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Brief Reports

Indian Pediatrics 1999; 36:379-383 

Early Experiences with High Frequency Ventilation in Neonates

K.K. Diwakar
Nalini Bhaskaranand

 From the Department of Pediatrics, Kasturba Medical College, Manipal - 576 119, india.

Repr{nt requests:'Dr. K.K. Diwakar. Head, Neonatal Division, Associate Professor, Department of Pediatrics, Kasturb"a Medical College, Manipal, Karnataka 576119, India.

Manuscript received: June 9, 1998; Initial review completed: August II, 1998;
Revision accepted: November 16, 1998

High frequency ventilation (HFV) has proved useful in treating respiratory failure in both preterm and term infants. Improving arterial oxygenation, lesser barotrauma and the reduction in the incidence of airleaks are the commonly reported advantages of HFV. Despite its popularity in other countries, not many centers in India are using HFV. We are presenting our early experience with HFV.

Subjects and Methods

A retrospective analysis of infants who had received HFV at the NICU of the Kasturba Medical College, Manipal over a 2 year period (December 1995-December 1997) was carried out. Conventional mandatory ventilation (CMV) was delivered by time cycled pressure limited ventilator (Infant star, Infrasonics) and HFV by HFV Infant star ventilator (HFV Star). Standard clinical and biochemical monitoring were performed in all neonates. All infants were initially commenced on CMV at rates ranging from 40-80, inspiratory time of 0.33-0.5 sec, positive end expiratory pressure (PEEP) of 3-5 cm of water and peak inspiratory pressure (PIP) at 25-28 cm of water. The switch over to HFV was done when the PaO2 dropped below 60 torr with FIO2 of 0.9 on a MAP of to cm of water. In two infants, one with a rapidly reaccumulating pneumothorax and the other with pulmonary hemorrhage, HFV was commenced before the set criterion for switch-over was fulfilled. All infants fulfilling the critria for switch-over could not be commenced on HFV, as only one ventilator in our NICU was equipped with the HFV module. Therefore, only 18 infants could be treated with HFV. Infants who received HFV for a period less than 24 h were excluded from this study.

HFV was commenced at a frequency of 10Hz (600 breaths/min), and amplitude adequate to obtain adequate chest vibration. The Star HFV ventilator has a fixed inspiratory time of 18 milliseconds, so the I : E ratio on HFV mode is never greater than 1 : 2.7. Mean airway pressure (MAP) was initially increased to 1-2 cm above that of CMV. Along with the HFV background, tidal breaths at rates of 20-25/min were delivered. The background tidal breaths were gradually reduced to 10-20, based on individual requirements of the patients. The PaCO2 was optimized by adjusting the amplitude (Power or ΔP). In the rare situation where the PaCO2 continued to be high despite ΔP being maximum, the frequency was lowered. Satisfactory HFV settings were based on improvement in oxygenation. Attempts to decrease the MAP was made when a 20% reduction of PIO2 was achieved. The ventilator parameters were adjusted to obtain optimal oxygenation at the lowest MAP. Regular chest X-rays were taken to detect overexpansion of the lung as assessed by lung field density and the liver being pushed below the 9th rib. Once the infant was stabilized, improvement of respiratory status was determined by the decreasing requirement of FIO2. The infants were weaned off HFV when FIO2 approached 0.4 The MAP was reduced, then ΔP decreased, and finally changed over to CMV at low ventilator settings permitting easy weaning off the ventilator.

The outcome parameters included Oxygenation index (OI) on Gonventional mandatory ventilation (Ol-CMV) before commencing HFV and the OI at the time of maximum PaO2 on HFOV (OI-HFV). The effects of HFV on airleaks and outcome of infants were also evaluated.

Non-parametric test (Wilcoxan or Mann Whitney) and the Fisher's exact test were applied where appropriate, to evaluate statistical difference between two groups, p
0.05 was considered significant.


Thirteen of the 18 infants received HFV for more than 24 h (mean 71 h) and were included in this study. The indications and clinical characteristics Of these infants are provided in Table I. The most common reasons for ventilation were perinatal asphyxia(1) and pneumothoraces.


Study Characteristics

Characteristics Survivors (n=4) Died (n=9) Total; (n=13)
Birth weight (g)-Mean (SD) 2805(413) 2661 (789) 2705 (680)
Gestation (weeks)-Mean (SD) 37 (1) 37 (1) 37 (1)
Male: Female 2:2 7:2 9:4
Perinatal asphyxia with PPHN 1 4 5
MAS with Perinatal asphyxia 2 2 4
Hyaline Mombrane disease 1 1 2
Pneumonia 0 2 2
Pneumothorax 1* 7** 8

PPHN: Persistent pulmonary hypertension of the newborn; MAS: Meconium aspiration syndrome. (*resolved on HFOY; **persisted despite HFY).

