Hubbry Logo
Cold pressor testCold pressor testMain
Open search
Cold pressor test
Community hub
Cold pressor test
logo
7 pages, 0 posts
0 subscribers
Be the first to start a discussion here.
Be the first to start a discussion here.
Cold pressor test
Cold pressor test
Cold pressor test
View on Wikipedia
from Wikipedia
Cold pressor test
Purposemeasuring changes in blood pressure

The cold pressor test is a cardiovascular test performed by immersing the hand into an ice water container, usually for one minute, and measuring changes in blood pressure and heart rate. These changes relate to vascular response and pulse excitability. Some research suggests that the outcome of the cold pressor test can help to predict hypertension in patients; however other studies have failed to confirm this.[1][2][3][4]

Other measures can also be obtained from the cold pressor such as pain threshold and pain tolerance.[5][6][7] This is done by requiring a participant to place their hand in the cold pressor for as long as they can. Once pain is present, they let the researcher know. Once the pain is unbearable, the participant removes their hand. This provides a measure of threshold (first feeling pain) and tolerance (total time minus threshold). This method is the most frequently used application of the cold pressor task. Comparable in terms of pain elicitation is the hot water immersion test, the equivalent to the cold pressor using hot water. The hot water immersion test (HIT) is equally capable of triggering a pain response without the confounding of baroreflex activation.[8]

Physiology

[edit]

Sensory afferent nerves trigger a systemic sympathetic activation leading to marked vasoconstriction. The result is an elevated pulse pressure (normal is 40mm Hg), due to catecholamine release. This increased pressure fills the ventricle to a greater extent, but stroke volume decreases due to an increase in afterload.[citation needed]

References

[edit]

Further reading

[edit]
Revisions and contributorsEdit on WikipediaRead on Wikipedia

Cold pressor test

View on Grokipedia
from Grokipedia
The cold pressor test (CPT) is a simple, used to evaluate activation, cardiovascular reactivity, and pain sensitivity by immersing a participant's hand or foot in ice-cold water, typically at 0–10°C, for up to 1–3 minutes while monitoring physiological responses such as and . Developed in the early by Edgar A. Hines Jr. at the , the test originated as a method to quantify variability in response to cold stress, with normal systolic increases below 20 mmHg and hyperreactive responses at 25 mmHg or higher indicating potential autonomic or vascular issues. Physiologically, immersion triggers afferent sensory nerve activation, leading to sympathetic noradrenergic outflow that causes , elevated systolic (often by 10–20 mmHg in healthy individuals), and modest increases (3–5 beats per minute), while also inducing a slowly mounting sensation to assess threshold and tolerance. In healthy subjects, the response involves both and compensatory via β2-adrenergic receptors and , but it is blunted in conditions like or autonomic disorders. Originally employed to predict hypertension risk— with long-term studies showing hyperreactors at higher odds of developing the condition—the CPT has expanded to applications in autonomic testing (e.g., for or failure), experimental research (measuring tolerance via immersion duration), and evaluations of vascular in diseases like or Parkinson's. Standard protocols emphasize ethical safeguards, such as excluding those with cardiovascular risks, using circulating water baths for consistency, and limiting immersion to prevent discomfort, with no reported adverse effects in large cohorts.

Introduction

Definition and purpose

The cold pressor test (CPT) is a noninvasive experimental procedure in which a participant immerses a hand or foot in ice-cold water, typically maintained at 0–5°C, to induce acute and activation. This method reliably stimulates nociceptors, particularly cold-sensitive C-fibers, without causing tissue damage during brief exposures of up to several minutes, ensuring participant safety while eliciting consistent physiological responses. The primary purposes of the CPT include evaluating and threshold by measuring the duration of immersion until voluntary withdrawal or reported pain intensity. It also assesses stress reactivity through induced autonomic and cardiovascular responses, such as elevations in and , providing insights into sympathetic function. Additionally, the test is employed to examine endothelial function by observing vascular reactivity, such as changes in coronary blood flow or vasodilation, which can indicate underlying cardiovascular health. Overall, the CPT facilitates the study of individual differences in perception and reactivity, influenced by factors like age, sex, and psychological coping strategies.

