呼衰竭Respiratory Failure英文课件

Respiratory FailureDr. Sat SharmaUniv of ManitobaRESPIRATORY FAILUREn“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 FAILUREnDefinition 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.nClinically Respiratory failure is defined as PaO2 50 mmHg.Respiratory system includes:CNS (medulla) Peripheral nervous system (phrenic nerve) Respiratory muscles Chest wall Lung Upper airway Bronchial tree Alveoli Pulmonary vasculature Potential causes of Respiratory FailureHYPOXEMIC RESPIRATORY FAILURE(TYPE 1)nPaO2 50 mmHgnHypoxemia is always presentnpH depends on level of HCO3nHCO3 depends on duration of hypercapnianRenal response occurs over days to weeksAcute Hypercapnic Respiratory Failure (Type II)nAcutenArterial pH is lownCauses- sedative drug over dose- acute muscle weakness such as myasthenia gravis- severe lung disease: alveolar ventilation can not be maintained (i.e. Asthma or pneumonia) Acute on chronic:nThis occurs in patients with chronic CO2 retention who worsen and have rising CO2 and low pH.nMechanism: respiratory muscle fatigueCauses of Hypercapnic Respiratory failurenRespiratory centre (medulla) dysfunctionnDrug over dose, CVA, tumor, hypothyroidism,central hypoventilationnNeuromuscular disease Guillain-Barre, Myasthenia Gravis, polio, spinal injuriesnChest wall/Pleural diseases kyphoscoliosis, pneumothorax, massive pleural effusionnUpper airways obstruction tumor, foreign body, laryngeal edemanPeripheral airway disorder asthma, COPDClinical and Laboratory Manifestation(non-specific and unreliable)nCyanosis - bluish color of mucous membranes/skin indicate hypoxemian- unoxygenated hemoglobin 50 mg/L - not a sensitive indicator nDyspnea - secondary to hypercapnia and hypoxemianParadoxical breathingnConfusion, somnolence and comanConvulsionsASSESSMENT OF PATIENTnCareful historynPhysical ExaminationnABG analysis -classify RF and help with cause Clinical & Laboratory ManifestationsnCirculatory changes - tachycardia, hypertension, hypotensionnPolycythemia - chronic hypoxemia - erythropoietin synthesisnPulmonary hypertensionnCor-pulmonale or right ventricular failureManagement of Respiratory Failure PrinciplesnHypoxemia may cause death in RFnPrimary objective is to reverse and prevent hypoxemianSecondary objective is to control PaCO2 and respiratory acidosis nTreatment of underlying diseasenPatients CNS and CVS must be monitored and treated Oxygen TherapynSupplemental O2 therapy essential ntitration based on SaO2, PaO2 levels and PaCO2nGoal is to prevent tissue hypoxianTissue hypoxia occurs (normal Hb & C.O.) - venous PaO2 20 mmHg or SaO2 40% - arterial PaO2 38 mmHg or SaO2 60 mmHg(SaO2 90%) or venous SaO2 60%nO2 dose either flow rate (L/min) or FiO2 (%) Risks of Oxygen Therapy: - very high levels(1000 mmHg) CNS toxicity and seizures - lower levels (FiO 60%) and longer exposure: -capillary damage, leak and pulmonary fibrosis - PaO 150 can cause retrolental fibroplasia - FiO 35 to 40% can be safely tolerated indefinitely - PaCO may increase severely to cause respiratory acidosis, somnolence and coma - PaCO increase secondary to combination of a) abolition of hypoxic drive to breathe b) increase in dead space MECHANICAL VENTILATIONnNon invasive with a masknInvasive with an endobronchial tube nMV can be volume or pressure cycled For hypercapnia: - MV increases alveolar ventilation and lowers PaCO2, corrects pH - rests fatigues respiratory muscles nFor hypoxemia: - O2 therapy alone does not correct hypoxemia caused by shunt- Most common cause of shunt is fluid filled or collapsed alveoli (Pulmonary edema)POSITIVE END EXPIRATORY PRESSURE (PEEP)nPEEP increases the end expiratory lung volume (FRC)nPEEP recruits collapsed alveoli and prevents recollapsenFRC increases, therefore lung becomes more compliantnReversal of atelectasis diminishes intrapulmonary shuntnExcessive PEEP has adverse effects - decreased cardiac output - barotrauma (pneumothorax, pneumomediastinum) - increased physiologic dead space - increased work of breathingPULMONARY EDEMAnPulmonary edema is an increase in extravascular lung waternInterstitial edema does not impair functionnAlveolar edema cause several gas exchange abnormalitiesnMovement 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 coefficientnLung edema is cleared by lymphaticsAdult Respiratory distress Syndrome (ARDS)nVariety of unrelated massive insults injure gas exchanging surface of LungsnFirst described as clinical syndrome in 1967 by Ashbaugh & Petty nClinical terms synonymous with ARDS Acute respiratory failure Capillary leak syndrome Da Nang Lung Shock Lung Traumatic wet Lung Adult hyaline membrane diseaseRisk 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 coagulopathy 12.5% Two or more of the above 24.6% PATHOPHYSIOLOGY AND PATHOGENESISnDiffuse damage to gas-exchanging surface either alveolar or capillary side of membrane nIncreased vascular permeability causes pulmonary edemanPathology: fluid and RBC in interstitial space, hyaline membranesnLoss of surfactant: alveolar collapse CRITERIA FOR DIAGNOSIS OF ARDSnClinical history of catastrophic event Pulmonary or Non pulmonary (shock, multi system trauma) nExclude chronic pulmonary diseases left ventricular failure Must have respiratory distress tachypnea 20 breath/minute Labored breathing central cyanosis CXR- diffuse infiltrates PaO2 O.6 Compliance 50 ml/cm H2O increased shunt and dead space ARDSMANAGEMENT OF ARDSnMechanical ventilation corrects hypoxemia/respiratory acidosisnFluid management correction of anemia and hypovolemianPharmacological intervention Dopamine to augment C.O. Diuretics Antibiotics Corticosteroids - no demonstrated benefit early disease, helpful 1 week laternMortality continues to be 50 to 60%