Arrythmias - Therapy Flashcards

1
Q

What is a sinus arrhythmia?

A

Heart rate and rhythm will vary with respiration. May increase heart rate on inspiration.

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2
Q

What is sinus Tachycardia?

A

Remaining sinus rhythm on the heart rate goes above 100 beats per minute. Can be classified to superventricular arryhthmias and ventricular arrhythmias.

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3
Q

What are common superventricular arrhythmias?

A
  • Atrial fibrilation
  • SVT
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4
Q

What are common ventricular arrhythmias ?

A
  • Ventricular Tachycardias ( ventrical arrhythmias emanate within the ventrical and can be regular or complex tachycardia)
  • Ventricular Fibrillation (they may be disorganised irregular rhythms that aren’t assoiated with cardiac output at all)
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5
Q

Is atrial and ventricular fibrillation organised or chaotic?

A

In atrial and ventricular fibrillation there is chaotic ventricular discharge within the myocardial tissue and there is no organised myocardial contraction

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6
Q

What is sinus Brachycardia?

A

If the heart rate drops below 60 beats per minute. This becomes a problem when it drops below 30 beats per minute and is associated with other symptoms

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7
Q

What is the resting membrane potential of myocardial tissue?

A

Resting membrane potential of myocardial tissue is -90millivolts and is dependand on the exchange of sodium and potassium. Largely dependant on sodium potassium atpase exchange pumpm on the surface of all cells.
potassium is intracellular cation
sodium is extracellular cation

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8
Q

What is memebrane potential?

A

Membrane potential is due to an uneven distribution of charges across the cell membrane.

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9
Q

What is the Class I Vaugh-Williams Classified Drug?

A

Class I is sodium channel blockers.
They are used in both ventricular and atrial tachycardia.

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10
Q

How does sodium channel blockers work?

A

They use dependance so they cross the membrane quickly and be more active when the heart is pumping more quickly. Higher the heart rate the more effective the drugs are.
Sodium channel blockers are responisble for the depolarisation of the tissue within the purkinje fibres and normal muscles cells of the myocardium.

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11
Q

What is the most common socium channel blocker used?

A

Flacenide. Class IC. Most likely sodium channel blocker for us to come across in clinical practice. It is used to maintain sinus rhythm in patients with atrial fibrillation and is used to control SBP. It cannot be used in patients who have previous history of ischaemic heart disease or structural heart disease as these patients could develop malignant arrhythmias.

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12
Q

What are the main side effects of anti-arythmics?

A

Can cause problems with arrhythmia. Can induce arrhythmia particular in patients who have underlying cardiac disease

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13
Q

How does sodium channel blockers impact the action potential?

A

Slows down phase 1 depolarisation of the ventrical site off the myocardium and it shortens the plateau phase.

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14
Q

What are the class II of Vaugh-William classified drugs?

A

Class II is beta blockers

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15
Q

How doe beta blockers work?

A

Beta blockers reduce sympathetic simulation of the heart that leads to prolongation of phase 4 depolarisation within nodal tissue - within SA node and AV node. It also reduces excitability of the noncardiac tissue by polonging the refactory period.

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16
Q

How do beta blockers have a negative effect on contractility?

A

Beta blockers have a negative effect on contractility because it slowly reduces the length of the muscle phase so less calcium goes into the cell and calcium is required for contractility.

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17
Q

What are beta blockers first line choice for?

A

Beta blockers are first line choice for atrial fibrillation and are reduced to the risk of ventricular tachycardia post MI or malignant arrhythmias post MI

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18
Q

What are the class III drugs of Vaugh-Williams classification of drugs?

A

Class III is potassium channel blockers.

19
Q

How do potassium channel blockers work?

A

Pottassium cannel blockers prolong the repolarisation phase and increase the effective refactory periods so they help stabilise the myocardium.

20
Q

Where are potassium channel blockers used?

A

Generally used in dysrythmias and or tachyrythmias that are difficult to treat

21
Q

What is a common potassium channel blocker used?

A

Common potassium channel blocker used is amiodarone. This is used mostly in patients who have ventricular tachycardia and occasionally in superventricular tachycardia. Amiodarone can be used in patients to manage atrial fibrilation and flutter if they are resistant to other drugs to maintain a patients sinus rhythm

22
Q

What are side effects of Amiodarone?

