Download acute respiratory failure (arf)

ACUTE
RESPIRATORY FAILURE (ARF)
Alicja Sniatkowska MD, PhD
Department of Pediatric Anaesthesiology
and Intensive Therapy
University of Medical Sciences in Poznan
Pathophysiology
of
Acute Respiratory Failure
Definition of ARF
According to the most clinicians:
Based upon the resulting abnormalities in arterial
oxygen and carbon dioxide levels
arterial oxygen tension (PaO2) is less than 60 mmHg at rest
breathing room air
arterial carbon dioxide (PaCO2) may be elevated, normal or low
Mechanisms
of Abnormal Gas Exchange
•
•
•
•
•
•
Hypoventilation
Ventilation-perfusion mismatching
Shunting
Diffusion impairment
Reduction in inspired oxygen concentration
Increased venous desaturation with cardiac dysfunction plus one or
more of the above 5 factors
Hypoventilation
• Characteristic abnormality in patients with
depressed central system function
inadequate chest movements
neuromuscular or skeletal diseases
• If the lungs are normal or near normal the rise of PaCO2 will be accompanied by a
corresponding fall in PaO2, for example:
„pure” hypoventilation is present if PaO2 is 50 and PaCO2 80 mmHg
which are changed from their normal values by about 40 mmHg
but
in contrast if PaO2 is only 30 mmHg with PaCO2 of 80 mmHg in the same patient
hypoventilation alone cannot explain the hypoxemia – presence of additional inadequate
ventilation
Ventilation-Perfusion Mismatching
Alveoli that are ventilated
must also be perfused !!!
V/Q Mismatching
V/Q mismatching is a common mechanism for both hypoxemia and carbon dioxide retention
Latter effect can be minimazed or eliminated by increasing minute volume (MV) – so may
result in overcompensation with a decrease in PaCO2 below normal ranges
Mild V/Q – corrected by increasing the inspired oxygen concentration (FiO2)
linear relationship
Severe V/Q – the rate of rise in PaO2 with increasing FiO2 decreases
curvilinear relationship
Very severe V/Q – effect of increasing FiO2 becomes similar to that seen with
shunts
Fig. Effects on arterial PO2 of changing inspired oxygen concentration
(FiO2 in the presence of increasing V/Q mismatching)
Mild V/Q
Severe V/Q
Very severe V/Q
Shunting
Right-to-left shunting of mixed venous blood through the lungs is the
major cause of hypoxemia in patients with acute lung injury,
including:
- cardiogenic pulmonary oedema
- noncardiogenic pulmonary oedema
- pulmonary embolism
Normal right-to-left shunt is approximately 2 to 3 %
unoxygenated blood from the bronchial, mediastinal veins goes emptying
directly into the left ventricle
Relationship between FiO2 and PaO2
according to severity of shunting
Extensive left-lung pneumonia caused respiratory failure;
the mechanism of hypoxia is intrapulmonary shunting
Diffusion Impairment
Diffusion impairment is the failure of the equilibration of the pulmonary
capillary blood with the alveolar gas
Normally the pulmonary capillary blood equilibrates with the alveolar gas in about 1/3 of the
time it takes to pass through the alveolar capillaries..........
So,
***In the cases of inadequate diffusion – we have a wide margin - before the clinical symptoms
of hypoxemia occurs
***Diffusing capacity must fall below 20% - before any change in PaO2 is seen
Abnormally rapid blood flow (e.g. in septic shock...)
... diffusion impairment does not cause hypoxemia
because...
the lung can increase its diffusing capacity by
recruiting additional pulmonary capillaries
Acid-base Disturbances
in ARF
Normal regulation of acid-base balance depends on three systems
in the body:
1.
2.
3.
Lungs
Kidneys
Body buffer systems
3a *carbonic acid ** phosphates***protein
3b intracellular-extracellular ion shifts
Regulate
pH 7,4
PaCO2 40 mmHg
bicarbonate 24mmol/l
in a normal person living at sea level
The accurate interpretation of a patient’s acid-base balance requires
integration of information from several different sources, incl.:
•
•
•
•
clinical history
physical examination
arterial blood gas analysis
Measurements of electrolites
Acid-base Normogram
The nomogram rates values of pH, pCO2 and HCO3 that would be expectated for
simple respiratory and metabolic acid-base disturbances.
