Chaper 13

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Zhao Mingyao
BMC.ZZU
2006-05-10
• Respiration
= ventilation + gas exchange
Ventilation: alveoli enlarging to set up P gradient
airway fluency to let gas flow
gas exchange: area
distant
efficiency (V/Q)

------ physiology view

 1.Concept
Respiratory system fails to adequately
oxygenate the blood with/without retention of
carbon dioxide, it is generally defined as a
PaO2 < 60mmHg, with /without PaCO2
>50mmHg
 Respiratory failure
External respiratory dysfunction
Blood gas abnormal
Effects on body
2.Classification
According to
(1)duration
Acute : hours to days
Chronic: over months to years

(2)primary site
Central : head injury, encephalitis
Peripheral: asthma, pneumonia, emphysema
(3)blood-gas
Type I : PaO2 
Type II: PaO2  + PaCO2 
(4)pathogenesis
ventilation
blood gas exchange: diffusion
V/Q
Section 1 Etiology and
pathogenesis
 Major Causes of ~

CNS and nerves

Respiratory muscles,
chest wall and pleura
Disorders

pulmonary airway
and gas-exchange
Mechanism of RF
Ventilatory disorders

Diffusion disorders

mismatching ventilation-perfusion

Right-to-left shunting of blood

mechanism
1. Ventilatory disorders
• Respiration(does work)
= dynamic force
overcomes
resistant force
(elastic ~ + nonelastic ~)

----physics view
hypoventilation

restrictive ~ Extralung

intralung

Central airway ~

obstructive ~
Peripheral airway ~
(1)Restrictive ventilatory
disorders

Alveoli distensibility 
1)Extrapulmonary causes

CNS: drugs, infections, Cerebrovascular accident

Respiratory muscles:
fatigue, atrophy, hypokalemia
Chest wall and pleura
Fracture of ribs, pleura fibrosis

restrictive
2)Intrinsic disease

Pulmonary elastic structure 

Alveolar surfactant substance

restrictive
Function of surfactant substances
1.Reduces surface tension,
2. Increases compliance, stabilize
alveoli

keep alveoli dry;

prevent pulmonary edema
3)Blood gas change

PACO2
PAO2=PiO2  ——————
R
– PAO2 P O2 in alveoli
– PiO2 ： PO2 in inhaling air
– PACO2 ： PCO2 in alveoli
– R ： respiratory quotient
PCO2 in alveoli

0.863Vco2
PaCO2= PACO2 = ——————
VA
– PACO2 ： PCO2 in alveoli
– Vco2 ： CO2 production/min
– VA ： alveolar ventilation volume
 Blood-Gas changes
Ventilatory Restrictive
disorder obstructive

Alveolar ventilatory volume 

PaO2 and PaCO2  proportionately

PaO2 + PaCO2 
(2)Obstructive ventilatory disorders

Tracheobronchial tree narrowing

1)Central airway obstruction

Airway above or below

carina

Variable narrowing
Fixed narrowing
Variable outside thorax---inspiratory dyspnea
inspiration expiration
Variable inside thorax---expiratory dyspnea

inspiration expiration
 *Fixed narrowing

Intense scar
infiltration tumors
external compression
2)Peripheral airway obstruction
peripheral airway: diameter <2mm

Characteristics:
thinner wall, without cartilage support
caliber changes with respiration
close junction with adjacent tissues
 Peripheral airway obstruction

mucosa edema
fibrosis
inflammatory infiltration thickness
secretions in lumen
diameter
 Isobaric point

Normal person Emphysema patient

expire expire
Mechanism of RF due to COPD
 CNS, NS
Extrapulmonary Respiratory muscle
Ventilation disorders

Restrictive Chest wall, pleura

Elastic structure
intrapulmonary
Surfactant substances 

outside inspiratory
variable
Central inside expiratory
Obstructive fixed  both
Peripheral isobaric point upshift
caliber decrease

expiratory
 3)Blood gas change
• PO2 ?
• PCO2 ?
 2. Diffusion disorder
a disruption in the exchange of O2 or CO2
or both across the alveolar-capillary
membrane
Causes:
Diffusion distance
Diffusion area
Diffusion time
 1) Diffusion area

Alveolar area : 80m2

at rest: 40 m2
Causes of decreased area:
Emphysema
Pulmonary tumor
Pulmonary lobectomy
• 

260m2

85 m2.
 2) Diffusion distance
Pulmonary edema, congestion
Pulmonary fibrosis
Alveolar epithelium hyperplasia

Alveolar-capillary membrane
thickness
Surfactant
lining
Alveolar
epithelium
Epithelial
basement
Interstitial
space

