Effects of pain and arousal on the control of breathing

Ward, Denham S.; Karan, Suzanne

doi:10.1007/s005400200028

Cited by 12 publications

(7 citation statements)

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“…Pain has a clear influence on ventilation (Ward & Karan, 2002), with the activation of cutaneous nociceptors resulting in hyperventilation and a ß2 mmHg decrease in P ET,CO 2 (Sarton et al 1997). Likewise, higher sensations of pain associated with dehydration in the present study induced a 2 mmHg reduction in P ET,CO 2 (Fig.…”

Section: Discussionsupporting

confidence: 65%

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Mild dehydration modifies the cerebrovascular response to the cold pressor test

Perry

Bear

Lucas

et al. 2015

Experimental Physiology

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New Findings r What is the central question of this study?The cold pressor test (CPT) is commonly used to investigate cerebrovascular regulation. Despite blood viscosity per se being able to modulate cerebral blood flow, it is unknown whether hydration status alters this response, nor is it commonly reported. We investigated the effects of mild dehydration on the cerebrovascular response to the CPT. r What is the main finding and its importance?The main finding from this study is that when compared with euhydration, mild dehydration reduced cerebral blood flow via a decrease in the partial pressure of end-tidal CO 2 . This demonstrates that hydration status is an important modulator of the cerebrovascular response to the CPT and should be reported and controlled for.The cold pressor test (CPT) is widely used in clinical practice and physiological research. It is characterized by a robust autonomic response, with associated increases in heart rate (HR), mean arterial pressure (MAP) and mean middle cerebral artery blood flow velocity (MCAv mean ). Hydration status is not commonly reported when conducting this test, yet blood viscosity alone can modulate MCAv mean , potentially modifying the MCAv mean response to the CPT. We investigated the effect of mild dehydration on the physiological response to the CPT in 10 healthy men (mean ± SD: age 28 ± 5 years; body mass 83 ± 5 kg). All participants completed two CPTs, cold water (0°C) immersion of both feet for 90 s, with the order of the euhydration and dehydration trials counterbalanced. Beat-to-beat MCAv, MAP, HR and breath-by-breath partial pressure of end-tidal CO 2 (P ET,CO 2 ) were measured continuously. Participants' pain perception was measured 1 min into the CPT using a visual analog scale (no pain = 0; maximal pain = 10). Dehydration significantly elevated plasma osmolality and urine specific gravity and reduced body mass (all P < 0.01). The MAP and HR responses were not different between treatments (both P > 0.05). After 90 s of immersion, the change in MCAv mean from baseline was less in the dehydration compared with the euhydration trial (change 0 ± 5 versus 7 ± 7 cm s −1 , P = 0.01), as was P ET,CO 2 (change −3 ± 2 versus 0 ± 3 mmHg, P = 0.02). Dehydration was associated with greater relative pain sensation during the CPT (7.0 ± 1.3 vs 5.8 ± 1.8, P = 0.02). Our results demonstrate that mild dehydration can modify the cerebrovascular response to the CPT, with dehydration increasing perceived pain, lowering P ET,CO 2 and, ultimately, blunting the MCAv mean response.

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Section: Discussionsupporting

confidence: 65%

“…Pain has a clear influence on ventilation (Ward & Karan, ), with the activation of cutaneous nociceptors resulting in hyperventilation and a ∼2 mmHg decrease in

P_{ET, C O_{2}}

(Sarton et al . ).…”

Section: Discussionmentioning

confidence: 99%

Mild dehydration modifies the cerebrovascular response to the cold pressor test

Perry

Bear

Lucas

et al. 2015

Experimental Physiology

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“…Few reports exist for models of combined effects of propofol with remifentanil on respiratory depression, despite the frequency with which agents are combined in anesthesia, and those that do are based on data derived from healthy volunteers (Nieuwenhuijs et al, 2003;Olofsen et al, 2010). Respiratory control is determined by multiple processes, in which intrinsic feedback is provided by arterial pH levels and concentrations of O 2 and CO 2 (Lloyd et al, 1958;Dahan et al, 1990;Ward and Karan, 2002). Feedback mechanisms regulate respiratory drive, which changes the alveolar minute ventilation.…”

Section: Introductionmentioning

confidence: 99%

“…Modulation of the respiratory system occurs via several physiologic processes (Lloyd et al, 1958;Dahan et al, 1990;Ward and Karan, 2002). This makes estimation of model parameters difficult, even in controlled conditions and ventilation studies.…”

mentioning

confidence: 99%

Modeling Respiratory Depression Induced by Remifentanil and Propofol during Sedation and Analgesia Using a Continuous Noninvasive Measurement of pCO2

