At the rates provided with HFJV and HFOV, tidal volumes are often smaller than those with conventional ventilation. Generally speaking, the higher the respiratory rate, the lower the tidal volume. At moderate to high rates (≥ 8 Hz), tidal volumes can be less than anatomic dead space.
Although numerous mechanisms are active during HFV to establish gas exchange (Figure 10-3), normal convection and molecular diffusion are the primary mechanisms affecting gas exchange. Other principles enhance molecule diffusion and the dispersion of gases in the airway. With HFPV, tidal volume is also dependent on the pressure control setting.
More than one mechanism of gas transport may operate in various regions of the lung during high-frequency ventilation. Moreover, mechanisms may act synergistically. Gas velocities decrease from the airway opening to alveolus. (Chang HF. Mechanisms of gas-transport during ventilation by high-frequency oscillation. J Appl Physiol Respir Environ Exerc Physiol. 1984; Mar; 56(3):553-563.)
Frequency, I:E ratio, and pressure amplitude are the three variables affecting ventilation during HFOV. Tidal volume during HFOV is also affected by rate. As rate is decreased, tidal volume increases and vice versa. Pressure amplitude (the pressure developed as the oscillator forces gas into the airway) and a longer inspiratory time also increase the tidal volume (Table 10-2). Neonates are generally ventilated at high rates (10-15 Hz) and low-pressure amplitudes (20-30 cm H2O), which generate very small tidal volumes. Adults are ventilated at lower rates (3-8 Hz) and higher pressure amplitudes (60-90 cm H2O). With neonates, the bias flow in the circuit is about 10 L/min, whereas with adults the bias flow is about 30 L/min range. In adults, tidal volumes approaching those delivered by conventional mechanical ventilation (3-4 mL/kg) are possible at 3 Hz and 90 cm H2O pressure amplitude. During HFOV, it is not possible for the patient to trigger the ventilator; heavy sedation, and sometimes paralysis, is needed to ensure patient-ventilator synchrony. In the setting of a high Paco2 and maximal ventilator settings, the cuff may be deflated, which clears CO2 from the central airway and endotracheal tube. Oxygenation with HFOV is determined by Fio2 and mean airway pressure (P̄aw). P̄aw is similar to positive end-expiratory pressure (PEEP) in its effect on oxygenation, since at the alveolar level there is minimal pressure change during HFOV (particularly at high rates).
Table 10-2HFOV settings in adults ||Download (.pdf) Table 10-2 HFOV settings in adults
• Frequency: 3-8 Hz; the highest that allows acceptable
• Pressure amplitude: 60-90 cm H2O
• I:E ratio: 1:2
• Bias flow: 30 L/min
• Mean airway pressure: 25-35 cm H2O
It is estimated that as little as 15% of the inspiratory pressure amplitude is transmitted to the alveolar level through an 8-mm internal diameter endotracheal tube at 8 Hz. With smaller tubes and more rapid rates, less pressure is transmitted. With a pressure amplitude of 60 cm H2O (30 cm H2O above and 30 cm H2O below P̄aw during inhalation and exhalation, respectively) at 8 Hz with an 8-mm internal diameter tube, the alveolar pressure would fluctuates 4.5 cm H2O above and below the P̄aw. A lung recruitment maneuver is often performed when HFOV is initiated, by increasing P̄aw for a short time and then decreasing it to the lowest level that maintains oxygenation. In adults, P̄aw during HFO are generally set at 25 and 35 cm H2O.
With HFJV the tidal volume is affected by the gas that is entrained via the conventional ventilator. Estimation of tidal is currently not possible during HFOV and HFPV. With HFJV and HFPV, oxygenation is controlled in the same manner as during conventional ventilation. PEEP and Fio2 are set to achieve the desired oxygenation status.