Historical development

The cold pressor test originated in the late as a diagnostic tool for cold-induced allergies, with Bayard T. Horton at the employing hand immersion in water at approximately 15°C to provoke urticaria in susceptible individuals. This precursor laid the groundwork for systematic physiological assessment using cold stimuli. In 1932, Edgar A. Hines Jr. and George E. Brown formalized the test at the , adapting it to measure reactivity as a predictor of ; their protocol involved immersing the hand in ice water (4–5°C) for up to three minutes while monitoring systolic and diastolic responses, classifying increases of ≥25 mmHg systolic or ≥20 mmHg diastolic as hyperreactive. Their seminal 1932 paper examined responses in 79 individuals, establishing the test's reliability for identifying prehypertensive states and influencing its adoption in cardiovascular research. Following , the test gained prominence in psychophysiological studies of autonomic function and stress reactivity, with longitudinal cohorts—such as medical students tested between 1948 and 1964—demonstrating that exaggerated responses predicted development over decades. By the mid-20th century, researchers expanded its scope beyond screening; in 1941, Stewart Wolf and James D. Hardy investigated the test's -inducing properties, documenting how immersion elicited a progressive deep ache due to local cooling, which informed early models of experimental thresholds and sensory mechanisms. This shift marked the test's integration into broader psychosomatic research, including autonomic responses to stressors, as reviewed in the psychophysiological literature of the . In the , the cold pressor test has evolved into a versatile tool for and stress paradigms, with functional MRI applications revealing central processing and sympathetic activation during immersion. A 2021 review highlighted its growing role in assessing autonomic integrity across clinical populations, from to psychiatric disorders, underscoring adaptations like the socially evaluated variant for enhanced stress induction. More recent adaptations include remote administration for clinical use (as of 2024) and combined use with physiological measures like for studying anxiety responses (2025). This progression reflects a transition from a focused cardiovascular predictor to a multifaceted probe in interdisciplinary research.

Methodology

Standard procedure

The standard procedure for the cold pressor test begins with thorough preparation to ensure participant safety and accurate baseline data. Participants are seated comfortably in a quiet, temperature-controlled room free from distractions to minimize external influences on physiological responses. The non-dominant hand, typically the left, is selected for immersion to preserve functionality in the dominant hand for daily activities. A bath is prepared by combining and to maintain a between 0°C and 5°C, with continuous stirring or circulation to ensure uniformity; a is used to verify the periodically. is obtained, explaining the test's purpose, expected sensations, and right to withdraw at any time. Baseline measurements, such as , , and subjective ratings (often using a 0-10 visual analog scale, VAS), are recorded after a brief rest period of 5-10 minutes. The immersion protocol involves instructing the participant to fully submerge the selected hand up to the in the cold water bath, with the palm facing upward and fingers extended but unclenched to promote even exposure. Participants are directed to keep the hand motionless during immersion to avoid altering sensory input through movement. The commences upon full submersion, with the maximum duration set at 3 minutes to balance assessment of with risk minimization. Throughout the procedure, participants provide periodic intensity ratings, typically every 15-30 seconds, using a standardized scale like the VAS to track subjective experience without prompting withdrawal. Termination occurs based on predefined criteria to prevent harm: voluntary withdrawal by the participant if becomes intolerable, attainment of a high threshold (e.g., 8/10 on the VAS), or completion of the 3-minute duration. Upon ending the immersion, the hand is immediately removed and dried with a , followed by warming if needed (e.g., in room-temperature water or with a ) to alleviate discomfort. The experimenter closely monitors for adverse reactions, such as excessive numbness, , or signs of distress, and ensures prompt cessation if any occur. Post-immersion, recovery is observed until baseline physiological parameters normalize, typically within 5-10 minutes.

