The relationship between pain and hypertension is potentially of great pathophysiological and clinical interest, but is poorly understood.
The perception of acute pain initially plays an adaptive role, which results in the prevention of tissue damage. The consequence of ascending nociception is the recruitment of segmental spinal reflexes through the physiological neuronal connections.
In proportion to the magnitude and duration of the stimulus, these spinal reflexes cause the activation of the sympathetic nervous system, which increases peripheral resistances, heart rate, and stroke volume.
The response also involves the neuroendocrine system, and, in particular, the hypothalamic-pituitary-adrenal axis, in addition to further activation of the sympathetic system by adrenal glands.
Below is where it gets interesting:
However, in proportion to an elevation in resting blood pressure, there is a contemporary and progressive reduction in sensitivity to acute pain, which could result in a tendency to restore arousal levels in the presence of painful stimuli.
So, when you’re injured, the acute pain increases your blood pressure, which then reduces your pain sensitivity so you can continue to function. This could explain soldiers who don’t immediately realize they’ve been wounded.
Nowadays, the phenomenon of being able to suppress reactions to nociception (the nerve impulse itself) in emergencies is taken as proof that it’s possible to mentally control our pain. But this only happens with acute pain, when distress and pain raise blood pressure to provide temporary relief.
The pathophysiological pattern is significantly different in the setting of chronic pain, in which the adaptive relationship between blood pressure and pain sensitivity is substantially reversed.
The connection between acute or chronic pain and cardiovascular changes is supported observationally, but some of this indirect evidence is confirmed by experimental models and human studies.
The pain regulatory process and functional interaction between cardiovascular and pain regulatory systems are briefly reviewed. Various data obtained are described, together with their potential clinical implications.
While it is widely recognized that pain can raise blood pressure (BP) acutely, the evidence that hypertension is associated with a reduced sensitivity to acute pain is less known
Therefore, in the setting of acute pain, an inverse relationship between resting BP levels and pain sensitivity defines a clinical feature called “hypertension-associated hypoalgesia.”
This condition is believed to reflect homeostatic feedback that helps to restore arousal levels in the presence of acutely painful stimuli.
This review summarizes the available information about the possible pathophysiological mechanisms underlying these two different conditions, and suggests their potential clinical implications.
Acute Pain and BP Response
The ability to adapt to an acute pain stimulus is an important contributor to quality of life. Acute pain is considered a warning alarm to prevent danger and to maximize survival. Adaptation to pain is the result of a complex endogenous pain regulatory network made of both descending inhibitory and descending facilitatory pathways.
Reactions to stressors typically involve either short- or long-term compensatory changes in cardiovascular, endocrine, immune, and somatosensory systems, which tend to maintain adequate physiological function against the imbalance created by the stressors
In nature, acute pain signals by tissue trauma and sensitization inhibits normal behavior in a protective manner to minimize risk and promote tissue healing. Although unpleasant, acute pain promotes survival.
Acute pain generates increasing sympathetic nerve activity.
Several studies have reported that acute or chronic hypertension is associated with behavioral hypoalgesia in rats.
In humans, different painful stimuli have been studied, such as tooth pulp, electrical stimulation, and thermal stimulation. All studies confirmed the same association of the rat model reaction, finding the same hypertension-associated hypoalgesia.
In other words, BP correlates positively with the pain threshold and negatively with the perception of the intensity of the painful stimulus in acute pain models.
At this point, investigators should ask themselves the classic “chicken and egg” question: is the hypoalgesia secondary to hypertension or does it contribute to the genesis of hypertension? Some evidence would seem to show that hypoalgesia in hypertensive rats is present at a young age, even before they develop hypertension. On the other hand, hypoalgesia is not observed in all rats that have undergone the clipping of the renal artery in experimental models. Finally, the administration of antihypertensive drugs has never demonstrated a significant reduction of hypoalgesia.[
At the moment we only know that the increase in pain threshold and reduced perception of painful stimuli may be mediated by an increase in the inhibitory descending pathways, and that this central activity may be associated with the development of arterial hypertension
Moreover, resting BP is inversely correlated with acute pain sensitivity in healthy normotensive patients, and presurgical resting systolic BP is inversely associated with acute postsurgical pain intensity
Chronic Pain and Hypertension
In chronic pain, the relationship between hypertension and pain sensitivity is completely reversed.
In patients with chronic low back or orofacial pain, elevated BP levels at rest were associated with an increased sensitivity to acute pain and a higher intensity of chronic pain
The observed alterations in the BP-pain sensitivity relationship are likely to reflect wider alterations in endogenous pain regulatory systems related to chronic pain.
As previously defined, the pain regulatory system is represented by both pain inhibitory and facilitatory pathways. There is evidence suggesting that activity in both of these pathways is altered in chronic pain conditions.
This dysfunction may be related to the sensitivity of baroreceptors, which appears to be decreased in chronic pain. Alternatively, the explanation may lie in an impairment of the descending inhibitory pain pathways normally activated by an increase in the stimulation of baroreceptors.
A positive relationship between resting BP and clinical chronic pain intensity has been observed.
They also suggested that the pain regulatory dysfunction reflected in this positive BP-chronic pain relationship is progressive, in relation to the duration of pain (more than 2 years).
That condition would be supported by a gradual exhaustion of pain inhibitory systems or gradual changes in baroreceptor function.
A retrospective study has directly examined the question of hypertension as it relates to chronic pain.
The results suggest that if the alterations related to chronic pain in the functional interactions between the cardiovascular and pain systems reflect the failure of overlapping systems, it may be possible to have an increased prevalence of hypertension in a chronic pain population.
#”may be possible” is so vague as to be meaninglesss
In this study, it was shown that the intensity of chronic pain was a significant predictor of hypertensive status, independent of the effects of age, race, ethnicity, and parental hypertension.
These results suggest the possibility that chronic pain may be associated with increased risk of hypertension.