Respiratory failure is characterized by severe dysfunction of pulmonary ventilation and/or oxygenation caused by various diseases, resulting in hypoxia and retention of carbon dioxide. It is defined as a PaO2 of less than 8.0 kPa (60 mmHg), and/or a PaCO2 of greater than 6.67 kPa (50 mmHg). The main causes are ventilation dysfunction due to airway obstruction or limitation, and oxygenation dysfunction due to pulmonary edema, interstitial lung disease, or ARDS. The key pathophysiological changes are hypoxia, retention of carbon dioxide, and acidosis, which can affect multiple organ systems and lead to complications.

1. Respiratory failureRespiratory failure

2. DefinitionDefinition
• Severe dysfunction of pulmonarySevere dysfunction of pulmonary
ventilationventilation and/orand/or oxygenationoxygenation caused bycaused by
various diseases, characterized byvarious diseases, characterized by
hypoxiahypoxia and/orand/or retention of carbonretention of carbon
dioxidedioxide, manifested as, manifested as multiple systemicmultiple systemic
syndromessyndromes with a series ofwith a series of
pathophysiologic changespathophysiologic changes

3. • The standard for definitionThe standard for definition ::
• PaO2<8.0kPa (60mmHg), and/orPaO2<8.0kPa (60mmHg), and/or
PaCO2>6.67kPa(50mmHg), under thePaCO2>6.67kPa(50mmHg), under the
circumstances as at sea-levelcircumstances as at sea-level
atmospheric pressure, at rest indoor,atmospheric pressure, at rest indoor,
excluding the interference of otherexcluding the interference of other
diseases such as intracardiac shuntdiseases such as intracardiac shunt

4. ClassificationClassification
• History & CourseHistory & Course
1.1. Acute: no primary pulmonary D, accordant toAcute: no primary pulmonary D, accordant to
the standard of RF in several Hrs or daysthe standard of RF in several Hrs or days
2.2. Chronic: long history of chronic pulmonary D,Chronic: long history of chronic pulmonary D,
e.g. COPD, interstitial D, etce.g. COPD, interstitial D, etc
• PathophysiologyPathophysiology
1.1. Hypoventilation, airway obstructionHypoventilation, airway obstruction
2.2. Oxygenation (gas exchange disorder), ARDSOxygenation (gas exchange disorder), ARDS
3.3. Combination of the above: COPDCombination of the above: COPD
• Site of Primary DiseasesSite of Primary Diseases
1.1. PeripheralPeripheral
2.2. CentralCentral

5. • Arterial gas analysisArterial gas analysis
1.1. Type Ⅰ:Type Ⅰ: hypoxia, PaOhypoxia, PaO22<8.0kPa, no significant<8.0kPa, no significant
change of PaCO2, common in acute RF, morechange of PaCO2, common in acute RF, more
related to gas exchange disorderrelated to gas exchange disorder
2.2. Type Ⅱ:Type Ⅱ: hypoxia (PaOhypoxia (PaO22<8.0kPa), with retention<8.0kPa), with retention
of carbon dioxide (PaCO2>6.67kPa), commonof carbon dioxide (PaCO2>6.67kPa), common
in chronic RF, more related to hypoventilationin chronic RF, more related to hypoventilation

6. • EtiologyEtiology
1.1. Pump RF:Pump RF: insufficiency of respiratory driveinsufficiency of respiratory drive
(center), or limited respiratory movement(center), or limited respiratory movement
(paralysis of peripheral nerve, fatigue of(paralysis of peripheral nerve, fatigue of
muscles, thoracic deformity, etc)muscles, thoracic deformity, etc)
2.2. Lung RF:Lung RF: caused by airway obstruction,caused by airway obstruction,
pulmonary parenchymal or interstitial D orpulmonary parenchymal or interstitial D or
pulmonary vascular D.pulmonary vascular D.

7. EtiologyEtiology
• In terms of pathogenesis:In terms of pathogenesis:
hypoventilation, oxygenation, or thehypoventilation, oxygenation, or the
combinationcombination
• Ventilation dysfunctionVentilation dysfunction
1.1. ObstructiveObstructive
• Chronic bronchitis, COPD, late stage of asthma, sleepChronic bronchitis, COPD, late stage of asthma, sleep
apnea, bronchial foreign body, oppression ofapnea, bronchial foreign body, oppression of
inflammatory granuloma, tumor or enlarged LNinflammatory granuloma, tumor or enlarged LN
1.1. LimitedLimited

8. • LimitedLimited
1.1. Diseases of Chest wall: such as thoracicDiseases of Chest wall: such as thoracic
deformity, trauma, Rheumatic Arthritis(centraldeformity, trauma, Rheumatic Arthritis(central
type), severe pleural adhesion and hypertrophytype), severe pleural adhesion and hypertrophy
2.2. Diaphragmatic movement limited by abdominalDiaphragmatic movement limited by abdominal
surgery, exuberant ascites, huge mass, etcsurgery, exuberant ascites, huge mass, etc
3.3. Limited lung expansion: pleural effusion,Limited lung expansion: pleural effusion,
pneumothorax, atelectasis, lung consolidation,pneumothorax, atelectasis, lung consolidation,
etcetc
4.4. CNS diseases: cerebral injury, tumor, stroke,CNS diseases: cerebral injury, tumor, stroke,
encephalitis, etcencephalitis, etc
5.5. Neuromuscular D, such as poliomyelitis,Neuromuscular D, such as poliomyelitis,
myasthenia gravitas, progressive myatrophy,myasthenia gravitas, progressive myatrophy,
etcetc
6.6. Respiratory center inhibited by drugs such asRespiratory center inhibited by drugs such as
morphine, barbitals, & other sedatives,morphine, barbitals, & other sedatives,
pesticidespesticides

