Glyceryl Trinitrate (GTN) Spray Flashcards

1
Q

GTN Indications

A
  1. Myocardial ischaemia
  2. Cardiogenic pulmonary oedema
  3. Control of hypertension associated with autonomic dysreflexia
  4. Control of hypertension (usually in conjunction with Labetalol) prior to fibrinolytic treatment for STEMI, or during inter-hospital transfer for STEMI
  5. STEMI
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2
Q

GTN Contraindications

A
  1. Known severe allergy
  2. Systolic BP less than 110 mmHg
  3. Heart rate less than 40/minute
  4. Heart rate more than 150/minute
  5. Ventricular tachycardia
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3
Q

GTN Cautions

A
  1. STEMI, particularly STEMI involving the right ventricle. GTN may cause a significant fall in cardiac output and if there are signs of low cardiac output GTN should be withheld
  2. The patient is frail
  3. Signs of shock
  4. Dysrhythmia
  5. Has taken a phosphodiesterase inhibitor in the last 24 hours
  6. Known aortic or mitral stenosis
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4
Q

GTN Dose for Myocardial Ischaemia

A

0.4 mg every five minutes. Consider increasing interval to ten minutes if caution is present

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5
Q

GTN Dose for STEMI

A

O.4 mg with caution. Withhold if signs of poor perfusion are present

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6
Q

GTN Dose for cardiogenic pulmonary oedema

A

0.8 mg every five minutes. Consider increasing the dosing interval to ten minutes if a caution is present. Increase the dose and frequency is patient is not improving

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7
Q

GTN Dose for Control of Hypertension

A

0.4 mg every five minutes

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8
Q

GTN Route and Administration

A
  • IS, sprayed under tongue
  • If administered in presence of a caution;
    > patient should be sublime
    > IV assess should have been obtained whenever possible
    > the dosing interval should be increased to ten minutes
    > Be ready to administer 0.9% sodium chloride IV if there is a significant fall in cardiac output or blood pressure
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9
Q

GTN Common Adverse Effects

A
  1. Hypotension
  2. Flushing
  3. Headache
  4. Tachycardia
  5. Feeling light-headed
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10
Q

GTN Mechanism of Action

A
  • It is a vasodilator that acts on smooth muscle to cause venous and arterial vasodilation, with the predominant effect being on veins.
  • The MOA is not clear, but it results in the formation of nitric oxide which is a vasodilator causing;
    > A reduction in venous return (preload) to the heart reducing the ventricular filling and cardiac output which reduces myocardial oxygen demand
    > Arterial dilation which reduces peripheral resistance (after load) to the heart hence reducing the myocardial oxygen demand
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