COPD Flashcards

1
Q

The mechanisms by which excess oxygen administration causes hypercarbia are controversial and complex. they include

A

ū Reversal of hypoxic pulmonary vasoconstriction, causing high levels of CO2 in poorly ventilated alveoli to diffuse back into the circulation.
ū Decreased ventilatory drive.
ū Decreased CO2 buffering capacity of haemoglobin.
ū Absorption of CO2 from alveoli beyond obstructed airways.
ū The higher density of oxygen compared with air causing increased work of
breathing.

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2
Q

signs of C02 levels rising

A

The signs of a rising carbon dioxide level are usually confusion, drowsiness, agitation and a falling level of consciousness.

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3
Q

mild to moderate treatment

A
  • Follow the patient’s COPD action plan if they have one.
  • Measure and record the patient’s peak expiratory flow rate (PEFR) before and after treatment if a PEFR meter is available.
  • Administer bronchodilators:
    a) Use the patient’s metered dose inhaler (MDI) if it is available, or
    b) Administer 5 mg of salbutamol nebulised in combination with 0.5 mg of
    ipratropium nebulised if the patient’s MDI is unavailable.
  • Administer 40 mg of prednisone PO.
  • Consider the possibility that transport may not be required if the patient rapidly improves with only one dose of nebulised bronchodilators.
  • Administer further doses of salbutamol as required.
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4
Q

severe COPD treatment

A
  • Measure and record the patient’s PEFR before and after treatment if a PEFR meter is available, but this is not a priority.
  • Administer 5 mg of salbutamol nebulised in combination with 0.5 mg of ipratropium nebulised.
  • Administer continuous salbutamol until improvement occurs.
  • Gain IV access.
  • Begin transport without delay, providing most treatments en route.
  • An ICP may administer midazolam in 0.5 mg doses IV, sparingly for severe anxiety provided the patient is able to obey commands at all times.
  • Prednisone administration is not a priority. Administer 40 mg of prednisone PO if the patient improves sufficiently to be able to swallow tablets.
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5
Q

imminent arrest treatment

A
  • Administer adrenaline IV in addition to bronchodilators as described for severe COPD:
    a) Administer an adrenaline infusion via an infusion pump. Start at a rate of 0.5 mg/hour and adjust the rate to the patient’s condition, or
    b) Place 1 mg of adrenaline into a 1 litre bag of 0.9% sodium chloride (1:1,000,000):
    ū Administer as an infusion. Start at 2 drops/second and adjust the rate to the patient’s condition, or
    ū Administer a bolus of 0.01 mg adrenaline (10 ml) IV every 1-2 minutes as required.
  • Do not administer midazolam.
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6
Q

COPD non transport requirements

A

ū Known COPD, and
ū Improves to their usual respiratory state, and
ū An SpO2 greater than or equal to 88% when breathing air, andū Observed by ambulance personnel for a minimum of 20 minutes following completion of the last bronchodilator administration, and
ū Observed to mobilise in a way that is normal for the patient, and
ū Able to see a doctor (preferably by their own GP) within two days, and
ū Provided with a prednisone pack (if appropriate), an information sheet and
the information within it is explained to them and to any carers.

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7
Q

COPD is a term used to encompass

A

chronic inflammatory and destructive diseases within the lung, including chronic bronchitis and emphysema. The bronchoconstriction present in COPD is not completely reversible.

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8
Q

COPD should be suspected in patients with

A

chronic respiratory illness, particularly if they have risk factors such as: age over 50 years, long-term exposure to cigarette smoke (including second hand exposure), or long-term exposure to environmental or industrial pollutants.

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9
Q

mild charecteritistcs

A

Patients with mild to moderate COPD are short of breath, able to speak in sentences, moving enough air to generate wheeze, usually have some chest and/or neck indrawing, have an SpO2 that is near their normal level and a normal level of consciousness.

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10
Q

severe characteristics

A

Patients with severe COPD are very short of breath, usually only able to speak a few words with each breath, may not be moving enough air to generate wheeze, usually have severe chest and/or neck indrawing, may be in the tripod position, may have an SpO2 that is significantly below their normal level and may have agitation.

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11
Q

Patients with imminent respiratory arrest are

A

Patients with imminent respiratory arrest are extremely short of breath, usually unable to speak, may not be moving enough air to generate wheeze or to have chest and/or neck indrawing, usually have a rapidly falling SpO2 and usually have severe agitation and/or a falling level of consciousness.

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12
Q

Consider assisting the patient’s ventilation (without added oxygen unless hypoxia is severe), using a manual ventilation bag if:

A

ū
ū
SpO2 continues to fall below 80% despite treatments, or
The patient is becoming exhausted, or
The patient is suspected of developing hypercarbic respiratory failure despite lowering the oxygen flow.

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13
Q

Differentiating COPD from asthma

A
  • It is necessary to distinguish COPD from asthma because the treatments are different.
  • Patients with asthma are usually symptom free between attacks.
  • Patients with COPD usually have a history of smoking and are not symptom free between attacks.
  • Age is not a very useful factor for differentiating COPD from asthma. Some young patients have COPD and some older patients have asthma.
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14
Q

Differentiating COPD from cardiogenic pulmonary oedema

A
  • Cardiogenic pulmonary oedema may produce a wheeze that sounds like COPD. Differentiating COPD from cardiogenic pulmonary oedema is not always easy:
    ū Cardiogenic pulmonary oedema is the likely diagnosis when the patient has been supine (for example in bed) and the wheeze is worse bilaterally in the lower zones. The patient is often hypertensive, clammy and peripherally vasoconstricted.
    ū COPD is the likely diagnosis if it is associated with a productive cough and the wheeze is evenly heard through all lung fields. The patient is usually normotensive and not peripherally vasoconstricted.
  • Some patients may have a history of both COPD and cardiogenic pulmonary oedema. In this setting they may be able to tell you which condition is causing their shortness of breath.
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