13 respiratory failure


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13 respiratory failure

  1. 1. Respiratory failure Guo Yubiao, M.D & Ph.D Pulmonary & Critical Care Medicine The first Affiliated Hospital of Sun-Yat Set University
  2. 2. Male, 32 Fever, cough with sputum for 3 days No finding on physical examination Diagnosis : pneumonia X - ray : shadow in left lower lobe August 16, 2003 August 20, 2003 <ul><li>Acute shortness of breath </li></ul><ul><li>Anxiety </li></ul><ul><li>RR 40/min, Cyanosis </li></ul><ul><li>ABG : PaO2 61mm Hg(FiO2 1.0) </li></ul><ul><li>PaCO2 35 mmHg, pH 7.20 </li></ul><ul><li>X-ray : clouded glass </li></ul><ul><li>Diagnosis : ARDS </li></ul><ul><li>Acidosis </li></ul>
  3. 3. Intubation via mouth tracheotomy Monitoring and ventilation
  4. 4. Contents 0f outline <ul><li>Definition </li></ul><ul><li>Etiology & Pathogenesis </li></ul><ul><li>Classification </li></ul><ul><li>Clinical manifestations </li></ul><ul><li>Diagnosis </li></ul><ul><li>Treatment </li></ul>
  5. 5. Introduction <ul><li>Be a frequently encountered medical problem </li></ul><ul><li>A major cause of death in China </li></ul><ul><li>Mortality from COPD, which ends in death from respiratory failure, continues to increase </li></ul><ul><li>More than 70% of patients with pneumonia are attributed to respiratory failure </li></ul><ul><li>About 1/3 patients in ICU in the United States, about 500 000 persons, receive mechanical ventilation each year </li></ul>
  6. 6. Introduction (cont.) <ul><li>Short-term survival is more than 80% for acute respiratory failure not preceded by additional lung disease or systemic illness </li></ul><ul><li>Multi-system organ failure or pre-existing renal, liver, or chronic gastrointestinal disease with malnutrition substantially worsens outlook </li></ul><ul><li>About 17% of patients placed on mechanical ventilation require assistance for more than 14 days </li></ul><ul><li>Among those requiring this amount of mechanical ventilation, elderly patients have a 9% survival and younger patients a 36% survival </li></ul>
  7. 7. Definition <ul><li>Be a clinical syndrome of respiratory and metabolism dysfunction caused by any condition that severely affects the lung’s ability to maintain arterial oxygenation or carbon dioxide elimination. </li></ul><ul><li>Both acute or chronic respiratory failure may be divided into two main categories. </li></ul><ul><ul><li>A failure of gas exchange – hypoxemia </li></ul></ul><ul><ul><li>A failure of ventilation – hypercapnia </li></ul></ul>
  8. 8. Classification <ul><li>According to pathophysiology and arterial blood gas analysis: </li></ul><ul><ul><li>Type I: A failure of gas exchange </li></ul></ul><ul><ul><ul><li>Hypoxemia, PaO2 < 60 mmHg </li></ul></ul></ul><ul><ul><li>Type II: A failure of ventilation </li></ul></ul><ul><ul><ul><li>PaO 2 < 60 mmHg, PaCO 2 > 50 mmHg </li></ul></ul></ul><ul><ul><li>PaO 2 > 60 mmHg, PaCO 2 >50 mmHg </li></ul></ul><ul><ul><ul><li>Iatrogenic </li></ul></ul></ul>
