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Respiratory Failure. Respiration  external respiration ( pulmonary ventilation and gas exchange in lung )  transport of gas  internal respiration.

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Presentation on theme: "Respiratory Failure. Respiration  external respiration ( pulmonary ventilation and gas exchange in lung )  transport of gas  internal respiration."— Presentation transcript:

1 Respiratory Failure

2

3 Respiration  external respiration ( pulmonary ventilation and gas exchange in lung )  transport of gas  internal respiration

4 1.respiratory insufficiency The condition in which the lungs can not take in sufficient oxygen or expel sufficient carbon dioxide to meet the needs of the cells of the body. Also called pulmonary insufficiency. The condition in which the lungs can not take in sufficient oxygen or expel sufficient carbon dioxide to meet the needs of the cells of the body. Also called pulmonary insufficiency. Respiratory failure concept and classification

5 2. respiratory failure normal reference values : normal reference values : PaO 2 < 60mmHg ( 8kPa ) PaO 2 < 60mmHg ( 8kPa ) with or without PaCO 2 > 50mmHg ( 6.67kPa ) with or without PaCO 2 > 50mmHg ( 6.67kPa ) RFI = PaO2/FiO2 ≤ 300 Respiratory failure is a syndrome in which the respiratory system fails in one or both of its gas exchange functions: oxygenation and carbon dioxide elimination. In practice, respiratory failure is defined as a PaO 2 value of less than 60 mm Hg while breathing air or a PaCO 2 of more than 50 mm Hg.

6 3 . classification ( 1 ) according to PaCO 2 ( 1 ) according to PaCO 2 ■ Ⅰ ) ■ hypoxemic (Group Ⅰ ) respiratory failure a PaO 2 of less than 60 mm Hg with a normal or low PaCO 2. Cause of: Edema, Vascular disease, Chest Wall. ■ ■ hypercapnic (Group Ⅱ ) respiratory failure a PaO 2 low 60 mm Hg and PaCO 2 of more than 50 mm Hg. Cause of: Airway obstruction, Neuromuscular disease.

7 ( 4 ) according to duration ■ acute respiratory failure ■ acute respiratory failure ■ chronic respiratory failure ■ chronic respiratory failure ( 3 ) according to primary site ■ central respiratory failure ■ central respiratory failure ■ peripheral respiratory failure ■ peripheral respiratory failure ( 2 ) according to pathogenic mechanism ■ ventilatory disorders ■ ventilatory disorders ■ gas exchange disorders ■ gas exchange disorders

8 ventilatory disorders gas exchange disorders respiratory failure obstructive ventilatory disorders disorders restrictive ventilatory disorders etiology and pathogenesis 【 classification of respiration failure mechanism 】 diffusion disorders ventilation-perfusion ventilation-perfusionmismatching

9 Ⅰ. ventilatory disorders 1. restrictive ventilatory disorders 1. restrictive ventilatory disorders Restrictive hypoventilation is caused by the diseases that affect the distensibility of the alveolar. Restrictive hypoventilation is caused by the diseases that affect the distensibility of the alveolar.

10 Respiratory movement forced breathing

11 Respiratorymovement disorder disorder neuro-muscular disorders decreased strength, myasthenia gravis decreased strength, myasthenia gravis hypoxia, acidosis Respiratory movement ↓ Respiratory movement ↓ Depression of CNS damage of CNS drug overdose ▲ Disorders of the respiratory muscles alveolar distensibility Restrictiveventilatory disorders disorders respiratory failure

12 ● decrease of pulmonary surfactantsand increase of ● decrease of pulmonary surfactants and increase of surface tension force surface tension force ● diffuse interstitial fibrosis decreased lung compliance ▲ decreased lung compliance decreased thoracic compliance of lung ▲ decreased thoracic compliance of lung deformity of thorax, fracture of several ribs, tension pneumothorax, thickened constrictive pleural layer. pneumothorax, thickened constrictive pleural layer.

13 2. obstructive ventilatory disorders ■ obstructive ventilatory disorders are caused by the diseases which share the common characterestic of causing enough narrowing within the tracheobronchial tree to increase resistance to the flow of air.原因和机制 etiology ■ etiology asthma, emphysema, chronic bronchitis, and bronchiectasis.

