asthma lecture

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Asthma Asthma Maneesha Sabharwal, MD Maneesha Sabharwal, MD NYU/Bellevue Emergency Medicine Residency, NY, NYU/Bellevue Emergency Medicine Residency, NY, USA USA February 2015 February 2015

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  • AsthmaManeesha Sabharwal, MDNYU/Bellevue Emergency Medicine Residency, NY, USAFebruary 2015

  • OutlinePathophysiologyClinical featuresMedical managementDecision to intubationVentilator managementVentilator troubleshootingCoding asthmaticIndications for admission

  • Asthma PathophysiologyPredisposing FactorsTrigger = Exposure to an AntigenImmune response Mast cells, eosinophils, T-lymphocytes, macrophages, neutrophils, and epithelial cellsInflammatory responseReversible airflow obstructionSymptoms: recurrent episodes of wheezing breathlessness, chest tightness and coughing

  • Predisposing FactorsGeneticsAgeRace Gender

  • Common Asthma TriggersAllergic TriggersDust mitesMoldCertain foodAnimal danderPollenNon-Allergic TriggersExerciseViral Respiratory InfectionsCold or humid airEmotional StressMedications (aspirin, NSAIDs, beta blockers)Air pollutionChemicals

  • Immunology of AsthmaIgE-dependent release of mediators from mast cellshistamineleukotrienetryptaseprostoglandinsDirectly contracts airway smooth muscle

  • Consequences of Bronchial InflammationReduction in the airway diameter caused by smooth muscle contraction, vascular congestion, bronchial wall edema, thick secretionsContinuum from acute bronchospasm to airway inflammation and permanent airway remodelingIncreased work of breathing from severe airflow resistance due to bronchial mucosal inflammation and edema, constriction of bronchial smooth muscle, and mucus in the bronchial lumenIncreased intrathoracic pressure from air trapping, which further increases the work of breathing, decreases preload, and increases afterloadDepletion of catecholamines during prolonged exacerbationsDehydration through insensible losses

  • Physiologic Consequences of Airflow ObstructionIncreased airway resistanceDecreased maximum expiratory flow ratesAir trappingIncreased airway pressureBarotraumaAdverse hemodynamic effectsVentilation-perfusion imbalanceHypoxemia, HypercarbiaIncreased work of breathingPulsus paradoxusRespiratory muscle fatigue with ventilatory failure

  • Clinical FeaturesTriadDyspneaWheezingCough

  • History of Present IllnessSymptomsCoughWheezingShortness of breathChest tightnessSputum productionFeverHistoryLast hospital admissionIntensive Care admissions?Steroid useIntubations# of puffs of albuterol daily, medicationsBest spirometry measureSocial History: smoking, living conditions (roaches)

  • Asthma Classification

  • Signs and Symptoms of a severe asthma exacerbationBreathlessness at restMust sit upright, cant lie downCant speak full sentences, fragmented speechRR>30Using accessory musclesDiffuse inspiratory and expiratory wheezingTachycardic >120Hypoxia
  • Signs of Impending Respiratory FailureDrowsy/confusedAbsence of wheezing or air entryBradycardiaSlowed respirationHypercapniaPEFR < 25% of predicted (100-150 L/min)Respiratory acidosis: rising PCO2 on VBG

  • Medical Management of Asthma Outline

    Initial StabilizationMedicationsBilevel: Non-invasive ventilationRescue MeasuresIntubation

  • Initial ManagementPlace the patient on telemetry, pulse oximetry and capnography monitoringOxygen via nasal cannula or non-rebreatherTwo peripheral intravenous linesIntravenous fluidsReplaces insensible losses from increased work of breathingIntravascular volume should be replaced because hypotension often occurs after the initiation of positive pressure ventilation.

  • MedicationsNebulized: Albuterol, IpratropriumCorticosteriodsMagnesiumBeta 2 agonist

  • NebulizersBeta 2-agonist: AlbuterolMOA: Bronchodilation via Beta-2 receptorsAlbuterol vs L-albuterol: Levalbuterol provides little to no advantage over less-expensive racemic albuterol.Anti-cholinergic agents: Ipratroprium MOA: Blocks the action of acetylcholine at parasympathetic sites in bronchial smooth muscle causing bronchodilationExpert Panel Report III recommend the addition of ipratropium for patients with severe exacerbations

