Indian J Pediatr 1993; 60 : 109-117

Mechanical Ventilation in Pediatrics Praveen K h i l n a n i

Pediatric Intensive Care Unit, Henrico Doctors' Hospital, Richmond, Virginia, U.S.A hildren are not miniature adults.

C This statement holds true while treat ing a child with respiratory failure requiring mechanical ventilation. A knowledge of the physiologic differences is hllportant to understand the principles uf mechanical ventilation in pediatric patients. Respiratory bronchioles, alveolar ducts and alveoli grow in number until 8 years of age, and continue to grow hi size until adulthood. 1'2 Pores of Kohn coculecting alveoli are not developed until 1 year of age, and Channels of Lambert which connect alveoli to larger airways do not develop until 5 years of age.3-5 This results in poor collateral gas circulation in the airways and alveoli. In children, the majority of airway resistance lies in lower airways as compared to adults where nasal passages alone may be responsible for 60% of total airway resistance. Furthermore, due to softer cartilage supporting the airway, collapse of the airway is more common with relatively smaller changes of airway pressure. 6 Children have a relatively ~nlall functional residual capacity (-TolUnle of air in the lungs at the end of nornlal expiration), and a higher oxygen COnsumption compared to adults. Theretore, normal children tend to have relaI~eprint requests : Dr Praveen Khilnani, Director, Pediatric Intensive Care Unit, Henrico Doctors' Hospital, 1602 Skipwith Road, Richmond, VA 23229, U.S.A.

tively shallow breaths at a rate higher than adults. When a child is in respiratory distress, the respiratory rate increases ultimately progressing to slowing respirations, progressing to gasping followed by apnea or cardiorespiratory arrest. It is therefore extremely important to recogulize tachypnea, agitation, nasal flaring, grunting, retractions as early signs of hypoxemia and respiratory failure. Cyanosis, lethargy and bradycardia are late signs dangerously close to cardiorespiratory arrest. Close monitoring of the patients' clinical status, and appropriate initiation of respiratory support and mechanical ventilation in this group of patients can prevent mortality, and in most cases significant morbidity. Mechanical Ventilation - Basic C o n c e p t

Movement of air in and out of the lungs is initiated by generating a pressure differential between mouth pressure and alveolar pressure. This can be achieved by decreasing alveolar pressure (negative pressure ventilation, spontaneous breathing) or by increasing mouth pressure (positive pressure ventilation). 8 (Table 1.) Mechanical ventilation cycle consists of an inspiratory phase and an expiratory phase._ 1. Inspiratory Phase This essentially consists of three components: initiation, maintenance and termi-

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TABLE1. Indications for Mechanical Ventilation Resuscitation after cardiac arrest/ circulatory failure Hypoventilation and apnea Respiratory failure due to lung disease Neuromuscular diseases causing muscle wee kness or paralysis Elective hyperventilation for increased intracranial pressure Postoperative/anesthetic recovery

nation of inspiratory phase. Initiation of inspiratory phase may be, (i) controUed when: ventilator controls all the ventilation while the patients has minimal or no respiratory effort; (ii) IMV (Intermittent Mandatory Ventilation). 7 This mode is incorporated to enable the patient to breathe spontaneously while being mechanically ventilated at a preset rate; (iii) Patient Triggered: Negative pressure generated by the spontaneously breathing patient triggers the ventilator to begin inspiratory flow to the patient. It is important to understand the difference between controlled vs. IMV (Intermittent M a n d a t o r y Ventilation) modes of ventilation. IMV mode essentially ensures that the gas flow from the ventilator is continuous at all ventilator settings. If the patient were to start breathing spontaneously while being mechanically ventilated, :the patient can get inspiratory,flow c o n t i n u o u s l y as compared ,to,controlled m o d e when the gas flow from the ventilator occt~rs only during the inspiratory phase of the cycle. Therefore, during controlled ventilation, the patient gets n o flow during.spontaneous inspiratory effort.