  9. 9. Classification <ul><li>According to the involved site </li></ul><ul><ul><li>Central respiratory failure </li></ul></ul><ul><ul><ul><li>Change of respiratory rhythm and frequency </li></ul></ul></ul><ul><ul><li>Peripheral respiratory failure </li></ul></ul><ul><ul><ul><li>Dyspnea </li></ul></ul></ul><ul><li>According to onset of respiratory failure </li></ul><ul><ul><li>Acute, develops in seconds or hours </li></ul></ul><ul><ul><li>Chronic, develops in days or longer, elevated HCO3- </li></ul></ul><ul><ul><li>Acute onset of Chronic respiratory failure </li></ul></ul><ul><ul><li>Have no definitive borderline </li></ul></ul><ul><li>According to mechanisms </li></ul><ul><ul><li>Pump failure </li></ul></ul><ul><ul><li>Lung failure </li></ul></ul>
  10. 10. Etiology <ul><li>Airway obstruction </li></ul><ul><ul><li>Airway inflammation, tumor, foreign bodies, fibrosis scar COPD and asthma </li></ul></ul><ul><li>Alveolar or interstitial lung diseases </li></ul><ul><ul><li>pneumonia, emphysema, pulmonary tuberculosis, diffuse interstitial pulmonary fibrosis, pulmonary edema </li></ul></ul><ul><li>Pulmonary vascular diseases </li></ul><ul><ul><li>Pulmonary embolism, pulmonary vasculitis </li></ul></ul><ul><li>Chest wall or pleural diseases </li></ul><ul><ul><li>Flail chest caused by trauma, pneumothorax, severe spinal deformity, massive pleural effusion </li></ul></ul><ul><li>Neuromuscular diseases </li></ul><ul><ul><li>Cerebrovascular diseases, craniocerebral trauma, cerebritis and sedative-hypnotic, poliomyelitis, polyneuritis, myasthenia gravis </li></ul></ul>
  11. 11. Respiratory Pump Failure (泵衰竭) <ul><li>Pump failure is caused by dysfunction of respiratory pump </li></ul><ul><li>Low respiratory drive due to central or peripheral nervous system diseases, neuromuscular junction problem or f atigue of respiratory muscles -> hypoventilation </li></ul><ul><li>manifested as type Ⅱ respiratory failure </li></ul>
  12. 12. Lung Failure (肺衰竭) <ul><li>Lung failure is caused by disorder of lung parenchyma, pulmonary vascular or airway obstruction </li></ul><ul><li>Airway obstruction -> hypoventilation , manifested as type Ⅱ respiratory failure </li></ul><ul><li>Disorder of lung parenchyma -> dysfunction of oxygenation, manifested as hypoxemia </li></ul><ul><li>Disorder of pulmonary vascular system -> ventilation/perfusion mismatch, manifested as hypoxemia </li></ul>
  13. 13. Mechanisms & Pathophysiology <ul><li>Hypoxemia </li></ul><ul><ul><li>Alveolar ventilation ↓ </li></ul></ul><ul><ul><li>FiO 2 ↓ </li></ul></ul><ul><ul><li>Diffusion abnormality </li></ul></ul><ul><ul><li>V/Q mismatch </li></ul></ul><ul><ul><li>A-V shunt </li></ul></ul><ul><li>Hypercapnia( CO2 retention) </li></ul><ul><ul><li>CO 2 production ↑ </li></ul></ul><ul><ul><li>Alveolar ventilation ↓ </li></ul></ul>
  14. 15. Mechanisms of hypoxemia <ul><li>FiO2 ↓ </li></ul><ul><ul><li>Altiplano or under a deep well </li></ul></ul><ul><ul><li>PAO2 & PaO2 ↓ </li></ul></ul><ul><li>Hypoventilation </li></ul><ul><ul><li>VA = VE – VD </li></ul></ul><ul><ul><li>The diffusion capacity of CO2 is 20 times of that of O2 </li></ul></ul>25 20 15 10 5 肺泡分压 (kPa) 0 2 4 6 8 10 肺泡通气量 (l/min) P A CO2 P A O2 P A C O 2 =0.863*VC O2 /VA
  15. 16. Mechanisms of hypoxemia –– Diffusion abnormality ( 弥散障碍 ) <ul><li>The factors that influence rate of gas diffusion across the respiratory membrane include: </li></ul><ul><ul><li>the partial pressure difference of the gas between the two sides of the membrane, </li></ul></ul><ul><ul><li>the surface area of membrane </li></ul></ul><ul><ul><li>the time of contact between blood and alveoli </li></ul></ul><ul><ul><li>the permeability of the membrane </li></ul></ul><ul><li>Diffusion abnormality manifested as hypoxemia </li></ul>100 80 60 40 动脉氧分压 0.25 0.5 0.75 血液通过肺泡毛细血管时间