  • CorticosteroidsGive to patients who have:moderate (peak expiratory flow
  • MagnesiumMOA: bronchodilator activity due to inhibition of calcium influx into airway smooth muscle cellsTwo systematic reviews concluded that it is helpful in the subgroup of patients with severe exacerbations. Not useful in mild/moderate exacerbations.Dose: give 2 g IV over 20 minutes for life-threatening exacerbations and exacerbations that remain severe after one hour of intensive bronchodilator therapyContraindicated in ESRD/renal insufficiencyMonitor for Mg toxicity - can cause muscle weakness

  • Beta 2 AgonistsBeta 2 agonists - Epinepherine IM and terbutaline SQEpinephrine IM vs nebulizedEpi dose: 0.3 to 0.5 mg IM (eg, 0.3 to 0.5 mL of 1 mg/mL [also labeled 1:1000] solutionTerbutaline IV - Expert panel doesnt recommend the use of IV beta 2 agonists and IV isoproterenol because of the danger of myocardial toxicity.Subcutaneous - 0.25 mg/dose; may repeat in 15-30 minutes (maximum: 0.5 mg/4-hour period

  • Non-invasive VentilationBiPAPInsufficient evidence to recommend its use, but often usedBronchoconstriction results in fatigue of the respiratory muscles and the inhalation support will ultimately help them exhale and decrease air trapping. IP 8 = PSEP = peep 2-4, these patients have autopeep, but the machine doesnt sense this peep, so a little peep helps them initiate a breathCan use nebulizers through BiPAP

  • Rescue MeasuresLidocaineHelioxKetamine

  • LidocaineMechanism: may attenuate the rise in airway resistance (as seen with asthma exacerbations)IV: 1-1.5mg/kg before rapid sequence intubationEvidence unclear if it decreases bronchospasmMultiple RCT have shown that it can suppress cough reflexesContraindicated in 2nd and 3rd degree heart block

  • HelioxTheoretical benefits:Low density so reduces airflow resistance and improves airflow dynamicsUsing a helium-oxygen mixture results in a smaller particle size, which may improve drug penetration to the small airwaysDecreases work of breathing and improves ventilationInsufficient evidence to recommend the use in the treatment of all asthmatic attacksRoutine use not recommended, but consider heliox-driven albuterol nebulization to improve delivery of drug in severe/life-threatening exacerbations or after one hour of intensive conventional therapy

  • KetamineMOA: noncompetative NMDA receptor antagonist that blocks glutamate, has bronchodilatory propertiesProduces a cataleptic-like states that helps the patient maintain breathing and helps them tolerate the facemaskNon-dissociative dose: 1mg/kg/hrMany case series have demonstrated improvement in oxygenation, ventilation, bronchospasm and pulmonary function, but another RCT failed to demonstrate benefit. Overall, large randomized trials to assess the effectiveness of ketamine in the intubation of asthmatics are lackingNo evidence of the use of a drip

  • Decision to IntubateThis is a clinical decision, no definitive guidelines:Is there failure of airway maintenance or protection?Is there failure of oxygenation or ventilation?Is deterioration, particularly of the airway, anticipated? (ie, What is the expected clinical course?)Clinical findings that portend imminent respiratory arrest:inability to maintain respiratory effort (ie extreme fatigue)depressed mental statusCyanosis

  • Rapid sequence IntubationPreoxygenation: often not possibleconsider BVM or NIVV for higher O2 concETT size - 8.0 or 9.0 because larger diameter will minimize airway resistancePretreatment: IV Lidocaine 1-1.5mg/kg 2-3min before inductionSedation: ketamine/propofol - have bronchodilatory propertiesCase reports suggest that propofol has bronchodilatory effects, but causes hypotension, so less desirable.Paralytic agent is a must: need first pass successRocuronium, Vecuronium

  • Post-intubation ManagementHOB at 30 degreesRepeat CXR for ETT placementOrogastric tubeFoleyDeep Sedation: allow asthma pt to rest respiratory muscles ABG w/in 30 min to assess ventilation and oxygentation

  • Post-intubation goalsMaintain adequate oxygenation Permissive hypercapnia Minimize airway pressuresDeeply sedate: to avoid tachypnea/rest respiratory muscles, prevent asynchrony with the ventilatorparenteral opioids w/ non-histamine releasing opioids (fentanyl)May need paralyticContinue nebulizers through the ventilator

  • Ventilator settingsGoal: prevent air trapping, breath stackingProlonged I:E ratio: Increasing the inspiratory flow rate (80L/min) will shorten the inspiratory time, increase the expiratory time, and allow the patient more time to exhaleTV 6-8cc/kg of IBW: Decreasing the TV causes less lung inflation and gives the patient a smaller volume to exhale before the next breathRR = 10 (start low): Decreasing the RR increases the expiratory time and allows the patient more time to exhaleLow TV and RR will result in elevated PaCO2, which is considered permissive hypercapnia.

