COPD Tintinalli Chapter 69

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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




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