1. Chaper 13
Respiratory failure
Zhao Mingyao
BMC.ZZU

2. Respiration = ventilation + gas exchange
Ventilation: alveoli enlarging to set up P gradient
airway fluency to let gas flow
gas exchange: area
distance
efficiency (V/Q)
physiology view

4. 1.Concept of Repiratory Failure
Respiratory system fails to adequately oxygenate the blood with/without retention of CO2, it is generally defined as a PaO2 < 60mmHg, with /without PaCO2 >50mmHg

5. 2.Classification of ~ (1)duration (2)primary site
According to
(1)duration
Acute : minutes to days
Chronic: over months to years
(2)primary site
Central : head injury, encephalitis
Peripheral: asthma, pneumonia, emphysema

6. (3)blood-gas Type I : PaO2  Type II: PaO2  + PaCO2  (4)pathogenesis
ventilation
blood gas exchange: diffusion
V/Q
anatomy shunt
----O2 exchange 
----alveolar hypoventilation

7. Section 1 Etiology and pathogenesis
Respiration
= ventilation + gas exchange

8. Mechanism of RF 1. Hypoventilation (1)restrictive ~ (2)obstructive ~
Extralung
intralung
(1)restrictive ~
(2)obstructive ~
Ventilatory disorders ()
Central airway ~
Peripheral airway ~

9. Ventilation (does work)
= dynamic force
overcomes
resistant force
(elastic ~ + nonelastic ~)
----physics view

10. (1) Restrictive ~ Major Causes: CNS and nerves
Respiratory muscles, chest wall and pleura
Lung( Alveoli) distension 
distensibility
Alveoli distensibility 

11. 1)Extrapulmonary disease
①CNS:
②Respiratory muscles:
③Chest wall and pleura:
Lung distension drugs, infections, Cerebrovascular accident fatigue, atrophy, hypokalemia
Fracture of ribs, pleura fibrosis
Acute organophosphorus poisoning 抑制 acetylcholinesterase，AChE causes

12. Lung distension  Pneumonia, fibrosis ,congestion Pulmonary edema &
2)Intrinsic disease
①Pulmonary elastic structure 
Lung distension  Pneumonia, fibrosis ,congestion Pulmonary edema &
②Alveolar surfactant substance

13. Function of surfactant substances
1. Reduces surface tension
2. Increases compliance, stabilize alveoli
Keep alveoli dry;
Prevent pulmonary edema

14. 3)Blood gas change PACO2 PAO2=PiO2  ———— R PAO2 P O2 in alveoli
Alveolar;arterial
PAO P O2 in alveoli
PiO2 ： PO2 in inhaling air
PACO2 ：PCO2 in alveoli
R：respiratory quotient

15. PCO2 in alveoli 0.863Vco2 PaCO2= PACO2 = —————— VA
PACO2 ： PCO2 in alveoli
Vco2：CO2 production/min
VA ：alveolar ventilation volume

16. Blood gas change PACO2 R 0.863Vco2 PaCO2= PACO2 = —————— VA
PAO2= PiO2  —————— R
Alveolar;arterial PACO2 ： PCO2 in alveoli
Vco2：CO2 production/min
VA ：alveolar ventilation volume
0.863Vco2
PaCO2= PACO2 = —————— VA 16

17. Blood-Gas changes Ventilatory disorder Restrictive obstructive
Alveolar ventilatory volume 
PaO2 and PaCO2  proportionately
PaO2 + PaCO2 

18. (2) Obstructive ventilatory disorders
Tracheobronchial tree narrowing

19. Airway narrowing 1)Central airway obstruction
Airway above or below carina
Airway narrowing
Variable narrowing
Fixed narrowing

20. outside thorax---inspiratory dyspnea
Variable
expiration
inspiration
outside thorax---inspiratory dyspnea

21. Retractions ( supraclavicular, intercostal and subcostal areas)
retraction of soft tissue on inspiration
concave 
a depression 
indentation 
hollow 
Retractions ( supraclavicular, intercostal and subcostal areas)
on inspiration

22. Variable
inspiration
expiration
inside thorax---expiratory dyspnea

23. 2)Peripheral airway obstruction

24. Peripheral airway (Φ <2mm )
1. thinner wall, without cartilage support
2. caliber changes with respiration
3. close junction with adjacent tissues
diameter
Characteristics

