Lever: Treatment of Rhythm Disturbances Flashcards

1
Q

Common conditions of the heart?

How many drugs for heart problems are currently available?

A

Normal Heart Rhythms

  • normal electrical activity
  • normal excitation-contractile coupling
  • ectopics

Bradycardias

  • AV/SND conduction disorders, often supportive treatment or withdrawal of current drugs

Tachycardias

  • Automaticity/triggered activity
  • Re-entrant mechanisms

Less than <20 drugs are available for rhythm disturbances

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2
Q

Types of arrhythmias and the therapy used for them?

A

Simple → complex
either because condition OR its comorbidities are complicated

Benign → malignant

  • Drug Therapy: to supress the substrate causing the arrhythmias or the triggers
    • not curative
    • SE profile
    • Interactions
  • Drug/device/intervention interface: we need a combination of treatments for optimal outcome
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3
Q

Cardiac Devices available are, where do they go?

A
  • Single chamber AAI/VVI (R)
  • Dual chamber DDD (R) programmed to do both, may use 2 wires
  • Pacemaker vs ICD (cardioverter defibrillator)

  • Usually inserted underneath the clavicle*
  • ONLY SUPPLY SLOW HEARTBEATS, racing tachycardias will not work*
  • Rate support
  • AV synchrony
  • VV synchrony (CRT device)
  • Other;
    • vasovagal syncope devices
    • monitors
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4
Q

Why do we give a pacemakers??

Why do we give defibrillators and CRT

A
  • Give pacemakers for patients with bradycardic indications
    • high grade AV block, symptomatic sinus node disease
    • DOn’t usually give to those with a risk of sudden cardiac death, BUT could do be if they don’t want ICD and have long QT syndrome, or have a pacemaker and drugs
  • Defibrillators -ICD
    • Those who have aborted Sudden CD (rescued from Vt or VF) or sustained VT in structural heart disease
    • High risk for SCD***
  • Cardiac Resynchronisation Therapy (CRT)
    • Ventricle that’s not working properly, LBBB, cardiomyopathy w. symptoms
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5
Q

A sinus tachycardia. When is it appropriate and when is it inappropriate

A

Appropriate: fever, thyrotoxicosis, pain
Treat the cause of the ST!!

Inappropriate: no drivers, ST, automaticity problem, sinus node reentry

Can give a small amount of b blocker to treat the symptoms (like sweatyness, shakey and fast HR) if you have a particular reason to treat - eg. big performance. But you expose to adverse effects

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6
Q

What is an ectopic beat?

A
  • Beat in the atria or ventricle that arrives before you expect it to
    • Atrial ectopic beat: Narrow QRS response
    • Ventricular ectopic: broad as we are no longer using the Purkinje system
  • Common -often only felt if we are resting
  • Clinical significance
    • Majority are benign (increase with age)
    • Distraction and activity mutes most of these
    • Very aware of them when we are unwell, our brain become more aware, can be frightening!
  • Assessment:
    • examination- exclusion, history very important
    • Appropriate tests ECG, Echo, holter
  • Treatment
    • reassurance of the patient as the treatment can cause more issue
    • Suppressive Rx (caution SE/ADR)
      • Betablockade
      • Class I agents
    • Severe symptoms + focus → ablation
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7
Q

Common Treatments of Ectopic beats are?

A
  • Assessment
  • Reassurance
  • Drug therapy
  • Withdrawal of drug Rx
  • Management of underlying condition
  • Devices
  • Intervention (surgical/ablation)
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8
Q

Drug therapy for Heart surgery: general summary?

A
  • Anti-arrhythmics cover a range of classes
    • each have their own modes of action and come with their own risks/pro-arrhymthmic profile
  • Major side effects are common
  • Can have co-morbidities with other drugs
  • Can have a pro-arrhythmic effect
  • Can interact with other drugs/devices
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9
Q

Describe Class I heart drug therapy agents.

A

Sodium channel blockers

  • Often use popafenon and flecainide

IA​

  • Reduce Vmax and prolong AP widening QRS and QT
  • quinidine, procainamide
  • rapid on/offset

IB

  • No effect of Vmax, shorten AP and refractory period
  • mexiletine, phenytoin,
  • fast on/offset

IC -

  • Reduce Vmax, slow conduction, little to no effect of refractory period
  • flecainide, popafenone,
  • slow on/offset
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10
Q

Describe Class II, III and IV heart drug therapy agents.

A

Class II: Beta-blockers

  • “olol” propanolol, metoprolol, atenolol
  • slow down sinus node and AV conduction

Class III: K+ channel blockers → increase repolarisation

  • Sotalol: has Class II activity in low doses and Class III in high doses
  • amiodarone

Class IV: Slow Calcium channel blocker

  • nifedipine
  • also helpful for hypertension
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11
Q

How do anti-arrhythmics work

A
  • affect different places; cell membrane, ANS, vagal tone
    • Vagal tone:
      • increased: decreases heart rate, decreases SA automaticity, slower conduction through the AV node
      • Decreased: Increased heart rate, increased SA automaticity, faster conduction through the AV node
  • Cell membrane activity affects; conduction velocity, length of refractory period, automaticity of the SA or AV node
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12
Q

What is the class of anti-arrhythmics most commonly used clincially?

