3. What is HFOV?
• HFOV provides small tidal volumes (not really a tidal
volume, but an Amplitude, usually referred to as Delta
P: P) usually equal to, or less than, the dead space;
150 millilitres, at a very fast rate (Hertz-Hz) of
between 4-5 breaths per second.
• The delivery of tidal volumes of dead space or less at
very high frequencies enables the maintenance of a
minute volume.
• Lungs are kept open to a constant airway pressure via
a mean pressure adjust system.
• HFOV allows for the decoupling of oxygenation from
ventilation: it allows the clinician to separately adjust
either oxygenation or ventilation.
6. Open Lung Ventilation Strategy
Volume
Pressure
Zone of Overdistention
Safe
window
Zone of
Derecruitment
and
atelectasis
Goal is to avoid injury zones
and operate in the safe window
Froese, CCM, 1997
7. INJURY
INJURY
CMV
HFOV
• During CMV, there are swings between the zones of
injury from inspiration to expiration.
• During HFOV, the entire cycle operates in the “safe
window” and avoids the injury zones.
8. Ventilator Induced Lung Injury
Volutrauma
Caused by high lung volume
Barotrauma
Caused by excess airway pressure
Atelectotrauma
Caused by repetitive closing/opening of collapsed
alveoli
Biotrauma
Caused by mechanical stresses which triggers the
inflammatory cytokine cascade Organ Faulire
9. So What??
Reduce the
Risk of VILI
Allows
Recruitment of
Alveolar Space
Improves V/Q
Matching
Decoupling of
Oxygenation
from
Ventilation
Safer
Mode of
Ventilation for
Patients with
Decreased Lung
Compliance
10. Comparison
Ventilator Rate Volume
Conventional Ventilator 1 to 120 4 to 20 cc/kg
Sensor Medics 3100B 60 to 900 0.1 to 1.5 cc/kg
Conventional Ventilator: active
inspiration with passive
expiration
HFOV: active inspiration with
active expiration
11. How does it do that?
HFOV provides small tidal volumes
(not really a tidal volume, but an Amplitude, usually
referred to as Delta P
usually equal to, or less than, the dead space; 150
ml
at a very fast rate of between 180-900 breaths per
minute
3 – 15 Hz
12. How does it do that?
Convection (bulk flow) ventilation
Asymmetrical velocity profile
Taylor dispersion
Molecular diffusion
Pendelluft
Cardiogenic mixing
13. How does it do that?
HFOV keeps the lungs/alveoli open at a constant,
less variable, airway pressure
This prevents the “inflate/deflate, inflate/deflate”
cycle, which has been shown to damage alveoli and
further complicate lung disease
14. How does it do that?
Further, HFOV allows for the decoupling of
oxygenation from ventilation:
It allows the clinician to separately adjust either
oxygenation or ventilation
It is believed that HFOV may enhance gas mixing
and improve V/Q matching
15.
16.
17. How does the machine ventilate the
patient?
Follow ME to
The Machine
18. Inadequate oxygenation/CO2
elimination that cannot safely
be treated without potentially
toxic ventilator settings and,
thus, increased risk of
ventilator Induced lung injury
(VILI)
ARDS
Air Leak
Syndrome
Broncho-Pleural
Fistula
20. Hertz = BPM
Power
(Amplitude ∆
P)
Bias FlowFiO2
mPaw
Inspiratory
time %
25 – 40
LPM
100%
5 above
mPaw on
CMV
Power 4
Amp 45 –
55
cmH2O
Hz 5 to 6 33%
Oxygenatio
n Ventilation Constant
21. • Resuscitation bag with PEEP valve attached to an O2
source
• Airway is suctioned and patent before starting HFOV
• Adequate titration of sedation and analgesia
• Initiation of neuromuscular blockade (Don’t forget the
train of four)
• Make sure patient is well hydrated and normotensive.
• Starting of HFOV may induce hypotension; volume
expanders and inotropic support should be available
22. • Set Bias Flow at 25 - 40 LPM.
• Set Amplitude 45 – 60 cm H2O (Power of 4.0) and increased it to
achieve chest wiggle down to the level of the groin (mid-thigh).
• Inspiratory time percent (It %) is started at 33%.
• Frequency starts at 5 Hertz (Hz) . Watch pH if low (< 7.2) you may
set it at 4 Hertz.
• Set Mean Paw at 5 cm H2O above patient’s Mean Paw on CMV.
• Set FiO2 at 100 %
• Set high pressure alarm at 5 cm H2O above mean Paw, and low
pressure alarm at 5 cm H2O below mean Paw.
23. • ABG should be obtained within 30 to 60 mins post-HFOV
initiating.
• CXR 1 to 4 hours post-HFOV initiating, (ordered).
Achieving optimal lung volume: (assess
initial CXR)
CXR showed good lung expansion to the level of T8 –
T9 posterior, if not increase mean Paw by increments
of 1 to 2 cm H2O. ( To maximum of 35 H2O)
24. • Hypercapnia / Respiratory Acidosis:
Increase the amplitude by 5 cm H2O to maximum
Amp =(3 X mean Paw) not to exceed 100 cm H2O.
Decrease Hz by 1 to minimum of 3 Hz.
Generate ETT leak.
Creating a Cuff Leak
The Cuff Leak is indicated for high PaCO2 with no response
to Amp and Hz. (Amp ≥ 100 cmH2O and Hz ≤ 3.5) and with
optimal mPwa.
1. Assess the patency of the EET, suction the tube.
2. Assess appropriate lung volumes.
3. If both 1 and 2 are fine, then proceed with the procedure.
4. Withdraw air from the cuff with a syringe to create a drop
of 5 cmH2O in the mPaw.
5. Increase the bias flow to adjust the mPaw to the set level.
25. • Hypocapnia / Respiratory Alkalosis
Decrease amplitude by increments of 5 cm H2O to the
minimum amplitude that gives adequate chest wiggle.
Increase the frequency by 1 to achieve 5 to 6 Hz.
Allow 30 minutes between
changes – use ABGs to
guide
26. • Worsening Oxygenation
Increase FiO2 by 5% as needed to FiO2 of 100%.
Increase mean Paw by 2 cm H2O as needed to
maximum of 35 cm H2O.
Consider Recruitment Manoveuver.
Recruitment Maneuver
RMs is indicated at commencement of HFOV and if SpO2
decreases > 5% with suctioning, positioning, or any other
procedure.
Before the RM:
• To be conducted only after assessment of adequacy of
cardiovascular function and volume status. (Patient is
hemodynamically stable)
• ICU Consultant or Registrar must be in attendance during
procedure.
RM Procedure
1. Set high airway pressure alarm to 50 cmH2O.
2. Inflate cuff to occlude leak. (if cuff was deflated to establish a
leak to acceptable cuff pressure 22 – 28 cm H2O )
3. Set HFOV to standby (Stop the piston).
4. Increase mPaw to 40 – 45 cmH2O for 40 – 60 secs (watch BP
and decrease mPaw immediately if MAP < 60 mmHg or fall
more than 20 mmHg).
5. Return mPaw to previous setting.
6. Reset cuff leak.
7. Restart piston.
27. If increased PaCO2 with pH
< 7.2 despite maximum ΔP,
frequency of 3 Hz, and cuff
leak. (ensure ETT patency)
or/and failure to wean FiO2
to ≤ 60% within 24 hours.
Then Consider inhaled nitric
oxide and/or prone position
Return to
conventiona
l
28. • Consider trial of CV when FiO2 ≤ 40% and mPaw < 22
cmH2O
• Set up conventional ventilator / standby
• Set ventilator on PCV, PC 20cm H2O (to achieve Vt of
approx 6 mL/Kg), PEEP 10 to 15 cm H2O (to achieve
mean Paw 20 cm H2O +/- 2), FiO2 5% > HFOV setting,
RR 15 to 20 BPM, I:E ratio 1:1 to 1:3 (Ti 0.85 t0 1.2 sec).
