1. Ann Parker Cardiology Pharmacist Frimley Health
Cardiac Medication
Ann Parker
Cardiology Pharmacist
Frimley Health

2. Aims Overview of: Anti-arrhythmic medication Anticoagulation in AF
Medication in heart failure
And an opportunity for you to ask questions

3. Electrical conduction system of the heart
Inherent rate – rate at which cells spontaneously initiate impulses. Atria beats/min. AV node beats. Vetricles beats.
Depolarisation ( the movement of charged ions across a cell membrane ) results in myocardial contraction. At resting state K+ in the cell and Na+ and Ca+ outside
When an electrical impulse spreads through the muscle from the SA node the Na+ pump channels open and the K+ closes, electrolytes change place across the cell membrane

4. Arrhythmia
When the electrical impulses that coordinate heartbeats are not working properly, making the heart beat too fast/slow or inconsistently.
Many heart arrhythmias are harmless.
Some may cause troublesome and even potentially fatal symptoms.
We all occasionally experience irregular heartbeats, which may feel like a racing heart or fluttering.

6. Digoxin Works by inhibiting the sodium- potassium pump
Helps to control heart rate, particularly in the irregular atrial fibrillation
Increases cardiac contractility
Medical use first described in 1785

7. Vaughan -Williams Classification
Class I - sodium channel blockers eg Disopyramide, Flecainide, Mexilitine
Class II- Betablockers
Class III- potassium channel blockers eg Amiodarone
Class IV- calcium channel blockers eg Verapamil, Diltiazem

8. Sodium channel blockers eg mexilitene, flecainide
slows conduction in the heart
makes the heart tissue less sensitive (reduce ventricular response)
Side effects -dizziness, heartburn, nausea, nervousness, trembling, unsteadiness
usually reversible and dose-related.

9. Betablockers
Reduce the effect of adrenaline on the heart (sympathetic nervous system blockade)
Slow the heart by depressing sinus node function and AV node conduction
Can help maintain sinus rhythm
Protective of the heart as reduce oxygen demand
depression of sinus node (natural pacemaker) function and atrioventricular node (electrical relay station between the upper and lower chambers of the heart conduction

11. Potassium channel blockers eg amiodarone
increases the refractory period via sodium and potassium channel effects
has beta blocker like and calcium channel blocker like actions on the SA and AV node
slows intra-cardiac conduction
These electrophysiologic effects are reflected in a decreased sinus rate of 15 to 20%, increased PR and QT intervals of about 10%, the development of U-waves, and changes in T-wave contour. These changes should not require discontinuation of Amiodarone as they are evidence of its pharmacological action, although Amiodarone can cause marked sinus bradycardia or sinus arrest and heart block. On rare occasions, QT prolongation has been associated with worsening of arrhythmia

13. Act in the AV node to prolong conduction time and refractory period

14. Anticoagulation in AF, why?
Risk of stroke assesses usings CHADsVASc score

15. Congestive heart failure
CHADS2VASc
Risk Factor
Score
Congestive heart failure 1
Hypertension
Age >75years 2
Diabetes
Stroke
Vascular disease
Age years
Sex category (female)

16. HASBLED Hypertension Abnormal renal and liver function Stroke Bleeding
Labile INRs
Elderly
Drugs or alcohol

17. Anticoagulation Warfarin
NOACs (or DOACs) eg. apixaban, dabigatran, rivaroxaban

18. Warfarin affects the body’s ability to synthesise vitamin K which is used in production of factors 2, 7, 9 and 10.

20. Heart failure treatment
Type – LVSD of HFPEF
Angiotensin converting enzyme inhibitors (ACEI)
Betablockers
Aldosterone antagonists
Angiotensin receptor neprilysin inhibitor (ARNI)
Natriuretic peptides (NPs) are a family of hormones that help maintain sodium and fluid balance. Natriuretic peptides (NPs) are a family of hormones that help maintain sodium and fluid balance.

22. References https://www.pinterest.com/pin/404338872771327665/