Arteries
How should it happen that, if you tie the arteries, immediately the parts not only become torpid, and frigid, and look pale, but at length cease even to be nourished?
—WILLIAM HARVEY, ON THE MOTION OF THE HEART AND BLOOD IN ANIMALS, 1628
POINTS TO REMEMBER:
In a case of suspected arterial vascular disease, the worst thing you can do is fail to measure the blood pressure in all four extremities.
It is possible to produce a bruit in any vessel by exerting sufficient pressure with a stethoscope.
Listen for carotid bruits as a sign of vascular disease. Further evaluation of a bruit may be advisable depending on symptoms, other findings, and the availability of safe interventions.
Always think of temporal arteritis in a person over the age of 50 with persistent unexplained pain above the neck.
An ankle-brachial systolic pressure index (ABI) less than 0.5 is limb threatening, even in the presence of palpable pedal pulses.
Palpation, auscultation, and the special maneuver of taking the blood pressure are all oriented to the same purpose: determining occlusion and flow. Therefore, this chapter is organized by region (or by specific vessel) rather than in the usual manner by method of investigation.
There are four points to remember in examining the arteries.
In patients with atrial fibrillation or any other condition producing wide beat-to-beat variation in stroke volume, it is a good idea to palpate the arterial pulse on both sides at the same time. Thus, the relative strength of each side during the same stroke volume can be compared. Otherwise, one runs the risk of missing all but the most blatant degrees of decrease in arterial pulsation, especially as the arterial pressure is less useful (Chapter 6). (This is also a good general rule of examination even if the patient is not in atrial fibrillation.)
A bruit can be consistently produced over any vessel if one compresses it sufficiently with the stethoscope. (This misadventure is most likely to visit those who are not aware of the possibility of its occurring.)
Meador’s Rule1: The worst thing you can do in a case of suspected arterial vascular disease is to fail to measure the blood pressures in all appropriate portions of the extremities. This may seem self-evident but needs to be emphasized to the neophyte who believes that simple palpation will often suffice. Such neophytes should note that peripheral vascular surgeons with years of experience do not rely on palpation but quantitate their observations with pressure measurements, often with the use of a Doppler, even though their diagnostic acumen may be the equal of the laboratory’s.
Patients with palpably normal pulses may still have arterial insufficiency, as may be demonstrated by the special maneuvers described in this chapter.
Carotid (and Vertebral) Arteries
Inspection
One branch of the internal carotid artery is accessible to direct inspection in the fundus. The plaque of Hollenhorst is a sign of an ulcerated atheromatous plaque in the ipsilateral carotid system (see Chapter 10).
Palpation: Pulse Wave Contour
The carotid artery is most easily found by placing your index and third fingers on the thyroid cartilage and slipping them laterally between the trachea and the sternocleidomastoid. Palpate gently and low in the neck to avoid the carotid sinus.
Although all arteries have a recordable pulse wave contour, the carotid artery is the best artery for detecting it in terms of cardiac assessment.
Examine Fig. 18-1 and see whether you can tell the significance of each of the tracings. Then read on. Tracing A is a normal one for comparison.
Pulsus Parvus et Tardus2
Pulsus parvus et tardus is a sign of aortic stenosis (see Chapter 17) and may also be called the anacrotic pulse because of the anacrotic notch, indicated on the pulse wave contour (Fig. 18-1B) by the arrow. I can almost never feel the notch. Also, the exact rate of rise of the carotid upstroke is poorly estimated by clinical examination (Spodick et al., 1982). However, in cases of severe aortic stenosis, the upstroke is so delayed that one can learn to detect it at the bedside.
False Positives
Carotid upstroke may also be measurably decreased because of any left ventricular outflow obstruction (e.g., idiopathic hypertrophic subaortic stenosis [IHSS]), any significant vascular obstruction
(e.g., atheroma between the left ventricle and the carotid artery), or any decrease in forward stroke volume (e.g., congestive heart failure, mitral insufficiency, or ventricular septal defect with a left-to-right shunt).
(e.g., atheroma between the left ventricle and the carotid artery), or any decrease in forward stroke volume (e.g., congestive heart failure, mitral insufficiency, or ventricular septal defect with a left-to-right shunt).
