Mechanisms
of respiratory
insufficiency
-
Introduction
Mechanisms of
respirator insufficiency
-
introduction
-
necessary
values:
tidal volume (TV) 500 me
breathrate (BR) 1 41 min
gases
anterial
central renow
y
C02 40
mm4g
46
100
40
↑
o2
1)
C
hypoxia
↳alsolar hypoxemia
240/hypencapma
under normalsituation the
gas exchange on almoto-
capillary
membrane is perfect
P
I
composition of acterial and
alveolar gasses
is
the same
4 A0z
=
4a82 i
pAC02 =
paCon
↑e feet
⑧ ↓
the
same
exchange
--
composition
-T
Further we wie,darinema
ofrespirator insufficiency
Antionof restiein
sufficiency
-
paon
60
many (w9oz
-paCO2>
50
mang
-
90%)
saturation curve
of
hemoglobin
2-
60-90
Sa
9
Fin
1) meof 3 libs
- >
pain
an inspiriem
->
superficial breathing
7 =
low TV
I
->
compensator teasphoe
minute
(v)TV. BR =
ventilation
↳ or mal: 500. 14=7000ml/min
FX of:250.28
=7000 Me/a-
ribs
↓
total ventilation is the
same
attendbene
We mustconsider anatomic
dead space, approx.
150 me.
Real almost ventilation is:
normal:
(500-150).14- 1900inFxof
ribs.(250 -
150).28
=
2800m
- min
relationship
between
al role
4 a CO2
in
t
In case
of his Fx the
pacient
has
hypercapnia.
This mechanism is called
① molarhypoventilation
type 2
results:
- -
respiratory
1) T4aC02 I insufficient-
2) ↓pa O2
J
=ventilatory
failure
-
hypercapaic
ces
of causes file)
muscle weakness, myasthenia
gravis, yogaeaeopathy,
opiates, yathology of C
Ns,
o
beberation of airways,
unstable chestwall, pain...
2 -
5
further
mechanisms
reset really in
resin insuff
#normal
17 ↓ 02
but 2) on even 202
lowen
E
I
↳yoxemia faile
3=
oxygenation dysfunction
airtig
Type
1
lung
is ill
Type
2
lung
is
healthy,
but other
-
on
extwe ne
respiratory
illness
components
an ill
of lung
2) monaryemboss
Je/min
-endead
② space
-
↳
embolus
5-2) min I
Rightlung
is ventilated, '
butnotperfused
with
blood!
-space
washed ventilation!->
i
->
actually A powertreation (2.5?)
=>
↑
202
↓02
-> compensatory hyperventilation
↳ Why does hypoventilation decrease ?
3100, although total or delivery is sufficient,
3)Loban premonia-
iy
e
ovale +
pulmonary
ypertension
I
exchange
preserved perfusion
M
dright-to-left)
⑤Enemonamyshant
-02
I both inflow-
4cor,
and
outgro
is venous
blood
prcO2
11
compensatiny
penventilation
↑O
*w.
i
y ox-;
ble
4 ↑ A 02
puCOn I mixed blood
↑
C02 >
4 C02 > PACO2
4202 -402 <4A02
causes ·
meumonia, severelung
edema, atlectasis,
alwolambleedina
re1s
intrap we no
any shant?
1) Sp
eventilation
of healthy
a soli
->
will decreate CO2
- does not
change P2 (why ?)
2) delivery of
external
oxy from
-> does not
change 2 (Why?)
-> does not
change 20(why?)
-> actually compensation is
almost
impossible
- >
necessary
to that
transe
premonia -> ATB
↳ a telectasis ->
bronchoscopy
Cdrainage of
pleural effusion
4) -nary fibrosis
wide me d
alsolo-->
capillary membrane
->
mireddiffusion
(
less
importantmechanism
gas
concentrations
I
normally, the
in alveoliand
blood are equiliit
backed in as of
the capillary
long th
-
problem
more
for
↓
Or than for 202
big
tional
dyspnea reserve
and hypoxemia
20PD, asthma,
& failure-
inhomogeneity
of lung impairment
->
somewhere lower ventilation
(i),
somewhere lower perfusion (a)
⑤
-perfusion mismatch
->
3 =
vamismatch)
-the most importantmechanism
shuntand
dead space
are
extreme variants
-
Anemonaryvasoconstrictionoptimizes
aratios
without
h.p.r. the
lang
function would be
impaired
even in healthy lungs
C
esmin norm
-
I
B·
.e/min 0.5
l/min
evailing I ↑
revailin
I g
perfusion ventilation
over ventilation
b fusionOwen ve
=renous -wasted
admixture
ventilation
2.shurt"] E 17
dead
-paa"
1)itis
possible to
compensate
·
for it with
hyperventilation
on with a
delivery of [Why?I
0xzse4