14 ■ Obstruction is located in the airway inside the thorax : expiratory dysnea ■ Obstruction is located in the airway outside the thorax : inspiratory dysnea 1 ) central airway obstruction defined as airway obstruction between the glottis and the carina + expire inspire three depression sign

15 2 ) peripheral airway obstruction 2 ) peripheral airway obstruction smaller airways less than 2 mm in diameter. smaller airways less than 2 mm in diameter. equal pressure point (EPP) In forced expiration, the point where intrapleural pressure and alveolar pressure are equal. Determinants of airway closure are the intrinsic caliber of peripheral airways. Smooth muscle tone, thickness of the wall, mechanical properties of the surface film, and secretions in the lumen,bingding effect of attachments of the surrounding lung parenchyma. lung parenchyma.

16 EPP moves distally as expiration progresses because as air leaves the alveolar unit, the pressure in the alveolar decreases hence the pressure in the airway decreases as well. Peripheral airway obstruction may be caused by: specific chemical mediators (such as histamine, leukotrienes, prostaglandins ), other substances released during inflammatory and allergic responses. forced expiration

17 1 ) Low PaO 2 : PaO 2 < 60mmHg 2 ) PaCO 2 change : A. hypoventilation : high PaCO 2. A. hypoventilation : high PaCO 2. R=40/50 mmHg=0.8 ; R=40/50 mmHg=0.8 ; B. part hypoventilation: Low PaO 2 and normal or low PaCO 2. B. part hypoventilation: Low PaO 2 and normal or low PaCO The alteration of blood gas

18 Ⅱ. gas-exchanging dysfunction Ⅱ. gas-exchanging dysfunction 1. diffusion disorders The diffusion impairment is characterized by a disruption in the exchange of O 2 or CO 2 or both across the alveolar-capillary membrane. Causes: reduction and/or thicken of alveolar-capillary membrane or reduction of the diffuse time.

19 1 ) etiology of diffusion disorders 1 ) etiology of diffusion disorders ■ reduction of diffusion membrane area Abnormalities of diffusion may not cause arterial hypoxia in Abnormalities of diffusion may not cause arterial hypoxia in persons at rest unless they are extremely severe. persons at rest unless they are extremely severe. (total: 80 mm 2; at rest: 30~40 mm 2 ) (total: 80 mm 2; at rest: 30~40 mm 2 ) Causes: emphysema, pneumonia, lobectomy Causes: emphysema, pneumonia, lobectomy increase of diffusion membrane thickness ■ increase of diffusion membrane thickness edema, fibrosis, capillary vessel dilatation edema, fibrosis, capillary vessel dilatation decreased time of blood contacts with alveolar ■ decreased time of blood contacts with alveolar

20 AA V A Q V A / Q Top 1.2L/min 0.4L/min 3.0 Middle 1.8L/min 2.0L/min 0.9 Bottom 2.1L/min 3.4L/min 0.6 ···· 2. ventilation/perfusion imbalance The dysfunction of gas exchange can arise secondary to ventilation /perfusion mismatching.

21 asthma, chronic bronchitis, obstructive emphysema, fibrosis, edema V A / Q ↓ part alveolar ventilatory ↓ V A / Q ↓ part alveolar ventilatory ↓ functional shunt↑ >30% respiratory failure · · 1) type and cause of ventilation-perfusion-mismatching 1) type and cause of ventilation-perfusion-mismatching (1) decreased ratio of V A /Q underventilated in relation to their perfusion underventilated in relation to their perfusion ··

22 (2) increased ratio of V A /Q poor perfusion in relation to their ventilation with air poor perfusion in relation to their ventilation with air ·· pulmonary artery embolization, DIC in lung, vessels contract, pulmonary arteritis, dead space like ventilation V A /Q ↑ poor perfusion↓ dead space like ventilation V A /Q ↑ poor perfusion↓ respiratory failure · ·

23 pulmonary consolidation,At electasis anatomical-like shunt increased of ▲ increased of anatomical-like shunt bronchiectasis anatomic shunt ↑ Pulmonary A-V shunt open↑ true shunt↑ Respiratory failure increased of anatomical shunt ▲ increased of anatomical shunt 3 ) increased of anatomical shunt Right-to-left shunts or anatomic shunt Right-to-left shunts or anatomic shunt

24 Ⅲ. Acute respiratory distress syndrome ( ARDS ) [concept] ARDS is a clinical description of severe lung injury characterized by increased permeability of alveolar-capillary membranes, development of protein-rich pulmonary edema, marked hypoxemia refractory to increase in inspired oxygen concentration, and the absence of left ventricular failure. ARDS is a clinical description of severe lung injury characterized by increased permeability of alveolar-capillary membranes, development of protein-rich pulmonary edema, marked hypoxemia refractory to increase in inspired oxygen concentration, and the absence of left ventricular failure.