Measurement and assessment

The cold pressor test involves quantifying both subjective and objective responses to cold-induced pain and stress. Pain assessment primarily relies on self-report scales to capture intensity and duration. The Visual Analog Scale (VAS), a continuous line from 0 (no pain) to 100 (worst imaginable pain), or the Numeric Rating Scale (NRS), an 11-point scale from 0 (no pain) to 10 (worst pain), is used to rate pain intensity at baseline, during immersion, and post-withdrawal. Pain tolerance is measured as the elapsed time in seconds from the start of hand immersion to voluntary withdrawal, often with a maximum duration of 3 minutes to standardize exposure. Cardiovascular responses are monitored to evaluate sympathetic activation. Blood pressure (BP) is typically assessed using an oscillometric on the non-immersed arm for intermittent measurements every 30-60 seconds, or continuously via finger devices like the Nexfin system. (HR) is recorded via electrocardiogram (ECG) for precise beat-to-beat intervals or on the or finger for non-invasive monitoring. The pressor response is calculated as the change from baseline, with an increase in systolic BP exceeding 20 mmHg indicating heightened reactivity. Additional metrics include , measured with a probe on the immersed hand to track , and subjective stress ratings via VAS (0-100, from calm to extreme stress). Post-test recovery is assessed by continuing BP and HR monitoring for 5-10 minutes until values return to baseline, providing insight into autonomic recovery dynamics. Data analysis focuses on mean changes from baseline, with individual variability emphasized due to factors like sex differences; for instance, females often exhibit shorter times compared to males. Tolerance data may require log transformation to address , and responses are averaged across trials for reliability.

Physiological Responses

Pain and sensory mechanisms

The cold pressor test elicits primarily through the activation of peripheral nociceptors in the skin, specifically cold-sensitive Aδ and C fibers, which respond to temperatures below approximately 15°C. These thinly myelinated Aδ fibers mediate the initial sharp, pricking sensation, while unmyelinated C fibers convey the subsequent dull, burning, or aching . Upon immersion in ice water (typically 0–5°C), the rapid drop in skin temperature stimulates these nociceptors, generating action potentials that propagate via primary afferents to the dorsal horn of the . From there, the signals ascend through the , a key pathway for transmitting nociceptive and thermal information to higher centers. The pain pathway continues with integration in the , where nociceptive inputs are relayed and processed, before projecting to the somatosensory cortex for localization and intensity perception. This central processing contributes to the characteristic slow-building nature of cold pressor pain, which intensifies over time due to progressive tissue cooling and that reduces blood flow, exacerbating local hypoxia and stimulating ongoing firing. Unlike acute thermal injuries, the standard test duration (up to 1–2 minutes) does not cause actual tissue damage, as the cold stimulus remains below the threshold for or cellular destruction, allowing full recovery upon withdrawal. Central modulation of cold pressor-induced pain involves endogenous opioid systems and descending inhibitory pathways from brainstem structures like the periaqueductal gray, which can attenuate nociceptive transmission at the spinal level. The test itself serves as a conditioning stimulus to activate diffuse noxious inhibitory controls (DNIC), demonstrating how supraspinal mechanisms release opioids to suppress pain signals. Individual variability in pain experience arises from differences in central sensitization, where repeated exposure may lead to habituation in some, or heightened responses due to genetic or psychological factors influencing opioid receptor function. Sensory experiences typically begin with an innocuous sensation that transitions to a deep aching pain within 10–30 seconds, reflecting the dual activation of thermoreceptors and nociceptors without progressing to inflammatory damage.

