Adult COPD Flashcards

1
Q

COPD should be suspected in anyone over the age of 40 with….

A
  • smoking history (or ex-smoker)
  • dyspnoea that is progressive, persistent and worse with exercise
  • chronic cough
  • chronic sputum production
  • family history of COPD.
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2
Q

COPD exacerbation S+S

A
  • increased dyspnoea
  • increased cough
  • increased sputum production
  • complete removal of wheeze in these patients may not be possible due to chronic airway disease
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3
Q

Indications for the removal of Bi-PAP or CPAP include:

A
  • Ineffective (cardiac/respiratory arrest, mask intolerance, decreasing respiratory effort, nil improvement after 1 hour of treatment)
  • Deteriorating vital signs
  • Risk to patient (loss of airway control, copious secretions, active vomiting, paramedic judgement of clinical deterioration)
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4
Q

Mgx SD3 Exacerbation of COPD

A

1) R+R
2) Position - Seated/Upright
3) O2 - Nebuliser 8-10L/min initial
4) Salbutamol 10mg NEB
5) Ipratropium Bromide 500mcg NEB
6) IV Access
7) Dexamethasone 8mg IV
8) Sitrep MICA - up/downgrade/cancel
9) O2 Reassess - NP titrate 88-92%
10) Reassess VSS 5/60
11) Extrication - Wheelchair to stretcher
12) Load Signal? MICA?

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5
Q

COPD Differential Diagnosis

A

1) COPD
2) Asthma
3) Anxiety
4) Hyperventilation
5) Chest Infection
6) Pneumonia

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6
Q

Mgx of Deteriorating COPD pt

A

MICA - CPAP/BiPAP
Assisted Ventilations with 100%O2 if inadequate TV or RR
Load Signal 1 to nearest appropriate hospital

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7
Q

Definition of COPD

A

Chronic, progressive, reversible obstructive pulmonary disease characterised by difficult expiration. Three common pulmonary obstructive diseases: asthma, chronic bronchitis, emphysema

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8
Q

Pathophysiology of Chronic Bronchitis

A

Prolonged exposure to irritants

Hyper secretions of thick and sticky mucous due to enlargement of goblet cells and mucous glands

Fibrosis, bronchospasm and oedema with impaired mucocillary function

Increased size and number of mucous glands – susceptible to infections

Bronchial wall thickening – obstruction

Difficulty with expansion

Gas trapping – Co2 retention

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9
Q

Chronic Bronchitis Definition

A
  • Abnormal permanent enlargement of gas exchange in airways due to inflammatory changes and excessive mucous production. Mainly affects the bronchi
  • Characterised by a chronic cough for three consecutive months over the space of two years
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10
Q

Emphysema Definition

A

Lung tissue destruction and abnormal permanent enlargement of gas exchange airways. Mainly affects alveoli

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11
Q

Emphysema Pathophysiology

A

Prolonged exposure to irritants

Toxins cause airway epithelial inflammation and activation of macrophages and neutrophils

Elastin breakdown and loss of elastic recoil

Pulmonary capillary destruction causes V/Q mismatch

Decreased expiratory flow rate and increased WOB

Compensate SOB by hyperventilating

Gas trapping causes resp acidosis

SHOCK, COMA, DEATH

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12
Q

Oxygen Therapy Critical Illnesses

A
  • Cardiac Arrest and/or Resuscitation
  • Major Trauma/Head Injury
  • Shock
  • Severe Sepsis
  • Anaphylaxis
  • Status Epilepticus
  • Ketamine Sedation
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13
Q

Oxygen Therapy Chronic Illnesses

A
  • COPD
  • Neuromuscular Disorders
  • Cystic Fibrosis
  • Bronchiectasis
  • Severe Kyphoscoliosis
  • Obesity
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14
Q

Salbutamol Presentation

A

5 mg in 2.5 mL polyamp
pMDI (100 mcg per actuation)

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15
Q

Salbutamol Pharmacology

A

A synthetic beta adrenergic stimulant with primarily beta 2 effects

Actions: Causes bronchodilatation

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16
Q

Salbutamol Indications

A

Respiratory distress with suspected bronchospasm:
- asthma
- severe allergic reactions
- COPD
- smoke inhalation
- oleoresin capsicum spray exposure

17
Q

Salbutamol Contraindications

A

Nil

18
Q

Salbutamol Precautions

A

Large doses of Salbutamol have been reported to cause intracellular metabolic acidosis

19
Q

Salbutamol Side Effects

A

Sinus tachycardia
Muscle tremor (common)

20
Q

Salbutamol Onset/Peak/Duration Times

A

Onset: 5 – 15 minutes
Peak: n/a
Duration: 15 – 50 minutes

21
Q

Ipratropium Bromide Presentation

A

250 mcg in 1 mL nebule or polyamp

22
Q

Ipratropium Bromide Pharmacology

A

Anticholinergic bronchodilator

Actions: Allows bronchodilatation by inhibiting cholinergic bronchomotor tone (i.e. blocks vagal reflexes which mediate bronchoconstriction)

23
Q

Ipratropium Bromide Indications

A
  1. Severe respiratory distress associated with bronchospasm
  2. Exacerbation of COPD irrespective of severity
24
Q

Ipratropium Bromide Contraindications

A

Known hypersensitivity to Atropine or its derivatives

25
Q

Ipratropium Bromide Precautions

A
  1. Glaucoma
  2. Avoid contact with eyes
26
Q

Ipratropium Bromide Side Effects

A

Headache
Nausea
Dry mouth
Skin rash
Tachycardia (rare)
Palpitations (rare)
Acute angle closure glaucoma secondary to direct eye contact (rare)

27
Q

Ipratropium Bromide Onset/Duration/Peak times

A

Onset: 3 - 5 minutes
Peak: 1.5 - 2 hours
Duration: 6 hours

28
Q

Difference between Salbutamol and Ipratropium Bromide?

A

Salbutamol is a synthetic beta adrenergic stimulant with primarily beta 2 effects which causes bronchodilatation

Ipratropium Bromide is an anticholinergic bronchodilator which promotes bronchodilatation by inhibiting cholinergic bronchomotor tone (i.e.
blocks vagal reflexes which mediate bronchoconstriction)

29
Q

Why do Emphysema patients become hypoxic?

A
  • Emphysema is caused by the destruction of alveoli and small bronchioles in the lung
  • Gas exchange is inhibited as a result
  • CO2 builds up in the blood stream resulting in hypoxia
30
Q

Why are there no repeat doses of nebulised medications in the AV COPD guideline?

A
  • COPD is an irreversible condition which is the result of destruction of the alveoli
  • Nebulised medications aim to reduce smooth muscle constriction which is not the
    primary problem of this disease state unlike asthma
  • Therefore giving high doses of bronchodilators in short periods of time is not beneficial
31
Q

Name two signs/symptoms that would lead you to suspect COPD in an adult > 40 years of age?

A
  • Smoking history (or ex-smoker)
  • Dyspnoea that is progressive, persistent and worse with exercise
  • Chronic cough
  • Chronic sputum production
  • Family history of COPD