Rehabilitation management of the chronic pain-hypertension synergy: Proposal of an evidence-informed framework

Abstract

Background: Chronic pain and hypertension (HTN) have a significant societal impact worldwide. Both lead to consumption of substantial healthcare resources and dollars. The pathophysiology of chronic pain and HTN are each complex and multifactorial. Chronic pain has been associated with an increased risk of comorbid HTN. There are numerous common factors related to the development, progression, and prognosis of patients with chronic pain and HTN. Though the cardiovascular and pain regulatory systems are structurally and functionally intertwined, the exact physiological interactions between chronic pain and HTN are less understood. Many systems, including the central and autonomic nervous systems, play a role in the development and interaction of these two complex conditions. In collaboration with other healthcare providers, physical therapists play a critical role in managing those with chronic pain and HTN.

Objectives: This masterclass aims to develop physical therapists' knowledge and understanding regarding 1) the epidemiological and physiological relationship between chronic pain and HTN, and 2) screening, examination, and management of the patient with chronic pain and HTN, including appropriate referral.

Discussion: Improving understanding of the relationship between chronic pain and HTN should assist clinicians in appropriate management strategies for such patients. Physical therapy should be an essential component in the management of patients with chronic pain and HTN. By collaboratively addressing both health conditions, there is a window of opportunity to play a role in mitigating the burden of these conditions and promoting a healthier society.

Keywords: Cardiovascular disease; Epidemiology; Examination; Exercise; Physical therapy; Risk factors.

Fig. 1

The relationship between chronic pain, hypertension, and associated factors.

Fig. 2a

(A) Along with the secondary projections that sends signals to supraspinal centers, the noxious stimulus additionally travels through the somato-autonomic reflex, which increases sympathetic arousal and produces increased blood pressure. (B) Increased blood pressure leads to baroreceptor stimulation which triggers the baroreflex, inputting sensory information into the central nervous system. Alterations in baroreceptor sensitivity may limit the ability for the autonomic system to stimulate the central autonomic network which includes the nucleus of the solitary tract and the locus coeruleus. (C) Signals from the baroreceptor triggers the central autonomic network. (D) This reinforces sympathetic output and pain inhibition via noradrenergic pathways, decreasing pain stimulus. Adapted with permission from Bruehl et al. pain and blood pressure model.

Fig. 2b

Alterations in the pain and blood pressure model may include noradrenergic exhaustion where a reduction in norepinephrine which normally modulates pain. Another possibility in this region includes facilitatory mechanisms with changes in receptor type may promote symptoms. Adapted with permission from Bruehl et al. alterations in the pain and blood pressure model.

Fig. 3

Decision-making algorithm to identify and manage patients with elevated blood pressure.