Oxygenation Index: All infants showed an improvement in oxygenation on HFV as evident from the lowering of OI(Table //). The differences in the OI-CMV and OI-HFV were significant (Wilcoxan test-p <0.005). Four of the 13 infants commenced on HFV survived. The differences between OI-CMV, OI-HFV and the duration of HFV between the survivors and those who died were not significant (Table II). The median time for attaining best OI-HFV was less among the survivors (17.5 h vs 31 h); however, this difference was statistically not significant. Eight infants had pneumothoraces on CMV. Pneumothorax resolved in one of them after commencing HFV. This infant was one of the survivors. The pneumothorax persisted despite HFV in the remaining 7, till they died. Seven of the 9 infants who died had persistent pneumothorax (Fisher's exact test: p <0.02).



 Changes in Oxygenation

Characteristics [median (range)] Survivors (n=4) Died (n=9)
Total (n=13)
Pre-switch over on CMV      
PIP (cm H2O) 30 (27-33) 32 (23-35) 32 (23-35)
PEEP (cm H2O) 4 (4-6) 4.5 (3-5) 4 (3-6)
a/A ratio 0.08 (0.05-0.13) 0.08 (0.06-0.17) 0.08 (0.05-0.17)
OI (OI-CMV)* 28.4 (12.5-38) 21 (11.7-42.4) 27.7 (11.7-42.5)
a/A - at best Pao2 0.2 (0.15-0.35) 0.15 (0.09-0.54) 0.16 (0.09 - 0.54)
a/A - at 24 h 0.15 (0.10-0.19) 0.1 (0.02-0.2) 0.11 (0.02-0.2)
OI - at best PaO2 (OI-HFOV)* 9 (6.3 - 13.1) 10 (3.1 - 16.8) 10 (3.1-16.8)
OI - at 24h 11.4 (9.27-20.9) 16.2 (6.2 113.3) 14.9 (6.2-113.3)
Time to OI-HFOV (h) 17.5 (1-22) 31 (10-70) 18 (1-70)
Duration of HFOV (h) 90.5 (25-208) 56  (28-142) 68 (25-142)

Progressive hypoxia despite HFV was the cause of death in all infants. Three of these infants had associated pulmonary hemorrhage. Hyperinflation of the lung and asymmetric regional distension were seen in two patients. One of these had MAS while the other had pneumonia. Manoeuvres like reduction in MAP and increasing the frequency aimed at decreasing the hyperinflation were unsuccessful as these resulted in the drop of Pa02 to hypoxic levels.


The present study consisted of term or near term infants. HFV was resorted to when infants continued to be hypoxic despite optimal conventional ventilation. The oxygenation index decreased in all infants who were commenced on HFV. The improvement of oxygenation on HFV has been reported by other workers also(2,3). However, they had evaluated the effect of HFV on premature infants with respiratory distress syndrome(2,3) and had excluded infants who had infection(3). The greater efficiency of HFV in volume recruitment of the lung results in better oxygenation of the patient at MAP lower than that required by conventional ventilation(4,5). Further, on HFV the lung can be ventilated on the "deflation limb" of its pressure volume curve(4,6). The CO
2 tends to blowout very fast on HFV. Therefore, frequent arterial blood gases to adjust the ΔP is required. The efficiency of HFV for CO2 blowout has been attributed to multiple mechanisms like bulk convection, pendeluft effect and molecular diffusion(5). This would enable CO2 elimination at lower peak pressures in cases of barotrauma(4). These benefits were duly considered in 8 infants of the present study who had pneumothorax on CMV. Despite the predicted benefits of HFV in reducing barotrauma(4) and airleaks(3,7), pneumothorax persisted in 7 infants despite commencing HFV. It was seen that elevation of ΔP to reduce PaCO2 often led to reaccumulation of pneumothorax in these patients. Attempts to reduce PaC02 at lower. ΔP by reducing the frequency were unsuccessful and resulted in a drop in PaO2, especially at frequency < 8. This could be because of reduced ventilation of the apices of the lung at lower frequencies or due to asynchrony with the resonant frequency of the lung(5).

