The cardiovascular and pain regulatory systems are structurally and functionally intertwined. In healthy individuals, these interconnections produce blood pressure (BP)-related hypoalgesia, in which a noxious stimulus triggers elevated BP to initiate a reduction in pain experience (Supplemental material 1).18,19 A noxious stimulus travels through the somato-autonomic reflex, which increases BP through sympathetic arousal (Fig. 2a). Increased BP leads to baroreceptor stimulation, triggering the baroreflex and associated pathway in the central nervous system (CNS). The baroreceptor system is vital to cardiovascular regulation. It consists of a negative feedback loop in which electrical activity changes in arterial baroreceptors, resulting from BP alteration, initiate compensatory changes in heart rate, cardiac contractility, and vascular tone.20 This feedback system processes information within the cardiovascular cranial nerve branches into the lower brain stem. Brain signaling reinforces sympathetic output and descending modulation of noxious stimuli via noradrenergic pathways to reduce the painful experience. Once reduction in noxious and pain signaling occurs, there is a reduction in activation within this baroreflex and associated pathways, allowing BP to return to baseline.

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 model26.

(0.28MB).

Although BP-related hypoalgesia has been postulated to respond to acute pain stimulus, it is important to highlight this mechanism has demonstrated mixed results in conjunction with exercise. Exercise inherently is thought to produce an increase in BP that attenuates the baroreceptor related mechanism.21 Research on isometric exercises found that increases in BP has not consistently corresponded to alterations in pain perception.22 These findings suggest that other physiological mechanisms may be at play aside BP alone such as endogenous opioids, cannabinoids and growth hormones which have been hypothesized to be produced during exercise.21

Altered central nociceptive processing may occur with chronic pain, leading to nociplastic pain.23 While various mechanisms are associated with nociplastic pain, including hyperexcitability of nociceptive pathways, another potential feature of the condition is impaired descending inhibitory mechanisms. Descending noradrenergic inhibition can be profoundly effective in modulating pain, and may be impaired in individuals with HTN and chronic pain.24,25 Chronic pain is associated with reduced magnitude of BP-related hypoalgesia, suggesting maladaptive processes occurring within the cardiovascular regulatory systems (Supplemental Material 1). These are potentially relevant to comorbid cardiovascular risk in chronic pain.26 Possible reasons for this altered relationship between BP and pain sensitivity include exhaustion of certain pain-inhibiting pathways, changes in baroreceptor function, increased inflammation, and other contributing factors (Fig. 2b).

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 model26.

(0.31MB).

Chronic pain conditions may mask sinister pathology requiring assessment and intervention from another health care practitioner. Unfortunately, clinicians are more likely to discount symptoms that patients with chronic pain report and are less inclined to provide intervention, particularly when evidence for a particular pathology is lacking and/or the patient reports high pain intensity.50,51 It is imperative that health care providers continue to screen and examine throughout the episode of care, even if patients are improving. For instance, Hensley and Emerson report on a patient with chronic left upper quarter pain who was improving with management provided by the physical therapist. A change in presentation during the episode of care warranted referral for further medical workup, leading to a diagnosis of lung cancer.52 Moreover, patients with chronic pain and HTN should be evaluated for signs and symptoms consistent with post-exertional malaise/post-exertional neuroimmune exhaustion (PEM/PENE),53 because pain is a common component of PEM/PENE. PEM/PENE is a clinical hallmark of myalgic encephalomyelitis (ME) and ME-like conditions, such as subtypes of Long Covid54-57 and post-treatment Lyme disease.58 These conditions are important to be aware of because exercise recovery responses are impaired in people with PEM/PENE.59-63 In those with PEM/PENE, exercise should not be considered as a frontline intervention.64

