COPD Tintinalli Chapter 69

1
COPDTintinalli Chapter 69

• Dr. Batizy
• Slides by
• David R. Fisher, D.O.
• September 20, 2005

2
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 lt 40 years old

3
Epidemiology

• Men gt 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 gt 65, one year mortality post ICU
  discharge is 59

4
COPD

• Consider diagnosis if
• Chronic cough
• Sputum production
• Dyspnea
• Exposure to risk factors for disease

5
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

6
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
• a1-antitrypsin deficiency (1 of patients with
  COPD)
• Diet

7
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

8
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

9
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

10
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

11
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

12
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 breathing

13
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

14
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 lt 80 predicted FEV1/FVC lt70
• Once disease progresses, percentage of predicted
  FEV1 is better measure of disease severity

15
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

16
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

17
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

18
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
• Pneumococcal vaccine recommended

19
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
  US

20
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

21
Treatment of Chronic Compensated COPD

• ß2-agonists
• Relax smooth muscle
• Stimulates ß2 -adrenergic receptors
• Long-acting ß2 agonists
• Salmeterol or formoterol
• May improve overall symptoms and health status
• Short-acting ß2 agonists
• May improve exercise capacity
• Less convenient to use

22
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 ß2-adrenergic agents
• Bothered by side effects of ß2-adrenergic agents
• Regular use of inhaled ipratropium has been shown
  to improve health status

23
Treatment of Chronic Compensated COPD

• Combination of ß2 -agonists with ipratropium may
  improve bronchodilation more than either drug
  alone
• If symptoms increasing with optimization of the
  above drugs, theophylline may be helpful

24
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 lt50
• Those with predicted and recurrent exacerbations
  requiring antibiotic treatment or systemic
  corticosteroids

25
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

26
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

27
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

28
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

29
Acute Exacerbations of COPD

• Complications may be neglected or minimized by
  the patients clinical distress
• Pneumonia
• Pneumothorax
• Pulmonary embolism
• Acute abdomen
• Differential diagnosis
• Asthma
• CHF
• Pneumonia
• PE
• TB
• Metabolic disturbances

30
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

31
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

32
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

33
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

34
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

35
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

36
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, ßNP, CTA chest, D-dimer

37
Treatment of Acute Exacerbations of COPD

• Goals of treatment
• Correct tissue oxygenation
• Alleviate reversible bronchospasm
• Treat underlying etiology of exacerbation
• Factors influencing therapy
• Patients 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

38
Treatment of Acute Exacerbations of COPD

• Oxygen
• First goal is to alleviate hypoxemia with desired
  PaO2 greater than 60 mm Hg or SaO2 of gt 90
• May be accomplished by
• Nasal canula
• Simple face mask
• Venturi mask
• Non-rebreather mask with reservoir and one-way
  valve

39
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

40
Treatment of Acute Exacerbations of COPD

• ß2-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

41
Treatment of Acute Exacerbations of COPD

• Anticholinergics
• First line COPD therapy
• Ipratropium and glycopyrrolate
• Similar short term improvements in airflow
  obstruction as ß2-agonists
• Repeat dose timing not well studied
• Side effects minimal but include dry mouth and
  metallic taste
• Efficacy of combination with ß2-agonists evidence
  conflicting

42
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

43
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 typical in studies

44
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

45
Indications for Invasive Mechanical Ventilation

• Severe dyspnea with
• Use of accessory muscles
• Paradoxical abdominal motion
• Respiratory frequency gt 35 bpm
• Life-threatening hypoxemia
• PaO2 lt 50 mm Hg or PaO2/FIO2 lt200 mm Hg
• Severe acidosis (phlt7.25) and hypercapnia (PaCO2
  gt 60 mm Hg)

46
Indications for Invasive Mechanical Ventilation

• Respiratory arrest
• Somnolence, impaired mental status
• Cardiovascular complications
• Hypotension
• Shock
• Heart failure
• Noninvasive positive pressure ventilation failure

47
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

48
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

49
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

50
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

51
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

52
ED Management of Exacerbations of COPD

• Assess severity of symptoms
• Administer controlled oxygen therapy
• Perform ABG measurement after 20-30 minutes if
  SaO2 remains lt 90 or if concerned about
  symptomatic hypercapnia
• Administer bronchodilators
• ß2-agonists and/or anticholinergic agents by
  nebulization or MDI with spacer
• Consider adding IV methylxanthine if needed

53
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 ventilation

54
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

55
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

56
Hospitalize for Acute Exacerbation of COPD

• Significant comorbidities
• Newly occurring arrhythmias
• Diagnostic uncertainty
• Older age
• Insufficient home support

57
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

58
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 a1-antitrypsin deficiency.

59
V-Fib

• 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
• CAD
• More common than Vtach in hypothermia

60
V-Tach

• 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
• 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