Values lying out-side the bands suggest the presence of mixed disorder
Oxygen Delivery
Adequate systemic oxygen delivery depends on :
Cardiac output (Q)
Level of hemoglobin
Saturation
system
cardiovascular
hematologic
respiratory
•
•
•
•
•
100ml of arterial blood contains about 20 ml of oxygen
Normal resting cardiac output (CO) – 6 L/min
It means 1200ml of oxygen is delivered per minute
Normal resting consumption is about 300 ml/min
900 ml remains in the mixed venous blood (CvO2)
1g of hemoglobim carries 1,34 ml of oxygen when fully saturated
The ability of hemoglobin to bind oxygen at normal PaO2 levels and to give it
up at lower levels is described by the:
oxyhemoglobin disociation curve (fig.)
The normal oxyhemoglobin dissociation curve
at pH 7,4 and 37oC
Fig.
Hypothermia and
alkalemia shift the curve
to the left
Fever and acidemia
shift the curve
to the right
Oxygen Delivery Estimation
The adequacy of oxygen delivery could be estimate by measuring the mixed
venous PO2 – PvO2
PvO2 – about 40 mmHg
PvO2 < 30 mmHg – anaerobic cellular metabolism with lactic acid
production
Abnormalities of arterial oxygen content (CaO2), oxygen consumption
(VO2) and cardiac output (CO) are common in critically ill patients
Macrocirculation vs Ovygenation
1.
Oxygen extraction in the lungs
OXYGENATION
SaO2, PaO2, PCO2
2.
Oxygen transport from the lungs to the organs
MACROHAEMODYNAMICS
BP, MAP, CVP, HR,CO, CI, SVI, SVR
HB/Htk, CRT
3.
Oxygen extraction in the tissues
O2ER, ScvO2, SvO2, lactate clearance
CONSUMPTION
DO2 (Oxygen Delivery)
Extraction
in the lungs
Transport
from the
lungs into the
tissues
Extraction in
the tissues
VO2 : DO2
CO x (CaO2 – CvO) : CO x CaO2
1.
SpO2, SaO2, PaO2
CaO2 = SaO2 x Hb x 1,34
CvO2 = SvO2 x Hb x 1,34
2.
DO2 = CO x CaO2 ml/min x m2
CO x (SaO2 x Hb x 1,34) + (0,003 x PaO2)
DO2Index = DO2/BSA
3.
VO2
CO x (CaO2 – CvO2)
900 - 1100 ml/min
520 - 600 ml/min/m2
200 – 270 ml/min
(4 - 8 ml/min/kg)
VO2Index = VO2/BSA
110 - 160 ml/min/m2
4.
O2ER = VO2 / DO2 = (SatO2 – ScvO2):SatO2
0,2 – 0,3 (śr. 24%)
> 0,5 = kwasica
5.
ScvO2 / SvO2
> 70% / > 65%
Vincent JL. Crit Care Clin. 1996;12(4):995-1006. Review.
Comparison of variables
• O2ER disorder in the shock leads to the „pO2 gap”, when pcapO2
achieve the level lower then pvO2,e.g. Shunting
• „pO2 gap” – higher in sepsis in comparison to hypovolemic shock
DO2
CO
fluids, inotropes
Hb
RBC
SO2
oxygenation/mechanical ventilation
Edwards LifeSciences
ScvO2
Normal ≥
70%
Low ≤
70%
SaO2
Do nothing
Low
(hypoxemia)
Normal
≥ 95%
Oxygen therapy,
increased PEEP
Cardiac
output
High
>2,5 L/min/m2
Low
<2,5 L/min/m2
hemoglobin
SVV
> 8 g/dl
stress, anxiety,
pain
high VO2
< 8 g/dl
anemia
< 12% myocardial
dysfunction
> 12%
hypovolemia
Analgesia,sedation
Blood transfusion
Dobutamine
Fluid challenge
de Oliveira CF et al. Intensive Care Med. 2008 Jun;34(6):1065-75.
We conclude that goal-oriented resuscitation with the current ACCM/PALS
guidelines can improve morbidity and mortality when supplemented by
ScvO monitoring.
These2 findings may have a significant impact on the outcome of children and
adolescents with septic shock.
Lemson J et al. J Crit Care. 2011 Aug;26(4):432.e7-12.
EVLWI (Extravascular Lung Water Index)
GEDVI
(Global End-Diastolic Volume Index)
Lemson J et al. Crit Care. 2010;14(3):R105.
EVLWI vs Chest X-Ray
• Extravascular lung water index measured in critically ill children using the transpulmonary thermodilution technique does not correlate with a chest x-ray score of pulmonary edema.
• Extravascular lung water in critically ill children does not correlate with parameters of oxygenation.