 FIGURE 18-1 Carotid pulse wave contours. See text. |
False Negatives
Unfortunately, carotid upstroke increases in the aged because of the changed compliance of their atherosclerotic vessels. Thus, in the elderly, the decreased carotid upstroke of aortic stenosis plus the increased upstroke due to age may yield an upstroke that seems to be within the range of normal values, albeit for a younger population (Flohr et al., 1981). This is not an artifact due to unskilled palpation but can be demonstrated with external carotid pulse tracings.
Corrigan Pulse
The Corrigan, or Watson water hammer, pulse (Fig. 18-1C) was first described by de Vieussens. One hundred years later, Corrigan and Hope, Irish clinicians, noted that many patients with aortic insufficiency had a de Vieussens pulse. Later still, Watson described the pulse as feeling like a water hammer, a Victorian child’s toy. This pulse can also be easily detected at the radial artery.
A Teaching Trick
To make a water hammer, take a piece of thin-walled glass laboratory tubing and seal one end in a Bunsen burner. Add water about one third of the way up. Heat the open end so that you will be able to close it quickly, then boil the water to produce steam while the open end is still workable.
As the steam flows out the hot end of the tubing, seal it off quickly. Permit the tube to cool for a few minutes. After the steam condenses, the tube will contain water under a vacuum.
Holding the tube in your hand, turn it so that the water is at the top. The sensation caused by the water falling through the vacuum is what Watson felt in his patients’ pulses.
False Positives
Like many of the old signs of aortic insufficiency, the Watson water hammer pulse is actually a sign of wide pulse pressure and/or a high stroke volume being ejected down a relatively lax vascular tree. Thus, any condition marked by high stroke volume/high flow/wide pulse pressure has been found to produce a water hammer pulse.
Additionally, mitral insufficiency may rarely have a Corrigan pulse.
False Negatives
Mild cases of aortic insufficiency have insufficient flow to cause a water hammer pulse.
Bisferiens Pulse
The first type of bisferiens pulse (a pulse with two systolic peaks, shown in Fig. 18-1D) is supposedly sensitive for the diagnosis of IHSS. However, it has been found in combined aortic stenosis and insufficiency (Wood, 1956). In aortic stenosis, it seems to indicate a good cardiac reserve (McAlpin and Kattus, 1965).
The other type of bisferiens pulse (Fig. 18-1E), also called a dicrotic pulse, was initially described in febrile patients, especially in those with typhoid fever, and attributed to “arterial relaxation.” Recently, however, it has been described in young patients with elevated peripheral resistance and low stroke volume. Disease states have included primary myocardial disease, hypertensive cardiovascular disease, ischemic heart disease, primary pulmonary hypertension, and pericardial tamponade. In afebrile patients at rest, a marked dicrotic pulse may be a sign of severe functional impairment of the myocardium. Early case descriptions may have been of patients who had typhoid myocarditis or a low stroke volume secondary to severe dehydration from diarrhea (Ewy et al., 1969).
Auscultatory evidence of pulsus bisferiens may be sought as follows (McAlpin and Kattus, 1965). While auscultating over the brachial artery, gradually increase the pressure of the stethoscope bell, using the edge closest to the heart to indent the brachial artery. Eventually, one will hear the usual indentation systolic bruit, which, in cases of pulsus bisferiens will—at a critical pressure somewhere below systolic—split into two short bruits.
This technique detected bisferiens pulses that were otherwise detectable only by utilizing graphic recordings of the pulse wave.
Carotid Shudder
Evidence for a peculiar systolic tactile phenomenon called a carotid shudder was first presented in 1945 (Evans and Lewes, 1945). At the time, the sign was believed to occur only in conjoined aortic stenosis and aortic incompetence and not in either lesion in the absence of the other. The carotid artery tracings (Fig. 18-1F) showed that the systolic peak was replaced by a number of rough undulations, which apparently produced the tactile sensation of “shuddering” or “shivering.” Dr Eugene D. Robin of California also taught a variation of this sign in which the systolic undulations were so fine that the tactile sensation was more like a cat purring. Whereas coarse shudders are invariably palpable, fine shudders are at times felt and at other times not perceived (Alpert et al., 1976).
