Capnometric feedback training decreases 24-h blood pressure in hypertensive postmenopausal women.

BACKGROUND: High normal resting pCO2 is a risk factor for salt sensitivity of blood pressure (BP) in normotensive humans and has been associated with higher resting systolic BP in postmenopausal women. To date, however, no known studies have investigated the effects of regular practice of voluntary mild hypocapnic breathing on BP in hypertensive patients. The objective of the present research was to test the hypothesis that capnometric feedback training can decrease both resting pCO2 and 24-h BP in a series of mildly hypertensive postmenopausal women. METHODS: A small portable end tidal CO2 (etCO2) monitor was constructed and equipped with software that determined the difference between the momentary etCO2 and a pre-programmed criterion range. The monitor enabled auditory feedback for variations in CO2 outside the criterion range. 16 mildly hypertensive postmenopausal women were individually trained to sustain small decreases in etCO2 during six weekly sessions in the clinic and daily sessions at home. 24-h BP monitoring was conducted before and after the intervention, and in 16 prehypertensive postmenopausal women in a control group who did not engage in the capnometric training. RESULTS: Following the intervention, all 16 capnometric training participants showed decreases in resting etCO2 (- 4.3 ± 0.4 mmHg; p < .01) while 15 showed decreases in 24-h systolic BP (- 7.6 ± 2.0 mmHg; p < .01). No significant changes in either measure was observed in the control group. In addition, nighttime (- 9.5 ± 2.6; p < .01) and daytime (- 6.7 ± 0.2 mmHg) systolic BP were both decreased following capnometric training, while no significant changes in nighttime (- 2.8 ± 2.2 mmHg; p = .11) or daytime (- 0.7 ± 1.0 mmHg; p ≤ .247) systolic BP were observed in the control group. CONCLUSIONS: These findings support the hypothesis that regular practice of mild hypocapnic breathing that decreases resting etCO2 reliably decreases 24-h blood pressure in hypertensive postmenopausal women. The extent to which these effects persist beyond the training period or can be observed in other hypertensive subgroups remains to be investigated.

Derangement of PaCO2 requires physician attention in acute carbon monoxide poisoning.

The objective was to describe the prevalence of derangement of the partial pressure of arterial carbon dioxide (PaCO2) and to determine the association between PaCO2 and adverse cardiovascular events (ACVEs) in carbon monoxide (CO)-poisoned patients. Additionally, we evaluated whether the derangement of PaCO2 was simply secondary to metabolic changes. This retrospective study included 194 self-breathing patients after CO poisoning with an indication for hyperbaric oxygen therapy and available arterial blood gas analysis at presentation and 6 h later. The incidence rate of hypocapnia at presentation after acute CO poisoning was 67.5%, and the mean PaCO2 during the first 6 h was 33 (31-36.7) mmHg. The most common acid-base imbalance in 131 patients with hypocapnia was primary respiratory alkalosis. The incidence rate of ACVEs during hospitalization was 50.5%. A significant linear trend in the incidence of ACVEs was observed across the total range of PaCO2 variables. In multivariate regression analysis, mean PaCO2 was independently associated with ACVEs (odds ratio 0.051; 95% confidence interval 0.004-0.632). PaCO2 derangements were common after acute CO poisoning and were not explainable as a mere secondary response to metabolic changes. The mean PaCO2 during the first 6 h was associated with ACVEs. Given the high incidence of ACVEs and PaCO2 derangement and the observed association between the mean PaCO2 and ACVEs, this study suggests that (1) PaCO2 should be monitored in the acute stage to predict and/or prevent ACVEs and (2) further investigation is needed to validate this result and explore the early manipulation of PaCO2 as a treatment strategy.

Effects of acupuncture at GB20 on CO2 reactivity in the basilar and middle cerebral arteries during hypocapnia in healthy participants.

