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Dr. Md Mostafizur Rahman
Year 1 resident (pediatric
cardiology)
Dr. Azmery Saima
Year 3 resident (Neonatology)
BSMMU
Welcome
To
Seminar on HFV
Case scenario 2
A baby 28 weeker 1000g born by NVD due to
premature labour, mother did not get antenatal
corticosteroid. just after delivary baby has severe
respiratory distress.If we want to avoid long term
complications regarding respiratory system what
should be the management plan?
Outline
Introduction
Why HFV
Types of HFV
Indications
Mechanism of ventilation
Settings( Initiation and weaning)
Monitoring and routine care on HFV
Complications
Evidences
Case scenario 1
B/O Rina 18 hours old diagnosed as preterm(32 week)
with very low birth weight (1420g) respiratory distress
syndrome. baby on mechanical ventilation for last 12
hours with the following set up- mode SIMV, Rate 55,
pressure 20/6,FiO2 100%.Baby has persistent respiratory
distress, not maintaining saturation on conventional
mechanical ventilation with that set up. ABG reveals
severe respiratory acidosis. pH 7.03, PCO2 120, PO2 65,
HCO3 30.8
What should be the further respiratory management?
Mechanical ventilation
• Definition: It is a device to inflate the lungs artificially
by positive pressure.
Mechanical ventilation Normal ventilation
History
The earliest breathing machine
was the Drinker respirator. It
was invented in 1928 and was
known as an ‘iron lung’ for
people whose breathing
muscles had been paralyzed
by polio. They used negative
pressure to help patients
breathe while lying inside the
iron lung’s airtight chamber.
In 1949, American engineer
John Haven Emerson
developed an positive pressure
anesthetic ventilator.
High frequency ventilation
Definition- High frequency ventilation is a form of
mechanical ventilation that uses small tidal volume
sometimes less than anatomic dead space and very rapid
ventilatory rates (2 to 20 Hz or 120 to 1200 cycles/min).
• Tidal volume 1-3 ml/kg.
• Both isnspiration and expiration are active.
Assisted ventiltion of the neonate, Goldsmith 6th edition
High frequency oscillatory ventilation
HFOV in our NICU
1915,
Dr. Henderson studied
small tidal volumes and
rapid rates
1950-1970
Dr. Emerson,
Dr. Bird, Dr. Bunnell studied
HFV
1970’s
Success with animal
studies
1980’s
Four received FDA
approval
1990’s
HFOV
emerged
2000’s
HFOV for Adults
1991
1995 2001
???
HistoryofHigh FrequencyVentilation
Types of high frequency ventilation
1.High frequency flow interruption
(HFFI)
2.High frequency jet ventilation
(HFJV)
3.High frequency oscillator ventilation
(HFOV)
Why HFV?
• Small tidal volumes limits alveolar over distension .
• Higher MAP Better alveolar recruitment.
• Constant Paw during inspiration and expiration
preventing end alveolar collapse.
Ventilator Initiated Lung Injury
• All forms of positive pressure ventilation (PPV) can
cause ventilator induced lung injury (VILI).
• VILI is the result of a combination of the following
processes:
1. Barotrauma
2. Volutrauma
3. Atelectrauma
4. Biotrauma
Slutsky, Chest, 1999
Barotrauma
• High airway pressures during PPV can cause lung
overdistension with gross tissue injury.
• This injury can allow the transfer of air into the interstitial
tissues at the proximal airways.
• Clinically, barotrauma presents as pneumothorax,
pneumomediastinum, pneumopericardium, and
subcutaneous emphysema.
Slutsky, Chest, 1999
Volutrauma
• Lung overdistension can cause diffuse alveolar damage at the
pulmonary capillary membrane.
• This may result in increased epithelial and microvascular
permeability, thus, allowing fluid filtration into the alveoli
(pulmonary edema).
• Excessive end-inspiratory alveolar volumes are the major
determinant of volutrauma.
Atelectrauma
• Mechanical ventilation at low end-expiratory volumes may be
inefficient to maintain the alveoli open.
• Repetitive alveolar collapse and reopening of the under-
recruited alveoli result in atelectrauma.
• The quantitative and qualitative loss of surfactant may
predispose to atelectrauma.
Biotrauma
• In addition to the mechanical forms of injury, PPV
activates an inflammatory reaction that perpetuates
lung damage.
• Even ARDS from non-primary etiologies will result in
activation of the inflammatory cascade that can
potentially worsen lung function.
• This biological form of trauma is known as biotrauma.
HFOV is used to prevent
ventilator induced lung
injury
Pressure and Volume Swings
•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.
Indications of HFV
1.When conventional ventilation fails
– reduced compliance,RDS/ARDS,meconium aspiration ,BPD
,pneumonia,atelectases, lung hypoplasia
Other: PPHN
2.When conventional ventilation fails
Prematures relative: PIP > 22 mbar absolute: PIP > 25 mbar
Newborns relative: PIP > 25 mbar absolute: PIP > 28 mbar
3.Primary mode of ventilation in extreme prematurity.
