Drugs & Arrhythmia (Lever) Flashcards
What are some causes of Bradycardias
- Physiological mediated
- Atrioventricular node and sinus node conduction disorders
- Neural mediated
What are some causes of Tachycardias
Automaticity/triggered activity. Re-entrant mechanisms.
- Atrial
- Junctional (supraventricular tachycardia (SVT)
- Ventricular (scar, ‘normal’ hearts)
What are the different types of Cardiac Devices for arrythmias?
What are the different functions of Cardiac Devices?
Different types include:
- Single chamber AAI (atrial) or VVI (ventricular) (R)
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First letter- chamber the pacemaker is placed, and the 2nd is the chamber you are listening to, and the 3rd- what it does
- T= triggered
- I= Inhibited
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First letter- chamber the pacemaker is placed, and the 2nd is the chamber you are listening to, and the 3rd- what it does
- Dual chamber DDD (both atrial and ventricular) (R)
- Pacemaker vs ICD (implantable cardioverter defibrillator)
- Pacemakers treat slow heartbeats (anti-bradycardic)
- Defibrillator control fast heartbeats (anti-tachycardic)
Functions include:
- Rate support
- Atrioventricular (AV) synchrony
- Ventriculoventricular (VV) synchrony via CRT (cardiac resynchronization therapy) device
Other devices include vasovagal syncope devices, monitors.
What are the indicators for Device Support?
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Pacemaker used in
- high grade AV block,
- symptomatic sinus node disease
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Defibrillator used in
- aborted SCD (sudden cardiac death)/ sustained VT in structural heart disease
- High risk of SCD *
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CRT used in (Cardiac Resynchronization Therapy)
- cardiomyopathy
- LBBB (left bundle branch block)
Use of these devices are also accompanied by some risks (venous stenosis, valve infections, pneumothorax at time of implant)
What are some common conditions for Sinus Tachycardia?
Appropriate
- Fever, thyrotoxicosis, pain etc.
- Most of time, treat cause of sinus tachycardia
Inappropriate
- No drivers
- ?ST
- ?Automaticity
- ?Sinus node re-entry
- Requires drug therapy
Describe the Clinical significance of Ectopic Beats
How do atrial vs ventricular ectopic beats present in an ECG?
Ectopic beats are common, which involves beat of ventricles out of expectation. Majority is benign.
- Atrial ectopic beats have narrow QRS complex (indicates normal conduction through His-Purkinje system)
- _Ventricular ectopic beat_s have wide QRS complex (slower conduction)
Symptomatic state proportional to number of factors (prematurity of ectopic, distraction/activity)
How do you assess ectopic beats?
Examination for exclusion. Appropriate tests include ECG/echocardiogram/Holter.
Describe the Summary of Treatment for Ectopic Beats
Summary of Treatment
- Assessment and reassurance
- Make sure ectopy is benign then reassure patients
- Exclude malignancy by taking thorough history and family history of syncope, sudden cardiac death
- Suppressive drug therapy (caution with side effects/adverse drug reactions SE/ADR)
- Beta blockers, class I agents (?)
- Drug withdrawal might cause problems
- Management of underlying condition
* Device and surgical/ablation intervention (severe symptoms + focus → ablation)
Describe the Class 1 Antiarryhtmic drug therapy
- Na+ channel agents (predominantly blocking)
- IA = quinidine, procainamide, disopyramide (rapid onset/offset)
- ↓ Vmax, prolong AP (prolong refractoriness, slow conduction velocity).
- widens QRS interval, prolongs QT interval
- may enhance AV conduction, so may be co-prescribed with rate-slow drugs (AV nodal)
- IB = mexiletine, phenytoin, lidocaine (fast onset/offset)
- no effect Vmax
- shorten AP (shorten refractory)
- IC (most clinical use) = flecainidine, popafenone (slow onset/offset)
- ↓ Vmax
- prolong AP
- no effect on refractoriness, slow conduction velocity
Describe the Class 2 Antiarrthymic drugs
- β-blockers, which block β-adrenergic Rs in SNS
- = metoprolol, propanolol, , sotalol (low dose = class II activity, high dose = class III activity)
- cardio-selective (β1) and non-cardio-selective (β1 and β2) properties
- slows AV node conduction to treat atrial and ventricular arrhythmia
- can also treat hypertension, post-infarction (reduce mortality rate), HF
- side effects = bradycardia, fatigue; asthma/wheeze, depressed moods, constipation
- some patients on chronic β blockade require permanent pacing to manage bradycardia
- fatigue is a common side effect, but may diminish over time
- contraindications = asthma, but not chronic obstructive pulmonary disease (COPD)
Describe the Class 3 Antiarrthymic drugs (Vaughan Williams Classification)
- K+ channel blocker, can also affect sodium and calcium channels
- = sotalol, amiodarone, ibutilide.
