REVIEW ARTICLE |
https://doi.org/10.5005/ijrc-1-1-21 |
Basic neonatal and paediatric mechanical ventilation
Email eribain@yahoo.co.in
Assistant Professor, Department of Respiratory Therapy Manipal College of Allied Health Sciences, Manipal
Professor of Paediatrics and Head, Neonatal Intensive Care Unit, Kasturba Medical College, Manipal
Abstract
Neonatal and paediatric ventilation is highly challenging in respiratory care. Management of the 'little ones' on ventilator is a difficult task. A strong knowledge about basic respiratory physiology and lung mechanics of newborns, gives us the easier application of providing both noninvasive and invasive ventilation. Respiratory distress is mainly assessed by Downes' score, clinical conditions and arterial blood gases. Different modes of ventilation describe the easier ability for gentler ventilation and lung protective strategy. Humidification is essential as the upper airway is bypassed and it can prevent hypothermia. This review will explore the ventilatory support in neonates and paediatric age group.
Keywords: Neonatal, mechanical ventilation, pulmonary physiology, modes of ventilation, humidification.
How to cite this article: Shilla E, Lewis L. Basic neonatal and paediatric mechanical ventilation. Ind J Resp Care 2012; 1:21-7.
Introduction
Neonatal and paediatric mechanical ventilation is currently one of the most clinically challenging situations in respiratory care. The neonatal and paediatric population encompasses a broad range of weight, ages, sizes and diseases. Therefore, ventilator practices can vary widely. Children are not small adults and infants are not small children.1 To manage neonatal and paediatric ventilation effectively, one must combine the principles and knowledge as how airway anatomy, pulmonary physiology and pathophysiology are affected by various diseases. One of the most common reasons for intensive care admission is need for mechanical ventilation for acute or impending respiratory failure.
Since the introduction of mechanical ventilation in neonatology in the 1960s, mortality rates of preterm infants have decreased dramatically.2 The introduction of neonatal intensive care, including mechanical ventilation, during the 1960s and its widespread application in the 1970s was associated with increased survival of very low birth weight infants and was shown to be more cost effective in infants of 1 to 1.5 kg birth weight compared with infants weighing less than 1 kg.3 Assessment of respiratory distress and clinical condition of these neonates is essential in order to support them with positive pressure ventilation. Different modes of ventilation describe the easier ability for gentler ventilation and lung protective strategy. Application of humidification is essential as the upper airway is bypassed.
Basic concepts
Anatomy: Infants are nose breathers because of the large omega-shaped soft epiglottis, positioned high in the larynx (at the level of C4 in the infants versus C6 in the adult). This tends to obscure the laryngeal inlet. Partial or complete occlusion of the nasopharyngeal airway may increase the work of breathing and contribute to respiratory failure. The narrowest part of the infant airway is cone shaped cricoid cartilage in the subglottic region. The cross-sectional area between the vocal cords is widened during inspiration and narrowed during expiration. This action allows infant to generate intrinsic positive end expiratory pressure (PEEP) grunting to stabilise their cartilaginous, relatively elastic and flaccid chest, which has a tendency to collapse. Infant’s ribs are aligned horizontally allowing for less anteroposterior movements during respiration. Breathing is primarily diaphragmatic. The soft and compliant chest wall can cause two specific pathological conditions: i) rapid and serious impairment of breathing efficiency and ii) inward distortion of the rib cage and waste of energy through sucking in of the rib cage rather than air.
Basic understanding of pulmonary mechanics is necessary when ventilating an infant or a child. The most important elements are elastic recoil, compliance, resistance and time constant.
Elastic recoil: Newborn has low elastic recoil of the chest because it is nonossified and has low total muscle mass, with a low percentage of slow-muscle fibres in both the diaphragm and intercostal muscle. Very little airway pressure is needed to expand the chest wall during inspiration. This explains why muscle relaxation is rarely needed in the young infant during controlled ventilation. The major force contributing to elastic recoil in the newborn is the surface tension at the air-liquid interface in distal bronchioles and alveoli. As described by Laplace’s law (P=2T/r), the pressure (P) needed to counteract the tendency of bronchioles to collapse is directly proportional to the surface tension (T) and inversely proportional to the radius (r). A decrease in surface tension in surfactant deficiency state (hyaline membrane disease) or after inactivation of surfactant (acute respiratory distress syndrome) increases the tendency of distal airways to collapse.