9. • Oxygenation dysfunctionOxygenation dysfunction
1.1. Pulmonary edemaPulmonary edema caused by cardiac or other Dcaused by cardiac or other D
2.2. Chronic pulmonaryChronic pulmonary interstitial Dinterstitial D such as primarysuch as primary
interstitial fibrosis, sarcoidosis, silicosis, radiointerstitial fibrosis, sarcoidosis, silicosis, radio
pneumonia, oxygen intoxication, etcpneumonia, oxygen intoxication, etc
3.3. Occlusive pulmonary vascular D:Occlusive pulmonary vascular D: pulmonarypulmonary
embolism and infarction, thrombosisembolism and infarction, thrombosis
4.4. ARDS (acute respiratory distress syndrome)ARDS (acute respiratory distress syndrome)

10. PathogenesisPathogenesis
1.1. Alveolar insufficient ventilationAlveolar insufficient ventilation
2.2. Ventilation/perfusion mismatchingVentilation/perfusion mismatching
3.3. Diffusion dysfunctionDiffusion dysfunction
4.4. Increased intrapulmonary shuntIncreased intrapulmonary shunt
5.5. Respiratory muscular fatigueRespiratory muscular fatigue

11. 1. Alveolar insufficient ventilation1. Alveolar insufficient ventilation
• Normal ventilation depends on:Normal ventilation depends on:
• Airway, thoracic and pulmonary complianceAirway, thoracic and pulmonary compliance
• Obstruction orObstruction or  compliancecompliance→→ insufficientinsufficient
ventilationventilation →hypoxia and retention of→hypoxia and retention of COCO22..

12. • PaPaCO 2CO 2 equation, which show theequation, which show the
relationship between Parelationship between PaCO 2CO 2 and alveolarand alveolar
ventilationventilation
• PaPaCO2CO2 = 0.863= 0.863 ×× (VCO(VCO22//VAVA))
• VCOVCO2:2: Minute production of COMinute production of CO22 ----relativelyrelatively
invariableinvariable
• VA: Minute alveolar ventilationVA: Minute alveolar ventilation
• Negative relationship betweenNegative relationship between VA &VA & PaPaCO2CO2
• VAVA ＝＝ VE—VD. VE: minute ventilation; VD:VE—VD. VE: minute ventilation; VD:
physiologic dead (ineffective) volumephysiologic dead (ineffective) volume
 VE andVE and ↑↑VDVD →→  VAVA→ hypoxia and retention of→ hypoxia and retention of
COCO22

13. 2. Ventilation/perfusion2. Ventilation/perfusion
mismatchingmismatching
• Effective gas exchange realized byEffective gas exchange realized by
matched alveolar ventilation & bloodmatched alveolar ventilation & blood
perfusionperfusion
1.1. N: ventilation 4L/N: ventilation 4L/Min; perfusion:Min; perfusion: 5L/5L/Min;Min;
V/Q≈0.8V/Q≈0.8
2.2. V/QV/Q>>0.8: N ventilation, but0.8: N ventilation, but perfusion, termedperfusion, termed
as dead-volume effect, occurrs in shock oras dead-volume effect, occurrs in shock or
pulmonary embolismpulmonary embolism
3.3. V/QV/Q<<0.8: insufficient ventilation, but N0.8: insufficient ventilation, but N
perfusion, termed as “shunt effect”, occurs inperfusion, termed as “shunt effect”, occurs in
atelectasis or pulmonary edemaatelectasis or pulmonary edema

14. 3. Intrapulmonary shunt increase3. Intrapulmonary shunt increase
• N: shuntN: shunt <<5%--physiologic shunt5%--physiologic shunt
∀ ↑↑ shunt:shunt: in severe chronic bronchopulmonary D–in severe chronic bronchopulmonary D–
pathologic shuntpathologic shunt
• ShuntShunt →hypoxia, which is difficult to be improved even→hypoxia, which is difficult to be improved even
by high-concentration of oxygen therapyby high-concentration of oxygen therapy

15. 4. Diffusion dysfunction4. Diffusion dysfunction
• Gas exchange realized via respiratoryGas exchange realized via respiratory
membrane—alveolar-capillary membranemembrane—alveolar-capillary membrane
• Composed of 6 layers: surfactant,Composed of 6 layers: surfactant,
alveolar epithelium, alveolar basicalveolar epithelium, alveolar basic
membrane, interstitia, capillary basicmembrane, interstitia, capillary basic
membrane and capillary endotheliummembrane and capillary endothelium
• Average thickness: 0.7μmAverage thickness: 0.7μm

16. • Diffusion effect is determined byDiffusion effect is determined by
• Equation:Equation: D = dD = d ×× AA ×× （（ P1--P2P1--P2 ）） /T/T
• D: diffusion amountD: diffusion amount
• Membrane area (A)Membrane area (A)
• Thickness (T)Thickness (T)
• Diffusion coefficient: (d)Diffusion coefficient: (d)
• Differential pressure betweenDifferential pressure between
alveoli and capillary (P1—P2)alveoli and capillary (P1—P2)

17. • InIn COPD, alveolar injuryCOPD, alveolar injury → Area reduced→ Area reduced
• In pulmonary edema & interstitial fibrosis →In pulmonary edema & interstitial fibrosis →
thickness increasedthickness increased
• Diffusion coefficiency of CODiffusion coefficiency of CO22 is 20is 20
times of Otimes of O22 , so diffusion dysfunction, so diffusion dysfunction
is for Ois for O22 only in most casesonly in most cases

18. 5. Respiratory muscular fatigue5. Respiratory muscular fatigue
• Important part of “respiratoryImportant part of “respiratory
pump”pump”
• ReasonsReasons
1.1. Insufficient drive of Respiratory centerInsufficient drive of Respiratory center
2.2. Neuromuscular DNeuromuscular D
3.3. Respiratory burden increasedRespiratory burden increased
4.4. Energy support insufficiencyEnergy support insufficiency

