Survey
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
* Your assessment is very important for improving the workof artificial intelligence, which forms the content of this project
Feature Articles Pressure-controlled ventilation in children with severe status asthmaticus* Ashok P. Sarnaik, MD, FAAP, FCCM; Kshama M. Daphtary, MD; Kathleen L. Meert, MD, FAAP; Mary W. Lieh-Lai, MD, FAAP; Sabrina M. Heidemann, MD, FAAP Objective: The optimum strategy for mechanical ventilation in a child with status asthmaticus is not established. Volume-controlled ventilation continues to be the traditional approach in such children. Pressure-controlled ventilation may be theoretically more advantageous in allowing for more uniform ventilation. We describe our experience with pressure-controlled ventilation in children with severe respiratory failure from status asthmaticus. Design: Retrospective review. Setting: Pediatric intensive care unit in a university-affiliated children’s hospital. Patients: All patients who received mechanical ventilation for status asthmaticus. Interventions: Pressure-controlled ventilation was used as the initial ventilatory strategy. The optimum pressure control, rate, and inspiratory and expiratory time were determined based on blood gas values, flow waveform, and exhaled tidal volume. Measurement and Main Results: Forty patients were admitted for 51 episodes of severe status asthmaticus requiring mechanical ventilation. Before the institution of pressure-controlled ventilation, median pH and PCO2 were 7.21 (range, 6.65–7.39) and 65 torr (29 –264 torr), respectively. Four hours after pressure-con- A sthma remains one of the most common causes of hospitalization in children despite considerable advances in our understanding of its pathophysiology and management (1). Severe acute exacerbations of asthma, which are refractory to pharmacologic interventions, are potentially life threatening and may require mechanical ventilation. Morbidity and *See also p. 191. From the Division of Critical Care Medicine, Department of Pediatrics, Children’s Hospital of Michigan, Wayne State University School of Medicine, Detroit, MI. Presented, in part, at the American College of Chest Physicians Annual Meeting, Philadelphia, PA, November 2001. Address requests for reprints to: Ashok P. Sarnaik, MD, Children’s Hospital of Michigan, 3901 Beaubien, Detroit, MI 48201. E-mail: [email protected] Copyright © 2004 by the Society of Critical Care Medicine and the World Federation of Pediatric Intensive and Critical Care Societies DOI: 10.1097/01.PCC.0000112374.68746.E8 Pediatr Crit Care Med 2004 Vol. 5, No. 2 trolled ventilation, median pH increased to 7.31 (6.98 –7.45, p < .005), and PCO2 decreased to 41 torr (21–118 torr, p < .005). For patients with respiratory acidosis (PCO2 >45 torr) within 1 hr of starting pressure-controlled ventilation, the median length of time until PCO2 decreased to <45 torr was 5 hrs (1–51 hrs). Oxygen saturation was maintained >95% in all patients. Two patients had pneumomediastinum before pressure-controlled ventilation. One patient each developed pneumothorax and subcutaneous emphysema after initiation of pressure-controlled ventilation. All patients survived without any neurologic morbidity. Median duration of mechanical ventilation was 29 hrs (4 –107 hrs), intensive care stay was 56 hrs (17–183 hrs), and hospitalization was 5 days (2–20 days). Conclusions: Based on this retrospective study, we suggest that pressure-controlled ventilation is an effective ventilatory strategy in severe status asthmaticus in children. Pressure-controlled ventilation represents a therapeutic option in the management of such children. (Pediatr Crit Care Med 2004; 5:133–138) KEY WORDS: status asthmaticus; ventilators; mechanical; intensive care; child; preschool; child; adolescent mortality rates among patients receiving mechanical ventilation can be considerable. Markedly increased airway resistance and prolonged time constant are characteristic features of respiratory mechanics in asthma. Traditionally, volume control has been the preferred mode of ventilation (2– 4). However, as tidal volume is delivered with constant flow in traditional volume-controlled ventilation (VCV), relatively less obstructed airways with shorter time constant are likely to receive more volume throughout inspiration