Compliance: Lung compliance is very low (3.5 ml/cm H2O) at birth and increases rapidly during the first week to about 5-6 ml/cm H2O. Reduced lung compliance is seen in neonates with congenital pathologies characterised by small lung volumes with primary or secondary surfactant deficiency, with restrictive lung disease and with bronchopulmonary dysplasia. Reduced compliance also can be seen in obstructive lung disease combined with high lung volumes, such as asthma and bronchiolitis.
Resistance: Airway resistance refers to the inherent capacity of the air conducting system (airway and endotracheal tube) and tissues to oppose airflow and is expressed as change in pressure per unit change in flow. It depends on the radius and length of the airways and gas flow rates. Airway resistance in spontaneously breathing infants is normally 20-30 cm H2O/L/s. Values in intubated infants are 50-150 cm H2O/L/s consequent to a narrow endotracheal tube (ETT).4 In hyaline membrane disease (HMD), the resistance is usually normal while in the case of meconium aspiration syndrome, the airway resistance is markedly increased.
Time constant: The concept of time constant in the lung represents how fast pressure equilibrates between the circuit and the alveoli. The time constant is a mathematic and physiologic concept that is not consistently applied clinically. It is the product of multiplying compliance and resistance. The time constant relates to both inspiratory and expiratory filling of the lungs. Mouth pressure or proximal pressure equilibrates with alveolar pressure in three or five time constants. In a healthy newborn this is 0.33 s. In premature infants with respiratory distress syndrome with decreased lung compliance, time constant can be as short as 0.05 s.5 Hence the pressure equilibrium will occur in 0.15-0.25 s, which is the minimal inspiratory time required to ensure complete delivery of the tidal volume. In meconium aspiration syndrome, the airway resistance is high resulting in longer time constant. An intervention to improve compliance (surfactant treatment or recruitment manoeuvres) produces a longer time constant by improving compliance.6
Mechanical ventilation
Indications: The three major indications for mechanical ventilation in the paediatric and neonatal age group are to secure the upper airway, improve gas exchange and reduce work of breathing. Common objectives of ventilation are three-fold: i) To support gas exchange by improving alveolar ventilation in order to achieve acceptable oxygenation, ii) to restore and maintain adequate functional residual capacity in order to prevent or reopen atelectasis, improve oxygenation and lung compliance and iii) to reduce work of breathing in the presence of high airway resistance and / or reduced compliance, which causes ineffective spontaneous breathing.
Respiratory failure is diagnosed by two or more criteria from the following clinical and laboratory criteria:
Clinical criteria: Retraction, grunting, respiratory rate more than 60 breaths/minute in neonates or more than 35 breaths/minute in children, central cyanosis, intractable apnoea, decreased activity and movement.
Laboratory criteria: PaCO2 > 60 mm Hg, PaO2 < 50 mm Hg or SpO2 < 80% with FiO2 of 1.0, pH < 7.25.
Retractions typically indicate a significant loss of lung volume. The infant then attempts to recruit alveolar volume by increasing respiratory efforts but the excessively complaint neonatal chest wall make this effort somewhat futile in most cases. Grunting often accompanies retractions, particularly in the neonate with respiratory distress syndrome (RDS). Grunting is an expiratory effort against a partially closed glottis that elevates the end-expiratory pressure in an attempt to increase residual volume and oxygenation. Retraction and grunting are the ominous signs of respiratory failure in neonates and infants. If significant retraction and grunting are observed in an infant, early ventilatory assistance should be considered.
Modes of ventilation can be pressure, volume or flow controlled. Ventilation can be fully supported or partially supported.
Control mode (CMV): To attain complete control, the patient-triggering mechanism is made inactive and all breaths are delivered at a preset volume or pressure, frequency and inspiratory flow rate.7 Patient should be paralysed or sedated to avoid asynchrony between ventilator inflation and patient breathing efforts. The disadvantage of this mode is that asynchrony may cause complication such as pneumothorax. Such situation may occur in acute respiratory distress syndrome (ARDS) or asthma.
