Respiratory Failure

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RESPIRATION
4 distinct mechanisms:
Ventilation
Gas exchange External respiration
Transport of oxygen and carbon dioxide in the
blood
Internal respiration

2
 The Process of External Respiration

PiO2 159mmHg

Pulmonary
ventilation PAO2 102mmHg
PACO2 40mmHg

Pulmonary
gas exchange PaO2 40mmHg
PaCO2 46mmHg
PvO2 100mmHg
PvCO2 40mmHg 3
Definition of RF
Disorders of external respiratory function

PaO2 <60 mmHg (8.0kpa) while breathing air

at rest, with or without PaCO2 >50
mmHg(6.67kpa).

judgment standard: PaO2 <60 mmHg , PaCO2 >50

mmHg
hypoxia with (or without) respiratory acidosis
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Respiratory failure (RF):
It is a condition in which respiratory
function is inadequate to meet body’s needs
during exertion.

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Classification
1. According to blood gas:
1) typeⅠ(hypoxemic RF) :
PaO2 <60 mmHg (8.0kpa)
2) type Ⅱ (hypercapnic RF) :
PaO2 <60 mmHg (8.0kpa) ,
with PaCO2 >50 mmHg(6.67kpa)

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2. According to primary site
central
peripheral
3. According to duration
acute
chronic

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 Section 1
Causes and pathogenesis of
respiratory failure

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• Pathogenesis of RF:

Disorders of external respiratory function

pulmonary ventilation disturbance

pulmonary gas exchange disturbance

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Ⅰ.pulmonary ventilation disturbance

i. Types and Causes

restrictive hypoventilation
obstructive hypoventilation

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• Causes of RF

Disorders of:
Central Nervous System
Spinal Cord
Neuromuscular System
the chest wall and pleura
the airway

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component elements causing ventilation
disturbance
Airway
thorax wall
straitness
damaged
or block
Inhibition of R. center

Lung elastic
High spinal resistance
cord increased
damaged
weakness
of
R. M

Anterior
angle cell
damaged phrenic nerve
damaged 12
• Restrictive hypoventilation:

Causes and mechanisms:

 impaired activity of respiratory muscle (dysfunction
of CNS, neural, muscle etc.)
 decreased compliance of thorax (chest
malformation ,
pleura fibrosis)
 decreased compliance of lungs (pulmonary edema ,
inflammation , fibrosis, insufficient surfactant)
 thorax fluidify or pneumothorax
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2. Obstructive hypoventilation :

central airway obstruction

peripheral airway obstruction

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 1) central airway obstruction:

above the forf ic ation (between the glottis and the

carina)

（
obstruction locates out of thorax paralysis,
edema or inflammation of vocal cords ）
inspiratory dyspnea

obstruction locates within thorax

expiratory dyspnea

why?
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 Phase of Phase of Phase of Phase of
expiration inspiration expiration inspiration
(Ptr > Patm) (Ptr <Patm) (Ptr<Ppl) (Ptr>Ppl)

Patm Patm
Ptr Ptr
Ptr
Ptr

Ppl Ppl

The effects on the phase of The effects on the phase of

respiration on an extrathoracic respiration on an intrathoracic
variable obstruction variable obstruction
Ptr—intratrachel pressure
Ppl—pleural pressure
Patm—atmospheric pressure
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 ）
2) peripheral airway obstruction (diameter <2mm :

peripheral airway character ：

；
Wall: thin,without cartilage support

Diameter changes with respiration；

keep tight connection to

surrounding alveoli

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causes and mechanism:
chronic obstructive pulmonary disease
，
(chronic bronchitis emphysema),
severe pneumonia, atelectasis ,etc.
→ equal pressure point is moved up
expiratory dyspnea

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 point that
Intra-airway pressure
= extra-airway pressure

Equal pressure point

normal person makes Emphysema patients makes

forced expiration
forced expiration 19
ii. Alteration of PaO2 ，PaCO 2 in
pulmonary ventilation disturbance

PaO2↓
PaCO2↑ （ type II RF）

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Ⅱ . Pulmonary gas exchange
disturbance

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22
Pulmonary gas exchange disturbance

diffusion impairment
VA / Q mismatch
anatomic shunt

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i. Diffusion impairment

Causes:
area of R-M
thickness of R-M
diffusion time

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1. Area of R-M

Normal adult R-M: 80 m2

At rest, used R-M:35~40 m2

，
area of R-M : atelectasis pulmonary
，
consolidation lobar resection,
emphysema

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2. Thickness of R-M : pulmonary edema, fibrosis,
formation of pulmonary hyaline membrane, hydremia

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Alteration of PaO2 , PaCO2

PaO2↓
PaCO2 : N or ↓
according to compensatory ventilation
why?

