Formative Assessment for Simulation Training (FAST)—COPD Exacerbation
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SCENARIO ALGORITHM
SET UP
Sim Man w/ live video feed & mic OR
older standardized patient
Instructor will control Sim Man and
monitor case from video room and be
voice of patient if possible
Resident will play role of RN
ECG available @ monitor
CXR available @ monitor
slkdjf
ABG, CBC, Chem 10, trop available
Need Bipap/CPAP and/or vent
PRE ARRIVAL
 65 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% T99.9
ARRIVAL
 No change
 PMH—COPD (1 hosp in past yr), DMII,
HTN, HLP
 Meds—Albuterol, Spiriva, Metformin,
Zestoretic, Lipitor, ASA
 All—None
 SH—Tob x 1 ppd x 40 yrs, quit 5 yrs ago;
no ETOH; retired, lives c wife
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PRIMARY SURVEY
ABCs WNL except tachypnea/tachycardia
as above; bilateral wheezing, some
accessory muscle use, mild to mod
distress/ill appearing
SECONDARY SURVEY
Pt slowly decompensates and requires
NPPV and/or intubation
LABS & IMAGES
 CXR—COPD w/o evid of PNA
 Labs—see handout
 ECG—COPD—Rt axis dev, P pulmonale,
and RBBB
DISPOSITION
ICU
Date:
Examiner:
Examinee(s):
Learning Objectives:
1. Assess patient as stable vs. unstable and diagnose COPD exacerbation
2. Conduct appropriate work up of COPD exacerbation and COPD staging
3. Discuss adjunctive therapy for a COPD exacerbation, including non-invasive positive pressure
ventilation
4. Review the indications for intubation of a COPD patient and basic ventilator therapy
CRITICAL ACTIONS
Place safety net—IV, O2, monitor
& begin ABCs
MS
ME
NI
SUSTAIN
IMPROVE
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 doses
Tx in ER/Ward then move to ICU
Demonstrate effective
communication including closed
loop feedback
TOTAL
ABG: 7.33/55/49/18
CBC: 12.5/15.2/45.8/185 diff 70% neutron, 6 bands
CMP: 130/4.0/117/18/24/1.2/190 nl LFT’s, alk phos, Ca/Mg/Phos
CK/Trop: wnl, d-dimer: wnl, BNP: wnl
MS = Milestone
ME = Meets Expectations
NI = Needs Improvement
Formative Assessment for Simulation Training (FAST)—COPD Exacerbation
Introduction
The 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:
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Cough increases in frequency and severity
Sputum production increases in volume and/or changes character
Dyspnea increases
Causes of an Acute Exacerbation of a COPD Patient
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Superimposed infection
Continued smoking
Non-compliance
Lack of usual medications or oxygen therapy
Spontaneous pneumothorax
The single best predictor of exacerbations was a history of exacerbations, regardless of COPD severity.
Typical Signs of a Patient with a COPD Exacerbation
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Pursed lip breathing
Cyanosis
Use of accessory muscles
Intercostal retractions
Barrel chest
Hyper-resonant chest
Wheezing, rhonchi, rales
Prolonged expiratory phase
Tachycardia
Mental status changes w/sig hypoxia, elevated CO2
Signs of CHF if cor pulmonale (Pulm HTN) –JVD, LE edema, hepatomegaly
Initial Action and Primary Survey
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ABC’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 Testing
Since 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 pneumonia
Formative Assessment for Simulation Training (FAST)—COPD Exacerbation
Chest 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
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Low voltage, right axis deviation and rightward axis deviation
P pulmonale- peaked P waves in II, III, aVF, rt axis deviation, RBBB, low voltage QRS
Right atrial hypertrophy
Tachycardia
Multifocal 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.
pH
Normal ABG 7.4
Compensated 7.39
Decompensated <7.35
PCO2 Pa02 O2 Sat
40
60-90 >95%
50
60-90 >92%
Rising Falling <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 nonresponders 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)::
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Inadequate response of symptoms to outpatient management
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Marked increase in dyspnea
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Inability to eat or sleep due to symptoms
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Worsening hypoxemia
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Worsening hypercapnia
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Changes in mental status
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Inability to care for oneself (ie, lack of home support)
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Uncertain diagnosis
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High risk comorbidities including pneumonia, cardiac arrhythmia, heart failure, diabetes mellitus, renal failure, or liver failure
Acute respiratory acidosis justifies hospitalization.
Treatment: In general, treatment revolves around use of bronchodilators, corticosteroids, and antibiotics to treat superimposed infection.
Formative Assessment for Simulation Training (FAST)—COPD Exacerbation
 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 37 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 H 2O, 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 minute
Pearls and Pitfalls
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Assess what patient factors may have caused the exacerbation
Always consider alternate diagnoses such as PE, ACS, pneumonia, and CHF in the COPD patient
Give oxygen early and give enough
Use a combination of bronchodilators, steroids, and consider antibiotics in moderate and severe exacerbations
Start NIPPV early in patients who have persistent increased work of breathing
Formative Assessment for Simulation Training (FAST)—COPD Exacerbation
Formative Assessment for Simulation Training (FAST)—COPD Exacerbation
Formative Assessment for Simulation Training (FAST)—COPD Exacerbation
Appendices:
Initial ABG:
pH: 7.33
PCO2: 55
PO2: 49
Bicarb: 18
Subsequent ABG (after appropriate intervention):
pH: 7.38
PCO2: 45
PO2: 70
Bicarb: 19
Other labs:
CBC: 12.5/15.2/45.8/185
CMP: 130/4.0/117/18/24/1.2/190
CK: wnl
Trop: wnl
d-dimer: wnl
BNP: wnl
Formative Assessment for Simulation Training (FAST)—COPD Exacerbation
Formative Assessment for Simulation Training (FAST)—COPD Exacerbation
Formative Assessment for Simulation Training (FAST)—COPD Exacerbation