25. Peripheral airway obstruction
1.mucosa edema 2.fibrosis 3.inflammatory
infiltration
4.secretions in
lumen
thickness
Bronchial asthma Chronic obstructive emphysema Chronic bronchitis
diameter

26. Isobaric point upshift in Emphysema
Isobaric point 10 20 25 10 15 20 20 20 20 20 30 20
+35 35 20 20 25
+35 20
Normal expire
Emphysema expire
Isobaric point upshift in Emphysema

27. Mechanism of RF due to COPD?
a correlation between the increase in inflammation in the lungs and a loss of activity in an enzyme responsible for switching off inflammatory genes and cells, called histone deacetylase (HDAC).

28. Ventilation disorders Restrictive
CNS, NS
Ventilation disorders
Respiratory muscle
Extrapulmonary
Chest wall, pleura
Restrictive
Elastic structure
intrapulmonary
Surfactant substances 
outside
inspiratory
variable
Central
inside
expiratory
Obstructive
resistance
force
fixed 
both
Peripheral
isobaric point upshift
caliber decrease
expiratory

29. 3)Blood gas change
PO2 ?
PCO2 ?

30. 2. Diffusion disorder
a disruption in the exchange of O2 or CO2 or both across the alveolar-capillary membrane

31. Total diffusion AREA is large
50~100 m2
Diffusion PATH is very small, <1 µm

32. 1) Diffusion area  Alveolar area : 80m2 at rest: 40 m2
Causes of decreased area:
Emphysema
for an average size adult Ventilation area
Pulmonary tumor
Pulmonary lobectomy

33. 2) Diffusion distance  Pulmonary edema, congestion Pulmonary fibrosis
Alveolar epithelium hyperplasia
Hyaline membrane
Alveolar-capillary membrane thickness

34. 3) Diffusion time ↑ alveolar normal Thick alveolar membrane Pul vein
Pul Artery

35. 3) Blood gas change distance PaO2 area  solubility
Blood stream time 
solubility
PaCO2 Normal or or 
diffusion ability
Diffusion disorder

36. 3. Mismatching Ventilation/perfusion

37. 1)V/Q Causes: Mechanism:
Bronchial asthma, chronic bronchitis, obstructive pulmonary emphysema, pulmonary fibrosis
Mechanism:
venous admixture
alveolar ventilation 
V/Q<0.8
Perfusion normal
(functional shunt)

38. 2)V/Q Causes: Mechanism:
Pulmonary arteriosclerosis, pulmonary thrombosis bronchiectasis, pulmonary tuberculosis
Mechanism:
alveolar ventilation normal
deadspace-like ventilation
V/Q>0.8
perfusion 

39. Gas exchange disorder diffusion area ↓ diffusion distant ↑
efficiency (V/Q)
V/Q ↓ －functional shunt
V/Q ↑ －dead space-like
ventilation
anatomy shunt ↑ Bronchial vein dilating
Arterial-venous short-way

40. 3)Blood gas change V/Q: ventilation  V/Q: perfusion  PaO2 ,
PaCO2 N or  or 

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

42. 3)Blood gas change
PO2 ?
PCO2 ?

43. Respiratory failure restrictive inadequate alveolar ventilation
summary
restrictive
inadequate alveolar ventilation
ventilatory
(PaO2↓
PaCO2↑)
obstructive
Respiratory failure
diffusion disorder
Gas exchange
（PaO2↓
PaCO2↑↓N）
Ventilation-perfusion dismatching
Anatomic shunt（V/Q=0）

44. Mechanism of ARDS ? ?

45. Mechanism of ARDS Pathogenic factors
Inflammatory cells and platelet activated
Release proteinase,
inflammatory mediators
Microthrombosis
Alveolar-capillary membrane damaged
Permeability 
(continue)

46. hypoxemia pulmonary edema diffusion disorder atelectasis
functional shunt
bronchus spasm
dead space-like ventilation
vascular constriction
microthrombosis

47. Section 2 Alterations of function and metabolism in ~

48. Acid-base, electrolytes
Respiratory
failure
Acid-base, electrolytes
disorder
abnormal blood-gas
reaction of
systems
compensation
decompensation