19. PathophysiologyPathophysiology
• Key or basic changes: hypoxia,Key or basic changes: hypoxia,
retention of CO2, and acidosisretention of CO2, and acidosis
• Systemic changes includingSystemic changes including
1.1. Central nervous systemCentral nervous system
2.2. Respiratory systemRespiratory system
3.3. Circulatory systemCirculatory system
4.4. Digestive systemDigestive system
5.5. And othersAnd others

20. 1. Influence on CNS1. Influence on CNS
• Determined by the severity, velocity andDetermined by the severity, velocity and
durationduration
• Hypoxia:Hypoxia: cerebral cortex most sensitive, Ocerebral cortex most sensitive, O22
consumption: 3mlconsumption: 3ml ／／ 100g100g ／／ Min. abrupt halt forMin. abrupt halt for
20Sec20Sec→spasm and coma; if hypoxia occurs→spasm and coma; if hypoxia occurs
slowly →slowly → attention and orientation →deliriumattention and orientation →delirium
→coma→coma
• Retention of CO2:Retention of CO2: headache and excitementheadache and excitement
→somnolence →coma (CO2 anesthesia)→somnolence →coma (CO2 anesthesia)
• Both hypoxia & retention of CO2:Both hypoxia & retention of CO2: brainbrain
vascular dilation,vascular dilation, ↑↑permeability,permeability, ↑↑intracranialintracranial
pressurepressure →cerebral edema→cerebral edema

21. 2. Influences on respiratory system2. Influences on respiratory system
• Hypoxia (PaO2Hypoxia (PaO2<<8kPa) stimulate respiration via8kPa) stimulate respiration via
chemical receptor in carotid & aortic body.chemical receptor in carotid & aortic body.
attention:attention: >>50% O2 inhalation may induce R.50% O2 inhalation may induce R.
inhibition, so 16% is recommended.inhibition, so 16% is recommended.
• COCO22– strong respiratory stimulant. 5% CO2– strong respiratory stimulant. 5% CO2
inhalationinhalation ↑↑ ventilation 3-4 times, butventilation 3-4 times, but >>12%12% →→
R. inhibitionR. inhibition
• PaCOPaCO22 ＞＞ 10.7kPa, no stimulation on R. center.10.7kPa, no stimulation on R. center.
At this time, hypoxia is the only trigger forAt this time, hypoxia is the only trigger for
ventilation, that’s why high-dose O2 therapy mayventilation, that’s why high-dose O2 therapy may
reduce ventilationreduce ventilation → aggravate retention of→ aggravate retention of CO2CO2
→pulmonary encephalopathy→pulmonary encephalopathy

22. 3. Influence on circulatory3. Influence on circulatory
systemsystem
• Hypoxia:Hypoxia: slightslight →sympathetic nerve→sympathetic nerve (+)(+)
→tachycardia,→tachycardia, ↑↑myocardial retraction,myocardial retraction, ↑↑output,output,
↑↑Bp. Severe hypoxia →arrhythmia, bradycardia,Bp. Severe hypoxia →arrhythmia, bradycardia,
myocardial retraction (-),myocardial retraction (-), output.output. outputoutput
→pulmonary vascular retraction →pulmonary A→pulmonary vascular retraction →pulmonary A
hypertension →RV hypertrophy →cor pulmonalehypertension →RV hypertrophy →cor pulmonale
• Retention of CO2:Retention of CO2: slightslight →→sympatheticsympathetic
nerve (+); severe retention → bradycardia,nerve (+); severe retention → bradycardia,
output and Bp, skin vessel dilationoutput and Bp, skin vessel dilation
→dermatorrhea (excessive sweat), facial flush→dermatorrhea (excessive sweat), facial flush

23. 4. Influence on hematology4. Influence on hematology
• Secondary erythrocytosisSecondary erythrocytosis
• Increase the burden of heartIncrease the burden of heart
• Hypoxia and toxinHypoxia and toxin →capillary injury→capillary injury
→→DICDIC

24. 5. On digestive and urinary5. On digestive and urinary
systemsystem
• HypoxiaHypoxia →dyspepsia, abdominal→dyspepsia, abdominal
distention, nausea, vomiting, stress ulcer,distention, nausea, vomiting, stress ulcer,
gastrointestinal bleedinggastrointestinal bleeding
• Lobular necrosis,Lobular necrosis, ↑↑enzymes and bilirubinenzymes and bilirubin
• Retraction of renal artery, renal perfusionRetraction of renal artery, renal perfusion
reduced, GFRreduced, GFR ; imbalance of acid-base; imbalance of acid-base
and electrolyteand electrolyte

25. 6. On acid-base & electrolyte6. On acid-base & electrolyte
• Retention of CORetention of CO22 →→ PaCOPaCO22 ↑↑,, respiratoryrespiratory
acidosisacidosis
• pH may be in normal range, because itpH may be in normal range, because it
determined by the ratio of PaCOdetermined by the ratio of PaCO22 /HCO3/HCO3--
..
• pH calculated by Henderson-HanalbachpH calculated by Henderson-Hanalbach
equation:equation:
• pH = 6.1 + (pH = 6.1 + (--
HCOHCO33 )/PaCO)/PaCO22
• pH is normal: termed as compensatorypH is normal: termed as compensatory
respiratory acidosis, or else,respiratory acidosis, or else,
decompensatory respiratory acidosisdecompensatory respiratory acidosis

26. • If acidosis in tissue fluid, KIf acidosis in tissue fluid, K ＋＋
transferred outward,transferred outward,
while Nawhile Na ＋＋
and Hand H ＋＋
inwardinward →cellular acidosis,→cellular acidosis,
extracellular hyperpotassemiaextracellular hyperpotassemia
∀↑↑PaCO2PaCO2 →hypochloremia & hypochloremia→hypochloremia & hypochloremia
alkalosisalkalosis
• Therapy on typeTherapy on type Ⅱ RF, administration of glucose,Ⅱ RF, administration of glucose,
uretics and glucocorticoidsuretics and glucocorticoids →→loss of Kloss of K ＋＋
→→ hypopotassemia andhypopotassemia and hypochloremia alkalosishypochloremia alkalosis
• AlkalosisAlkalosis →→ left shift of oxygenation curveleft shift of oxygenation curve →→
O2 releaseO2 release →aggravate hypoxia, inhibit→aggravate hypoxia, inhibit
respirationrespiration