A

Class 1C

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13
Q

Where else could you use Class II anti-arrhythmics (beta-blockers)?

A
  • hypertension
  • post myocardial infarction
  • Heart failure
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14
Q

Why is it important to read up on class III antiarrhythmics?

A

Because these drugs are commonly used and have important drug-drug interactions. eg; amiodarone and warfarin

Can also interact with devices!

Sotalol and amiodarone are frequently proarrhythmic

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15
Q

Classic side effect of Class IV drug verapamil?

A

Ankle oedema

due to excessively dilated peripheries

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16
Q

Digoxin?

A
  • Increases parasympathetic activity
  • Slows the atrial rate
  • slows AV nodal conduction
17
Q

Adenosine?

A
  • Purine nucleotide
  • Typically administered by IV (bolus and flush)
  • Causes transient AV node block (and some SA node effect)
18
Q

Pro-arrhythmia?

A

Important if you’re older and female

  • Major and potentially fatal clinical problem (up to 5%)
  • Mechanisms:
    • prolongation of repolarization
    • development of EADs which cause torsades
    • alterations in reentry pathways
    • Can cause acquired LQT
  • Increased risk of proarrhythmia in HF
19
Q

The commonest type of a regular narrow tachycardia?

A

AV Nodal Re-entrant Tachycardia

  • AV nodeduality
  • Ectopic trigger
  • ‘Safe’ SVT
  • Can be easily aborted
  • Medical therapy
    • eg; adenosine; transient AV block, be careful with how much you use
  • Ablation therapy
    • AV damage: don’t damage everything → you’ll ruin the main pacemaker
    • Curative
    • 10% recurrence
20
Q

AV Re-entrant Tachycardia alternative

A
  • Short circuit using an accessory reentry pathway
  • Action potential safety
  • Treated with: medical and ablation therapy
  • People can be born with this eg; meatloaf
    • Counterclockwise: narrow (normal system)
    • Clockwise: broad (not using purkinje system)
21
Q

What’s this rhythm disturbance?

A

an irregularly irregular ventricular rhythm disturbance

Therefore its atrial fibrillation!

22
Q

Describe atrial fibrillation

A
  • Common especially with increasing afe “irregularly irregular”
  • interestingly many people don’t know they have it
  • Varying symptoms
    • stroke
    • rate-related cardiomyopathy
  • Morbidity/mortality
  • Rate vs rhythm control (what will reduce their two issues the most??)
    • drug: things that slow down the AV node; b-blockers and Ca antagonists
    • device
    • intervention - ablation to remove triggers
  • Anticoagulation issues: balance with the risk of treating and not treating
  • Comorbidities
23
Q

Whats the fundamental process of AF ablation?

A
  • Ablate around the pulmonary veins (bringing back fresh red blood from the lungs) in loops. This separates them from the atria and is done as these can provide unwanted stimulus due to firing off lots of ATP.
  • Tries to ring off and ‘contain’ the ectopics that these can cause
24
Q

Common anticoagulants available in NZ

A

Warfarin

dabigatran

Heparin

DOACs

25
Q

The chance of SCD increases with…

What does this mean for screening?

A
  • myocardial infarction
  • reduced EF

It’s the general adult population as a group who are more likely. But this risk is nowhere near as large as someone who had a previous cardiac-related event. Do we screen the general public? how far can our preventative measure go?

26
Q

Venticular tachycardia

A
  • Reentrant or automatic trigger around or in scar tissue
  • VT invades rest of ventricles
  • Call for help! (111 in the hospital 777)
  • Broad complex;
    • activating chamber through cell-cell contact
    • Not using normal His-Purkinje network
  • Atria cont. to activate and contract independently
27
Q

What do you do if someones in VT/VF?

A

Emergency management:

  • 777 in hospital
  • resuscitation

THEN treat underlying pathology

  • ischaemia
  • bradycardia
  • structural disease
  • metabolic or drug causes
28
Q

Amiodarone

A
  • Dirty drug
  • Side effects and toxicity high
  • Loading issues: pulmonary, thyroid toxicity
  • Maintenance
    • TFTs/LFTs
    • lung function
  • Drug interaction
    • warfarin
29
Q

So now we know that treating someone isn’t just throwing drugs at them, its …..

A
  • Rx of underlying cause
    • CAD/hypertension/OSA/obesity etc
  • Rx of comorbidities
  • Specific tachycardia treatments
    • drug/device/intervention
  • Prophylaxis
  • Important interactions: