Some Clinical Aspects on the Carotid Sinus Mechanism

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28. Erik Ask-Upmark, Lund. Some Clinical Aspects on the Carotid Sinus Mechanism. The mechanism of the carotid sinus is physiologically defined thus:-an increase of pressure within the sinus will cause a drop of the blood pressure, a retardation of the heart and a respiratory reflex in the general direction of an apnoe; a decrease of pressure within the sinus will bring about the contrary effects :-increased. blood pressure, cardiac acceleration and hyperpnoe. The response thus elicited is established by means of a reflex in which the carotid sinus is sending impulses through the sinus nerve to the glosso- pharyngeus and by means of this nerve to the brain stem. The efferent pathway is represented by the vagus and the sympathetic system; the tone of vagus is stimulated, the tone of sympathetic inhibited by an increased pressure in the sinus and the contrary goes for a decreased intrasinal tension. From clinical point of view it is important to remember that the carotid sinus faces on the one side the heart and the systemic circu- lation, on the other side the brain and the cerebral circulation. The different clinical applications to the sinus mechanism may be centered around these two systems. As to the cardiovascular system the following clinical entities will be briefly discussed:-hypertension, myocardosis, paroxysmatic tachycardia, angina pectoris, pulmonary oedema. Hypertension :-In animals several authors have provoked a vascular hypertension by severing the four hitherto known “buffer- nerves” of the blood pressure (from the carotid sinus and the aortic arch) provided that certain experimental requirements have been fulfilled. Without entering more closely upon this experimental hypertension which has been discussed amply elsewhere (ASK- UPMAHK 1934) it may be said that its reality has been doubted by

Transcript of Some Clinical Aspects on the Carotid Sinus Mechanism

28. Erik Ask-Upmark, Lund.

Some Clinical Aspects on the Carotid Sinus Mechanism.

The mechanism of the carotid sinus is physiologically defined thus:-an increase of pressure within the sinus will cause a drop of the blood pressure, a retardation of the heart and a respiratory reflex in the general direction of an apnoe; a decrease of pressure within the sinus will bring about the contrary effects :-increased. blood pressure, cardiac acceleration and hyperpnoe. The response thus elicited is established by means of a reflex in which the carotid sinus is sending impulses through the sinus nerve to the glosso- pharyngeus and by means of this nerve to the brain stem. The efferent pathway is represented by the vagus and the sympathetic system; the tone of vagus is stimulated, the tone of sympathetic inhibited by an increased pressure in the sinus and the contrary goes for a decreased intrasinal tension.

From clinical point of view i t is important to remember tha t the carotid sinus faces on the one side the heart and the systemic circu- lation, on the other side the brain and the cerebral circulation. The different clinical applications to the sinus mechanism may be centered around these two systems.

As to the cardiovascular system the following clinical entities will be briefly discussed:-hypertension, myocardosis, paroxysmatic tachycardia, angina pectoris, pulmonary oedema.

Hypertension :-In animals several authors have provoked a vascular hypertension by severing the four hitherto known “buffer- nerves” of the blood pressure (from the carotid sinus and the aortic arch) provided tha t certain experimental requirements have been fulfilled. Without entering more closely upon this experimental hypertension which has been discussed amply elsewhere (ASK- UPMAHK 1934) i t may be said that its reality has been doubted by

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other investigators. In man it has been discussed whether not hypertension might depend upon the elimination of the buffer nerves by means of pathological alterations of their vascular receptor- area. The receptors are situated in the adventitia and i t may well be that an arteriosclerotic intima might block the pressure impulses within the sinus on their way to the receptors in the outer layer of the vascular wall. If such be the case, however, an increased pres- sure within the sinus would not become adjusted any longer and a permanent hypertension hence result. This explanation must howe- ver be considered as erroneous since there is no correlation between the occurrence of hypertension and the occurrence of morphological alterations of the vascular wall in the receptor areas of the buffer nerves (KEELE and others). I t is moreover to be remembered that hypertension generally precedes arteriosclerosis and not the con- verse.

Myocardosis. I t has been stated by WENCKEBACH (1914) that if a slight pressure upon the sinus region does cause a marked bradycardia this should indicate a bad condition of the heart and particularly the myocard whereas the converse should not be true. I t will appear, however, as if this conclusion would be exaggerated. The prononcia- tion of the response upon a pressure exerted on the sinus may depend upon various factors but is obvious that the most con- spicuous one is represented not by the condition of the heart but by the condition of the sinus. If a marked arteriosclerosis is present there may be a calcified shell in the intima of the sinus, against which the nervous receptors are particularly liable to become com- pressed by a pressure exerted transcutaneously. I t is a well ascer- tained fact that the pronounced responses of a pressure over the sinus are to be obtained particularly in older individuals with arteriosclerosis and on the other hand i t is well known that the carotid sinus represents an arterial region in which the arteriosclero- tic changes are liable to occur at an early stage and become amply developed.

Paroxysmatic tachycardia. Already in 1880 BENSON and PREISEN- DORF pointed out that this condition may be treated by a pressure in the neck which had to be exerted over the sinus region whereas pressure elsewhere in the neck was of no effect. This observation has been confirmed by numerous investigators and it may be said that a pressure upon the sinus should always be tried when dealing

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with this disorder. Most recently REGNIER has pointed out tha t this pressure sometimes has to be rather considerable and of sufficient duration in order to obtain the effect wanted. Pathophysiologically i t seems reasonable to consider the response, if response there is, as depending upon an inhibition of the sympathetic tone and a sti- mulation of the vagus tone.

