Cardiac Arrhythmia (Basic Concepts)
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What is Arrhythmia?
When heart deviates from the normal rhythm is called arrhythmia.
Normal Cardiac Rhythm and Its Criteria:
Normal cardiac rhythm has following criteria:
Heart rate is better 60 – 100 beats/min.
Every heart beat should be originated from SA Node.
All cardiac impulses should be passed through normal conduction pathway
Cardiac impulse should be passed through normal pathway with normal velocity
On the basis of heart rate arrhythmia can be classified as
1. Tachyarrhythmia – Tachycardia
2. Bradyarrhythmia- Bradycardia
When heart rate is more than 100 bpm we call Tachy arrhythmia, which are further classified as:
a. Simple Tachyarrhythmia – Tachycardia
When heart rate is between 100 – 150 bpm
b. Paroxysmal Tachyarrhythmia – Tachycardia
When heart rate is between 150 – 250 bpm
c. Flutter (Atrial or Ventricular Flutter):
When heart rate is between 250 – 350 bpm
d.Fibrillation (Atrial or Ventricular Fibrillation):
When heart rate is more than > 350 bpm
If heart rate is less than 60 beats/min we call Brady Arrhythmias, which are further classified as:
a. Bradyarrhythmia- Bradycardia
When heart rate is between 40 – 60 bpm
b. Bradyarrhythmia- Bradycardia
When heart rate is between 20 – 40 bpm
c. Severe Bradyarrhythmia- Bradycardia:
When heart rate is less than 20 bpm
On the basis of main site where abnormal rhythm is generated, we can classify arrhythmias as:
Any abnormal rhythm which comes from SA Node, called as Sinus arrhythmia.
2. Atrial Arrhythmia:
Those abnormal rhythms which are due to abnormal activity within the atrial myocardial tissue are called atrial arrhythmias.
3. Junctional arrhythmias (Nodal Arrhythmia)
When there are, abnormal rhythms related with AV Node or related with junction between the atrium and ventricle called junctional arrhythmias.
4. Ventricular arrhythmias
If there is abnormal rhythm originating due to abnormalities with the ventricles we call them
Sinus arrhythmias, atrial arrhythmias and junctional arrhythmias are also called supra ventricular arrhythmias are also called arrhythmias because these arrhythmias are generated above the ventricles.
Mechanism of Cardiac Arrhythmias
Re-entry (Circus moment)
It is defined as: “Property of any excitable tissue which can undergo depolarization spontaneously.”
How automaticity is increased?
SA Node works as a pace maker because it has tendency to undergo depolarization spontaneously.
In SA Node, cell have leaky Na+ channels, when Na+ enters into cell, the RMP cannot really rest because incoming Na+ will take RMP towards threshold, when RMP reaches up to threshold, there is opening of voltage-gated Ca++ channels, this produces Ca- dependent depolarization and then opening of voltage-dependent K-channels and K+ efflux occurs and membrane become again repolarized.
When you stimulate SA Node with epinephrine or nor-epinephrine, stimulating the Beta-adrenergic receptors, eventually leading to phosphorylation of some additional Ca++ channels and additional Ca++ comes in, this added ca++ helps the cells to move RMP towards threshold potential more rapidly and these is frequent production of action potential. In this way, normal automaticity is enhanced after the action of epinephrine on SA Node.
2. Triggered Automaticity:
In ventricular cells, RMP keeps on resting until the nearby cells throw some cations into the cells and these cells will undergo depolarization and it has long plateau phase due to k+ efflux and entering of Ca++ at the same time.
Repolarization takes place only due to K+ efflux in ventricular arrhythmias, early after depolarization and delayed after depolarization.
3. Re-entry (Circus movement)
If there is a scarred area in the heart, when electrical current comes to this area, on one side it moves well and form other side it cannot move due to blockage. The side on which it moves slowly, when it will come back it will find excitation behind the blockage and this current will enter into the area back and this current will start moving around this dead area. This situation is seen when total time taken by cardiac impulse around an area is longer than the time reacquired for a blocked area to recover from the refractive phase and becomes excitable and starts moving rapidly. This is called circus movement.
Sinus Arrhythmia and ECG Patterns
Physiological Sinus Arrhythmia
One of the major Parasympathetic outflow called Vagus that controls the automaticity of SA Node. Vagus has inhibitory influence on S.A Node and heart rate will go down and whenever Vagus itself inhibited, heart rate will go up.
