Carotid Artery Compression in Vascular Headache
Carotid artery pressure may be used as an aid in the diagnosis of migraine and migrainoid headaches (referred to collectively as “vascular headaches”). If the patient is seen early in the attack while the cephalalgia still has its characteristic pulsatile quality, the patient is asked to rate his pain on a scale of 0 to 10. Damping of the pulse wave contour by ipsilateral carotid compression will, early in attacks of vascular headache, be accompanied by a diminution in the pain score. After the compression is released, the pain score tends to return toward the original higher score within just a few beats. This pain relief must be shown not to be replicated with placebo neck stimulation (i.e., rubbing the mastoid process, pinching the skin over the carotid artery without compressing it, etc.). Furthermore, the test is useless once the headache has passed through the pulsatile pain phase and is in the steady pain phase.
This is one of the four criteria associated with vascular headache. To diagnose a vascular headache, any three need to be present in the patient. The others are (a) unilateral pain, (b) throbbing onset, and (c) relief by ergot alkaloids.
Carotid Sinus Reflex
Historic Background
The carotid sinus reflex qua reflex was elucidated by Hering, who is probably best remembered for the Hering-Breuer4 reflex.
A Method (after Lown and Levine, 1961)
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Tilt the (recumbent) patient’s head backward and to the side so that either one of the carotid sinuses can be readily palpated. The sinus is usually situated just below the angle of the jaw at the level of the uppermost portion of the thyroid cartilage (
Fig. 18-2).
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Massage the carotid sinus with pressure directed medially and posteriorly, compressing the artery and the sinus against the vertebral spine.
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Apply vigorous massage for not more than 5 seconds at a time. The procedure may be repeated after several seconds’ rest.
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Never massage both carotid bodies at the same time.

If this technique is carefully followed, adverse consequences are extremely uncommon. These primarily result from interference with cerebral blood flow. Accordingly, the maneuver should be avoided in patients with historic or physical evidence of cerebrovascular disease (e.g., a carotid bruit) and in patients over the age of 75. Patients with coronary insufficiency may develop
asystole (
Lown and Levine, 1961). In a study of 1,000 patients 50 years or older who had a history of syncope or unexplained falls, diagnostic carotid sinus massage provoked transient neurologic symptoms in 1% and persistent neurologic complications in 0.1% (
Richardson et al., 2000).

A safer way of slowing the heart rate without medication in older patients, in whom there is some risk of dislodging a carotid plaque, is to use the oculocardiac reflex (see
Chapter 26) (L. Huntoon,
personal communication, 2004).
Customary Response
The carotid sinus baroreceptors send the afferent impulses to the cardiac and the vasomotor centers in the medulla via cranial nerve IX. The efferent arc involves stimulation of parasympathetic (vagal) activity, which immediately slows conduction in the SA and AV nodes, causing a chronotropic and bradydromic
5 effect on the heart. After several seconds, there is also an independent inhibitory effect on the sympathetics, causing a drop in blood pressure through vasodilatation. The carotid sinus reflex results in a variable effect on respiratory rate (
Lown and Levine, 1961).
It is well recognized that most subjects with cardiovascular disease have a brisk carotid sinus reflex but many normal subjects do not. Some type of cardiac response is elicited in 82% of persons over the age of 40 but in only 18% of those under 40, possibly because of the coexistence of cardiovascular disease in the older group.
Slowing of the sinus rhythm is seen in only 5% of normal subjects. A fall in the systolic blood pressure occurs in 60% of subjects. Again, the figure is higher for older subjects and for those who have cardiovascular disease. Less hypotension is evoked in healthy soldiers.
Some Differential Diagnoses of Arrhythmias Made with the Carotid Sinus Pressure
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Regular bradycardia. A sinus bradycardia gradually slows further during carotid sinus massage. As with many second-degree heart blocks, in paroxysmal atrial tachycardia with a 3:1 AV block, an effective carotid sinus reflex can cause an irregular or jerky slowing of the heartbeat with an irregular or jerky reacceleration when the pressure is removed.