Cardiovascular and autonomic effects

The cold pressor test (CPT) elicits a robust activation in response to the cold stimulus, primarily through engagement of the locus coeruleus-norepinephrine (LC-NE) system, which drives the release of catecholamines such as norepinephrine and epinephrine from the and sympathetic endings. This neuroendocrine response is mediated by afferent activation in the immersed limb, leading to central processing that amplifies efferent sympathetic outflow to vascular and cardiac tissues. Direct recordings of muscle sympathetic activity during CPT confirm a marked increase in burst frequency, often doubling or tripling baseline levels within the first minute of immersion. These sympathetic changes manifest in pronounced hemodynamic responses, characterized by a rapid elevation in systolic (typically 10–20 mmHg above baseline) and (3–5 beats per minute), attributable to alpha-adrenergic-mediated peripheral and beta-adrenergic stimulation of . Diastolic also rises, often by 5–15 mmHg, due to heightened total peripheral resistance from widespread arteriolar constriction, while increases correspondingly to support the enhanced sympathetic drive. In healthy individuals, these alterations reflect an integrated cardiovascular to the acute stress, with most prominent in the skin and skeletal muscle beds. The CPT further serves as a tool to evaluate endothelial function, particularly through assessment of post-immersion recovery in forearm blood flow, measured via venous occlusion strain-gauge plethysmography to quantify vascular reactivity and nitric oxide-dependent . This method detects the forearm's ability to restore hyperemic flow after cold-induced , providing insights into endothelial integrity independent of large-vessel responses. During the recovery phase, sympathetic activation subsides progressively, with blood pressure and heart rate returning to baseline over 5–10 minutes as catecholamine levels decline and mechanisms restore . Exaggerated or prolonged responses in this phase, such as delayed normalization of vascular tone, indicate heightened autonomic reactivity.

Clinical and Research Applications

Diagnostic uses

The cold pressor test (CPT) serves as a valuable diagnostic tool in clinical settings to identify individuals at risk for various cardiovascular and neurological conditions by eliciting and measuring acute physiological responses to cold-induced stress. In hypertension screening, the test, particularly via the standardized Hines-Brown protocol, evaluates blood pressure reactivity to predict future essential hypertension. Individuals classified as "reactors"—those exhibiting a systolic blood pressure increase of at least 20 mmHg during the test—are deemed at higher risk, with longitudinal studies validating this association in middle-aged adults, where hyperreactors showed a significantly elevated incidence of hypertension over 20-30 years of follow-up. In clinics, the CPT aids in screening for , a key precursor to . Assessment of diameter response during the test reveals abnormalities, such as paradoxical , which correlate with presence and predict adverse cardiovascular events like in hypertensive patients with otherwise normal angiograms. Recent applications include its use in evaluating hemodynamic responses in , where paradoxical blood pressure reductions may indicate disease-specific autonomic alterations (as of March 2025). Additionally, CPT-derived has prognostic significance in patients with ischemia and nonobstructive . For evaluating pain disorders, the CPT integrates with quantitative sensory testing (QST) protocols to quantify hypo- or in patients with conditions. In , patients often display heightened sensitivity, rating the cold-induced as more intense and showing faster neural processing of the stimulus compared to healthy controls, indicating central sensitization. Similarly, in sufferers, the test elicits exaggerated perception and autonomic responses, such as altered pupillary parasympathetic activity during interictal periods, helping differentiate migraine-related sensory dysregulation from other headaches. The CPT also assesses autonomic disorders by examining vasoconstrictive and cardiovascular responses in conditions like and Raynaud's phenomenon. In , the test detects residual sympathetic activation through elevations, confirming partial integrity of autonomic pathways despite overall dysfunction. For Raynaud's, immersion provokes exaggerated digital , leading to unique increases in and visible color changes in extremities, aiding of vasospastic tendencies. These responses help clinicians evaluate the severity of autonomic imbalance and guide therapeutic interventions. Emerging protocols include of the CPT, enhancing feasibility for assessing pain sensitivity in clinical populations with mobility limitations (as of 2024).

