呼吸衰竭英文

1、Respiratory Failure,Dr. Sat SharmaUniv of Manitoba,RESPIRATORY FAILURE,“inability of the lung to meet the metabolic demands of the body. This can be from failure of tissue oxygenation and/or failure of CO2 homeostasis

2、.”,RESPIRATORY FAILURE,Definition Respiration is gas exchange between the organism and its environment. Function of respiratory system is to transfer O2 fr

3、om atmosphere to blood and remove CO2 from blood.Clinically Respiratory failure is defined as PaO2 50 mmHg.,Respiratory system includes:,CNS (medulla)

4、 Peripheral nervous system (phrenic nerve) Respiratory muscles Chest wall

5、 Lung Upper airway Bronchial tree Alveol

6、i Pulmonary vasculature,,Potential causes of Respiratory Failure,HYPOXEMIC RESPIRATORY FAILURE(TYPE 1),PaO2 <60mmHg with normal or low PaCO2 ? normal or hi

7、gh pHMost common form of respiratory failureLung disease is severe to interfere with pulmonary O2 exchange, but over all ventilation is maintainedPhysiologic causes: V/Q mismatch and shunt,HYPOXEMIC RESPIRATO

8、RY FAILURE CAUSES OF ARTERIAL HYPOXEMIA,1.?FiO22.Hypoventilation (? PaCO2) Hypercapnic 3. V/Q mismatch Respiratory failure (eg.COPD)4. Dif

9、fusion limitation ?5. Intrapulmonary shunt - pneumonia - Atelectasis

10、 - CHF (high pressure pulmonary edema) - ARDS (low pressure pulmonary edema),,Causes of Hypoxemic Respiratory

11、 failure,Caused by a disorder of heart, lung or blood. Etiology easier to assess by CXR abnormality:- Normal Chest x-ray Cardiac shunt (right to left) Asthma, C

12、OPD Pulmonary embolism,Hyperinflated Lungs : COPD,Causes of Hypoxemic Respiratory failure (cont’d.),Focal infiltrates on CXR Atelectasis Pneumonia,An example of intrapulmonary shunt,Causes of Hypoxemic Respirat

13、ory Failure (cont’d.),Diffuse infiltrates on CXRCardiogenic Pulmonary EdemaNon cardiogenic pulmonary edema (ARDS)Interstitial pneumonitis or fibrosisInfections,Diffuse pulmonary infiltrates,Hypercapnic Respiratory Fa

14、ilure (Type II),PaCO2 >50 mmHgHypoxemia is always presentpH depends on level of HCO3HCO3 depends on duration of hypercapniaRenal response occurs over days to weeks,Acute Hypercapnic Respiratory Failure (Type II),

15、AcuteArterial pH is lowCauses- sedative drug over dose- acute muscle weakness such as myasthenia gravis- severe lung disease: alveolar ventilation can not be ma

16、intained (i.e. Asthma or pneumonia) Acute on chronic:This occurs in patients with chronic CO2 retention who worsen and have rising CO2 and low pH.Mechanism: respirat

17、ory muscle fatigue,Causes of Hypercapnic Respiratory failure,Respiratory centre (medulla) dysfunctionDrug over dose, CVA, tumor, hypothyroidism,central hypoventilationNeuromuscular disease

18、 Guillain-Barre, Myasthenia Gravis, polio, spinal injuriesChest wall/Pleural diseases kyphoscoliosis, pneumothorax, massive pleural effusionUpper airways obstruction

19、 tumor, foreign body, laryngeal edemaPeripheral airway disorder asthma, COPD,Clinical and Laboratory Manifestation(non-specific and unreliable),Cyanosis

20、 - bluish color of mucous membranes/skin indicate hypoxemia- unoxygenated hemoglobin 50 mg/L - not a sensitive indicator Dyspnea

21、 - secondary to hypercapnia and hypoxemiaParadoxical breathingConfusion, somnolence and comaConvulsions,ASSESSMENT OF PATIENT,Careful historyPhysic

22、al ExaminationABG analysis -classify RF and help with cause 1) PaCO2 = VCO2 x 0.863

23、 VA2) P(A-a)02 = (PiO2 - PaCO2) – PaO2 RLung function

24、 OVP vs RVP vs NVPChest RadiographEKG,Clinical & Laboratory ManifestationsCirculatory changes - tachycardia, hypertension, hypotensionPolycythemia

25、 - chronic hypoxemia - erythropoietin synthesisPulmonary hypertensionCor-pulmonale or right ventricular failure,Management of Respiratory Failure Principles,Hypoxemia may cause

