hi everyone today we will be talking
about respiratory failure and
indications of mechanical ventilation
the way we're going to approach this is
based on the respiratory failure
pathophysiology in order to sustain
oxygenation and alveolar ventilation the
respiratory system has to be able to
overcome any load that is put on the
system this load could be resistive
loads such as in patients with asthma
elastic load such as patients with
pneumonia Pommery edema or hay RDS or
high minute ventilation loads such as
patients with severe sepsis and the
patient will be able to overcome that
load by having adequate neuromuscular
competence that will provide the work of
breathe required to overcome that load
so if you put the work of twins in the
middle here and it is a product of
respiratory rate and muscle strains this
work of breathe would be needed to
overcome any resistive load of the
Airways any
clusters Lord of the lung or the chest
wall or any minute ventilation Lord of
the body if the work of breathe is
enough the patient will have adequate
oxygenation and ventilation based on
that we can classify respiratory failure
into four different categories number
one respiratory failure due to increased
resistance respiratory failure due to
decreased compliance or increased
elastance number three respiratory
failure due to increased minute
ventilation and number four respiratory
failure due to decreased neuromuscular
competence
we will be giving example of each of
this categories a six-year-old boy with
asthma coming to emergency room with
severe respiratory distress tachycardic
at 26 per minute and taking 26 per
minute tachycardic at 130 per minute
they are phoretic wheezing and using
accessory muscles however when you do a
bee gees insured it shows that PS 7.47
pco2 30 po2 88 and saturation 95% so the
problem of this patient has increased
resistive load and this will give you a
high time constant in expiratory phase
which is a hard come off or the product
of resistance multiplied by compliance
we have increased resistance here this
will be manifested with prolonged
expiration and Asia has wheezes he may
have inflated chest if he developed
dynamic hyperinflation syndrome the
patient will increase his response rate
and the muscle strains in order to
overcome that increased resistance and
they will increase work of breathe if he
is able to provide that you will have
had adequate oxygenation and ventilation
and this will be manifested by deep
private academia using of accessory
muscles and that later stage he may show
signs of strain and he will call him to
respiratory failure so at this stage our
patient is showing balanced rest present
resistive load and neuro muscular
competence he has an increased resistive
load due to bronchospasm however he was
able to increase his neuromuscular
competence and overcome that node so he
killed the system in balance if this
patient gets tired or or if you give him
2 milligrams of midazolam you're going
to tip the balance off and the patient
you know muscular combat
will not be able to balance the
increased resistive load and this
patient will go into respiratory failure
indicated by decreasing pH and
increasing pco2 the second example is an
patient with pneumonia and going into a
RDS he already presented with
respiratory of 38 systolic pressure of
70 heart rate of 135 and he was using
accessory muscles with rapid shallow
breathing he was intubated his own fio2
of 90% PS 7.19 BC or 230 po2 57 he has a
high a gradient indicating shunting
process due to who due to his pneumonia
and here this
he was hyperventilating and having
combined metabolic acidosis and
metabolic alkalosis
this patient has increased resistance
I'm sorry increased elastance Lord due
to lung problem and his heart C or time
constant the history time constant
constant constant is decreased and it's
manifested by rapid shallow breathing
this patient had increased work of
breathing creased response rate and the
muscle strength trying to overcome this
decreased compliance or he creased
elastance however he was not able to
maintain that and he presented with
rapid shallow breathing
he used accessory muscles and he showed
signs of strain he was hypoxemic already
healthy was placed on mechanical
ventilation so he was already in
respiratory failure when he presented he
had an increased elastance load and he
could not overcome that elastance note
he had an increased neuromuscular
competence but it was not enough to
overcome death to overcome that
Stan's lot thus he presented with
respiratory failure the third case is a
patient who has been in the hospital
