4 What causes a weaker and delayed pulse in the left arm as compared to the right?

It depends on the patient’s age: in younger individuals, it is usually coarctation, in the elderly, it is instead an atherosclerotic obstruction or a dissection of the aorta. Depending on the level of obstruction, asymmetry and delay in pulses may only affect the lower extremities. Hence, the need to examine all peripheral pulses, especially in symptomatic or hypertensive patients. A pulse asymmetry can be confirmed by comparing systolic pressure of the two arms or by comparing that of lower extremities to upper extremities.

5 What is Raynaud’s phenomenon?

An exquisite sensitivity of hands and fingers to cold, but also to smoking and emotional stress. Upon exposure to the trigger, fingers exhibit a typical “triple response,” which very appropriately for Raynaud follows the colors of the French flag: initial pallor and blanching (white), followed by cyanosis (blue), and finally by rubro (red). Eventually, the fingers slowly return to their baseline color. Numbness, tingling, or pain accompanies this response. The white-blue-red response may at times be out of sequence, with patients exhibiting a blue-white-red response or even single-color responses (only blue or white).

6 What causes Raynaud’s phenomenon?

A spasm of the digital arteries, resulting in ischemia of the fingers, with pallor at first and cyanosis later (due to increased oxygen extraction from trapped and noncirculating erythrocytes). The final stage of redness coincides with the reperfusion that follows release of the arterial spasm. This also is the phase mostly characterized by numbness or pain (a bit like the numbness and pain experienced in legs that have “fallen asleep”). Severe vasospasm may even lead to infarction and dry gangrene.

7 How can Raynaud’s phenomenon be artificially triggered?

By immersing the patient’s hand in a bucket of iced water.

8 What is the clinical significance of Raynaud’s phenomenon?

It can precede several important disorders, including:

9 Who was Raynaud?

Maurice Raynaud (1834–1881) was one of the great 19th-century French physicians. The son of a university professor, he graduated in Paris at age 28 with a thesis describing his famous syndrome, which made him an instant celebrity. An excellent clinician and a beloved teacher, he also was passionately interested in literature, history, and the arts. In fact, all his life he sought the chair of Medical History at the University of Paris, but he died before this could come through. His contributions to medical knowledge included the book Medicine in Molière’s Time and an article on the Greek physician Asclepiades of Bithynia (an opponent of Hippocratic medicine and the unrivaled authority of his times, who treated celebrities like Cicero, Crassus, and Marc Antony). In 1881, Raynaud wrote an address to the International Medical Congress of London titled “Skepticism in Medicine, Past and Present,” but died before delivering it.

10 What is Allen’s test? What does it mean?

It is a bedside test for patency of the deep palmar arch and of radial/ulnar arteries (Fig. 22-5). Hence, a good way to learn about the risks of radial artery puncture and/or cannulation.

Figure 22-5 Allen’s test.

(From James EC, Corry RJ, Perry JF: Principles of Basic Surgical Practice. Philadelphia, Hanley & Belfus, 1987.)

11 Isn’t the test conducted by simultaneously compressing the ulnar and radial arteries?

Yes, it may be. This is, in fact, a variant of the Allen’s test, conducted as follows (see Fig. 22–5):

12 How do you report the results of an Allen’s test?

By indicating (1) the name and side of the artery compressed (for example, RR for right radial) and (2) refill time expressed in seconds. Thus a RR5/RU3 means that it took 5 seconds to refill the capillary bed of the right palm after releasing the right radial artery, and 3 seconds after releasing the right ulnar artery. Arteries with >15 seconds refill time should not be cannulated. Instead, the contralateral hand should be instrumented.

13 Who was Allen?

Edgar V. Allen (1900–1961) was an American physician. A native of Nebraska and a graduate of that state’s university, Dr. Allen eventually moved to the Mayo Clinic, where in 1947, he became professor of medicine. His contributions include the clinical use of coumarin anticoagulants and a landmark textbook of peripheral vascular diseases.

14 Can peripheral pulses be absent in normal individuals?

Yes. Dorsalis pedis and tibialis posterior are undetectable in 10% of healthy subjects. Congenital loss of one of the arteries usually leads to compensatory increases in the other. Still, only fewer than 2% of healthy subjects lack both pedal pulses. Hence, this is usually an important clue to the presence of peripheral vascular disease (see question 16).

15 What is peripheral vascular disease (PVD)?

An obstructive condition of the lower extremity arteries, also referred to as peripheral arterial disease. Usually caused by atherosclerosis, it affects 8–12 million Americans, with a steadily growing incidence. Although one half of all patients never experience symptoms, the condition represents a risk marker for many other diseases, such as diabetes, hypertension, coronary artery disease, cerebrovascular disease, and aneurysms. Hence, PVD patients have a fourfold to sixfold increase in cardiovascular mortality.

16 What are the symptoms of PVD?

Mostly symptoms of arterial insufficiency, such as exertional limb weakness, resting limb pain (or paresthesia), and poor healing of sores or ulcerations. The classic symptom, however, is claudication (from the Latin term for limping)—i.e., intermittent limb pain, usually triggered by activity. This affects different parts of the lower extremity, depending on which artery is compromised. Yet, whether obstruction is high or low, both pedal pulses are absent in PVD, an important diagnostic clue (see Table 22-1).

Table 22-1 Symptoms of Peripheral Vascular Disease

17 What are the physical findings of PVD?

(1) Decreased or absent pulses (as previously indicated); (2) atrophic changes in the foot (such as loss of hair, discoloration of skin, decreased warmth, impaired nail growth, pallor following elevation, and rubor following dependency); (3) vascular bruits (over the involved artery—iliac, femoral, or popliteal); and (4) increased venous filling time.

18 Can these findings predict severity of the disease?

No. Vascular bruits and other signs only indicate presence of disease; they do not correlate with severity. For severity, the standard assessment is the ankle-to-arm systolic pressure index (see Chapter 2, questions 117–119). Still, in diabetic patients with significantly abnormal ankle–brachial indexes, the following symptoms/signs predict more severe disease: (1) age greater than 65, (2) history of peripheral vascular disease or claudication in less than one block, (3) diminished foot pulses, and (4) venous filling time longer than 20 seconds.

19 What is an increased venous filling time?

It is the abnormally slow (re)filling of foot veins in peripheral vascular disease. To test for it:

20 What is a capillary refill time (CRT)?

A generally accepted bedside method for assessing peripheral perfusion. To test for it:

Still, these figures have little scientific foundation. In fact, CRT is often longer in women, the elderly, a cold environment, and poor ambient lighting. Hence, a normal CRT indicates good peripheral perfusion, but a prolonged one must be interpreted in view of other parameters, such as sex, age, blood pressure, heart rate, cardiac output, and level of consciousness.

21 What is the Buerger’s test?

Another bedside maneuver for assessing arterial perfusion to the leg. It consists of examining the color of the patient’s leg: first when elevated and then when lowered. Hence, it consists of two stages (Table 22-2). The test is considered positive for PVD when it elicits excessive pallor with elevation and intense rubor with dependency.

Table 22-2 Buerger’s Test