4.Air leak syndromes (pneumothorax, PIE)
5.Congenital diaphragmatic hernia.
Advantages of HFV
1.Small tidal volume- prevents alveolar
overdistension and volutrauma.
2.High MAP- Improved alveolar recruitment leading
to better oxygenation.
3.Smaller gradient between inspiration and
expiration pressures- prevents cyclical
overdistension and collapse of alveoli and hence less
atelectrauma.
4.Low peak pressures- reduce barotrauma.
CV HFOV
Contraindications
The only relative contraindications for the use of
HFV is pulmonary obstruction.
Mechanism of gas exchange
• HFV Provides augmented gas distribution by means
of numerous gas transport mechanisms.
Convection ventilation( bulk flow)
Pendelluft effect
Taylor dispersion
Asymmetric velocity profiles
Cardiogenic Mixing
Molecular diffusion
Collateral Ventilation
Assisted ventiltion of the neonate, Goldsmith 6th edition
Mechanism of gas exchange
Pendelluft effect
Not all regions of the lung have the same compliance
and resistance. Therefore, neighbouring units with
different time constants are ventilated out of phase,
filling and emptying at different rates. Due to this
asynchrony these units can mutually exchange gas, an
effect known as pendelluft. By way of this mechanism
even very small fresh-gas volumes can reach a large
number of alveoli and regions.
Mechanism of gas exchange
Pendelluft effect - in which regional differences in time constants for
inflation and deflation cause gas to recirculate among lung units and
improve gas exchange.
Mechanism of gas exchange
• Taylor dispersion- in which augmented diffusion
occurs because of turbulant air currents that results
from interection between axial velocity and the radial
concentration gradient.
• The relationship between:
Axial velocity profile (Turbulence)
The diffusion of gases in motion and
The branching network of the lungs.
High frequency ventilation:current status, AAP
Taylor dispersion
Asymmetrical velocity
Airflow moves through the
airways in a u-shape formation. At
the center of the lumen air will
move at a faster velocity, than air
that is closest to the wall.
Asymmetry Occurs with rapid
respiratory cycles. Gases (O2) at
the center of the lumen will
advance further into the lungs as
gases (CO2) along the wall of the
airway moves out towards the
mouth.
• Asymmetrical Velocity Profiles
• Inspiration
The high frequency bulk flow creates a “bullet”
shaped flow profile, with the central molecules
moving further down the airway than those
molecules found on the periphery of the airway.
• Expiration
The velocity profile is blunted so that at the
completion of each return, the central molecules
remain further down the airway and the peripheral
molecules move towards the mouth of the airway.
Mechanism of gas exchange
As the heart beats the
heart provides additional
peripheral mixing by
exerting pressure against
the lungs during
contraction of the heart.
This pressure promotes
the movement of gas flow
through the neighboring
parenchymal regions.
Molecular diffusion
Maintaining a constant
distending pressure with
HFV within the lungs
along with movement of
gas molecules promotes
gas diffusion across the
alveolar membrane, at a
faster rate.
Mechanism of gas exchange
Control variables of HFV
1.Mean airway pressure (Paw)/ MAP
2.Amplitude / oscillatory volume (∆P)
3.Oscillatory frequency
4.The gas transport coefficient (DCO2)
Variables
1. Mean airway pressure (Paw)- Average airway pressure
throughout the respiratory cycle.
Paw should be 2-5 cm H2O higher than the previous
conventional ventilation.
Range of Paw are 3-25 mbar
In CPAP-HFOV mode, Paw equals the set PEEP.
In IMV-HFOV mode, Paw also depends on PIP and frequency.
If Paw ↑ → ↑ oscilatory volume→ ↓ PCo2
2. Amplitude -oscilatory volume (∆P)
Amplitude is the maximum extent of a vibration or
oscillation.
referred as delta p.
it is analogous to PIP on conventional ventilation.
Amplitude is increased until there is visible chest wall
vibration.
If amplitude ↑ → ↑ oscillatory volume → ↓PCo2→improve
oxygenation
3.Frequency- Number of cycles per unit of time.
measured in units of Hertz. ( 1 Hz = 60 breaths/min)
Usually set as 15 Hz for premature infants with RDS.
at low frequency large volumes are obtained whereas
above 10 hertz volumes become very small.
↓ Oscillatory frequency → ↑ oscillatory amplitude,
↑oscillatory volume → ↓ Pco2
Time X
Lower frequencies have
a larger volume
displacement and
improved CO2
elimination.