49. 1. Acid-base and electrolytes disturbance
Respiratory acidosis
type II ~
retention of CO2
K+ 
Metabolic acidosis---hypoxia
zymolysis
anaerobic glycolysis 
lactic acid 
K+ 

50. Respiratory alkalosis
type I RF with hyperventilation
K+ 
Mixed acidosis
Res acidosis & met acidosis
type II RF---hypoxia and hypercapnia
K+ 
Res acidosis & met alkalosis
Remove CO2 too fast
hypokalemia

51. 2.Alternation of respiratory system
Respiratory frequency
Respiratory rhythm
Causes:
Primary diseases
PaO2 , PaCO2

52. 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

53. Respiratory center + + - - PaO2 (30 ~ 60mmHg) PaCO2(<70mmHg)
peripheral chemoreceptor
central chemoreceptor + +
Respiratory center - -
PaO2 
PaCO2 
<30mmHg
>70mmHg

54. 3. Alternation of circulatory system
Mild and medium
PaO2
Circulatory center
PaCO2
Severe

55. Pulmonary heart disease (cor pulmonale )
~ 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
cor pulmonale

56. 4. Alternation of CNS
Pulmonary encephalopathy: Cerebral dysfunction caused by severe respiratory failure
Manifestation
Excitation, headache, dysphoria
Confusion, drowsiness, coma
Death

57. Mechanism of Pulmonary encephalopathy
Membrane potential
Hypoxemia---ATP
Na+ pump
brain edema
Cerebral vessels dilation
Hypercapnia---
Cell acidosis
PaCO2>80mmHg
CO2 narcosis

58. PaO2、 PaCO2 changes and CNS changes
PaO2 60 : intelligence，eyesight decrease mildly
40-50: mental manifestation
20 : irreversible damage of neural cells
PaCO2 >80, CO2 narcosis,
CNS symptoms
mmHg mmHg mmHg millimetre(s) of mercury 毫米汞柱(液压单位)
mmHg

59. Section 3 principles of prevention and treatment
I. Treat primary causes
II. Relieve hypoxia and hypercapnia
III. Treat other complications
control infection

60. Oxygen administration
1. Type I : <50% O2
2. Type II : continuously
Low concentration: <30% O2
Low current amount: L/min
PaO2 = 60mmHg

61. Decreasing PaCO2 Relieve obstruction Increase drive of respiration
for type II RF, CO2 can’t be reduced too fast
Increase drive of respiration
Mechanical ventilator
Nutrition supply

62. Airway Foreign Bodies Heimlich method
儿童在进食、玩耍瓜子、豆类、花生、扣子等物时，常因突然惊吓、跌倒、哭笑等将异物吸入气管。成人多因口中含物，如铁钉等不慎吸入，或因昏迷时将呕吐物、假牙吸入气管。气管受到异物刺激，突然出现剧烈咳嗽、喘鸣、呼吸和吞咽困难、声音嘶哑、面色苍白，继之变为青紫，甚而失去知觉，昏倒在地。若不及时抢救，异物完全堵塞气管，超过4分钟就会危及生命，即使抢救成功，也会留下瘫痪、失语等严重后遗症。如果仅堵塞部分气管，但又咯不出来，就可能发生肺炎、肺不张。因此，最关键的措施是在现场即刻将异物排出。
　　急救方法
　　现场急救最为理想的办法是美国医学会推荐的海利希手法。海利希手法适用于自救，也可用于互救。
　　1、站位急救法：救护者站在患者身后，用双臂围绕患者腰部，一手握拳，拳头的拇指侧顶在患者的上腹部（脐稍上方）；另一手握住握拳的手，向上、向后猛烈挤压患者的上腹部。挤压动作要快速，压后随即放松。
　　2、卧位急救法：患者仰卧，救护者两腿分开跪在患者大腿外侧的地面上，双手掌叠放在患者脐稍上方，向下、向前快速挤压，压后随即放松。
　　3、儿童急救法：让患儿俯卧在两腿间，头低脚高，然后用手掌适当用力在患儿的两肩胛骨间拍击4次。拍背不见效，可让患儿背贴于救护者的腿上，然后，救护者用两手食指和中指用力向后、向上挤压患儿中上腹部，压后即放松，可重复几次，必要时急送医院。
Heimlich method

64.                                                                                                     
                                                                                                    
                                                                                                    
Thank you!