Assist/Control Mode (A/C): The volume or pressure, frequency and inspiratory flow rate are preset and the ventilator supports every breath. The patient is allowed to use his/her own ventilatory drive to trigger the ventilator and receive every breath at the preset volume or pressure. If the patient fails to take a breath during the specific period, the ventilator delivers the defined breath at a preset rate. A/C is then defined as patient triggered and machine triggered continuous mandatory ventilation.8 The advantage of the A/C mode is that every breath delivered to the patient, whether patient or machine triggered, has a guaranteed volume or pressure. The disadvantage is that in neonates, infants and small children with high respiratory rate, hyperventilation, hyperinflation and respiratory alkalosis can occur. The work of breathing may be increased, especially for patients who are not breathing in synchrony with the ventilator or who are 'fighting the ventilator'. If the sensitivity of the triggering mechanism is not adequately set, then the patient’s inspiratory effort may be increased and result in an increase in oxygen consumption.9
Synchronised intermittent mandatory ventilation (SIMV): The ventilator presets a rate for mandatory breaths and attempts to synchronise the breaths with the patient’s spontaneous effort. If no patient effort is sensed within the specific window of time, a mandatory breath is given. Airway pressure or flow is usually the triggering mechanism for SIMV Small volumes and rapid rates characterise an infant’s spontaneous breathing effort, which makes synchronising ventilatory inflation difficult. With the latest advances in sensor technology, SIMV is now a feasible option in neonates and infants.10,11
Pressure support ventilation (PSV): Pressure support ventilation is a flow-cycled but time-limited mode that supports each spontaneous breath. It is patient triggered ventilation where patient initiates inspiration, expiration, frequency and determines to a certain extent minute ventilation. This enhances patient’s comfort and ventilatory synchrony. To use this mode the neonate needs to have sufficient ventilatory drive. This mode comes with a back up mode when apnoea is detected.12
Continuous Positive Airway Pressure (CPAP): It can be used as a noninvasive type of ventilation. It is a gentle method of providing respiratory support to spontaneously breathing neonates. The pressure applied is continuous, during both inspiration and expiration. CPAP is used to maintain lung expansion under conditions that cause alveoli and small airways to collapse or filled with fluid.13 This constant application of positive pressure helps to open up the alveoli and increase the functional residual capacity (FRC) of the lung. Hence, better gas exchange and recruitment takes place. The condition where CPAP can be applied includes RDS, postextubation, meconium and other aspiration syndromes, pulmonary oedema, pneumonia, congestive heart failure, resuscitation in delivery room, high chest compliance and pulmonary haemorrhage. CPAP can also be used to treat apnoea of prematurity whereby it may stimulate breathing or help maintain airway patency. CPAP can be delivered by mechanical ventilator CPAP, bubble nasal CPAP and infant flow nasal CPAP.
Setting ventilator parameters
Peak inspiratory pressure (PIP): It is the positive pressure that opens up the alveoli. PIP is regulated by a combination of flow rate, respiratory rate and I:E (inspiratory : expiratory) ratio. For an appropriate PIP, the infant’s age, weight, gestational age, severity of the disease, lung compliance, airway resistance and time constant of the lung must be considered. Excess of PIP may lead to air leak. Initial PIP may be determined by manual ventilation with a pressure gauge by taking the average PIP required to obtain bilateral chest movement, colour and oxygen saturation. PIP can be adjusted to achieve a desired tidal volume.
A PIP of < 20 cm H2O is considered low whereas PIP > 20 cm H2O is considered high. Low PIP is associated with fewer side effects and may allow normal lung development to occur more rapidly. Ventilation may be insufficient and if PIP is too low, generalised atelectasis may occur.
High PIP may help to re-expand atelectasis, increase oxygenation (PaO2) and carbon dioxide (CO2) elimination and reduce pulmonary vascular resistance. However, the use of high PIP impedes venous return, reduces cardiac output acutely and in the long term, is associated with chronic lung disease.