  16. 17. Mechanisms of hypoxemia <ul><li>Ventilation/perfusion mismatch ( 通气 / 灌流失衡 ) </li></ul><ul><li>Shunt (肺动 - 静脉分流) </li></ul>V/Q=0.8 V/Q>0.8 V/Q<0.8 Q > V (A-V shunt) Normal V > Q (dead space effect)
  17. 18. ( 二 ) 通气 / 血流比例 V/Q 肺泡死腔通气 V/Q > 0.8 静 - 动脉分流 V/Q < 0.8 正常通气 / 血流 V/Q 0.8 VD PaCO 2 - PeCO 2 VT PaCO 2 Qs CcO 2 - CaO 2 Q T CcO 2 - CvO 2 V A 4.2L(R2.1, L2.1) Q 5.0L(R2.5, L2.5) 见于肺不张, ARDS 见于 COPD 正常 Mechanisms of hypoxemia
  18. 19. Mechanisms of hypoxemia <ul><li>Oxygen consumption, (VO2 ) ↑: fever, chill, dyspnea, twitch (eg, 500ml/min) </li></ul><ul><li>Oxygen delivery (DO2 )↓ , Palev O2 ↓ </li></ul>800 100 20 10 肺泡氧分压 2 4 6 8 10 肺泡通气量 (l/min) 400 动脉氧分压 (kPa)
  19. 20. Mechanisms of hypercapnia <ul><li>CO2 production↑: </li></ul><ul><li>• fever, infection, sepsis, epilepsy </li></ul><ul><li>Alveolar ventilation ↓ • neuromuscular diseases or fatigue of respiratory muscles • obstructive ventilation disorder </li></ul>
  20. 21. Influence of hypoxemia Central nervous system <ul><li>Oxygen consumption of brain- -3 ml/100g·min </li></ul><ul><li>If jugular vein PaO2 <20mmHg : unconsciousness, coma </li></ul><ul><li>PaO2 <20mmHg : irreversible damage to nerve cells in several minutes (4~5min) </li></ul><ul><li>Mild hypoxemia : impaired concentration, disorientation, hypomnesia </li></ul><ul><li>Severe hypoxemia : dysphoria, unconsciousness, coma </li></ul>
  21. 22. Influence of hypoxemia Cardiovascular system <ul><li>Myocardium oxygen consumption : 10 ml/100g/min </li></ul><ul><li>Early stage of acute hypoxia–stimulation of sympathetic nerve->HR  、 BP  、 CO  </li></ul><ul><li>Chronic hypoxia -> small pulmonary arteries contraction -> pulmonary hypertension  — Cor pulmonale </li></ul>
  22. 23. <ul><li>PaO 2 ↓ (<60mmHg) -> stimulate the chemoreceptors -> stimulate respiratory center -> strengthen respiratory movement, MV  , respiratory distress </li></ul><ul><li>PaO 2 ↓(<30mmHg) -> inhibition of respiratory center>stimulation of respiratory center -> respiratory depression </li></ul><ul><li>Hyperventilation ->CO 2 ↓ -> inhibition of respiratory center </li></ul><ul><li>Severe hypoxemia -> slow shallow irregular respiration or Cheyne-Stokes respiration </li></ul>Influence of hypoxemia Respiratory system
  23. 24. Influence of hypoxemia haematological system <ul><li>Chronic hypoxemia ->stimulate hematopoiesis of bone marrow -> EPO production  RBC   haemoglobin saturation & O 2 Delivery capacity  </li></ul><ul><li> blood viscosity  , blood stream resistance  -> cardiac load & CO   hypoxemia and blood viscosity  -> the risk of DIC  </li></ul>
  24. 25. Influence of hypoxemia Renal & Digestive system <ul><li>Renal blood vessels contraction, blood supply ↓when accompany with hypotension, DIC -> Renal failure </li></ul><ul><li>Gastric mucosal erosion, necrosis, ulcer and bleeding Hepatic cell impairment by hypoxia -> ALT↑ , jaundice </li></ul>
  25. 26. Influence of hypercapnia Central nervous system <ul><li>Cerebral blood flow : PaCO2  0.133kPa , blood flow  4% -> headache, intracranial pressure  </li></ul><ul><li>Cerebrospinal fluid : H+ 、 HCO 3 、 CO 2 enter blood-brain barrier -> [H+]  ->stimulate subcortex & excitability  </li></ul><ul><li>Consciousness : dizziness, asterixis, somnolence, coma, convulsion </li></ul><ul><li>Peripheral nerves : sympathetic nerve, adrenal gland, distal nerves , catecholamine(CA)  </li></ul>
