Glyceryl Trinitrate (GTN) Spray Flashcards
1
Q
GTN Indications
A
- Myocardial ischaemia
- Cardiogenic pulmonary oedema
- Control of hypertension associated with autonomic dysreflexia
- Control of hypertension (usually in conjunction with Labetalol) prior to fibrinolytic treatment for STEMI, or during inter-hospital transfer for STEMI
- STEMI
2
Q
GTN Contraindications
A
- Known severe allergy
- Systolic BP less than 110 mmHg
- Heart rate less than 40/minute
- Heart rate more than 150/minute
- Ventricular tachycardia
3
Q
GTN Cautions
A
- 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
- The patient is frail
- Signs of shock
- Dysrhythmia
- Has taken a phosphodiesterase inhibitor in the last 24 hours
- Known aortic or mitral stenosis
4
Q
GTN Dose for Myocardial Ischaemia
A
0.4 mg every five minutes. Consider increasing interval to ten minutes if caution is present
5
Q
GTN Dose for STEMI
A
O.4 mg with caution. Withhold if signs of poor perfusion are present
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
7
Q
GTN Dose for Control of Hypertension
A
0.4 mg every five minutes
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
9
Q
GTN Common Adverse Effects
A
- Hypotension
- Flushing
- Headache
- Tachycardia
- Feeling light-headed
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