A mechanism-based approach to pain has been proposed to improve pain management. A mechanisms-based approach integrates and builds on the biopsychosocial models by defining specific pathobiology in pain processing, and external factors influence an individuals’ pain experience.23 Pathobiological categories in pain processing include nociceptive, nociplastic, and neuropathic pain. These are further defined in Table 1. Recent recommendations have proposed features that discriminate between these three categories.65,66 It is important to recognize that more than one category can simultaneously contribute to an individual’s pain experience. In addition, consideration of pain-relevant psychological and motor factors must be given, as they may play a role in the maintenance of an individual's pain.23 Interventions have been proposed that can be matched to specific pain mechanisms.23,67 For instance, a patient with LBP predominantly driven by a nociceptive source can be managed with interventions that target biomechanics, such as posture education, strengthening weak musculature, and stretching structures deemed inflexible/hypomobile. Alternatively, if the pain is driven predominantly from a nociplastic source, it is unlikely that treatment targeting mechanics alone will improve outcomes. Pain neuroscience education (PNE) can be a crucial addition to exercise and manual therapy to assist these patients.68,69 It should be noted that there is a paucity of evidence demonstrating that a mechanism-based approach to pain provides better benefits to patient outcomes compared to a thorough biopsychosocial assessment and person-centered management plan.

While the standard patient interview and physical examination is critical, physical therapists may use additional testing, including quantitative sensory testing (QST), to help determine pain mechanism(s) involved. These tests include palpation, pain pressure threshold, temporal summation, and conditioned pain modulation. It should be noted that these tests have several limitations as stand-alone pieces of an evaluation.12,75 Firstly, they are indirect measures of CNS excitability and inhibition of pain pathways. Secondly, there is a general lack of consensus on normative and predictive values. Thirdly, findings from these tests do not always correlate with symptoms intensity or improvement in symptoms.76–78 Finally, funding for equipment and time to perform QST may not be widely available across rehabilitation settings. There are, however, cheaper, alternative testing equipment that can be used to perform QST measures.79,80

Physical therapists possess the expertise to assess vital signs throughout the episode of care, not only to conduct health screenings and gather patient history but also to ensure safety and appropriateness prior to initiating exercise interventions. They are positioned to expedite the World Health Organization’s initiative to reduce prevalence of undiagnosed or uncontrolled HTN.1 The specific parameters to attend to in order to mitigate threats to accurate BP measurement is available from the American Heart Association for reference.86 Appropriate BP management is likely to reduce the risk of negative cardiovascular/cerebrovascular-related sequelae, and improve societal health.87–90 Vital sign assessment should include monitoring at rest, during aerobic activity, and during recovery. This testing approach can reveal BP readings that place the patient at risk for an adverse event.1,12,16,91,92Fig. 3 provides guidelines for assessment and management based on patient vitals during different stages of rest, aerobic testing/exercise, and during recovery to ensure safety and optimal health outcomes. It includes specific BP measures and corresponding clinical decision making.

Fig. 3.

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

(0.53MB).

Multiple common risk factors should be considered when evaluating a patient with chronic pain and HTN. Assessment tools are identified and described in Table 1. As able, the health care team should work with the patient to mitigate these risk factors. Providers should also consider pain medications that can elevate BP. Risk of systolic/diastolic HTN can increase with consumption of non-steroidal anti-inflammatory drugs (e.g., naproxen), serotonin norepinephrine reuptake inhibitors (e.g., duloxetine), and tricyclic antidepressants (e.g., amitriptyline).93,114

Educational material should be provided in an accessible format to the patient. Education should be provided regarding:

• 1)

  What their BP reading means relative to healthy BP.

• 2)

  How to accurately measure BP at home for consistent comparison.

• 3)

  Warning signs and symptoms that require a consultation with a physician or an emergency room visit.

• 4)

  The potential bi-directional relationship between chronic pain and HTN, and how management targeting a patient-centered approach can assist with management of both.

• 5)

  Associated risk factors, particularly modifiable risk factors like stress, sleep, physical activity, and diet, related to chronic pain and HTN. Stress, for example, can be addressed through teaching coping strategies using the eliminate-change-accept approach and/or by increasing greenspace exposure.115 Educating on the importance of sleep and sleep hygiene can be tailored to address any sleep-related dysfunction.116 Clinicians should consider a referral to a psychologist, sleep specialist, and/or dietitian when deemed appropriate.

• 6)

  Factors related to predominant pain mechanism(s). Modifiable biomechanical factors that may be further perpetuating symptoms should be discussed. PNE could be incorporated when the clinical picture is dominated by nociplastic pain, or when maladaptive pain perceptions and/or coping strategies are present.68 Clinicians should aim to improve patients’ knowledge of pain processing within the nervous system, engaging patients in a discussion regarding their pain and attempting to reconceptualize the patient’s understanding and beliefs about their pain as needed.117 Recent evidence has shown beneficial effects of PNE in chronic musculoskeletal pain69 and fibromyalgia.117

Exercise can provide both acute and chronic changes in pain and BP.118–120 While exercise can increase BP during activity, there is a drop in BP for up to several hours after exercise in those with and without HTN.118,121 As suggested above, vitals should be measured throughout the plan of care to ensure safe delivery of exercise. Chronic adaptations in BP response to various forms of exercise are outlined in Supplementary Material 3. It should be noted that current data do not differentiate chronic changes in exercise between those with and without chronic pain. These changes should be used and interpreted with caution in patients with chronic pain.

