PEEP itself provides an obstruction to exhalatory flow, with the potential to worsen intrinsic air trapping.
Another approach to the intubated asthmatic individual is the use of pressure support ventilation. Pressure support assistance during inspiration helps overcome the resistance to airflow and decreases work of breathing. The patient determines the rate, inspiratory and expiratory times, and flow pattern. High levels of PEEP are applied to match the intrinsic PEEP created by the air trapping, titrated to the clinical assessment of the patient’s work of breathing. By remaining unparalyzed, the patient contributes to the reversal of hyperinflation with active exhalation. Although only case reports on this approach are published to date, the possibility of minimizing the use of paralytics in patients already at risk of muscle weakness caused by corticosteroid use is attractive and bears further investigation.
Bronchiolitis is the result of airway inflammation, with subsequent secretions and cellular debris, resulting in obstructive pulmonary disease. As a viral process, there is no specific therapy and treatment is supportive. Multiple pharmacologic interventions, including β-2 agonists, racemic epinephrine, and corticosteroids, have been studied without convincing evidence of their efficacy.
Nasal CPAP is frequently used for respiratory support in the sick individual with bronchiolitis. High-flow nasal cannula appears to be a potential alternative, although further study is warranted.
Those with RSV pneumonia frequently meet ALI and ARDS criteria, and therapy is directed in that manner.
Extracorporeal Membrane Oxygenation
Extracorporeal membrane oxygenation (ECMO) has been used for cases of refractory respiratory and cardiorespiratory failure since its widespread deployment in the late 1970s and early 1980s. Overall survival is 57% in pediatric patients (30 days to 18 years old), with wide variation based on diagnosis, ranging from 39% (pertussis) to 83% (asthma).
As ECMO circuits have become more compact and easier to manage, and greater expertise has been developed, ECMO has been offered to more complex patients. Patients can be considered eligible candidates even after prolonged mechanical ventilation for longer than 14 days.
The impact of mechanical ventilation time before initiation of extracorporeal life support on survival in pediatric respiratory failure: a review of the extracorporeal life support registry.
The degree of hypoxemia, as described by PaO2/Fio2 ratio, SaO2/Fio2 ratio, OI, or OSI, and alveolar dead space fraction (PaCO2-PETCO2/PaCO2), is associated with increased risk of death.
Although the prevalence of asthma in the pediatric population has increased in recent years, the outcome in even those with respiratory failure is generally good. The rate of invasive mechanical ventilation ranges from 3% to 47%, with an overall mortality rate of 7% to 8%.
similar to adult survivors. Although most children will have physiologic evidence of obstructive or restrictive disease after discharge from the hospital, pulmonary function continues to recover over the first year after the acute illness.
although bronchodilators may be needed during exercise or an intercurrent viral illness.
Outcome reports vary, likely related to the timing of the follow-up. It has been suggested that patient evaluations should occur 6 to 12 months after the acute illness, after which any significant recovery of pulmonary function is unlikely.
The value of end-tidal CO2 monitoring when comparing three methods of conscious sedation for children undergoing painful procedures in the emergency department.
Report of the American-European Consensus conference on acute respiratory distress syndrome: definitions, mechanisms, relevant outcomes, and clinical trial coordination.
The impact of mechanical ventilation time before initiation of extracorporeal life support on survival in pediatric respiratory failure: a review of the extracorporeal life support registry.
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