PERIPHERAL VASCULAR DISEASES 



12 I 7 



relative quantitative, qualitative, and temporal roles 

 of the many contributing factors such as the numerous 

 effects of disease of other organ systems. All of these 

 factors must be carefully integrated in order to decide 

 upon the type, amount, and time of administering 

 various therapeutic measures. 



Progress in the basic understanding of peripheral 

 vascular disease has been slow. Because of the enor- 

 mous number of variables and the complex nature 

 of these diseases, the clinical physiologist has had 

 great difficulty in elucidating underlying patho- 

 physiologic mechanisms. No small hindrance to this 

 progress has been the nature of the experimental 

 animal himself, namely, man. Nowhere else in 

 physiology does nondestructive observation place its 

 strictest limitations. Available counterparts of spon- 

 taneously acquired human peripheral vascular disease 

 are rare indeed in lower animals. 



The History 



The detection, clarification, and interpretation of 

 a patient's own experience with his altered circula- 

 tion (symptoms) may be just as important to the 

 clinician and clinical physiologist as graphic record- 

 ings of circulatory parameters may be to the basic 

 physiologist. For this reason, it seems worthwhile 

 to discuss briefly the important aspects of this means 

 of investigation. Where known, the physiologic 

 mechanisms underlying these symptoms will be noted. 



Several general aspects of the history are note- 

 worthy. Age, sex, and race are important; e.g., arterio- 

 sclerosis is more common in the aged; Raynaud's 

 disease is much more frequent in females; and 

 Buerger's disease is extremely rare in Negroes and 

 women (74). Because of their predisposing influences 

 on subsequent vascular disease, a past history of poly- 

 cythemia, frostbite, thrombophlebitis, diabetes mel- 

 litus, and many other disease states is important. 

 Occupational factors should be explored, e.g., the 

 predisposition to Raynaud's phenomenon seen in 

 truck drivers and pneumatic hammer operators. 

 Evaluation of environmental influences such as 

 temperature, humidity, and body position is also 

 important. The effects of drugs may be important, 

 e.g., ergot, nicotine, and sympathicomimetic agents. 

 Evaluation of emotional and other psychic factors 

 are also of considerable importance. 



More specific aspects of the history are as follows: 



symptoms of arterial disease. Among the common 

 symptoms associated with reduced arterial flow are 



pain, tenderness, fatigue, paresthesia, altered sensa- 

 tions ranging from hyperesthesia to anesthesia, muscle 

 cramps, and sensitivity to thermal change. Pain may- 

 be divided into three main groups: intermittent 

 claudication, rest pain due to ischemic neuritis, and 

 rest pain associated with trophic changes. 



Intermittent claudication characteristically is pain 

 produced by exercise and relieved with rest. It may 

 appear in any muscle group and is usually due to 

 organic arterial obstruction. It is related to the degree 

 and or rate of work (in the physiologic sense) over 

 a certain time interval performed by a particular 

 muscle group with its compromised circulation. 

 Increasing the amount or rate of work produces a 

 more rapid onset, a more severe degree of pain, or 

 both. With reference to the lower extremities, clini- 

 cians attempt to quantitate claudication in terms of 

 onset of pain after walking a certain distance (claudi- 

 cation distance) or after walking a certain period of 

 time (claudication time) at a prescribed pace. This 

 symptom usually starts as a sense of "fatigue" then 

 progresses to a "cramping" pain. A major charac- 

 teristic of claudication is relief with rest. When post- 

 exercise relief does not ensue within 5 to 10 min, 

 another cause for the pain is suspected. 



"Vasospastic claudication" is a term used to 

 describe a syndrome in which peripheral arterial 

 pulsations are normally present at rest but disappear 

 during exercise. The affected limb may then become 

 pale and typical claudicatory distress occur (43). 

 From clinical studies it is considered that the majority 

 of this comparatively small group of patients have 

 partial segmental occlusion of large arteries proximal 

 to the site of claudication (36) and that superimposed 

 arterial spasm is responsible for the ischemic mani- 

 festations on exercise. 



The exact mechanism of intermittent claudication 

 is not clear. That claudication is not clue to muscle 

 cramps has been repeatedly stressed, since the muscles 

 are flaccid during the attack, and it is not due to 

 vascular spasm of small vessels because the vessels to 

 the muscles are dilated rather than constricted with 

 exercise. Claudication indicates insufficient blood 

 supply to the painful muscles to meet the increased 

 metabolic needs of the muscle during exercise. 



It appears that there are at least two basic require- 

 ments for the production of intermittent claudication : 

 /) oxygen lack and 2) muscular contraction in the 

 presence of this anoxia (36). In this regard it should 

 be noted that claudicatory pain has been produced 

 in severely anemic patients with patent arteries (78) 

 and that it has been produced by exercising normal 