compared with more obstructed airways with longer time constant. This would result in uneven ventilation, higher peak inspiratory pressure, and a decrease in dynamic compliance. It has been suggested that pressure-controlled mode is better suited for mechanical ventilation in asthma (5, 6). With pressurecontrolled ventilation (PCV), because of a constant inflation pressure, relatively less obstructed lung units with shorter time constant would achieve pressure equilibration earlier during inspiration compared with more obstructed areas. Thus, units with shorter time constants would attain their final volume earlier in inspiration whereas those with longer time constants would continue to receive additional volume later in inspiration. This would result in more even distribution of inspired gas, delivery of more tidal volume for the same inflation pressure, and improved dynamic compliance compared with VCV. A disadvantage of PCV is that the delivered tidal volume will vary depending on the respiratory system resistance. In a disease such as asthma with potentially rapid changes in airway resistance, the tidal volume received by the patient may change dramatically for the same amount of inflation pressure. This would necessitate frequent changes in pressure control level to accommodate changes in resistance. Pressure-regulated volume control may be more advanta133 geous than PCV because it guarantees tidal volume by regulating inflation pressure in the face of changing dynamic compliance. However, pressure-regulated volume control is a relatively new mode of ventilation, not available in most ventilators, and therefore not well studied. The objective of our study is to describe our experience using PCV in the initial management of children with status asthmaticus according to a predetermined strategy. MATERIALS AND METHODS Study Population. Medical records of children receiving mechanical ventilation for status asthmaticus, admitted to the intensive care unit (ICU) of Children’s Hospital of Michigan between January 1, 1995, and December 31, 2000, were reviewed. Patients who were intubated before admission and extubated within 4 hrs of admission, and those who had suffered cardiopulmonary arrest and met clinical criteria of brain death on admission, were excluded. The Wayne State University Human Investigation Committee approved the study and waived the need for informed consent. Ventilatory Strategy. All patients were managed with PCV as the initial ventilatory mode. Puritan Bennett 7200 (Nellcor Puritan Bennett, Pleasanton, CA), VIP Bird (Bird Products, Palm Springs, CA), and Siemens 900C (Siemens-Elma, Solna, Sweden) were used for mechanical ventilation. All patients received a positive end-expiratory pressure of 4 cm H2O. The level of pressure control (peak inspiratory pressure ⫺ positive end-expiratory pressure) was initiated at 25–30 cm H2O for patients age 1–5 yrs and at 30 –35 cm H2O for patients ⬎5 yrs of age. Respiratory rate was initially set at 12–16 breaths/min for patients age 1–5 yrs and at 10 –12 breaths/min in patients ⬎5 yrs. The inspiratory to expiratory ratio was set at 1:4. Exhaled tidal volume and flow-time curve on ventilator waveform graphics were continuously monitored. Pressure control was adjusted by changes of 2–5 cm H2O to achieve an exhaled tidal volume of 10 –12 mL/kg. In general, the increase in pressure control was limited to 50 cm H2O. Ventilatory rate, inspiratory time, and expiratory time were selected to ensure near-complete return of expiratory flow to baseline and to achieve the desired exhaled tidal volume. Pressure control, rate, inspiratory time, and expiratory time were subsequently adjusted to maintain pH ⬎7.3 and PCO2 ⬍50 torr or exhaled tidal volume of 10 –12 mL/kg. The FIO2 was adjusted to maintain SpO2 ⬎95%. The optimal settings for each patient were defined as the combination of pressure control, rate, and inspiratory time within the initial 8 hrs that resulted in the first observed decline in PCO2 that was sustained on subsequent blood gas determinations. Pressure control was reduced by 2–5 cm H2O with improvement in airway obstruction 134 as indicated by exhaled tidal volume ⬎12 mL/kg and resolution of respiratory acidosis. Patients were weaned from mechanical ventilation when their flow waveforms demonstrated an exhalation phase short enough to allow