• A chest x-ray score of pulmonary edema in critically ill children does not correlate with parameters of
oxygenation.
PEDIATRIC CONSIDERATIONS
The respiratory pump includes:
1. the nervous system with central control
(ie, cerebrum, brainstem, spinal cord, peripheral nerves)
2. respiratory muscles
3. chest wall.
Differences among pediatric children
include the following:
•
•
•
•
•
Infants
and
young
children
have
fewer
alveoli
than
do
adults.
The number dramatically increases during childhood, from approximately 20 million after
birth
to
300
million
by
8
years
of
age.
Therefore, infants and young children have a relatively small area for gas exchange.
The alveolus is small. Alveolar size increases from 150-180 to 250-300 µm during childhood.
Collateral ventilation is not fully developed; therefore, atelectasis is more common in
children than in adults. During childhood, anatomic channels form to provide collateral
ventilation to alveoli. These pathways are between adjacent alveoli (pores of Kohn),
bronchiole
and
alveoli
(Lambert
channel),
and
adjacent
bronchioles.
This important feature allows alveoli to participate in gas exchange even in the presence of
an obstructed distal airway.
Smaller intrathoracic airways are more easily obstructed than larger ones.
With age, the airways enlarge in diameter and length.
Infants and young children have relatively little cartilaginous support of the airways.
As cartilaginous support increases, dynamic compression during high expiratory flow rates
is prevented.
Features of note in pediatric patients
•
•
•
•
•
The respiratory center is immature in infants and young children and leads to
irregular respirations and an increased risk of apnea.
The ribs are horizontally oriented. During inspiration, a decreased volume is
displaced, and the capacity to increase tidal volume is limited compared with that
in older individuals.
The small surface area for the interaction between the diaphragm and thorax
limits displacing volume in the vertical direction.
The musculature is not fully developed. The slow-twitch fatigue-resistant muscle
fibers in the infant are underdeveloped.
The soft compliant chest wall provides little opposition to the deflating tendency
of the lungs. This leads to a lower functional residual capacity (FRC) in pediatric
patients than in adults, a volume that approaches the pediatric alveolus critical
closing volume.
ARF / ARDS
Definition of Acute Respiratory
Failure (ARF)
The term of ARF is defined very various by many authors:
1.
Primary disorder in gas exchange
(in contrast to acute ventilatory failure)
2.
Any disruption in the function of the respiratory system
(which is consist of the central nerwous system control center, efferent and
afferent nervous pathways, as well as muscles, lungs, pleura)
3.
The best def. described ARF as condition resulting in an abnormally low arterial
oxygen tension with or without an abnormally high arterial carbon dioxide tension
Two types of ARF
1.
Type 1 (termed nonventilatory, hypocapnic or normocapnic)
- is manifested by an abnormally low PaO2 with PaCO2 either low or normal
- disease process involving the lungs:
*acute lung injury
**ARDS (adult resipratory distress syndrome)
2.
Type 2 (ventilatory or hypercapnic)
- is manifested by hypoxemia as well as hypercapnia
- failure of alveolar ventilation
decrease in minute ventilation
increase in total dead space
*depression of CNS control of ventilation
**exacerbations of chronic obstructive pulmonary disease
(COPD)
Ventilation – perfusion relationships change
during the course of the illness,
so the type of respiratory failure may change
Remember – type1 and type2 do not
represent specific disease entities
but rather two manifestations of ARF
Assessment of Severity
Respiratory rate
• Tachypnoe
is the usual response to the respiratory difficulty but is also seen with
metabolic acidosis and psychological disturbances
tab. normal respiratory rates
Age
Breaths/minute
<1
1-5
5-12
>12
30-40
20-30
15-20
12-16
Increased work of respiration
• Recession
in younger children and infants the increased compliance of the chest will
make the recession a common sign, in older children
(>7 years) it signifies severe respiratrpy problems
• Use of accessory muscles
nasal flaring may indicate mild increase in work of breathing while
sternomastoid and ather muscles use indicates increased and severe
respiratory effort
• Grunting
Is due to decreased lower airway compliances
- characteristically seen in infants
- sign of severe respiratory difficulties
- may disappear in a fatigued child
Effectiveness of breathing
The colour of skin and mucus membrane gives a subjective assessment od
cyanosis.