Experimental applications

The cold pressor test (CPT) serves as a reliable for inducing acute, controllable stress in settings, enabling researchers to investigate psychological, neurophysiological, and behavioral responses without ethical concerns associated with more invasive stressors. In experimental contexts, it facilitates the study of stress reactivity, processing, and individual variability, often integrated with biomarkers like assays or imaging techniques to test hypotheses in controlled cohorts. This utility stems from its ability to elicit predictable yet variable responses, allowing for the isolation of factors such as emotional regulation or pharmacological influences. In stress and research, the CPT induces acute physiological stress, prompting investigations into hypothalamic-pituitary-adrenal (HPA) axis activation, including release and its modulation by anxiety or strategies. For instance, studies have used the CPT to examine blunted ACTH and responses in individuals with (PTSD), revealing HPA dysregulation compared to healthy controls, which informs models of trauma-related resilience. The socially evaluated cold pressor test (SECPT), a incorporating elements like monitoring, amplifies al distress and has been widely adopted to study anxiety amplification and mechanisms in vulnerability to . Additionally, repeated CPT exposures demonstrate in the stress response multiplex, including attenuated and cardiovascular reactivity, providing insights into adaptive processes in regulation. Pain modulation experiments leverage the CPT to evaluate interventions that alter nociceptive thresholds and tolerance, focusing on both pharmacological and psychological mechanisms. Researchers have employed it to assess analgesic efficacy, such as the dose-dependent pain relief from intravenous administration of compounds like GSK3858279, which reduced cold-induced pain intensity in healthy participants. In psychological domains, the CPT tests placebo effects, where mere possession or expectation of an analgesic—without administration—enhances comparably to active use, highlighting the role of cognitive anticipation in endogenous release. Furthermore, it has been used to probe hypnotizability's influence on diffuse noxious inhibitory controls, showing greater pain inhibition in highly hypnotizable individuals during conditioning stimuli. Integration with neuroimaging techniques, particularly (fMRI), allows the CPT to map real-time brain activation patterns associated with and stress processing. During immersion, it elicits robust blood-oxygen-level-dependent (BOLD) signals in the insula and (ACC), regions central to affective evaluation, with increased activation correlating to perceived intensity. Distraction tasks combined with CPT reduce ACC activation, demonstrating top-down modulation of networks, while brainstem regions like the show heightened responses to cold stress in ultra-high field imaging. These findings have advanced understanding of neural circuits in acute , often contrasting responses in healthy versus clinical populations. Studies on individual differences utilize the CPT to explore variations in pain and stress reactivity influenced by biological and experiential factors. Sex differences are prominent, with females exhibiting lower thresholds and shorter tolerance times at standardized water temperatures (e.g., 5°C), attributed to estrogen-modulated . Genetic factors, such as polymorphisms in stress-related genes, interact with environmental influences like use to alter responsiveness in group-based SECPT protocols. research reveals that repeated CPT sessions lead to diminished autonomic and subjective responses over time, varying by individual baseline resilience, which informs models of sensitization in chronic conditions.

