Week 5/6 - A - Cardiac Arrhythmias - A.V.N.R.T/A.V.R.T/A.V Block - symptoms, Ix, Types, Treatment (drugs+pacemaker) Flashcards
(36 cards)
Describe the normal spread of electrical activity throughout the heart? What is the normal pacemaker of the heart?
Normal electrical activity pathway * SA node (pacemaker cells of the heart here) –> * Av node –> * Bundle of His –> * Left (anterior / posterior) and right bundle branches –> * Purkinje Fibres
Cardiac arrhythmias are a disturbance of the heart rate or rhythm and are generally named depending on their * Anatomical site or chamber of origin * Rate * Mechanism Where do supraventricular arryhtmias oriignate? Where do ventricular arrhythmias originate? What is bradycardia and what is tachycardia?
Supraventricular arrhythmia originate above the ventricle eg SA node, atrial muscle, AV node or Bundle of His Ventricular arrhythmia originate either in the ventricular muscles of fasicles of the conducting system (uncommon eg Left or right bundle branches) Bradycardia - heart rate 100bpmm
What are the different types of supaventricular arrhythmias? Those originating in atria, AV node
* Sinus arrhythmia * Atrial fibrillation * Atrial flutter * Supraventicular tachycardia - technically includes A.Fib and A.FLutter - usually used to classify * Av Nodal re-entry tachycardia (AVNRT) * AV re-entry tachycardia(AVRT) AV block (heart block) * Sinus bradycardia
Name different examples of ventricular rhythms
Ventricular ectopics aka Premature ventricular complexes Ventricular tachycardia Ventricular fibrillation
Many different causes of arrhythmia - eg abnormal anatomy, autonomic nervous system, metabolic causes, inflammatory causes, drugs, genetics What are ectopic beats?
Ectopic beats are beats or rhythms that originate in places other than the SA node
Defects in impulse conduction include re-entry circuits, conduction blocks (AV block) and accessory tracts Normally an action potential is conducted through 2 areas in an AV nodal conduction However why does this not result in a double beat?
This is because the action potential travel separate ways and the potentials will cancel each other out if they ‘collide’
How do AV nodal re-entry circuits arise? What are the two main things required for a re-entry circuit to develop?
The electrical signal does not complete the normal circuit, instead an alternative circuit loops back upon itself. This develops a self-sustaining circuit which has rapid and abnormal activation. Requires - 1. unidirectional block- inhibiting anterograde conduction and allowing slowed retrograde conduction
We have discussed AV blocks previously - Sum up the types
* 1st degree AV block - Regular tachycardia with PR interval >0.2seconds and no progressive lengthening * 2nd degree AV block * Mobitz Type 1 - progressive PR lengthening until there is a missed beat (pwave without a QRS following) * Mobitz Type 2 - constant PR interval then a missed beat 3rd degree AV block - no relationship between p waves and QRS due to no communication between atria/ventricle - often ectropic escape beat present
Defects in impulse conduction * Discussed the re-entry circuits (AVNRT) * Conduction block Some individuals possess electrical pathways in parallel to the AV node - an accessory tract pathway (these are AV rentrant/reciprocal tachycardias (AVRT) How does AVRT result in tachyarrythmias?
Accessory pathways allow for electrical activity to bypass the resting atrial myocytes creating a circuit atria-AVN-ventricles-accessory pathway-atria) The ventricles therefore recieve impulses from both the normal and accessory pathway which can result in tachyarrythmias
Name a common accessory pathway? What is a congenital condition where there is accessory conduction pathway between atria and ventricles resulting in slurred upstroke of the QRS? What is seen on ECG?
The bundle of Kent is an abnormal extra or accessory conduction pathway between the atria and ventricles that is present in a small percentage of the general population. Wolf Parkinson White syndrome - * Slurred QRS * QRS >0.12s * PR interval
What causes the delta wave in WPW syndrome?
This is causes due to pre-excitation of the ventricles due to the accessory pathway causing the ventricular contraction Reduces the PR time also
What are the symptoms of a cardiac arrhythmia?
* Palpitations - pounding heart * Shortness of breath * Dizziness * Loss of cosnciousness - syncope (fainting) * Feeling faint- presyncope * Sudden cardiac death * Angina, heart failure
What investigations are carried out to diagnose a cardiac arrhythmia? What are the different types of ECG?
