gas exchange is a complex process
to support the absorption of oxygen and
release of carbon dioxide about five to
eight liters of air per minute are
brought in and out of the lungs
and about three tenths of a liter of
oxygen is transferred from the alveoli
to the blood each minute even when the
person is at rest
at the same time a similar volume of
carbon dioxide moves from the blood to
the alveoli and is exhaled
when there is tachypnea a condition in
which patients breathe at a faster rate
usually in case of respiratory distress
and impairment of respiratory system due
to other causes even more air pumps in
sometimes even more than 100 liters
due to compromised function of lungs in
copd or other respiratory disorders the
co2 washout will be slower and hence
there will be retention of carbon
dioxide
the normal level of carbon dioxide in
blood is between 35 to 45 that is our
phco2
the increased level of carbon dioxide in
blood can cause neuromuscular
dysfunction and often lead to poor
prognosis
the condition is called co2 narcosis
one of the hallmark features of carbon
dioxide narcosis is a depressed level of
consciousness in this video we will look
at the causes pathophysiology diagnosis
and complications along with some key
features of carbon dioxide narcosis
so let's get started
for understanding co2 narcosis we need
to understand hypercapnia
hyper means excessive and capnia is
derived from the greek word capnos means
smoke or carbon dioxide
together excessive amount of carbon
dioxide in blood is called hypercapnia
the amount of co2 dissolved in blood is
called paco2 or partial pressure of
carbon dioxide in blood
an increased level of paco2 in blood
above normal is hypercapnia
so what's normal
in arterial blood the level of paco2 is
between 35 to 45 anything that's above
is hypercapnia
it has two types in general acute and
chronic
we have explained hypercapnia in detail
in other video check it out for now
acute hypercapnia is the driving force
behind co2 narcosis
so the etiology of co2 narcosis is
depend on the cause of acute hypercapnia
let's understand the etiology of co2
narcosis or causes in detail
although the etiology is complex it's
useful to categorize the potential
causes into three categories decreased
minute ventilation increased physiologic
dead space and increased carbon dioxide
production
number one
decreased minute ventilation first what
is minute ventilation
minute ventilation also known as total
ventilation is a measurement of the
amount of air that enters the lungs per
minute
it is the product of respiratory rate
and tidal volume
the minute ventilation is the
respiratory rate into tidal volume
now what are the causes of minute
ventilation
as we know the central nervous system
controls respiration
more particularly the respiratory
centers in the medulla
the central respiratory center in the
medulla integrates feedback from
multiple inputs into a respiratory drive
that controls our minute ventilation
anything that affects the central
respiratory center can have an impact on
minute ventilation
minute ventilation is raised in cases of
sedatives medication overdose stroke and
hypothermia
although the medulla functions to
control the respiratory drive many
peripheral nerves and respiratory
muscles are needed to perform
respirations
the decreased respiratory neuromuscular
function can decrease minute ventilation
also deformity of the thoracic cage can
impact tidal volumes therefore
decreasing minute ventilation
next increased physiologic dead space
increase in physiologic dead space is
one of the cause of hypercapnia
so what is physiologic dead space
dead space represents the volume of
ventilated air that does not participate
in gas exchange
the two types of dead space are
anatomical dead space and physiologic
dead space
anatomical dead space is represented by
the volume of air that fills the
conducting zone of respiration made up
by the nose trachea and bronchi
one can see an increase in the value of
physiologic dead space in lung disease
states where the diffusion membrane of
alveoli does not function properly or
when there are ventilation or perfusion
mismatch defects
third cause of hypercapnia is anything
that increases co2 production
this group is more likely to contribute
only partially to hypercapnia and is not
usually the primary cause but it can
occur in conditions that increase
metabolic rates
environmental exposure to areas rich in
carbon dioxides such as volcanoes or
geothermal activity puts patients at
risk for carbon dioxide poisoning
it can lead to sepsis thyrotoxicosis or
fever
now we know what causes co2 narcosis
it's time to understand its
pathophysiology
carbon dioxide is fundamental for blood
circulation in the brain
changes in paco2 and blood are thought
to cause changes in the ph of the
cerebral spinal fluid
changes in the ph of the cerebral spinal
fluid cause smooth muscles to relax or
constrict
when paco2 levels rise cerebral blood
vessels dilate when they fall cerebral
blood vessels constrict
so smooth muscle relaxation in patients
with co2 narcosis causes dilation of
cerebral blood vessels which increase
cerebral blood flow and potentially
increasing intracranial pressure
which results in a depressed level of
consciousness
but here patient baseline paco2 is
important to consider in the development
of co2 narcosis
normal individuals do not experience
alterations in consciousness until paco2
is greater than 75
patients with chronic hypercapnia may
not experience alterations in
consciousness until paco2 exceeds 90.
according to current understanding
hypercapnia alters neurotransmitter
levels involved in consciousness