Pathophysiology Of Respiratory Failure And Use Of .

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Pathophysiology of RespiratoryFailure andUse of Mechanical VentilationPuneet Katyal, MBBS, MSHIOgnjen Gajic, MDMayo Clinic, Rochester, MN, USA

DefinitionRespiratory failure is a syndrome of inadequategas exchange due to dysfunction of one or moreessential components of the respiratory system:nChest wall (includingpleura anddiaphragm)n Airwaysn Alveolar–capillaryunitsnPulmonary circulationn Nervesn CNS or Brain Stemn

Respiratory SystemBrainSpinal cordNervesIntercostalmusclesg:LunAlUnralve oitChest wallAirwayPleuraDiaphragm

EpidemiologyIncidence: about 360,000 cases per year in theUnited Statesn 36% die during hospitalizationn Morbidity and mortality rates increase with ageand presence of comorbiditiesn

ClassificationnType I or Hypoxemic (PaO2 60 at sea level): Failure ofoxygen exchangenIncreased shunt fraction (QS/QT)nnnDue to alveolar floodingHypoxemia refractory to supplemental oxygenType II or Hypercapnic (PaCO2 45): Failure toexchange or remove carbon dioxidennDecreased alveolar minute ventilation (VA)Often accompanied by hypoxemia that corrects withsupplemental oxygen

ClassificationnType III Respiratory Failure: Perioperative respiratoryfailurenIncreased atelectasis due to low functional residual capacity(FRC) in the setting of abnormal abdominal wall mechanicsnnnOften results in type I or type II respiratory failureCan be ameliorated by anesthetic or operative technique, posture,incentive spirometry, post-operative analgesia, attempts to lowerintra-abdominal pressureType IV Respiratory Failure: ShocknType IV describes patients who are intubated and ventilatedin the process of resuscitation for shocknGoal of ventilation is to stabilize gas exchange and to unload therespiratory muscles, lowering their oxygen consumption

ClassificationnRespiratory failure may beAcuten Chronicn Acute on chronicnn E.g.:acute exacerbation of advanced COPD

Pathophysiology: MechanismsnHypoxemic failureVentilation/Perfusion (V/Q) mismatchn Shuntn Exacerbated by low mixed venous O2 (SvO2)nnHypercapnic failureDecreased minute ventilation (MV) relative todemandn Increased dead space ventilationn

Pathophysiology:Etiologic CategoriesnNervous systemfailure (Type II)nCentralhypoventilationn NeuropathiesnnMuscle (pump)failure (Type II)Muscular dystrophiesn MyopathiesnNeuromusculartransmission failure(Type II)nnMyasthenia gravisAirway failure(Type II)Obstructionn Dysfunctionn

Pathophysiology:Etiologic CategoriesnChest wall and pleuralspace failure (Type II)nnnnnKyphoscoliosisMorbid nAlveolar unit failure(Type I)nnnCollapseFlooding: edema, blood,pus, aspirationFibrosisvasculature failure (Type I)nPulmonaryembolismnPulmonary hypertension

CausesnType I respiratory failurennPneumoniaCardiogenic pulmonary edemannNon-cardiogenic pulmonary edemannnnnnPulmonary edema due to increased hydrostatic pressurePulmonary edema due to increased permeabilityAcute lung injury (ALI)Acute respiratory distress syndrome (ARDS)Pulmonary embolism (see also type IV respiratory failure)Atelectasis (see also type III respiratory failure)Pulmonary fibrosis

CausesnType II respiratory failurennnCentral hypoventilationAsthmaChronic obstructive pulmonary disease (COPD)nHypoxemia and hypercapnia often occur together*Neuromuscularnnnnnand chest wall henia gravisObesity Hypoventilation Syndrome

CausesnType III respiratory failurennnnnInadequate post-operative analgesia, upper abdominalincisionObesity, ascitesPre-operative tobacco smokingExcessive airway secretionsType IV respiratory failurennnCardiogenic shockSeptic shockHypovolemic shock

Diagnosis: HistorynnnnnSepsis suggested by fever, chillsPneumonia suggested by cough, sputum production,chest painPulmonary embolus suggested by sudden onset ofshortness of breath or chest painCOPD exacerbation suggested by history of heavysmoking, cough, sputum productionCardiogenic pulmonary edema suggested by chest pain,paroxysmal nocturnal dyspnea, and orthopnea

Diagnosis: HistoryNoncardiogenic edema suggested by thepresence of risk factors including sepsis,trauma, aspiration, and blood transfusionsn Accompanying sensory abnormalities orsymptoms of weakness may suggestneuromuscular respiratory failure; as would thehistory of an ingestion or administration ofdrugs or toxins.n Additional exposure history may help diagnoseasthma, aspiration, inhalational injury and someinterstitial lung diseasesn

