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)
-
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
-
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?
-
Pacemaker used in
- high grade AV block,
- symptomatic sinus node disease
-
Defibrillator used in
- aborted SCD (sudden cardiac death)/ sustained VT in structural heart disease
- High risk of SCD *
-
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
Diagnose
Atrial fibrillation
