Cardio- Antiarrhythmic drugs Flashcards

1
Q

Name some Cardio Selective beta blockers?

A

Atenolol

Bisoprolol

Cardio-Selective

Metaprolol

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2
Q

What is the acute management for ACS

A

MONA

Morphine 10mg and metoclopramide 10mg

Oxygen- if stats <94%

Nitrates- (GTN spray)

Aspirin 300mg

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3
Q

What is the STEMI management?

A

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)

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4
Q

What is the thrombolysis?

A

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.

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5
Q

What are some of the examples of thrombolytic agents?

A

stroptokinase, alteplase, tenecteplase

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6
Q

What is management for NSTEMI?

A

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

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7
Q

What is the treatment for unstable angina treatment?

A
  1. MONA
  2. Offer fondaparinux to patients who do not have a high bleeding risk, unless coronary angiography is planned within 24 hours of admission
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8
Q

What is an alternative to fondaparinux?

A

Offer unfractionated heparin as a alternative to fonaparinux to patients who are likely to undergo coronary angiography within 24 hours of admission.

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9
Q

Secodnary prevention medical management of ACS

A

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)

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10
Q

What is the triple therapy for heart therapy?

A

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

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11
Q

What is the function of neprolysin?

A

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.

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12
Q

Vaughan-Williams Classification of Antiarrhythmic Drugs

Name the 4 classes

A

I- Sodium channel blockers

II- Beta adrenergic blockers

III- Potassium channel blockers

IV- Calcium channel blockers

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13
Q

Mechanism of Sodium channel blockers?

Sodium channel blockers can be split into?

A

A- Na channle blockade, prolonged refractoriness

B- Na channel blockase, little effect on refractoriness

C- Na channle blockade, slight prolongation of refractoriness

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14
Q

Mechanism of Beta adernerigc blockers?

A

Indirect Ca channel blockade by attenuation of adrenergic activation.

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15
Q

Mechanism of Potassium channel blockers?

A

Prolong action potential refractoriness, delay repolarisation

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16
Q

Mechanism of Calcium channel blockers?

A
17
Q

Examples of sodium channel blockers type A?

A

Quinidine

Disopyramide

Procainamide

18
Q

Examples of sodium channel blockers type B?

A

Lidocaine

Phenytoin

Mexilitine

19
Q

Examples of sodium channel blockers type C?

A

Flecainide

Propafenone

Ethmozine

20
Q

Examples of Beta adrenergic blockers?

A

Propanolol

Esmolol

Sotalol

21
Q

Examples of Potassium Channel Blockers?

A

Amiodarone

Ibuttilide

Dofetillide

Dronedarone

22
Q

Examples of Calcium Channel Blockers?

A

Verapamil

Diltiazem

23
Q

Where does each class of the Vaughan- William classification antiarrhythmic drugs affect the cardiac action potential

A

Phase 0 - Class 1

Phase 1

Phase 2 - Class 4

Phase 3 - Class 3

Phase 4 - Class 2

24
Q

Mechanism of action of Class 1 sodium channel blockers (lecture)

A

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
25
Q

What is brugada syndrome?

A

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)

26
Q

How iis brugada syndrome inherited?

A

Familial clustering and autosomal dominant inheritance has been demonstrated (can be sporadic)

27
Q

Which mutation is related to brugada syndrome?

A

SCN5A

28
Q

Brugrada syndrome can be unmasked or augmented by factors such as ____ ____ _____

A

Fever

ischaemia

hypokalemia

29
Q

Clinical manidestations of brugada syndrome?

A

Life threatening ventricular arrhythmias and sudden death

30
Q

What class of drug is flecainide?

A

Class 1 C

31
Q

Importance of flecainide in brugada syndrome

A

can use it in patients to diagnose brugada syndrome

32
Q

Effects of felcainide on sodium channel?

A

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

33
Q

What type of drug is Ajmaline

A

Class IA

34
Q

Effects of ajmaline?

A

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)