During inspection vagus is inhabited and heart rate will go up. During expiration vagus is stimulated and heart rate will go down. This phenomenon is called Physiological Sinus Arrhythmia.
During inspiration, heart rate goes up and R-R distance decrease and in a given time more P-wave and QRS complex.
During expiration, heart rate goes down and R-R distance will increase.
There is increased activity in the sinus, commonly seen during exercise, fever and thyrotoxicosis ( ↑ T3, ↑ T4 ). Excessive stimulation to SA Node, it will generate depolarization more frequently and heart rate will go up.
In ECG, P – Wave is produced more frequently followed by QRS complex in a given time.
There is something which inhibits SA node, so heart rate is less than 60/mint commonly seen in Athletes, Hypothyroidism and Cholestatic jaundice.
In ECG P – Wave are appearing less frequently followed by QRS complex in given time R-R distance will become more.
Sick Sinus Syndrome
SA Node is behaving pathological fashions, for some time it may be firing faster than the normal and at other time it may be firing slower than normal.
Atrial Abnormal Rhythm and ECG
Atria produces electrical activity at the rate of 120 – 250 beats/mint. In this case, you can see multiple P – wave and after those P – Wave you may find QRS complex.
à Atrial activity is very fast as compared to ventricular activity.
In this case, electrical activity in atria becomes very fast. There is special type of waves which are not well-recognized P – waves, these Characteristic waves are called F – Waves having saw tooth appearance.
It means very fast rhythm in the atrium.
There are more than one foci in the atria producing electrical activity having vectors directed in different directions at a given time.
In ECG, base line shows just some fluctuations producing small waves called as F – Waves.
Atrial Tachyarrhythmias may precipitate with ventricular tachyarrhythmias.
We must terminate atrial tachyarrhythmias. If we cannot terminate atrial tachyarrhythmias, then we should slow down AV – Node by Following groups of Drugs.
Ca++ Channel blockers
Digitalis (Vagotonic drugs)
This is a specialized electrical window between the atria and ventricles through which current can pass from atria to ventricles.
SA node has high automaticity.
Atria and ventricles are responsible for contraction.
AV Node has slow conduction.
Purkinje system has fast conduction.
Function of AV node is to conduct the current from atria to ventricles with extremely slow velocity. When current enters in AV node and exists from AV node, there is a delay of 0.1 second. The importance of this delay allows the atria to comfortably empty their blood into ventricles. When atria have completed their systole only then current will release into ventricles and ventricular systole starts.
When junctional tissues become so fast, Junctional Tachyarrhythmias are produced.
When junctional tissues become too slow, Junctional Bradyarrhythmias are produced.
Why AV node is a slow conductor?
AV node cells are small in size.
There are few gap junctions between these cells.
AV nodal cells have small diameter
RMP of AV nodal cells is -60mV.
Why current passes rapidly through Purkinje system?
Purkinje cells are larger in size.
The cells are present along the axis of the current
There are more gap junctions between the cells.
Diameter of the cell is more.
RMP of these cells is -90mV.
Junctional Blocks, Nodal Blocks, Heart Blocks
In normal cardiac cycle:
P-Wave: atrial depolarization.
PR segment: Duration for which the current is held in AV node.
QRS Complex: Ventricular depolarization which further has three steps:
Major ventricular depolarization
T Wave: Ventricular Re-polarization
PR Interval: P-Wave + PR segment
Anything which makes AV Node slower, then the PR segment will become longer and automatically PR interval will be longer.
Heart blocks are defined as:
There is unusual block to electrical activity when it is trying to pass from atria to ventricles.
Drugs that can cause Heat Blocks are:
Calcium channels blockers.
Digitalis (vagotonic drugs)
Types of Heart Blocks.
There are three degrees of Heart Blocks.
First Degree Heart Block:
Every current from atria is allowed to go ventricles but it is held in AV Node for unusual longer duration.
This is pathological prolongation of PR interval i.e. more than .22 sec.
In ECG, every P-wave is followed by QRS Complex.
Second-degree heart block.
Some of the atrial activity is conducted down and some of it is not conducted to ventricles, it means in ECG, all the P-waves are not followed by QRS complex.
It is subdivided into two important types:
Mobitz-I:There is progressive elongation of PR- interval until one P-Wave is not followed by QRS complex.