Inspiratory phase is maintained by a forward gas flow which can be generated by tile ventilator working as a constant or nonconstant pressure or flow generator. Inspiratory phase can be terminated when a preset volume is delivered (volume cycling) or a preset inspiratory time limit is reached (time cycling), or a preset pressure is reached (pressure cycling) (Table 2). In neonates (Sechrist ventilator), both time and pressure cycling is commonly used. In respiratory distress syndrome (hyaline membrane disease), initially the lung compliance is low; therefore, higher peak inspiratory pressure (PIP) is required to deliver the necessary tidal volume. As the lung compliance improves, the same preset PIP achieves a higher tidal volume. Therefore, PIP needs to be weaned to prevent over inflation of fl~e lungs and pneumothorax. Volume cycling is difficult to use in neonates because of smaller tidal volumes (50-60 cc), leak around endotracheal tube, and volume lost in air compression in circuit (compressible volume)? In older children (> 10 kg), volume cycling is preferable due to proportionally small compressible volume relative to larger tidal TABLE2. Commonly Used Ventilators in Pediatric Intensive Care Unit Pressure and Time Cycled Ventilators Baby Bird Bournes BP~200 Sechrist Healthdyne Siemens-Serve Biomed Newport

Volume Cycled Ventilators Bennett MA - I MA - II Engstrom Emerson Newport

1993;Vol.60. No. 1 volumes. Furthermore, cuffed endotracheal tubes may be used in older children to minimize the leak around the tube. Volume cycling is indicated when airway resistance is high (asthma, bronchiolitis) or when pulmonary compliance is very low (pulmonary edema, adult respiratory distress syndrome). In these cases, pressure cycled ventilators may not consistently deliver an adequate lidal volume at a given PIP if the compliance gets worse, or airway resistance increases due to bronchospasm or secretions. The main disadvantage of pressure cycling is inadequate ventilation if airway resistance increases, or compliance decreases because same preset pressure will reach earlier (at a lower tidal volume). The main disadvantage of volume cycling is inadequate ventilation if the circuit has a leak (volume is lost), or if the circuit is too long or too compliant, volume may be lost in expanding the circuit or due to compression (compressible volume). Adult circuit compliance is 4 ml/cm H20 (4 ml volume is lost for every cm H20 increase in peak airway pressure). In pediatrics, this could be a significant volume lost in compression. It is therefore recommended that pediatric circuit compliance should be no more than I m l / c m H20.1~ The duration of inspiratory phase can be controlled by regulating the inspiratory time. Once a particular inspiratory time has been set, frequency of ventilation can be changed by changing the expiratory time. Normally, the minimum recommended inspiratory time is 0.5 sec. Higher inspiratory times are required in diseases where airway resistance is high or the compliance is very low to deliver

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adequate tidal volume and improve oxygenation by increasing mean airway pressure (Figure 1). The purpose is to fill the alveoli with higher time constants (Table 3). One time constant is the time required to fill 63% of alveolus given a constant gas flow (average time constant in infants = 0.15 sec.). Normally, three to five times constants are required to fill an alveolus to its capacity. (0.45-0.75 sec.) lnspiratory times higher than I sec., although occasionally used, pose an increased risk of pneumothorax specially when inspiratory time exceeds the expiratory time. Normally recommended I : E (Inspiratory : Expiratory) ratio is 1 : 2. It is important to remember whether inspiratory phase is terminated by volume, pressure or time cycling, the goal of ventilation can be achieved if the fol-

E

o.9.

20-

10.

~

0

f 6

.%4 3

Seconds

Fig. !. Factors that improve mean airway pressure during mechanical ventilation are : (i) increased inspiratory flow rate; (i0 increased peak inspiratory pressure (PIP); (iiO increased inspiratory time; (iv) increased PEEP; (v) increased ventilator rate. Area under curve represents the mean airway pressure. (Reproduced with permission from Goldsmith JP and Karotkin EH, editors. Assisted Ventilation of ~he Neonate, Philadelphia: WB Saunders Co, 1988.