27. Clinical manifestationClinical manifestation
• typeⅠtypeⅠ
• Typical: dyspnea, esp. exertional.Typical: dyspnea, esp. exertional.
• Tachypnea, cyanosis, waving nose,Tachypnea, cyanosis, waving nose, ↑↑assistantassistant
R. movementR. movement
• In early stage, attention & orientation disordersIn early stage, attention & orientation disorders
→delirium, tachycardia,→delirium, tachycardia, ↑↑ BpBp →→ spasm, coma,spasm, coma,
bradypnea,bradypnea, BpBp
• Manifestation in other systemManifestation in other system

28. • Type Ⅱ RFType Ⅱ RF
• Similar with typeⅠSimilar with typeⅠ
• Besides, headache, somnolence, sleep rhythmBesides, headache, somnolence, sleep rhythm
disorder, warm skin, facial flush, bulladisorder, warm skin, facial flush, bulla
conjunctiva edemaconjunctiva edema
• Pulmonary encephalopathyPulmonary encephalopathy

29. Diagnosis & DifferentiationDiagnosis & Differentiation
DiagnosisDiagnosis
• Combination of history, signs andCombination of history, signs and
results of arterial gas analysisresults of arterial gas analysis
• If accompanied with neuropsychicIf accompanied with neuropsychic
presentations, be distinguished frompresentations, be distinguished from
1.1. StrokeStroke
2.2. Severe imbalance of acid-base and electrolyteSevere imbalance of acid-base and electrolyte
3.3. Infectious intoxicated encephalopathyInfectious intoxicated encephalopathy

30. TreatmentTreatment
• AIMAIM
• Correct hypoxia and retention of COCorrect hypoxia and retention of CO22
• Etiological therapy: different with various DEtiological therapy: different with various D
• Emphasis on treatment of aggravationEmphasis on treatment of aggravation
stage in chronic RFstage in chronic RF

31. Main principlesMain principles
1.1. Airway opening & ventilationAirway opening & ventilation
improvementimprovement
2.2. Oxygen therapyOxygen therapy
3.3. Antibiotics and infection controlAntibiotics and infection control
4.4. Regulation of acid-base & electrolyteRegulation of acid-base & electrolyte
disorderdisorder
5.5. Nutrition & supportive measurementsNutrition & supportive measurements
6.6. othersothers

32. 1.Airway opening & ventilation1.Airway opening & ventilation
improvementimprovement
1.1. Phlegm excretionPhlegm excretion
2.2. BronchodilatorsBronchodilators
3.3. HeparinHeparin
4.4. SteroidsSteroids
5.5. Respiratory stimulantsRespiratory stimulants
6.6. Airway intubation or incisionAirway intubation or incision
7.7. Mechanical ventilationMechanical ventilation

33. • Phlegm excretionPhlegm excretion
1.1.Phlegm dilation: infusionPhlegm dilation: infusion >>20002000 ～～ 2500ml, but2500ml, but
monitoring CVP (central vein pressure);monitoring CVP (central vein pressure);
inhalation of nebulized 2inhalation of nebulized 2~~4% carbonate natrium4% carbonate natrium
––monitoring cardiac function
2.2.active cough (position alternation) is encouragedactive cough (position alternation) is encouraged
3.3.expectorantsexpectorants

34. • BronchodilatorsBronchodilators
1.1.ββ22 selective inhalation agents isselective inhalation agents is
recommendedrecommended
2.2.AnticholinergicsAnticholinergics
3.3.Theophyllines: monitor blood drugTheophyllines: monitor blood drug
concentrationconcentration

35. • HeparinHeparin
1.1. Non-specific anti-inflammatory. Anti-allergicNon-specific anti-inflammatory. Anti-allergic
actionaction
2222  Viscosity of blood and airway excretions.Viscosity of blood and airway excretions.
Dosage: 50Dosage: 50 ～～ 100 m g/day, duration: 1 week.100 m g/day, duration: 1 week.
3.3. Examination for platelet counting, clotting andExamination for platelet counting, clotting and
bleeding time, and prothrombin time beforebleeding time, and prothrombin time before
administrationadministration

36. • SteroidsSteroids
2 Airway spasm, inflammation andAirway spasm, inflammation and
excretionexcretion
• Methylpredisolone inhalation isMethylpredisolone inhalation is
recommended (recommended (5 times of pharmacologic5 times of pharmacologic
effect, lower inhibition on HPA axiseffect, lower inhibition on HPA axis). 2). 2~~4mg/kg4mg/kg

37. • Respiratory stimulantsRespiratory stimulants
• Indication: significant retention of CO2Indication: significant retention of CO2
→respiration inhibited→respiration inhibited
• Drugs: CoramineDrugs: Coramine
• Mechanism: directly stimulates R. center, andMechanism: directly stimulates R. center, and
stimulates chemical receptors in carotid andstimulates chemical receptors in carotid and
aortic body. Administration: 0.375×7aortic body. Administration: 0.375×7~~10+ 500ml10+ 500ml
ivgtt, or together with lobelineivgtt, or together with lobeline
• Contraindication: R. muscular fatigue or airwayContraindication: R. muscular fatigue or airway
obstruction is not relievedobstruction is not relieved

38. • Airway intubation or incisionAirway intubation or incision
1.1. Indication: not relieved by bronchodilators andIndication: not relieved by bronchodilators and
phlegm excretionsphlegm excretions
2.2. Methods: intubation & incisionMethods: intubation & incision
3.3. Intubation: commonly used, via nasal cavity,Intubation: commonly used, via nasal cavity,
22~5cms above carina of trachea~5cms above carina of trachea