Anaemia, poor perfusion, hypercapnia and poor lighting can complicate the assessment
Effect of respiration on other organs
• Cardiovascular system – hypoxia initially causes a tachycardia which leads
to bradycardia (more severe and pre-terminal)
• CNS – hypoxia leads to drowsiness and eventually coma
Etiologies of ARF
Brain
Spinal cord
Neuromuscular system
Thorax and Pleura
Upper airway
Cardiovascular
Lower Airway and Alveoli
Disruption of any link in
the chain may lead to the
development of acute
respiratory failure
Etiology of ARF
Examination
• LOOK
colour, sweating, distress, high respiratory rate, use of accessory muscles,
evidence of exhaustion, chest wall movements, jugular venous pulsation
• FEEL
tracheal position, chest expansion, percussion, subcutaneous ephysema
• LISTEN
breath sounds, vocal resonance will help
• ACT
identify and treat immediately, life threatening problems that are within your
capacity or call early for appropiate assistance
Adult Respiratory Distress Syndrome
(ARDS)
• Common cause of Acute Respiratory Failure
• There are similarities to Infant Respiratory Distress Syndrome
• Originally we thought that a lack of surfactant played an etiologic role but
later the defect of surfactant was found
• They were also the first groups describing the beneficial effect of positive
end-expiratory pressure (PEEP) in the treatment
• ARDS is associated with the high mortality
150,000 patients per year and
more than 75% need greater than 50% FiO2
ARDS
Bilateral airspace infiltrates on chest radiograph film secondary to acute respiratory distress
syndrome that resulted in respiratory failure
Criteria for Diagnosing of ARDS
The new Berlin definition of ARDS - 2012
Ioannis Pneumatikos1, MD, PhD, FCCP
Vasilios Ε. Papaioannou2, MD, MSc, PhD
PNEUMON Number 4, Vol. 25, October - December 2012
LIS score
Parameter
Finding
Value
Rx.Torax
no alveolar consolidation
0
alveolar consolidation de 1 quadrant
1
alveolar consolidation de 2 quadrant
2
alveolar consolidation de 3 quadrant
3
alveolar consolidation de 4 quadrant
4
score 0: no lung injury
score 0.1 - 2.5: mild-to-moderate lung injury
score > 2.5: severe lung injury (ARDS)
Hypoxemia
PaO2/FIO2 > 300
PaO2/FIO2 225 - 299
PaO2/FIO2 175 - 224
PaO2/FIO2 100 - 174
PaO2/FIO2 < 100
0
1
2
3
4
PEEP
PEEP <= 5 cm H2O
PEEP 6 - 8 cm H2O
PEEP 9 - 11 cm H2O
PEEP 12 - 14 cm H2O
PEEP >= 15 cm H2O
0
1
2
3
4
Pulmonary Compliance
compliance >= 80 mL/cm H2O
0
compliance 60 - 79 mL/cm H2O
1
compliance 40 - 59 mL/cm H2O
2
compliance 20 - 39 mL/cm H2O
3
compliance <= 19 mL/cm H2O
4
Causes of ARDS
Clinical stages of ARDS
Four phases
• Injury
• Apparent stability
• Respiratory insufficiency
• Terminal stage
Injury (1)
• Usually no evident clinical signs
• Chest roentgenogram may be clear
• Up to 6 hours
Apparent stability (2)
• Hyperventilation
• Abnormalities in chest roentgenogram
reticular infiltrates representing perivascular fluid
accumulation and interstitial oedema
• 12-24 hours
Respiratory insufficiency (3)
• Next 12-24 hours
• X-ray – five-lobed alveolar and interstitial infiltrate „snow
storm” picture
• Tachypnoe, crackles
• Severe reduction in PaO2 even high oxygen concentration
is given
Terminal stage (4)
• Persistent severe hypoxemia despite the administration of
100 percent oxygen
• High carbon dioxide retention
• The occurence of multiorgan dysfunction syndrome
(MODS)
Pathophysiology of ARDS
Primary site of injury in ARDS – alveolar-capillary membrane
Swelling and retraction of the capillary endothelial cells leads to increased alveolar
permeability and interstitial oedema
Increased interstitial fluid produces noncompliant lungs
Continuating process leads to alveolar oedema and alveolar collapse
Microatelectasis and alveolar disruptions and haemorrhagic oedema
Surfactant (phospholipoprotein produced by 2 types of pneumocyte) has decreased
activity
ARDS
Mechanism of Lung Injury
Mediators characteristic and responsible for producing and
sustaining the intense inflammatory response
•
•
•
•
•
•
•
•
•
•
•
•
Arachidonic acid and its metabolites such as prostaglandins, leukotriens, tromboxane A2
Serotonin
Histamine
ß-endorfin
Fibrin and fibrin degradation products (FDP)
Superoxides
Polymorphonuclear lukocytes
Platelets
Free fatty acids
Bradykinin
Proteolytic enzymes
Lysosomes
Treatment
There is no specific therapy for
ARDS!!!