spontaneous breathing in between machine-delivered breaths and their PCO2 values were ⬍45 torr. Pharmacologic paralysis was stopped before weaning. Patients were weaned according to physician preference by decreasing PCV synchronized intermittent mandatory ventilation rate, by providing pressure support, by changing to VCV, or by combining VCV with pressure support. Baseline Patient Characteristics. Age, gender, race, past medical history, current home medications, referral source, and medications administered before and after mechanical ventilation were recorded. Reasons for intubation and mechanical ventilation were categorized as a) cardiorespiratory arrest; b) respiratory arrest (absent or agonal respirations); c) respiratory acidosis (pH ⱕ7.32 with PCO2 ⱖ50 torr), with clinical impression of respiratory fatigue (severe retractions, inability to speak a complete sentence, obtunded sensorium and diaphoresis); and d) clinical impression of respiratory fatigue without documented respiratory acidosis. Outcome Measures. Ventilator settings and arterial or capillary blood gas values were recorded before initiation of PCV, within 1 hr of starting PCV, and at 4, 8, and 12 hrs after initiation of PCV. Duration of mechanical ventilation, intensive care and hospitalization, complications, and mortality also were noted. Complications evaluated included pneumothorax, pneumomediastinum, subcutaneous emphysema, the need for fluid resuscitation and vasopressor agents, and neurologic morbidity. Fluid resuscitation was provided for hypotension and/or clinical impression of hypovolemia (cold, clammy extremities and decreased urine output). Vasopressor agents were started for hypotension resistant to fluid resuscitation. Statistical Analysis. Categorical variables are represented by the absolute count and percentage in each category. Continuous variables are represented by the median and range. Both capillary and arterial blood gas values were used for analysis of pH and PCO2. Since all patients received albuterol nebulization with 100% oxygen delivered through the inspiratory limb of the ventilator, the actual FIO2 delivered to the patient could not be accurately determined. Therefore, PaO2/FIO2 values were omitted from statistical interpretation. Blood gas measurements over time were compared using Wilcoxon signed ranks test. We considered p ⬍ .05 to be significant. RESULTS During the study period, 278 patients were admitted to the ICU for management of status asthmaticus. Of these, 56 episodes in 45 patients received mechanical ventilation. Four patients were rapidly weaned off mechanical ventilation and extubated within 4 hrs of admission and were excluded from the analysis. One patient sustained cardiorespiratory arrest at home, was resuscitated, but was clinically brain dead on arrival to the ICU and also was excluded from analysis. The remaining 40 patients were admitted for 51 episodes of status asthmaticus; 34 patients were admitted once, two patients were admitted twice, three patients were admitted three times, and one patient was admitted four times. Twenty-one patients (41%) were intubated and mechanically ventilated for respiratory acidosis, 19 (37%) for clinical impression of fatigue, and 11 (22%) for respiratory arrest. Baseline characteristics of patients are shown in Table 1. The racial distribution of patients reflects our referral base for medical/surgical emergencies. Medical therapy administered before and during institution of PCV is shown in Table 2. All episodes were managed with sedatives and analgesics, and 46 episodes were managed with neuromuscular blocking agents from the initiation of PCV. Sedation and analgesia were achieved with midazolam and morphine. Ketamine was used as an adjunct sedative in six patients. Vecuronium was used for pharmacologic paralysis. All episodes were treated with inhaled albuterol and intravenous corticosteroids, and 94% received intravenous theophylline (7). Sodium bicarbonate or tris-(hydroxymethyl) aminomethane was administered in 11 episodes for metabolic acidosis. Antibiotics were given in five episodes for suspected bacterial infection. Arterial catheters were placed in 45 episodes. Bronchoscopy was performed in five for management of mucus plugging. Ventilator settings that achieved the most satisfactory gas exchange within the first 8 hrs in age groups 1–5 yrs, 6 –10 yrs, and 11–18 yrs are shown in Table 3. Blood pH and PCO2 on admission and at 1, 4, 8, and 12 hrs after institution of PCV are shown in Table 4. Seven patients had PCO2 ⬍45 torr, 21 patients (41%) had PCO2 between 45 and 70 torr, 12 patients (24%) had PCO2 between 71 and 99 torr, and eight patients (16%) had PCO2 ⱖ100 torr before initiation of PCV. Blood gases were not obtained before PCV in three patients because emergent intubation and mechanical ventilation were clinically deemed necessary. Of the ten patients with PCO2 ⬍45 torr or nondocuPediatr Crit Care Med 2004 Vol. 5, No. 2 Table 1. Baseline characteristics (n ⫽ 51) Age, yrs Males Race African-American White Hispanic Reason for intubation Respiratory arrest Respiratory acidosis Clinical impression of fatigue Previous ICU admission for status asthmaticus Previous mechanical ventilation for status asthmaticus Home medications Inhaled -agonists Inhaled corticosteroids Oral corticosteroids Theophylline Referral source Emergency room General ward Another hospital a 9.0 (0.8–17) 32 (63)b 49 (96) 1 (2) 1 (2) 11 (22) 21 (41) 19 (37) 26 (51) 18 (35) 51 (100) 19 (37) 4 (8) 6 (12) 26 (51) 5 (10) 20 (39) ICU, intensive care unit. a Data are median (range); bdata are absolute counts (%). Table 2. Medical therapies (n ⫽ 51) Inhaled Albuterol Ipratropium bromide Isoproterenol Helium-oxygen Intravenous Corticosteroids Theophylline Isoproterenol Magnesium sulfate Ketamine Terbutaline Subcutaneous Epinephrine Terbutaline Before PCV During PCV 51 (100) 21 (41) 8 (16) 0 51 (100) 24 (47) 0 25 (49) 51 (100) 28 (55) 6 (12) 7 (14) 0 3 (6) 51 (100) 48 (94) 21 (41) 9 (18) 6 (12) 0 33 (65) 3 (6) 0 0 PCV, pressure-controlled ventilation. Data are absolute counts and percentages. mented PCO2 before PCV, eight were intubated for clinical impression of respiratory fatigue and two for respiratory arrest. Noninvasive ventilation was not used in any of these patients. For patients with PCO2 ⬎45 torr within 1 hr of starting PCV, the median length of time until PCO2 decreased to ⬍45 torr was 5 hrs (1–51 hrs). SpO2 was maintained above 95% in all patients throughout the ICU stay. Patients were weaned from mechanical ventilation by decreasing the PCV synchronized intermittent mandatory ventilation rate in 28 episodes, by providing pressure support in eight episodes, by changing to VCV in five episodes, and by Pediatr Crit Care Med 2004 Vol. 5, No. 2 combining VCV with pressure support in ten episodes. The duration of mechanical ventilation was 29 hrs (4 –107 hrs), intensive care 56 hrs (17–183 hrs), and hospitalization 5 days (2–20 days). Complications encountered are shown in Table 5. Of note, fluid resuscitation was provided in 78% of episodes. Two patients had pneumomediastinum at admission before institution of PCV. In both patients, pneumomediastinum resolved during PCV. One patient each developed pneumothorax and subcutaneous emphysema after initiation of PCV. Subcutaneous emphysema resolved spontaneously and pneumothorax resolved after insertion of a single chest tube while PCV was continued. All patients survived without neurologic morbidity including polyneuropathy associated with the use of steroids and neuromuscular blocking agents. DISCUSSION Despite maximum medical therapy, mechanical ventilation may be needed to manage respiratory insufficiency resulting from airway obstruction in severe status asthmaticus. Mechanical ventilation in patients with airway obstruction may be associated with significant morbidity and mortality rates. The goal of mechanical ventilation in status asthmaticus is two-fold: to provide sufficient gas exchange to ensure survival until reversal of airway obstruction is accomplished, and to minimize complications associated with such support. The two modes of mechanical ventilation that are com- monly used are PCV and VCV. In PCV, a predetermined airway pressure is maintained for a set period of inspiratory time. The delivered tidal volume depends on airway resistance and dynamic compliance. In VCV, a predetermined tidal volume is delivered throughout the inspiratory phase. The resultant peak airway pressure is a dependent variable determined by airway resistance and dynamic compliance. Dynamic compliance is greatly influenced by flow-resistive properties of the lung. In diseases with increased airway resistance, dynamic