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COPD
Tintinalli Chapter 69
Dr. Batizy
Slides by
David R. Fisher, D.O.
September 20, 2005
1
Epidemiology
• 4th most common killer in US
• 3rd most common cause of hospitalization in the US
• Only leading cause of death increasing in prevalence
• 10% prevalence in 55-85 yrs
• Rare < 40 years old
2
Epidemiology
• Men > Women
– Prevalence in women doubled in the past few decades
• Increased female smoking
• Prevalence highest in countries with most cigarette use
• Mortality of hospitalized is 5-14%
– ICU mortality is 24%
– If age > 65, one year mortality post ICU discharge is 59%
3
COPD
• Consider diagnosis if:
– Chronic cough
– Sputum production
– Dyspnea
– Exposure to risk factors for disease
4
COPD
• 85% with chronic bronchitis primary
– Defined in clinical terms
– Productive cough for 3 months in 2 successive years
• Other causes of cough have been ruled out
• 15% with emphysema primary
– Defined by anatomic pathology
– Abnormal permanent enlargement of air spaces distal
to terminal bronchioles
• Accompanied by destruction of walls without obvious
fibrosis 5
Risk factors
• Smoking
– 80-90% of those with COPD are smokers
– 15% of smokers develop clinically significant COPD
– Mortality increased
• Early starting age
• Total pack-years
• Current smoking status
• Other
– Respiratory infections
– Occupational exposures
– Ambient air pollution
– Passive smoke exposure
– α1-antitrypsin deficiency (1% of patients with COPD)
– Diet
6
Pathophysiology
• Insidious onset
– Early changes imperceptible clinically
• Small increase in peripheral airway resistance or lung compliance
• Dyspnea and hypersecretion often requires decades of disease
• Sedentary lifestyle prevents unmasking exertional dyspnea
• May attribute symptoms to aging, poor conditioning, obesity or allergies
– Early abstinence of smoking from onset of disease:
• May eliminate symptoms and result in physiologic improvement
• Once disease established, abnormalities may persist and progress
despite cessation
7
Pathophysiology
• Impedance to expiratory airflow
– Increased resistance or decreased caliber
• Throughout the small bronchi and bronchioles
– Airway inflammation
• Occurs in bronchioles and lung parenchyma
– Airflow obstruction
• Airway secretions
• Mucosal edema
• Bronchospasm and bronchoconstriction from impaired elasticity
– Exaggerated airway resistance
• Reduced total minute ventilation and increased respiratory work
• Alveolar hypoventilation results in hypoxemia and hypercarbia
8
Emphysema Pathophysiology
V/Q mismatch
– Destruction of alveolar architecture + vascular destruction
• Reduced matched alveolar and capillary surface area for diffusion of gas
• Resultant unmatched regions where ventilation is wasted
• Hypoxemia results
Aberrant neurochemical and proprioceptive ventilatory
responses in chronic airflow obstruction
– Ventilatory response to hypercarbia may be blunted during sleep
– Ventilatory drive and dyspnea exaggerated despite normal
pulmonary inflation
9
Emphysema Pathophysiology
• Pulmonary arterial hypertension supervenes as
chronic airflow obstruction progresses
– Right ventricle hypertrophies and later dilates with the
evolution of overt cor pulmonale
– Low-output state of pulmonary circulation translates into low
left ventricular output
– Arterial hypoxemia increases as effects of right-to-left shunt
of poorly oxygenated mixed venous blood are exaggerated
– Right ventricular pressure overload associated with atrial
and ventricular arrhythmias 10
Clinical Findings of Chronic Compensated COPD
• Hallmark symptoms: exertional dyspnea and cough
• Chronic productive cough
• Minor hemoptysis frequent
• Clinical findings
– Tachypnea
– Accessory respiratory muscle use
– Pursed-lip exhalation
• Expiratory wheezing 11
Clinical Findings of Chronic Compensated COPD
• Prolonged expiratory time
• Coarse crackles
– Uncleared secretions move about the central airways in dominantly
bronchitic disease
• Emphysematous disease
– Expansion of the thorax
– Impeded diaphragmatic motion
– Global diminution of breath sounds
• Weight loss frequent
– Poor dietary intake and excessive caloric expenditure for the work of
12
breathing
Clinical Findings of Chronic Compensated COPD
• Plethora due to secondary polycythemia