39. • Airway intubation or incisionAirway intubation or incision
• Incision: intubation is not effective, or longIncision: intubation is not effective, or long
period of mechanical ventilation is required.period of mechanical ventilation is required.
Advantages: significant reduction of deadAdvantages: significant reduction of dead
volume and consumption of respiratoryvolume and consumption of respiratory
movement, convenient for phlegm clearancemovement, convenient for phlegm clearance
and diet. Disadvantages: more nosocomialand diet. Disadvantages: more nosocomial
infections, difficult for nursinginfections, difficult for nursing

40. • Indication: ineffective by all aboveIndication: ineffective by all above
treatments, or oxygenation disorderstreatments, or oxygenation disorders
• AIM: improve ventilation & gasAIM: improve ventilation & gas
exchange, reduce consumption of R.exchange, reduce consumption of R.
movementmovement
• Methods: non-invasive or invasive.Methods: non-invasive or invasive.
Mechanical ventilationMechanical ventilation

41. • Indications for non-invasiveIndications for non-invasive
mechanical ventilationmechanical ventilation
1.1.Moderate to severe dyspnea, accompanied withModerate to severe dyspnea, accompanied with
assistant muscle involvement and paradoxicalassistant muscle involvement and paradoxical
thoracic-abdominal respirationthoracic-abdominal respiration
2.2.Moderate to severe acidosis (pH 7.30~7.35)Moderate to severe acidosis (pH 7.30~7.35)
and hypercapnea (Pand hypercapnea (PCO2CO2 45~60mmHg)45~60mmHg)
3.3.R>25tpmR>25tpm
• At least met 2 itemsAt least met 2 items

42. • Exclusive standard (any 1 of items)Exclusive standard (any 1 of items)
1.1.Respiratory inhibition or apneaRespiratory inhibition or apnea
2.2.Unstable circulatory system (hypotension,Unstable circulatory system (hypotension,
arrhythmia, or myocardial infarction)arrhythmia, or myocardial infarction)
3.3.Somnolence, abnormal consciousness, notSomnolence, abnormal consciousness, not
cooperatedcooperated
4.4.Abnormal swallowing reflex, severe upper digestiveAbnormal swallowing reflex, severe upper digestive
bleedingbleeding
5.5.Large amount of viscous airway excretionLarge amount of viscous airway excretion
6.6.Recent facial or gastroesophageal surgeryRecent facial or gastroesophageal surgery
7.7.Nasopharyngeal abnormality, cephalofacial injuryNasopharyngeal abnormality, cephalofacial injury
8.8.Severe fatnessSevere fatness
9.9.Severe gastrointestinal distentionSevere gastrointestinal distention

43. • Indications for invasive M. ventilationIndications for invasive M. ventilation
1.1. NIPPVNIPPV failed or existence of contraindicationsfailed or existence of contraindications
2.2. severe dyspnea,severe dyspnea, accompanied with assistant muscle involvement &accompanied with assistant muscle involvement &
paradoxical thoracic-abdominal respirationparadoxical thoracic-abdominal respiration
3.3. RR>>35tpm35tpm
4.4. Life threatened hypoxia,Life threatened hypoxia, POPO22<< 45~60 or PO45~60 or PO22/FIO/FIO22 <<200mmHg200mmHg
5.5. Acidosis (Acidosis (pHpH <<7.257.25) & hypercapnea (P) & hypercapnea (PCO2CO2 45~6045~60))
6.6. Respiratory inhibition or apneaRespiratory inhibition or apnea
7.7. severe circulatory complications such as hypotension,severe circulatory complications such as hypotension,
arrhythmia, or myocardial infarction, heart failurearrhythmia, or myocardial infarction, heart failure
8.8. Somnolence, abnormal consciousnessSomnolence, abnormal consciousness
9.9. Other complications:Other complications: metabolic disturbance, infectious intoxication,metabolic disturbance, infectious intoxication,
pneumonia, pulmonarypneumonia, pulmonary thromboembolism, pleural effusion, etc.thromboembolism, pleural effusion, etc.

44. Mode selectionMode selection
• Determined by 2 factorsDetermined by 2 factors
1.1. Autonomic respiratory capability or R. driveAutonomic respiratory capability or R. drive
2.2. Aim for mechanical ventilationAim for mechanical ventilation

45. • CMVCMV
• Controlled Mode of VentilationControlled Mode of Ventilation
• For acute attack of COPD patientsFor acute attack of COPD patients
• Provide sufficient tidal volume, reduceProvide sufficient tidal volume, reduce
respiratory consumption, relieve R. muscularrespiratory consumption, relieve R. muscular
fatiguefatigue
• If autonomic R reversed and infection controlled,If autonomic R reversed and infection controlled,
→→ SIMV PSV, in order to practice the capacitySIMV PSV, in order to practice the capacity
of autonomic respiration –preparation for stop M.of autonomic respiration –preparation for stop M.
ventilationventilation
• SIMV: simultaneous intermittent mode of ventilationSIMV: simultaneous intermittent mode of ventilation
• PSV: pressure support ventilationPSV: pressure support ventilation

46. • Indexes setupIndexes setup
• FiO2 (oxygenation flow fraction):FiO2 (oxygenation flow fraction):
>50%--alert for intoxication>50%--alert for intoxication
• VVTT (tidal volume)(tidal volume)
1.1. 66~~10ml/kg, generally10ml/kg, generally
2.2. Regulated in real time by the results ofRegulated in real time by the results of
arterial gas and dynamic changes ofarterial gas and dynamic changes of
respirationrespiration
3.3. Aim:Aim: avoiding too much high airway pressureavoiding too much high airway pressure
((high pressure cause injuryhigh pressure cause injury))
4.4. For patients with reduced effectiveFor patients with reduced effective
ventilation volume (ARDS), 6ventilation volume (ARDS), 6 ～～ 8ml/kg8ml/kg
is recommendedis recommended

