The independent effects of hydrostatic pressure and hypercapnic breathing during water immersion on ventilatory sensitivity and cerebrovascular reactivity.

Head out water immersion (HOWI) induces ventilatory and hemodynamic changes, which may be a result of hydrostatic pressure, augmented arterial CO2 tension, or a combination of both. We hypothesized that the hydrostatic pressure and elevated CO2 tension that occur during HOWI will contribute to an augmented ventilatory sensitivity to CO2 and an attenuated cerebrovascular reactivity to CO2 during water immersion. Twelve subjects (age: 24±3 y, BMI: 25±3 kg/m2) completed HOWI, waist water immersion with CO2 (WWI+CO2), and WWI where a rebreathing test was conducted at baseline, 10, 30, and 60 minutes, and post. PETCO2, minute ventilation, expired gases, blood pressure, heart rate, and middle cerebral artery blood velocity were recorded continuously. PETCO2 increased throughout all visits (p£0.011), was matched during HOWI and WWI+CO2 (p³0.264), and was greater during WWI+CO2 vs. WWI at 10, 30, and 60 minutes (p<0.001). When HOWI vs. WWI+CO2 were compared, the change in ventilatory sensitivity to CO2 was different at 10 (0.59±0.34 vs. 0.06±0.23 L/min/mmHg, p<0.001), 30 (0.58±0.46 vs. 0.15±0.25 L/min/mmHg, p<0.001), and 60 minutes (0.63±0.45 vs. 0.16±0.34 L/min/mmHg, p<0.001), while there were no differences between conditions for cerebrovascular reactivity to CO2 (p³0.163). When WWI+CO2 vs. WWI were compared, ventilatory sensitivity to CO2 was not different between conditions (p³0.642), while the change in cerebrovascular reactivity to CO2 was different at 30 minutes (-0.56±0.38 vs. -0.30±0.25 cm/s/mmHg, p=0.010). These data indicate that during HOWI ventilatory sensitivity to CO2 increases due to the hydrostatic pressure, while cerebrovascular reactivity to CO2 decreases due to the combined effects of immersion.

Carotid body chemosensitivity is not attenuated during cold water diving.

Tonic carotid body (CB) activity is reduced during exposure to cold and hyperoxia. We tested the hypotheses that cold water diving lowers CB chemosensitivity and augments CO2 retention more than thermoneutral diving. Thirteen subjects [age: 26 ± 4 yr; body mass index (BMI): 26 ± 2 kg/m2) completed two 4-h head-out water immersion protocols in a hyperbaric chamber (1.6 ATA) in cold (15°C) and thermoneutral (25°C) water. CB chemosensitivity was assessed with brief hypercapnic ventilatory response ([Formula: see text]) and hypoxic ventilatory response ([Formula: see text]) tests before dive, 80 and 160 min into the dive (D80 and D160, respectively), and immediately after and 60 min after dive. Data are reported as an absolute mean (SD) change from predive. End-tidal CO2 pressure increased during both the thermoneutral water dive [D160: +2 (3) mmHg; P = 0.02] and the cold water dive [D160: +1 (2) mmHg; P = 0.03]. Ventilation increased during the cold water dive [D80: 4.13 (4.38) and D160: 7.75 (5.23) L·min-1; both P < 0.01] and was greater than the thermoneutral water dive at both time points (both P < 0.01). [Formula: see text] was unchanged during the dive (P = 0.24) and was not different between conditions (P = 0.23). [Formula: see text] decreased during the thermoneutral water dive [D80: -3.45 (3.61) and D160: -2.76 (4.04) L·min·mmHg-1; P < 0.01 and P = 0.03, respectively] but not the cold water dive. However, [Formula: see text] was not different between conditions (P = 0.17). In conclusion, CB chemosensitivity was not attenuated during the cold stress diving condition and does not appear to contribute to changes in ventilation or CO2 retention.

Carotid body chemosensitivity at 1.6 ATA breathing air versus 100% oxygen.