Frequency ()
4. Gas transport co efficient (DCo2)
In conventional ventilation the product of tidal volume and
frequency, known as minute volume or minute ventilation, aptly
describes pulmonary gas exchange. Different study groups have
found that CO2 elimination in HFO however correlates well with
VT2 x f
Here, VT and f stand for oscillatory volume and frequency, re
spectively. This parameter is called ‘gas transport coefficient’,
DCO2.
An increase in DCO2 will decrease pCO2
Variables in oxygenation
• The two primarily variables that control oxygenation are:
– FiO2
– Mean airway pressure (Paw)
Variables in ventilation
• The two primarily variables that control ventilation are:
– Tidal volume (P or amplitude)
• Controlled by the force with which the oscillatory
piston moves. (represented as stroke volume or P)
– Frequency ()
• Referenced in Hertz (1 Hz = 60 breaths/second)
• Range: 3 - 15 Hz
Initial settings
Depends on pathology
• Optimal lung volume strategy-
maximize recruitment of alveoli.
• Low volume srategy-
minimise lung trauma.
Settings of HFV
HFV: Start
MAP(PEEP): 2-5mbar above MAP of conventional
ventilation; if necessary, increase MAP until pO2 (↑)
after 30 min: X-ray: 8-9 rib level
IMV Rate: 3bpm
Pressure: 2 to 5 mbar below conventional ventilation
HFV frequency: 10 Hz
HFV amplitude: 100% watch thorax vibrations
HFV volume: about 2 to 2.5 ml/kg
“Wiggle Factor”
• Chest movement after initiation of HFOV indicates good
ventilation.
• If chest oscillation is diminished or absent consider:
1. Decreased pulmonary compliance
2. ETT disconnect
3. ETT obstruction
4. Severe bronchospasm
• If the chest oscillation is unilateral, consider:
1. ETT displacement (right mainstem)
2. Pneumothorax
HFV Continuation
Hypoxia: increase MAP up to 25 mbar max (if CVP does not
increase)
alternatively: apply sustained inflation at low lung volume ,apply
sigh manoeuvre every 20 minutes for 10 to 20 seconds at 10 to
15 mbar above MAP
Hyperoxia: reduce FiO2 down to about 0.6 – 0.3 very carefully,
decrease MAP
Hypercapnia: Increase DCO2
Amplitude 100%
Decrease HF-frequency
Increase MAP (above 10 mbar)
HFV Continuation
Hypocapnia: decrease DCO2
decrease amplitude
increase frequency
reduce MAP (below 8 mbar)
Overinflation: reduce MAP
decrease frequency
discontinue HFO
Hypotension: volume expansion
Dopamine/Dobutamine
reduce MAP
discontinue HFO
Monitoring during HFV
Ventilation parameters
Blood gases
Blood pressure, heart rate
CVP if possible
Sedation
Suctioning
Urine output
Chest radiograph (expiratory)
Lung function if possible
Humidification
It is essential to adequately humidify (90%) the breathing
gas. Otherwise severe irreversible damage to the trachea
may result. Viscous secretion could obstruct bronchi and
deteriorate the pulmonary situation. Excessive
humidification on the other hand can lead to
condensation in the patient circuit, the ET tube and the
airways, completely undoing the effect of HFV.
Weaning
HFV: Weaning
1. Reduce FiO2 to 0.3 – 0.5
2. Reduce MAP by 1 to 2 mbar per hour until (8) to 9 mbar;
then increase IMV rate
3. Reduce amplitude
4. Continue ventilation with IMV/SIMV and weaning
5. Extubation from HFV is also possible if respiratory
activity is sufficient
Strategies for various lung diseases
HFV for diffuse homogeneous lung diseases
Goals: lung expansion less barotrauma
begin with MAP 2 to 5 mbar above that of conventional
ventilation
then increase MAP until pO2 rises by 20 to 30 mmHg, or
CVP increases, or signs of overinflation appear
reduce FiO2 to 0.3 – 0.5 then continue weaning.
Strategies..
HFV for inhomogeneous lung diseases
Goals: improved oxygenation and ventilation at minimum
MAP
Risk: partial overexpansion
– begin with MAP like or below that of conventional
ventilation
– HFV frequency low, e.g. 7 Hz
– then increase MAP until PO2 slightly rises; keep MAP
constant; if respiratory situation fails to improve return to
conventional ventilation.
Strategies...
HFV with air leaks
Goal: improved oxygenation and ventilation at minimum
MAP; (accept lower pO2 and higher pCO2)
– Do not superimpose IMV!
– Begin with MAP like or below that of conventional
ventilation
– HFV frequency low, for example, 7 Hz
– Reduce pressure prior to FiO2
– Continue HFV for 24 to 48 hours after improvement
Strategies..
HFV in pulmonary hypertension of the newborn (PPHN)
Goals: to optimize lung volume and perfusion; to improve
hypoxia and hypercapnia while minimising barotrauma
– HFV frequency: <10 Hz
– HFV amplitude: 100%
– MAP: on the level of conventional ventilation; increase as
needed for oxygenation in 1 mbar in the presence of airleaks,
MAP as low as possible; reduce MAP very carefully! observe
cardiac function!