Capillary
basement
Capillary
endothelium
Total diffusion AREA is large
50~100 m2

Diffusion PATH is very

small, <1 µm
3) Diffusion time
alveolar

normal

Thick alveolar
membrane

Pul vein
Pul Artery
3) Blood gas change
distance
area  PaO2
time 

solubility
diffusion ability PaCO2 N or or 

Diffusion disorder
3. Mismatching Ventilation/perfusion
 1)V/Q
Causes:
Bronchial asthma, chronic
bronchitis, obstructive pulmonary
emphysema, pulmonary fibrosis

Mechanism:
alveolar ventilation  venous
V/Q<0.8 admixture
Perfusion normal
(functional
shunt)
airway pulmonary artery

Less
ventilated

venous admixture
2)V/Q
Causes:
Pulmonary arteriosclerosis, pulmonary thrombosis
bronchiectasis, pulmonary tuberculosis

Mechanism:
alveolar ventilation
normal deadspace-like
V/Q>0.8 ventilation
perfusion 
 airway
pulmonary
artery

perfusion

deadspace-like ventilation
gas exchange disorder

diffusion area ↓
diffusion distant ↑ V/Q ↓ － functional shunt

efficiency (V/Q)

V/Q ↑ － dead space-like

ventilation
3)Blood gas change

PaO2 , PaCO2 N or

4.Anatomic shunt (Right-to-left
shunt)
Causes:
atelectasis, pulmonary consolidation
, bronchiectasis, A-V shunt open
Mechanism:
Admixture with unoxygenated bl
ood
Venous
admixture Anatomic shunt

Hypoxia
 3)Blood gas change
• PO2 ?
• PCO2 ?
 restrictive
inadequate
ventilatory
alveolar
(PaO2↓ obstructive
ventilation
respiratory PaCO2↑)
failure
diffusion disorder

Gas exchang Ventilation-perfusion

e dismatching
（ PaO2↓
PaCO2↑ ↓
Anatomic
N） shunt （ V/Q=0
）
 100 nm.

100 nm.

SARS-Associated Coronavirus
Section 2 alterations of function
and metabolism
 Respiratory
failure

Acid-base, electrolytes
abnormal blood-gas
disorder

reaction of
systems

compensation decompensation
1.Acid-base and electrolytes
disturbance
Respiratory acidosis
retention of CO2 K+ 

Metabolic acidosis---hypoxia
lactic acid  K+ 
Respiratory alkalosis
type I RF with hyperventilation K+ 

Mixed acidosis
hypoxia and hypercapnia
Respiratory acidosis and metabolic alkalosis ?

Remove CO2 too fast for chronic type II

hypokalemia
2. Alternation of respiratory syst
em

Respiratory frequency
Respiratory rhythm

Causes:
Primary diseases
PaO2 , PaCO2
• the shallow and rapid RR does
not increase O2 supply

Effective alveolar ventilation

= (tidal volume – dead space)×RR
(500 – 150) × 12 = 4.2 L normal
(250 – 150) × 24 = 2.4 L shallow & rapid
(250 – 150) × 6 = 0.6 L shallow & slow
(1000 – 150) ×24= 20.4 L deep & rapid
Cheyne-Stokes breathing

RC inhibited
 PaO2 (30 ~ 60mmHg) PaCO2(<70mmHg)

peripheral chemoreceptor central chemoreceptor

+ +

respiratory center

- -

PaO2  PaCO2 
<30mmHg >70mmHg
3.Alternation of circulatory
system
Mild and medium
PaO2
PaCO2 Circulatory center
Severe
 Pulmonary heart disease
~ caused by pulmonary disease with the
characteristics of pulmonary hypertension

Mechanism:
(1)Pulmonary hypertension---arteriolar constriction
(2)Pulmonary blood flow resistance---RBC  
(3)Myocardial function---hypoxia, acidosis
(4)forced expiration and inspiration
 4.Alternation of CNS
Cerebral dysfunction caused by severe respiratory
failure called pulmonary encephalopathy

Manifestation
Excitation, headache, dysphoria
Confusion, drowsiness, coma
Death
Mechanism:
Membrane potential
Hypoxemia---ATP
Na+ bump brain
edema
Cerebral vessels dilation
Hypercapnia---
Cell acidosis

PaCO2>80mmHg CO2 narcosis

 PaO2 、 PaCO2 changes and CNS changes

PaO2: 60 mmHg:intelligence ， eyesight decrease

mildly

40-50 mmHg: mental manifestation

20 mmHg: irreversible damage of neural cells
PaCO2 >80 mmHg, CO2 narcosis,
CNS symptoms
 Section 3 principles of
prevention and treatment
Principle for treatment
I. Treat primary causes

II. Relieve hypoxia and hypercapnia

III. Treat other complications

control infection
 Oxygen administration
1. Type I : <50% O2

2. Type II : continuously

Low concentration: <30% O2

Low current amount: 1-2 L/min

PaO2 = 60mmHg
 Decreasing PaCO2
Relieve obstruction
for type II RF,
Increase drive of respiration
CO2 can’t be
Mechanical ventilator reduced too
fast
Nutrition supply
end