OBJECTIVES: The acupoint GB20 is known to affect vertebrobasilar blood flow regulation. However, no previous study has used transcranial Doppler imaging to examine whether acupuncture at GB20 has a selective effect on blood flow in various cerebral arteries, such as the basilar artery (BA) and the middle cerebral arteries (MCAs). Therefore, this study sought to determine the specific effects of GB20 acupuncture on cerebral blood flow (CBF). MATERIALS AND METHODS: Blood flow velocity and CO(2) reactivity were measured by transcranial Doppler imaging with a 2-MHz pulsed Doppler probe observed through both temporal windows for the MCAs and through the suboccipital window for the BA before and after GB20 acupuncture treatment in 15 healthy young male volunteers. The changes in hyperventilation-induced CO(2) reactivity and corrected blood flow velocities at 40 mmHg (CV40) were assessed for the BA and both MCAs. Blood pressure and heart rate were measured before and after the acupuncture treatment. RESULTS: CO(2) reactivity in the BA increased significantly after GB20 acupuncture treatment compared with baseline (p=0.041). In contrast, CO(2) reactivity in both MCAs remained unchanged. The CV40 in the BA and the MCAs showed no change after the GB20 acupuncture treatment. The mean heart rate decreased significantly after the GB20 acupuncture, whereas the mean blood pressure showed no change. CONCLUSIONS: This study demonstrated that acupuncture treatment on GB20 increases CO(2) reactivity specifically in the BA, with no effect in the MCAs. These results clinically support the use of GB20 to treat disorders of posterior cerebral circulation and support the idea that particular acupoints affect specific brain regions and cerebral arteries.

Targeting pCO(2) in asthma: pilot evaluation of a capnometry-assisted breathing training.

OBJECTIVES: This pilot study aimed to evaluate the feasibility and potential benefits of a novel biofeedback breathing training for achieving sustained increases in pCO(2) levels. METHODS: Twelve asthma patients were randomly assigned to an immediate 4-week treatment group or waiting list control. Patients were instructed to modify their respiration in order to change levels of end-tidal pCO(2) using a hand-held capnometer. Treatment outcome was assessed in frequency and distress of symptoms, asthma control, lung function, and variability of peak expiratory flow (PEF). RESULTS: We found stable increases in pCO(2) and reductions in respiration rate during treatment and 2-month follow-up. Mean pCO(2) levels rose from a hypocapnic to a normocapnic range at follow-up. Frequency and distress of symptoms was reduced and reported asthma control increased. In addition, mean PEF variability decreased significantly in the treatment group. CONCLUSIONS: Our pilot intervention provided evidence for the feasibility of pCO(2)-biofeedback training in asthma patients.

Cerebral artery blood velocity in normal subjects during acute decreases in barometric pressure.

To investigate the effect of acute changes in barometric pressure on regional cerebral perfusion we studied the middle cerebral artery (MCA) blood velocity in five healthy male volunteers by means of a low-pressure chamber. The MCA blood velocity, arterial blood and respiratory gases were measured at the barometric pressures of 1, 0.8, 0.65, and 0.5 atmospheres. The observed blood velocity (Vo) showed no systematic changes. Decreases in barometric pressure induced hypoxia and hypocapnia. When normalizing the MCA blood velocity (Vn) to a standard P(CO2) (5.3 kPa), thereby correcting for the hypoxic induced hypocapnia, we obtained an inverse relationship between cerebral artery blood velocity and arterial blood oxygen content (CaO2). The oxygen supply to the brain, estimated as the product of Vo and CaO2, decreased with lowering of the barometric pressure. However, the product of Vn and CaO2 remained constant. This suggests the existence of a regulatory mechanism attempting to maintain a constant oxygen supply to the brain during acute changes in CaO2, if the hyperventilation induced decrease in PCO2 can be omitted. In the artificial situation of a low pressure chamber, our findings are quite similar to those obtained at sea level. This indicates that the underlying mechanisms of control of cerebral blood flow do not change during acute exposure to altitude.