Hyperoxia reduces the ventilatory response to hypercapnia by suppressing carotid body (CB) activation. This effect may contribute to CO2 retention during underwater diving due to the high arterial O2 content associated with hyperbaria. We tested the hypothesis that CB chemosensitivity to hypercapnia and hypoxia is attenuated during hyperbaria. Ten subjects completed two, 4-h dry dives at 1.6 atmosphere absolute (ATA) breathing either 21% O2 (Air) or 100% O2 (100% O2). CB chemosensitivity was assessed using brief hypercapnic ventilatory response ([Formula: see text]) and hypoxic ventilatory response ([Formula: see text]) tests predive, 75 and 155 min into the dives, and 15 and 55 min postdive. End-tidal CO2 pressure increased during the dive at 75 and 155 min [Air: +9 (SD 4) mmHg and +8 (SD 4) mmHg versus 100% O2: +6 (SD 4) mmHg and +5 (SD 3) mmHg; all P < 0.01] and was higher while breathing Air (P < 0.01). [Formula: see text] was unchanged during the dive (P = 0.73) and was not different between conditions (P = 0.47). However, [Formula: see text] was attenuated from predive during the dive at 155 min breathing Air [-0.035 (SD 0.037) L·min·mmHg-1; P = 0.02] and at both time points while breathing 100% O2 [-0.035 (SD 0.052) L·min·mmHg-1 and -0.034 (SD 0.064) L·min·mmHg-1; P = 0.02 and P = 0.02, respectively]. These data indicate that the CB chemoreceptors do not appear to contribute to CO2 retention in hyperbaria.NEW & NOTEWORTHY We demonstrate that carotid body chemosensitivity to brief exposures of hypercapnia was unchanged during a 4-h dive in a dry hyperbaric chamber at 1.6 ATA regardless of breathing gas condition [i.e., air (21% O2) versus 100% oxygen]. Therefore, it appears that an attenuation of carotid body chemosensitivity to hypercapnia does not contribute to CO2 retention in hyperbaria.

Mask fatigue.

Extended wearing of mask, which has become a part of routine life, has led to the emergence of 'mask fatigue'. Mask fatigue is defined as the lack of energy that accompanies, and/or follows prolonged wearing of a mask. This communication describes the various aspects of mask fatigue, and shares pragmatic tips on its reduction. This discussion is relevant to all health care professionals and to general public to some extent, in the present scenario.

Secondary Response to Chronic Respiratory Acidosis in Humans: A Prospective Study.

INTRODUCTION: The magnitude of the secondary response to chronic respiratory acidosis, that is, change in plasma bicarbonate concentration ([HCO3-]) per mm Hg change in arterial carbon dioxide tension (PaCO2), remains uncertain. Retrospective observations yielded Δ[HCO3-]/ΔPaCO2 slopes of 0.35 to 0.51 mEq/l per mm Hg, but all studies have methodologic flaws. METHODS: We studied prospectively 28 stable outpatients with steady-state chronic hypercapnia. Patients did not have other disorders and were not taking medications that could affect acid-base status. We obtained 2 measurements of arterial blood gases and plasma chemistries within a 10-day period. RESULTS: Steady-state PaCO2 ranged from 44.2 to 68.8 mm Hg. For the entire cohort, mean (± SD) steady-state plasma acid-base values were as follows: PaCO2, 52.8 ± 6.0 mm Hg; [HCO3-], 29.9 ± 3.0 mEq/l, and pH, 7.37 ± 0.02. Least-squares regression for steady-state [HCO3-] versus PaCO2 had a slope of 0.476 mEq/l per mm Hg (95% CI = 0.414-0.538, P < 0.01; r = 0.95) and that for steady-state pH versus PaCO2 had a slope of -0.0012 units per mm Hg (95% CI = -0.0021 to -0.0003, P = 0.01; r = -0.47). These data allowed estimation of the 95% prediction intervals for plasma [HCO3-] and pH at different levels of PaCO2 applicable to patients with steady-state chronic hypercapnia. CONCLUSION: In steady-state chronic hypercapnia up to 70 mm Hg, the Δ[HCO3-]/ΔPaCO2 slope equaled 0.48 mEq/l per mm Hg, sufficient to maintain systemic acidity between the mid-normal range and mild acidemia. The estimated 95% prediction intervals enable differentiation between simple chronic respiratory acidosis and hypercapnia coexisting with additional acid-base disorders.

Peripheral chemosensitivity is not blunted during 2 h of thermoneutral head out water immersion in healthy men and women.