– IMV: rate 0 to 15 (30) bpm;
– reduce O2 prior to MAP
– Maintain HFV for 24 to 48 hours after recovery
Always: minimal handling, perhaps sedation or relaxation
Complications
1. Irritation- require more sedation.
2. hemodynamics- high MAP can jeopardies venous
return and cardiac output and also increase
puolmonary vascular resistance, Hypotension
3.Air trapping
4.Overinflation
5.Necrotizing tracheobronchitis
6.Intracranial haemorrhages.
Evidences
• Randomized study of high-frequency oscillatory ventilation
in infants with severe respiratory distress syndrome. HiFO
study group,April 1993.
• When the HFOV and CV groups were compared with control
for birth weight strata, study site, and inborn versus outborn
status, HFOV significantly reduced the development of air leak
syndrome in those patients who entered the study without
the syndrome. We conclude that HFOV, when the strategy
employed in this study is used, provides effective ventilation,
improves oxygenation, and significantly reduces the
development of air leak syndrome in infants with severe
respiratory distress syndrome.
Evidences
Pediatrics. 1996 Dec;98(6 Pt 1):1044-57.
The Provo multicenter early high-frequency oscillatory
ventilation trial: improved pulmonary and clinical outcome in
respiratory distress syndrome.Gerstmann DR, Minton SD,
Stoddard RA, Meredith KS, Monaco F, Bertrand JM, Battisti O,
Langhendries JP, Francois A, Clark RH.
When used early with a lung recruitment strategy, HFOV after
surfactant replacement resulted in clinical outcomes consistent
with a reduction in both acute and chronic lung injury. Benefit
was evident for preterm infants both less than or equal to 1 kg
and more than 1 kg.
• In addition, early HFOV treatment may have had a
more global effect on patient health throughout the
hospitalization, resulting in reduced morbidity and
decreased health care cost.
Evidences
N Engl J Med. 2002 Aug 29;347(9):643-52.
High-frequency oscillatory ventilation versus conventional
mechanical ventilation for very-low-birth-weight
infants.Courtney SE, Durand DJ, Asselin JM, Hudak ML,
Aschner JL, Shoemaker CT; Neonatal Ventilation Study
Group.
Here was a small but significant benefit of high-frequency
oscillatory ventilation in terms of the pulmonary outcome
for very-low-birth-weight infants without an increase in the
occurrence of other complications of premature birth.
Evidence
As a primary mode
Elective high frequency ventilation compared to
conventional mechanical ventilation in the early
stabilization of infants with respiratory distress -
Cochrane-March 2015
Insufficient evidence exists to support the routine use of
high frequency oscillatory ventilation instead of
conventional ventilation for preterm infants.
• High frequency oscillatory ventilation is a way of
providing artificial ventilation of the lungs that
theoretically may produce less injury to the lungs and
therefore reduce the rate of chronic lung disease. This
review of the evidence from 19 randomised controlled
trials showed that although a small protective effect
towards the lungs can be seen, this moderate benefit is
highly variable between studies and should be weighed
against possible harm.
Looking towards the future
• A great deal remains unknown about HFOV:
– the exact mechanism of gas exchange
– the most effective strategy to manipulate ventilator settings
– the safest approach to manipulate ventilator settings
– a reliable method to measure tidal volume
– the appropriate use of sedation and neuromuscular blockade
to optimize patient-ventilator interactions
• Additional research in these and other issues related to HFOV
are necessary to maximize the benefit and minimize the
potential risks associated with HFOV.
References
• Goldsmith: Assisted ventilation of the neonate
• Pediatric and neonatal mechanical ventilation-praveen khilnani
• Dragger manuals – high frequency ventilation basics and practical
application
• High frequency ventilation: current status, pediatrics in review
• Priebe GP, Arnold JH: High-frequency oscillatory ventilation in
pediatric patients. Respir Care Clin N Am 2001; 7(4):633-645
• RPA newborn care guideline
• Arnold JH, Anas NG, Luckett P, Cheifetz IM, Reyes G, Newth CJ,
Kocis KC, Heidemann SM, Hanson JH, Brogan TV, et al.: High-
frequency oscillatory ventilation in pediatric respiratory failure: a
multicenter experience. Crit Care Med 2000; 28(12):3913-3919
References
• Arnold JH: High-frequency ventilation in the pediatric
intensive care unit. Pediatr Crit Care Med 2000; 1(2):93-99
• Slutsky, AS: Lung Injury Caused by Mechanical Ventilation.