  26. 27. Influence of hypercapnia Cardiovascular system <ul><li>HR  , CO  , BP  </li></ul><ul><li>With stimulation of sympathetic nerve, the skin and abdominal vessels contract while coronary vessels dilate </li></ul><ul><li>Severe hypoxia and hypercapnia -> directly inhibit cardiovascular center -> depressed cardiac function, dilated vessels -> BP↓, arrhythmia </li></ul><ul><li>Acute severe hypercapnia -> ventricular fibrillation or cardiac arrest especially during intubation procedure </li></ul><ul><li>PaCO2 enhance cardiac inhibition by vagus </li></ul>
  27. 28. Influence of hypercapnia Respiratory system <ul><li>Stimulate respiratory center -> strengthen respiratory movement, Ventilation  </li></ul><ul><li>(PaCO2  0.133 kPa , Ventilation volume  2 L/min) </li></ul><ul><li>Slight contraction of small pulmonary arteries </li></ul><ul><li>Directly relax the bronchial smooth muscle </li></ul><ul><li>PAO2  </li></ul><ul><li>PaCO2  -> rightward shift of the oxyhaemoglobin dissociation curve (ODC) </li></ul>
  28. 29. pH  pH  26.6mmHg
  29. 30. Influence of hypercapnia urinary system <ul><li>Mild CO2 retention ->dilation of renal blood vessels -> renal blood flow  -> urine  </li></ul><ul><li>PaCO2 > 8 kPa, pH   ->renal blood vessels spasm -> renal blood flow  </li></ul><ul><li>HCO3 and Na+ reabsorption  -> urine  </li></ul>
  30. 31. Influence of hypoxemia & hypercapnia Acid-base balance and electrolytes <ul><li>Severe hypoxia -> inhibition of cellular energy metabolism -> insufficient energy production, production of lactic acid ↑ -> sodium-potassium pump failure -> metabolic acidosis, hyperkalemia -> PCO 2 ↑ </li></ul><ul><li>Respiratory acidosis and metabolic acidosis </li></ul><ul><li>pH is determined by HCO 3 /PaCO 2 ratio </li></ul><ul><li>Slow CO 2 retention -> compensated by kidney, decreased elimination of HCO 3 - </li></ul><ul><li>( It takes 1 ~ 3 days for kidney to compensate ) </li></ul>pH = HCO 3 - PaCO 2
  31. 32. Clinical manifestation Acute respiratory failure (1) <ul><li>Dyspnea </li></ul><ul><li>Dyspnea is a early symptom of respiratory failure. </li></ul><ul><li>Increased breath rates </li></ul><ul><li>Change in breath rhythm: Cheyne-Stokes respiration, Biot’s respiration </li></ul><ul><li>Accessory respiratory muscles involved in </li></ul><ul><li>breathing -> “three depressions sign” </li></ul>
  32. 33. <ul><li>Cyanosis: </li></ul><ul><li>Cyanosis is a typical sign of hypoxia, indicating arterial oxygen saturation lower than 90%. </li></ul><ul><li>The extent of cyanosis is associated with content of reduced hemoglobin. So it is less readily detectable if anemia is present and more readily seen in polycythemia. </li></ul><ul><li>Peripheral cyanosis is associated with stasis, in which oxyhemoglobin is reduced more than it normally is because of the prolonged peripheral blood transit time, while the PaO2 could be normal. </li></ul><ul><li>Central cyanosis results from arterial hypoxemia. </li></ul>Clinical manifestation Acute respiratory failure (2)