Fraction of inspired oxygen (FiO2): Appropriate use of O2 is highly therapeutic in most cases of neonatal cardiopulmonary disease. In addition to relieving hypoxaemia, its action as a pulmonary vasodilator in case of persistent pulmonary hypertension of the neonates may be invaluable.14 Excessive variation in O2 administration has been implicated as one of the provocative factors for retinopathy of prematurity with subsequent retinal scarring and loss of vision, as well as in bronchopulmonary dysplasia, leading to O2 or ventilatory dependency. 15,16 Accurate measurement of O2 administration and PaO2 or 22 oxygen saturation is mandatory in any neonate requiring O2 therapy.
A simple method to determine the FiO2 needed for a desired arterial oxygen tension PaO2 is derived from the arterial-to-alveolar oxygen tension ratio. Assuming constant barometric pressure and stable lung conditions, the equation simplifies to:
FiO2 desired = PaO2 desired × FiO2 known/PaO2 known
Since prolonged exposure to high levels of oxygen may be toxic, the lowest acceptable FiO2 should be used.17 However, high levels of oxygen may be necessary to correct hypoxaemia when treating severe lung disease or persistent pulmonary hypertension of the newborn.
Tidal volume: The tidal volume control on a microprocessor ventilator adjusts flow or time to derive an increase in tidal volume. Research has shown that the largest contribution to ventilator-induced lung injury results from lung over distension caused by excessive tidal volume (volutrauma), followed by the repetitive opening and closing of the terminal lung units (atelectrauma).18 Hence it is emphasised that the setting of lower tidal volume improves tidal volume monitoring and setting of adequate PEEP level. The tidal volume setting for neonates varies from 4 to 6 ml/kg in low birth weight premature infants, 5 to 8 ml/kg in term infants, and 7 to 10 ml/kg in paediatric age group and adolescent patients.18,19 Lower volumes have been shown to be effective for patients with restrictive lung disease such as RDS and ARDS.20,21 Tidal volume should be corrected for compressible volume loss or a proximal flow sensor should be used. During pressure controlled ventilation, increasing the pressure limit may also increase tidal volume. An increase in pressure limit causes the initial flow to increase. The result is larger decelerating flow waveform and a larger tidal volume.
Flow rate: The flow rate will directly affect mean airway pressure. Inspiratory flow should be set to match the peak inspiratory demands and depends largely on the patient’s spontaneous effort, work of breathing or patient-ventilator synchrony. Too much or not enough flow can increase the work of breathing or cause dyssynchrony.22,23 The flow required for spontaneous breathing is provided by means of continuous flow or a demand valve that is triggered by the patient’s inspiratory effort.9
Frequency: The respiratory rate can determine the minute ventilation and CO2 elimination. The frequency varies with the disease condition of the lung, complications, infants' age and clinical response. Generally taking the basic knowledge, as the compliance decreases, time constant decreases and faster is the respiratory rate. Higher rates are commonly used in persistent pulmonary hypertension (PPHN) to induce respiratory alkalosis and decrease pulmonary vascular resistance (PVR). Caution needs to be exercised with higher rates of more than 60 breaths per minute (bpm) in neonates because it may lead to air trapping, inadvertent PEEP, decreased venous return and cardiac output.24 For infant, toddler, child and adolescent, the respiratory rate ranges from 25-40 bpm, 20-35 bpm, 18-25 bpm and 12-20 bpm respectively.26
Inspiratory time and I:E ratio: Inspiratory time and I:E ratio directly affect the mean airway pressure. The inspiratory time usually set for neonates is 0.25-0.5 s, in infants 0.60-0.90 s and for toddlers and children its 1-1.2 s.25 An I:E ratio of 1:2 to 1:3 is usually considered. It should be kept as physiological as possible.