This sign is useful but insensitive (i.e., most patients with combined aortic insufficiency and stenosis do not have it). Furthermore, the carotid shudder may be less diagnostic than originally thought
(Table 18.1). In a study of carotid pulse tracings of 73 patients with advanced aortic disease documented by cardiac catheterization, neither the fine nor coarse undulations had any significance other than indicating the presence of aortic valve disease, being found in isolated stenosis or insufficiency as well as in combined lesions (Alpert et al., 1976).
(Table 18.1). In a study of carotid pulse tracings of 73 patients with advanced aortic disease documented by cardiac catheterization, neither the fine nor coarse undulations had any significance other than indicating the presence of aortic valve disease, being found in isolated stenosis or insufficiency as well as in combined lesions (Alpert et al., 1976).
TABLE 18.1 Incidence of carotid shudders in patients with proven aortic valve disease | |||||||||||||||
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The carotid shudder does not guarantee the presence of a major lesion. I have detected this sign in patients with no aortic regurgitation and no aortic valve systolic gradient at cardiac catheterization. Others had no significant stenosis as judged by the Doppler velocity display. All had calcification of the aortic ring and the aortic valve as demonstrated by echocardiogram.
Other false positives result from carotid obstruction and kinking.
Palpation: Inequalities of Carotid Pulsations
Pulsus Alternans (Inequality Across Time)
Figure 18-1G does not represent bigeminy because the beats occur at perfectly regular intervals.
Pulsus alternans is an important sign of myocardial failure caused either by a primary myocardial problem or by an overwhelming challenge to the myocardium, for example, from a greatly increased peripheral vascular resistance. It may also occur during tachycardia.
Inequality Between Sides
A weakened carotid pulse on one side probably signifies ipsilateral occlusion of the common carotid. Other causes of unequal carotid pulsations are aortic aneurysm, double aortic arch, atypical coarctation, and cervical rib syndromes (Silverstein et al., 1960b). However, if the carotid and the superficial temporal pulses are both missing only on one side, then there is probably ipsilateral occlusion of the common carotid (Silverstein et al., 1960b).
Auscultation (Including the Vertebral Arteries) for Neck Bruits3
A Method
Listen over the carotid artery high in the neck and inch downward toward the precordium in order to help distinguish a carotid bruit from a transmitted heart murmur. Be sure to listen with the bell of the stethoscope over the bifurcation of the common carotid at the level of the upper border of the thyroid cartilage (Gilroy and Meyer, 1962). Also, listen in the subclavian fossa just posterior to the sternocleidomastoid, immediately above its clavicular origin, and over the posterior neck. (Remember that the subclavian artery is the origin of the vertebral artery.)
Bruits at the top of the neck are thought to be more important than those at the base that do not radiate, especially if the latter can be altered by subclavian compression (David et al., 1973; Ziegler et al., 1971). It has also been said that an important bruit is one that is high pitched or loud (Duncan et al., 1975). However, agreement of physicians on the intensity, pitch, or duration of a bruit is only fair (κ < 0.4), whereas agreement on the presence or location of the bruit is substantial (κ = 0.67) (Chambers and Norris, 1985).
Carotid Compression
Owing to increased flow, a carotid bruit may be intensified by compression of the contralateral artery. However, carotid compression should not be used as a routine diagnostic maneuver for carotid occlusion, especially in older patients, because it has caused serious complications such as hemiplegia (Silverstein et al., 1960a,b) and even death (Webster et al., 1955). Precautions are described in Chapter 9 and in the discussion of special maneuvers (vide infra).Continuous Neck Bruits
A continuous murmur over a partially obstructed artery indicates that the gradient continues to exist in both systole and diastole. This situation is found with high-grade stenosis. There are many conditions that produce a false positive (Table 18.2).
Auscultating for Heart Sounds in the Neck
Suppression of the heart sounds over the carotids on turning the head (Gilroy and Meyer, 1962) and softness of the heart sounds (determined both clinically or by phonocardiographic display) have been advocated as signs of obstructive disease of the carotids (Kartchner and McRae, 1969).
