Cardiovascular Pharmacology Flashcards
ACS drugs
Oxygen Glyceryl trinitrate (GTN) Morphine Aspirin Entonox
Aspirin (Acetylsalicylic acid)
Analgesic
Anti-inflammatory
Anti-platelet properties
Non competitive inhibitor of platelet prostaglandins COX1 and COX 2
Reduceded thromboxane production renders platelets functionless for their 10-12 day life span
By inactivating COX 1 and 2 enzymes:
Stomach ulcers can occur
Reduces temperature
Reduces inflammation
Reduces clot formation
Q. How do we overcome first pass effect in the LAS?
A. Chewed aspirin is absorbed by lymphatic system
Cox 1
Produces prostaglandins that protect stomach wall via mucous secretion
cox 2
Produces prostaglandins at site of inflammation – transmits pain information.
Used in the synthesis of thromboxane (a product made by platelets to make blood clot)
GTN - Why its given sublingually?
To avoid hepatic first pass effect which would completely metabolise the drug rendering it inactive
GTN
Potent vasodilator
Converted by the body to nitric oxide
Reduces afterload & pre-load
Acts primarily on veins
Reduces blood pressure
What does the sympathetic nervous system do to the heart?
It speeds up the heart using adrenaline as a neurotransmitter (and as a hormone)
How does the parasympathetic nervous system effect the heart?
It slows the heart using acetylcholine (Ach) as a neurotransmitter
Amiodarone
In cardiac arrest the guidance is currently to give Amiodarone 300mg to resistant VT.
The theory being that this Type III antiarrhythmic will calm the ventricles down and allow an organized rhythm to arise.
Class III antiarrhythmic
Prolongs phase 3 of action potential
Blocks K+ and inactivated Na+ channels
Adrenaline
Sympathomimetic
- It mimics the action of the sympathetic nervous system
1st drug in cardiac arrest
Onset in 90 secs with duration of ~ 5 mins
Adrenaline has positive inotropic and chronotropic effects
The adrenaline given IM in anaphylaxis will ensure vasoconstriction and boost blood pressure.
In some cases of anaphylaxis it is lack of tone in the blood vessels that causes death
Cardiac medication Types
Cardiac medications are classed into three types:
Inotropic
Affects cardiac contraction
Dromotropic
Affects cardiac conduction
Chronotropic
Affects the rate
What drug is an α1, β1 and β2 agonist
Adrenaline affects α1, β1 and β2 receptors
α1 and β1 receptors affect the heart
β2 receptors affect the lungs
α1 and β1 - 1 heart
Β2 - 2 lungs
Atropine
Atropine is an acetylcholine antagonist.
It’s an antimuscarinic and anticholinergic agent.
Instead of increasing the amount of adrenaline, use a drug that will block the slowing effects of ACh on the heart.
SA node will revert to its normocardic rhythm of 60 – 100
Action of Atropine at SA node = The Vagus nerve is releasing Ach causing slower heart rate. Atropine blocks Ach receptor sites causing the slowing effect to reduce, increasing heart rate.
Anaphylactic shock - Our pharmacological treatment needs to combat:
Widespread histamine release
Widespread vasodilation and low BP
Bronchoconstriction leading to hypoxia
High levels of O2 target saturation 94-98%.
Administer IM adrenaline.
Consider fluid therapy.
Consider Chlorphenamine.
Consider Hydrocortisone.
Consider nebulised salbutamol for bronchospasm.
Anaphylaxis is likely when all of the following 3 criteria are met:
• Sudden onset and rapid progression of symptoms
• Life-threatening Airway and/or Breathing and/or Circulation problems
• Skin and/or mucosal changes (flushing, urticaria, angioedema)
The following supports the diagnosis: Exposure to a known allergen for the patient
Chlorphenamine (Piriton)
Antihistamine – H1 receptor antagonist
Histamine release, due to inflammatory response in anaphylaxis, causes loss of tone in blood vessels
Prevents further histamine release
But does not reverse loss of tone that has already occurred
Hydrocortisone
Corticosteroid
Reduces uncontrolled inflammation
Complicated method of action
May take hours for action to be seen
Improves long term prognosis
Hypovolemic Shock
Multiple causes such as D&V, trauma etc Key is to support circulation O2 as indicated Fluids as indicated Trauma – tranexamic acid Post-partum haemorrhage - syntometrine
Tranexamic acid
Haemorrhage Ladder
Surgery Tranexamic acid Tourniquet / haemostatic gauze Haemorrhage control dressing Direct pressure and elevation Simple dressing
This is an antifibrinolytic compound which promotes clotting by preventing the breakdown of clots
It is the first medication that should be used in major trauma when a significant haemorrhage is suspected.
Side Effects
Rapid injection might rarely cause hypotension.
Presentation
Ampoules containing 500mg tranexamic acid in 5ml
Dosage
Adults and children over 12 years old 1g IV/IO. Given over 10 minutes.
Two ampoules of tranexamic acid should be drawn up and injected into the 100ml bag of 0.9% saline (located in the drug pack)
The 100ml bag should then be inverted a couple of times to ensure the contents is mixed and run through the giving set
This should then be given over 10 minutes whilst conveying the patient to the major trauma centre.
Requires a ‘drug added’ label
If given the patient must be conveyed to the Major Trauma Centre unless the patients airway becomes compromised and unmanageable then divert to the nearest trauma unit
There is no evidence to currently support the administration of tranexamic acid to medical bleeding or obstetric haemorrhage.
A risk versus benefit decision should be taken before instituting IO access purely to administer tranexamic acid
Tranexamic acid - 7 steps
Ensure administration is not delaying on scene time Draw up TXA and add to 100ml saline Drug added label Run through giving set Attach to cannula 10ml aliquots Handover
Syntometrine
Post partum haemorrhage after uterine massage has failed
Contains oxytocin and ergometrine
Uterus has hormone receptor sites for hormone oxytocin
Oxytocin causes contraction of the uterus – prevents bleeding.
Oxytocin is short acting
Ergometrine is long lasting and ensures sustained contraction of uterine wall