Limitations and Variations

Potential risks and contraindications

The cold pressor test (CPT) carries several short-term risks, primarily related to prolonged exposure to cold water, which can lead to or if immersion exceeds the recommended 3-minute limit. These risks arise from rapid and heat loss in the immersed limb, potentially impairing local circulation and tissue integrity, though such complications are uncommon when protocols are followed. Additionally, the test induces sympathetic activation, elevating and , which may impose rare cardiac strain in vulnerable individuals, including transient arrhythmias or increased myocardial oxygen demand leading to ischemia in those with . Serious adverse events are rare, with no long-term physical or psychological effects reported in large cohorts. Contraindications for the CPT include Raynaud's disease, open wounds or fractures on the hand, uncontrolled , and , as these conditions heighten the risk of exacerbated , , or reactions. Caution is advised for elderly individuals due to impaired and circulation, children owing to potential for heightened distress or vasovagal responses, and pregnant persons because of possible autonomic and exclusion in safety protocols. Individuals with a history of cardiovascular disorders, fainting, seizures, or cold should also be excluded to prevent adverse outcomes. Adverse events from the CPT are generally mild and infrequent, including nausea, dizziness, or panic-like responses triggered by pain and stress, with vasovagal reactions occurring in approximately 1.6% of cases, though severe incidents are rare. To mitigate these, monitoring protocols involve continuous observation by trained personnel, limiting immersion to 3 minutes maximum, and immediate post-test warming of the hand with dry towels or warm water to restore circulation and prevent prolonged discomfort. Ethical considerations emphasize obtaining that clearly describes the anticipated discomfort and , allowing participants voluntary withdrawal at any time, in line with (IRB) guidelines for research involving experimental induction. This ensures the test's benefits in clinical or research contexts outweigh potential harms.

Modifications and alternatives

One modification to the standard cold pressor test involves immersing both feet in ice water instead of a single hand, which addresses potential biases from upper limb laterality effects and allows hands to remain free for concurrent measurements or tasks. This bilateral foot immersion variant follows a similar protocol, with feet submerged up to the ankles in 2–3°C water for up to 3 minutes, though participants may withdraw early if tolerance is exceeded, and it elicits comparable or enhanced hemodynamic and neuroendocrine responses compared to hand immersion. Temperature adjustments are commonly applied for sensitive populations to improve tolerability and safety. For instance, warmer at 10°C is recommended in pediatric studies to minimize distress while still activating cold receptors, contrasting with the typical 0–5°C used in adults. Shorter immersion durations, such as 30 seconds to 1 minute, are also employed in children to reduce excessive discomfort and enhance feasibility, often within fixed-time paradigms that prioritize intensity ratings over full tolerance assessment. Alternatives to the cold pressor test include quantitative sensory testing (QST), which uses precise cold stimuli like thermodes or cooled metal probes to determine detection and thresholds with greater control and standardization than full limb immersion. QST protocols typically apply brief (3-second) contacts at temperatures from 0–50°C, averaging multiple trials to quantify A-delta and C-fiber responses, making it suitable for detailed profiling where the cold pressor test's variability may limit precision. For assessing non-physical stressors, the (TSST) serves as a alternative, involving and arithmetic tasks under evaluation to induce and cardiovascular responses without , though it requires more setup time. A hybrid option, the socially evaluated cold pressor test (SECPT), adds observational elements to hand immersion for amplified but retains some physical components. Technological enhancements include automated immersion devices that maintain consistent water flow and temperature (2–4°C) during foot protocols, reducing experimenter variability and enabling precise timing for repeated trials. Integration with wearable sensors, such as photoplethysmography (PPG), impedance plethysmography (IPG), and (ECG) devices, facilitates real-time cardiovascular monitoring during the test, with IPG showing superior accuracy for estimation even under cold-induced motion artifacts, supporting remote or applications. These adaptations are particularly useful in addressing risks like excessive by allowing closer physiological oversight.