47. • Breath rateBreath rate
1.1. 1212 ～～ 16tp, for patients with COPD and asthma16tp, for patients with COPD and asthma
2.2. More rapid frequency in D of limited ventilationMore rapid frequency in D of limited ventilation
such as ARDS, assisted with lower VT, whichsuch as ARDS, assisted with lower VT, which
benefit for overcoming elastic resistance andbenefit for overcoming elastic resistance and
cardiovascular side effectscardiovascular side effects
• I/E (ratio of inspiration to expiration)I/E (ratio of inspiration to expiration)
1.1. 1:2, generally.1:2, generally.
2.2. Smaller I/E (Smaller I/E (<<1/2), elongate expiratory time,1/2), elongate expiratory time,
helpful for exhalation, frequently used in COPDhelpful for exhalation, frequently used in COPD
and asthmaand asthma
3.3. I/E >1, even 2:1 ventilation, used in ARDS,I/E >1, even 2:1 ventilation, used in ARDS,
helpful for gas distribution & oxygenationhelpful for gas distribution & oxygenation

48. • Time of Positive end-inspiratoryTime of Positive end-inspiratory
pressurepressure
1.1. Period between end of inspiration and start of expirationPeriod between end of inspiration and start of expiration
2.2. In general,In general, << 2020 ％％ respiratory cyclerespiratory cycle
3.3. Longer: benefit gas distribution, reduce dead-volumeLonger: benefit gas distribution, reduce dead-volume
ventilation, but increased average airway pressure andventilation, but increased average airway pressure and
harmful to hemodynnamicsharmful to hemodynnamics
• PEEP: Positive end-expiratory pressurePEEP: Positive end-expiratory pressure
• For patients with COPD, endogenous PEEP exist,For patients with COPD, endogenous PEEP exist,
because ofbecause of ↑↑airway resistance andairway resistance and thoracic-thoracic-
pulmonary elastic retraction. Proper PEEP (2-5cmH2O)pulmonary elastic retraction. Proper PEEP (2-5cmH2O)
improve alveolar ventilation and oxygenationimprove alveolar ventilation and oxygenation
• While in ARDS, PEEP is key to improve oxygenationWhile in ARDS, PEEP is key to improve oxygenation

49. • Complications in M. ventilationComplications in M. ventilation
• Atmospheric pressure injuryAtmospheric pressure injury
1.1. Such as interstitial, mediastinal, subcutaneousSuch as interstitial, mediastinal, subcutaneous
emphysema, or pneumothoraxemphysema, or pneumothorax
2.2. Prevention: limit & avoid abrupt increase ofPrevention: limit & avoid abrupt increase of
airway pressureairway pressure
• HypotensionHypotension
1.1. Occurred when insufficient effective bloodOccurred when insufficient effective blood
volume, excessive Vvolume, excessive VTT, or too high PEEP, or too high PEEP
2.2. Prevention:Prevention: monitoring cardiovascular function (CVPmonitoring cardiovascular function (CVP
by Swan-Ganz catheter), compensate blood volumeby Swan-Ganz catheter), compensate blood volume

50. • Nosocomial infectionNosocomial infection
1.1. Occurrence rateOccurrence rate : 9: 9 ～～ 6767 ％％ , death rate: 33, death rate: 33
～～ 7676 ％％
2.2. ReasonsReasons: poor resistance, administration of: poor resistance, administration of
wide-spectrum antibiotics, intubation & incision,wide-spectrum antibiotics, intubation & incision,
phlegm aspiration, etcphlegm aspiration, etc
3.3. Pulmonary infectionPulmonary infection is most commonis most common
• PreventionPrevention
1.1. Avoid cross-infectionAvoid cross-infection
2.2. Use antibiotics reasonablyUse antibiotics reasonably
3.3. Stop M. ventilation as soon as possibleStop M. ventilation as soon as possible

51. • Other complicationsOther complications
1.1. Insufficient or excessive ventilationInsufficient or excessive ventilation
2.2. Gastrointestinal bleedingGastrointestinal bleeding
3.3. Dysfunction of liver & kidneyDysfunction of liver & kidney
4.4. Oxygen intoxicationOxygen intoxication
5.5. Dependence on M. ventilation, etc.Dependence on M. ventilation, etc.

52. • Indications for weaningIndications for weaning
1.1. Primary D is controlledPrimary D is controlled
2.2. Reversion of autonomic respiration to someReversion of autonomic respiration to some
degreedegree
3.3. Monitoring of autonomic respiration by aMonitoring of autonomic respiration by a ＴＴ --
type tube or CPAP mode, the indexes are fortype tube or CPAP mode, the indexes are for
reference only. CPAP: continuous positivereference only. CPAP: continuous positive
airway pressureairway pressure
4.4. Currently, mainly relied on integral analysis andCurrently, mainly relied on integral analysis and
experienceexperience

53. • Procedure for weaningProcedure for weaning
1.1. CMV→SIMV+PSV→PSV→ weaning from M.CMV→SIMV+PSV→PSV→ weaning from M.
ventilationventilation
2.2. Patients with COPD need long period of M.Patients with COPD need long period of M.
ventilation and have difficulty in weaningventilation and have difficulty in weaning
(which caused VAP, ventilation-weaning(which caused VAP, ventilation-weaning
associated pneumonia)associated pneumonia)
3.3. Recent evidence suggest: non-invasive M.Recent evidence suggest: non-invasive M.
ventilation used before weaning is very helpfulventilation used before weaning is very helpful
to shorten period of assistant ventilation, toto shorten period of assistant ventilation, to
reduce the occurrence of VAP and otherreduce the occurrence of VAP and other
nosocomial infectionsnosocomial infections

54. 2. Oxygen therapy2. Oxygen therapy
• Important for RF, the mode isImportant for RF, the mode is
determined by different types of RFdetermined by different types of RF
1.1. Non-controlled: FiONon-controlled: FiO22 no need to be strictly controlled,no need to be strictly controlled,
but regulated by clinical status; More in patientsbut regulated by clinical status; More in patients
without ventilation disorderwithout ventilation disorder
2.2. Controlled: FiO2 is controlled strictly. Aim: PaO2Controlled: FiO2 is controlled strictly. Aim: PaO2
<<8.0kPa—correct hypoxia to some degree, but not8.0kPa—correct hypoxia to some degree, but not
inhibit the excitant action on carotid & aortic body,inhibit the excitant action on carotid & aortic body,
more helpful for typeⅡ RF. For patients with COPD,more helpful for typeⅡ RF. For patients with COPD,
FiO2 ranges within 25FiO2 ranges within 25 ～～ 30% (130% (1 ～～ 2L/Min).2L/Min).