Paradoxical acceleration of the ventricular rate during carotid sinus stimulation is a specific clue to a 2:1 block. The vagally induced slowing of atrial impulses permits the previously blocked alternate impulse (which had reached the AV node when it was refractory to conduction) to now pass through. Thus, conduction is now 1:1 and the ventricular rate is faster (
Fig. 18-3).
(Complete heart block is not affected by carotid sinus pressure but can be identified by observing the variability in the first heart sound [S1] [see
Chapter 17].)
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Regular rhythm, with the rate between 70 and 100. Such a rhythm is naturally assumed to result from a normal sinus mechanism. However, if carotid sinus pressure produces an abrupt slowing or halving of the rate, with a jerky return after the pressure is released, it should suggest to you that the mechanism is not sinus but rather atrial flutter or paroxysmal atrial tachycardia with block.
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Rapid regular rhythm. When the heart rate is regular and rapid (between 120 and 300 beats per minute), carotid sinus stimulation is useful even if you cannot study the patient with an electrocardiogram (ECG).
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If the carotid sinus stimulation abruptly stops the tachycardia, but the rhythm remains slow (<100 beats per minute) and regular after the release of pressure, one was probably dealing with paroxysmal atrial tachycardia.
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If carotid stimulation temporarily slows the ventricular rate, you can be sure that the arrhythmia is not ventricular tachycardia.
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If the slowing of the rate with carotid sinus pressure is smooth and gradual with a similar smooth and gradual return to the original rate after release, it must be sinus tachycardia. This smooth deceleration and reacceleration has been likened to a train slowing down (without stopping) at a station to pick up a mailbag and then speeding up to its original rate.
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If recovery from the temporary slowing is jerky, you must again think of atrial flutter or paroxysmal atrial tachycardia with block.
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Rapid, irregular rhythm. If the original rate is rapid and irregular but the slowed heart rate is regular, atrial fibrillation has been excluded. However, if the heart slows while maintaining an irregular rhythm but exercise accelerates and regularizes it, the differential diagnosis includes atrial flutter, premature beats, or paroxysmal atrial tachycardia with block (
Lown and Levine, 1961).
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Digitalis intoxication. Because digitalization may sensitize the carotid sinus reflex, carotid sinus stimulation can be used as a nonpharmacologic test for the presence of digitalis intoxication even before the characteristic arrhythmias occur spontaneously. If such stimulation produces advanced degrees of heart block,
ectopic beats with fixed coupling, or the emergence of rapid and regular ventricular response in a patient with atrial fibrillation (representing conversion to a nodal ventricular rhythm while the atria continue to fibrillate), digitalis intoxication is highly likely, especially if carotid sinus stimulation did not previously cause these events in a particular patient.
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For the very advanced student 2:1 AV block and 2:1 sinus exit block. There is no electrocardiographic way to distinguish a 2:1 AV block from a 2:1 sinus exit block, a distinction that can be significant both in terms of underlying diagnosis and, in the case of the former, in the use of drugs that could further slow AV conduction. Should carotid sinus pressure increase the block (slow the pulse), the diagnosis of AV block would seem secure. Conversely, if there were no effect, the test would be suggestive of sinus exit block, although it would not be definitive.
It was formerly taught that the right carotid artery should be massaged to affect the sinus node and that the left carotid should be massaged to affect the AV node. I know of no data to support this. Can you think of a good senior medical student project based upon the testing of such a hypothesis?
The Levine Test
Carotid sinus massage sufficient to produce bradycardia may relieve chest pain due to angina pectoris. Although the Levine test was first described by Wassermann, his eponym was already associated with a serologic test (for syphilis). The test is known today as the Levine test for the man who popularized it.
A Method:
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Have an attendant (or the patient if no one else is available) hold the stethoscope over the precordium so that you can listen for the bradycardia. Both your hands are now free so that one can be used to brace the patient’s head and one can be used to massage the carotid sinus by the method described earlier in this chapter.
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Establish that the pain is still present.
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Massage the right carotid first. If this does not produce appreciable cardiac slowing, massage the left.
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Once slowing has occurred, ask the patient whether the pain has become worse.