Hannam

Borrat

Trocóniz

et al. 2015

Journal of Pharmacology and Experimental Therapeutics

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Respiratory depression is a common adverse effect of propofol and remifentanil. We aimed to develop a model for respiratory depressant effects of propofol with remifentanil in patients undergoing endoscopy with sedation. Data were available for 136 patients undergoing endoscopy with sedation. Participants randomly received infusions of propofol and remifentanil. Predicted plasma concentrations, outputted by infusion pumps, were available. Transcutaneous arterial pressure of carbon dioxide (pCO 2 ) was measured. Data were analyzed using nonlinear mixed-effects modeling methods. Covariate relationships were investigated for age, noxious stimuli (endoscopy tube insertion), and A118G genotype for the m-opioid receptor (OPRM1). Participants had a median ( An indirect-effect model with a "modulator" compartment best described pCO 2 data (P , 0.001) over a direct-effect model. Remifentanil inhibited pCO 2 removal with an IC 50 of 1.13 ng/ml and first-order rate constant (k e0 ) of 0.28 minute 21. Propofol affected the modulator compartment with an IC 50 of 4.97 mg/ml (no effect-site compartment). Propofol IC 50 and remifentanil k e0 were reduced with increasing age. Noxious stimuli and genotype were not significant covariates. An indirect-effect model with a rebound mechanism can describe remifentanil-and propofolinduced changes in pCO 2 in patients undergoing noxious procedures. The model may be useful for identifying optimal dosing schedules for these drugs in a combination that provides adequate sedation but avoids respiratory depression.

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“…Possible influences of ischemic pain on the postexercise pressor response were recognized in the classic study by Alam and Smirk (1937) but were dismissed per the subjects’ characterization of the occlusion-provoked sensation as “tiredness or heaviness” and not discomfort or pain, an argument that has since been invoked by many authors. However, activation of nociceptive pathways could stimulate breathing without involving arousal of higher centers (Ward and Karan, 2002). Similarly, activation of skeletal muscle ASIC receptor-mediated nociceptive pathways has been shown to contribute to the pressor reflex during regional circulatory occlusion after muscle contraction in decerebrated cats, without the animals’ conscious perception of pain (McCord et al, 2009).…”

mentioning

confidence: 99%

Mechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading

Poon

Tin

2013

Respiratory Physiology & Neurobiology

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Patients with chronic heart failure (CHF) suffer increased alveolar VD/VT (dead-space-to-tidal-volume ratio), yet they demonstrate augmented pulmonary ventilation such that arterial PCO2 (PaCO2) remains remarkably normal from rest to moderate exercise. This paradoxical effect suggests that the control law governing exercise hyperpnea is not merely determined by metabolic CO2 production (V̇CO2) per se but is responsive to an apparent (real-feel) metabolic CO2 load false(V˙normalCO2ofalse) that also incorporates the adverse effect of physiological VD/VT on pulmonary CO2 elimination. By contrast, healthy individuals subjected to dead space loading also experience augmented ventilation at rest and during exercise as with increased alveolar VD/VT in CHF, but the resultant response is hypercapnic instead of eucapnic, as with CO2 breathing. The ventilatory effects of dead space loading are therefore similar to those of increased alveolar VD/VT and CO2 breathing combined. These observations are consistent with the hypothesis that the increased series VD/VT in dead space loading adds to V˙normalCO2o as with increased alveolar VD/VT in CHF, but this is through rebreathing of CO2 in dead space gas thus creating a virtual (illusory) airway CO2 load within each inspiration, as opposed to a true airway CO2 load during CO2 breathing that clogs the mechanism for CO2 elimination through pulmonary ventilation. Thus, the chemosensing mechanism at the respiratory controller may be responsive to putative drive signals mediated by within-breath PaCO2 oscillations independent of breath-to-breath fluctuations of the mean PaCO2 level. Skeletal muscle afferents feedback, while important for early-phase exercise cardioventilatory dynamics, appears inconsequential for late-phase exercise hyperpnea.

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Effects of pain and arousal on the control of breathing

Cited by 12 publications

References 57 publications

Mild dehydration modifies the cerebrovascular response to the cold pressor test

Mild dehydration modifies the cerebrovascular response to the cold pressor test

Modeling Respiratory Depression Induced by Remifentanil and Propofol during Sedation and Analgesia Using a Continuous Noninvasive Measurement of pCO2

Mechanism of augmented exercise hyperpnea in chronic heart failure and dead space loading

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