Chest 1999; 116(1):9S-14S
• dos Santos CC, Slutsky AS: Overview of high-frequency
ventilation modes, clinical rationale, and gas transport
mechanisms. Respir Care Clin N Am 2001; 7(4):549-575
• Duke PICU Handbook (revised 2003)
• Duke Ventilator Management Protocol (2004)
THANK YOU

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seminar on hfv - high frequency ventilation dr saima

  • 1. Dr. Md Mostafizur Rahman Year 1 resident (pediatric cardiology) Dr. Azmery Saima Year 3 resident (Neonatology) BSMMU Welcome To Seminar on HFV
  • 2. Case scenario 2 A baby 28 weeker 1000g born by NVD due to premature labour, mother did not get antenatal corticosteroid. just after delivary baby has severe respiratory distress.If we want to avoid long term complications regarding respiratory system what should be the management plan?
  • 3. Outline Introduction Why HFV Types of HFV Indications Mechanism of ventilation Settings( Initiation and weaning) Monitoring and routine care on HFV Complications Evidences
  • 4. Case scenario 1 B/O Rina 18 hours old diagnosed as preterm(32 week) with very low birth weight (1420g) respiratory distress syndrome. baby on mechanical ventilation for last 12 hours with the following set up- mode SIMV, Rate 55, pressure 20/6,FiO2 100%.Baby has persistent respiratory distress, not maintaining saturation on conventional mechanical ventilation with that set up. ABG reveals severe respiratory acidosis. pH 7.03, PCO2 120, PO2 65, HCO3 30.8 What should be the further respiratory management?
  • 5. Mechanical ventilation • Definition: It is a device to inflate the lungs artificially by positive pressure. Mechanical ventilation Normal ventilation
  • 6. History The earliest breathing machine was the Drinker respirator. It was invented in 1928 and was known as an ‘iron lung’ for people whose breathing muscles had been paralyzed by polio. They used negative pressure to help patients breathe while lying inside the iron lung’s airtight chamber. In 1949, American engineer John Haven Emerson developed an positive pressure anesthetic ventilator.
  • 7. High frequency ventilation Definition- High frequency ventilation is a form of mechanical ventilation that uses small tidal volume sometimes less than anatomic dead space and very rapid ventilatory rates (2 to 20 Hz or 120 to 1200 cycles/min). • Tidal volume 1-3 ml/kg. • Both isnspiration and expiration are active. Assisted ventiltion of the neonate, Goldsmith 6th edition
  • 9. HFOV in our NICU
  • 10. 1915, Dr. Henderson studied small tidal volumes and rapid rates 1950-1970 Dr. Emerson, Dr. Bird, Dr. Bunnell studied HFV 1970’s Success with animal studies 1980’s Four received FDA approval 1990’s HFOV emerged 2000’s HFOV for Adults 1991 1995 2001 ??? HistoryofHigh FrequencyVentilation
  • 11. Types of high frequency ventilation 1.High frequency flow interruption (HFFI) 2.High frequency jet ventilation (HFJV) 3.High frequency oscillator ventilation (HFOV)
  • 12.
  • 13. Why HFV? • Small tidal volumes limits alveolar over distension . • Higher MAP Better alveolar recruitment. • Constant Paw during inspiration and expiration preventing end alveolar collapse.
  • 14. Ventilator Initiated Lung Injury • All forms of positive pressure ventilation (PPV) can cause ventilator induced lung injury (VILI). • VILI is the result of a combination of the following processes: 1. Barotrauma 2. Volutrauma 3. Atelectrauma 4. Biotrauma Slutsky, Chest, 1999
  • 15. Barotrauma • High airway pressures during PPV can cause lung overdistension with gross tissue injury. • This injury can allow the transfer of air into the interstitial tissues at the proximal airways. • Clinically, barotrauma presents as pneumothorax, pneumomediastinum, pneumopericardium, and subcutaneous emphysema. Slutsky, Chest, 1999
  • 16. Volutrauma • Lung overdistension can cause diffuse alveolar damage at the pulmonary capillary membrane. • This may result in increased epithelial and microvascular permeability, thus, allowing fluid filtration into the alveoli (pulmonary edema). • Excessive end-inspiratory alveolar volumes are the major determinant of volutrauma.
  • 17. Atelectrauma • Mechanical ventilation at low end-expiratory volumes may be inefficient to maintain the alveoli open. • Repetitive alveolar collapse and reopening of the under- recruited alveoli result in atelectrauma. • The quantitative and qualitative loss of surfactant may predispose to atelectrauma.
  • 18. Biotrauma • In addition to the mechanical forms of injury, PPV activates an inflammatory reaction that perpetuates lung damage. • Even ARDS from non-primary etiologies will result in activation of the inflammatory cascade that can potentially worsen lung function. • This biological form of trauma is known as biotrauma.
  • 19. HFOV is used to prevent ventilator induced lung injury
  • 20. Pressure and Volume Swings •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.