12 lead ECG or continous ECG monitoring as below * Stress ECG for exercise related arrythmias or myocardial ischaemia * 24 hour Holter ECG * If an in patient - can use telemetry - monitors RR, SPo2 and ECG Echo - looking for structural disease in the heart Measure electrolytes
We know there are many different types of arrhythmia. Before we discuss them and how they are treated, lets take a look at the anti-arrhythmic drugs Anti-arrhythmic drugs generally inhibit specific ion channels and can be classified pharmacologically based upon their effects upon the cardiac action potential What is this classification known as?
The Vaughn Williams classification The scheme defines four classes I, II, III and IV, with class I subdivided into subclasses Ia, Ib and Ic Some drugs eg adenosine and digoxin do not fit into this classification system
Firstly, discuss what ion channels are involved in each of the stages of the SA node action potential?
SA NODE Spontaneous pacemaker potential - K+ efflux superimposed on a slow Na+ influx (funny current), transient Ca++ influx through T-type Ca channels Rising phase -Ca++ influx (L-type channels) Falling phase - closure of L-type Ca++ channels and K+efflux
Now, discuss what ion channels are involved in each of the stages of the myocyte action potential?
Cardiac myocyte Phase 0 - Fast Na+ influx Phase 1 - Closure of Na+ channels, and transient K+ efflux Phase 2 - Mainly Ca++ influx Phase 3 - Closure of Ca++ channels and K+ efflux Phase 4 - back to resting membrane potential
Vaughn Williams Anti-arrhythmic drug classification * The scheme defines four classes I, II, III and IV, with class I subdivided into subclasses Ia, Ib and Ic How does each class of anti-arrhythmic drug work?
* Class 1 - Target the voltage activated sodium channels - prolonging the action potential and slowing the heart rate
* Class II agents - Decrease rate of depolarisation in SA and AV nodes
* Class III agents - Target voltage activated K+ channels plus others - prolongs AP duration increasing refractory period
* Class IV - Target L-typevoltage activate Ca++ channels - slows conduction in SA an AV nodes and decreases contraction force
Try and name the different drugs in each anti-arrhythmic classification Which anti-arrhythmic drugs are rate controllers and which are rhythm controllers?
Rate control Class II - Beta blockers - eg metoprolol Class IV -L-type Ca++ channel blockers - eg verapamil and dilitiazem Rhythm control Class I - Na+ channel blockers disopryamid, lignocaine, flecainide Class III - K+ channel blockers as well as others - amiodarone
For SVTs, available drugs include Class II (BB), Class IV (CCB), amiodarone, ADENOSINE AND DIGOXIN For VTs, available drugs include BB and Amiodarone (Class I drugs not really used but technically work for both atrial and ventricle arhythmia) How does adenosine work?
Adenosine is give IV It activates A1-adenosine receptors This cause opening of K+ channels causing potassium efflux and briefly hyperpolarising the AV node Useful for terminating SVTs caused by re-entry involving AV node, SA node or atrial tissue
How does digoxin work? What is it used to treat? Why is it a ‘dirty drug’?
Digoxin stimulates vagal activity –> slows conduction and prolongs the refractory period in AV node and bundle of His - delays AV node conduction Used to treat heart failure and Afib Used to treat Afib and heart failure Has a very narrow therapeutic index
What are the side effects of digoxin? How can it cause ventricular arrhythmias?
Digoxin side effects If in digoxin toxicity, can cause nausea and vomiting, yellow vision, bradycardia and heart block Digoxin can also increase ventricular irritability which produces ventricular arrhythmias - bad
We have now discussed the anti-arryhthmic drugs used in cardiac arrhythmia. Let’s discuss the different arrhythmias and the treatment options What is a normal sinus arrhythmia and why does it arise? Describe what is seen on the ECG?
Considered to be a physiological variant - Occurs due to physiological changes in cardiac timing due to changes in vagal tone during respiration ECG meets all the criteria for normal sinus rhythm PR interval 0.12-02s Every pwave followed by a QRS, every QRS preceded by a pwave But, irregular RR interval
What is bradycardia define as? When is it physiological?What can cause it? What type of MI is it common in?
Bradycardia is a heart rate <60bpm Can be physiological ie if patient is young and fit Can be caused by sinus drugs eg bblocker, digoxin, ischaemia It is common in inferior STEMIs - this is because the right coronary artery supplies the SA and AV node in most people
Bradycaria can be eg sinus, heart block, AF with slow ventricular response When is medication given to treat sinus bradycardia and what drug?
Medication is given to treat bradycardia if there are adverse signs of deterioration ie haemodynamic shock, syncope, myocardial ischaemia Atropine is given If this fails, transcutaneous pacing me be required