Diagnosis: Physical FindingsnnnHypotension usually with signs of poor perfusionsuggests severe sepsis or massive pulmonary embolusHypertension usually with signs of poor perfusionsuggests cardiogenic pulmonary edemaWheezing suggests airway obstruction:nnnnBronchospasmFixed upper or lower airway pathologySecretionsPulmonary edema (“cardiac asthma”)

Diagnosis: Physical FindingsStridor suggests upper airway obstructionn Elevated jugular venous pressure suggests rightventricular dysfunction due to accompanyingpulmonary hypertensionn Tachycardia and arrhythmias may be the causeof cardiogenic pulmonary edeman

Diagnosis: Laboratory WorkupnABGnnnQuantifies magnitude of gas exchange abnormalityIdentifies type and chronicity of respiratory failureComplete blood countnnnnAnemia may cause cardiogenic pulmonary edemaPolycythemia suggests may chronic hypoxemiaLeukocytosis, a left shift, or leukopenia suggestive ofinfectionThrombocytopenia may suggest sepsis as a cause

Diagnosis: Laboratory WorkupnCardiac serologic markersTroponin, Creatine kinase- MB fraction (CK-MB)n B-type natriuretic peptide (BNP)nnMicrobiologyRespiratory cultures: sputum/trachealaspirate/broncheoalveolar lavage (BAL)n Blood, urine and body fluid (e.g. pleural) culturesn

Diagnostic InvestigationsnChest radiographynnElectrocardiogramnnIdentify chest wall, pleural and lung parenchymalpathology; and distinguish disorders that causeprimarily V/Q mismatch (clear lungs) vs. Shunt(intra-pulmonary shunt; with opacities present)Identify arrhythmias, ischemia, ventriculardysfunctionEchocardiographynIdentify right and/or left ventricular dysfunction

Diagnostic InvestigationsnPulmonary function tests/bedside spirometrynnnIdentify obstruction, restriction, gas diffusion abnormalitiesMay be difficult to perform if critically illBronchoscopynnnObtain biopsies, brushings and BAL for histology, cytologyand microbiologyResults may not be available quickly enough to avertrespiratory failureBronchoscopy may not be safe in the if critically ill

Respiratory Failure:ManagementnABC’sEnsure airway is adequaten Ensure adequate supplemental oxygen and assistedventilation, if indicatedn Support circulation as neededn

Respiratory Failure:ManagementnTreatment of a specific cause when possiblen Infectionn Antimicrobials,nsource controlAirway obstructionn Bronchodilators,nglucocorticoidsImprove cardiac functionn Positiveairway pressure, diuretics, vasodilators,morphine, inotropy, revascularization

Respiratory Failure:ManagementnMechanical ventilationnNon-invasive (if patient can protect airway and ishemodynamically stable)n Mask:nusually orofacial to startInvasiven Endotrachealtube (ETT)n Tracheostomy – if upper airway is obstructed

Respiratory FailureSecure airwayNeed for endotrachealintubation or tracheostomy?Supplemental oxygen as neededTreat underlying conditionYesInvasive mechanicalventilationNoNon-invasivemechanical ventilationFails

Indications for MechanicalVentilationnnnnnCardiac or respiratory arrestTachypnea or bradypnea with respiratory fatigue orimpending arrestAcute respiratory acidosisRefractory hypoxemia (when the PaO2 could not bemaintained above 60 mm Hg with inspired O2 fraction(FIO2) 1.0)Inability to protect the airway associated with depressed levelsof consciousness

Indications for MechanicalVentilationnnnnShock associated with excessive respiratory workInability to clear secretions with impaired gas exchangeor excessive respiratory workNewly diagnosed neuromuscular disease with a vitalcapacity 10-15 mL/kgShort term adjunct in management of acutely increasedintracranial pressure (ICP)

Invasive vs. Non-invasiveVentilationnConsider non-invasive ventilation particularlyin the following settings:COPD exacerbationn Cardiogenic pulmonary edeman Obesity hypoventilation syndromen Noninvasive ventilation may be tried in selectedpatients with asthma or non-cardiogenic hypoxemicrespiratory failuren

Goals of MechanicalVentilationnImprove ventilation by augmenting respiratoryrate and tidal volumenAssistance for neural or muscle dysfunctionn Sedated,comatose or paralyzed patientn Neuropathy, myopathy or muscular dystrophyn Intra-operative ventilationCorrect respiratory acidosis, providing goals of lungprotective ventilation are metn Match metabolic demandn Rest respiratory musclesn

Goals of MechanicalVentilationnCorrect hypoxemiaHigh F IO2n Positive end expiratory pressure (PEEP)nnImprove cardiac functionDecreases preloadn Decreases afterloadn Decreases metabolic demandn

Permissive HypercapnianVentilation strategy that allows PaCO2 to riseby accepting a lower alveolar minute ventilationto avoid specific risks:Dynamic hyperinflation (“auto-peep”) andbarotrauma in patients with asthman Ventilator-associated lung injury, in patients with, orat risk for, ALI and ARDSnnContraindicated in patients with increasedintracranial pressure such as head trauma