Asymmetric regional distension can occur in disease where regional heterogeneities of resistance and compliance exist(5). Reduction in the MAP pressure need not necessarily relieve alveolar over inflation, as expiratory flow would be low and choke points could develop resulting in gas trapping(5). Despite observing that air trapping was not a significant problem among preterms on HFV, Alexander and Milner(8) have cautioned that regional variations in distribution of pressure could possibly result in gas trapping. We encountered regional hyperinflation on HFV in cases of pneumonia and meconium aspiration syndrome. The non-uniform involvement of the lung in both these cases led to progressive regional gas trapping. Ventilatory adjustments made to reduce gas trapping resulted in inadequate oxygenation. There was little to choose between adequate oxygenation and progressive. regional gas trapping. The management resulted in predictable fatality. Unsatisfactory response to HFV has been observed in meconium aspiration syndrome by other workers also(9). Conventional ventilation has been recommended by other workers in such situations( I 0). As observed by others(3) none of our patients developed a pneumothorax for the first time on HFV. However, among the 8 infants who had developed pneumothorax on CMV, it resolved only in one after commencing HFV. We therefore feel that in infants, HFV is not necessarily curative for pneumothorax, specially in non-uniform lung diseases like meconium aspiration syndrome.

The association of mortality with persisting pneumothorax cannot be ignored. Seven of the 9 (78%) infants who died in the present study had persistent pneumothorax. It was interesting to observe that the infant in whom the pneumothorax resolved after commencing HFV was a survivor. lf with better use rexpertise, HFV can live up to its reputation of resolving airleaks, this mode of ventilation could possibly contribute to reduction in mortality.

The role of HFV as an alternative mode when CMV is unsatisfactory has always been appreciated(10, 11). Four of the 13 (30%) infants who were unsatisfactorily ventilating on conventional ventilation survived after commencing HFV. Most of these infants were term infants, with the often associated problems of perinatal asphyxia, PPHN and meconium aspiration. The importance of HFV as rescue therapy in term infants with severe hypoxic respiratory failure(10) could be appreciated more under circumstances like ours where facilities like nitric oxide ventilation or ECMO are not available for neonatal care.

It must be remembered that the improvement in oxygenation (reducing OI), as ob- served in other studies on high frequency ventilation(12), does not necessarily improve the survival. While accepting, that survival would depend on many factors, the importance of better oxygenation in influencing the outcome can never be ignored.

We join others(9) in saying that HFV would be useful in treating near term infants with hypoxemia unresponsive to conventional ventilation. Though HFV did not increase the incidence of airleak syndrome, in our experience its efficacy in resolving the pneumothorax was not satisfactory. We have presented our early experiences with HFV. Improvement in clinical expertise would undoubtedly fetch better results. The small sample size precludes drawing any major conclusions. Larger studies would be required to ascertain the efficacy of HFV.



1. Carter BS, Haverkamp AD, Merenstein GD. The definition of acute perinatal asphyxia. Clin Perinatol1993; 20: 287-304.

2. Gerstmann DR, Minton SD, Stoddard RA, Meredith KS, Monaco F, Bertrand JM, et al. The provo multicenter early high frequency oscillatory ventilation tria1: Improved pulmonary and clinical outcome respiratory distress syndrome. Pediatrics 1996; 98: 1044-1057.

3. HIFI study group. Randomized study of high- frequency oscillatory ventilation in infants with severe respiratory distress syndrome. J Pediatr 1993; 122: 609-619.

4. McCulloch PR, Froese AD. High frequency ventilation. Anesth Clin North Am 1987; 5: 873-891.

5. Froese AB, Bryan AC. High frequency ventilation. Am Rev Respir Dis 1987; 135: 1363- 1374.

6. Harris TR, Wood BR. Physiologic principles. In: Assisted Ventilation of the Neonate. 3rd edn. Eds. Goldsmith JP, Karotkin EH. Philadelphia, W.B. Saunders Co, 1996; pp 21-68.

7. Mayes TC, Jefferson LS, David Y, Louis PT, Fortenberry JD. Management of malignant airleak in a child with neonatal high frequency oscillatory ventilator. Chest 1991; 100: 263- 264.

8. Alexander J, Milner AD. Determination of gas trapping during high frequency oscillatory ventilation. Acta Paediatr 1997; 86: 268-273.

9. Carter JM, Gerstmann DR, Clark RH, Snyder G, Cornish JD, null DM, et at. High frequency oscillatory ventilation and extracorporeal membrane oxygenation for treatment of acute neonatal respiratory failure. Pediatrics 1990; 85: 159-164.

10. Kinsella JP, Abman SH. Clinical approaches to the use of high-frequency oscillatory ventilation in neonatal respiratory failure. J Perinatol 1996; 16: 552-555.

11. Fox R. High-frequency ventilation. Lancet 1991; 337: 706-707.

12. Engle W A, Yader MC, Andreoli SP, Darragh RK, Langefeld CD, Hui SL. Controlled prospective randomized comparison of high-frequency jet ventilation and conventional ventilation in neonates with respiratory failure and persistent pulmonary hypertension. J Perinatol 1997; 17: 3-9.



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