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.
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.
(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).
(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
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)
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.
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.
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.
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.)
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.
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.
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.
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).
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.