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Chaper 13. Respiratory failure. Zhao Mingyao BMC.ZZU. Respiration = ventilation + gas exchange Ventilation: alveoli enlarging to set up P gradient airway fluency to let gas flow gas exchange: area distance
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Chaper 13 Respiratory failure Zhao Mingyao BMC.ZZU
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
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
Acute : minutes to days Chronic: over months to years Central : head injury, encephalitis Peripheral: asthma, pneumonia, emphysema 2.Classification of ~ According to (1)duration (2)primary site
(3)blood-gas Type I : PaO2 Type II: PaO2 + PaCO2 (4)pathogenesis ventilation blood gas exchange: diffusion V/Q anatomy shunt
Section 1 Etiology and pathogenesis Respiration = ventilation + gas exchange
Mechanism of RF 1. Hypoventilation Extralung intralung (1)restrictive ~ (2)obstructive ~ Central airway ~ Peripheral airway ~
Ventilation (does work) = dynamic force overcomes resistant force (elastic ~ + nonelastic ~) ----physics view
(1) Restrictive ~ Major Causes: CNS and nerves Respiratory muscles, chest wall and pleura Lung( Alveoli) distension Alveoli distensibility
1)Extrapulmonary disease ①CNS: ②Respiratory muscles: ③Chest wall and pleura:
2)Intrinsic disease ①Pulmonary elastic structure ②Alveolar surfactant substance
Function of surfactant substances 1. Reduces surface tension 2. Increases compliance, stabilize alveoli Keep alveoli dry; Prevent pulmonary edema
3)Blood gas change PACO2PAO2=PiO2 ———— R • PAO2 P O2 in alveoli • PiO2: PO2 in inhaling air • PACO2:PCO2 in alveoli • R:respiratory quotient
PCO2 in alveoli 0.863Vco2 PaCO2= PACO2 = —————— VA PACO2: PCO2 in alveoli Vco2:CO2 production/min VA:alveolar ventilation volume
Blood gas change PACO2 PAO2= PiO2 —————— R • 0.863Vco2 • PaCO2= PACO2 = ——————VA
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 expiration inspiration outside thorax---inspiratory dyspnea
Retractions ( supraclavicular, intercostal and subcostal areas) on inspiration
Variable inspiration expiration inside thorax---expiratory dyspnea
Peripheral airway (Φ <2mm ) 1. thinner wall, without cartilage support 2. caliber changes with respiration 3. close junction with adjacent tissues
Peripheral airway obstruction 1.mucosa edema 2.fibrosis 3.inflammatory infiltration 4.secretions in lumen thickness diameter
0 0 Isobaric point 10 20 25 10 15 20 20 20 20 20 30 20 35 +35 20 20 +35 25 20 Normal expire Emphysema expire Isobaric point upshift in Emphysema
CNS, NS Ventilation disorders Respiratory muscle Extrapulmonary Chest wall, pleura Restrictive Elastic structure intrapulmonary Surfactant substances outside inspiratory variable Central expiratory inside 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
Total diffusion AREA is large 50~100 m2 Diffusion PATH is very small, <1 µm
1) Diffusion area Alveolar area : 80m2 at rest: 40 m2 Causes of decreased area: Emphysema Pulmonary tumor Pulmonary lobectomy
2) Diffusion distance Pulmonary edema, congestion Pulmonary fibrosis Alveolar epithelium hyperplasia Alveolar-capillary membrane thickness
3) Diffusion time↑ alveolar normal Thick alveolar membrane Pul vein Pul Artery
3) Blood gas change distance PaO2 area Blood stream time solubility PaCO2 Normal or or diffusion ability Diffusion disorder
1)V/Q Causes: Bronchial asthma, chronic bronchitis, obstructive pulmonary emphysema, pulmonary fibrosis Mechanism: venous admixture alveolar ventilation V/Q<0.8 Perfusion normal (functional shunt)
2)V/Q Causes: Pulmonary arteriosclerosis, pulmonary thrombosis bronchiectasis, pulmonary tuberculosis Mechanism: alveolar ventilation normal deadspace-like ventilation V/Q>0.8 perfusion
Gas exchange disorder diffusion area ↓ diffusion distant ↑ efficiency (V/Q) V/Q ↓ -functional shunt V/Q ↑ -dead space-like ventilation
3)Blood gas change V/Q(-) V/Q: ventilation V/Q: perfusion V/Q V/Q PaO2 , PaCO2 N or or
4.Anatomic shunt (Right-to-left shunt) Causes: atelectasis, pulmonary consolidation, bronchiectasis, A-V shunt open Mechanism: Admixture with unoxygenated blood
3)Blood gas change PO2 ? PCO2 ?
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)
Mechanism of ARDS Pathogenic factors Inflammatory cells and platelet activated Release proteinase, inflammatory mediators Microthrombosis Alveolar-capillary membrane damaged Permeability (continue)
pulmonary edema diffusion disorder hypoxemia atelectasis functional shunt bronchus spasm dead space-like ventilation vascular constriction microthrombosis
decompensation compensation Respiratory failure Acid-base, electrolytes disorder abnormal blood-gas reaction of systems
1. Acid-base and electrolytes disturbance Respiratory acidosis type II ~ retention of CO2 K+ Metabolic acidosis---hypoxia anaerobic glycolysis lactic acid K+
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