Cardiac dysrhythmia (arrhythmia and irregular heartbeat) is a large and heterogeneous group of conditions in which there is abnormal electrical activity in the heart.

The heart beat may be too fast or too slow, and may be regular or irregular.

Each heart beat originates as an electrical impulse from a small area of tissue in the right atrium of the heart called the sinus node or sino-atrial node which generates a Sinus Rhythm.

The SA Node paces the heart in the normal rate range of 60 to 100 per minute.

The impulse initially causes both atria to contract, then activates the atrioventricular (or AV) node which is normally the only electrical connection between the atria and the ventricles (main pumping chambers). The impulse then spreads through both ventricles via the Bundle of His and the Purkinje fibres causing a synchronised contraction of the heart muscle and, thus, the pulse. In adults the normal resting heart rate ranges from 60 to 80 beats per minute. The resting heart rate in children is much faster.

The causes of the cardiac arrhythmias are usually one or a combination of the following abnormalities in the rhythmicity-conduction system of the heart:

Abnormal rhythmicity of the pacemaker

Shift of the pacemaker from the sinus node to another place in the heart

Blocks at different points in the spread of the impulse through the heart

Abnormal pathways of impulse transmission through the heart

Spontaneous generation of spurious impulses in almost any part of the heart

Cardiac dysrhythmias are often first detected by simple but nonspecific means:

auscultation of the heartbeat with a stethoscope, or

feeling for peripheral pulses. (cannot usually diagnose specific dysrhythmias,

but can give a general indication of the heart rate and whether it is regular or irregular. Not all the electrical impulses of the heart produce audible or palpable beats; in many cardiac arrhythmias, the premature or abnormal beats do not produce an effective pumping action and are experienced as "skipped" beats).

The simplest specific diagnostic test for assessment of heart rhythm is the electrocardiogram. A Holter monitor is an EKG recorded over a 24-hour period, to detect dysrhythmias that may happen briefly and unpredictably throughout the day.

Tachycardia means fast heart rate, usually defined in an adult person as faster than 100 beats per minute.

This electrocardiogram is normal except that the heart rate, as determined from the time intervals between QRS complexes, is about 150 per minute instead of the normal 72 per minute.

Bradycardia means a slow heart rate, usually defined as fewer than 60 beats per minute. Bradycardia is shown by the electrocardiogram.

Any circulatory reflex that stimulates the vagus nerves causes release of acetylcholine at the vagal endings in the heart, thus giving a parasympathetic effect. Perhaps the most striking example of this occurs in patients with carotid sinus syndrome.

In these patients, the pressure receptors (baroreceptors) in the carotid sinus region of the carotid artery walls are excessively sensitive. Therefore, even mild external pressure on the neck elicits a strong baroreceptor reflex, causing intense vagal-acetylcholine effects on the heart, including extreme bradycardia.

During atrial fibrillation the atria show chaotic depolarisation with multiple foci. Mechanically the atria stop contracting after several days to weeks of atrial fibrillation, the result of the ultra-rapid depolarisations that occur in the atria, typically around 400 bpm, but up to 600 bpm. At the AV node 'every now and then' a beat is conducted to the ventricles, resulting in an irregular ventricular rate, which is the typical ECG characteristic of atrial fibrillation.

During atrial flutter the atria depolarize in an organized circular movement. This is caused by re-entry. The atria contract typically at around 300 bpm, which results in a fast sequence of p-waves in a saw-tooth pattern on the ECG. For most AV-nodes this is way to fast to be able to conduct the signal to the ventricles, so typically there is a 2:1, 3:1 or 4:1 block, resulting in a ventricular frequency of 150, 100 or 75 bpm respectively

In normal tissue, if a single Purkinje fiber forms two branches (1 & 2), the action potential will travel down each branch. An electrode in a side branch off of branch 1 would record single, normal action potentials as they are conducted down branch 1 and into the side branch. If branches 1 & 2 are connected together by a common, connecting pathway (branch 3), the action potentials that travel into branch 3 will cancel each other out.

Reentry (bottom panel) can occur if branch 2, for example, has a unidirectional block. In such a block, impulses can travel retrograde (from branch 3 into branch 2) but not orthograde.  When this condition exists, an action potential will travel down the branch 1, into the common distal path (branch 3), and then travel retrograde through the unidirectional block in branch 2 (blue line). Within the block (gray area), the conduction velocity is reduced because of depolarization.