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THE INDIANJOURNALOF PEDIATRICS TABLE3. Time Constant

A measure of how quickly an alveolar unit fills (or empties). Resistance x compliance One time constant fills it 63% Two time constants fill it 87% Three time constants fill it 95% Three to five constants are required to fill or empty an alveolus lowing criteria are met: (i) adequate chest rise (indicating adequate tidal volume) during inspiration; (ii) normal colour and oxygen saturation; (iii) absence of acidosis, hypercarbia or hypoxia on arterial blood gases.

2. Expiratory phase

1993;Vol. 60. No. 1 e m p h y s e m a (PIE) m a y also occur. 13 PEEP should be avoided in situations where the patient has hypovolemia, pneumothorax, increased intracranial pressure, pericardial tamponade or air trapping (asthma). Long expiratory time, three to four times that of inspiratory time may be needed in conditions with air trapping such as asthma to give time for adequate emptying of the alveoli.

3. Initial Ventilator Settings Regardless of the age of the patient or the lung condition, hand bagging with anesthesia (Mapleson type) bag with in line airway pressure manometer can be Used to assess the peak airway pressure required to achieve adequate chest expansion. This is by far the best clinical method to get a feel fo~ lung and chest compliance. Based on the above information, approximate initial ventilator setting s can be chosen. Following guidelines (Table 4) may be used to select initial ventilator settings depending on tile age of the patient and lung pathology. Oxygen saturation, adequate chest rise and blood gases should then be monitored, and the ventilator settings may be adjusted accordingly.

Expiration is a passive process in most ventilators. Currently, all the ventilators being manufactured have the capability of delivering PEEP (Positive End Expiratory Pressure) 11 as well as CPAP (Continuous Positive Airway Pressure). n PEEP prevents complete deflation (collapse) of alveoli during expiration and improves the distribution of volume to slow alveoli which have longer time constants (recruitment). PEEP also increases the m e a n airway pressure thereby improving oxygenation. Main 4. Respiratory Care and Monitoring 14"1~ indications for the use of PEEP are All patients on the ventilator need repneumonia, atelectasis, ARDS (Adult peated assessment of oxygenation and Respiratory Distress Syndrome) and ventilation. PaO 2 and oxygen saturations pulmonary edema. PEEP values higher are good indicators of oxygenation. than 10 cm of water m a y decrease PaCO 2 is the best indicator of ventilation. cardiac output by compressing the heart Arterial blood gases may be d r a w n from (Tamponade effect) and by reducing the anindwelling arterial line. Clinically, the venous return to the heart. Barotrauma importance of monitoring chest moveresulting in pneumothorax, pneumome- ments and breath sounds cannot be diastinum and p u l m o n a r y interstitial overemphasized.

1993;Vol.60. No. 1

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TABLE4. Guidelines for Initial Ventilator Settings Tidal volume Rate Inspiratory I:E Ratio PEEP PIP (Cm (ml) (breaths/min)time (sec) (Cm of H20 ) of H20 ) Hyaline membrane disease, * Pneumonia Meconium aspiration * syndrome RSV Bronchiolitis 10-15 ml/kg Asthma 10-15 ml/kg Pulmonary edema 10-15 ml/kg Adult respiratory distress 10-15 ml/kg syndrome Head injury 10-15 ml/kg Congestive heart failure 10-15ml/kg ~r :t.~b

20-30

0.6-1

1:2

4-6

20-25

30-40

0.6-1

1:2

5-7

25-30

20-25 15-20 20-25 20-25

0.5 0.5 0.6-0.8 0.6-0.8

1:3 1:4 1:2 1:2

4-5 0-2 6-8 8-10

** ** ** **

25-30 20-25

0.5 0.6-0.8

1:2 1:2

0-2 4-5

** **

Determined by flow, inspiratory time and preset pressure; Determined by preset tidal volume.; PEEP Positive end expiratory pressure.

