Ipratropium Flashcards

1
Q

Preparation of ipratropium

A

Ampoule containing 0.5 mg in 2 ml

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2
Q

Indications for ipratropium

A

Bronchospasm in conjunction with the initial dose of salbutamol

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3
Q

Contraindications of ipratropium

A

None

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4
Q

Precautions for ipratropium

A

None

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5
Q

Administration of ipratropium

A

Nebuliser in combination with the initial salbutamol administration.

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6
Q

Dosage of ipratropium

A

0.5 mg

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7
Q

Onset of effect of ipratropium

A

3-5 minutes

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8
Q

Mechanism of action ipratropium

A

Ipratropium is an anticholinergic agent. It inhibits the action of acetylcholine, the neurotransmitter released from the vagus nerve. In doing so ipratropium reduces parasympathetic mediated bronchospasm.

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9
Q

Pharmacokinetics

A

Following inhalation of nebulised ipratropium, 10-30% is absorbed in the lungs, while the major part of the dose is swallowed and passes into the GI tract.
It is excreted predominantly via the urine.

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10
Q

Duration of effect
for ipratropium

A

Approximately 6 hours

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11
Q

Common adverse effects from ipratropium

A

Nausea
Dry mouth
Blurred vision
Tachycardia and palpitations
It may worsen pre-existing glaucoma if repeat doses are given.

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12
Q

Interactions of ipratropium

A

No common interactions.

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13
Q

Preparation of Glucagon

A

Ampoule containing 1mg as powder within a ‘hypo-kit’

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14
Q

Indications for glucagon

A

Hypoglycaemia when the patient cannot swallow glucose or food or when IV access cannot be obtained

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15
Q

Contraindications for glucagon

A

None

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16
Q

Precautions for glucagon

A

None

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17
Q

Administration of glucagon

A

Dissolve the powder using the syringe within the ‘hypo-kit’. Give IM. The preferred IM site is the lateral thigh. If this site is not suitable use the lateral upper arm.

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18
Q

Dosage for glucagon

A

Adults and children aged 5 years and over: 1 mg
Children aged less than 5 years: 0.5 mg
Do not repeat

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19
Q

Onset of effect
for glucagon

A

5-10 minutes (depending on absorption)

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20
Q

Mechanism of action for glucagon

A

Glucagon increases the blood glucose level by stimulating glycogenolysis. This causes stored glycogen to be broken down into glucose, predominantly within the liver.

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21
Q

Duration of effect
for glucagon

A

10-30 minutes

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22
Q

Common adverse effects
for glucagon

A

None

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23
Q

Interactions for glucagon

A

No common interactions

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24
Q

Additional information
for glucagon

A

Glucagon relies on stored glycogen being available to exert its effect. If glycogen stores are not available, glucagon may be ineffective. Examples when this may occur are if the patient:
has undergone strenuous exercise
not eaten food for more than 12 hours
is suffering from adrenal insufficiency
is suffering from chronic hypoglycaemia
is suffering from alcohol- induced hypoglycaemia.
Glucagon also inhibits the tone and motility of the smooth muscle in the gastrointestinal tract , but is not recommended in the setting of esophageal obstruction.

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25
Q

(Preparation of GTN)

A

Metered dose bottle delivering 0.4 mg doses

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26
Q

Indicationsof GTN

A

Myocardial ischaemia or cardiogenic pulmonary oedema

27
Q

Contraindications of GTN

A

Systolic BP less than 100 mmHg or
HR less than 40/min or
HR greater than 130/min

28
Q

(Preparation of GTN)

A

Metered dose bottle delivering 0.4 mg doses

29
Q

Indicationsof GTN

A

Myocardial ischaemia or cardiogenic pulmonary oedema

30
Q

Precautions for GTN

A

Small, fail or physiologically unstable
Inferior STEMI - GTN may result in a significant fall in cardiac output in a patient suffering from a
STEMI involving the right ventricle because:
STEMI involving the right ventricle can result in a significant reduction in right ventricular contractility. This causes blood flow from the right side of the heart to the left side of the heart to become largely dependent on venous pressure within the inferior vena cava and the superior vena cava.
GTN predominantly dilates veins and can result in a significant fall in venous pressure. In a patient with STEMI involving the right ventricle, this may cause a significant fall in cardiac output.
Poor perfusion - Poor perfusion indicates reduced cardiac output. It is important to administer GTN with caution due to the reduction in preload that results from GTN administration, as this will further reduce cardiac output
Dysrhythmia is present - in general, when dysrhythmia is present, preload and/or afterload is compromised. Administration of GTN will reduce the preload and afterload, and therefore reduce cardiac output. Therefore, in instances where GTN is indicated and a dysrhythmia is present, GTN should be administered with this in mind
The patient has taken a drug for erectile dysfunction in the last 24 hours - there is a range of medicines (with multiple different names) used for erectile dysfunction and some of them (particularly sildenafil) are also used in the treatment of pulmonary hypertension. These medicines are long acting (12-24 hours) inhibitors of one of the subtypes of the enzyme phosphodiesterase. Inhibition of phosphodiesterase results in an enhanced effect of nitric oxide, which is a vasodilator. GTN may interact with such medicines, causing severe and prolonged hypotension if they have been taken within the last 24 hours. GTN is not contraindicated in this setting, but if used there must be a very strong indication and it must be used in 0.4 mg doses. If in doubt seek medical advice
Known aortic stenosis - these patients already have a reduced cardiac output and left ventricular strain. GTN in these patients will cause venous dilation, reducing preload and further reducing cardiac output. This may result in a substantial fall in cardiac output.

