Introduction - Uniformed Services Academy of Family Physicians



SCENARIO ALGORITHMSET UPSim Man w/ live video feed & mic OR older standardized patientInstructor will control Sim Man and monitor case from video room and be voice of patient if possibleResident will play role of RNECG available @ monitorCXR available @ monitorABG, CBC, Chem 10, trop availableNeed Bipap/CPAP and/or ventPRE ARRIVAL65 yo male with inc SOB, cough, yellow sputum x 1 day; “cold” symptoms x 3 days HR 125 BP 138/79 RR 30 Pox 84% T99.9ARRIVALNo changePMH—COPD (1 hosp in past yr), DMII, HTN, HLPMeds—Albuterol, Spiriva, Metformin, Zestoretic, Lipitor, ASAAll—None SH—Tob x 1 ppd x 40 yrs, quit 5 yrs ago; no ETOH; retired, lives c wifePRIMARY SURVEYABCs WNL except tachypnea/tachycardia as above; bilateral wheezing, some accessory muscle use, mild to mod distress/ill appearingSECONDARY SURVEYPt slowly decompensates and requires NPPV and/or intubationLABS & IMAGES CXR—COPD w/o evid of PNA Labs—see handoutECG—COPD—Rt axis dev, P pulmonale, and RBBBDISPOSITIONICUDate: Examiner: Examinee(s):Learning Objectives: Assess patient as stable vs. unstable and diagnose COPD exacerbationConduct appropriate work up of COPD exacerbation and COPD stagingDiscuss adjunctive therapy for a COPD exacerbation, including non-invasive positive pressure ventilationReview the indications for intubation of a COPD patient and basic ventilator therapyCRITICAL ACTIONSMSMENISUSTAINIMPROVEPlace safety net—IV, O2, monitor & begin ABCs?ID COPD exacerbation and pt as unstable. ??Take thorough history and ID time of onset??Give nebs??Give abx??Give steroids??Place pt on BIPAP and/or intubate and choose appropriate settings??Choose appropriate sedation agents and dosesTx in ER/Ward then move to ICU??Demonstrate effective communication including closed loop feedbackTOTALABG: 7.33/55/49/18MS = Milestone CBC: 12.5/15.2/45.8/185 diff 70% neutron, 6 bandsME = Meets ExpectationsCMP: 130/4.0/117/18/24/1.2/190 nl LFT’s, alk phos, Ca/Mg/PhosNI = Needs ImprovementCK/Trop: wnl, d-dimer: wnl, BNP: wnlslkdjfIntroductionThe Global Initiative for Chronic Obstructive Lung Disease (GOLD) defines an exacerbation of chronic obstructive pulmonary disease (COPD) as an acute increase in symptoms beyond normal day-to-day variation. This generally includes an acute increase in one or more of the following cardinal symptoms:Cough increases in frequency and severitySputum production increases in volume and/or changes characterDyspnea increasesCauses of an Acute Exacerbation of a COPD Patient Superimposed infectionContinued smokingNon-complianceLack of usual medications or oxygen therapySpontaneous pneumothoraxThe single best predictor of exacerbations was a history of exacerbations, regardless of COPD severity.Typical Signs of a Patient with a COPD Exacerbation Pursed lip breathingCyanosisUse of accessory musclesIntercostal retractionsBarrel chestHyper-resonant chestWheezing, rhonchi, ralesProlonged expiratory phaseTachycardiaMental status changes w/sig hypoxia, elevated CO2Signs of CHF if cor pulmonale (Pulm HTN) –JVD, LE edema, hepatomegalyInitial Action and Primary SurveyABC’s: Begin by assessing airway, breathing, and circulation. Obtain vital signs including the pulse oximetry reading.Give Oxygen. Apply controlled oxygen to all hypoxic patients who present with suspected COPD. In general, use a delivery system such as a Venturi mask or nasal cannula. Avoid routine use of a non-rebreather mask with 15 L/min of oxygen, unless the patient is not responding to lower flow rates. In some patients with chronic carbon dioxide retention, high flow oxygen may cause respiratory depression with the rapid rise in oxygen depressing the central ventilatory drive.Safety net: Place the ill patient on the monitor, attach continuous pulse oximetry, and insert an intravenous line. Observe the patient’s work of breathing and mental status, looking for signs of respiratory distress and fatigue. COPD patients MAY require immediate intubation or non-invasive ventilatory support.Diagnostic TestingSince COPD patients are typically older with a history of smoking and multiple co-morbidities they require a broad differential diagnosis such as CHF, acute coronary syndrome, pulmonary embolus, pneumothorax, pericardial effusion, and pneumoniaChest X-Ray: chest radiograph is the most common study necessary in evaluating the COPD patient. A typical chest x-ray will show increased AP diameter, flattening of the diaphragm, decreased lung markings and the absence of another acute abnormality, such as pneumothorax, pulmonary edema or infiltrate. Significant abnormalities such as pneumonia, pulmonary edema or pneumothorax will require a change in therapy.Electrocardiography: EKG is rarely specific in COPD, but frequently necessary in the evaluation of elderly patients with multiple co-morbidities to help exclude other disease processes. Common EKG Features of COPD Low voltage, right axis deviation and rightward axis deviationP pulmonale- peaked P waves in II, III, aVF, rt axis deviation, RBBB, low voltage QRSRight atrial hypertrophyTachycardiaMultifocal atrial tachycardia (rare, but specific to COPD)Laboratory Testing: arterial blood gas (ABG) if the patient is critically ill and not responding to standard treatment. Evaluate for degree of hypoxia, acidosis, and CO2 retention. Serial arterial blood gases may be needed to assess trends in the ill patient.pHPCO2Pa02O2 SatNormal ABG7.44060-90>95%Compensated7.395060-90>92%Decompensated<7.35RisingFalling<92%Several studies may be indicated to exclude other diagnoses: d-dimer (with subsequent chest CT angiography if positive) in patients felt to be at risk for PE or in non-responders to standard treatment. Cardiac enzymes may be