Mobitz-II:There is no variation of PR Interval.
PR- Interval is stable, but somewhere P-wave may not be followed by QRS Complex.
2:1 Second Degree Heart Block:
When these are after two P-Waves one QRS-T is there. For every two P-waves there is one QRS complex.
Third Degree Heart Block:
When there is more suppression of AV node, whatever P-waves are coming, they are unable to go down. None of the atrial activity can pass to the ventricles. The new pacemaker will be developed and now ventricles will be driven by this new pacemaker. Now atria are paced in a different way and ventricles are paced in a different way.
Usually SA node may be driving atrium at the rate of 80 bpm and maybe this new pacemaker may be producing ventricular depolarization just 40 bpm.
Now the activities of atria and ventricles are dissociated from each other, these activities are no more synchronized.
In ECG, there is no relationship between P-wave and QRS. P-waves are totally independent of QRS complexes.
There is something wrong at the junction, it means around or near the AV node there is pathology precipitating tachycardia.
In this case, there is an abnormal connection between atria and ventricles. This connection is called Bundle of Kent, i.e. faster than AV-node.
Some people born with this anomaly, when current passes through this Bundle of Kent, this pathway is faster than AV-node, eventually PR-segment will be shorter. There are myocardial cells between bundle of Kent and bundle of His. These myocardial cells conduct the current with moderate speed. Due to that area a small vector is made and this vector considered with depolarization of septal muscle, this can lift the needle gradually up that is why particular wave is produced. This pathological situation is called Wolf Parkinson white syndrome.
When these patients take caffeine or alcohol or do some exercise or become anxious, making AV node fast and precipitate dangerous tachyarrhythmias.
Let us imagine the patient has taken caffeine and develops some irritable foci producing ectopic current. This current enters into bundle of Kent and passes through it and goes downward, re-enter into area which is just came out of refractive phase, it starts rotating (circus movement). This rotation takes 0.4 seconds and heart rate will become 140 bpm.
So these patients should avoid alcohol, caffeine, smoking and stress.
In another example, in AV node, two types of pathways are produced and one pathway conducts fast and another conducts slowly. It may happen that the current from the fast pathway moves down as well as re-enter, this is called intranodal re-entrant phenomenon.
This is completing the cycle every 0.3 seconds and starts shooting down the current on the ventricles every 0.3 seconds and heart rate will go to 180-200 bpm.
Massage the carotid sinus: it stimulates strong vagal outflow that will inhibit AV node.
Drugs: Verapamil injection (IV) or any other drug which can inhibit AV node.
Ventricular arrhythmias are produced by irritable foci in the ventricles.
When myocardial cells develop ischemia, oxygen supply is less and ATP level is less, eventually NA/K pumps will not work. Whatever Na coming in, is being trapped into cells this accumulated Na makes the RMP less negative, taking the RMP toward THP.
During ischemia, membrane of the cells is physically injured and the membrane becomes more leaky and more cations (Na+ and Ca+) will enter into the cells.
Whenever cations will be loaded, RMP will become less negative and it will start fluctuating the RMP and when it touches THP and pathological action potential is produce. This is called Ectopic Firing. When the patients of ischemic heart diseases get angry, excited or tense, more adrenaline will bind with beta-1 adrenergic receptors, consequently causing phosphorylation of calcium channels and more calcium will come in and the cells become further loaded with cations.
When there is ectopic firing, in ECG abnormal QRS complex is appeared (wider QRS complex), because the current is not passing through normal high-velocity pathway.
These abnormal QRS complexes called ventricular premature beats, because this ventricular focus fires before the normal beat come.
If they start appearing frequently then it is a dangerous sign.
When one ectopic foci has fired many times repetitively, this is called Ventricular Tachycardia.
When one foci may start firing and driving the ventricles somewhere between 250-350 electrical stimulations per minute.
When ventricular flutter continues for significant time, the mechanical activity cannot follow so fast electrical activity and cardiac output will dangerously drop, then hundreds of areas of sever ischemia will appear in the heart and every area will start firing on its own, this is called Ventricular Fibrillation.
In Ventricular Flutter, there is one or two centers which are firing very rapidly, but in Ventricular Fibrillation there are many centers (ectopic foci) which are firing very rapidly.
If we don’t treat the ventricular fibrillation, it will lead to a straight line on ECG i.e. death.