Peripheral arterial disease pathophysiology

Nonpharmacologic interventions such as smoking cessation and walking exercise programs have the ability to positively impact several of the pathophysiologic abnormalities present in patients with peripheral arterial disease. 

Peripheral arterial occlusion can be the initial manifestation of cardiac or systemic disease. At times, patients with chronic stable claudication may experience abrupt shortening of the distance at which claudication occurs, and this may be the only symptomatic evidence of an acute arterial occlusion either by embolization of by thrombus formation on a pre-existing arterial stenosis. The situation is not chronic and stable any more, but acute and unstable. As ischemia becomes more severe, the patient with chronic peripheral arterial disease develops ischemic pain at rest. The pathophysiologic mechanisms and the clinical presentation parallel the evolution of chronic stable angina pectoris to unstable angina and acute coronary syndromes. 

This chapter will review the available studies that report the incidence and prevalence of peripheral vascular disease in both type 1 and type 2 diabetic patients. It will focus not only on risk factors associated with the development of peripheral arterial disease, but also touch on pathophysiologic changes that may help to account for some epidemiologic trends. Lastly, it will highlight differences between diabetic and nondiabetic subjects concerning localization of disease and its association with mortality and limb loss. 

A common reason for diuretic use is for reduction of peripheral or pulmonary edema that has accumulated as a result of cardiac, renal, or vascular diseases that reduce blood delivery to the kidney. This reduction is sensed as insufficient effective arterial blood volume and leads to salt and water retention and edema formation. Judicious use of diuretics can mobilize this interstitial edema without significant reductions in plasma volume. However, excessive diuretic therapy may lead to further compromise of the effective arterial blood volume with reduction in perfusion of vital organs. Therefore, the use of diuretics to mobilize edema requires careful monitoring of the patient s hemodynamic status and an understanding of the pathophysiology of the underlying illness. 

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