with Uri tract infection was recovering
but showed signs of diaphoresis dyspnea
and hypotension
he was breathing at 3 liters per minute
of oxygen respiratory it was 42 systolic
but palapa shot 65 and heart rate 150
his pH was seven point four zero B co2
20 and po2 of 80 saturation ninety-five
percent he has the humans mass with a
gradient of 124 he has significant high
minute ventilation secondary to high
metabolism secondary to sepsis
he has metabolic acidosis and
respiratory alkalosis indicating
increased demand so his problem is not a
resistive load and it is not in
elastance Lord he has increased minute
ventilation load because of severe
sepsis
so his increased main ventilation is
required and increased work of breathing
so he had an increased response rate and
increase muscle strength the wall of
green was able to provide adequate
oxygenation and ventilation for this
patient manifested with Robins deep
tachypnea use of accessory muscles this
patient may have signs of strain at
later stage so you can see here that
there was there was a balance between
the increased minute ventilation Lord
and the neuromuscular competence the
patient was able to increase his work of
breathe in in order to meet the demands
of his body so pH was 7.4 c40 miss your
to 2010 po2 of Haiti
however at later stage this patient may
get tired and his neuromuscular
competence would not be enough to
overcome that increased load and it will
tip off the almost Lord competence and
the patient would go into respiratory
failure pH is going down here 7.29 pco2
35 in 2002 67 the last case is a patient
with who was a 27 year old being
evaluated in emergency room for a
keyword decreased level of consciousness
his own lumière ph 7.19 B co2 is
elevated at 65 and po2 is decreased at
65 in analyzing his ABCs you can see
that he has a normal or slightly
elevated a gradient indicating
hypoventilation status or
hyperventilation process the beige is
hyperventilating with a high B co2 and
he has acute respiratory and metabolic
acidosis so the problem is not a
resistive load over here elastic elastic
load it is not in minute ventilation his
problem actually is in the competence in
the neuromuscular competence he may have
a problem in decreased transmission
drives such as in lesions of the brain
drugs or hypothyroidism he may have a
problem with the muscle strains strains
such as electrolyte problem hypokalemia
for example fatigue myopathy or
malnutrition or he may her he may have a
problem in the neuromuscular connection
as in ALS myasthenia gravis
guillain-barré a or pata visible so the
work of peas for him his lower than
normal and that is not enough to
maintain adequate harsh nation and
ventilations mean it's mainly
ventilation problem
there is no - take there is no VQ
mismatch
- cause hypoventilation hypoxemia the
hypoxemia that he has is the result of
his hyperventilation this patient may
present with a low res graduate he will
have a low tidal volume if you measure
the fatica pass he will be low and if
you measure the negative inspiratory
force will be no also and the Lord here
is normal there is no problem with the
elastance
resistance or the minute ventilation
however neuromuscular competence is
decreased so is not able to provide the
basic needs of the body and that's why
he presented with hypercapnia
respiratory failure pco2 65 with
respiratory acidosis so based on that
now you can understand a respective
failure in a different way than the
traditional way of hypoxemic respective
a failure versus hypercapnia special
failure and you can look at the path of
physiology it could be just one elastic
Lord problem such as abdominal
distension scientists compartment
syndrome I mean dural effusion
pneumothorax room fracture it could be
long elastic load such as pulmonary
edema atelectasis pneumonia or dynamic
hyperinflation the Lord could be
resistive loss such as him Broca's
person with asthma bronchiolitis and
COPD exacerbation with bronchitis could
be dima secretions or scarring of the
airways saw or could be upper airway
obstruction
the third law it could be a high minute
ventilation load such as in excessive
calories hypovolemia poor money
impulsive or sepsis on the other side we
may have a normal lord however the neuro
competence could be
affected such as in impaired respiratory
drive in brainstem lesions drug overdose
I bow tie realism in bear neural
transmission such as malenko's I'd
totally serve spinal cord lesions
guillain-barré a myasthenia gravis
neuromuscular blockers or could be
muscle weakness such as electrolyte
abnormalities fatigue hypoperfusion
hypoxemia myopathy thank you very much