Treatment of ARDS must
be individualized as a variety
of causes may produce this syndrome
Directions of treatment of ARDS
1.
Maintainence adequate tissue oxygenation
of vital organs, particularly the brain and heart
2.
Treatment of underlying cause of lung damage
Treatment of ARDS
•
Mechanical ventilation
non-invasive and invasive
small volumes 5-6 ml/kg b.w.
•
PEEP
•
Appropriate antibiotic therapy
when infection is present and severe sepsis or septic shock is responsible for ARDS
•
Immunologic therapy
•
Proper fluid balance
•
Haemofiltration or haemodiafiltration
•
Prevention and control of multiorgan dysfunction or failure
•
Proper and good nursing care
Tracheal intubation - MSOAPP
M = Monitors
(heart rate, blood pressure, pulse oximetry, capnography for CO2 detection)
S = Suction and catheters
O = Oxygenation with a bag-valve mask
A = Apparatus
(laryngoscope, endotracheal tubes appropriate for the patient's age and endotracheal tubes 0.5
size smaller and larger, stylets, oral airways)
P = Pharmacy
(medications for amnesia and paralysis)
P = People
(respiratory therapist, nurse, a skilled set of hands)
Oxygen Therapy
The initial treatment for hypoxemia is to provide supplemental
oxygen.
High-flow (>15 L/min) oxygen delivery systems include a Venturi-type
device that places an adjustable aperture lateral to the stream of
oxygen. Oxygen is mixed with entrained room air, and the amount of
air is adjusted by varying the aperture size. The oxygen hoods and
tents also supply high gas flows.
Low-flow (<6 L/min) oxygen delivery systems include the nasal
cannula and simple face mask.
Humidified high-flow nasal cannula (HHFNC)
Although no single universally accepted definition is available for
what constitutes HHFNC therapy in neonates, a widely used and
reasonable definition is optimally warmed (body temperature) and
humidified respiratory gases delivered by nasal cannula at flow rates
of 2-8 L/min.[2 ]
In 2004, the US Food and Drug Administration (FDA) approved a
device specifically for the provision of HHFNC in neonates:
Vapotherm 2000i (Vapotherm, Inc, Stevensville, MD). This devices
delivered molecular vapor with 95-100% relative humidity at body
temperature through nasal cannula at flow rates between 5-40
L/min.
Continuous positive airway pressure (CPAP)
CPAP may be indicated if lung disease results in severe oxygenation
abnormalities such that an FiO2 greater than 0.6 is needed to
maintain a PaO2 greater than 60 mm Hg.
CPAP in pressures from 3-10 cm H2 O is applied to increase lung
volume and may redistribute pulmonary edema fluid from the alveoli
to the interstitium.
CPAP enhances ventilation to areas with low V/Q ratios and improves
respiratory mechanics.
If a high concentration of FiO2 is needed and if the patient does not
tolerate even short periods of discontinued airway pressure,
positive-pressure ventilation should be administered.
Noninvasive positive-pressure ventilation (NPPV)
Noninvasive mechanical ventilation refers to assisted ventilation
provided with nasal prongs or a face mask instead of an
endotracheal or tracheostomy tube.
This therapy can be administered to decrease the work of breathing
and to provide adequate gas exchange.
NPPV can be given by using a volume ventilator, a pressurecontrolled ventilator, or a device for bilevel positive airway pressure
(BIPAP or bilevel ventilator).
Mechanical ventilation
A primary strategy for mechanical ventilation should be the avoidance of
high peak inspiratory pressures and the optimization of lung recruitment.
In adults with acute respiratory distress syndrome (ARDS), a strategy to
provide low tidal volume (6 mL/kg) with optimized positive end-expiratory
pressure (PEEP) offers a substantial survival benefit compared with a
strategy for high tidal volume (12 mL/kg).
According to the permissive hypercapnia strategy in ARDS, arterial CO2 is
allowed to rise to levels as high as 100 mm Hg while the blood pH is
maintained at greater than 7.2 by means of the intravenous administration
of buffer solutions. This is done to limit inspiratory airway pressure to
values less than 35 cm H2 O.
PEEP should be applied to a point above the inflection pressure such that
alveolar distention is maintained throughout the ventilatory cycle.