  • 21. Indications of HFV 1.When conventional ventilation fails – reduced compliance,RDS/ARDS,meconium aspiration ,BPD ,pneumonia,atelectases, lung hypoplasia Other: PPHN 2.When conventional ventilation fails Prematures relative: PIP > 22 mbar absolute: PIP > 25 mbar Newborns relative: PIP > 25 mbar absolute: PIP > 28 mbar 3.Primary mode of ventilation in extreme prematurity. 4.Air leak syndromes (pneumothorax, PIE) 5.Congenital diaphragmatic hernia.
  • 22. Advantages of HFV 1.Small tidal volume- prevents alveolar overdistension and volutrauma. 2.High MAP- Improved alveolar recruitment leading to better oxygenation. 3.Smaller gradient between inspiration and expiration pressures- prevents cyclical overdistension and collapse of alveoli and hence less atelectrauma. 4.Low peak pressures- reduce barotrauma.
  • 24. Contraindications The only relative contraindications for the use of HFV is pulmonary obstruction.
  • 25. Mechanism of gas exchange • HFV Provides augmented gas distribution by means of numerous gas transport mechanisms. Convection ventilation( bulk flow) Pendelluft effect Taylor dispersion Asymmetric velocity profiles Cardiogenic Mixing Molecular diffusion Collateral Ventilation Assisted ventiltion of the neonate, Goldsmith 6th edition
  • 26. Mechanism of gas exchange Pendelluft effect Not all regions of the lung have the same compliance and resistance. Therefore, neighbouring units with different time constants are ventilated out of phase, filling and emptying at different rates. Due to this asynchrony these units can mutually exchange gas, an effect known as pendelluft. By way of this mechanism even very small fresh-gas volumes can reach a large number of alveoli and regions.
  • 27. Mechanism of gas exchange Pendelluft effect - in which regional differences in time constants for inflation and deflation cause gas to recirculate among lung units and improve gas exchange.
  • 28. Mechanism of gas exchange • Taylor dispersion- in which augmented diffusion occurs because of turbulant air currents that results from interection between axial velocity and the radial concentration gradient. • The relationship between: Axial velocity profile (Turbulence) The diffusion of gases in motion and The branching network of the lungs. High frequency ventilation:current status, AAP
  • 30. Asymmetrical velocity Airflow moves through the airways in a u-shape formation. At the center of the lumen air will move at a faster velocity, than air that is closest to the wall. Asymmetry Occurs with rapid respiratory cycles. Gases (O2) at the center of the lumen will advance further into the lungs as gases (CO2) along the wall of the airway moves out towards the mouth.
  • 31. • Asymmetrical Velocity Profiles • Inspiration The high frequency bulk flow creates a “bullet” shaped flow profile, with the central molecules moving further down the airway than those molecules found on the periphery of the airway. • Expiration The velocity profile is blunted so that at the completion of each return, the central molecules remain further down the airway and the peripheral molecules move towards the mouth of the airway.
  • 32. Mechanism of gas exchange As the heart beats the heart provides additional peripheral mixing by exerting pressure against the lungs during contraction of the heart. This pressure promotes the movement of gas flow through the neighboring parenchymal regions.
  • 33. Molecular diffusion Maintaining a constant distending pressure with HFV within the lungs along with movement of gas molecules promotes gas diffusion across the alveolar membrane, at a faster rate.
  • 34. Mechanism of gas exchange
  • 35. Control variables of HFV 1.Mean airway pressure (Paw)/ MAP 2.Amplitude / oscillatory volume (∆P) 3.Oscillatory frequency 4.The gas transport coefficient (DCO2)
  • 36.
  • 37. Variables 1. Mean airway pressure (Paw)- Average airway pressure throughout the respiratory cycle. Paw should be 2-5 cm H2O higher than the previous conventional ventilation. Range of Paw are 3-25 mbar In CPAP-HFOV mode, Paw equals the set PEEP. In IMV-HFOV mode, Paw also depends on PIP and frequency. If Paw ↑ → ↑ oscilatory volume→ ↓ PCo2
  • 38. 2. Amplitude -oscilatory volume (∆P) Amplitude is the maximum extent of a vibration or oscillation. referred as delta p. it is analogous to PIP on conventional ventilation. Amplitude is increased until there is visible chest wall vibration. If amplitude ↑ → ↑ oscillatory volume → ↓PCo2→improve oxygenation
  • 39. 3.Frequency- Number of cycles per unit of time. measured in units of Hertz. ( 1 Hz = 60 breaths/min) Usually set as 15 Hz for premature infants with RDS. at low frequency large volumes are obtained whereas above 10 hertz volumes become very small. ↓ Oscillatory frequency → ↑ oscillatory amplitude, ↑oscillatory volume → ↓ Pco2
  • 40. Time X Lower frequencies have a larger volume displacement and improved CO2 elimination. Frequency ()
  • 41. 4. Gas transport co efficient (DCo2) In conventional ventilation the product of tidal volume and frequency, known as minute volume or minute ventilation, aptly describes pulmonary gas exchange. Different study groups have found that CO2 elimination in HFO however correlates well with VT2 x f Here, VT and f stand for oscillatory volume and frequency, re spectively. This parameter is called ‘gas transport coefficient’, DCO2. An increase in DCO2 will decrease pCO2
  • 42.
