69 Chronic Obstructive Pulmonary Disease Rosens Emergency Medicine Fifth Edition

1
69 Chronic Obstructive Pulmonary DiseaseRosens
Emergency Medicine Fifth Edition

• ??? ??? ??
• ??? ??? ??

2
PERSPECTIVE

• COPD afflict more than one forth of all adults
  and are the forth leading cause of death overall
• COPD refers to a triad of distinct disease
  processes that, as a rule, coexist
  asthma(airway reaction), emphysema(airway
  collapse) and bronchitis(airway inflammation)

3
PRINCIPLES OF DISEASEThree-Component Division
and Synthesis
4
Permutation of combinations of bronchitis (B),
asthma (A), and emphysema (E).
5
PRINCIPLES OF DISEASEPathophysiology

• Asthma
• Bronchocontriction
• Usually suspected and diagnosed
• Directly and quickly respond to drug therapy
• Mucus plugging
• In small bronchi and bronchioles is the steady
  component
• The pathology found consistently in patients
  dying of asthma

6
PRINCIPLES OF DISEASEPathophysiology-emphysema

• Emphysema
• Gradual destruction of alveolar septi and
  obliteration of the pulmonary capillary bed
• Elastase-antielastase hypothesis
• elastase is elaborated by PMN and abundant in
  chronic smoker
• Ventilatory drive increase and maintain a near
  normal PO2
• Hypoxia-induced pulmonary hypertension (-) and
  cor pulmonale (-) but a syndrome of pulmonary
  cachexia ()

7
PRINCIPLES OF DISEASEPathophysiology

• Bronchitis
• Affect both small and large bronchi and pulmonary
  capillary bed is relatively undamaged
• Most bronchitis are viral origin
• bacteria including pneumococcus, H.Influenzae,
  Moraxella catarrhalis, and Neisseria species
  probably contribute further inflammatory change.
• ABGs reveal hypoxia and hypercapnia
• fails to increase minute volume,and the chronic
  hypoxia leads to pulmonary hypertension with cor
  pulmonale and polycythemia

8
(No Transcript)
9
PRINCIPLES OF DISEASECritical Episodes

• Disease-Related Factors - Acute
• Pneumothorax
• Most common and most treatable Chest pain(-) in
  elders
• A small pneumothorax cant be R/O by PE and is
  easily missed on inspiratory CXR.
• Large pulmonary embolism
• Suspected with chronic bronchitis who
  deteriorates quickly with no other apparent cause
• Lobar atelectasis
• Secretions,dehydration, impaired cough,
  quadriplegia, polio. or other NM disorder impair
  diaphragmatic motion
• A deviated trachea, unilateral decreased lung
  expansion, and decreased breath sounds

10
PRINCIPLES OF DISEASECritical Episodes

• Disease-Related Factors Subacute
• Acute bronchitis(allergic or infective)
• The most common aggravating cause
• Episodic cough and expectoration with ordinary
  fever(-) and leukocytosis(-)
• Pneumonia(cause death in many patients)
• Cough , fever, leukocytosis and toxicity are less
  seen with more nonspecific and subtle symptoms
• Infiltrate may or may not be seen
• Small pulmonary emboli
• Worsening dyspnea, coexisting decrement in PCO2
  and PO2
• Helical CT and identification of DVT by Doppler US

11
PRINCIPLES OF DISEASECritical Episodes

• Disease-Related Factors Subacute
• Pulmonary compression(e.g., obesity, ascites.
  Gastric distention, pleural effusion)
• Segmental atelectasis
• CXR show linear horizontal streaking or small
  flarelike shadows or normal
• Hypoxemic reactive patients with a protracted
  wheezing course unresponsive to bronchodilators
• Trauma(e.g., rib fractures, pulmonary contusion)
• Neuromuscular and metabolic diseases
• K ?, Mg ?, Ca ? and P ? Paraplegia, polio and MG
• Neomycin kanamycin interfere with motor
  end-plate function

12
PRINCIPLES OF DISEASECritical Episodes

• Disease-Related Factors Chronic
• Cigarettes, air pollutants, childhood respiratory
  illness, ?-antitrypsin deficiency
• Unrelated treatable chronic pulmonary disease
  (brochiectasis, TB, sarcoidosis)
• Subacute LV failure produce cardiac asthma

13
PRINCIPLES OF DISEASECritical Episodes

• Patient-Related Factors
• Noxious habits
• Noncompliance

14
PRINCIPLES OF DISEASECritical Episodes

• Physician-Related Factors
• Insufficient therapy
• Do not understand the proper usage of MDI
• Inappropriate therapy(e.g.,deleterious drugs)
• Produce bronchospasm (aspirin, propranolol,
  reserpine, cholinergics, opiates, and all drug
  with prostaglandin-1 inhibiting action)
• sedatives