Several mechanisms have been suggested as to why exercise is effective for managing chronic pain and HTN. Namely, there are improvements in pain regulation systems through EIH; improvements in autonomic regulation through decreasing sympathetic tone and vagal inhibition; increases in circulatory and intraarticular anti-inflammatory markers, and changes in brain chemical makeup, activation, and connectivity.122

If deemed safe to begin an exercise program, factors such as current activity level, patient’s previous response to exercise, patient beliefs, readiness to begin an exercise program, predominant pain mechanism(s), health conditions, and current medications need to be considered. Integrating exercise in the plan of care in those with chronic pain can be challenging. Nijs et al outline a stepwise approach to assist with implementing exercise for patients with chronic pain.123 This includes an individually tailored plan that may involve:

• 1)

  Goal setting plus identifying body functions, activity limitations, participation restrictions, and contextual factors related to pain

• 2)

  Shared decision making

• 3)

  Tackling maladaptive beliefs about pain and physical activity

• 4)

  Improving lifestyle factors that can optimize exercise, such as sleep, diet, and stress

• 5)

  Identification of activities that are avoided (managed with graded activity) versus persisted (managed with pacing and acceptance-based interventions).

Table 2 provides proposed guidelines for clinical-decision making regarding exercise parameters in patients with chronic pain and HTN.119,122,124–126 Aerobic, resistance, and isometric exercise have demonstrated effectiveness in managing patients with chronic pain or HTN.119,122,124–126 Exercise can be tailored to best meet the demands of the patient. For instance, if a patient has significant pain at the knee yet can tolerate regional exercise at other body sites, clinicians can consider titrating exercise at these other and less painful sites.127

Moderate intensity aerobic exercise has been a staple element of HTN management at all stages.136,137 High intensity aerobic exercise is safe and also appears to promote substantial decreases in BP in those with HTN, although there are limited high quality studies supporting this approach.128 Moreover, higher intensity training may not be tolerated in those with chronic pain, particularly early on during the rehabilitation process. It is important to recognize that, although exercise and lifestyle change are important management strategies in those with HTN, pharmacological intervention may be indicated in those with higher BP and/or those at higher risk for a cardiovascular event.93 Moderate to high intensity aerobic exercise has also been recommended for the best analgesic effect. However, Vaegter and Jones21 suggested that even very short-duration aerobic exercise can elicit EIH, which implies that intensity, or permutations of intensity and duration, may be more critical for achieving analgesia after aerobic exercise than either variable alone.

Depending on the patient’s pain and BP response to aerobic exercise/testing, resistance and/or isometric exercise may be a necessary and effective first step to address chronic pain and HTN. There is promising research emerging on the effects of isometric exercise and BP management.136,138 Large increases in BP can take place with resistance and isometric exercise.121 If there is a concern for large increases in BP, clinicians should consider using smaller musculature to begin.138

Emerging data suggest that meditation and/or breathing control exercises for 15-20 min/day can reduce BP in those with HTN 39 and improve ability in those with chronic musculoskeletal pain.136,139 Research on mindfulness meditation has demonstrated significant pain relief and greater activation in brain regions associated with cognitive modulation of pain, including the orbitofrontal, subgenual anterior cingulate, and anterior insular cortex.140

Manual therapy intervention has shown to increase PPT and facilitates impaired conditioned pain modulation in persons with lateral epicondylalgia of at least 6 weeks duration; however, the effects on BP were not reported.141,142 Yung et al found that non-thrust mobilization targeting the cervical spine in those with non-chronic neck pain results in acute changes in systolic BP.143 Other trials are underway investigating the effects of manual therapy on BP in those with HTN.144 While studies are limited, it seems plausible that improving pain may alter intertwined mechanisms involving chronic pain and HTN and reduce BP. Future studies are warranted.