• Hypercarbia in advanced disease
– Cyanosis
– Tremor
– Somnolence
– Confusion
• Findings of secondary pulmonary hypertension with or without
cor pulmonale may be present
• Physical signs of ventricular dysfunction
– Often disguised or underestimated
• Seemingly more overwhelming signs of respiratory disease
• Pulmonary hyperinflation prohibits adequate auscultation 13
Diagnosis of Chronic Compensated COPD
• Examination of:
– Lung mechanics
– ABGs
– Evaluation of ventilatory response patterns
– Tests of respiratory muscle performance
– Metabolic assessment
– Non-invasive survey of hemodynamic reserve
• Most valuable tools for determining disease severity are PFTs
– Ratio of FEV1 to FVC used to diagnose mild COPD
• FEV1 < 80% predicted + FEV1/FVC <70%
• Once disease progresses, percentage of predicted FEV1 is better measure of
disease severity
14
Diagnosis of Chronic Compensated COPD
• ABGs
– Early stages of COPD:
• Mild to moderate hypoxemia
• No evidence of hypercapnia
– As disease progresses:
• Hypoxemia becomes more severe
• Hypercapnia becomes more evident
– Worse during:
• Exacerbations
• Exercise
• Sleep
15
Diagnosis of Chronic Compensated COPD
Radiographs
– Often misleading
– Mild chronic airflow obstruction not likely to be radiographically
apparent
– Right or left ventricular enlargement may not produce relative
enlargement of the cardiac silhouette
– Radiographs are valuable for complications such as
pneumothorax, pneumonia, pleural effusion and pulmonary
neoplasia
16
Diagnosis of Chronic Compensated COPD
• Radiographs
– Bronchitic disease
• Associated with subtle or absent x-ray findings
– Emphysematous disease
• Associated with remarkable signs of hyperaeration:
– Increased AP diameter
– Flattened diaphragms
– Increased parenchymal lucency
– Attenuation of pulmonary arterial vascular shadows despite only
mild-to-moderate physiologic alterations
17
Treatment of Chronic Compensated COPD
• Healthy lifestyle
– Regular exercise
– Weight control
– Smoking cessation
• Only therapeutic intervention that can reduce the accelerated decline
in lung function
• Reduces COPD mortality along with long-term oxygen therapy
– Pulmonary rehab can improve exercise capacity and quality
of life
• Recommended in moderate to severe COPD
18
– Pneumococcal vaccine recommended
Treatment of Chronic Compensated COPD
• Oxygen
– Primary goal of long-term oxygen therapy:
• Increase baseline PaO2 to 60 mm Hg or SaO2 to 90% at rest
– Use has been demonstrated to reduce mortality
– Start with patients with:
• ABG showing PaO2 of 55 mm Hg
• SaO2 below 88%
• PaO2 of 56-59 mm Hg with signs of:
– Pulmonary hypertension
– Cor pulmonale
– Polycythemia
– Home oxygenation 30% of all COPD related costs in US19
Treatment of Chronic Compensated COPD
• Pharmacotherapy
– No evidence it alters progression of COPD
– Does provide:
• Symptom relief
• Control of exacerbations
• Improved quality of life
• Improved exercise performance
– Inhaled bronchodilators used:
• PRN for mild to moderately obstructed patients with intermittent
symptoms
• On a regular basis to prevent or decrease symptoms
20
Treatment of Chronic Compensated COPD
• β2-agonists
– Relax smooth muscle
– Stimulates β2 -adrenergic receptors
– Long-acting β2 –agonists
• Salmeterol or formoterol
• May improve overall symptoms and health status
– Short-acting β2 –agonists
• May improve exercise capacity
• Less convenient to use
21
Treatment of Chronic Compensated COPD
• Anticholinergics
– Facilitate bronchodilation
• Block acetylcholine on muscarinic-3 receptors
– Ipratropium bromide
• Drug of choice:
– Patients with persistent symptoms
» Refractory to β2-adrenergic agents
» Bothered by side effects of β2-adrenergic agents
– Regular use of inhaled ipratropium has been shown to
improve health status
22
Treatment of Chronic Compensated COPD
• Combination of β2 -agonists with ipratropium
may improve bronchodilation more than either
drug alone
• If symptoms increasing with optimization of the
above drugs, theophylline may be helpful
23
Treatment of Chronic Compensated COPD
• Systemic corticosteroids
– Evidence lacking for long-term use for all patients with COPD
– 20-30% of patients with COPD improve when given chronic
oral steroids
• Inhaled corticosteroids
– Indicated only if:
• Documented spirometric response to inhaled corticosteroids