A

thyroid (hyper and hypo thyroidism), pulmonary fibrosis, corneal deposits, LFT abnormalites slate grey pigmentation

23
Q

What are Class IV drugs of Vaugh-Williams Classification system of drugs?

A

Calcium channel blockers

24
Q

When are calcium channel blockers used?

A

Calcium channel blockers are generally used in patients who are tolerant of beta blockers. Are also used for proxysmal superventricular tachycardia and rate control of atrial fibrillation and flutter

25
How does calcium channel blockers work?
Calcium is important for the phase 4 depolarisation in the nodal tissue and also voltage gated calcium channels are reponsible for phase 0 of rapid depolarisation within the mantle tissue Calcium channel blockers have the effect that they have slow discharge from the SA node and slow conduction from the AV node and so slow the heart rate down. They reduce contractility and reduce the amount of calcium going into the myocardial cells and have a negativy ionotropic effect.
26
What is class V drugs of the vaugh-williams classification of drugs?
Other Arythmics
27
What are the main other arythmics?
Main ones are digoxin and adenosine.
28
How does digoxin work?
Digoxin inhibts the sodium potassium ATPase pump in myocardial tissue. It has a complex effect on cardiac action potential as it reduces the refactory period in myocardium. It increases plateu phase so has a postive ionotropic effect . It also increases vagal tone and slows SA/AV node conduction
29
In which patients is digoxin used?
Digoxin is used in patients with atrial dysrhythmias. Acutely in patients with atrial fibrillation, atrial flutter and SVT (rarely). Is aslo beneficial on the symptoms of heart failure because it has a positive ionotropic effect
30
Why is digoxin used more in elederly patients?
Half life of digoxin is prolonged and it is increased in renal failure because it is excreted unchanged by the kidneys. Commonly used in elderly patients who often may have renal impairment
31
What are the common side effects of digoxin?
xantopasia (GI upset), bradycardia, tachycardia, nausea and vomiting, arrhythmias - ventricular tachycardia and ventricular fibrillation
32
What are the signs of digoxin toxicity?
A reverse tick may appear on the ST segment in lateral leads. Some people may say they be seeing a yellow glow around objects or yellowing in their vision, signiciant nausea, palapatations - this may develop reverse tick on ecg st segment which suggests that the patient is toxic to digoxin.
33
What is the treatment of digoxin toxicity?
Stop the digoxin, has a very long half life however so if patient is at signifcant risk then use moclonal anitbody digibind which will help reduce the oxygen level rapidly and increases excretion by the kidneys. If there is low potassium then there is risk of significant arrhythmias in which toxicity is increased.
34
How does adenosine work?
Adenosine is a nuceloside organic compound. It binds to adenosine receptors in the AV node. It slows /blocks conduction through AV node. This is used to convert paroxysmal superventricular tachycardia to sinus rhythm It can also help diagnose atrial flutter
35
What are the side effects of anti-arrhytmias?
All anti-arrhythmias can cause arrhythmias.
36
What is warfarin?
- Warfarin is an oral anticoagulant. - Warfarin therapy is monitered by INR normal is 1.
37
What are the adverse effects of anticoagualation with warfarin?
bleeding, interaction with multiple other drugs and problematic in pregnancy (fetal and placenta bleeding and teratogenic effects)
38
What is warfarin metabolised by?
Warfarin is metabolised by the cytochrome p450 system.
39
What are the characteristics of the "ideal" anticoagulant?
- Oral - No need for monitoring - No interaction with food or drugs - Given once or twice a day/fixed dose irrespective of body weight/age - As effective as warfarin - Safer than warfarin
40
What are the characteristics of warfarin?
- oral - needs monitoring - interacts with a lot of different drugs and can interact with food.
41
What are direct oral anticoagulants?
Apaxiban - rivaroxaban edoxaban
42
does apaxiban have drug interactions?
Apixaban has multiple drug interactions but less problematic then warfarin.
43
What are the pharmodynamics of apixaban?
Still interacts with things that increase bleeding e.g aspirin, NSAIDS or SSRI’s
44
What is the pharmokinetics of apixaban?
Antiepileptics eg carbazapine reduces apixaban effectiveness so it is best to avoid. Multiple theoretical interactions eg amiodarone/dronedarone, verapamil, conazole antifungals. No advice is given for most