CVS: Arrhythmia Flashcards
What is arrhythmia?
Abnormalities in heart rhythm. Arrhythmias lead to incorrect filling and ejection, incorrect CO and thus the symptoms of: Palpitations, dizziness, fainting, fatigue, cardiac arrest, blood coagulation (stroke, MI)
- Causes: Cardiac ischemia (MI, angina), heart failure, hypertension, heart block, excess symp stimulation
- Origin: Supraventricular (above ventricles- SAN, atria, AVN). Or ventricular.
- Effect : Tachycardia or Bradycardia
Describe AF and SVT
Describe heart block, VT and VF
Give the Mechanisms of arrhythmogenesis
Abnormal Impulse Generation due to:
Automatic rhythms - increased SAN activity, ectopic activity
Triggered rhythms – Early-after depolarisations (EADs), delayed-after depolarisations (DADs)
Abnormal Conduction due to:
Re-entry electrical circuits in heart- eg an ischaemic area which changes conduction
Conduction block
What is ectopic pacemaker activity?
Pacemaker activity is initiated in SAN but other areas can have pacemaker activity to ‘safeguard’ if SAN becomes damaged- eg the AVN, bundle of His, Purkinje fibres.
These low Hz ‘pacemaker’ areas are greatly enhanced by symp activity, if they become the predominant signals then this is ectopic pacemaker activity
They cause continuous symp stimulation, causing stress, HF and arrhythmia
What is EAD and DAD?
EADs: A.potentials during the refractory period. Due to altered ion channel activity e.g. abnormal increase in Na or Ca channel activity
DADs: in phase 4, after repolarization but before another a.potential would normally occur.
RyR becomes leaky; Ca2+ leaks out from RyR into cytosol. This Ca2+ stimulates Na/Ca exchanger, removing Ca and bringing Na+ into the cell= depolarisation
What is reentry (in abnormal impulse conduction)?
In a general conduction pathway, a.potentials stop conducting because surrounding tissue is refractory
But, myocardium damage means that some areas of the heart are more conductive than others – produces RE-ENTRY pathways. It can cause premature impulses to generate inappropriate a.potentials.
What is another type of abnormal impulse conduction which is not reentry?
Heart block from fibrosis/ischaemic damage of conducting pathway. Often AVN issue
1st degree: Conduction slows down between atria and ventricles. P-R interval >0.2 s
2nd degree: >1 atria impulses fail to stimulate ventricles
3rd degree (complete block): atria and ventricles beat independently of one another. Ventricles contract slowly depending on what ectopic pacemaker sets the rate (e.g. Bundle of his, ventricular tissue).
What is the main goal in the treatment of arrhythmias?
Restore sinus rhythm and normal conduction. Prevent more arrhythmia. To achieve this, anti-arrhythmic drugs:
- Reduce conduction velocity
- Alter refractory period of cardiac action potentials
- Reduce automaticity (decrease EADs, DADs, Ectopic beats)
Briefly outline the classes of antiarrhythmic drugs
Class I : Na+ channel blockers slow down ap generation (non-nodal tissue)
Class II : β blockers reduce excitability
Class III : K+ channel blockers (non-nodal tissue)
Class IV : Ca2+ channel blockers
Non-classified drugs
Describe Class I drugs – Na+ channel blockers
Eg Lidocaine: block Na+ channels in non-nodal tissue (atria/ventricles) in their inactivated state.
It is a fast dissociating drug, meaning that it comes off the channel in <0.5s. So, it has a greater effect on higher ap Hz (see diagram). Hence useful for fast arrhythmia, e.g. VT and VF. Overall this is a use dependence property.
Describe class II drugs- beta blockers
Symp nerve stimulation activates β1 receptors, increasing SAN and AVN firing rate. Also increase ventricular excitability at AVN. These effects are pro-arrhythmic
β1 blockers, e.g. atenolol, bisoprolol reduce VT after myocardial infarctions caused by increase in sympathetic nerve activity
Slows initiation of pacemaker potentials in SAN, and slows conduction through AVN to reduce ventricular firing rate in SVT
Describe Class III drugs – K+ channel blockers
Class III, e.g. amiodarone:
Inhibit K+ channels responsible for repolarisation in atria/ventricles (not K+ channels in SAN/AVN). This prolongs repolarisation and the refractory period. Na+ channels are in-activated, no more ap’s can be fired – prevent arrhythmias
Used for SVT and VT
Describe Class IV drugs – Ca2+ channel antagonists
Block L-type voltage-gated Ca2+ channels found mainly in nodal tissue (but also Phase 2 of atria/ventricle). Reduces pacemaker potential Hz
L-type Ca2+ channels also found on vsmcs for vasoconstriction – so blockers can relax blood vessels and decrease bp
Class IV, e.g. Verapamil (more cardiac specific), diltiazem (cardiac and vascular smooth muscle). Used to control ventricular response rate in SVT
Describe the non classified drugs
Adenosine: Decreases activity in SAN and AVN. Used for SVT
Atropine: Muscarinic antagonist. Reduces parasymp activity. May treat sinus bradycardia (very low HR) after MI
Digoxin: Increases vagus nerve activity which increases Ach release, activating more muscarinic receptors which slows HR and conduction. Used for AF. Inhibits the Na/K pump which increases Ca levels and therefore contractility
What is an issue of class III drugs?
Class III drugs increases QT duration of ECG, causing long QT syndrome. This can generate unwanted EADs and DADs= arrhythmia. It can create a Torsades de pointes (ventricular tachycardia) on an ECG.
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