55. • MethodsMethods
1.1. Unilateral nasal catheterUnilateral nasal catheter
2.2. Bilateral nasal catheterBilateral nasal catheter
3.3. Air diluted VenturiAir diluted Venturi
• Calculation for oxygen concentration:Calculation for oxygen concentration:
FiO2FiO2 ＝＝ 2121 ＋＋ 4×oxygen flow (L/min)4×oxygen flow (L/min)

56. 3. Infection control3. Infection control
• Infection is the commonest trigger forInfection is the commonest trigger for
RFRF
• In RF,In RF, airway excretionairway excretion↑↑, mucosal edema,, mucosal edema,
bronchial spasm, lower resistancebronchial spasm, lower resistance →→
susceptible tosusceptible to infection, hard to be controlledinfection, hard to be controlled
• Emphasis on reasonable administrationEmphasis on reasonable administration
of antibioticsof antibiotics
1.1. Based on result of repeated culture andBased on result of repeated culture and
sensitivity testsensitivity test
2.2. Experience: GExperience: G ＋＋
coccus or Gcoccus or G——
bacillusbacillus

57. 4. Correction of disturbance of acid-4. Correction of disturbance of acid-
base & electrolytebase & electrolyte
• R. acidosisR. acidosis
1.1. Key measurement: Improve alveolarKey measurement: Improve alveolar
ventilation,ventilation, PaCO2PaCO2
2.2. Generally, alkaline drugs not required, whichGenerally, alkaline drugs not required, which
only used when PHonly used when PH<<7.2, or airway obstruction7.2, or airway obstruction
not improved in short time, or accompaniednot improved in short time, or accompanied
with metabolic acidosis. 5% Na HCO3with metabolic acidosis. 5% Na HCO3--
100ml100ml
ivdrop.ivdrop.

58. • Metabolic acidosisMetabolic acidosis: lactic acid: lactic acid ↑↑,,
improve ventilation, correct hypoxiaimprove ventilation, correct hypoxia
• Metabolic alkalosisMetabolic alkalosis
1.1. Caused by hypopotassemia orCaused by hypopotassemia or
hypochloremiahypochloremia
2.2. →→left shift of oxygenation curve,left shift of oxygenation curve,
aggravate hypoxiaaggravate hypoxia
3.3. More dangerous, more difficult forMore dangerous, more difficult for
weaningweaning
4.4. Prevention: chloridion & potassiumPrevention: chloridion & potassium
compensationcompensation

59. • Disturbance of electrolyteDisturbance of electrolyte
• Hypopotassemia, hypochloremia, andHypopotassemia, hypochloremia, and
hyponatremia is commonhyponatremia is common
• Severe hyponatremia is corrected by infusion ofSevere hyponatremia is corrected by infusion of
10% chloride natrium (diluted in 3%). Attention:10% chloride natrium (diluted in 3%). Attention:
rapid infusion may aggravate heart failurerapid infusion may aggravate heart failure

60. 5. Nutrition & supportive therapy5. Nutrition & supportive therapy
• Malnutrition is common, becauseMalnutrition is common, because
1.1. High consumption exist in both ARDS & COPD-High consumption exist in both ARDS & COPD-
acute attackacute attack
2.2. Insufficient ingestion, malabsorptionInsufficient ingestion, malabsorption
3.3. Oxygen consumption in mechanical ventilationOxygen consumption in mechanical ventilation
• MalnutritionMalnutrition → lower immunity, and reduce both of→ lower immunity, and reduce both of
central and peripheral drivecentral and peripheral drive
• Improve nutritional status is vitalImprove nutritional status is vital
• Basic everyday energy support (BEE) calculated byBasic everyday energy support (BEE) calculated by
Harris-Benedict equationHarris-Benedict equation ：：
• BEE (M)=66.47+13.75W+5H-6.8A(kcal)BEE (M)=66.47+13.75W+5H-6.8A(kcal)
• BEE (F)=655+9.68W+1.7H-4.68A(kcal)BEE (F)=655+9.68W+1.7H-4.68A(kcal)
• W: weight (kg), H: height (cm), A: age (year)W: weight (kg), H: height (cm), A: age (year) 。。
• For patients with COPD, the value is rectified by multiplyFor patients with COPD, the value is rectified by multiply
a coefficiency (1.16 for M, 1.19 for F)a coefficiency (1.16 for M, 1.19 for F)

61. • Ratio of nutrientsRatio of nutrients
• CarbohydrateCarbohydrate <<40%: excessive40%: excessive →→↑↑CO2 andCO2 and
respiratory burdenrespiratory burden
• Protein:Protein: 1.51.5~~2g/kg/d, even higher for ARDS.2g/kg/d, even higher for ARDS.
More accurate compensation is regulated byMore accurate compensation is regulated by
nitrogen balance.nitrogen balance. Energy: nitrogenEnergy: nitrogen
=100~150kcal:1g=100~150kcal:1g
• Administration ofAdministration of calcium, phosphate,calcium, phosphate,
magnesiummagnesium