• If FEV1 is <50%
• Those with predicted and recurrent exacerbations requiring antibiotic
treatment or systemic corticosteroids
24
Treatment of Chronic Compensated COPD
• Mobilization of Secretions
– Generous oral fluid intake
– Atmospheric humidification
– Avoidance of antihistamine and decongestant agents
– Limitation of antitussives helps mobilize respiratory
secretions
– Effect of expectorants questionable 25
Acute Exacerbations of COPD
• Decompensation usually due to worsening of airflow obstruction from:
– Superimposed respiratory infection
– Increased bronchospasm
– Respiratory pathology
• Pulmonary embolism
• Interference with respiratory drive
• Cardiovascular deterioration
• Smoking
• Non-compliance with medications
• Noxious environmental exposures
• Uses of medications that prevent bronchorrhea
• Adverse response to medication
– Disordered ventilatory drive
• Misuse of oxygen therapy, hypnotics or tranquilizers
• Metabolic disturbances and inadequate oxygen delivery independent of respiratory
function may cause decompensated COPD
26
Acute Exacerbations of COPD
• Frequently result in progressive hypoxemia
– Signs
• Tachypnea
• Tachycardia
• Systemic hypertension
• Cyanosis
• Change in mental status
– Most life threatening complication is hypoxemia
• Arterial saturation less than 90%
• Increased work of breathing increases muscle production of CO2
• Alveolar ventilation is often unable to increase to prevent CO2 retention
and respiratory acidosis
• Signs of hypercapnea include mental status changes and hypopnea
27
Acute Exacerbations of COPD
• Primary complaints dyspnea and orthopnea
• Intensified effort to ventilate is further dramatized by:
– Sitting-up-and-forward position
– Pursed-lip exhalation
– Accessory muscle use
– Diaphoresis
• Pulsus paradoxus may be noted during blood pressure
recording
28
Acute Exacerbations of COPD
• Complications may be neglected or minimized by the patient’s
clinical distress:
– Pneumonia
– Pneumothorax
– Pulmonary embolism
– Acute abdomen
• Differential diagnosis:
– Asthma
– CHF
– Pneumonia
– PE
– TB
– Metabolic disturbances 29
Diagnosis of Acute Exacerbations of COPD
• Medical history
• COPD history
• Assessment of oxygenation
• Physical examination
• Bedside PFTs if available
• Assessment of sputum
• Chest X-ray
30
Diagnosis of Acute Exacerbations of COPD
• Oxygenation
– Pulse oximetry may identify hypoxemia
• Cannot identify hypercapnia or acid-base disturbances
– No correlation between FEV1 and oxygenation
– PaO2 of less than 60 mm Hg or SaO2 of less than 90 % in
room air indicates respiratory failure
– Hypercapnia or pH of less than 7.30
• Likely experiencing a life-threatening episode of ventilatory failure
• Need intensive management in the ED and ICU
31
Diagnosis of Acute Exacerbations of COPD
• Bedside PFTs
– May provide rapid objective assessment of therapy
– Patient cooperation is essential
• Patients commonly too dyspneic to do
– Not recommended during an acute exacerbation
– If able to cooperate:
• Peak expiratory flow rate less than 100 L/minute or FEV1 less than
1.00 L in a patient without chronic severe obstruction indicates a
severe exacerbation 32
Diagnosis of Acute Exacerbations of COPD
• Bedside PFTs
– Sequential measurements can be very helpful in
determining response to therapy
– Signs on physical examination and physician
estimates of pulmonary function are inaccurate
– Measurement of FEV1 is preferred to PEFR
• Allows comparison with baseline studies and published
guidelines
33
Diagnosis of Acute Exacerbations of COPD
• Assessment of sputum
– Changes in volume and color
• Especially increase in purulence
• Suggests a bacterial etiology for the exacerbation
• Indicates need for antibiotics
34
Diagnosis of Acute Exacerbations of COPD
• Radiographic abnormalities common in COPD
exacerbations
– May elucidate underlying etiology of exacerbation
• Pneumonia
– May identify an alternative diagnosis such as CHF
35
Diagnosis of Acute Exacerbations of COPD
• ECGs
– May reveal concurrent disease processes:
• Ischemia
• MI
• Cor pulmonale
• Arrhythmias such as MAT
• Theophylline level if taking
• Other
– Order based on clinical picture
• CBC, lytes, βNP, CTA chest, D-dimer
36
Treatment of Acute Exacerbations of COPD
• Goals of treatment
– Correct tissue oxygenation