15
CLINICAL FEATURESAsthma(Reactive Airways Disease)

• Wheezing is classic sign of asthma, but cough,
  dyspnea or chest pain may be predominant.
• Wheezing with rapid onset, high pitched, and
  relieved by bronchodilators(gt25 ?FEV1) is due to
  bronchospasm
• Clinical deterioration occurs over days and when
  wheezing is unrelieved by broncho-dilators ?
  consider mucus plugging
• Clouding of consciousness suggest carbon dioxide
  narcosis and impending respiratory failure

16
CLINICAL FEATURESAsthma(Reactive Airways Disease)

• The number of words expressible at one time is an
  excellent measurement of FEV1
• Higher pitched wheezes is severe than the lower
• A silent chest suggest little air exchange and is
  ominous
• Diaphoresis, visible retractions, and accessory
  muscle use should concern the EP, if persistent
• The degree of tachycardia can be a useful
  parameter but may be related to ?-agonist
  therapy.

17
(No Transcript)
18
CLINICAL FEATURESEmphysema(Airways Collapse)

• Typically thin, anxious, alert and oriented,
  dyspneic and tachypneic dyspnea is the hallmark
• Purse lips on expiration(puffing)
• A sedentary existence, chronically hunched
  forward and supporting the torso with elbows on
  knees produces a tanning and induration of the
  skin just proximal to the knees

19
CLINICAL FEATURESEmphysema(Airways Collapse)

• CXR show lung overinflation, low immobile
  diaphragms and ? AP diameter with a large
  retrosternal airspace
• PE hyperresonance, ?BS with faint
  end-expiratory rhonchi
• Despite air hunger, the patient has good color
  (pink) and near normal ABG levels
• The heart is small and hypodynamic , the BP low

20
(No Transcript)
21
CLINICAL FEATURESChronic Bronchitis(Airway
Inflammation and Secretions)

• Cough is the hallmark
• Acute ventilatory failure with irritable
  somnolence and asterixis ()
• Chronic ventilatory failure and cor pulmonale
  account for the peripheral edema, anasarca, and
  chronic external jugular distention
• Severe secretions is evidenced by scattered
  rhonchi and rales
• Chronic visceral congestion causes hepatomegaly,
  hepatojugular reflex may lead digestive
  disturbance

22
CLINICAL FEATURESChronic Bronchitis(Airway
Inflammation and Secretions)

• Cardiac examination
• Subxiphoid or retrosternal heave signifies
  chronic RVH
• S4 suggests decreased LV compliance
• S3 indicates LV failure
• Holosystolic blowing murmur of TR is secondary to
  RV and tricuspid ring dilation
• CXR
• Normal lung volume, hyperaeration of ULF, coarse
  reticulation of LLF, slightly enlarged globular
  cardiac silhouette with pleural effusion
  impingement on the retrosternal airspace by RV on
  lateral view

23
(No Transcript)
24
DIAGNOSTIC STRATEGIESPulse Oximetry and ABG
Analysis

• Pulse oximetry is a fifth vital sign
• Hypoxia when Sat lt 95 in many COPD patients Sat
  lt 90 indicate severe hypoxia
• The change from baseline or in response to
  therapy is more important than absolute levels
• ABG is more reliable than FEV1
• pH and Pco2 can be helpful when correlated to
  known baseline levels
• immediate airway and ventilatory management
  depends on clinical findings in conjunction with
  pulse oximetry

25
DIAGNOSTIC STRATEGIESChest Radiography

• Routine CXR, though challenged,is appropriate in
  patients with acute exacerbations of COPD

26
DIAGNOSTIC STRATEGIESForced Expiratory Volume
and Peak Expiratory Flow Rate

• PFTs are more useful in asthma
• PFTs add little to decision making and correlate
  poorly to ABGs
• A FEV1 of greater than 40 of predicted may
  identify patents for discharge

27
DIAGNOSTIC STRATEGIESSputum Examination

• Gram stain correlates poorly with cultures
• Sputum culture is more appropriate when patient
  is acutely ill, has infiltrate, and is being
  admitted.
• Sputum evaluation is diagnostic for TB,
  Legionella, fugal, and PCP.

28
DIAGNOSTIC STRATEGIESElectrocardiogram (ECG)

• RVH?cor pulmonale but unable DD from BVH
• P pulmonale ?COPD but may due to acute increases
  in RA pressure
• Low QRS voltage, clockwise rotation, and poor R
  wave progression
• Continuous ECG monitoring is helpful for
  detection of dysrhythmias associated with COPD
  exacerbations and should be used in moderate to
  severe AE

29
DIAGNOSTIC STRATEGIESMiscellaneous Blood Tests

• Theophylline level
• theophylline toxicity may be part of
  exacerbation, normal level ? no toxicity
• CBC
• Polycythemia associated with chronic hypoxia
• ? WBC infection or hyperadrenergic state of
  acute dyspnea

30
DIFFERENTIAL CONSIDERATIONS

• Cardiac asthma acute pulmonary edema
• Pulmonary embolism and pneumothorax
• ARDS, pulmonary fibrosis, pulmonary effusions,
  and pneumonia
• Myocardial ischemia and pericardial effusions
• Metabolic acidosis and shock states