compliance can be sharply reduced at higher respiratory rates because of an increase in air flow. Another important consideration in mechanical ventilation is that of time constant, a product of static compliance and resistance. Time constant is a reflection of the amount of time that is necessary for equilibration of proximal airway pressure and alveolar pressure. Asthma is a predominantly obstructive airway disease characterized by long time constant requiring a relatively long time for approximation of pressure at proximal airway and alveoli during inspiration and expiration. Expiratory time constant is prolonged even more because of a greater increase in expiratory resistance resulting from an upstream (closer to the terminal airways) displacement of the equal pressure point and narrowing of airways during expiration. As opposed to disorders of static compliance with short time constants such as acute respiratory distress syndrome that can be managed with relatively faster respiratory rates, disorders of resistance such as asthma require relatively slow rates for adequate ventilation. Insufficient inspiratory time would result in decreased tidal volume, whereas incomplete exhalation would result in dynamic hyperinflation and auto positive end-expiratory pressure. Ventilator strategies for patients with asthma should include relatively low respiratory rates with long expiratory times. The degree of airway obstruction is not uniform in asthma and varies in different lung units. Thus, there may be considerable regional variation in time constants. It could be argued that in status asthmaticus, PCV is a better strategy than VCV, which is the traditionally recommended mode of ventilation (2– 4). With VCV, tidal volume is delivered at a relatively constant flow rate so that relatively less obstructed airways with shorter time constants are likely to receive more volume throughout inspira135 Table 3. Optimal ventilator settings 1–5 Yrs (n ⫽ 20) 36 (20–45) 14 (10–20) 1.0 (0.6–1.2) 1:4 (1:3–1:5) 4 Peak inspiratory pressure, cm H2O Rate, breaths/min Inspiratory time, secs I:E ratio PEEP, cm H2O 6–10 Yrs (n ⫽ 13) 11–18 Yrs (n ⫽ 18) 38 (26–49) 12 (10–14) 1.0 (1.0–1.25) 1:4 (1:3–1:5) 4 40 (30–60) 12 (8–12) 1.2 (1.0–1.8) 1:4 (1:2–1:5) 4 I:E, inspiratory/expiratory; PEEP, positive end-expiratory pressure. Data are median (range). Table 4. Blood gas values over time pH PCO2, torr Before PCV Within 1 Hr of PCV 4 Hrs After PCV 8 Hrs After PCV 12 Hrs After PCV 7.21 (6.65–7.39) (n ⫽ 48) 65 (29–264) (n ⫽ 48) 7.22 (6.95–7.47) (n ⫽ 51) 59 (24–115) (n ⫽ 51) 7.31a (6.98–7.45) (n ⫽ 51) 41a (21–118) (n ⫽ 51) 7.34a (7.07–7.49) (n ⫽ 46) 38a (23–98) (n ⫽ 46) 7.38a (7.17–7.55) (n ⫽ 43) 37a (16–76) (n ⫽ 43) PCV, pressure-controlled ventilation. a p ⬍ .01 by Wilcoxon’s signed ranks test compared with values obtained before PCV. Data are median and range. Table 5. Outcomes (n ⫽ 51) Duration of mechanical ventilation, hrs Duration of ICU stay, hrs Duration of hospitalization, days Complications Need for fluid resuscitation Need for vasopressors Pneumothorax Pneumomediastinum Subcutaneous emphysema Neurologic morbidity Death 29 (4–107)a 56 (17–183) 5 (2–20) 40 (78)b 4 (8) 1 (2) 0c 1 (2) 0 0 a Data are median (range); bdata are absolute counts (%); ctwo patients had pneumomediastinum before initiation of pressure-controlled ventilation. tion compared with more obstructed airways with longer time constants. This will result in uneven ventilation, higher peak inspiratory pressure, and decrease in dynamic compliance. With PCV, because of the constant inflation pressure, relatively less obstructed lung units with shorter time constants will achieve pressure equilibration during early inspiration and more obstructed areas with longer time constants will continue to receive additional volume in late inspiration. This will result in more even distribution of inspired gas, delivery of more tidal volume for the same inflation pressure, and improved dynamic compliance. There are isolated case reports of PCV and pressure support ventilation in patients with status asthmaticus who required mechanical ventilation (6, 8). This is the 136 only study reported that describes the use of PCV exclusively in managing severe respiratory failure from status asthmaticus. It is also the second largest study describing the outcome of children with