Positive end expiratory pressure (PEEP): PEEP is the pressure applied at the end of expiration. PEEP improves gas exchange by improving PaO2, recruiting collapsed alveoli, increasing functional lung volume, decreasing intrapulmonary shunting and improving lung compliance.26 A conservative but acceptable PaO2 is 45 to 65 mm Hg for neonates younger than 33 weeks of gestation and 60 to 80 mm Hg for paediatric patients at an FiO2 of 0.40 to 0.50. PEEP usually begins with 3 to 5 cm H2O, with an increase made in increments of 2 cm H2O.27,28
Mean airway pressure: Mean airway pressure is the most critical factor that determines the optimal gas exchange as it correlates with lung volume. Improvement of PaO2 directly relates to increase in airway pressure. Mean airway pressure determines the area under the curve (pressure time waveform) from the beginning of inspiration to the beginning of the next inspiration divided by the total cycle time. An equation for this is as follows:
MAP= PIP × Ti / TCT + PEEP × Te / TCT
Where MAP = Mean airway pressure; PIP = Peak inspiratory pressure; Ti = inspiratory time; TCT = total cycle time; Te = Expiratory time; PEEP = Positive end expiratory pressure.29
Initial ventilator settings
Depends on underlying lung condition, gestation and weight of the neonate, the PIP is set based on the chest rise and retractions on clinical examination and severity of lung condition (Table 1).
Lung condition | PIP (cm H2O) |
Normal | 12 |
Mild disease | 13-15 |
Moderate disease | 16-20 |
Severe disease | 20-25 |
PEEP is set between 4-6 cm H O. Neonates with hyaline membrane disease will require higher PEEP to open up the collapsed alveoli. Ventilator rate (VR) must be adjusted between 40-60 breaths / min and based on underlying lung pathology. Concentration of inspired oxygen (FiO2) is adjusted based on target saturation. The target saturation for preterm neonates below 32 weeks of gestation will be 8892%.
Lung protective strategy: It is essential to choose the correct mode and appropriate ventilation strategy to enhance patient ventilatory synchrony, reduce leak and decrease days of ventilation.30 Optimal lung volume and pressure is the key to lung protection. Permissive hypercapnoea is another ventilator strategy which allows the PaCO2 to be a little higher than normal. This is a valuable tool for lung protection in premature neonates. A study done by Kraybill et al showed that infants ventilated with higher PaCO2 had lower risk of developing chronic lung disease. 31
Humidification: Humidification is essential when the tracheal tube bypasses the normal humidifying, filtering and warming system of the upper airway. Therefore, heat and humidity must be provided to prevent hypothermia, drying of airway secretions and necrosis of airway mucosa. Filtration of dry gases before humidification also is needed because of the contamination sometimes found in medical gas lines. A heated water humidifier is necessary to ensure that inspired gases are delivered at or near body temperature.
A modern servo-controlled heated humidifier, with its high and low temperature alarms and heated wires preventing accumulation of condensation, should provide adequate humidification with proper operation. Heated wire circuits are adopted because of the frequency with which condensation needed to be drained and because of infection control considerations. The heated wire circuits are intended to enable the clinician to heat the gas inside the circuit to a temperature above that at which it left the humidifier, ensuring adequate absolute humidity without condensation in the circuit.
Summary
The different modes of ventilation and ventilation strategies are designed to prevent ventilatory induced lung injury (VILI). New ventilators are equipped with patient-triggered ventilation which has more patient-ventilator synchrony to improve gas exchange and recruitment of lungs. Future neonatal and paediatric ventilation appears to be better and more promising. Ventilator management protocols are essential to improve the care of these delicate patients.
References
1. Mellins RB, Chernick V, Doershuk CF, Downes JJ, Sinclair JC, Waring WW Respiratory care in infants and children. Am Rev Respir Dis 1972; 105:461-83.
2. van Kaam AH, Rimensberger PC. Lung-protective ventilation strategies in neonatology: what do we know—what do we need to know? Crit Care Med 2007; 35: 925-31.
3. Henderson-Smart DJ, Wilkinson A, Raynes-Greenow CH. Mechanical ventilation for newborn infants with respiratory failure due to pulmonary disease. Cochrane Database Syst Rev 2002; 4: CD002770.
4. Manczur T, Greenough A, Nicholson GP, Rafferty GF. Resistance of pediatric and neonatal endotracheal tubes: influence of flow rate, size and shape. Crit Care Med 2000; 28:1595-8.
5. Carlo WA, Martin RJ. Principle of neonatal assisted ventilation. Pediatr Clin North Am 1986; 33:221-37.
6. Couser RJ, Ferrara TB, Ebert J, Hoekstra RE, Fangman JJ. Effect of exogenous surfactant therapy on dynamic compliance during mechanical breathing in preterm infants with hyaline membrane disease. J Pediatr 1990; 116:119-24.