– Alleviate reversible bronchospasm
– Treat underlying etiology of exacerbation
• Factors influencing therapy
– Patient’s mental status
– Degree of reversible bronchospasm
– Recent medication usage and evidence of potential toxicity
– Prior history of exacerbation courses, hospitalizations and intubation
– Presence of contraindications to any drug or class of drugs
– Specific causes or complications related to the exacerbation
37
Treatment of Acute Exacerbations of COPD
• Oxygen
– First goal is to alleviate hypoxemia with desired
PaO2 greater than 60 mm Hg or SaO2 of > 90 %
– May be accomplished by:
• Nasal canula
• Simple face mask
• Venturi mask
• Non-rebreather mask with reservoir and one-way valve
38
Treatment of Acute Exacerbations of COPD
• Oxygen
– Need to increase PaO2 must be balanced against the
possibility of producing hypercapnia
• Monitoring of oxygenation and CO2 levels with ABGs is imperative
– Improvement after administration of supplemental oxygen
may take 20-30 minutes to achieve a steady state
– If adequate oxygenation is not achieved or respiratory
acidosis ensues, assisted ventilation may be required
39
Treatment of Acute Exacerbations of COPD
• β2-Adrenergic agonists
– First line agent in management of acute, severe COPD
– Aerosolized forms preferred due to minimized systemic
toxicity
– May give q 30-60 minutes prn as tolerated
– Side effects include tremors, anxiety and palpitations
– Should have monitor if suspected or known heart disease
40
Treatment of Acute Exacerbations of COPD
• Anticholinergics
– First line COPD therapy
– Ipratropium and glycopyrrolate
– Similar short term improvements in airflow obstruction as β2-
agonists
– Repeat dose timing not well studied
– Side effects minimal but include dry mouth and metallic taste
– Efficacy of combination with β2-agonists evidence conflicting
41
Treatment of Acute Exacerbations of COPD
• Corticosteroids
– Short course of 7-14 days of systemic steroids
improves FEV1 in acute exacerbations of COPD
– Optimal effective dose is 1-3 times the maximal
physiologic adrenal secretion rate
• Equivalent to 60-180 mg prednisone daily
– Hyperglycemia is the most common adverse effect
42
Treatment of Acute Exacerbations of COPD
• Antibiotics
– All guidelines recommend concurrent antibiotic treatment in
COPD exacerbations if evidence of infection
– Studies show small benefit in resolution of obstruction and
symptoms
– Benefits more apparent in severe exacerbations
– Direct antibiotic choices at S. pneumoniae, H. influenzae
and M. catarrhalis
– Little evidence regarding duration of treatment but 3-14 days
43
typical in studies
Treatment of Acute Exacerbations of COPD
• Methylxanthines
– Role of theophylline and aminophylline controversial
– Routine use not supported unless little relief with other
medications or in those already using with sub-therapeutic
levels
– Formulas for loading doses and IV maintenance dose
infusions
44
Indications for Invasive Mechanical Ventilation
• Severe dyspnea with:
– Use of accessory muscles
– Paradoxical abdominal motion
• Respiratory frequency > 35 bpm
• Life-threatening hypoxemia:
– PaO2 < 50 mm Hg or PaO2/FIO2 <200 mm Hg
• Severe acidosis (ph<7.25) and hypercapnia (PaCO2 >
60 mm Hg) 45
Indications for Invasive Mechanical Ventilation
• Respiratory arrest
• Somnolence, impaired mental status
• Cardiovascular complications
– Hypotension
– Shock
– Heart failure
• Noninvasive positive pressure ventilation failure 46
Treatment of Acute Exacerbations of COPD
• Assisted ventilation
– Main goals to rest ventilatory muscles and to
restore gas exchange to a stable baseline
– Noninvasive positive pressure ventilation can be
delivered via a nasal mask, full face mask or
mouthpiece
– No mode has been shown to be superior 47
Treatment of Acute Exacerbations of COPD
• Assisted ventilation
– Patients who receive noninvasive positive pressure
ventilation have better outcomes:
• Intubation rates
• Short-term mortality rates
• Symptomatic improvement
• Length of hospitalization in patients with respiratory failure
– Disadvantages
• Slower correction of gas-exchange abnormalities
• Risk of aspiration
• Inability to control airway secretions directly
• Possible complications of gastric distension and skin necrosis
48
Treatment of Acute Exacerbations of COPD