25 [etiology] shock from any cause, shock from any cause, multisystem trauma, multisystem trauma, infection including bacterial and nonbacterial pneumonia, infection including bacterial and nonbacterial pneumonia, inhaled toxic substances, inhaled toxic substances, overdose of some drug, overdose of some drug, acute pancreatitis. acute pancreatitis.

26 1 . direct injury of damage factor 2 . indirect injury of inflammation medium [ pathogenesis of ARDS]

27 [Mechanisms of respiratory failure] 1. diffusion disorders damage of alveolar-capillary membrane increased permeability diffusion disorders diffusion disorders ARDS 2. ventilatory disorders edema, type Ⅱ alveolar epithelial cells damage decreased lung volume ▲ edema, type Ⅱ alveolar epithelial cells damage decreased lung volume airway obstruction obstructive ventilatory restrictive ventilatory disorders disorders disorders disorders inflammation medium bronchia spasm respiratory failure ▲ inflammation medium bronchia spasm respiratory failure 3 . V A /Q mismatching

28 Effects of respiratory failure 1.Acid-base disturbances & disorders of electrolyte balance 2.Alteration of the respiratory system peripheral chemoreceptor peripheral chemoreceptor ■ PaO 2 ↓ < 60mmHg respiratory center(+) respiratory movement↑ < 30mmHg respiratory center (-) respiratory movement ↓ < 30mmHg respiratory center (-) respiratory movement ↓ ■ PaCO2↑ central chemoreceptor (+) respiratory movement↑ > 80mmHg respiratory center (-) respiratory movement ↓ > 80mmHg respiratory center (-) respiratory movement ↓

29 3. Alteration of the respiratory system 3. Alteration of the respiratory system compensatory reaction ■ compensatory reaction PaO 2 <60 mmHg , PaCO 2 increase cardiovascular center(+) PaO 2 <60 mmHg , PaCO 2 increase cardiovascular center(+)  increase in cardiac output : increase in stroke volume and heart rate  redistribution of blood flow injurious changes ■ injurious changes PaO 2 80 mmHg cardiovascular center(-) PaO 2 80 mmHg cardiovascular center(-)  rate slow, decreased blood pressure  cardiac output decrease  pulmonary hypertension

30 ■ difficulty breathing Restricted diastolic co pulmonale ■ co pulmonale ■ pulmonary arterial embolism, capillary damage co pulmonale afterload to right ventricle ↑ chronic pulmonary hypertension Pulmonary vascular wall thickening and hardening ■ PaO 2 ↓ blood resistance ↑ blood resistance ↑ pulmonary vasoconstriction RBC ↑ blood viscosity ↑ Stenosis ■ Hypoxia, acidosis myocardial systolic and diastolic function(-) and diastolic function(-)

31 (2) Hypercapnia: CO 2 nacosis. (2) Hypercapnia: CO 2 nacosis. a condition of confusion, tremors, convulsions, and possible coma that a condition of confusion, tremors, convulsions, and possible coma that may occur if blood levels of carbon dioxide increase to 80 mm Hg or higher. may occur if blood levels of carbon dioxide increase to 80 mm Hg or higher. (1) Hypoxia: the nervous system is very sensible to oxygen lack. < 40~50 mmHg, serious but reversible deterioration in cerebral function < 40~50 mmHg, serious but reversible deterioration in cerebral function ( orientation, arithmetic tasks, memory) occurs, and restlessness and ( orientation, arithmetic tasks, memory) occurs, and restlessness and confusion are common. confusion are common. < 30 mmHg, loss of consciousness results. < 30 mmHg, loss of consciousness results. < 20 mmHg, irreversible damage of neural cells. < 20 mmHg, irreversible damage of neural cells. 功能和代谢 4. Alteration of the nervous system 4. Alteration of the nervous system

32 ■ Brain cell injury lysosomal membrane stability↓ lysosomal enzyme release nerve cell necrosis GABA↑ GABA↑ CSF pH↓ < 7.25 EEG slow or stop PaCO 2 ↑, acidosis Cerebral vasodilation Cerebral blood flow↑ PaCO 2 ↑, acidosis Cerebral vasodilation Cerebral blood flow↑ hypoxia vascular endothelial damage extracellular brain edema hypoxia vascular endothelial damage extracellular brain edema edema on brain cell Vascular compression edema on brain cell Vascular compression Increased cerebral anoxia Increased cerebral anoxia ■ cerebrovascular injury Intracranial pressure ↑ pulmonary encephalopathy [pulmonary encephalopathy] [pulmonary encephalopathy]

33 4. Alteration of the renal function 4. Alteration of the renal function 5. Alteration of the digestive system 5. Alteration of the digestive system

34 Thanks for attention


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