31
Q

Precautions for GTN

A

Small, fail or physiologically unstable
Inferior STEMI - GTN may result in a significant fall in cardiac output in a patient suffering from a
STEMI involving the right ventricle because:
STEMI involving the right ventricle can result in a significant reduction in right ventricular contractility. This causes blood flow from the right side of the heart to the left side of the heart to become largely dependent on venous pressure within the inferior vena cava and the superior vena cava.
GTN predominantly dilates veins and can result in a significant fall in venous pressure. In a patient with STEMI involving the right ventricle, this may cause a significant fall in cardiac output.
Poor perfusion - Poor perfusion indicates reduced cardiac output. It is important to administer GTN with caution due to the reduction in preload that results from GTN administration, as this will further reduce cardiac output
Dysrhythmia is present - in general, when dysrhythmia is present, preload and/or afterload is compromised. Administration of GTN will reduce the preload and afterload, and therefore reduce cardiac output. Therefore, in instances where GTN is indicated and a dysrhythmia is present, GTN should be administered with this in mind
The patient has taken a drug for erectile dysfunction in the last 24 hours - there is a range of medicines (with multiple different names) used for erectile dysfunction and some of them (particularly sildenafil) are also used in the treatment of pulmonary hypertension. These medicines are long acting (12-24 hours) inhibitors of one of the subtypes of the enzyme phosphodiesterase. Inhibition of phosphodiesterase results in an enhanced effect of nitric oxide, which is a vasodilator. GTN may interact with such medicines, causing severe and prolonged hypotension if they have been taken within the last 24 hours. GTN is not contraindicated in this setting, but if used there must be a very strong indication and it must be used in 0.4 mg doses. If in doubt seek medical advice
Known aortic stenosis - these patients already have a reduced cardiac output and left ventricular strain. GTN in these patients will cause venous dilation, reducing preload and further reducing cardiac output. This may result in a substantial fall in cardiac output.

32
Q

Dosage for GTN

A

0.4 - 0.8 mg GTN. Repeat every 2-5 minutes.

33
Q

Mechanism of action of GTN

A

GTN is a vasodilator. GTN dilates veins and arteries but the predominant effect is on veins. The exact mechanism of action is not clear but it appears that GTN results in the formation of nitric oxide, which is a vasodilator. GTN causes:
Venous dilation, which causes peripheral pooling of blood, reducing venous return and preload. This reduces ventricular filling and cardiac output, which reduces myocardial work and myocardial oxygen demand.
Arterial dilation, reducing peripheral resistance and afterload. This reduces the force the left ventricle must overcome to eject blood into the systemic circulation, reducing myocardial oxygen demand.
A small amount of dilation of the coronary arteries. This increases the supply of blood to the myocardium.

34
Q

Onset of effect of GTN

A

1-2 minutes

35
Q

Duration of effect of GTN

A

The vasodilator effects of GTN are relatively short and usually last 10-30 minutes. However, in some patients the effect on blood pressure may be quite prolonged, lasting several hours (even in the absence of drugs for erectile dysfunction).

36
Q

Duration of effect of GTN

A

Duration of effect

37
Q

Interactions of GTN

A

The effects of GTN will be increased in patients taking beta blockers and other anti-hypertensive medications.
There is a range of medicines used for erectile dysfunction and some of them (particularly sildenafil) are also used in the treatment of pulmonary hypertension. Interaction with these can result in prolonged hypotension.

38
Q

Preparation of salbutamol

A

Ampoule containing 5 mg in 2.5 ml

39
Q

Indications of salbutamol

A

Bronchospasm resulting from:
Asthma
CORD
Airway burns or smoke inhalation

40
Q

Contraindications of salbutamol

A

None

41
Q

Precautions of salbutamol

A

None

42
Q

Administration of salbutamol

A

Administration: salbutamol is nebulised, initially in conjunction with ipratropium. Any subsequent doses are nebulised with salbutamol alone.