  • 43. Variables in oxygenation • The two primarily variables that control oxygenation are: – FiO2 – Mean airway pressure (Paw)
  • 44. Variables in ventilation • The two primarily variables that control ventilation are: – Tidal volume (P or amplitude) • Controlled by the force with which the oscillatory piston moves. (represented as stroke volume or P) – Frequency () • Referenced in Hertz (1 Hz = 60 breaths/second) • Range: 3 - 15 Hz
  • 45. Initial settings Depends on pathology • Optimal lung volume strategy- maximize recruitment of alveoli. • Low volume srategy- minimise lung trauma.
  • 46. Settings of HFV HFV: Start MAP(PEEP): 2-5mbar above MAP of conventional ventilation; if necessary, increase MAP until pO2 (↑) after 30 min: X-ray: 8-9 rib level IMV Rate: 3bpm Pressure: 2 to 5 mbar below conventional ventilation HFV frequency: 10 Hz HFV amplitude: 100% watch thorax vibrations HFV volume: about 2 to 2.5 ml/kg
  • 47. “Wiggle Factor” • Chest movement after initiation of HFOV indicates good ventilation. • If chest oscillation is diminished or absent consider: 1. Decreased pulmonary compliance 2. ETT disconnect 3. ETT obstruction 4. Severe bronchospasm • If the chest oscillation is unilateral, consider: 1. ETT displacement (right mainstem) 2. Pneumothorax
  • 48. HFV Continuation Hypoxia: increase MAP up to 25 mbar max (if CVP does not increase) alternatively: apply sustained inflation at low lung volume ,apply sigh manoeuvre every 20 minutes for 10 to 20 seconds at 10 to 15 mbar above MAP Hyperoxia: reduce FiO2 down to about 0.6 – 0.3 very carefully, decrease MAP Hypercapnia: Increase DCO2 Amplitude 100% Decrease HF-frequency Increase MAP (above 10 mbar)
  • 49. HFV Continuation Hypocapnia: decrease DCO2 decrease amplitude increase frequency reduce MAP (below 8 mbar) Overinflation: reduce MAP decrease frequency discontinue HFO Hypotension: volume expansion Dopamine/Dobutamine reduce MAP discontinue HFO
  • 50. Monitoring during HFV Ventilation parameters Blood gases Blood pressure, heart rate CVP if possible Sedation Suctioning Urine output Chest radiograph (expiratory) Lung function if possible
  • 51. Humidification It is essential to adequately humidify (90%) the breathing gas. Otherwise severe irreversible damage to the trachea may result. Viscous secretion could obstruct bronchi and deteriorate the pulmonary situation. Excessive humidification on the other hand can lead to condensation in the patient circuit, the ET tube and the airways, completely undoing the effect of HFV.
  • 52. Weaning HFV: Weaning 1. Reduce FiO2 to 0.3 – 0.5 2. Reduce MAP by 1 to 2 mbar per hour until (8) to 9 mbar; then increase IMV rate 3. Reduce amplitude 4. Continue ventilation with IMV/SIMV and weaning 5. Extubation from HFV is also possible if respiratory activity is sufficient
  • 53. Strategies for various lung diseases HFV for diffuse homogeneous lung diseases Goals: lung expansion less barotrauma begin with MAP 2 to 5 mbar above that of conventional ventilation then increase MAP until pO2 rises by 20 to 30 mmHg, or CVP increases, or signs of overinflation appear reduce FiO2 to 0.3 – 0.5 then continue weaning.
  • 54. Strategies.. HFV for inhomogeneous lung diseases Goals: improved oxygenation and ventilation at minimum MAP Risk: partial overexpansion – begin with MAP like or below that of conventional ventilation – HFV frequency low, e.g. 7 Hz – then increase MAP until PO2 slightly rises; keep MAP constant; if respiratory situation fails to improve return to conventional ventilation.
  • 55. Strategies... HFV with air leaks Goal: improved oxygenation and ventilation at minimum MAP; (accept lower pO2 and higher pCO2) – Do not superimpose IMV! – Begin with MAP like or below that of conventional ventilation – HFV frequency low, for example, 7 Hz – Reduce pressure prior to FiO2 – Continue HFV for 24 to 48 hours after improvement
  • 56. Strategies.. HFV in pulmonary hypertension of the newborn (PPHN) Goals: to optimize lung volume and perfusion; to improve hypoxia and hypercapnia while minimising barotrauma – HFV frequency: <10 Hz – HFV amplitude: 100% – MAP: on the level of conventional ventilation; increase as needed for oxygenation in 1 mbar in the presence of airleaks, MAP as low as possible; reduce MAP very carefully! observe cardiac function! – IMV: rate 0 to 15 (30) bpm; – reduce O2 prior to MAP – Maintain HFV for 24 to 48 hours after recovery Always: minimal handling, perhaps sedation or relaxation
  • 57. Complications 1. Irritation- require more sedation. 2. hemodynamics- high MAP can jeopardies venous return and cardiac output and also increase puolmonary vascular resistance, Hypotension 3.Air trapping 4.Overinflation 5.Necrotizing tracheobronchitis 6.Intracranial haemorrhages.
