Chaper 13: Zhao Mingyao

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.Concep t 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 (1)duration

According to

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 – PiO2

P O2 in alveoli ：

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 disorder

Restrictive 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 secretions in lumen

thickness diameter

Isobaric point

Normal person expire

Emphysema patient expire

Mechanism of RF due to COPD

CNS, NS Respiratory muscle Chest wall, pleura

Extrapulmonary

Restrictive intrapulmonary

Elastic structure

Surfactant substances 

variable

d noi t ali t ne V

Central

Obstructive

outside inspiratory insideexpiratory

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  time  solubility diffusion ability

PaO2 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  Perfusion normal

venous V/Q<0.8 admixture (functional shunt)

airway

pulmonary artery

Less ventilated

venous admixture

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

Mechanism: alveolar ventilation normal perfusion 

V/Q>0.8

deadspace-like ventilation

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-toleft shunt) Causes: atelectasis, pulmonary consolidation, bronchiectasis, A-V shunt open Mechanism: Admixture with unoxygenated blood

Venous admixture

Hypoxia

Anatomic shunt

3)Blood gas change • PO2 ? • PCO2 ?

ventilatory (PaO2↓ respiratory PaCO2↑) failure Gas exchange （ PaO2↓ PaCO2↑ ↓N ）

inadequate alveolar ventilation

restrictive obstructive

diffusion disorder Ventilation-perfusion dismatching Anatomic shunt （ V/Q=0 ）

100 nm.

100 nm.

SARS-Associated Coronavirus

Section 2 alterations of function and metabolism

Respiratory failure

abnormal blood-gas

Acid-base, electrolytes disorder

reaction of systems compensatio n

decompensatio n

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

Mixed acidosis hypoxia and hypercapnia

K+ 

Respiratory acidosis and metabolic alkalosis ? Remove CO2 too fast for chronic type II hypokalemia

2. Alternation of respiratory system 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) peripheral chemoreceptor +

PaCO2(<70mmHg ) central chemoreceptor +

respiratory center PaO2  <30mmHg

PaCO2 >70mmHg 

3.Alternation of circulatory system Mild and medium PaO2

Circulatory center

PaCO2 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 Hypercapnia---

PaCO2>80mmHg

Cerebral vessels dilation Cell acidosis

CO2 narcosis

brain edema

O2 、 PaCO2 changes

and CNS chang

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 Increase drive of respiration Mechanical ventilator Nutrition supply

for type II RF, CO2 can’t be reduced too fast

end