Inspired gases should be adequately humidified. Cascade type or high molecular output heated humidifiers, and heated inspiratory and expirtory tubing to minimize water condensation within the system may be used. All ventilators should have an inspiratory line pressure alarm to detect excessive airway pressure, obstruction and sudden loss of pressure (ventilator disconnect or circuit leak). Alarms for gas supply, apnea, inspired 0 2 concentration and gas temperature are also desirable. When using a cuffed endotracheal tube, cuff presSures must be checked frequently. High volume low.pressure cuffs are currently recommended. Cuff pressures greater than 20 cm H20 predispose to tracheal Tnucosal ischemia with subsequent necrosis. As a general rule, cuff should b e inflated just enough to obliterate the leak around the endotracheal tube. Frequent Suctioning of the endotracheal tube is r~ecessary to ensure patency of the tube.

The endotracheal tube should be well secured, and placement should be checked to prevent later right mainstem bronchial intubation, or accidental extubation. Flexion at the neck advances the endotracheal tube further in the trachea, hyperextension at the neck may increase the risk of accidental extubation. If PEEP greater than 10 cm of H20 is used (e.g. ARDS), hemodynamic monitoring may be required to monitor cardiac output by placing a pulmonary artery catheter. A need for daily chest x-rays should be individualized. Sedative agents and muscle relaxants are frequently needed in the pediatric intensive care unit to enable effective ventilation. These medications can be used on an intermittent dosing schedule or as a continuous infusion (Table 5). Usually sedation alone is sufficient. In patients requiring maximal ventilatory support and higher oxygen concentration, muscle relaxants m a y

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have to be used in addition to sedatives. 15 It is important to understand that agitation frequently results from hypoxemia. Causes of hypoxemia should be looked for (i.e., mucus plug obstruction, right mainstem bronchus intubation or atelectasis) and treated. In most cases, agitation does not require further sedation to prevent the patient from "fighting the ventilator." Chest physical therapy (percussion, vibration) and postural drainage with frequent suctioning are important maneuvers to keep the upper and lower airways clear of secretions, as well as to prevent atelectasis. I6 5. Weaning from Mechanical Ventilationl~,18 Weaning from the ventilator essentially requires a patient with improving clinical condition supported by improved

blood gases, oxygen saturation and chest X-rays. Normal fluid and electrolyte balance in addition to normal neurological and cardiovascular status are vital for predicting successful weaning and extubation. Once these criteria are met and the child has a decreasing 0 2 requirement with normal oxygen saturations, decreased secretions, absence of nasal flaring or suprasternal and intercostal retractions, extubation can usually be accomplished (Table 6). There is no standard technique of weaning. As a general rule, all ventilator parameters and inspired oxygen concentrations have to be reduced to minimal levels before mechanical ventilation is discontinued. When ventilating with a pressure cycled ventilator, peak inspiratory pressures can be weaned step wise alternating with the ventilator rate. Weaning of oxygen concentration should

TABL~5. Sedatives and Muscle Relaxants in P1CU Sedative Analgesics Intravenous Dose Duration of Action

Continuou~ Infusion

Midazolam

0.05-0.1 mg/kg

2 hours

Fentanyl

2-10 mcg/kg*

30-60 min.

Morphine

0.1 mg/kg

4 hours

Loading dose 0.05 mg/kg IV Maintenance 0.025 mg/kg/hr Loading dose 2-10 mcg/kg IV Maintenance 1-5 mcg/kg/hr Loading dose 0.05-0.1 mg IV Maintenance 0.02 mg/kg/hr

Lorazepam Diazepam Phenobarbital

0.05-0.1 mg/kg 0.1-0.2 mg/kg 2-3 mg/kg

4-6 hours 4-6 hours 8-12 hours

0.1 mg/kg 0.1 mg/kg 0.5 mg/kg 0.5 mg/kg 1-2 mg/kg

50-60 rain. 25-35 rain. 20-30 rnin.

Muscle Relaxants

Pancuronium Vecuronium Atracurium d-Tubocurarine Succinyl choline

* mcg - micrograms

5-15 rain.