Factors Affecting the Intensity of Murmurs
The variables that affect the intensity of bruits, both over the carotids and over other arteries, include the distance between the
stethoscope and the occlusion (the intensity of sound diminishes according to the inverse square law), the velocity of blood flow, the density of the blood, and the size of the stenotic orifice.
stethoscope and the occlusion (the intensity of sound diminishes according to the inverse square law), the velocity of blood flow, the density of the blood, and the size of the stenotic orifice.
TABLE 18.2 Continuous carotid bruits as a sign of carotid stenosis (including evocation by contralateral carotid compression) | ||||||||
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False Negatives
The absence of a bruit is not so helpful because there may be total occlusion of the vessel (Matthews, 1961). Also, some significant lesions do not produce a bruit.
False Positives
With carotid vessels, as with others, a systolic bruit can be produced in a completely normal vessel merely by pressing hard enough to indent the vessel with the stethoscope, thus causing stenosis with turbulence. In fact, failure to produce a murmur under such circumstances could be considered as evidence that the vessel is thrombosed.
Other conditions that produce noises in the neck include venous hums (see Chapter 19) and transmitted heart murmurs (see Chapter 17). The murmur of valvular aortic stenosis is usually transmitted into the carotid arteries. While it decreases in intensity as it is transmitted up the neck, this murmur may be louder in the neck than it is at the second intercostal space near the sternum. Also, the murmurs due to the ruptured chordae tendineae of the mitral valve and the systolic ejection murmur due to severe aortic regurgitation may be heard in the neck (Hurst et al., 1980).
A supraclavicular bruit, common in children but also heard in adults, may result from increased arterial flow or the velocity of left ventricular ejection (Hurst et al., 1980).
Carotid Disease and Stroke
The main reason for auscultating for cervical carotid bruits in symptomatic patients is to look for a surgically correctable lesion. Numerous studies, using different methods, have reported widely varying results for the diagnosticity of carotid and subclavian bruits.
Symptomatic Patients
In symptomatic patients, the likelihood ratio (LR) for high-grade carotid stenosis was found, in two studies, to be 1.6 or 3.2 when bruits were present and 0.6 or 0.3 when bruits were absent (Sauvé et al., 1993).
Symptomatic means having transient ischemic attacks (TIAs), in which strokelike symptoms last only for minutes to hours. The classic TIA due to atherosclerotic lesions of the common or the internal carotid is amaurosis fugax. One may be able to see the causative embolus—the plaque of Hollenhorst—on retinal examination.
Characteristically, patients report a black or dark shade spreading across the visual field of the affected eye and disappearing after a few minutes. Less commonly, in severe carotid stenosis, transient visual loss due to hypoperfusion occurs under circumstances that increase retinal oxygen demand (such as exposure to bright light) or decrease perfusion pressure (such as postural change). In very rare circumstances, it occurs postprandially when splanchnic blood flow is increased at the expense of other regions. Patients report scotomata in a blotchy pattern, as if “mud had been thrown over the bathroom walls,” lasting minutes to hours (Levin and Mootha, 1997).
Patients with “dizziness,” generalized subjective weakness, “blurry vision,” syncope or near syncope, or transient positive visual phenomena such as “floaters” are not considered to be symptomatic for possible carotid stenosis (Lanzino et al., 2009).
Focal carotid bruits (those heard only over a well-localized region of the bifurcation of the artery in the region of the upper border of the thyroid cartilage) had the best correlation with high-grade stenosis in one study, increasing in frequency with increasing degrees of stenosis, peaking in the 70% to 89% range and becoming less common as the stenosis exceeded 90% (Sauvé et al., 1994). Others found that a focal bruit was no more accurate than a diffuse bruit in predicting moderate-to-severe stenosis in the ipsilateral carotid (Ingall et al., 1989).
