Cardiovascular Pharmacology Flashcards

1
Q

ACS drugs

A
Oxygen
Glyceryl trinitrate (GTN)
Morphine
Aspirin
Entonox
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2
Q

Aspirin (Acetylsalicylic acid)

A

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

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3
Q

Cox 1

A

Produces prostaglandins that protect stomach wall via mucous secretion

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4
Q

cox 2

A

Produces prostaglandins at site of inflammation – transmits pain information.

Used in the synthesis of thromboxane (a product made by platelets to make blood clot)

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5
Q

GTN - Why its given sublingually?

A

To avoid hepatic first pass effect which would completely metabolise the drug rendering it inactive

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6
Q

GTN

A

Potent vasodilator

Converted by the body to nitric oxide

Reduces afterload & pre-load

Acts primarily on veins

Reduces blood pressure

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7
Q

What does the sympathetic nervous system do to the heart?

A

It speeds up the heart using adrenaline as a neurotransmitter (and as a hormone)

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8
Q

How does the parasympathetic nervous system effect the heart?

A

It slows the heart using acetylcholine (Ach) as a neurotransmitter

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9
Q

Amiodarone

A

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

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10
Q

Adrenaline

A

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

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11
Q

Cardiac medication Types

A

Cardiac medications are classed into three types:

Inotropic
Affects cardiac contraction

Dromotropic
Affects cardiac conduction

Chronotropic
Affects the rate

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12
Q

What drug is an α1, β1 and β2 agonist

A

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

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13
Q

Atropine

A

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.

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14
Q

Anaphylactic shock - Our pharmacological treatment needs to combat:

A

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.

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15
Q

Anaphylaxis is likely when all of the following 3 criteria are met:

A

• 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

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16
Q

Chlorphenamine (Piriton)

A

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

17
Q

Hydrocortisone

A

Corticosteroid

Reduces uncontrolled inflammation

Complicated method of action

May take hours for action to be seen

Improves long term prognosis

18
Q

Hypovolemic Shock

A
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
19
Q

Tranexamic acid


A

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

20
Q

Tranexamic acid - 7 steps

A
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
21
Q

Syntometrine

A

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