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Oxygenation of Blood

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 PO2 PCO2( kPa )

13.33 PaO2
PvCO2
10.67 6.13

8.00

PvO2
5.33

2.67 PaCO2

0 0.25 0.50 0.75 s

Blood gas change when blood circulating through lungs

Real line stands for normal person;
broken line stands for patients with increased thickness of R-M
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ii. Ventilation-Perfusion
Mismatch

：
At rest

（V )： 4L
（Q) ： 5L
A ~

V /Q ： 0.8
~

ratio
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• Ventilation-Perfusion Coupling

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[Link] and Causes
1) Hypoventilation of Partial alveoli （V /Q↓）
A

functional shunt or
venous admixture

• Causes ：Disorders of trachea or alveolus

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functional shunt :
alveolar Ventilation （V ） ，
A

alveolar Perfusion (Q) have not VA / Q

accordingly , even due to inflammation

venous blood flowing through these units have not been

totally arterialized and mixes into arterial blood, this
process is called as functional shunt, also as venous
admixture.

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 O2 CO 2

⾎
V A ⾎
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 O 2↓ CO 2

⾎
V ⾎
V

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 （
2) Low perfusion of alveoli VA/Q↑ ）
“dead space”- like ventilation:

alveoli at diseased region have low perfusion,

while ventilation is not decreased,

alveolar ventilation can not be fully used.

：
• causes Disorders of pulmonary vessel(vessel
inflammation, occlusion, spasm ）
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 O2 CO 2

⾎
V A ⾎
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 O2 CO 2

⾎
V A ⾎
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2. Alteration of PaO2 ,PaCO2

PaO2

PaCO2
N ？
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 1) blood gas change in functional shunt
Asthma
[Link] VA / Q functional shunt

PaO2 ,PaCO2
)ld/lm( 2 OC dn a 2O . C

compensatory

respiration ventilation

PO2 and PCO2 health region diseased region

Dissociation curve of O2 and CO2
VA / Q VA / Q
PaO2 ↑ ，HbO2+ ， PaO2 ↓ ， HbO2 ↓
PaCO2 ↓ HbCO2 ↓ ，
PaCO2 ↑ HbCO2 ↑

PaO2 ↓ ， PaCO ?
2
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 2) blood gas change in dead space like
ventilation
p. embolism
P. arteritis, DIC VA / Q dead space like ventilation
)ld/lm( 2 OC dn a 2O . C

other region
Q

PO2 and PCO2

Dissociation curve of O2 and CO2 functional shunt

health region diseased region

VA / Q VA / Q
PaO2 ↓ ， HbO2 ↓ PaO2 ↑ ， HbO2 +
PaCO2 ↑ ， HbCO2 ↑ PaCO2 ↓ HbCO2 ↓ 41
iii. anatomic shunt(true shunt)
、
1 Under physiological condition
anatomic shunt:
bronchia vein

venous blood pulmonary vein

A-V communicating branch

true shunt: there are totally no gas exchange in the

blood flowing through anatomic shunt, so anatomic
shunt also called as true shunt.
： －
N 2% 3% 42
2、Under pathological condition
bronchiectasis flow of bronchial vein
shock flow of A-V shunt
true shunt
atelectasis
Consolidation like true shunt
of lung
PaO2 PaCO2± or or

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 summary
restrictive
Ventilation Hypoven-

disturbance tilation obstructive
（ PaO2↓
RF PaCO2↑ ）
Gas exchange diffusion impairment
disturbance
PaO2↓ V/Q mismatch
）
（V/Q=0）
PaCO2↑ ↓N
true shunt↑

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 Section 2
The functional and metabolic
changes in RF

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 Total change direction

.pmoC
hypoxemia ＜
PaO2 60mmHg
hypercapnia
＞
PaCO2 50mmHg
Dysf. of
Effects on
external R.
organ system

Dist. of acid-base electrolyte

＜30mmHg

.mocsiD
PaO2
PaCO2＞80mmHg

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 Ⅰ. Acid-base Disorders and
Electrolytes Disorders

i. Respiratory
Acidosis——type Ⅱ R
F : CO2 retention
Hyperkalemia:
ii. Metabolic Acidosis
H+-K+ exchange
——Hypoxia →
Secretion from distal renal
tubules ↓ production of lactic acid↑
hydrogen ion dissociate from H2CO3 excretion ↓
carbonic acid

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iii. Respiratory Alkalosis ----
type I RF
Hypoxia compensation hyperventilation
→ PaCO2 ↓
Hypokalemia

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Ⅱ. Respiratory system
1、Effects of PaO ↓and PaCO ↑
（1） PaO ↓
2 2

2
PaO2 ↓

stimulate peripheral inhibit respiratory center

chemoreceptor

excite respiration inhibit respiration

：
30mmHg<PaO2<60mmHg excite respiration
：
PaO2<30mmHg inhibit respiration
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(2) PaCO2↑
（ ）
• PaCO2 ↑ <80mmHg →stimulate center
chemoreceptor→respiratory center was
excited→ventilation ↑
• PaCO2>80mmHg ： respiratory center was
depressed
inhaling 30% O2

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The effects of PaO2↓and PaCO2 ↑ on R

PaO2↓ +
30~60mmHg peripheral
chemoreceptor -
<30mmHg Respiratory
center

PaCO2↑ center +
>50mmHg chemoreceptor
-

>80mmHg

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2. Primary disorders of respiratory system
1) pulmonary compliance↓
pulmonary juxtapulmonary-capillary
extend reflex receptor

rapid light R.
2) obstructive hypoventilation→ins/exp dyspnea
3) respiratory M. fatigue → contractibility of R.M. ↓
→ rapid light R.
4) central RF: slow light R.,R. rhythm disturbance
e.g.: tide-like R.

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 Tide-like R.(Cheyne-Stokes
Breathing)

Over low central excitability → [Link]→ PaCO2 ↑ → R.

center was stimulated →R occur→CO2was expelled out
→ R. central excitability became very low

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Ⅲ. cardiovascular system

mild PaO2 ↓and PaCO2 ↑can excite

cardiovascular center

Severe PaO2 ↓and PaCO2 ↑can inhibit

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1 、 vasoconstriction and vasodilatation
-blood redistribution：

• mild PaO2 ↓and PaCO2 ↑→ cardiovascular center →

sympathetic nerve →norepinephrine → α-receptor
→ vasoconstriction
• local metabolite(adenosine) → vasodilatation(heart)
• direct effect → vasodilatation

→ blood redistribution
skin, kidney, stomach-intestine: vasoconstriction
brain, heart: vasodilatation

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、Heart：
2
mild ： hear t rate ↑, myocardium
contraction
force ↑,CO↑
severe: heart rate ↓, myocardium contraction,
force ↓, CO↓ ,blood pressure↓
right heart failure

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3. Cor pulmonale
• concept: Cor pulmonale is right heart
hypertrophy and even failure, which is
caused by RF.
• Mechanism of Cor pulmonale :

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1) pulmonary hypertension ：
• pulmonary arteriole contraction：
，
hypoxemia hypercapnia →blood hydrogen ion [H+ ] ↑
→chemoreceptor → pulmonary artery contraction
：
• Pulmonary vessel becomes sclerosis, stegnosis
chronic RF → pulmonary arteriole contracts long-
standing and oxygen deficit long-term → pulmonary
vessel’s smooth muscle cell and fibroblast become
hypertrophy and proliferation.
• Some pulmonary disorders effects:
，
pneumonia pulmonary fibrosis → pulmonary vessel
became twist
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2) cardiac diastole and contraction were
confined ：
intrathoracic pressure ↑; hypoxemia, acidosis
3) resistance of blood flow is increased：
Hypoxemia compensation RBC increased
→blood became viscous

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Ⅳ. CNS
1. PaO2 ↓ ：
• PaO2 decreased to 60mmHg →intelligence
and

eyesight slight impairment
• PaO2 decreased to below 40~50 mmHg
→a series symptom of nerve and
consciousness.
• PaO2 decreased to 20mmHg → nerve cell
will become irreversible damaged
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2. PaCO2 ↑ ：
PaCO2 is higher than 80mmHg→ carbon
dioxide narcosis ：
headache, dizziness, dysphoria, flapping
tremor, mental disorder , drowsiness,
hyperspasmia, respiratory depression ,coma,
even death

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[Link] encephalopathy:
a kind of brain dysfunction caused by RF.

Mechanism:
1) brain vessel：
• hypoxia→ brain vessel dilation, blood f low↑ →brain
congestion
• acidosis → blood vessel endothelium(BVE)
permeability↑ → brain interstitial tissue edema

→ intracranial pressure ↑, to oppress brain vessel

→ischemia, hypoxia, acidosis became severe
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 ：
2) brain cell
• hypoxia → ATP↓,Na+-K+-ATPase↓→ brain cell edema
• acidosis → glutamic acid decarboxylase (GAD )
activity ↑ → GABA↑
• acidosis → phospholipase ↑ → lysosome enzyme
release → nerve cell and tissue damage

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Ⅴ. kidney ：
PaO2 sympathetic nervous system

renal blood vessel contract

renal blood flow

functional renal failure

(oliguria, azotemia, metabolic acidosis)

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Ⅵ. gastrointestinal tract ：
hypoxia and acidosis → excitation of sympathetic
nerve → gastrointestinal tract wall vessel
contraction (large amount of receptor) → ischemia
CO2 retention→↑activity of carbonic anhydrase
(CA) in acid cell in stomach →secrete more acid
→ pH of gastric juice ↓

→ gastrointestinal mucous membrane erosion,

necrosis, bleeding ulcer

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 Section 3
Treatment Principle

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• Etiology treatment
Correcting the cause and relieving the
hypoxia and hypercapnia
e.g. use of bronchodilators,
antibiotics for respiratory infections,
establishment of airway
(using endotracheal tube )

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2. Oxygen therapy
1) General Oxygen Therapy （typeⅠ）：<50%O 2

2) Controlled Oxygen Therapy （typeⅡ ）:

Continuous low concentration (<30%O2 )
Low flux (1~2L/min)

PaO2 =50 ~60mmHg

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