  33. 34. <ul><li>Neuropsychic symptoms: </li></ul><ul><li>Mental disorder, mania, coma, convulsion </li></ul><ul><li>Circulatory system: </li></ul><ul><li>Tachycardia, myocardial impairment, peripheral circulatory failure, hypotension, arrhythmia, cardiac arrest. </li></ul><ul><li>Digestive system : </li></ul><ul><li>Hepatic function impairment: ALT↑ </li></ul><ul><li>Gastrointestinal tract: mucosal erosion, stress ulcer, gastrointestinal bleeding </li></ul><ul><li>Urinary system: </li></ul><ul><li>Renal function impairment: BUN↑ </li></ul><ul><li>Proteinuria, hematuria, casts in urine </li></ul>Clinical manifestation Acute respiratory failure (3)
  34. 35. Clinical manifestation Chronic respiratory failure <ul><li>Dyspnea: </li></ul><ul><li>Excessive respiratory effort, prolonged expiration——rapid shallow breathing——slow shallow breathing, Cheyne-Stokes breathing (CO2 narcosis, severe respiratory depression) </li></ul><ul><li>Neuropsychic symptoms: </li></ul><ul><li>Irritation caused by increased PaCO2 in early stage: insomnia at night, drowsiness during the day </li></ul><ul><li>Depression caused by pulmonary encephalopathy in late stage: apathy, convulsion, coma, tendon reflex weakened or disappear </li></ul><ul><li>Circulatory system: </li></ul><ul><li>Peripheral vesodilation, skin congestion, warm and sweaty extremities, BP ↑ , CO ↑ , pulsus magnus, HR ↑ , pulsatile headache </li></ul>
  35. 36. Diagnostic criteria <ul><li>History of respiratory dysfunction that severely affects the lung’s ability to maintain arterial oxygenation or carbon dioxide elimination </li></ul><ul><li>Clinical manifestation of d yspnea and cyanosis </li></ul><ul><li>Blood gas analysis </li></ul><ul><ul><li>PaO2 < 60 mmHg, or plus </li></ul></ul><ul><ul><li>PaCO2 > 50 mmHg </li></ul></ul><ul><li>Breathing air on sea level and standard atmosphere pressure at rest </li></ul><ul><li>Exclude intracardiac shunt and decreased cardiac output , such as ventricular septal defect </li></ul><ul><li>In fact it is a pathophysiology & laboratory Diagnosis </li></ul>
  36. 37. Diagnostic criteria The acute respiratory distress syndrome (ARDS) <ul><li>ARDS is a process of nonhydrostatic pulmonary edema and hypoxemia associated with a variety of etiologies: </li></ul><ul><li>Progressive dyspnea and hypoxia which can not be relieved by oxygen therapy </li></ul><ul><li>Bilateral infiltrates on chest radiograph </li></ul><ul><li>PaO2/FiO2 <200 </li></ul><ul><li>Excluding patients with signs of heart failure or a pulmonary capillary wedge pressure (PCWP) >18 mmHg </li></ul>
  37. 38. Treatment (outline of principle) <ul><li>Etiology Management </li></ul><ul><li>Keep airway open </li></ul><ul><li>Oxygen therapy </li></ul><ul><li>Ensure adequate alveolar ventilation, correct CO2 retention </li></ul><ul><ul><li>Respiratory stimulant </li></ul></ul><ul><ul><li>Mechanical Ventilation </li></ul></ul><ul><li>General supportive care </li></ul><ul><ul><li>Transfer to ICU for critical care and treatment </li></ul></ul><ul><ul><li>Infection control </li></ul></ul><ul><ul><li>Management of electrolyte and acid-base disturbance </li></ul></ul><ul><ul><li>Management of cor pulmonale, pulmonary encephalopathy, multi-organ dysfunction syndrome(MODS). </li></ul></ul><ul><ul><li>Nutrition support </li></ul></ul>
  38. 39. Treatment Etiology Management <ul><li>Management of any underlying diseases : upper airway obstruction, severe pneumothorax, massive pleural effusions </li></ul><ul><li>Eliminate any factors that cause respiratory failure secondary to infection or shock </li></ul><ul><li>Any inducement leading to acute deterioration of chronic respiratory failure : infection, malnutrition, inappropriate medication usage </li></ul>