Asymptomatic Patients
An asymptomatic carotid bruit not caused by stethoscope indentation may be a marker for increased risk of stroke, either ipsilateral or contralateral to the bruit. There is skepticism on that score (Bergan et al., 1984), and it is important to remember that only about 50% of asymptomatic patients with carotid bruits have detectable carotid stenosis (Donaldson et al., 1987). In a cohort of 4,442 persons without a history of stroke or myocardial infarction, who were participating in the Systolic Hypertension in the Elderly Program, the incidence of stroke over a mean follow-up period of 4.2 years was 7.4% in those with carotid bruits and 5.0% in those without. The association was confounded by more important stroke risk factors, and in enrollees aged 70 years or more, there was no relation between a carotid bruit and a later stroke. Authors of the study concluded that their results “confirm the accepted notion that carotid bruits are a sign of generalized atherosclerosis, rather than a useful marker of clinically significant carotid artery disease” (Shorr et al., 1998). Thus, patients with bruits need a particularly careful examination for coronary artery disease, aortic aneurysm, or peripheral vascular disease (Hurst et al., 1980). Another study showed that patients with asymptomatic cervical bruits had a 3.4-fold higher risk of dying of ischemic heart disease (Heyman et al., 1980). However, a 5-year prospective study showed that the average annual stroke rate was three times as high (1.5%) in patients with bruits compared to those without bruits (0.5%) (Wiebers et al., 1990). A prospective study of patients with type 2 diabetes showed that patients with an incidental carotid bruit had a greater than sixfold higher incidence of stroke within 2 years than patients without a bruit (Gillett et al., 2003).
Carotid Duplex Scanning
Carotid duplex scanning is a considerably more accurate tool for detecting asymptomatic disease than is auscultation for bruits, with a reported sensitivity of 96% and a specificity of 85% for detecting a stenosis of greater than 70% (Rockman et al., 1997). Others note that carotid ultrasonography results are highly user dependent, with sensitivities for severe stenosis ranging from 72% to 97% and specificities ranging from 83% to 95% (Whitty et al., 1998). If the physician performs the test himself, he can obtain as many views as he needs to be certain of the results. Owing to Medicare cuts in allowed fees, the performance of the test is generally delegated to technologists these days and the interpreting physician is totally dependent on the data presented. Correlation of duplex scanning results with angiography results within each institution is recommended (Chang et al., 1995).
The recent addition of color to carotid duplex has improved the ability to distinguish between high-grade stenosis and occlusion.
What If the Results Are Positive?
The key question is whether patients should be referred for surgery if disease is found. Definitive answers are elusive for a number of reasons. One is the difficulty in conducting studies. In a population with a low ipsilateral stroke rate (2.5% annually), more than 3,000 patients would have to be studied to demonstrate a 50% reduction in the stroke rate in the surgical group (Wittgen and Brewster, 1997). Moreover, surgical outcomes are quite dependent upon the skill and experience of the surgeon and the preoperative state of the patient. In a review of the records of 6,038 patients who underwent carotid endarterectomy in Ontario in the period 1994 to 1997, the 30-day postoperative stroke or death rate was as high as 16% in patients with several risk factors. The risk factors included history of a prior TIA or stroke, atrial fibrillation, contralateral carotid occlusion, congestive heart failure, and diabetes mellitus (Tu et al., 2003).
Use of the duplex scan as a screening tool was stimulated by the results of the Asymptomatic Carotid Atherosclerosis Study, which showed a 53% reduction in the aggregate 5-year risk of ipsilateral stroke combined with any perioperative stroke or death in surgically treated patients (who also received medical treatment). The rate in surgically treated patients was 5.1% versus 11% in patients treated only with daily aspirin and risk-reduction measures (Executive Committee for the Asymptomatic Carotid Atherosclerosis Study, 1995). These results look less impressive when one considers that the probability of not having a stroke if surgery is deferred is 89% at 5 years (Rockman et al., 1997) or that surgery possibly prevents only one stroke per 100 persons per year. In contrast, only 8 symptomatic patients with high-grade (>70%) stenosis needed to be treated with carotid endarterectomy to prevent one stroke in a 2-year period (Barnett et al., 1998). Much of the benefit is lost if surgery is delayed more than 2 to 4 weeks after the symptomatic event (Lanzino et al., 2009).
