Cardio- Antiarrhythmic drugs Flashcards
Name some Cardio Selective beta blockers?
Atenolol
Bisoprolol
Cardio-Selective
Metaprolol
What is the acute management for ACS
MONA
Morphine 10mg and metoclopramide 10mg
Oxygen- if stats <94%
Nitrates- (GTN spray)
Aspirin 300mg
What is the STEMI management?
Primary PCI (if available within 2 hours of presentation)
Thrombolysis (if PCI not available within 2 hours)
THe local cardiac centre will advise about further management (such as further loading within asprin and ticagrelor)
What is the thrombolysis?
It involves injectin a fibrinolytic medication (they break diwn fibrin) that rapidly dissolve clots. There is a signifciant risk of bleeding which can make it dangerous.
What are some of the examples of thrombolytic agents?
stroptokinase, alteplase, tenecteplase
What is management for NSTEMI?
think of BATMAN
B- beta blockers unless contracindicated
A- aspirin 300mg stat dose
T- Ticagrelor 180mg stat dose (clopidogrel 300mg is an alternative)
M- morohine titrated to control pain
A- anticoagulant: Low Molecular Weight Heparin at treatment dose (eg enoaparin 1 mg/kg twice daily for 2-8 days)
N- Nitrates (eg GTN) to relieve coronary artery spasm
What is the treatment for unstable angina treatment?
- MONA
- Offer fondaparinux to patients who do not have a high bleeding risk, unless coronary angiography is planned within 24 hours of admission
What is an alternative to fondaparinux?
Offer unfractionated heparin as a alternative to fonaparinux to patients who are likely to undergo coronary angiography within 24 hours of admission.
Secodnary prevention medical management of ACS
Think of 6As
A- Asprin 75mg once daily
A- another anticoagulant eg clopidogrel or ticagrelor for up to 12 months
A- Atrovastatin 80mg once daily
A- ACE inhibitor (eg ramipril titrates as tolerated to 10mg once daily)
A- Atenolol (or other beta blocker tirated as hgih as tolerated)
A- Aldosterone antagonist for those with clinical heart failure (i.e eplerenone titrates to 50mg once daily)
What is the triple therapy for heart therapy?
ARNI- Angiotensin Receptor Neprolysi Inhibitor. This is a combo of Clasartan (ARB) and Sacubitril (neprolysin inhibitor). This combo replaces the old combo of ACEi and ARB
Beta Blocker
MRA- Mineralcorticoid Receptor Antagonist rg Spironolactone
What is the function of neprolysin?
Neprolysin breaks down BNP produced by the heart to help decrease cardiac output and hence reduced workload of the heart.
Therefore, by inhibiting neprolsin= increased BNP= good for workload of heart.
Vaughan-Williams Classification of Antiarrhythmic Drugs
Name the 4 classes
I- Sodium channel blockers
II- Beta adrenergic blockers
III- Potassium channel blockers
IV- Calcium channel blockers
Mechanism of Sodium channel blockers?
Sodium channel blockers can be split into?
A- Na channle blockade, prolonged refractoriness
B- Na channel blockase, little effect on refractoriness
C- Na channle blockade, slight prolongation of refractoriness
Mechanism of Beta adernerigc blockers?
Indirect Ca channel blockade by attenuation of adrenergic activation.
Mechanism of Potassium channel blockers?
Prolong action potential refractoriness, delay repolarisation
Mechanism of Calcium channel blockers?
Examples of sodium channel blockers type A?
Quinidine
Disopyramide
Procainamide
Examples of sodium channel blockers type B?
Lidocaine
Phenytoin
Mexilitine
Examples of sodium channel blockers type C?
Flecainide
Propafenone
Ethmozine
Examples of Beta adrenergic blockers?
Propanolol
Esmolol
Sotalol
Examples of Potassium Channel Blockers?
Amiodarone
Ibuttilide
Dofetillide
Dronedarone
Examples of Calcium Channel Blockers?
Verapamil
Diltiazem
Where does each class of the Vaughan- William classification antiarrhythmic drugs affect the cardiac action potential
Phase 0 - Class 1
Phase 1
Phase 2 - Class 4
Phase 3 - Class 3
Phase 4 - Class 2
Mechanism of action of Class 1 sodium channel blockers (lecture)
Block fast sodium channels thereby
- reducing the rate of Phase 0 depolarisation
- prolonging the effective refractory period
- increasing the threshold of excitability
- reducing phase 4 depolarisation
- also have local anaesthetic properties
What is brugada syndrome?
Brugada (brew-GAH-dah) syndrome is a rare, but potentially life-threatening heart rhythm disorder that is sometimes inherited. People with Brugada syndrome have an increased risk of having irregular heart rhythms beginning in the lower chambers of the heart (ventricles).
Due to a mutation in the cardiac sodium chammel (sodium channelopathy)
How iis brugada syndrome inherited?
Familial clustering and autosomal dominant inheritance has been demonstrated (can be sporadic)
Which mutation is related to brugada syndrome?
SCN5A
Brugrada syndrome can be unmasked or augmented by factors such as ____ ____ _____
Fever
ischaemia
hypokalemia
Clinical manidestations of brugada syndrome?
Life threatening ventricular arrhythmias and sudden death
What class of drug is flecainide?
Class 1 C
Importance of flecainide in brugada syndrome
can use it in patients to diagnose brugada syndrome
Effects of felcainide on sodium channel?
Depressant effect on the rapid sodium channel (phase 1)
Minimal increase in atrial and ventricular redractoriness in QT interval
Increase anterograde and retrograde redractoriness in AP pathway s
What type of drug is Ajmaline
Class IA
Effects of ajmaline?
evoloved to use a diagnostic took
very short half life
Produces right precordial ST elevation in susoected brugada cases
Can produce heart block in patietns with BBB and syncope
Can cause disppearance of delta wave in WPW (prolonging the AP anterograde ERP)