status asthmaticus who were intubated and mechanically ventilated. Risk factors for intubation in asthmatics include psychosocial problems, family dysfunction, low socioeconomic status, second-hand smoke exposure, parental history of allergy, prior intubation, intercurrent respiratory infection, prior hospitalization for asthma in the past year, excessive use of 2-agonist inhalers, and steroid dependence (9 –11). A number of these risk factors were evident in our patients (Table 1). Most children with status asthmaticus are medically managed without intubation and mechanical ven- tilation. Mechanical ventilation is most often reserved for children with actual or impending respiratory failure. Of 278 patients with status asthmaticus admitted to the ICU during the study period, only 56 (20%) required intubation. These findings are similar to those of Roberts et al. (12), who reported a 17% incidence of mechanical ventilation in asthmatic children from 11 pediatric ICUs. Little information is available in the literature regarding the specific indications for intubation in patients with asthma. Stein et al. (13) reported that 10% of asthmatic children intubated in the ICU had preceding respiratory arrest. Among adult studies, approximately 50% of asthmatics requiring intubation had cardiopulmonary arrest or coma (14, 15). It has been suggested that mechanical ventilation itself may be a cause of mortality and morbidity in patients with acute severe asthma. Studies of patients with severe asthma who received mechanical ventilation during the 1970s and 1980s have reported mortality rates as high as 23–38% (16 –18). More recent studies suggest that the mortality rate for ventilated asthmatics may be decreasing (19, 20). The greatest threats to survival in such patients are ineffective oxygenation and ventilation, and barotrauma. Darioli and Perret (21) proposed using permissive hypercapnia to minimize barotrauma in patients with asthma who need mechanical ventilation. Purported benefits of hypercapnia include a reduction in lung stretch, dilation of small airways, improvement in collateral ventilation, and attenuation of inflammatory processes (12). Several authors have reported decreased mortality rates with the use of controlled hypoventilation (14, 19, 20). However, there are no controlled studies demonstrating benefits of permissive hypercapnia compared with normocapnia. Moreover, hypercapnia and the resultant respiratory acidosis may be associated with undesirable consequences such as decreased catecholamine responsiveness, blunting of the effects of bronchodilators (22, 23), and increased intracranial pressure. We aimed at achieving normocapnia in our patients using the pressure control, respiratory rate, inspiratory time, and expiratory time required to deliver the necessary tidal volume and minute alveolar ventilation. More than 80% of our patients had PCO2 ⬎45 torr before the institution of PCV. All these patients had a steady decline in PCO2 after institution of PCV. All patients Pediatr Crit Care Med 2004 Vol. 5, No. 2 O ur retrospective study of 51 episodes in 40 pa- tients demonstrates the efficacy of pressure-controlled ventilation in treating children with acute respiratory failure from severe status asthmaticus. Pressure-controlled ventilation represents a therapeutic option in the management of such children. survived to be discharged from the hospital. The median duration of ventilation in our patients was 29 hrs (mean, 30 hrs; range, 4 –107 hrs). This compares favorably with that reported in other studies. Malmstrom et al. (24) reviewed the records of 59 children admitted on 66 occasions to the ICU who received mechanical ventilation for severe asthma. The details of the mode of ventilation or the ventilatory strategy were not mentioned. The mean duration of mechanical ventilation was 51 hrs with a range of 6 –216 hrs (24). Two other studies employing VCV as the mode of ventilation reported the mean duration of mechanical ventilation to be 23.9 hrs (range, 1.5–78 hrs) and 54 hrs (range, 20 –185 hrs) (25, 26). Studies in children combining VCV and permissive hypercapnia documented the mean duration of mechanical ventilation to be 32–54.3 hrs (4, 13, 27, 28). The duration of mechanical ventilation in adults with severe asthma is much longer, and the mean duration ranges from 36.1 hrs to 