indicated in patients who you suspect are at risk for an acute coronary syndrome. Obtaining a newly elevated BNP may suggest a component of congestive heart failure.Admission Criteria: 2004 position paper from the American Thoracic Society/European Respiratory Society (ATS/ERS)::Inadequate response of symptoms to outpatient managementMarked increase in dyspneaInability to eat or sleep due to symptomsWorsening hypoxemiaWorsening hypercapniaChanges in mental statusInability to care for oneself (ie, lack of home support)Uncertain diagnosisHigh risk comorbidities including pneumonia, cardiac arrhythmia, heart failure, diabetes mellitus, renal failure, or liver failureAcute respiratory acidosis justifies hospitalization.Treatment: In general, treatment revolves around use of bronchodilators, corticosteroids, and antibiotics to treat superimposed infection.Oxygen: goal of PaO2 of 60-70 and/or O2 sat of 90-94%. Venturi masks are preferred as they deliver precise FiO2. Nasal cannulae can provide flow rates up to 6 L (FiO2 40%). Avoid high flow O2—not necessary and may inc CO2 retention/dec resp drive.Bronchodilators: After oxygen, the use of bronchodilators to treat acute decompensation is the initial treatment. Inhaled albuterol, the preferred beta-agonist, provides the most rapid response in most patients. Even after multiple doses a clinical response may occur. The only limiting factor to ongoing use is tachycardia and other cardiovascular side effects such as ischemia. There is no role for long acting beta-agonists such as salmeterol in treatment of the acute exacerbation. Give albuterol (2.5mg) tx’s every 1-4 hrs. No role for cont albuterol nebs in COPD. Use of anti-cholinergic bronchodilators such as ipatropium bromide, is also first line therapy. Ipatropium is typically given every 4 hours (500mcg), not in stacked or repeated doses like albuterol. Systematic review has not shown combination therapy with beta-agonists to be superior, but it is frequently used.Steroids: An IV steroid such as methlyprednisolone OR prednisone orally should be started. The optimum regimen is not established, but typical regimens are 10-14 days. Corticosteroids have been shown to improve lung fxn, reduce treatment failure, dec hospital stay, and the need for additional medical therapy. Complications of steroid use are worsening hypertension, elevated blood sugars, gastritis, and even steroid psychosis. Usually PO doses(30-40mg qd) if going to ward, IV doses(60mg qd to qid) if going to ICU. No role for inhaled corticosteroids in COPD exacerbation.Antibiotics: Empiric antibiotics are used if signs of infection are present and in patients with moderate to severe exacerbations. Exam and historical features that suggest infection are dyspnea, color change of sputum, and increased volume of sputum. The optimal antibiotic regimen for the treatment of exacerbations of COPD has not been determined. Many options! ACP: Amoxil or Doxy or alternate (oral ceph, azith, etc) (mild/outpt); Levo/Moxiflox or 3rd gen ceph (mod to severe and/or recent abx use). Tx for 3-7 days.Others: no role for mucoactive agents (N-acetylcysteine), methylxanthines (theophylline) and/or chest physiotherapy.Adjunctive Therapy for Decompensated Patients: Continuing respiratory decompensation with worsening carbon dioxide retention and hypoxia despite standard treatment are indications for adjuctive therapy with non-invasive positive pressure ventilation (NPPV) or endotracheal intubation. The decision to initiate one of these adjunctive therapies can be a purely clinical one, based on overall assessment of work of breathing, or via direct measurement of arterial blood gases. There is no absolute guideline for level of carbon dioxide and it is not uncommon for severely affected patients to be awake and relatively stable with a PC02 over 60. However, worsening acidosis and unresponsive hypoxia are good markers for the need for adjunctive therapy.Non-invasive positive pressure ventilation is a mode of mechanical ventilation given by facemask or nasal prongs that aids oxygen delivery and decreases work of breathing. However, it should be started early before acute neurologic deterioration or respiratory depression occurs.. A reasonable approach is to initiate NPPV in a spontaneously triggered mode with a backup respiratory rate, an inspiratory pressure of 8 to 12 cm H2O, and an expiratory pressure of 3 to 5 cm H2O.Rapid sequence intubation (RSI ) may be necessary for airway control, correction of hypoxia, and correction of carbon dioxide retention. After intubation and sedation, the ventilator is set with a tidal volume of 5-7ml per kg of ideal body weight (best calculated by length measurement of the patient). The initial oxygen flow is typically 50-100% depending on pulse oximetry and blood gas measurement. The initial mode of ventilation is typically assist control or IMV/PSV (but not IMV or PSV alone) with a fixed number of ventilations being delivered even if the patient is paralyzed or taking insufficient breaths per minutePearls and PitfallsAssess what patient factors may have caused the exacerbationAlways consider alternate diagnoses such as PE, ACS, pneumonia, and CHF in the COPD patientGive oxygen early and give enoughUse a combination of bronchodilators, steroids, and consider antibiotics in moderate and severe exacerbationsStart NIPPV early in patients who have persistent increased work of breathingAppendices:Initial ABG:pH: 7.33PCO2: 55PO2: 49Bicarb: 18Subsequent ABG (after appropriate intervention):pH: 7.38PCO2: 45PO2: 70Bicarb: 19Other labs:CBC: 12.5/15.2/45.8/185CMP: 130/4.0/117/18/24/1.2/190CK: wnlTrop: wnld-dimer: wnlBNP: wnl ................
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