31
MANAGEMENT
32
MANAGEMENTVentilation and Oxygenation(1)

• Ventilation setting
• FIO2 100, TV 6-8 ml/kg, RR 8-10, inspiratory
  flow 80-100ml/min with AC mode
• Permissive hypercapnia over many hours for
  gradual normalization of pH and Paco2
• Low volume and rate prevent barotrauma
• F/U ABG 15-20 min later
• Hyperventilation alkalosis result in seizures and
  dysrhythmias, esp. coexisting hypokalemia
• ? iPEEP cause barotrauma ? intrathoracic
  pressure decreases CO ?monitor peak flow pressure
  and systemic BP

33
MANAGEMENTVentilation and Oxygenation(2)

• Nasal CPAP
• 5-10 cm H2O pressure
• BLPAP
• Expiratory positive airway pressure 2-4 cm H2O
• Inspiratory positive airway pressure 8-10 cm H2O

34
MANAGEMENTVentilation and Oxygenation(3)

• An inherent anxiety exist to use oxygen therapy
  because of the fear of apnea by removing the
  hypoxic drive to breath
• Breathing inappropriately slowly who is at
  highest risk of apnea
• Tachypnea suggests the central chemoreceptor are
  receptive to CO2 stimulus and respiratory drive
  will be maintained
• The most important factor in the decision to
  intubate is the patients clinical status

35
MANAGEMENTGeneral Drug Therapy

• ß-Agonists
• The nebulization dose albuterol 2.5- 5.0 mg
• 
  metaproterenol 10-15mg
• Able to tolerate 2 to 3 rapid successive doses of
  oxygen-nebulized ß-agonist
• Need to titrated if tremor, tachycardia, or
  ventricular ectopy are significant
• Terbutaline or epinephrine SC is only indicated
  in extremis
• Minor AE may receive MDI

36
MANAGEMENTGeneral Drug Therapy

• Anticholinergics
• Block muscarinic receptors and prevent smooth
  muscle contraction while ? release of secretion
  from submucosal glands.
• Ipratropium bromide, devoid of systemic effects,
  the nebulization dosage is 0.5mg every 4 hours
• Mild to moderate AE and stable cooperative
  patients can be candidates for MDI with multiple
  puffs initially, F/U 1 puff every minute until
  improvement

37
MANAGEMENTGeneral Drug Therapy

• Corticosteroids
• Decrease the relapse rate of AE and reduce
  treatment failure
• IV methyllprednisolone is prudent whereas a
  2-week oral prednisolone taper for severe
  exacerbations requiring admission
• Significant benefit from long-term inhaled
  corticosteroids.

38
MANAGEMENTGeneral Drug Therapy

• Methylxanthines
• Multiple modes of action bronchodilatation, ?
  dia-phragmatic contractility, stimulation of
  respiratory drive, inotropism, ? mucociliary
  clearance, and synergy with ß2-Agonists and
  Anticholinergics
• 5mg/kg IV over 10 to 15 min then 0.5mg/kg/hr if
  normal liver function
• 1mg/kg IV elevate a 2?g/ml in blood level (await
  blood level results before IV dose when patient
  on oral aminophylline)
• Lower dosing Alcoholism, old age, chronic liver
  disease, CHF, fever,erythromycin. ciprofloxacin
  or H2-blocker

39
MANAGEMENTOther Therapeutic agents
40
MANAGEMENTOther Therapeutic agents

• Mucokinetic Medications
• Nebulized water and saline and oral expectorants
  guaifenesin and saturated iodide are of no
  benefit
• Acetylcysteine cause reflex bronchoconstriction
• Clinical improvement with oral iodinated glycerol
  but can cause thyroid dysfunction
• Simple oral hydration is the easiest and safest
  agent

41
MANAGEMENTOther Therapeutic agents

• Respiratory Stimulants
• Not recommended for routine use in the ED
• Almitrine increase peripheral chemoreceptor
  sensitivity and improves ventilation-perfusion
  matching.

42
DIPOSITION

• Admission guideline
• Significant deviation from baseline
• Coexisting pulmonary infection or other inciting
  factor
• Failed outpatient management
• Lack improvement in the ED
• COPD c AE often need short stay admission
• Attention on
• Vaccination history(influenza and pneumococcal
  vaccines)
• The proper technique of inhaler use
• Evaluation of support systems and appropriate
  referrals
• Smoking cessation

43
KEY CONCEPTS

• COPD with AE has slow recovery periods and
  patient do not usually show dramatic improvement
  after therapy.
• ß-Agonists, anticholinergics, and corticosteroids
  are the mainstay of drug therapy.Theophylline has
  a limited role in management.
• Noninvasive ventilation provide another
  therapeutic option in the COPD patient with
  respiratory failure
• Acute complications are common aggravation
  factors which include pneumonia, pneumothorax,
  and pulmonary embolism.