If the heart rate has been slowed, the patient with angina pectoris behaves in a characteristic fashion: There is a pause before the answer is given, frequently with a look of uncertainty and puzzlement, “No doctor, the pain is all gone” or “It is letting up.” Disappearance or lessening of the pain occurs within several seconds of the onset of slowing of the heart though the heart may promptly reaccelerate. Generally, the pain does not recur. Of importance in the proper performance of the test is the exact wording of the question. The objective is to mislead the patient by suggesting that this maneuver has aggravated the chest discomfort. If, despite this misdirection, the patient says the pain has lessened or disappeared, one can be certain that the subjective change is real and has not been suggested by the examiner (
Lown and Levine, 1961).
I prefer not to lead witnesses, especially overly cooperative ones, in any direction. Therefore, I have modified the test as follows: I ask for a baseline measurement of pain on a 0 to 10 scale. Then, I ask what number the pain is during the pressure. Unless the pain has gone, I repeat the baseline and experimental measurements while performing placebo maneuvers: rubbing the mastoid, pinching the skin over the carotid sinus, and so forth. (Note that in a scientific study, the placebo should be used first half of the time and second half of the time.)
This test is diagnostic of angina pectoris when positive, provided that the same pain relief scores were not obtained with the placebo maneuvers. (However, if negative, it does not rule out angina pectoris as the cause of the chest pain.)
Carotid Sinus Reflex in Left Bundle Branch Block
Slowing the ventricular rate with carotid sinus massage may sometimes eliminate left bundle branch block temporarily, permitting you to inspect the ECG for the signs of anterior myocardial infarction, which can be impossible to detect in the presence of left bundle branch block.
Therapeutic Use of the Carotid Sinus Reflex in Pulmonary Edema
Carotid sinus stimulation has been found effective in alleviating pulmonary edema in 80% of hypertensive or ischemic cases. Relief is immediate and coincides with the onset of bradycardia. The episode may be completely reversed. Carotid sinus stimulation has been carried out intermittently (i.e., for no more than 5 minutes at a time) for as long as 30 minutes. If the reflex becomes extinguished on one side, a good response may be elicited by stimulating the other side. This technique has not been effective in the presence of atrial fibrillation or aortic valve disease (
Lown and Levine, 1961).
Carotid Sinus Syncope
When I was a medical student, I was told the following story:
Clinician Soma Weiss was once presented the case of a Boston streetcar conductor who experienced syncope every morning at a certain street corner but at no other time. Apparently, at this particular corner, the conductor had to turn the car and his head to the right. In those days, streetcar conductors wore wing collars (
Fig. 18-4). Weiss hypothesized that the stiff starched collar was pressing into the patient’s carotid sinus causing a reflex bradycardia or asystole. He tested the hypothesis by pressing with his fingers on the supine patient’s carotid sinus, reproducing the symptoms.
After hearing this story, I faithfully inquired about the tightness of the collar in all my patients admitted with syncope. However, by this time, the wing collar had given way to the modern low cut collar of soft cloth, so my inquiries were diagnostically fruitless, as I would have known had I read the original paper (
Weiss and Baker, 1933) instead of listening to stories:
This 65-year-old white streetcar motorman entered the hospital complaining of dizziness and fainting attacks. His symptoms began about 18 months previously when, one day while running his car, he suddenly felt very dizzy and lost consciousness. He started to fall, but was caught by a man standing behind him and regained consciousness immediately. He had another similar attack some months later while running the streetcar. Quite frequently, while working, he noticed dizziness and diplopia. These were always brought on by turning his head from side to side watching traffic. Moreover, he had eight or ten fainting attacks while at home reading. It was always his custom to wear a celluloid collar which was quite loose. When he sat reading, his neck slipped down into the
collar in such a fashion as to press against the right carotid sinus. This fact was not brought to light until we started our investigation. During the 18 months preceding that, he consulted several physicians, who were unable to find any cause for his fainting. Finally, he was examined by Dr Walter Burrage at the Massachusetts General Hospital, who pressed on the right carotid sinus and immediately precipitated a fainting attack. The patient stated that this was entirely similar to his spontaneous attacks. He was referred to us for study.