43
Q

Dosage of salbutamol

A

5 mg

44
Q

Onset of action of salbutamol

A

3-5 minutes

45
Q

Mechanism of action of salbutamol

A

Salbutamol is a beta 2 receptor agonist. Stimulating beta 2 receptors in the bronchial smooth muscle causes bronchodilation.

46
Q

Pharmacokinetics of salbutamol

A

Following nebulisation of salbutamol, only 10-20 % of the drug reaches the lungs. The other 80-90 % remains in the mouth, the stomach, or on the delivery device. The salbutamol that reaches the lungs acts rapidly and directly on the bronchial smooth muscle.
The active metabolite of salbutamol is 4’-o-sulfate ester. The half-life is between 2.7-5 hours; 77% of the dose is recovered in the urine after 48 hours.

47
Q

Duration of effect of salbutamol

A

1-2 hours

48
Q

Common adverse effects of salbutamol

A

Tremor
Tachycardia
Tachydysrhythmia Headache
Hypokalaemia

49
Q

Interactions of salbutamol

A

Salbutamol will be less effective in the presence of a non-selective beta blocker (such as propranolol).

50
Q

Preparation adrenaline

A

Ampoule containing 1 mg in 1 ml.

51
Q

Indications for adrenaline

A

Cardiac arrest
Anaphylaxis
Severe asthma
Severe bradycardia
Septic shock unresponsive to fluid loading
Stridor (nebulised)
Moderate to severe epistaxis (intranasal)

52
Q

Contraindications adrenaline

A

None

53
Q

Precautions of adrenaline

A

Myocardial ischaemia or tachydysrhythmias

54
Q

Administration of adrenaline

A

IM: undiluted. The preferred IM site is the lateral thigh. If this site is not suitable, use the lateral upper arm.
Nebulised: undiluted via a nebuliser mask

55
Q

Dose of adrenaline asthma

A

Asthma - adrenaline IM doses
Adults and children greater than or equal to 50 kg: EMT 0.5 mg adrenaline IM (Paramedics and ICPs can alter the dose if the patient is small, frail, or physiologically unstable)
Children less than 50 kg:

56
Q

Anaphylactic dose adrenaline

A

Anaphylaxis - IM doses
Adults and children greater than or equal to 50 kg: 0.5 mg adrenaline IV (Paramedics and ICPs can alter the dose if the patient is small, frail, or physiologically

57
Q

Stridor - nebulised adrenaline dose

A

5 mg adrenaline into the nebuliser bowl with a flow rate of 8L/min.

58
Q

Onset of effect of adrenaline

A

IM: 2-5 minutes (dependent on absorption) Nebulised: on contact with target site
IN: on contact with target site

59
Q

Mechanism of action of adrenaline

A

Adrenaline is an alpha and betaadreno-receptor agonist (stimulator).
Alpha one (α1) stimulation causes peripheral smooth muscle contraction, including vasoconstriction of blood vessels. Stimulates glycogenolysis and gluconeogenesis in the liver.
Alpha two (α2) receptors cause sedation and vasoconstriction.
Beta one (β1) a) stimulation causes primarily cardiac effects. Positive inotropic (increased force of contractility), chronotropic (increased heart rate) and dromotropic (increased conduction) effects of the heart
Beta two (β2) a) stimulation causes smooth muscle relaxation including coronary vasodilatation, venous dilatation, bronchodilation, non-pregnant uterine smooth muscle relaxation, GI smooth muscle relaxation, and sphincter constriction. In addition it also stabilises mast cell membranes reducing histamine release from mast cells.

60
Q

Pharmacokinetics of adrenaline

A

Adrenaline is metabolised by the liver and other tissues. Predominantly, adrenaline is taken up by sympathetic nerve endings.
The metabolites of adrenaline are excreted in the urine.

61
Q

Duration of effect
You of adrenaline

A

The cardiovascular effects last 2-15 minutes. The mast cell membrane effects may last for several hours.

62
Q

Common adverse effects
Of adrenaline

A

Tachycardia
Tachydysrhythmias
Myocardial ischaemia
Ventricular ectopy
Hypertension
Nausea
Vomiting
Tremor
Headache
Anxiety
Restlessness
Weakness
Dyspnoea
Cold extremities
Pallor
Sweating
Flushing or redness of the face and skin.

63
Q

Interactions of adrenaline

A

Increased doses may be required in patients taking beta blockers and/or calcium antagonists.

64
Q

Additional Information adrenaline

A

In general, a dose of 0.5 mg adrenaline IM is appropriate for the majority of adult patients. At Paramedic ATP and above, it is appropriate to reduce the dose to between 0.3-0.5 mg if the patient is small, elderly or has ischaemic heart disease.
Adrenaline administration can make a patient tachypnoeic and look or feel awful. It is important to differentiate this from a worsening of their underlying problem and not to automatically respond by giving more adrenaline.