  39. 40. Causes of Upper Airway Obstruction <ul><li>CNS depression-anesthesia, drug overdose </li></ul><ul><li>Cardiac arrest </li></ul><ul><li>Loss of consciousness </li></ul><ul><li>Foreign body or tumor </li></ul>
  40. 41. Treatment Keep airway open 保持气道通畅 <ul><li>Importance of airway open : </li></ul><ul><li>Airway obstruction: resistance ↑ -> WOB↑ </li></ul><ul><li>respiratory muscle fatigue </li></ul><ul><li>difficult to clear airway secretion -> infection deteriorate </li></ul><ul><li>atelectasis -> the surface area of gas exchange  </li></ul><ul><li>Complete airway obstruction -> apnea, death </li></ul><ul><li>Clear airway secretion : </li></ul><ul><li>mucolytics </li></ul><ul><li>manual suction </li></ul>
  41. 42. Treatment Keep airway open 保持气道通畅 <ul><li>Bronchodilators for patients with bronchospasm: </li></ul><ul><ul><li>β 2-adrenoreceptor agonist, anticholinergic, glucocorticoid, theophylline </li></ul></ul><ul><ul><li>Mode of administration : parenteral first and then inhale </li></ul></ul><ul><ul><li>Mechanical ventilation+ medications delivery </li></ul></ul><ul><ul><li>Airway humidify & nebulize </li></ul></ul><ul><li>Establishing artificial airway </li></ul><ul><ul><li>Endotracheal intubation </li></ul></ul><ul><ul><li>Tracheostomy </li></ul></ul>
  42. 43. Treatment Oxygen therapy <ul><li>Indications of oxygen therapy : </li></ul><ul><li>Pump failure: improve ventilation </li></ul><ul><li>Pneumonia, Pulmonary embolism, acute attack of asthma </li></ul><ul><li>Severe pulmonary edema, ARDS </li></ul><ul><li>Acute deterioration or worsening of COPD (pay attention to CO2 retention when giving oxygen therapy! ) </li></ul>
  43. 44. Treatment Oxygen therapy <ul><li>Inspired oxygen concentration: </li></ul><ul><li>Inspired oxygen concentration should be the lowest value that results in an oxygen saturation of over 90% (PaCO2 about 60mmHg). </li></ul><ul><li>High concentrations of inspired oxygen (>35%) are safe in patients with type Ⅰ respiratory failure, as there is no risk of CO2 retention. </li></ul><ul><li>While in patients with type Ⅱ respiratory failure, who are dependent on hypoxic drive for ventilation, oxygen therapy must be carefully controlled so that sufficient oxygen is supplied but without precipitating severe respiratory acidosis. </li></ul>
  44. 45. <ul><li>Oxygen delivery device: </li></ul><ul><li>① Nasal cannula/prongs: </li></ul><ul><li>Advantage: allow patients to eat, drink, expectorate and speak </li></ul><ul><li>Disadvantage: FiO2 delivered is not stable and affected by breathing; high flow rates irritate nasopharyngeal mucosa </li></ul><ul><li>Guide: Delivers 4% Oxygen per liter flow; </li></ul><ul><li>FiO2 (%)=21+4×oxygen flow rate (L/min) </li></ul><ul><li>Flow rates should be limited to less than 7L/min. </li></ul><ul><li>② Mask: </li></ul><ul><li>Simple oxygen mask, nonrebreathing mask with reservoir bag, Venturi mask. </li></ul><ul><li>Advantage: FiO2 delivered is comparatively stable and is adjustable; less irritative to nasopharyngeal mucosa </li></ul><ul><li>Disadvantage: inconvenient for patients to expectorate, eat and drink </li></ul>Treatment Oxygen therapy
  45. 46. Nasal cannula/prongs 鼻导管吸氧 <ul><li>鼻导管给氧的上限量为 6L/min ,大于这一流量时,由于管道和鼻咽内产生涡流,吸氧浓度不再增加。 </li></ul>