Ventricular tachycardia is defined as a sequence of three or more ventricular beats. The frequency must by higher than 100 bpm, mostly it is 110-250 bpm. Ventricular tachycardias often origin around old scar tissue in the heart, e.g. after myocardial infarction.

Ventricular fibrillation (VF or V-fib) is chaotic depolarisation of the ventricles. Mechanically this results in an arrested cardiac pump function and immediate death. VF can only be treated by immediate defibrillation. If you consider ventricular fibrillation in a conscious patient, than you should look for a technical problem with the ECG, eg. movement or electrical interference.

Ventricular Flutter is mostly caused by re-entry with a frequency of 300 bpm. The ECG shows a typical sinusoidal pattern. During ventricular flutter the ventricles depolarize in a circular pattern, which prevents good function.

Conduction disturbances can occur at the level of the sinoatrial (SA) node, the atrioventricular (AV) node and the bundle branch system. In atrioventricular block the conduction between atria and ventricles is disturbed, leading to an increased PQ interval or to P waves that are not followed by QRS complexes: atrial activity that is not followed by ventricular activity. Three degrees of block can be distinguished.

First degree AV block

In first degree AV block there is a prolongation of PQ duration (PQ time > 0.20 sec). Still every P wave is being followed by a QRS complex. First degree AV block is present in 16% of >90-year olds and is mostly caused by a degeneration of the conduction system. First degree AV block is relatively harmless. Although the PQ interval is prolonged, all P waves are followed by QRS complexes: there is no dropout of complexes.

Second degree AV block In second degree AV block not all p-

waves are being followed by QRS complexes: beat dropout occurs.

Second degree AV block can be categorized in 3 types:

Second degree AV block type I (Wenckebach)

the PQ interval prolongs from beat to beat up until the drop-out of one QRS complex

QRS complexes cluster (e.g. a 5:4 block or 4:3 block)

The PQ interval prolongs every consecutive beat The PQ interval that follows upon a dropped

beat is the shortest. The RR interval shortens (!) every consecutive

beat. The amount of block decreases during exercise

(e.g. a 4:3 block improves into a 6:5 block) The conduction disturbance in a type I block

originates in the AV node. Isolated second degree AV block type I is relatively benign and not a pacemaker indication.

Second degree AV block type II (Mobitz)

beats are dropped irregularly without PQ interval prolongation

no clustering of QRS complexes can be seen as in second degree block type

marks the starting of trouble and is a class I pacemaker indication.

c) High grade AV block High grade AV block is defined as two

or more p-waves not followed by QRS complexes

3. Third degree AV block is synonymous to total block: absence of atrioventricular conduction. The P-waves and QRS complexes have no temporal relationship, which is called to AV dissociation.

The ventricular rhythm can be nodal, idioventricular or absent. Absent ventricular rhythm results in asystole and death. During third degree AV block the blood supply to the brain can insufficient, leading to loss of consciousness

If the conduction system is dysfunctional, the QRS widens beyond 0.12 seconds. If the QRS complex is wider than 0.12 seconds this is mostly caused by a delay in the conduction tissue of one of the bundle branches:

Left Bundle Branch Block (LBBB)) Right Bundle Branch Block(RBBB) Intraventricular conduction delay

A bundle branch block causes a delay in the depolarization of the right (RBBB) or left (LBBB) ventricle.

In RBBB the QRS complex shows a second peak or R' in V1. Check V1 when QRS > 0.12 sec. When the "terminal force“(2nd half of QRS) of the QRS in V1 is below the baseline (i.e. QS wave), a LBBB is the most likely diagnosis. When the "terminal force" of the QRS in V1 is above the baseline (i.e. RSR' wave), it's a RBBB. If the QRS > 0.12 sec. but the morphological criteria of LBBB or RBBB do not apply, it is called 'intraventriculair conduction delay', a general term.

Criteria for left bundle branch block (LBBB)

QRS >0,12 sec Broad monomorphic R waves in I and

V6 with no Q waves Broad monomorphic S waves in V1,

may have a small r wave

Criteria for right bundle branch block (RBBB)

QRS >0,12 sec Slurred S wave in lead I and V6 RSR'-pattern in V1 where R' > R