American Thoracic Society - We help the world breathe - PULMONARY :: CRITICAL CARE :: SLEEP
| | More

Guidelines for Alternative Modes of Ventilation Used in the Management of Patients with ARDS


Neil MacIntyre, MD

Duke University Medical Center

Definition of refractory hypoxemia:
- Persistent hypoxemia despite use of the NIH ARDS Network ventilator management protocol (see below):
        - Assist control mode
        - Tidal volume 4-8 ml/kg predicted body weight (PBW)
        - Use either of the following PEEP-FiO2 Tables (Goal: PaO2 55-80 mmHg,
                                    SpO2 88-95%):

CONSERVATIVE PEEP APPROACH
FiO2  .30  .40  .40  .50  .50  .60  .70  .70  .70 .80  .90  .90  .90  1.0  1.0  1.0   1.0
PEEP   5    5     8     8    10   10   10   12  14  14   14   16   18   18   20   22   24
AGGRESSIVE PEEP APPROACH
FiO2  .30  .30  .40  .40  .50  .50  .60  .60  .70  .80  .80  .90  1.0  1.0
PEEP  12   14   14   16   16   18   18   20   20  20    22   22   22   24

- Lung protective goals not being met:
         - Plateau pressure => 35 cm H2O
         - FiO2 =>0.70

ALTERNATIVE VENTILATOR MODES

Airway Pressure Release Ventilation (APRV)

Definition: APRV uses patient or machine triggered, pressure targeted, time cycled breaths and permits superimposed spontaneous breaths. The unique feature of APRV is that it usually employs long inflation periods (i.e. several seconds) and short deflation periods (i.e. less than one second). This creates an “inverse ratio” like support pattern with most spontaneous breaths thereby occurring during the inflation period.

Theory: By lengthening inflation periods, additional lung recruitment can occur without adding additional expiratory pressure (PEEP) or tidal volume. Mean airway pressure can thus be increased without an increase in the end inflation plateau pressure. The superimposed spontaneous breaths may also provide more even ventilation distribution as well as augment cardiac filling. It is important to note that clinical trials to date with APRV are few and while results show that APRV provides effective support, it has not been shown to improve outcomes.

Initial settings: On many ventilators APRV is offered as a distinct mode although from an engineering perspective it is very similar to pressure targeted IMV. Unfortunately, these APRV modes go by a variety of proprietary names (e.g. APRV on Dräger devices, BiLevel on Covidien devices, BiPhasic on CareFusion (formerly Viasys) devices, and Bi-Vent on Maquet devices). When these devices are set in the APRV mode, there are 4 key settings – the inflation pressure (sometimes called “Phigh”), the deflation pressure or PEEP (sometimes called “Plow”), the inflation time (sometimes called “Thigh”), and deflation time (sometimes called “Tlow”). Machine rate per minute is thus 60 divided by (Thigh plus Tlow). Plow is generally set in the 0-8 cm H2O range and Phigh is set to provide a delivered inflation volume of 4-8 ml/kg PBW while limiting total applied pressure to <=35 cm H2O. The initial Tlow is set at 0.5-1 second and Thigh is adjusted to be as long as possible while still providing the necessary minute ventilation. Remember that the patient’s breathing throughout the ventilatory cycle adds to the total minute ventilation. In practice, Thigh is usually set in the 3-5 second range (with a 1 second Tlow, this translates to breathing frequencies of 10 to 15 inflations/deflations per minute). On some devices, pressure support can be added to the spontaneous efforts. However, this approach adds to the total end inflation pressure, may interfere with the gas mixing effects of unsupported breaths, has never been systematically evaluated, and thus is generally not recommended.

Subsequent settings: CO2 clearance is controlled by two adjustments – the delivered driving pressure (driving pressure for tidal volume is Phigh minus Plow) and the respiratory rate (i.e. the inflation/deflation rate). Oxygenation is controlled primarily by FiO2 and the mean airway pressure which, in turn, is controlled by the combination of Phigh, Plow and the Thigh:Tlow (I:E) ratio. If plateau pressure is <= 35 cm H2O, increasing Plow or increasing Thigh will increase mean airway pressure to improve oxygenation. Remember, however, that with a Plow increase, Phigh will have to also increase to maintain machine tidal volume. Also remember that as Thigh:Tlow increases, intrinsic PEEP can develop which, in a pressure targeted mode like APRV, will automatically reduce effective driving pressure and machine tidal volume. Phigh may thus have to be increased to maintain machine tidal volume. If plateau pressure is >35 cm H2O, consideration should be given to reducing Phigh (machine tidal volume) and extending Thigh as much as possible. Again, however, as Thigh:Tlow increases, intrinsic PEEP can develop with effects described above

Sedation/paralysis: Because spontaneous breathing is allowed, patients can often remain quite comfortable during APRV. However, the long periods of high inflation pressures and the rapid deflation/inflation events can lead to some discomfort and thus a need for sedation/analgesia with standard drugs such as benzodiazepines and opiods. On some devices, the inflation phase can be synchronized with patient effort (i.e. patient triggered) but whether this improves comfort is not clear. Importantly, unlike older forms of inverse ratio ventilation which did not permit spontaneous breathing, neuromuscular blockers are almost never indicated. Indeed, the elimination of spontaneous breaths with neuromuscular blockade removes the gas distribution benefits of spontaneous efforts – one of the putative benefits of APRV.

High Frequency Oscillatory Ventilation (HFOV)

Definition: High frequency ventilation is defined as mechanical ventilatory support using higher than normal breathing frequencies (ie >60 breaths/minute in adults). In practice, this can mean breathing frequencies approaching 900 breath/minute (ie 15 breaths/second or 15 Hz). Under these conditions, delivered tidal volumes are very low and often below anatomic dead space. Gas delivery systems on conventional ventilators are incapable of responding at these rates and thus specialized devices. High frequency oscillators operate by providing a continuous “bias” flow in the circuit and then oscillates the gas with a “to-and-fro” piston located near the opening of the artificial airway.

Theory: With very small tidal volumes delivered at very high frequencies, alveolar pressure swings are very small. Conceptually this can minimize cyclical overdistention and recruitment-derecruitment lung injury induced by conventional positive pressure ventilation. Indeed, some have described HFOV as essentially “CPAP with a wiggle”. With tidal volumes less than anatomic dead space, gas transport up and down the tracheobronchial tree must involve non-convective flow mechanisms such as Taylor dispersion, coaxial flow, augmented molecular diffusion and perhaps others. Alveolar-capillary gas transport involves maintaining alveolar patency in a fashion similar to CPAP. Thus, ventilation-perfusion matching and oxygenation correlate well with mean airway pressure (mPaw). Interestingly, mPaw during HFOV can be significantly higher than generally accepted injurious plateau pressures in conventional ventilation (ie as high as 40-45 cm H2O) without causing apparent lung injury. Why this is possible is not clear but probably is related to the minimal lung tissue cyclical stretch with HFOV.

Initial settings: The only device available for adult HFOV is the Sensormedics 3100B oscillator which is available with an exhalation filter. With this device, the important settings are frequency, power (the piston pressure swings generating the tidal volume), FiO2, and the mPaw. Most authorities recommend some form of recruitment maneuver (eg 30-40 cm H2O mPaw for 30-40 seconds) and a subsequent mPaw setting 5 cm H2O higher than what had been delivered with the conventional ventilator. The initial frequency is usually 5 Hz and the FiO2 is 1.0. The initial power setting (piston displacement force) is generally set at 5-6 and subsequently adjusted to see an obvious “chest wiggle”. There are two additional settings on HFOV. First, the inspiratory:expiratory ratio can be set - usually at 1:2. Second, the circuit bias flow can be set, generally near the maximum of 30-40 L/min to assure CO2 clearance and the maintenance of mPaw.

Subsequent settings: If the PaCO2 is higher than desired, power settings should be increased; if the PaCO2 is too low, power settings should be decreased. Some authorities also recommend deflating the endotracheal tube cuff to facilitate CO2 clearance.If power is maximum but the PaCO2 is still too high, frequency should be decreased by increments of 0.5 (this increases tidal volume). Deflating the endotracheal tube cuff is another technique that may facilitate CO2 clearance, but must be done with caution as it may decrease mPaw. As noted above, oxygenation is dependent primarily on the mPaw and the FiO2. Tables similar to the PEEP/FiO2 noted earlier can be used to titrate FiO2 and mPaw to reach oxygenation goals. An example is:

Mean Airway Pressure/FiO2 Table

Goal: 55 ≤ PaO2 ≤ 80
Goal: 88 ≤ SpO2 ≤ 95

Mean Airway Pressure

FiO2

<25

0.4-0.5

25-30

0.5-0.8

31-39

0.8-1.0

40-45

1.0

Once the patient has stabilized on HFOV, some authorities suggest increasing the frequency as much as possible so as to further minimize alveolar cyclical pressures. This is usually done by adjusting the power settings to maximal and increasing the frequency in 0.5 Hz increments until CO2 clearance becomes unacceptable (due to decreased tidal volumes). As patients improve, FiO2 and mPaw requirements come down. Generally, when the mPaw is 20-22 cm H2O and the FiO2 is 0.40-0.50, consideration can be given to returning the patient to conventional ventilation.

Sedation/paralysis: Neuromuscular blockade is probably reasonable in the first few hours of HFOV in order to optimize settings. Thereafter, however, paralysis should be avoided. Surprisingly, most patients tolerate HFOV quite well without excessive sedative/analgesic requirements. It is important to note that spontaneous breaths can occur during HFOV although inspiratory gas flow is limited by the set bias flow.

APRV References

  1. Stock MC, Downs JB, Frolicher DA. Airway pressure release ventilation. Crit Care Med 1987;15:462-466.
  2. Neumann P, Golisch W, Stromeyer A, et al. Influence of different release times on spontaneous breathing during airway pressure release ventilation. Intensive Care Med 2002;28:1742-1749.
  3. Putensen C, Mutz NJ, Putensen-Himmer G, et al. Spontaneous breathing during ventilatory support improves ventilation-prefusion distributions in patients with acute respiratory distress syndrome. Am J Respir Crit Care Med 1999;159:1241-1248.
  4. Kaplan LJ, Bailey H, Formosa V. Airway pressure release ventilation increases cardiac performance in patients with acute lung injury/ adult respiratory distress syndrome. Critical Care 2001;5:221-226.
  5. Putensen C, Zech S, Wriggle H, et al. Long term effects of spontaneous breathing during ventilatory support in patients with acute lung injury. Am J Respir Crit Care Med 2001;164:43-49.
  6. Rasanen J, Cane RD, Downs JB,et al. Airway pressure release ventilation during acute lung injury: a prospective multicenter trial. Crit Care Med 1991;19:1234-1241.
  7. Varpula T, Valta P, Niemi R, et al. Airway pressure release ventilation as a primary ventilatory mode in acute respiratory distress syndrome. Acta Anaesthesiol Scand 2004;48:722-731.
  8. Varpula T, Jousela I, Niemi R, et al. Combined effects of prone positioning and airway pressure release ventilation on gas exchange in patients with acute lung injury. Acta Anesth Scand 2003;47:516.
  9. Habashi NM. Other approaches to open lung ventilation: airway pressure release ventilation. Crit Care Med. 2005: 33: S228-40.

HFOV References

  1. Derdak S, Mehta S, Stewart TE, et al. High-frequency oscillatory ventilation for acute respiratory distress syndrome in adults: a randomized, controlled trial. Am J Respir Crit Care Med 2002;166:801-808.
  2. Bollen CW, van Well GT, Sherry T, et al. High-frequency oscillatory ventilation compared with conventional mechanical ventilation in adult respiratory distress syndrome: a randomized controlled trial. Crit Care 2005;9:430-439.
  3. Mehta S, Granton J, MacDonald RJ, et al. High-frequency oscillatory ventilation in adults: the Toronto experience. Chest 2004;126:518-527.
  4. Mehta S, Lapinsky SE, Hallet DC, et al. Prospective trial of high-frequency oscillation in adults with acute respiratory distress syndrome. Crit Care Med 2001;29:1360-1369.
  5. Ferguson ND, Chiche J-D, Kacmarek RM, et al. Combining high-frequency oscillatory ventilation and recruitment maneuvers in adults with early acute respiratory distress syndrome: the Treatment with Oscillation and an Open Lung Strategy (TOOLS) Trial pilot study. Crit Care Med 2005;33:479-486.

The ATS is providing this information about salvage therapies that are available as a resource for those interested in this information, but it is important to note that none of these therapies have been shown to improve survival for patients with ALI/ARDS and that the ATS is not recommending the use of these therapies.

Critical Care