Heart block is an abnormal delay or, in extreme cases, complete block in the conduction of the electrical impulse from the atria to the ventricles (A-V block) or in the specialized conducting network supplying the ventricles (bundle block).
Gerbezius, an early eighteenth-century German physician, described the pulse of a man he attended as being ‘so very slow, that before the subsequent pulsations followed that which went before, three pulsations would certainly have pass'd in another healthy person’. But it was two Dublin clinicians more than a century later who gave heart block and its effects the eponym Stokes-Adams syndrome. Adams and Stokes both reported patients with persistent pulse rates around 30. The exceptionally slow heart rates in these patients (and in others recognized subsequently) became from time to time even slower, causing them to pass out in a manner which could be confused with epilepsy or ‘apoplexy’. Such a black-out became known as a ‘Stokes- Adams attack’, occurring because the brain was deprived of blood flow when a ‘subsequent pulsation’ did not follow for far too long.
Fig. 1 Diagram of heart chambers showing spread of excitation and sites of heart block. (RA, LA: right and left atrium. RV, LV: right and left ventricle.)
The mechanism whereby, normally, the ‘subsequent pulsation’ follows after a proper interval of one second or less, depends on transmission of electrical signals from the heart's
pacemaker, the
sino-atrial (SA) node, through the atria to the only, and restricted, pathway through which it can reach the ventricles — via the
atrio-ventricular (AV) node and thence along the rapidly conducting modified muscle cells known as the
Bundle of His and its branching fibres, to spread through the whole ventricular muscle mass. Should the signal fail to get through, it cannot stimulate the ventricles to beat. But there are cells beyond the AV node which can take over as pacemakers, generating regular signals at a slower pace than that which is normally imposed. The SA node keeps firing off at its own faster rate, but to no avail as far as ventricular contraction is concerned. The
electrocardiogram (ECG) shows P waves and QRS complexes which are completely dissociated from one another. The QRS waves, and therefore the heart beats, are 40 or fewer per minute. This is the condition of complete, or third degree, heart block.
Fig. 2 ECG from a subject with partial heart block. The first five beats are normal. At the 'missed beats' the arrows point to P waves that are not followed by a QRS complex, indicating failure of transmission of activity from atria to ventricles. Each missed beat is followed by a normal one
The importance of the normal sequence of activation lies in the fact that a wave of contraction is initiated first in the atria then, after a brief delay, in the ventricles. The relative timing of this sequence, as well as the sequence itself, are important determinants of the effectiveness with which the heart pumps the blood. Since heart block is a major disturbance to the smooth progress of the triggering wave, its consequences can be serious.
There are lesser degrees of block, where some activations get through and others do not (shown by the presence of any isolated P waves) and in its mildest form there is simply a slowing down of transmission from atria to ventricles (shown by a prolonged P-R interval). It is also possible for just one of the main branches of the Bundle of His to be blocked.
The cause of heart block is damage to the conducting fibres, by deprivation of blood supply picking out that part of the heart when there is coronary artery disease, or as a result of infection; it may also be congenital.
Nowadays, heart block can be treated by implanting an artificial pacemaker to drive the ventricles.
— David J. Miller, Niall G. MacFarlane
See also electrocardiogram; heart; pacemaker.