As in screening for other conditions, the prevalence of disease in the population is extremely important. If the prevalence of carotid stenosis is that of the general population, less than 1%, then screening causes more strokes than it prevents. Only in populations with a prevalence of disease greater than 20%, as well as in centers with the best angiographic and surgical results, are significant benefits seen (Whitty et al., 1998).
The prevalence of disease is higher in patients seen by vascular surgeons. In a cohort of veterans, the presence of smoking, cardiac disease, or peripheral vascular disease was associated with an increased risk of greater-than-50% carotid stenosis. The prevalence rate among veterans with all three risk factors was nearly 18% (Fowl et al., 1991). In another study, nearly 25% of patients with claudication had carotid stenosis greater than 50% as was determined on duplex examination. This study also found that a low ankle-brachial systolic pressure index (ABI) (see Chapter 6) is highly predictive of carotid stenosis (Marek et al., 1996).
Of patients presenting with ophthalmologic findings of vascular disease (see Chapter 10), 70% were shown to have stenosis of the carotid artery greater than 50%. The findings included asymmetric hypertensive retinopathy, central or branch retinal artery occlusion, retinal plaques, venous stasis retinopathy, or ischemic optic neuropathy (Lawrence and Oderich, 2002).
The availability of less invasive therapy, namely carotid angioplasty and stenting, might change the risk: benefit analysis, but relative safety and efficacy compared with endarterectomy are not resolved as of 2009 (Lanzino et al., 2009).
Embolic Stroke
Because of its surgical implications, much attention has been focused on carotid artery disease, yet only about 22% of strokes can be clearly attributed to this cause. An embolus that causes a
stroke could come from a source other than an ulcerated carotid plaque. At least 15% of strokes (and probably many more) are the consequence of cardiac disease, including atrial fibrillation, ventricular aneurysm, or dilated cardiomyopathy. Another possibility is paradoxical embolization through a patent foramen ovale, which may be detected only by transesophageal echocardiography (Zhu and Norris, 1990) or transcranial Doppler ultrasonogram following the peripheral injection of microbubbles (see Chapter 17). Neurologists too must examine the heart and be aware of advanced cardiac imaging methods.
stroke could come from a source other than an ulcerated carotid plaque. At least 15% of strokes (and probably many more) are the consequence of cardiac disease, including atrial fibrillation, ventricular aneurysm, or dilated cardiomyopathy. Another possibility is paradoxical embolization through a patent foramen ovale, which may be detected only by transesophageal echocardiography (Zhu and Norris, 1990) or transcranial Doppler ultrasonogram following the peripheral injection of microbubbles (see Chapter 17). Neurologists too must examine the heart and be aware of advanced cardiac imaging methods.
Conclusions
More aggressive screening for carotid disease may be warranted if better treatments become available. Better still, a large portion of this chapter could be made obsolete by more effective treatments for generalized atherosclerosis. On the basis of barely discernible differences in local manifestations of a systemic disease, a vast and expensive effort has been made to optimize the use of an invasive procedure with significant risk and limited potential. In the meantime, this author makes the following recommendations:
Listen for carotid bruits as part of the general cardiovascular examination.
Obtain carotid duplex ultrasonography on patients with symptoms referable to the anterior cerebral circulation, whether they have a bruit or not.
If an asymptomatic patient has a bruit or undergoes a change in a previously heard bruit or is at high risk for a carotid stenosis, carotid duplex ultrasonography is indicated.
Do not focus exclusively on the extracranial carotids as a cause of stroke or TIA.
In advising patients, recognize that the risk of stroke or death resulting from carotid endarterectomy is highly dependent on the precise clinical indication and the available interventions.
Remember that vascular disease is a systemic disease that requires attention to medical risk factors. The systemic disease may be atherosclerosis, but it could also be temporal arteritis or another form of vasculitis.
Special Maneuvers
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)
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).
Massage the carotid sinus with pressure directed medially and posteriorly, compressing the artery and the sinus against the vertebral spine.
Apply vigorous massage for not more than 5 seconds at a time. The procedure may be repeated after several seconds’ rest.
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).
