THE CAROTID SINUS REFLEX IN HEALTH AND DISEASE

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Abstract
A clinical study of the effects of stimulation of the carotid sinus (by digital pressure) in 128 patients, 50 with normal cardiovascular systems, 42 with arterial hypertension, with or without arteriosclerosis, and 36 with arteriosclerosis without hypertension. In the normal group sinus stimulation had little or no effect (pulse rate, blood pressure, electrocardiogram) . In the other groups sinus stimulation had much more marked effects; systolic blood-pressure fell as much as 105 mm. (average 40), and pulse slowed by as much as 28 beats per minute (average 16 in the arteriosclerotic group) ; in patients with coronary disease cardiac slowing was marked and preexisting partial A-V block was exaggerated; in one case paroxysmal tachycardia was abolished by sinus stimulation. 15 patients with hypersensitive sinuses were studied in detail; all showed dizziness, fainting, and convulsions on sinus stimulation. In 6 the sinus was aneurysmally dilated, in 3 there was a tumor pressing on it, while the other 6 showed no pathological change. In 12 of these patients sinus stimulation caused cardiac slowing, sometimes asystole for 2-12 sec, and sometimes even lightest external pressure was effective ; blood-pressure fell in 10 of these cases. Electrocardiograms showed striking changes: complete asystole, A-V block (partial or complete), nodal rhythm, ventricular extrasystoles, bizarre complexes such as occur in ventricular fibrillation, inversion of T-waves, and some unexplained changes. Cardiac output and velocity of blood-flow, estimated by a dye-injection method (Hamilton) , showed a decrease on sinus stimulation. Cerebral blood-flow also showed a decrease, as evidenced by increase in the carotid-jugular O2 difference, but retinal vessels showed no striking changes. The effect of druga was also tested: epinephrine (intramuscularly) abolished all effects of sinus stimulation; atropine intramuscularly abolished the bradycardia but did not influence the other effects, and a small dose intraarterially (carotid) abolished the reflex ipsolaterally, not contralaterally; luminal did not affect it; novocaine block of the sinus nerve abolished the reflex. In one patient one sinus nerve was cut, in another a glossopharyngeal; in both there was a sharp temporary rise in blood pressure. In 3 patients with hyperactive sinus reflexes infusion of hista-mine or acetyl choline into a vein or carotid artery did not modify the response to sinus stimulation; CO2 inhalation was equally ineffective. It is suggested that hyperactive sinus reflexes may be responsible for some cases of dizziness, fainting, and convulsions, either because of fall in blood-pressure or contraction (spasm) of cerebral vessels, the latter in neurotic patients; that some cases of cardiac arrhythmias, including Adams-Stokes syndrome, are reflex in origin; that atropine has a central action on synapses of the sinus reflex. The convulsions occurring on stimulation of a hypersensitive sinus probably have nothing in common with epilepsy. Observations of other workers, indicating that sinus reflexes are not inactive in human hypertension, are confirmed.