0.1 mg/kg/hr 0.3-0.6 mg/kg/hr

THE INDIANJOURNALOF PEDIATRICS

1993;Vol.60. No. 1 continue simultaneously based on PaO 2 and oxygen saturation. In the authors experience, if peak pressure is weaned below 20 cm of H20, chances of airway closure and atelectasis increase. For example, in a patient w h o has been weaned down to a rate of 15 breaths/rain and PIP of 20 cm of H20, further weaning of rate is appropriate without weaning the PIP any further. The rate should be weaned to 4-6 breaths/min before extubation. While using a volume cycled ventilator, tidal volume and rate should be weaned step by step, and the patient's increased ability to breathe effectively should be closely monitored. As a guide!ine, the ventilator should deliver less than 30% of patient's minute ventilation before successful extubation can be accomplished (minute ventilation = tidal volume x respiratory rate). Some authors recommend the use of CPAP (continuous positive airway pressure) or pressure support ventilation 19 as a further weaning measure before extubation. CPAP enables the patient to breathe spontaneously via a continuous gas flow sufficient to maintain positive airway pressure, so that the patient effort required to initiate the spontaneous inspi-

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ration is minimized. Pressure support ventilation is a relatively new form of assisted ventilation in which the ventilator assists the patient's spontaneous effort by delivering a gas flow to achieve a preset pressure. Inspiratory phase is terminated when the inspiratory gas flow rate reaches a certain low level. Initiation of pressure support breath from the ventilator is entirely dependent on the negative pressure generated by the patient effort to open a demand valve. A back up ventilator rate should therefore be set, should the patient were to stop breathing due to muscle fatigue or central nervous system depression. Pressure support ventilation allows better synchrony between the patient and the ventilator when compared to IMV, pressure or volume cycled ventilation. 2~ It also allows the respiratory muscles to gradually train to bear the increasing load of breathing. An increase in respiratory rate and retractions at a given pressure support setting.indicate, that the patient may n o t .be ready to wean the pressure support any further, and may require a higher level of pressure support to achieve a slower respiratory rate. In the authors experience, pressure

TABLE6. Criteria for Weaning from Mechanical Ventilation General Weaning Criteria

Specific Criteria

Improving lung condition Stable cardiovascular status Improving chest x-rays Decreased secretions Normal hemoglobin Improving nutrition Normal fluid and electrolyte balance Intact airway reflexes

PaO 2 > 60 with FiO2 < 0.3 PaO2 to FiO2 ratio > 200 Vital capacity > 10-15 ml/kg Negative inspiratory force at least 20 cm H20 Minute ventilation < 10 litres/min PEEP < 10 PIP < 20 cm H20 rate < 10

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support ventilation mode is more useful on patients intubated with endotracheal tube size 4 m m or greater. Younger patients intubated with smaller endotracheal tubes have increased airway resistance, which may result in muscle fatigue caused by inability to generate negative pressure to initiate the pressure support breath from the ventilator. It is important to bear in mind that the majority of children will successfully wean from ventilatory support regardless of use of IMV, CPAP, T-tube or pressure support ventilation. Some patients take longer than others to wean. Factors that prolong the weaning process are slow resolution of the underlying disease process or ventilatory pump failure. 21 Various causes of ventilatory pump failure (Table 7) should be kept in mind while weaning. TABLE7. Ventilatory Pump Failure D e c r e a s e d respiratory m u s c l e capacity

Decreased respiratory center output (CNS disorders) Phrenic nerve injury Decreased muscle strength and/or endurance Malnutrition Prolonged neuromuscular blockade Muscle fatigue Electrolyte abnormalities Increased respiratory m u s c l e load Increased work of breathing Hyperinflation Lower airway obstruction Decreased respiratory system compliance Increased ventilatory requirements Increased CO2 production (e.g., excessive carbohydrate intake) Increased dead space Hypercatabolic states (e.g., sepis)