 FIGURE 18-2 The carotid sinus. (Adam, by Michelangelo. Detail from the Temptation and Expulsion, Sistine Chapel.) |
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 bradydromic5 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
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].)
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.
FIGURE 18-3 A: Ladder diagram of a 2:1 AV block. The vertical dashes in the row labeled a symbolize atrial depolarizations. The vertical dashes in the row labeled v symbolize ventricular depolarizations. The diagonals in the row labeled n represent nodal transmission. The rectangles indicate the refractory period in the nodal tissue, their breadth being proportional to duration. Note that alternate atrial impulses reach the node during the refractory period and thus are not transmitted to the ventricle. Because there are twice as many atrial impulses as ventricular ones, the block is called 2:1. B: The effect of carotid sinus pressure. The atrial rate is slowed, but the ventricular rate is paradoxically increased because the atrial impulses arrive after the refractory period (itself unchanged) has passed. Whenever carotid sinus pressure causes an increase in ventricular rate, consider that that may be the mechanism.
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).
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.
If carotid stimulation temporarily slows the ventricular rate, you can be sure that the arrhythmia is not ventricular tachycardia.
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.
If recovery from the temporary slowing is jerky, you must again think of atrial flutter or paroxysmal atrial tachycardia with block.
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).
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.
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:
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.
Establish that the pain is still present.
Massage the right carotid first. If this does not produce appreciable cardiac slowing, massage the left.
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.
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.
 FIGURE 18-4 A: A wing collar with tie removed to show how the stiff, starched, angled point of the wing collar might press the carotid sinus. B: Celluloid collars. This must be the type of collar that Armand’s wife stuck her finger under (see text). |
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.
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).
Subclavian Steal Syndrome
In patients complaining of neurologic or left-upper-extremity symptoms, especially if brought on by exercise, you should always compare the blood pressure and pulses of the left arm with those in the right in order to identify patients with the surgically reversible subclavian steal syndrome. The word “steal” refers to the exercise-induced theft of blood from the vertebral artery caused by occlusion of the subclavian artery proximal to the origin of the vertebral artery. Although at first it seems startling to consider, such occlusions actually lead to a reversal of flow (arteriographically demonstrated) in the ipsilateral, usually left, vertebral artery. In other words, the blood goes first to the brain, and then to the arm, bypassing the traffic jam in the subclavian. In the old days, we made the diagnosis by history. Typically, a man (60% of cases occur in men) in his fifties (±10 years) complained of sudden vertigo, ataxia, lightheadedness, confusion, headache, and/or visual disturbances while brushing his crew cut with his left hand. In one third of the cases, there are hemispheric rather than vertebrobasilar symptoms and these might include transient (or even completed) monoplegia or hemiplegia or, rarely, transient blindness. About 12% of patients have no neurologic symptoms but rather exhibit upper-extremity claudication,6 easy fatiguability, and weakness of an intermittent and transient (i.e., not strokelike) nature. Such symptoms can also accompany the neurologic symptoms in about 50% of the patients experiencing the latter.
In more than 85% of the patients, the syndrome is acquired (i.e., atherosclerotic) and left sided. On physical examination, such patients have absence or diminution of the left radial pulse (compared with the right) and/or a left brachial systolic blood pressure that is 20 mm Hg less than that on the right. The remainder either have a congenital or traumatic cause, right subclavian steal syndrome or bilateral disease, confounding the comparative study of the upper-extremity arterial circulation (Larrieu et al., 1979; Lawson et al., 1979).
Cases of a coronary subclavian steal, and of a concomitant cerebral and coronary subclavian steal, have been reported (Takach et al., 1997).
Internal Carotid Artery
Direct Palpation
The internal carotid cannot be palpated in the neck. A method for palpation in the posterior wall of the pharynx, under the pharyngopalatine muscle, has been described (Dunning, 1953). This is most commonly carried out by vascular surgeons intraoperatively.
Ocular Pressures
The determination of ocular pressures by ophthalmodynamometry or ocular plethysmography is primarily of historic interest (see discussion in Sapira [1990]). These are seldom used, having been replaced by the carotid duplex study, which is much more sensitive and probably about the same cost as the ophthalmologic consultation required to obtain the pressures.
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