PEEP as Method of Therapy in ARDS
• PEEP (Positive End-Expiratory Pressure)
Indications:
-
to obtain optimal distention of alveoli
to reverse alveolar collapse
to increase the FRC (Functional Residual Capacity)
to correct the progressive atelectasis
it allows to maintenance of adequate oxygenation with a decrease in required
oxygen concentration – help tp minimaze the potential toxic effect of high oxygen
tension
to stabilize fluid-filled alveoli
to improve ventilation of alveoli which were previosly sites of shunting or low
ventilation in reltion to perfusion
there is no evidence that use of PEEP decreases extravascular lung water
(in fact high lung volumes may it increase...)
Non-positive effects and consequences of using PEEP
•
•
•
•
•
Impaired venous return
Increased pulmonary vascular resistance
Reduced left ventricular afterload
Altered right and left ventricular geometry
Altered compliance
Optimal level of PEEP ?!
Controversial opinions (.... 5 cm H2O)
The goal of PEEP is to allow a reduction in the FiO2
to 50% or less
Haemodynamic effects of positive
pressure ventilation on cardiac output
Likely effect on cardiac output
Haemodynamic effect of positive pressure
Preload dependent
ventilation
Afterload dependent
RV preload ↓
↓
↑
RV afterload ↑
↓
↓
LV preload ↓
↓
↑
LV afterload ↓
↑
↑
Prone positioning
Prone positioning reduces compliance of the thoracoabdominal cage by
impeding the compliant rib cage.
Gases should distribute toward the sternal and anterior diaphragmatic
regions that become dependent on prone positioning.
Improved homogeneity of ventilation improves oxygenation.
This measure may cause a redistribution of blood flow, improving the V/Q
match.
Researchers in a multicenter randomized controlled clinical trial concluded
that prone positioning did not significantly reduce ventilator-free days,
mortality, or time to recovery in pediatric patients with acute lung injury.
but…………
Prone positioning in ARDS
Extracorporeal life support (ECLS)
ECLS:
blood is removed from the patient, passed through an artificial
membrane where gas exchange occurs, and is returned to the body
by either the arterial (venoarterial [VA]) or venous (venovenous [VV])
system.
VV ECLS has become the preferred method for patients of all age
groups who do not require cardiac support.
From 1980-1998 at the University of Michigan, 586 neonatal, 132
pediatric, and 146 adult patients were given ECLS for respiratory
failure, with survival rates of 88%, 70%, and 56%, respectively.
Complications Associated with the ARDS
History of mechanical ventilation
• 1928r. First „iron lungs”, Boston, creator - Emerson
• 1948r. Ventilator Bennett in the USA
• 1950r. Ventilator Engström in Sweden
• 1952r. Epidemy of poliomyelitis, Kopenhagen, dr Björn Ibsen
cause – respiratory insufficiency among 11% of pts
mortality among them 90%!!!
New Techniques
of Mechanical Ventilation
• Pressure Support Ventilation (PSV)
• Pressure Support Ventilation Back Up Rate (PSV BUR)
• Pressure Controlled Ventilation (PCV)
• Pressure Assisted Controlled Ventilation (PACV)
• Controlled Volume (CV)
• Assisted Controlled Volume (ACV)
• Synchronous Intermittent Mandatory Ventilation (SIMV)
High Frequency Ventilation (HFV)
• HFO
High Frequency Oscillation Ventilation
rates up to 6,000bpm
• HFJV
High Frequency Jet Ventilation
rates up to 600 bpm
the tidal volumes are usually smaller than dead space
volume and much faster rates are utilized
Potential Uses for
High-Frequency Ventilation
• HFOV combines small tidal volumes (smaller than the calculated
airway dead space) with frequencies of more than 1 Hz to
minimize the effects of elevated peak and mean airway pressures.
• HFOV has proven benefit in improving the occurrence and
treatment of air-leak syndromes associated with neonatal and
pediatric acute lung injury.
Prognosis
The prognosis depends on the underlying etiology leading to acute
respiratory failure.
• The prognosis can be good when the respiratory failure is not very very
severe event and not associated with prolonged hypoxemia.
• The prognosis may be fair when a new process is associated with chronic
respiratory failure secondary to a neuromuscular disease or thoracic
deformity. This may herald the need for long-term mechanical ventilation.
• The prognosis can vary when respiratory failure is associated with a
chronic disease with acute exacerbations.
• Respiratory failure may be the sign of an irreversible progressive disease
that leads to death.
THANK YOU FOR
YOUR ATTENTION