4.9 days (14, 15, 21, 29 –31). The median time for the PCO2 to return to normal was 5 hrs (1–51 hrs) in this study. This was considerably less than that reported by Dworkin and Kattan (28) (20.1 hrs) and Shugg et al. (27) (14.9 hrs), who used VCV and controlled hypoventilation in children with status asthmaticus. Pediatr Crit Care Med 2004 Vol. 5, No. 2 Despite eschewing permissive hypercapnia, the incidence of barotrauma (4%) was relatively low in our patients. It is of note that another two (4%) patients had pulmonary airleak before initiation of PCV. Furthermore, the pulmonary airleak in our patients was easily managed and still allowed continuation of PCV mode. In pediatric studies that used VCV without controlled hypoventilation, the incidence of barotrauma was 16 –33% (25, 26). Studies using permissive hypercapnia and limited peak inflation pressures reported the incidence of barotrauma ranging from zero in one study (24) to 15–20% in others (4, 13, 27, 32). The corresponding rates of barotrauma in adults who received VCV for asthma, with and without controlled hypoventilation strategies, were 4 –27% (14, 15, 19 –21) and 2–18% (29, 30), respectively. The incidence of barotrauma in our study using PCV strategy aimed at achieving normocapnia compares favorably with that reported in the literature. A large percentage (78%) of patients exhibited circulatory compromise manifested by cool, clammy extremities and reduced urine output. Circulatory compromise may have resulted from positive pressure ventilation, preexisting hypovolemia secondary to poor oral intake and increased insensible water losses, and increased venous capacitance following the use of sedative and paralytic agents. Patients with circulatory compromise improved after intravascular volume expansion with isotonic fluids. No other complications attributed to mechanical ventilation were encountered. A low tidal volume, high ventilatory rate strategy has been shown to be effective in reducing mortality rates in patients with acute respiratory distress syndrome (33). It should be noted, however, that acute respiratory distress syndrome is predominantly a disease of low compliance and short time constant as opposed to increased airway resistance as in status asthmaticus. The ventilatory strategy in our study was aimed at attaining a given minute alveolar ventilation necessary to achieve pH ⬎7.30 and PCO2 ⬍50 torr. This was accomplished by a combination of using a pressure control variable, using a relatively low ventilatory rate, and adjusting inspiratory/expiratory time to achieve exhaled tidal volume of 10 –12 mL/kg. Ventilator graphic waveform was continuously monitored to ensure near completion of exhalation to avoid auto positive end-expiratory pressure and decreased dynamic compliance. Older patients required higher peak inspiratory pressure and lower rates. Pressure control was decreased as exhaled tidal volumes increased and PCO2 decreased. Once sufficiently improved, the patients were rapidly weaned off the mechanical support by withdrawing pharmacologic paralysis and allowing spontaneous respirations in PCV or VCV modes with or without pressure support and decreasing the synchronized intermittent mandatory ventilation rate. Our retrospective study of 51 episodes in 40 patients demonstrates the efficacy of PCV in treating children with acute respiratory failure from severe status asthmaticus. PCV represents a therapeutic option in the management of such children. Randomized controlled trials are needed to compare the efficacy and complications of PCV and VCV. Furthermore, the superiority of normocapnic vs. hypercapnic strategy regarding duration of mechanical ventilation and complications needs to be investigated. REFERENCES 1. McCormick MC, Kass B, Elixhauser A, et al: Annual report on access to and utilization of health care for children and youth in the United States-1999. Pediatrics 2000; 105: 219 –230 2. Ackerman VL, Eigen H: Lower airway disease. In: Pediatric Critical Care. Second Edition. Fuhrman BP, Zimmerman JJ (Eds). St. Louis, MO, Mosby, 1998, pp 472– 476 3. Mutlu GM, Factor P, Schwartz DE, et al: Severe status asthmaticus: Management with permissive hypercapnia and inhalation anesthesia. Crit Care Med 2002; 30:477– 480 4. Cox RG, Barker GA, Bohn DJ: Efficacy, results, and complications of mechanical ventilation