  • 58. Evidences • Randomized study of high-frequency oscillatory ventilation in infants with severe respiratory distress syndrome. HiFO study group,April 1993. • When the HFOV and CV groups were compared with control for birth weight strata, study site, and inborn versus outborn status, HFOV significantly reduced the development of air leak syndrome in those patients who entered the study without the syndrome. We conclude that HFOV, when the strategy employed in this study is used, provides effective ventilation, improves oxygenation, and significantly reduces the development of air leak syndrome in infants with severe respiratory distress syndrome.
  • 59. Evidences Pediatrics. 1996 Dec;98(6 Pt 1):1044-57. The Provo multicenter early high-frequency oscillatory ventilation trial: improved pulmonary and clinical outcome in respiratory distress syndrome.Gerstmann DR, Minton SD, Stoddard RA, Meredith KS, Monaco F, Bertrand JM, Battisti O, Langhendries JP, Francois A, Clark RH. When used early with a lung recruitment strategy, HFOV after surfactant replacement resulted in clinical outcomes consistent with a reduction in both acute and chronic lung injury. Benefit was evident for preterm infants both less than or equal to 1 kg and more than 1 kg.
  • 60. • In addition, early HFOV treatment may have had a more global effect on patient health throughout the hospitalization, resulting in reduced morbidity and decreased health care cost.
  • 61. Evidences N Engl J Med. 2002 Aug 29;347(9):643-52. High-frequency oscillatory ventilation versus conventional mechanical ventilation for very-low-birth-weight infants.Courtney SE, Durand DJ, Asselin JM, Hudak ML, Aschner JL, Shoemaker CT; Neonatal Ventilation Study Group. Here was a small but significant benefit of high-frequency oscillatory ventilation in terms of the pulmonary outcome for very-low-birth-weight infants without an increase in the occurrence of other complications of premature birth.
  • 62. Evidence As a primary mode Elective high frequency ventilation compared to conventional mechanical ventilation in the early stabilization of infants with respiratory distress - Cochrane-March 2015 Insufficient evidence exists to support the routine use of high frequency oscillatory ventilation instead of conventional ventilation for preterm infants.
  • 63. • High frequency oscillatory ventilation is a way of providing artificial ventilation of the lungs that theoretically may produce less injury to the lungs and therefore reduce the rate of chronic lung disease. This review of the evidence from 19 randomised controlled trials showed that although a small protective effect towards the lungs can be seen, this moderate benefit is highly variable between studies and should be weighed against possible harm.
  • 64. Looking towards the future • A great deal remains unknown about HFOV: – the exact mechanism of gas exchange – the most effective strategy to manipulate ventilator settings – the safest approach to manipulate ventilator settings – a reliable method to measure tidal volume – the appropriate use of sedation and neuromuscular blockade to optimize patient-ventilator interactions • Additional research in these and other issues related to HFOV are necessary to maximize the benefit and minimize the potential risks associated with HFOV.
  • 65. References • Goldsmith: Assisted ventilation of the neonate • Pediatric and neonatal mechanical ventilation-praveen khilnani • Dragger manuals – high frequency ventilation basics and practical application • High frequency ventilation: current status, pediatrics in review • Priebe GP, Arnold JH: High-frequency oscillatory ventilation in pediatric patients. Respir Care Clin N Am 2001; 7(4):633-645 • RPA newborn care guideline • Arnold JH, Anas NG, Luckett P, Cheifetz IM, Reyes G, Newth CJ, Kocis KC, Heidemann SM, Hanson JH, Brogan TV, et al.: High- frequency oscillatory ventilation in pediatric respiratory failure: a multicenter experience. Crit Care Med 2000; 28(12):3913-3919
  • 66. References • Arnold JH: High-frequency ventilation in the pediatric intensive care unit. Pediatr Crit Care Med 2000; 1(2):93-99 • Slutsky, AS: Lung Injury Caused by Mechanical Ventilation. Chest 1999; 116(1):9S-14S • dos Santos CC, Slutsky AS: Overview of high-frequency ventilation modes, clinical rationale, and gas transport mechanisms. Respir Care Clin N Am 2001; 7(4):549-575 • Duke PICU Handbook (revised 2003) • Duke Ventilator Management Protocol (2004)