Post-extubation stridor due to laryngeal edema can be treated with intravenous decadron 0.2 m g / k g and racemic epinephrine aerosol treatment. Endotracheal intubation equipment with bag and mask, and suction equipment must be at the bedside before e x t u b a t i o n is attempted. After extubation has been accomplished, frequent clinical examination for signs of respiratory distress (i.e. grunting, retractions, tachypnea) and monitoring of oxygen saturation is necessary. Suctioning of secretions from the airway, chest physical therapy, bronchodilator aerosol treatments, oxygen therapy with humidification may be initially required to prevent the need for early reintubation. REFERENCES

1. Hilsop A, Reid L. Growth and development of the respiratory system. In : Davis JA, Doping J, eds. Scientific Foundations of Pediatrics. London : Heineman, 1974 : pp. 214-215. 2. Inselman LS, Mellins RB. Growth and development of the lung. J Pediatr 1981; 98 : 1-15. 3. Lambert MW. Accessory bronchiole-alveolar communications. J Path Bact 1955; 970 : 311-314. 4. Liebow AA. Recent advances in pulmonary anatomy. In : De Reuek AVS, O'Conner M, eds. Ciba Foundation. Boston : Little Brown and Company, 1962 : pp. 2-28. 5. Reid L. The embryology of the lung. In : De Reuck AVS, Porter R, eds. Ciba Foundation Symposium : Development of the Lung. Boston : Little Brown and Company, 1967 : pp. 109-124. 6. Nunn JF. Resistance to gas flow and airway closure. In : Applied Respiratory Physiology, 3rd edn. London : Butterworths, 1975 : 74-111.

1993;Vol. 60. No. 1 7. Downs JB, Perkins MH, Modell JH. Intermittent mandatory ventilation. Arch Surg 1974; 109 : 519-523. 8. McWilliams BC. Mechanical ventilation in pediatric patients. Clin Chest Med 1987; 8 : 597-609. 9. Robbins L, Crocker D, Smith RM. Tidal volume losses of volume-limited ventilators. Anesthes Analg 1967; 46:428-431. 10. Bartel LP, Bazile JR, Powner DJ. Compression volume during mechanical ventilation: Comparison of ventilators and tubing circuits. Crit Care Med 1985; 13 : 851-854. 1l. Tyler DC. Positive end-expiratory pressure : A review. Crit Care Med 1983; 11 : 300-308. 12. Gregory GA et al. Treatment of idiopathic respiratory distress syndrome with continuous positive airway pressure. N Engl JMed 1971; 284 : 1333-1340. 13. Hall RT, Rhodes PG. Pneumothorax and pneumomediastinum in infants with idiopathic respiratory distress syndrome receiving continuous positive airway pressure. Pediatrics 1975; 55 : 493-548. 14. Chatburn RL, Lough MD. Mechanical ventilation. In: Lough MD, Doershuk CF, Stern RC, eds. Pediatric Respiratory Therapy. Chicago : Year Book Medical Pub-

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lishers, 1985 : pp. 148-191. 15. Crone RK. Assisted ventilation in children. In: Gregory GA, ed. Respiratory Failure in the Child. New York : Churchill Livingstone, 1981 : pp. 17-29. 16. Shapiro BA, Harrison RA, Trout CA. Clinical application of respiratory care, 2nd edn. Chicago : Year Book Medical Publishers, 1979. 17. Tahvanainen J,Salmenpera M,Nikki P. Extubation criteria after weaning from intermittent mandatory ventilation and continuous positive airway pressure. Crit Care Med 1983; 11 : 702-707. 18. Klein EF Jr. Weaning from mechanical breathing with intermittent mandatory ventilation. Arch Surg 1975; 110 : 345-350. 19. Brochard L, Haft A, Lorino H et al. Pressure support decreases work of breathing and oxygen consumption during weaning from mechanical ventilation. Am Rev Resp Dis 1987; 135 (2) : A51. 20. MacIntyre NR. Respiratory function during pressure support ventilation. Chest 1986; 89 : 677-683. 21. Venkataraman ST, Orr RA. Mechanical ventilation and respiratory care. In : Fuhrman BP, Zimmerman JJ, eds. Pediatric Critical Care. St Louis : Mosby Year Book, 1992 : pp. 519-543.