notes by dr Claudio Italiano
Sick sinus syndrome (SSS), also called sinus dysfunction, or sinoatrial node disease ("SND"), is a group of abnormal heart rhythms (arrhythmias) presumably caused by a malfunction of the sinus node, the heart's primary pacemaker.
Tachycardia-bradycardia syndrome is a variant of sick sinus syndrome in which the arrhythmia alternates between slow and fast heart rates. Tachycardia-bradycardia syndrome is often associated with ischemic heart disease and heart valve disease.
This term refers to an irregular activity of the sinus node comprising very different situations. Sinus dysfunction syndromes are not necessarily linked to an organic alteration of the sinus node, the role played in them by indirect mechanisms, vagal and sympathetic stimuli above all, must not, in fact, be neglected or underestimated.
The sinus node (NS) consists of these cells and as it is equipped with the fastest automatism it controls the cardiac activity, triggering the action potentials in the common myocardium.
Thus, through a sodium-calcium exchange, the myocardial cells are excited (hence the use of calcium antagonists in therapy to adjust the rhythm). There are other structures that like the sinus node are equipped with automatic activity: among these the Atrioventricular Node (NAV), which is however equipped with a slower automatism, so it can act as a pacemaker only when the other path markers are, so to speak, turned off.
The refractory period, however, is a minimum interval between two action potentials, during which the common myocardium fails to be stimulated. The NAV has a refractory period, therefore, longer, since the frequency of its action potentials is shorter, but its physiological function is important, as we will see, in the supraventricular tachyarrhythmias where an excessive rhythm of the ventricular chambers contraction, causing a deficit of pump activity, would cause death by cardiovascular collapse.This is due to the fact that the ventricles if they contract quickly do not have time to fill and pump
These syndromes may occur in acute or chronic form:
-The acute forms, usually reversible and transitory, include the syndromes
arising in the course of pharmacological intoxications (from quinidine,
beta-blockers, lidocaine, amiodarone, digital, etc.), but also as a result of
metabolic disorders (hyperkalemia, ex.) or also due to excessive release of
acetylcholine at the parasympathetic terminations during acute ischemia (eg in
the acute phase of a myocardial infarction) or, finally, following cardioversion.
- The chronic forms, mostly stable and irreversible, usually the expression of
organic sinus lesions, can in turn be divided into two groups:
a) The first one including the electrocardiographic aspects:
• sinus-atrial blocks (1st, 2nd and 3rd degree).
• sinus arrests.
• junctional escapements.
b) The second group is represented by isolated sinus bradycardias, characterized
by a frequency lower than 55 / min., underlining that in these cases they
acquire relevance above all:
• Severe bradycardias
• Daytime bradycardias.
• The bradycardias that appear in the mature age (from 40 to 60 years).
In this nosological picture of the sinus node disease there are some syndromes
in which pacemaker dysfunction is associated with disturbances of rhythm or
conduction: the most classical of these associations is represented by the
so-called orecchiette disease.
Ambulatory monitoring of the electrocardiogram (ECG) may be necessary because arrhythmias are transient.
The ECG may show any of the following:
Inappropriate sinus bradycardia
Sinus arrest
Sinoatrial block
Tachy-Brady Syndrome
Atrial fibrillation with slow ventricular response
A prolonged asystolic period after a period of tachycardias
Atrial flutter
Ectopic atrial tachycardia
Sinus node reentrant tachycardia
Wolff-Parkinson-White syndrome
Electrophysiologic tests are no longer used for diagnostic purposes because of
their low specificity and sensitivity. Cardioinhibitory and vasodepressor forms
of sick sinus syndrome may be revealed by tilt table testing.
Artificial pacemakers have been used in the treatment of sick sinus syndrome.
Bradyarrhythmias are well controlled with pacemakers, while tachyarrhythmias
respond well to medical therapy.
However, because both bradyarrhythmias and tachyarrhythmias may be
present, drugs to control tachyarrhythmia may exacerbate bradyarrhythmia.
Therefore, a pacemaker is implanted before drug therapy is begun for the
tachyarrhythmia.
The 1st block indicates delay, the 2nd intermittent interruption, the 3rd
complete interruption of conduction +. The block of the second degree includes
the subdivision in I and II type depending on whether the conduction
progressively deteriorates, before the block or rather it stops abruptly. The
first type realizes the Wenckenbach phenomenon in which the block of the impulse
is usually preceded for 3-5 cycles by a progressive lengthening of the
conduction time; in the 2nd degree block an impulse can be blocked on a regular
basis, every pulse, every two, every three, etc.
Etiopathogenesis. Functional causes can cause blocking, e.g. vagal hypertonia,
sleep, digitalis effect, beta blockers, obstructive jaundice, intracranial
hypertension. Organic causes: sclerodegenerative processes, myocarditis, tumors,
Lenegre's disease, Lev's disease ..
Symptomatology.
The subject may feel palpitation, vertigo, angina pectoris, breath suspension,
cerebral hypoxia due to pump failure that goes under the name of MAS or
Morgagni-Adams-Stokes syndrome, with sudden syncope.
In the case of the sino-atrial block, the conduction disturbance resides between
the Keith-Flack sinus node and the atrial: the pulse usually arises from the
sinus node but is not transmitted to the atria.
Depending on the importance of the conduction disorder it is logical to describe
3 types of breast-atrial block:
- 1st degree SA block: in which the transmission of sinus impulse between the
sinus node and the atria is simply slowed down.
- 2nd degree SA block: in which the sinus impulse transmission is intermittently
blocked. Complete blockage can occur at the end of a series of sinus impulses
whose conduction becomes progressively slower at the sine-atrial junction, thus
creating a Luciani-Wenckebach-like block. The complete block can also occur once
in two, realizing then a SA block 2/1, or intermittently and variably (once in
three, once in four etc ....): SA block of the common type, like Mobitz.