in children with status asthmaticus. Pediatr Pulmonol 1991; 11:120 –126 5. Werner HA: Status asthmaticus in children. A review. Chest 2001; 119:1913–1929 6. Lopez-Herce J, Gari M, Bustinza A, et al: To the editor: On pressure-controlled ventilation in severe asthma. Pediatr Pulmonol 1996; 21:401– 403 7. Yung M, South M: Randomized control trial of aminophylline for severe acute asthma. Arch Dis Child 1998; 79:405– 410 8. Wetzel RC: Pressure-support ventilation in children with severe asthma. Crit Care Med 1996; 24:1603–1605 9. LeSon S, Gershwin ME: Risk factors for asthmatic patients requiring intubation: A comprehensive review. Allergol Immunopathol (Madr) 1995; 23:235–247 10. LeSon S, Gershwin ME: Risk factors for asth- 137 11. 12. 13. 14. 15. 16. 17. 138 matic patients requiring intubation. I. Observations in children. J Asthma 1995; 32: 285–294 Limthongkul S, Wongthim S, Udompanich V, et al: Status asthmaticus: An analysis of 560 episodes and comparison of mechanical and non-mechanical groups. J Med Assoc Thai 1990; 73:495–501 Roberts JS, Bratton SL, Brogan TV: Acute severe asthma: Differences in therapies and outcomes among pediatric intensive care units. Crit Care Med 2002; 30:581–585 Stein R, Canny GJ, Bohn DJ, et al: Severe acute asthma in a pediatric intensive care unit: Six years’ experience. Pediatrics 1989; 83:1023–1028 Kearney SE, Graham DR, Atherton ST: Acute severe asthma treated by mechanical ventilation: A comparison of the changing characteristics over a 17 yr period. Respir Med 1998; 92:716 –721 Braman SS, Kaemmerlen JT: Intensive care of status asthmaticus: A 10-year experience. JAMA 1990; 264:366 –368 Picado C, Montserrat JM, Roca J, et al: Mechanical ventilation in severe exacerbation of asthma. Eur J Res Dis 1983; 64:102–107 Webb AK, Bilton AH, Hanson GC: Severe bronchial asthma requiring ventilation. A review of 20 cases and advice on management. Postgrad Med J 1979; 55:161–170 18. Scoggin CH, Sahn SA, Petty TL: Status asthmaticus. A nine-year experience. JAMA 1977; 238:1158 –1162 19. Bellomo R, McLaughlin P, Tai E, et al: Asthma requiring mechanical ventilation: A low morbidity approach. Chest 1994; 105:891– 896 20. Williams TJ, Tuxen DV, Scheinkestel CD, et al: Risk factors for morbidity in mechanically ventilated patients with acute severe asthma. Am Rev Respir Dis 1992; 146:607– 615 21. Darioli R, Perret C: Mechanical controlled hypoventilation in status asthmaticus. Am Rev Respir Dis 1984; 129:385–387 22. Blumenthal JS, Blumenthal MN, Brown EB, et al: Effect of changes in arterial pH on the action of adrenaline in acute adrenaline-fast asthmatics. Dis Chest 1961; 39:516 –522 23. Mithoefer JC, Runser RH, Karetzky MS: The use of sodium bicarbonate in the treatment of acute bronchial asthma. N Engl J Med 1965; 272:1200 –1203 24. Malmstrom K, Kaila M, Korhonen K, et al: Mechanical ventilation in children with severe asthma. Pediatr Pulmonol 2001; 31: 405– 411 25. Wood DW, Downes JJ, Lecks HI: The management of respiratory failure in childhood status asthmaticus. Experience with 30 episodes and evolution of a technique. J Allergy 1968; 42:261–268 26. Simons FER, Pierson WE, Bierman W, et al: 27. 28. 29. 30. 31. 32. 33. Respiratory failure in childhood status asthmaticus. Am J Dis Child 1977; 131: 1097–1101 Shugg AW, Kerr S, Butt WW: Mechanical ventilation of paediatric patients with asthma: Short- and long-term outcome. J Paediatr Child Health 1990; 26:343–346 Dworkin G, Kattan M: Mechanical ventilation for status asthmaticus in children. J Pediatr 1989; 114:545–549 Luksza AR, Smith P, Coakley J, et al: Acute severe asthma treated by mechanical ventilation: 10 years experience from a district general hospital. Thorax 1986; 41:459 – 463 Higgins B, Greenining AP, Crompton GK: Assisted ventilation in severe acute asthma. Thorax 1986; 41:464 – 467 Zimmerman JL, Dellinger RP, Shah AN, et al: Endotracheal intubation and mechanical ventilation in severe asthma. Crit Care Med 1993; 21:1727–1730 Simpson H, Mitchell I, Inglis JM, et al: Severe ventilatory failure in asthma in children. Arch Dis Child 1978; 53:714 –721 The Acute Respiratory Distress Syndrome Network: Ventilation with lower tidal volumes as compared with traditional tidal volumes for acute lung injury and the acute respiratory distress syndrome. N Engl J Med 2000; 342:1301–1308 Pediatr Crit Care Med 2004 Vol. 5, No. 2