A n g i n a pectoris. Several authors (WASSERMANN, MANDELSTAMM and others) have observed a therapeutic effect of a pressure on the sinus in attacks of angina pectoris. I t may be difficult to account for this effect but i t seems reasonable to assume, a t least as con- tributing factors, on the one hand a decrease of the blood pressure (which of course often is increased during an attack), on the other hand a dilatation of the coronary vessels brought about by the increased vagotonus.

P u l m o n a r y oedenia of the cardiac type may be influenced in therapeutic direction by a pressure on the sinus (WASSERMANN). I t will appear as if this would be true particularly in those cases of pulmonary oedems in whom the blood pressure is high. The effect elicited may depend upon the derivation of blood from the lungs by means of the peripheric vasodilatation and thus be rather com- patible with the other therapeutics which have been suggested in such instances (amyl-nitrite, venae-section, hydrargan).

I t may finally be mentioned tha t HEYMANS and his collaborators consider the effect of digitalis as essentially depending upon the carotid sinus region, perhaps in the first line the system of the carotid body.

The possibility of provoking a STOKES-ADAM’S syndrome by means of a compression of the sinus receptors will be discussed below.

As to the clinical relation between the carotid sinus and the cerebral system three different conditions will be briefly touched upon : the syncope, the glossopharyngeal neuralgia and the behavi- our of the blood pressure in tumours of the brain.

Syncope. I t has been ascertained beyond reasonable doubt that there is a syndrome characterized by dizziness, fainting and occa- sionally convulsions that may be provoked by pressure on the carotid sinus. This pressure may under circumstances be slight enough, e. g. when shaving or putting on a stiff collar. That the reaction depends upon the carotid sinus is indicated firstly by the

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fact that pressure exerted elsewhere in the neck is without effect, secondly by the experience that these cases can be cured by surgical denervation of the sinus region. The anatomical appearance of this region may be entirely normal although in other instances an aneurysmatic dilatation of the sinus or a tumour of the carotid body may be found (it will be recalled that fainting is no uncommon symptom in cases of such tumours) and not infrequently an arte- riosclerosis of the sinus region. The mechanism by means of which the fainting is caused may be complicated. On the one hand the drop in blood pressure and heart rate, usually obtained, may be projected passively into the brain vessels as some kind of reflex-ADAM-STOKES. On the other hand fainting may in rare instances be obtained when no drop of the blood pressure can be registered. I t may be that a direct (reflex-) influence upon the cerebral vessels is present in such instances; evidences in this direction are the pallor to be observed in the face (WEISS) and particularly the fact tha t the convulsions, when appearing, usually may be ascribed to one of the hemispheres (that on the side of which the sinus is stimulated, ASK-UPMARK.) In certain cases the carotid sinus syncope does appear only during the periods of menstruation. The diagnosis is easy when the condition is remembered; when not i t may be mistaken for epilepsy or nar- colepsy. If pronounced the reaction may be dangerous; deaths have been observed and i t is anyway always advisable to examine the patients in recumbent position. Therapeutically, surgical denerva- tion of the sinus region may be considered1).

Glossopharyngeal neuralgia. Whether the carotid sinus may be involved in the development of this condition is unknown (in one case observed by FONIO the sinus region was transformed into a veritable aneurysm). This disease may however be cured by the intracranial severing of the ninth cranial nerve and since I have been able to show that the sinus fibres enter the brain stem by means of this nerve i t is obvious that vasomoter reactions may be elicited by the surgical manipulation of the nerve. Clinical observa- tions which I have had the opportunity to make seem to confirm this (lantern slides) whereas the division of certain other cranial nerves (the Vth and the VIIIth) does not provoke any regular vasomotor reaction. I t is thus obvious that the ninth nerve has to

1) In one case thus operated upon by CATTEL the result was good even 2 years after the operation (letter from CATTEL).

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be handled carefully during all operations in the posterior cranial fossa, not least in the acoustic tumours which may press upon the posterior bundle of cranial nerves and accordingly have to be freed from this bundle. Personal observations in a material of some 170 acoustic tumours are in line with this evidence.

Brain tumours do not unusually present a low blood pressure. In a material of approximately 500 intracranial tumours in indivi- duals aged 20-44 the blood pressure was thus < 100 in some 20%. One might be tempted to ask whether perhaps this low pressure might not be established from the sinus by means of the increased resistance to the carotid blood presented by an increased intra- cranial pressure. Such, however, cannot be the case since the low blood pressure does not present any correlation with the increased intracranial pressure; on the contrary i t has been found that tumours causing a more considerable increase of the intracranial tension are more liable to present a high blood pressure (presumably by means of the Cushing mechanism of bulbar anemia) whereas the low blood pressures are to be noted in tumours involving the basal structures of the brain.

Summarizing i t may be said that the carotid sinus is a structure of clinical importance, that essential hypertension and alterations of the blood pressure in brain tumours apparently have nothing to do with the sinus reflex but that this reflex may be involved on the one hand in certain conditions of the heart on the other hand in disorders with symtoms from the nervous system.