Accurate measurement of delivered tidal volumes in infants and children is essential during mechanical ventilation.

An accurate determination of the tidal volume (Vt) delivered to a patient’s lungs is essential when mechanically ventilating infants and children. Considering the small Vts used in ventilating infants and young children, small inaccuracies in Vt determination may result in significantly adverse conditions. Many conventional ventilators measure Vt at the expiratory valve. The determined values of these ventilators are often used clinically for important patient-care decisions; however, due to multiple circuit variables (such as circuit compliance, heaters, in-line suction devices, secretions, and condensation), the Vt measured at the expiratory valve of a ventilator does not accurately represent the Vt truly delivered.

A determination of Vt at the expiratory valve of a ventilator does not compensate for the volume of gas lost due to the distensibility of the ventilator circuit, nor does it compensate for the many different variations in the circuit setup. Since a significant volume of the gas that is delivered by the ventilator may be lost due to circuit conditions, it is essential to measure the Vt that reaches the endotracheal tube accurately in infants and small children. Vt determination at the endotracheal tube is more likely to represent the actual Vt of the patient’s lungs accurately than is Vt measured at the expiratory valve of the ventilator.

The volume of gas lost due to distensibility of the ventilator circuit is partially attributable to the compliance of the circuit. The compliance factor of a ventilator circuit is printed on its package or can be obtained from the circuit’s manufacturer. To determine the actual Vt delivery, one can employ a mathematical equation to correct for the circuit’s compliance. Theoretically, the effective Vt is defined as the Vt measured at the expiratory valve minus the volume of gas lost due to the distensibility of the circuit, calculated as the figure for peak inspiratory pressure minus positive end-expiratory pressure (PEEP) multiplied by circuit compliance.1 This equation, however, is based on a circuit-compliance factor that is derived using the circuit as it is packaged at room temperature in a manufacturing facility. The circuit-compliance factor does not consider uncontrolled variables such as heaters, in-line suction devices, adapters for end-tidal carbon dioxide monitors, changes in temperature, secretions, or condensation. Therefore, calculating the delivered Vt using an expiratory-valve measurement and the circuit-compliance factor would not be expected to give an accurate determination of the Vt actually delivered to the patient’s lungs. When Vts are measured using a pneumotachometer positioned between the ventilator circuit and the endotracheal tube, the ventilator circuit’s compliance and the confounding circuit variables are no longer pertinent factors.

Significant differences in ventilator-determined Vts, pneumotachometer-determined Vts, and calculated effective Vts exist, especially in neonates, infants, and young children who require small Vts. Cannon et al2 studied 98 conventionally ventilated infants and children. Respiratory parameters were measured both at the expiratory valve of the ventilator and using a pneumotachometer connected to a respiratory mechanics monitor. The pneumotachometer was placed between the ventilator circuit and the endotracheal tube.

Seventy patients were ventilated using infant circuits and 28 patients were ventilated using pediatric circuits. The mean age of the infant population was 2.8±2.3 months (median: 2.8 months), and the mean weight was 4.6±3.3 kg (median: 3.8 kg). The mean age of the pediatric patients was 8.7±5.6 years (median: 5.7 years) with a mean weight of 27.9±22.9 kg (median: 17 kg).

This study demonstrated that, for the 70 infants, the mean Vt measured by the respiratory mechanics monitor and the pneumotachometer at the endotracheal tube was significantly less than the Vt determined by either the ventilator display (39.4±21.5 mL versus 70.4±31.1 mL; P<.0001) or the calculated effective Vt (39.4±21.5 mL versus 59.2±28.8 mL; P<.0001). Thus, the mean Vt determined at the endotracheal tube was 56% of the mean Vt determined at the expiratory valve of the ventilator.

In the 28 pediatric subjects, the mean Vt measured by the respiratory mechanics monitor and the pneumotachometer was also significantly less than the Vt measured by the ventilator (135.3±75.8 mL versus 185.4±96.6 mL; P=.03). The pneumotachometer-measured Vt was, on average, 73% of that measured at the expiratory valve. For these older patients, there was no significant difference between the calculated effective Vt and the pneumotachometer-determined Vt.