- 3rd degree SA block: in which the sinus impulse transmission is permanently
blocked.
This classification of sinus-atrial blocks according to the degree of conduction
disturbance is theoretically justified and its reality is validated by
experimental, epicardial and endocavitary recordings.
In clinical electrocardiography it is not possible to record the pulses in the
sinus node: the only one to be recorded is the depolarization of the atria,
expressed by the waves P:
1 - 1st degree SA block: IT HAS NO EXPRESSION ELECTROCARDIOGRAPHY. It is not
possible to recognize a slowing of the conduction between the sinus node and the
atria, since in this case the P waves appear normal and regularly interspersed.
2 - 3rd degree SA block: Absence of P waves and junctional escapement rhythm. It
is possible to suspect a permanent blockage of sino-atrial conduction based on
the absence of P-waves and the existence of a junction rhythm at 40-50 per
minute (escapement rhythm). The absence of P waves can be confirmed by necessity
through the endocavitary registration.
3 - 2nd degree SA block: The only possibility in which the diagnosis of: SA
block can be performed on the electrocardiogram is that of the 2nd degree SA
block, that is intermittent: in fact every time the sinus impulse block is
produced it is easy to think about this possibility, since in this case the wave
P as the QRS complex are intermittently missing in the track; that is, there
appears to be no modification of the iso-electric line, where a P wave would
normally appear (atrial pause).
3.1 SENO-ATRIAL BLOCK WITH LUCIANI-WENCKEBACH PERIODS: three
electrocardiographic aspects can be observed, of which the first is the rarest:
• Progressive slowing of atrial rate, the interval between two waves P is
progressively lengthened until the sinus pause (abrupt absence of the wave P).
This aspect depends on the progressive lengthening of the conduction time from
the sinus node to the atria. This slowing down becoming more and more relevant
from one impulse to the next, finally leads to a complete block.
• Progressive acceleration of the atrial rate, in this case the interval between
2 waves P progressively shortens until the atrial pause. This aspect depends, as
the previous one, on the progressive extension of the breast-atrial conduction
time, but, contrary to what happens in the previous case, this elongation is
always less important from one impulse to the other and paradoxically manifests
itself with an acceleration progressive of the atrial rhythm until the pause.
• Alternation of acceleration and slowing of the atrial rhythm, which achieves a
ring-like appearance: this type of block depends on the alternation of the 2
previous mechanisms.
• In all cases: the interval between the 2 P waves framing the atrial pause must
be less than twice the PP interval immediately preceding and higher than the
following PP interval.
3.2 - sino-atrial block mobitz type:
It is the most commonly observed SA block:
• It is easily recognized by the appearance of intermittent atrial (and
ventricular) pauses, whose duration is a multiple of the PP interval of the
basic sinus rhythm.
However, the duration of the pause is often a bit shorter than the previous PP
interval, but also sometimes a bit longer.
So there are very different aspects.
• the SA block 2/1 is a particular aspect:
the sinus impulse induces atrial depolarization once in two: it results a
bradycardia completely comparable to sinus bradycardia, and in this case the
diagnosis of SA block 2/1 can be affirmed only if, from time to time, two
successive sinus impulses they manage to cross the sino-atrial junction. These
two successive pulses manifest themselves with a sharp doubling of the atrial
rate.
The differential diagnosis must be addressed with:
1 - Supraventricular rhythm disorders that reduce atrial rhythm:
• non-phasic sinus arrhythmia
• the atrial extrasystoles followed by a QRS complex, recognizable by the
precocity and the abnormality of the morphology of P.
• blocked atrial extrasystoles, which depolarize the sinus node and can thus
simulate a common type SA block. These are extrasystolic P waves, whose
anterograde conduction is blocked at the atrioventricular node level and which
are not followed by QRS complexes. These P waves, however, depolarize and
depress the sinus node retrograde, preventing the appearance of the following
sinus P wave. These ectopic waves can be difficult to recognize or be hidden in
the QRS complex or in the previous T wave, and then the pause that happens to
them can make a common SA block believe. Endocavital registration allows
rectification of the diagnosis by unmasking ectopic atrial activity.
• junctional extrasystoles: the diagnosis in this case is made easy by the
recognition of junctional QRS complexes, that is to say early, not preceded by a
P wave or preceded by a "retrograde" P wave (PR interval lower than 0 , 12
seconds and P waves of abnormal morphology).
It is necessary to distinguish two eventualities: the junctional extra-systolic,
followed by a true compensatory rest (see ESG), and the interpolated junctional
extra-systole, in which the P wave that follows the extra-systolic junctional
complex is hidden in the QRS complex or in the T-wave and remains blocked,
because it falls in the refractory period of the atrioventricular node).
- atrial paralysis, whose differential diagnosis with a 3rd degree SA block can
be made only by atrial electrical stimulation: the atrium is unhelpful in atrial
palsy, but excitable in the SA block.
1 - Idiopathic SA block: of the young subject or of the elderly subject (atrial
fibrosis, coronary atherosclerosis).
2 - Transient SA block: myocardial infarction (acute stage), digitalis
intoxication, hyperkalemia, immediate after-effects of cardioversion or
tachycardia, vagal reflex: vagal maneuvers, injection of adenosine triphosphate
(Striadyne) and other vagal reflexes, internal pains, stimulation of mucous
membranes, neurological or neuro-surgical syndromes, vasopressor injection.
3-1 chronic SA block: coronary insufficiency, aortic disease, arterial
hypertension, rhythmic atrium disease (see corresponding chapter).