13) Arrhythmia Flashcards
What is an Arrhythmia ?
> Symptoms
A disturbance in the cardiac cycle where the pacemaker functions incorrectly or there is abnormal contraction / contraction in the heart. This results in the rate or timing of the heart beat which insufficient to maintain cardiac output.
Symptoms: > Palpitations > Feeling Dizzy > Fainting > SOB
What are the 5 phases of Ventricular Normal Action Potentials ?
0 = Depolarisation occurs due to the movement of Na into the Cell
1 = Small amount of Depolarisation, K+
2 = The plateau stage occurs as the levels of Ca2+ and K+ movement are equal
3 = Repolarisation then occurs through efflux of K+
4 = Na/K ATPase then sets up the membrane potential in the refractory period
List some causes that can lead to Bradycardia
> Conduction blocks in the AVN, Bundle of His or Bundle Branches. This can be due to ischaemia of the node / tissue
> Sinus Bradycardia where the SAN has Slower DPs
List some causes that can lead to Tachycardia
> Ectopic Pacemaker activity either supra ventricular or ventricular -> Occurs in damaged areas e..g ischaemia or Mitral Stenosis
> After Depolarisation - abnormal depolarisation of myocytes
- Early before 2/3 or late 4
> Re Entry Loops Impulse is blocked and so travels in a retrograde way and re excites the area it came from., blockage can be due ischaemia
> Wolff Parkinson White Syndrome => Abnormal electrical conduction in the heart as impulses travel down the bundle of Kent resulting in a faster heart rate.
List some causes that lead to Fibrillations
> Ectopic Focal Points
High Blood Pressure
Mitral Valve Disease
Ischaemia
What is the mechanism of action of Class I AA drugs
> Example of drug and route of administration
> Uses
> Side effects
Blocks Na+ Channels => Slower Depolarisation (Affects Phase 0)
> SAN cells aren’t affected on these fasts Na Channels meaning rate is not controlled
> Rhythm Controlling Drugs
A: Quinidine (Oral or IV)
> AF, Flutter, Tachycardia and Brugada Syndrome
> Hypotension, Pro Arrhythmic (Torsades de points due to increased QT interval, Dizziness, confusion, Insomnia, Seizure, GI Effects
B: Lidocaine (IV)
> Tachycardia due to ischaemic heart disease
> Abdominal upset, CNS effects
C: Flecainide (Oral or IV)
> Supra Ventricular Fibrillation, Wolff Parkinson white syndrome
- DON’T give to patients with structural heart defects
> Proarrhythmia and sudden death with prolonged use ; Increased ventricular response to supraventricular arrhythmias therefore use for AVN blockers
What is the mechanism of action of Class II AA drugs
> Example of drug and route of administration
> Uses
> Side effects
Beta Blockers, thus blocks sympathetic nervous system and so funny current slope is decreased therefore less activation of AP in the SAN.
> Rate controlling Drug
> BisoprOLOL (Oral)
PropranOLOL (Oral + IV)
Use:
> Treating Sinus and Catecholamine dependent Tachycardia
> Converting Re entrant arrhythmia at AV node
> Protecting ventricles from high atrial rates (Slow AV conduction) in AF or Flutter
Side effects:
> Bronchospasm therefore do not give to patients with Asthma
> Hypotension
What is the mechanism of action of Class III AA drugs
> Example of drug and route of administration
> Uses
> Side effects
Potassium Blocker, increases the refractory period and therefore AP length. Prevents early DP.
> Rhythm controlling drug
> Amiodarone (Oral or IV)
Sotalol (Oral)
> Works for most arrhythmia but importantly Ventricular Tachycardia
Amiodarone > Pulmonary Fibrosis, Hepatic Damage, Thyroid Disease, Optic Neuritis, Increased LDL
Sotalol > Proarrhythmia, Fatigue, Insomnia
What is the mechanism of Action in Class 4 AA drugs
> Example of drug and route of administration
> Uses
> Side effects
CCB, slows down heart rate by preventing Calcium influx
> Rate Controlling
> Diltiazem (Oral)
Verapamil (Oral + IV)
> Controls ventricles during Supraventricular Tachycardia
Convert Supra ventricular Tachycardia
> Hypotension, Decreased CO, GI (Constipation), Asystole if b blocker is being used
What is the mechanism of Action of Adenosine
> Route of Administration
> Uses
Natural Nucleotide which binds to A1 Receptors and activates K+ Currents in AV and SA node and so decrease APD => Hyperpolarisation decreasing HR
> Rapid IV Bolus
> Convert Re Entrant Supraventricular Arrhythmias
What is the mechanism of Action of Vernakalant
> Route of Administration
> Uses
> Side Effects
Blocks Atrial Specific K+ Channels, slows atrial conduction
> IV bolus over 10 mins
> Convert Recent Onset Atrial Fibrillation to normal sinus rhythm
> Hypotension, AV Block, sneezing, taste disturbance
What is the mechanism of Action of Ivabradine
> Route of Administration
> Uses
> Side Effects
Blocks funny current, slows sinus node but does not effect blood pressure
> Oral
> Reduce inappropriate sinus tachycardia , Reduce HR in heart failing and angina
> Teratogen, Flashing lights
What is the mechanism of action of Cardiac Glycosides
> Give example
> Uses
> Side effect
Digoxin
> Enhances vagal activity, slows AV conduction and HR
> Reduce Ventricular Rates in AF and flutter
> Avoid in patients with renal failure
What is the mechanism of action of Atropine
> Uses
Selective Muscarinic Antagonist
> Block Vagal Activity to speed AV conduction and increase HR
> Treat Vagal Bradycardia