62. • PasswayPassway
• Enteric catheter-- safer:Enteric catheter-- safer: better forbetter for
maintenance of functional integrity of GI tract,maintenance of functional integrity of GI tract,
benefit for the growth of normal bacteria, whichbenefit for the growth of normal bacteria, which
inhibit the shift of bacteria & the production ofinhibit the shift of bacteria & the production of
toxin.toxin.
• Parenteric:Parenteric: including ivdrop, only used whenincluding ivdrop, only used when
EN is dangerous, e.g. comatous patientsEN is dangerous, e.g. comatous patients
(aspiration). EN should be used as soon as(aspiration). EN should be used as soon as
possiblepossible

63. 6. Treatment on other complications6. Treatment on other complications
• Improve cardiac functionImprove cardiac function
• Prevent against shock, DIC and arrhythmia, DICPrevent against shock, DIC and arrhythmia, DIC
• Pay much attention to DM and hypertensionPay much attention to DM and hypertension
• Severe airway structure, but without M.Severe airway structure, but without M.
ventilation, be alert for use of sedatives &ventilation, be alert for use of sedatives &
diureticsdiuretics

64. Appendices –antibioticsAppendices –antibiotics
• CephalosporinCephalosporin
• 44thth
generationgeneration
1.1. Wider spectrum, more effective on GWider spectrum, more effective on G ＋＋
coccus, especially for penicillin-coccus, especially for penicillin-
resistant S. pneumoniaeresistant S. pneumoniae
2.2. Stronger activity on GStronger activity on G--
bacillibacilli
3.3. More stable to β- lactamaseMore stable to β- lactamase

65. CephalosporinCephalosporin GG ＋＋ coccuscoccus G- bacilliG- bacilli
11stst
generationgeneration CephazolinCephazolin
(( 头孢唑啉头孢唑啉 ))
SensitiveSensitive
22ndnd
generationgeneration CefuroximeCefuroxime
(( 头孢呋辛头孢呋辛 ))
SensitiveSensitive SensitiveSensitive
33rdrd
generationgeneration CeftriaxoneCeftriaxone
(( 头孢曲松头孢曲松 ))
WeakWeak StrongStrong
44thth
generationgeneration CefepimeCefepime
（头孢吡肟（头孢吡肟 ))
StrongStrong StrongStrong

66. • CarbopenemCarbopenem
• Representatives: tienam composed of ImipenemRepresentatives: tienam composed of Imipenem
and cilastatin sodiumand cilastatin sodium
• Most effective in the worldMost effective in the world
• Quite stable to β- lactamase because of transQuite stable to β- lactamase because of trans
structure formed by hydroxyl lateral chain and β-structure formed by hydroxyl lateral chain and β-
lactate looplactate loop
• Cilastatin inhibit enzymes (degrade imipenem) inCilastatin inhibit enzymes (degrade imipenem) in
kidneykidney

67. • TienamTienam
1.1. Wide spectrum—aerobic or anaerobic GWide spectrum—aerobic or anaerobic G ＋＋
coccus and G- bacilli, including those withcoccus and G- bacilli, including those with
super β-lactamase (ESBL), and resistantsuper β-lactamase (ESBL), and resistant
against 3against 3rdrd
-generation cephalosporin-generation cephalosporin
2.2. Imipenem combine with PBP-2 and PBP-2IbImipenem combine with PBP-2 and PBP-2Ib
→induce rapid resolution,→induce rapid resolution,  production ofproduction of
endotoxinendotoxin

68. • QuinolonesQuinolones
• Representative: levoflaxacin (Representative: levoflaxacin ( 左旋氧氟沙星来立左旋氧氟沙星来立
信信 ))
• AdvantagesAdvantages
1.1. No need for cutaneous sensitivity testNo need for cutaneous sensitivity test
2.2. Oral administrationOral administration
3.3. Wide-spectrumWide-spectrum
4.4. Less side-effect on liver & kidneyLess side-effect on liver & kidney
5.5. Effective on intracellular pathogens such as legionellaEffective on intracellular pathogens such as legionella
and mycobacterium, mycoplasma, Chlamydia, etc.and mycobacterium, mycoplasma, Chlamydia, etc.
• DisadvantagesDisadvantages
1.1. Weaker effective on GWeaker effective on G++
coccuscoccus
2.2. Toxic to long bones and article, not recommended toToxic to long bones and article, not recommended to
be used in youth (be used in youth (<< ageage of 16)of 16)

69. • MacrolidesMacrolides
• Representative: erythromycin, roxithromycin,Representative: erythromycin, roxithromycin,
clarithromycin, azithromycinclarithromycin, azithromycin
• very effective on Gvery effective on G ＋＋ coccuscoccus
• Effective on atypical infectionsEffective on atypical infections

70. • AminoglycosidesAminoglycosides
• Representations: kanamycin, amikacin,Representations: kanamycin, amikacin,
netimicin, etimicin (netimicin, etimicin ( 爱大爱大 ))
• G- bacilliG- bacilli
• Toxin injury to Ear, auditory Nerve, kidneyToxin injury to Ear, auditory Nerve, kidney
• Etimicin more effective than gentamicinEtimicin more effective than gentamicin
• Netimicin, etimicin less side-effectNetimicin, etimicin less side-effect

71. • Anti fungus drugsAnti fungus drugs
• Representatives: Amphotericin B, ketoconazole,Representatives: Amphotericin B, ketoconazole,
fluconazolefluconazole
• Candida, cryptococcus, aspergillusCandida, cryptococcus, aspergillus
• Anti anaerobic bacteriaAnti anaerobic bacteria
• Penicillin, metronidazole, tinidazole,Penicillin, metronidazole, tinidazole,
chloromycetin, clindamycin. Erythromycin ischloromycetin, clindamycin. Erythromycin is
only against anaerobic coccus, metronidazoleonly against anaerobic coccus, metronidazole
against all anaerobic bacteriaagainst all anaerobic bacteria