- prolongs AP (prolong refractory period, increases rate of repolarization)
- may slow but not stop VT
- can affect defibrillation thresholds (variable individual response).
- Amiodarone ↑ DFTs
- Sotalol ↓ DFTs
- prescribed for atrial and ventricular arrhythmia
- toxicity level can build up cumulatively, therefore monitor patients frequently
Amiodarone can potentiate digoxin → reduce digoxin dose if administering with amiodarone
Describe the Class 4 Antiarrthymic drugs (Vaughan Williams Classification)
- slow Ca2+ channel blocker
- = verapamil, diltiazem
- affects mainly SA and AV nodes
- not pro-arrhythmic.
- side effect of verapamil = ankle swelling
Antiarryhtmics can affect…
1) Cell membrane
2) Autonomic nervous system
3) Vagal tone
Antiarrhythmic drugs affect _cell membrane activitie_s by…
- Conduction velocity
- Length of refractory period
- Automaticity of SA or AV node
How do Antiarrhythmic drugs affect the ANS?
- It also affect autonomic nervous system (vagal tone):
- ↑ vagal tone
- ↓ HR
- ↓ SA automaticity
- Slower conduction through the AV node
- ↓ vagal tone
- ↑ HR
- ↑ SA automaticity
- Faster conduction through the AV node
Describe the mechanism of pro-arrhythimic effect of Antiarrhythmic drugs
Mechanisms are:
- alterations in re-entry pathways
- prolonged repolarization
- development of early after-depolarizations, which cause torsades
- Torsades de pointes = specific form of polymorphic ventricular tachycardia with a long QT interval
- characterized by rapid, irregular QRS complexes, appear to be twisting around the ECG baseline
- increased risk of pro-arrhythmia in heart failure
How do you treat long QT intervals?
- acquired long QT due to some drugs given
- needs recurrent shock treatment
Describe what AV nodal re-entrant tachycardia can trigger
How can you treat this?
- due to AV node duality, ectopic trigger
- “safe” supra-ventricular tachycardia (SVT)
- medical therapy includes:
- preventative treatment (β blockers and Ca2+ channel blockers)
- acutely abort treatment
- (adenosine- transient AV block)
- ablation therapy is curative
what are the 2 types of AV re-entrant tachycardia?
- ante- vs ortho-dromic tachycardia (via accessory pathway)
- antedromic travels opposite to normal conduction pathway (wide QRS complex)
- orthodromic travels same direction as normal conduction pathway (narrow QRS complex)
Diagnose
Atrial fibrillation
Describe the symptoms and treatment of Atrial Fibrillation
Symptoms and Treatment
- Atrial fibrillation is common.
- There are varying symptoms (many are asymptomatic until complications develop such as stroke, rate related cardiomyopathy)
- There are morbidity/mortality issues, and co-morbidities.
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Rate vs rhythm control aims to reduce risk of complications. Control includes drug, device and intervention (?at AV)
- Note that restoring sinus rhythm hasn’t been proven to reduce risk of stroke
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Anticoagulation therapy for AF determined by scoring system. Common anticoagulants includes
- warfarin,
- heparin (good for short term, not for long term),
- DOACs .
- Atrial fibrillatini s not a diagnosis, it is a spectrum of disorders that present as AF.
Describe VT/VF
- caused by _reentrant or automatic trigge_r around or in scar tissue
- VT invades rest of ventricles
- broad complex due to:
- activating chamber through cell-cell contact
- not using normal conduction system (His-Purkinje network)
- Atria continue to activate and contract independently.
How do you manage VT/VF?
- Emergency Management
- 777
- Resuscitation
- Treat Underlying pathology
- Ischemia,
- bradycardia,
- structural disease,
- metabolic or drug causes
- ventricular support (anti-ischaemic, ACE inhibitor)
- antiarrhythmic (β blocker, class III, class I)
- device (ICD, pacemaker)
- intervention (surgery – CABG, ablation)
Describe the use of Amiodarone
Toxicity
Side Effects
- use to treat VT/VF
- loading issues and maintenance monitored by thyroid function tests/liver function tests, lung function
- drug interactions with warfarin and digoxin
Toxicity
- pulmonary fibrosis
- hypo- or hyper-thyroidism
- liver failure
- renal failure
- corneal deposits
Side Effects
- slight blue/red appearance on the face
- myalgias
- gait disturbance
- insomnia
- prolonged PT (↓ warfarin dosage)
- Digoxin toxicity (↓ digoxin dosage)
Describe the Treatment of Cardiac Rhythm Disturbances
Conclusion: Treatment Of Cardiac Rhythm Disturbances
- Rx for underlying cause (CAD (coronary artery disease)/hypertension/OSA/obesity, scar)
- Rx of co-morbidities
- specific tachycardia treatments (drugs/device/intervention)
- prophylaxis
- important drug interactions