• ABGs in 30 mins – reassess settings.
• Consider Recruitment Manoveuvre (RM).
Allow 30 minutes between
changes – use ABGs to
guide
30. • Chest “wiggle” factor–assess initially and routinely,
especially after any major re-positioning
• Auscultate the intensity of oscillation– must be equal
throughout chest
• ET tube position should be checked regularly
• Recognize the bad signs! - ↓chest wiggle, ↓ BP, ↓
SaO2
31. • Continuously assess chest vibration(chest wiggle factor)
o CWF depends on the amount of amplitude and lung
compliance
o Vibrations should be equal and continuous
o Visual assessment of the depth of wiggle :
Neonates from nipple line to umbilicus
Pediatrics from clavicle to hips
Adults from clavicles to mid thigh
32. • Chest wiggle factor: Absent or diminished
• Clinical sign for airway obstruction/ETT displacement
(notify RCP re; suctioning, increase power)
• If CWF present on one side suspect pneumothorax or
ETT has slipped down a bronchus
( check position of ETT, obtain CXR)
33. • Evaluation of chest expansion on CXR(T8-9)
• Check capillary refill, skin color , temperature
• Compare central with peripheral pulses
• Pulse oximeter: continuous non-invasive monitoring
• Blood Pressure
• Do not disconnect tubing during repositioning
(risk of alveolar collapse , loss of lung volume)
• After change of position check for chest wiggle, SpO2,
ETT placement
34. • When repositioning: minimum of two people ( nurse & RT)
• Do not suction for the first 24 unless necessary
• Suction using the clamp technique or use an in-line suction
catheter
• Obtain blood gas and CXR within the first hour of initiation
• Reposition carefully, ensure a smooth interface (free of kinks)
between ET tube and oscillator circuit
• Document: Amp, FiO2, Map, and Hz, and auscultation
assessment
35. • Lung Overdistension
• Pneumothorax
• ET Tube obstruction (caused by secretions)
• Tracheal inflammation and necrotizing tracheobronchitis
(oscillator circuit needs adequate humidification)
• Decreased cardiac output ( due to increased thoracic
pressure)
Editor's Notes
Biotrauma, a relatively newly described response to mechanical stresses, is characterized by the release of inflammatory mediators from cells within the lung [1]. These mediators can cause further injury to lung tissue and to other organ systems.
BIOTRAUMA — A number of studies have provided evidence that mechanical ventilation of injured lungs can exacerbate lung injury and lead to an additional inflammatory response [19,20]. Experimental animal data clearly demonstrate that over-stretching of lung cells and/or allowing recruitment/de-recruitment of the lung can lead to an increase in lung cytokines. Under conditions in which there is increased lung permeability, the cytokines may translocate from the alveolar space to the systemic circulation.
As an example, conventional ventilation in a rabbit model of lung injury produced severe hypoxemia and pathologic evidence of an influx of large numbers of neutrophils into the lung. This was in marked contrast to the results obtained in animals that were neutrophil-depleted with nitrogen mustard prior to lung lavage, in which the absence of neutrophilic infiltration was associated with an increased PaO2 [19]. These results suggested that mediators released from neutrophils could play a major role in ventilator-induced lung injury. High frequency oscillation in a similar lung lavage model produced a significant decrease in the concentration of inflammatory mediators, including thromboxane B2 and platelet activating factor, when compared to conventional mechanical ventilation [17,20].
Injurious forms of mechanical ventilation can also lead to an increase in cytokine concentrations in previously healthy lungs [21,22]. In studies of isolated, non-perfused ex vivo lungs, strategies which permitted overinflation of the lung (tidal volume of 15 mL/kg; PEEP of 10 cmH20) or those that allowed recruitment/de-recruitment (tidal volume of 15 ml/kg, PEEP of 0 cmH2O) produced a 3 to 6 fold increase in lung lavage cytokines, including inflammatory and antiinflammatory cytokines, and chemokines [16]. When zero PEEP was combined with a strategy using very high end-inspiratory lung volumes, a synergistic effect was observed with a 50 to 60 fold increase in lung lavage TNF-alpha concentrations. The increase in cytokines was associated with an increase in c-fos mRNA, an early response gene, suggesting that the concept of mechanotransduction (the conversion of cell or receptor deformation into biochemical responses) may play an important role in activating intracellular signal transduction pathways and leading to the development of biotrauma [21].
In experiments in which isolated lung cells were submitted to cyclic stretch (up to a 7 percent increase in diameter), increasing cell stretch increased release of a number of inflammatory mediators (eg, TNF-alpha, IL-6, IL-8, matrix metalloproteinase-9; show figure 3) [23]. The lung macrophage was the main source of these cytokines, which were associated with up-regulation of the transcription factor NF-kB. Dexamethasone prevented the increase in IL-8 and TNF-alpha.
Cytokines found in the lavage fluid may not be compartmentalized to the lung and may reach the systemic circulation [24]. As examples, one isolated perfused mouse model found that ventilation with high end-inspiratory stretch produced an increase in cytokines in the perfusate of the lungs [22]. A different group found that application of zero PEEP with a moderately large tidal volume (16 mL/kg) in an acid aspiration lung injury model in the rat resulted in an increase in serum TNF-alpha and MIP-2 over a four hour period [25]. When the same tidal volume was used with a higher PEEP level (5 cmH20), there was no significant increase in serum TNF-alpha.
These data suggest a mechanism (release of cytokines and/or inflammatory mediators into the systemic circulation) by which mechanical ventilation might effect systemic consequences and lead to the development of end-organ failure [2,26,27].
Another mechanism by which mechanical ventilation could produce systemic consequences is the translocation of bacteria from the lung into the circulation. High tidal volume ventilation with zero PEEP of lungs of dogs or rats, into which bacteria had been instilled, led to bacteremia in most of the animals. The addition of PEEP to the ventilation strategy was associated with a markedly lower incidence of bacteremia [28,29].
CLINICAL STUDIES — There are clinical data that suggest that the mechanisms described above may be relevant to humans [18]. In one randomized controlled trial in ARDS patients ventilated with either a conventional ventilatory strategy (tidal volume of 10 to 12 mL/kg; PEEP set at lowest value to maintain adequate oxygenation) or a protective strategy designed to minimize lung stress (PEEP above the lower inflection point; tidal volume such that the plateau pressure was less than the upper inflection point), there was a significant and marked decrease in lavage and serum cytokines in the ventilator group treated with the protective strategy over 36 hours [30].
The decrease in serum cytokines also may explain the decreased mortality observed in a 1998 study in which a high PEEP, low tidal volume strategy resulted in a 40 percent reduction in mortality [31]. A similar reduction in mortality in patients with ARDS ventilated with low tidal volumes was announced by the National Heart, Lung, and Blood Institute in 1999, when a study of 861 patients revealed significantly lower mortality (31 versus 40 percent) in patients treated with a low tidal volume strategy [3]. The study protocol compared an initial tidal volume of 6 mL/kg (and plateau pressure <30 cmH2O) with an initial tidal volume of 12 mL/kg (with plateau pressure <50 cmH2O); attempts were made to standardize PEEP and weaning protocols across both treatment groups.
Bulk flow can still provide conventional gas delivery to proximal alveoli with low regional dead space volumes.
Coaxial flow. Gas in the centre flows inward, while gas on the periphery flows outward. This can develop because of the asymmetric low profile of high velocity gases.
Taylor dispersion can produce a mixing of fresh and residual gas along the front of a flow of gas through a tube.
Pendelluft can mix gases between lung regions having different impedances.
Augmented molecular diffusion can occur at the alveolar level secondary to the added kinetic energy from the oscillations