• Assisted ventilation
– Contraindications
• Uncooperative or obtunded patient
• Inability of patient to clear airway secretions
• Hemodynamic instability
• Respiratory arrest
• Recent facial or gastroesophageal surgery
• Burns
• Poor mask fit
• Extreme obesity
49
Treatment of Acute Exacerbations of COPD
• Assisted ventilation
– Invasive ventilation should be considered in
patients with ventilatory or respiratory failure who
do not qualify for noninvasive positive pressure
ventilation
– Adverse events include pneumonia, barotrauma
and failure to wean
50
Treatment of Acute Exacerbations of COPD
• Other Options
– Little evidence to support use of mixture of helium
and oxygen or magnesium in the treatment of acute
COPD exacerbation
– Factors underlying the exacerbation, comorbidities
and other etiologies of dyspnea should be identified
and treated
51
ED Management of Exacerbations of COPD
• Assess severity of symptoms
– Administer controlled oxygen therapy
– Perform ABG measurement after 20-30 minutes if SaO2
remains < 90 % or if concerned about symptomatic
hypercapnia
• Administer bronchodilators
– β2-agonists and/or anticholinergic agents by nebulization or
MDI with spacer
• Consider adding IV methylxanthine if needed 52
ED Management of Exacerbations of COPD
• Add corticosteroids
– Oral or IV
• Consider antibiotics
– Increased sputum volume
– Change in sputum color
– Fever
– Suspicion of infectious etiology of exacerbation
• Consider noninvasive mechanical ventilation53
ED Management of Exacerbations of COPD
• Laboratory evaluation
– CXR
– CBC with differential
– Electrolytes
– ABG
– ECG
• At all times:
– Monitor fluid balance
– Consider subcutaneous heparin (DVT prophylaxis)
– Identify and treat associated conditions (CHF, arrhythmias)
– Closely monitor condition of the patient
54
Hospitalize for Acute Exacerbation of COPD
• Marked increase in intensity of symptoms such as
sudden development of resting dyspnea
• Severe background of COPD
• Onset of new physical signs
– Cyanosis, peripheral edema
• Failure of exacerbation to respond to initial medical
management
55
Hospitalize for Acute Exacerbation of COPD
• Significant comorbidities
• Newly occurring arrhythmias
• Diagnostic uncertainty
• Older age
• Insufficient home support
56
If stable to be discharged home:
• Arrange adequate supply of home oxygen if
needed
• Arrange adequate and appropriate
bronchodilator treatment
• Consider short course of oral corticosteroids
• Arrange for follow-up with their PCP 57
True/False Questions:
• 1. Chronic bronchitis is defined in clinical terms wheras emphysema is
defined by anatomic pathology.
• 2. Patients who receive noninvasive positive pressure ventilation have better
outcomes in terms of future intubation rate, short-term mortality rate, symptomatic
improvement and length of hospitalization in patients with respiratory failure.
• 3. Radiographic findings of patients with emphysematous disease are
associated with remarkable signs of hyperaeration including increased AP
diameter, flattened diaphragms and increased parenchymal lucency.
• 4. Complications that may be neglected or minimized in examining a patient
with COPD include pneumonia, pneumothorax, pulmonary embolism and
acute abdomen.
• 5. Risk factors for COPD include smoking, respiratory infections,
occupational exposures, ambient air pollution, passive smoke exposure
and α1-antitrypsin deficiency.
58
• The squiggly line
• Totally disorganized depolarization and contraction of ventricular myocardium
• No effective ventricular activity
• Absence of QRS complexes and P waves
•
•
•
May have coarse vs. fine VFib
Clinically associated with absent pulse and blood pressure
Etiology
V-Fib
– CAD
– More common than Vtach in hypothermia
59
• Three or more consecutive PVCs
• Wide bizarre appearing QRS Complex (0.12 s or greater)
• Most common rate 150-200
• Usually regular, may be slightly irregular
•
•
•
Fusion beats may be present, representing a combination of normally conducted sinus beats and ventricular ectopic
beats
VT may occur in paroxysms or sustained
Etiology
V-Tach
– Rare in patients without underlying heart disease
– Most common causes are ischemic heart disease, especially post MI
– Cardiomyopathy, MVP, drug toxicity, electrolyte imbalance and sympathomimetics are other causes
60
