I2l8 



HANDBOOK OF PHYSIOLOGY 



CIRCULATION II 



people while breathing air with low oxygen concen- 

 trations (40). It is noteworthy that intermittent 

 claudication may be produced in a normal limb by 

 exercise after artificial arrest of the blood supply. 

 In the normal limb following circulatory arrest, the 

 pain disappears quickly (usually within 3 sec) after 

 restoration of the circulation, but if arrest is main- 

 tained the pain persists, presumably because the 

 agents responsible for the pain are not inactivated in 

 the presence of an inadequate circulation. 



Lewis has shown that it is not oxygen lack itself 

 that causes the claudicatory pain but rather the 

 stimulation of sensory nerves by metabolic products 

 of muscular activity which are ordinarily inactivated 

 in the presence of an adequate blood supply with 

 sufficient oxygenation. The mediating agent or 

 agents from ischemic muscles to the pain-sensitive 

 nerve endings has been called "factor P" or "pain 

 factor." Apparently, it is a metabolic product of 

 muscle and is rather stable, acid, and nonvolatile. 

 Whether or not it is produced in increased quantities 

 or is inadequately neutralized, inhibited, or dis- 

 persed in the face of ischemia is not known. Few 

 definitive studies in this area are available. Among 

 the more important are those of Lewis et al. (47, 

 51 ) and Katz et al. (37). 



One observation that requires further exploration 

 is the relief of deep pain by the application of ethyl 

 chloride spray to the skin surface. Travell and 

 associates (98) have reported pronounced ameliora- 

 tion of claudicatory distress by this means. 



Ischemic neuritis is considered to be one of the 

 mechanisms of rest pain in arterial disease. This 

 type of pain, severe lancinating sensations and 

 paresthesias, is characteristic of stimulation of neural 

 elements. It is usually more troublesome at night 

 when the patient is in bed. The pain of ischemic 

 neuritis is found most frequently in vascular dis- 

 turbances associated with diabetes mellitus and 

 Buerger's disease. 



The pathogenesis of the symptoms due to ischemic 

 neuritis appears to be related to neural degeneration 

 secondary to impairment of blood flow through 

 the nutrient vessels of the nerves. In support ol 

 nerve degeneration is the associated reduction in 

 vibratory sense perception and pinprick sensation. 



Trophic changes may be responsible for pain occur- 

 ring in the resting state. These painful sites are areas 

 of ulceration and pre-ulceration which probably 

 cause sensory nerve irritation through inflammation 

 and ischemia. This type of pain is usually continuous 

 in nature. It is more common in Buerger's disease 



and in diabetic neuropathy probably because of 

 the involvement of nerves in the inflammatory 

 processes. 



The pain associated with occlusive arterial disease 

 is frequently accentuated by elevation and diminished 

 by dependency of the involved part. Excessive local 

 heat may be harmful and often increases the pain 

 because of increased metabolism with restricted 

 blood supply. Excessive cold may induce vascular 

 spasm and also accentuate pain and tissue damage. 



symptoms of venous disease. Symptoms due to 

 disease of the veins may include pain, muscle fatigue, 

 muscle cramps, and paresthesias. Many of the 

 symptoms of venous insufficiency (deep-vein throm- 

 bosis and obstruction, valvular incompetence, and 

 varicose veins) are due to congestion and edema of 

 the involved parts and therefore are affected by 

 gravity. These symptoms are accentuated by depend- 

 ency and diminished by elevation. Additional man- 

 ifestations of venous disease and their pathogenesis 

 will be found in subsequent sections. 



manifestations of capillary - and lymphatic 

 disease. These diseases are discussed in other parts 

 of this volume. 



Physical Examination and Simple Clinical 

 Tests of Vascular Function 



In the sense that the basic physiologist must define 

 the conditioning influences under which his labora- 

 tory experiments are conducted, so must the clinician 

 define the conditions under which he makes his 

 observations of disease processes. In this respect, 

 in the examination of his patient for peripheral 

 vascular disease, the clinician must make every 

 attempt to control influencing variables in the 

 environment. L T nder ideal conditions then, the 

 changes observed during a "steady state" estab- 

 lished by proper conditions for examination may be 

 assumed to be due to the disease itself. To this end, 

 standardization of the condition and technique of 

 the examination is necessary. 



The subject should rest supine in bed in a com- 

 fortable position with no constricting garments. 

 The environmental temperature and humidit) 

 should be in a comfortable range. The parts should 

 be dry and free from exposure to drafts. Blankets 

 may be applied, if necessary, but when employed 

 should cover all parts symmetrically. Local heat or 

 cold should be avoided. Other influencing factors 