  46. 47. Simple oxygen mask 常规面罩 <ul><li>常规面罩可提供较稳定的氧浓度,其输送的氧浓度大约为 70% -80% </li></ul><ul><li>但是这两种方法都不能精确地监测 FiO2 。因为随呼吸频率、每分钟通气量、室内空气的流动、输氧装置的放置等因素的不同而改变。故影响纠正低氧血症并防止高碳酸血症的发生的治疗观察。 </li></ul>
  47. 48. Venturi mask Venturi 面罩 <ul><li>Venturi 面罩可较精确地调整 FiO2 ,但面罩必须佩戴正确才能使预期的氧量得到输送 </li></ul>
  48. 49. Treatment Oxygen therapy <ul><li>Side effects </li></ul><ul><li>Inhibition of respiratory center in patients with type Ⅱ respiratory failure, who are dependent on hypoxic drive for ventilation  CO2 retention ↑ </li></ul><ul><li>Absorption atelectasis/denitrogenisation 吸收性肺不张 ): nitrogen is replaced by more absorptive oxygen </li></ul><ul><li>Oxygen poisoning : High concentrations of inspired oxygen  injury of pulmonary capillary epithelium </li></ul>
  49. 50. Treatment Ensure adequate ventilation, correct CO2 retention <ul><li>Respiratory stimulant: mainly used in CNS depression </li></ul><ul><li>Principles for respiratory stimulant ( 呼吸兴奋剂 ) : </li></ul><ul><ul><li>Maintain potency of airway to avoid respiratory muscles fatigue and deteriorate CO2 retention </li></ul></ul><ul><ul><li>Be cautious when used in patients with frequent convulsion caused by cerebral anoxia, cerebral edema </li></ul></ul><ul><ul><li>Suitable for patients with normal respiratory muscle strength </li></ul></ul><ul><ul><li>Not suitable for patients only with oxygenation failure </li></ul></ul><ul><ul><li>Avoid sudden withdrawal </li></ul></ul><ul><ul><li>Drug: coramine, lobeline, doxapram </li></ul></ul>
  50. 51. Treatment Non-invasive positive pressure ventilation, NIPPV <ul><li>Indications </li></ul><ul><li>Conscious and cooperative </li></ul><ul><li>Stable circulation </li></ul><ul><li>Be able to protect airway </li></ul><ul><li>No facial trauma, injury and deformity </li></ul><ul><li>Be endurable to mask </li></ul>
  51. 52. Different kind of masks 各款口鼻面罩
  52. 53. Treatment Mechanical ventilation <ul><li>Goals of Mechanical Ventilation: </li></ul><ul><ul><li>improve alveolar ventilation, decrease PaCO2; </li></ul></ul><ul><ul><li>improve pulmonary gas exchange; </li></ul></ul><ul><ul><li>Decrease work of breathing, reverse respiratory muscle fatigue. </li></ul></ul><ul><li>Indications for mechanical ventilation : </li></ul><ul><ul><li>apnea; </li></ul></ul><ul><ul><li>upper airway obstruction; impaired airway protection; </li></ul></ul><ul><ul><li>inadequate handling of secretions; </li></ul></ul><ul><ul><li>acute hypercapnia that is not quickly reversed by appropriate specific therapy; </li></ul></ul><ul><ul><li>severe hypoxemia; </li></ul></ul><ul><ul><li>progressive patient fatigue despite appropriate treatment. </li></ul></ul><ul><li>Adjust modes and settings for mechanical ventilation according to blood gas analysis and clinical judgment </li></ul>
  53. 54. Treatment Management of electrolyte and acid-base disturbance <ul><li>Respiratory acidosis </li></ul><ul><ul><li>improve alveolar ventilation </li></ul></ul><ul><li>Respiratory acidosis + metabolic acidosis </li></ul><ul><ul><ul><li>Etiology management of acidosis </li></ul></ul></ul><ul><ul><ul><li>improve alveolar ventilation </li></ul></ul></ul><ul><ul><ul><li>appropriate alkali supplement </li></ul></ul></ul><ul><li>Respiratory acidosis + metabolic alkalosis </li></ul><ul><ul><ul><li>Avoid Iatrogenic factors </li></ul></ul></ul>
  54. 55. Thank you!