The Vt values determined from both the expiratory valve and the pneumotachometer were bench tested to determine the validity of the values measured. These data were collected using a 15-cm noncompliant ventilator circuit with no distensible volume and no confounding variables. Data were obtained for both pressure-control ventilation and volume-limited ventilation. No significant differences were seen between the values calculated at the expiratory valve and the values determined by the respiratory mechanics monitor using a pneumotachometer placed at the endotracheal tube (P=.72). Thus, both monitoring methods accurately determine the volume of gas that passes through the monitoring device. The difference that was demonstrated in the study by Cannon et al2 was a result of the different location of the Vt measurement, not the device itself.

If the actual volume delivered to the lungs of critically ill infants and young children is not accurately known, the patient may be at risk for atelectasis, hypoxia, and hypercapnia. The presence of hypercapnia may or may not have clinical implications, depending on the clinical status of the patient; however, the development of atelectasis and hypoxia is likely to be a problem. If inadequate Vts are used and atelectasis develops, then increased airway pressures may be required to recruit the collapsed lung regions subsequently. This increase in airway pressure may increase the risk of secondary lung injury through the mechanism of shear injury.3,4 A confounding variable in this clinical scenario may be PEEP. An appropriate level of PEEP may prevent the development of atelectasis; however, ideal PEEP titration in small infants with high respiratory rates and dynamic pressure-volume curves is often difficult.

On the other hand, the clinician may attempt to compensate for the expected discrepancy between expiratory valve and endotracheal-tube Vt measurements by increasing the ventilator’s set delivered Vt for a given patient. Without an accurate determination of the delivered Vt at the endotracheal tube, however, the risk of overcompensation exists. Such overcompensation could produce overdistension, resulting in volutrauma and secondary lung injury.3,5-7 PEEP may again be a confounding variable; however, in this case, the use of excessive PEEP may further exacerbate the presence of overdistension.8

The accurate determination of delivered Vt, regardless of the PEEP level used, is essential in ventilating infants and young pediatric patients. With the use of a respiratory mechanics monitor and a pneumotachometer placed at the endotracheal tube, a more reliable measurement of the effective Vt that is actually delivered to a patient’s lungs can be obtained.

Donna S. Hamel, RRT, is pediatric clinical research coordinator, Department of Pediatric Critical Care Medicine, Duke Children’s Hospital, Duke University Medical Center, Durham, NC. Ira M. Cheifetz, MD, is associate professor, Chief of Pediatric Critical Care Medicine, and medical director of the PICU, Pediatric Respiratory Care, and ECMO.

 References 1. Wilson BG, Kern FH, Cheifetz IM, Meliones JN. Direct measurement via an inline pneumotachometer is necessary to determine effective tidal volume. Respir Care. 1995;40:1172. 2. Cannon ML, Cornell J, Tripp-Hamel DS, et al. Tidal volumes for ventilated infants should be determined with a pneumotachometer placed at the endotracheal tube. Am J Respir Crit Care Med. 2000; 162:2109-2112. 3. Dreyfuss D, Saumon G. Ventilator induced lung injury: lessons from experimental studies. Am J Respir Crit Care Med. 1998;157:294-323. 4. Mead J, Takishima T, Leith D. Stress distribution in lungs: a model of pulmonary elasticity. J Appl Physiol. 1970;28:596-608. 5. Dreyfuss D, Soler P, Basset G, Saumon G. High inflation pressure pulmonary edema. Am Rev Respir Dis. 1988;137:1159-1164. 6. Hickling KG, Henderson SJ, Jackson R. Low mortality associated with low lung volume pressure limited ventilation with permissive hypercapnia in severe respiratory distress syndrome. Intensive Care Med. 1990;16:372-377. 7. 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. 8. Cheifetz IM, Craig DM, Quick G, et al. Increasing tidal volumes and pulmonary overdistension adversely affect pulmonary vascular mechanics and cardiac output in a pediatric swine model. Crit Care Med. 1998;26:710-716.