  • Ventilator settings contAC volume controlFiO2: start at 40%desaturation will occur if air isnt moving or shunting occursExtrinsic PEEP - 2-4, low, maybe 0Intrinsic PEEP is due to air trapping, which must be minimizedExtrinsic PEEP is only needed if pt is initiating some spontaneous breathes because it will reduce the effort necessary to trigger inspirationPEEP not needed if pt is not breathing spontaneously.Plateau pressure: more accurate measure of distending pressuresThis is the pressure that the alveoli actually seesGoal is Pplat 30, you aren giving the patient enough time to exhale.Peak inspiratory pressure: not a reliable indicator of lung overdistension because it includes resistance of tube and upper airway

  • Why do we want to avoid intubating an asthmatic?Adverse effects of mechanical ventilation in asthma: dynamic hyperinflation air trapping and breath stacking creates intrinsic PEEP and elevates the plateau pressure (Pplat) which can cause: Cardiovascular collapseBarotraumaIncreased work of breathing

  • Dynamic hyperinflationCardiovascular collapse: stacking breathes --> increased intrathoracic pressure from air trapping--> decreased venous return and cardiac output.Barotrauma: keep Pplat
  • Coding asthmaticYour patient is desaturating/crashing/codingFirst thing you do is disconnect the patient from the ventilator because the #1 reason they are coding is that they are stacking breathes --> increased intrathoracic pressure from air trapping--> decreased venous return and cardiac output.

  • Coding AlgorithmDOPESD = Displacement of the tube: attach ETCO2 to confirm placementO = Obstruction of the tube: slip down a suction catheter, may not detect the mucous ballP = Pneumothorax: auscultate and check with the US for b/l lung sliding. If causing desaturation or hemodynamic instability, then it is a tension PTXE = Equipment: attach a BVM to the oxygen and eliminate the ventilatorS = Stacked breathes: disconnect the vent and physically decompress the chest

  • PneumothoraxDecompressionNeedleFinger Thoracostomy

  • PrognosisPrognosis:Status asthmaticus + mechanical ventilation Increased in-hospital mortality compared to patients who do not require mechanical ventilation (7 versus 0.2 percent)

  • Risk Factors for Death from Asthma

  • Indication for HospitalizationIndications for hospitalization: Use your clinical judgement!Peak Expiratory Flow Rate, risk factors, clinical signs and symptoms, compliance, access to expedite follow up.

  • Questions???

  • Thank you!Emergency Medicine residents at the Hue University of Medicine and PharmacyDr. Tran Thi Doan Trang - Director of Hue Central Hospital EmergencyDr. Tran Duc Lai - Chair of Hue University Emergency DepartmentDr. Heather Crane

    Inhaled antigens activate immunoglobulin E, mast cells, and T helper cells in the airway and induce the production of inflammatory mediators and cytokines. In turn, this initiates a cascade of reactions involving lymphocytes, mast cells, eosinophils, dendritic cells, macrophages, resident airway cells, and epithelial cells that perpetuate the inflammatory response, with further release of chemokines, cytokines, cysteinyl leukotrienes, and nitric oxide. Clearly, the inflammatory process is multicellular, redundant, and self-amplifying.rare reports of response to terbutaline in refractory asthma. The dose of terbutaline is 0.25 mg by subcutaneous injection every 20 minutes up to three doses. Terbutaline OR epinephrine may be used, but NOT bothAbsolute CI to lidocaine pretreatment: known lidocaine allergy and high grade heart block (Mobitz type II or third degree) in a patient without a functioning pacemaker. Can cause cardiac arrest in the setting of a high grade heart block.

    Needle decompression: Classic technique: insert needle at the 2nd or 3rd intercostal space, midclavicular line needle often doesnt reach, may hit great vessel can be safer if you needle decompress at chest tube insertion site - midaxillary line use longer needle from the central line kit. If there wasnt a PTX, there may be one now, and you may have to put in a chest tube! Pt will need serial CXR to determineFinger thoracostomy - possibly lower risk technique incision where you are going to put chest tube and just use your finger to relieve the tension and now you have time to place a sterile tube and if no PTX, then likely no chest tube is necessary, but will still need. Dont need hemostat, can blunt dissect through intercostals with your finger. also works in blunt traumatic arrest.