Routine physical examination was negative except for slight enlargement of the heart and generalized arteriosclerosis. Blood counts and urine were normal. Blood pressure was 136/72. Kahn [serologic test for syphilis] was negative. Electrocardiogram was normal. Both carotid arteries were readily palpable. Pressure on either carotid sinus caused slowing of the pulse, fall in blood pressure, dizziness, fainting and convulsions. Pulse and blood pressure measurements were made with the patient turning his head from side to side while wearing one of his celluloid collars. These movements caused pressure on the carotid sinuses and resulted in slight slowing of the heart rate, fall in blood pressure as much as 40 mm Hg systolic, sometimes dizziness, but not fainting. The patient was advised to wear a soft collar which he has done for the past month. In that time he has had no more attacks of dizziness or fainting.
As a Gallic footnote in the interest of truth, consider the following case report (
Roskam, 1930):
Last November 3, there presented in my consultation room a chief quarryman named Armand C. who was 53 years old and gave a history that before May of 1929 nothing particular had happened….
In May of 1929 the wife of our patient while helping him to put on a very tight collar slipped a finger between the rigid collar and his neck: Immediately her husband collapsed in a faint….
On the 3rd of November while in Liege on business he went to a barber. Here, when the razor went over his neck it provoked a sudden and prolonged syncope….
[This has been understood in English to mean a carotid sinus so sensitive that syncope occurred when the skin over the sinus was barely touched by a razor. It would not be possible to stimulate the carotid sinus in that way. No doubt what Armand remembered was the razor going over his neck. But when a barber shaves a customer’s neck, the thumb that is not holding the razor is used to straighten the customer’s skin, and this is done by pressing up the neck toward the angle of the jaw (i.e., over the carotid sinus), as the reader may observe by visiting a barber shop. Thus, I think the razor has been unjustly accused all these years, when the real culprit must have been the barber’s thumb pressing on the carotid sinus.]
I systematically searched by strong compression in many places of the carotid and paracarotid regions of my patient carefully going over the left carotid and above the region of the left carotid sinus but not getting any noticeable reaction. I then approached the carotid sinus itself going at the level of the thyroid cartilage to the inferior angle of the jaw. Hardly had I begun to compress—I hesitate to say I even touched it—when Armand C. cried in a voice strangled with anguish, “I’m going.” Immediately I ceased the compression which had been only an instant. Armand C. was pale as death, his lips without any color, his eyes dim, lying totally inert without consciousness, without movement, without pulse, without respiration. When the syncope went on more than 15 seconds after I had stopped pressing on him, I ausculted the precordial region with great attention: There was absolute silence. Finally, there supervened a grand mal seizure…. [The patient survived the episode and went back into normal sinus rhythm.]
Notice that this report predates that of Soma Weiss.
We previously noted that the carotid sinus reflex could be useful as a diagnostic tool or even a therapeutic one, although it was missing in many normal persons. Now, we have described a disease caused by a hyperactive carotid sinus reflex. The question is: At what point does a carotid sinus reflex merit the adjective “hyperactive”?
For screening purposes, a carotid sinus reflex is arbitrarily called
hyperactive (
Lown and Levine, 1961) if there is a greater than 50% slowing of the heart rate or a greater than 40 mm Hg drop in the systolic blood pressure (during carotid sinus massage). Of all the persons who meet these criteria, only one third will have symptomatic carotid sinus syncope. Thus, if the patient does not meet these criteria, a hyperactive carotid sinus reflex is ruled out. However, if a patient with syncope does meet the criteria for hyperactive carotid sinus reflex but the symptoms are not reproduced by carotid sinus massage, one still has not diagnosed carotid sinus syncope.
Carotid sinus syncope may be the mechanism for tussive (cough) syncope (
Wenger et al., 1980), which is most likely to
occur in patients with chronic obstructive pulmonary disease and well-developed thoracic musculature. Among the many other suggested mechanisms for tussive syncope are AV dissociation (
Saito et al., 1982), reflex vasodilation (
Chadda et al., 1986), or possibly decreased cerebral blood flow caused by increased venous pressure.
The prevalence of carotid sinus hypersensitivity has been found to be as high as 4% in asymptomatic adults and may be a contributory cause in 25% to 45% of older patients with unexplained syncope. Carotid sinus hypersensitivity was found in 35% of patients admitted with a fractured neck of the femur and in none of an age-matched control group admitted for elective hip surgery (
Richardson et al., 2000).