Mechanical VentilationF IO,2 PPEECorrect HypoxemiaRR, TVPrM eloadetab o , Aftlic er lde oadma ,ndEnhance Ventilation *Meet increasedmetabolicdemandCorrect respiratoryacidosis*Assistance for neural and/ormuscle dysfunctionOptimize cardiac functionHyperventilation may be used as a shortterm adjunct to treat acutely elevated ICP* Avoid ventilator induced lung injury and dynamic hyperinflation

Other Issues to Consider WhenInitiating Mechanical VentilationnDo not wait for frank respiratory acidosisespecially with evidence of:Inability to protect airwayn Persistent or worsening tachypnea (respiratory rate 35/minute)n Respiratory muscle fatiguennAlways consider risks and benefits of initiationand continuation of mechanical ventilation

Other Issues in Intubated &Mechanically Ventilated PatientsnnnAlways elevate the head of the bed 30º and use ulcerand DVT prophylaxis, unless contraindicatedUse lung protective ventilation strategy for patientswith Acute Lung Injury (TV 6 ml/kg ideal bodyweight, Plat pressure 30 cmH2O)Modify ventilator settings primarily to achieve patientventilator synchrony. If this fails, use the least amountof sedation required to achieve comfort and avoidunnecessary neuromuscular blockade

Other Issues in Intubated &Mechanically Ventilated PatientsnMonitor patient comfort, gas exchange,mechanics, and ventilator waveforms daily, ormore frequently if indicatednWhen minimal settings are required foroxygenation (FIO2 55%, PEEP 8) andpatient is hemodynamically stable, perform aspontaneous breathing trial daily

ReferencesnnnnnnnnnArora,V.K., Shankar, U. (1995). Acute Lung Injury. Lung India, Volume XIII, Number1, p 32-34.Behrendt C.F. (2000). Acute respiratory failure in the United States: Incidence and31-day survival. Chest, Volume 118, Number 4, p 1100-1105.Brochard L., Mancebo J., Elliott M.W. (2002). Noninvasive ventilation for acuterespiratory failure. European Respiratory Journal, Volume 19, Number 4, p 712-721Hall J.B., Schmidt G.A, Wood L. D.H. (2005). Principles of Critical Care, 3rd Edition.New York: McGraw-Hill /en/thumb/d/db/Alveoli diagram.png/300pxAlveoli diagram.png. Retrieved Nov., 16, 2006 from http://www.wikimedia.org.Hurford W.E. (2002). Sedation and paralysis during mechanical ventilation. RespiratoryCar, Volume 47, Number 3, p 334-346.Kasper D.L, Braunwald E., Fauci A.S., Hauser S.L., Longo D.L., Jameson J.L.,Isselbacher, K.L. (2004).Harrison's Principles of Internal Medicine, 16th Edition. New York:McGraw-Hill Professional.Masip J., Roque M., Sa nchez B., Ferna ndez R., Subirana M., Expo sito J.A., (2005).Noninvasive Ventilation in Acute Cardiogenic Pulmonary Edema: Systematic Reviewand Meta-analysis. Journal of the American Medical Association, Volume 294, Number 24, p3124-3130.Michael E. Hanley M.E., Welsh, C.H. (2003). Current Diagnosis & Treatment inPulmonary Medicine. New York: McGraw-Hill Professional.

ReferencesnnnnnnMidelton G.T., Frishman W.H., Passo S.S. (2002). Congestive heart failure andcontinuous positive airway pressure therapy: support of a new modality for improvingthe prognosis and survival of patients with advanced congestive heart failure. HeartDisease, Volume 4, Number 2, p 102-109.Plant P., Owen J., Elliott M. (2000). Early use of non-invasive ventilation for acuteexacerbations of chronic obstructive pulmonary disease on general respiratory wards:a multicentre randomised controlled trial. The Lancet, Volume 355, Issue 9219, p 19311935.Ryland B.P., Jr. emedicine- Ventilation, Mechanical. Retrieved Nov., 24, 2006 ma S. emedicine-Respiratory Failure. Retrieved Nov., 24, 2006 fromhttp://www.emedicine.com/med/topic2011.htmThe Acute Respiratory Distress Syndrome Network (2000). Ventilation with lowertidal volumes as compared with traditional tidal volumes for acute lung injury and theacute respiratory distress syndrome. New England Journal of Medicine, Volume 342,Number 18, p 1301-1308.Tobin, M.J. Principles and Practice of Mechanical Ventilation, 2nd Edition (2006). New York:McGraw-Hill Medical Publishing Division.

Classification nn Type III Respiratory Failure:Type III Respiratory Failure: Perioperative respiratory failure nn Increased atelectasis due to low functional residual capacity (( FRCFRC ) in the setting of abnormal abdominal wall mechanics nn Often results in type I or type II respiratory failure nn Can be ameliorat

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