26、death in RFPrimary objective is to reverse and prevent hypoxemiaSecondary objective is to control PaCO2 and respiratory acidosis Treatment of underlying diseasePatient’s CNS and CVS must be monitored and treated,Oxyg

27、en Therapy,Supplemental O2 therapy essential titration based on SaO2, PaO2 levels and PaCO2Goal is to prevent tissue hypoxiaTissue hypoxia occurs (normal Hb & C.O.) - venous PaO2 60 mmHg(SaO2 >

28、90%) or venous SaO2 > 60%O2 dose either flow rate (L/min) or FiO2 (%),Risks of Oxygen Therapy,O2 toxicity: - very high levels(>1000

29、mmHg) CNS toxicity and seizures - lower levels (FiO2 > 60%) and longer exposure: -capillary damage, leak and pulmonary fibrosis

30、 - PaO2 >150 can cause retrolental fibroplasia - FiO2 35 to 40% can be safely tolerated indefinitelyCO2 narcosis:

31、 - PaCO2 may increase severely to cause respiratory acidosis, somnolence and coma - PaCO2 increase secondary to combination of a) aboli

32、tion of hypoxic drive to breathe b) increase in dead space,MECHANICAL VENTILATION,Non invasive with a maskInvasive with an endobronchial tube MV can be volume or pressure cycled

33、 For hypercapnia: - MV increases alveolar ventilation and lowers PaCO2, corrects pH - rests fatigue

34、s respiratory muscles For hypoxemia: - O2 therapy alone does not correct hypoxemia caused by shunt- Most commo

35、n cause of shunt is fluid filled or collapsed alveoli (Pulmonary edema),POSITIVE END EXPIRATORY PRESSURE (PEEP),PEEP increases the end expiratory lung volume (FRC)PEEP recruits collapsed alveoli and prevents recollapse

36、FRC increases, therefore lung becomes more compliantReversal of atelectasis diminishes intrapulmonary shuntExcessive PEEP has adverse effects - decreased cardiac output

37、 - barotrauma (pneumothorax, pneumomediastinum) - increased physiologic dead space - increased work of breathing,PULMONARY

38、EDEMA,Pulmonary edema is an increase in extravascular lung waterInterstitial edema does not impair functionAlveolar edema cause several gas exchange abnormalitiesMovement of fluid is governed by Starling’s equation

39、 QF = KF [(PIV - PIS ) + ? ( ?IS - ?IV )? QF = rate of fluid movement

40、 KF = membrane permeability PIV & PIS are intra vascular and interstitial hydrostatic pressures ?IS and ?IV are interstitial and intravascular oncotic

41、pressures ? reflection coefficientLung edema is cleared by lymphatics,Adult Respiratory distress Syndrome (ARDS),Variety of unrelated massive insults injure gas exchanging surface of LungsFirst described as cli

42、nical syndrome in 1967 by Ashbaugh & Petty Clinical terms synonymous with ARDS Acute respiratory failure Capillary leak syndrome

43、 Da Nang Lung Shock Lung Traumatic wet

44、 Lung Adult hyaline membrane disease,Risk Factors in ARDS,Sepsis 3.8% Cardiopu

45、lmonary bypass 1.7% Transfusion 5.0% Severe pneumonia 12.0% Burn 2

46、.3% Aspiration 35.6% Fracture 5.3% Intravascular coagulopathy 12.5% Two or more of the

47、above 24.6%,PATHOPHYSIOLOGY AND PATHOGENESIS,Diffuse damage to gas-exchanging surface either alveolar or capillary side of membrane Increased vascular permeability causes pulmonary edemaPathology

48、: fluid and RBC in interstitial space, hyaline membranesLoss of surfactant: alveolar collapse,CRITERIA FOR DIAGNOSIS OF ARDS,Clinical history of catastrophic event Pulmonary or Non pulmonary (shock

49、, multi system trauma) Exclude chronic pulmonary diseases

50、 left ventricular failure Must have respiratory distress tachypnea >20 breath/min

51、ute Labored breathing central cyanosis

52、 CXR- diffuse infiltrates PaO2 O.6 Compliance <50 ml/cm H2O increased shunt and

53、dead space,ARDS,MANAGEMENT OF ARDS,Mechanical ventilation corrects hypoxemia/respiratory acidosisFluid management co

54、rrection of anemia and hypovolemiaPharmacological intervention Dopamine to augment C.O. Diuretics

55、 Antibiotics Corticosteroids - no demonstrated benefit early disease, helpful 1 week laterMort