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1、Respiratory FailureDr. Sat SharmaUniv of ManitobaRespiratory FailureDr. Sat ShaRESPIRATORY 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.” RESPIRATORY FAILURE“inability RESPIRATORY FAILUREDefi

2、nition Respiration is gas exchange between the organism and its environment. Function of respiratory system is to transfer O2 from atmosphere to blood and remove CO2 from blood.Clinically Respiratory failure is defined as PaO2 50 mmHg.RESPIRATORY FAILUREDefinition Respiratory system includes:CNS (me

3、dulla) Peripheral nervous system (phrenic nerve) Respiratory muscles Chest wall Lung Upper airway Bronchial tree Alveoli Pulmonary vasculature Respiratory system includes:CPotential causes of Respiratory FailurePotential causes of RespiratorHYPOXEMIC RESPIRATORY FAILURE(TYPE 1)PaO2 50 mmHgHypoxemia

4、is always presentpH depends on level of HCO3HCO3 depends on duration of hypercapniaRenal response occurs over days to weeksHypercapnic Respiratory FailurAcute Hypercapnic Respiratory Failure (Type II)AcuteArterial pH is lowCauses- sedative drug over dose- acute muscle weakness such as myasthenia gra

5、vis- severe lung disease: alveolar ventilation can not be maintained (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: respiratory muscle fatigueAcute Hypercapnic Respiratory Causes of Hypercapnic Respi

6、ratory failureRespiratory centre (medulla) dysfunctionDrug over dose, CVA, tumor, hypothyroidism,central hypoventilationNeuromuscular disease Guillain-Barre, Myasthenia Gravis, polio, spinal injuriesChest wall/Pleural diseases kyphoscoliosis, pneumothorax, massive pleural effusionUpper airways obstr

7、uction tumor, foreign body, laryngeal edemaPeripheral airway disorder asthma, COPDCauses of Hypercapnic RespiratClinical and Laboratory Manifestation(non-specific and unreliable)Cyanosis - bluish color of mucous membranes/skin indicate hypoxemia- unoxygenated hemoglobin 50 mg/L - not a sensitive ind

8、icator Dyspnea - secondary to hypercapnia and hypoxemiaParadoxical breathingConfusion, somnolence and comaConvulsionsClinical and Laboratory ManifeASSESSMENT OF PATIENTCareful historyPhysical ExaminationABG analysis -classify RF and help with cause 1) PaCO2 = VCO2 x 0.863 VA2) P(A-a)02 = (PiO2 - PaC

9、O2) PaO2 RLung function OVP vs RVP vs NVPChest RadiographEKG ASSESSMENT OF PATIENTCareful hClinical & Laboratory ManifestationsCirculatory changes - tachycardia, hypertension, hypotensionPolycythemia - chronic hypoxemia - erythropoietin synthesisPulmonary hypertensionCor-pulmonale or right ventricul

10、ar failureClinical & Laboratory ManifestManagement of Respiratory Failure PrinciplesHypoxemia may cause death in RFPrimary objective is to reverse and prevent hypoxemiaSecondary objective is to control PaCO2 and respiratory acidosis Treatment of underlying diseasePatients CNS and CVS must be monitor

11、ed and treated Management of Respiratory FailOxygen TherapySupplemental O2 therapy essential titration based on SaO2, PaO2 levels and PaCO2Goal is to prevent tissue hypoxiaTissue hypoxia occurs (normal Hb & C.O.) - venous PaO2 20 mmHg or SaO2 40% - arterial PaO2 38 mmHg or SaO2 60 mmHg(SaO2 90%) or

12、venous SaO2 60%O2 dose either flow rate (L/min) or FiO2 (%) Oxygen TherapySupplemental O2 Risks of Oxygen TherapyO2 toxicity: - very high levels(1000 mmHg) CNS toxicity and seizures - lower levels (FiO2 60%) and longer exposure: -capillary damage, leak and pulmonary fibrosis - PaO2 150 can cause ret

13、rolental fibroplasia - FiO2 35 to 40% can be safely tolerated indefinitelyCO2 narcosis: - PaCO2 may increase severely to cause respiratory acidosis, somnolence and coma - PaCO2 increase secondary to combination of a) abolition of hypoxic drive to breathe b) increase in dead space Risks of Oxygen The

14、rapyO2 toxi呼吸衰竭Respiratory-Failure-英文課件呼吸衰竭Respiratory-Failure-英文課件MECHANICAL VENTILATIONNon invasive with a maskInvasive with an endobronchial tube MV can be volume or pressure cycled For hypercapnia: - MV increases alveolar ventilation and lowers PaCO2, corrects pH - rests fatigues respiratory mus

15、cles For hypoxemia: - O2 therapy alone does not correct hypoxemia caused by shunt- Most common cause of shunt is fluid filled or collapsed alveoli (Pulmonary edema)MECHANICAL VENTILATIONNon inva呼吸衰竭Respiratory-Failure-英文課件呼吸衰竭Respiratory-Failure-英文課件POSITIVE END EXPIRATORY PRESSURE (PEEP)PEEP increa

16、ses the end expiratory lung volume (FRC)PEEP recruits collapsed alveoli and prevents recollapseFRC increases, therefore lung becomes more compliantReversal of atelectasis diminishes intrapulmonary shuntExcessive PEEP has adverse effects - decreased cardiac output - barotrauma (pneumothorax, pneumome

17、diastinum) - increased physiologic dead space - increased work of breathingPOSITIVE END EXPIRATORY PRESSU呼吸衰竭Respiratory-Failure-英文課件PULMONARY EDEMAPulmonary edema is an increase in extravascular lung waterInterstitial edema does not impair functionAlveolar edema cause several gas exchange abnormali

18、tiesMovement of fluid is governed by Starlings equation QF = KF (PIV - PIS ) + ( IS - IV ) QF = rate of fluid movement KF = membrane permeability PIV & PIS are intra vascular and interstitial hydrostatic pressures IS and IV are interstitial and intravascular oncotic pressures reflection coefficientL

19、ung edema is cleared by lymphaticsPULMONARY EDEMAPulmonary edemaAdult Respiratory distress Syndrome (ARDS)Variety of unrelated massive insults injure gas exchanging surface of LungsFirst described as clinical syndrome in 1967 by Ashbaugh & Petty Clinical terms synonymous with ARDS Acute respiratory

20、failure Capillary leak syndrome Da Nang Lung Shock Lung Traumatic wet Lung Adult hyaline membrane diseaseAdult Respiratory distress SynRisk Factors in ARDSSepsis 3.8% Cardiopulmonary bypass 1.7% Transfusion 5.0% Severe pneumonia 12.0% Burn 2.3% Aspiration 35.6% Fracture 5.3% Intravascular coagulopat

21、hy 12.5% Two or more of the above 24.6% Risk Factors in ARDSSepsis PATHOPHYSIOLOGY AND PATHOGENESISDiffuse damage to gas-exchanging surface either alveolar or capillary side of membrane Increased vascular permeability causes pulmonary edemaPathology: fluid and RBC in interstitial space, hyaline membranesLoss of surfactant: alveolar collapse PATHOPHYSIOLOGY AND PATHOGENESCRITERIA FOR DIAGNOSIS OF ARDSClinical history of catastrophic event Pulmonary or Non pulmonar

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