7. Branson RD, Chatburn RL. Technical description and classification of modes of ventilation operation. Respir Care 1992; 37:1026-44.
8. Greenough A, Greenall F. Patient triggered ventilation in premature neonates. Arch Dis Child 1988; 63:77-8.
9. Slutsky AS. Mechanical ventilation. American College of Chest Physicians' Consensus Conference. Chest 1993; 104:1833-59.
10. Reynolds EO. Pressure waveform and ventilator settings for mechanical ventilation in severe hyaline membrane disease. Int Anesthesiol Clin 1974;12: 259-80.
11. Sassoon CS. Mechanical ventilation design and function: the trigger variable. Respir Care 1992; 37:1056-69.
12. Sarkar S, Donn SM. In support of pressure support. Clin Perinatol 2007; 34:117-28.
13. Courtney SE, Barrington KJ: Continuous positive airway pressure and noninvasive ventilation. Clin Perinatol 2007; 34:73-92.
14. Peckham GJ, Fox WW. Physiologic factors affecting pulmonary artery pressure in infants with persistent pulmonary hypertension. J Pediatr 1978; 93: 1005-10.
15. Cunningham S, McColm JR, Wade J, Sedowofia K, McIntosh N, Fleck B. A novel model of retinopathy of prematurity simulating preterm oxygen variability in the rat. Invest Ophthalmol Vis Sci 2000; 41: 4275-80.
16. Jobe AH, Ikegami M. Prevention of broncho-pulmonary dysplasia. Curr Opin Pediatr 2001;13: 124-9.
17. Jenkinson SG. Oxygen toxicity. Clin Chest Med 1988; 9: 141-52.
18. Keszler M. Volume targeted ventilation. J Perinatol 2005; 25: S19-22.
19. Sinah SK, Donn SM. Volume controlled ventilation. In Goldsmith J, Karotkin E, editors. Assisted ventilation of the neonate. 4th ed. New York: WB Saunders; 2003.p.171-82.
20. Clark RH, Slutksy AS, Gerstmann DR. Lung Protective strategies of ventilation in neonate: what are they? Pediatrics 2000; 105:112-4.
21. Eisner MD, Thompson T, Hudson LD, et al. Acute Respiratory Distress Syndrome Network: Efficacy of low tidal volume ventilation in patients with different clinical risk factors of acute lung injury and acute respiratory distress syndrome. Am J Respir Crit Care Med 2001;164:231-6.
22. Kirby RR. Improving ventilator-patient interaction: reduction of flow dysynchrony. Crit Care Med 1997; 25:1630.
23. Jubran A. Inspiratory flow rate: more may not be better. Crit Care Med 1999;27:670-1.
24. Goldsmith J, Karotkin E, editors. Assisted ventilation of the neonate. 4th ed. New York: WB Saunders; 2003.p.158.
25. Walsh BK, DiBlasi RM, Czervinske MP, editors Perinatal and pediatric respiratory care. 3rd ed. Missouri: WB Saunders; 2010.p.326-51.
26. Suter PM, Fairely B, Isenberg MD. Optimum end expiratory pressure in patients with acute pulmonary failure. N Engl J Med 1975; 292:284-9.
27. Carroll CG, Tuman KJ, Braverman B, et al. Minimal positive end expiratory pressure (PEEP) may be "best PEEP". Chest 1988; 93:1020-5.
28. Nelson LD, Civetta JM, Hudson-Civetta J: Titrating positive end expiratory pressure therapy in patients with early moderate arterial hypoxemia. Crit Care Med 1987;15:14-9.
29. Oakes D. Editor. Oakes' neonatal/pediatric respiratory care: A critical care pocket guide. Orono: Health Educator Publications; 2009. p.10-11.
30. Donn SM, Sinha SK. Can Mechanical ventilation strategies reduce chronic lung disease? Semin Neonatol 2003;8:441-8.
31. Kraybill EN, Runyun DK Bose CL, Khan JH. Risk factors for chronic lung disease in infant with birth weight of 751 to 1000 grams. J Pediatr 1989; 115:115-20.