References

  1. https://www.sciencedirect.com/topics/medicine-and-dentistry/cold-pressor-test
  2. https://link.springer.com/article/10.1007/s10286-021-00796-4
  3. https://www.jpain.org/article/S1526-5900(05)00366-4/fulltext
  4. https://www.vumc.org/autonomic-dysfunction-center/cold-pressor-test
  5. https://www.ahajournals.org/doi/10.1161/01.hyp.25.1.71
  6. https://www.sciencedirect.com/science/article/pii/S0031938423002792
  7. https://pubmed.ncbi.nlm.nih.gov/2807514/
  8. https://pubmed.ncbi.nlm.nih.gov/16694857/
  9. https://onlinelibrary.wiley.com/doi/10.1111/j.1469-8986.1975.tb01289.x
  10. https://www.frontiersin.org/journals/pain-research/articles/10.3389/fpain.2024.1421709/full
  11. https://xmed.jmir.org/2025/1/e69472
  12. https://pubmed.ncbi.nlm.nih.gov/33712946/
  13. https://pmc.ncbi.nlm.nih.gov/articles/PMC8130774/
  14. https://pmc.ncbi.nlm.nih.gov/articles/PMC6339552/
  15. https://iastate.pressbooks.pub/curehumanphysiology/chapter/body-temperature-homeostasis/
  16. https://www.frontiersin.org/journals/physiology/articles/10.3389/fphys.2018.01863/full
  17. https://pmc.ncbi.nlm.nih.gov/articles/PMC9216420/
  18. https://pubmed.ncbi.nlm.nih.gov/16516820/
  19. https://pmc.ncbi.nlm.nih.gov/articles/PMC3588603/
  20. https://www.sciencedirect.com/science/article/abs/pii/S0022510X02000291
  21. https://www.sciencedirect.com/science/article/pii/S1526590009008098
  22. https://pubmed.ncbi.nlm.nih.gov/38284423/
  23. https://physoc.onlinelibrary.wiley.com/doi/10.14814/phy2.13985
  24. https://www.ahajournals.org/doi/pdf/10.1161/01.HYP.9.5.429
  25. https://pubmed.ncbi.nlm.nih.gov/19943060/
  26. https://journals.physiology.org/doi/full/10.1152/advan.00096.2015
  27. https://www.ahajournals.org/doi/10.1161/circulationaha.112.093245
  28. https://clinicaltrials.gov/study/NCT03083626
  29. https://journals.lww.com/mtmj/fulltext/2023/22010/blood_pressure_and_heart_rate_recovery_in_cold.26.aspx
  30. https://www.ahajournals.org/doi/pdf/10.1161/01.HYP.14.5.524
  31. https://www.ahajournals.org/doi/pdf/10.1161/01.hyp.6.3.301
  32. https://www.sciencedirect.com/science/article/pii/S0002914999804111
  33. https://www.atherosclerosis-journal.com/article/S0021-9150%2804%2900026-7/abstract
  34. https://www.medrxiv.org/content/10.1101/2025.03.10.25323710v1.full.pdf
  35. https://qims.amegroups.org/article/view/140137/html
  36. https://www.sciencedirect.com/science/article/abs/pii/S0165178100002237
  37. https://bmcneurol.biomedcentral.com/articles/10.1186/s12883-018-1043-2
  38. https://link.springer.com/article/10.1023/A:1018722002393
  39. https://pubmed.ncbi.nlm.nih.gov/11959161/
  40. https://journal.chestnet.org/article/S0012-3692%2816%2935233-3/fulltext
  41. https://pubmed.ncbi.nlm.nih.gov/6695950/
  42. https://www.sciencedirect.com/science/article/pii/S1526590005003664
  43. https://pmc.ncbi.nlm.nih.gov/articles/PMC4843861/
  44. https://pmc.ncbi.nlm.nih.gov/articles/PMC6204981/
  45. https://www.ajconline.org/article/S0002-9149(10)02119-3/fulltext
  46. https://www.tandfonline.com/doi/full/10.3109/10253890.2015.1053452
  47. https://www.sciencedirect.com/science/article/abs/pii/S0167876017303495
  48. https://www.sciencedirect.com/science/article/pii/S152659001200702X
  49. https://www.physio-pedia.com/Quantitative_Sensory_Testing_%28QST%29
  50. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8915716/
  51. https://pmc.ncbi.nlm.nih.gov/articles/PMC5314443/
  52. https://irispublishers.com/ojrat/fulltext/wearables-cardiovascular-monitoring-effects-of-cold-pressor-test-on-heart-rates-estimated-from-eCG-pPG-and-iPG-signals.ID.000541.php
Add your contribution
Related Hubs
User Avatar
No comments yet.