Carbon dioxide (CO2) retention occurs during water immersion, but it is not known if peripheral chemosensitivity is altered during water immersion, which could contribute to CO2 retention. We tested the hypothesis that peripheral chemosensitivity to hypercapnia and hypoxia is blunted during 2 h of thermoneutral head out water immersion (HOWI) in healthy young adults. Peripheral chemosensitivity was assessed by the ventilatory, heart rate, and blood pressure responses to hypercapnia and hypoxia at baseline, 10, 60, 120 min, and post HOWI and a time-control visit (control). Subjects inhaled 1 breath of 13% CO2, 21% O2, and 66% N2 to test peripheral chemosensitivity to hypercapnia and 2-6 breaths of 100% N2 to test peripheral chemosensitivity to hypoxia. Each gas was administered four separate times at each time point. Partial pressure of end-tidal CO2 (PETCO2), arterial oxygen saturation (SpO2), ventilation, heart rate, and blood pressure were recorded continuously. Ventilation was higher during HOWI versus control at post (P = 0.037). PETCO2 was higher during HOWI versus control at 10 min (46 ± 2 vs. 44 ± 2 mmHg), 60 min (46 ± 2 vs. 44 ± 2 mmHg), and 120 min (46 ± 3 vs. 43 ± 3 mmHg) (all P < 0.001). Ventilatory (P = 0.898), heart rate (P = 0.760), and blood pressure (P = 0.092) responses to hypercapnia were not different during HOWI versus control at any time point. Ventilatory (P = 0.714), heart rate (P = 0.258), and blood pressure (P = 0.051) responses to hypoxia were not different during HOWI versus control at any time point. These data indicate that CO2 retention occurs during thermoneutral HOWI despite no changes in peripheral chemosensitivity.

Transcutaneous carbon-dioxide partial pressure trends during six-minute walk test in patients with very severe COPD.

BACKGROUND: Transcutaneous carbon-dioxide partial-pressure (TCPCO2) can be reliably measured and may be of clinical relevance in COPD. Changes in TCPCO2 and exercise-induced hypercapnia (EIH) during six-minute walk test (6MWT) need further investigation. We aimed (1) to define patterns of TCPCO2 trends during 6MWT and (2) to study determinants of CO2-retention and EIH. METHODS: Sixty-two COPD patients (age: 63±8years, FEV1: 33±10%pred.) were recruited and TCPCO2 was recorded by SenTec digital-monitoring-system during 6MWT. RESULTS: Half of patients (50%) exhibited CO2-retention (TCPCO2[Δ]>4mmHg); 26% preserved and 24% reduced TCPCO2. Nineteen (31%) patients presented EIH (TCPCO2>45mmHg). EIH was associated to higher baseline-PCCO2, worse FEV1, lower inspiratory-pressures, underweight/normal BMI, and pre-walk dyspnea. Stronger determinants of CO2-retention were FEV1 and pre-walk dyspnea, whereas baseline-PCCO2 and pre-walk dyspnea better predict EIH. CONCLUSIONS: PCO2 response to 6MWT is highly heterogeneous; however, very low FEV1 and elevated baseline-PCCO2 together with pre-walk dyspnea increase the risk for CO2-retention and EIH. Overweight-BMI seems to carry a protective effect against EIH in very severe COPD.

Submissive hypercapnia: Why COPD patients are more prone to CO2 retention than heart failure patients.

Patients with late-stage chronic obstructive pulmonary disease (COPD) are prone to CO2 retention, a condition which has been often attributed to increased ventilation-perfusion mismatch particularly during oxygen therapy. However, patients with mild-to-moderate COPD or chronic heart failure (CHF) also suffer similar ventilatory inefficiency but they remain near-normocapnic at rest and during exercise with an augmented respiratory effort to compensate for the wasted dead space ventilation. In severe COPD, the augmented exercise ventilation progressively reverses as the disease advances, resulting in hypercapnia at peak exercise as ventilatory limitation due to increasing expiratory flow limitation and dynamic lung hyperinflation sets in. Submissive hypercapnia is an emerging paradigm for understanding optimal ventilatory control and cost/benefit decision-making under prohibitive respiratory chemical-mechanical constraints, where the need to maintain normocapnia gives way to the mounting need to conserve the work of breathing. In severe/very severe COPD, submissive hypercapnia epitomizes the respiratory controller's 'can't breathe, so won't breathe' say-uncle policy when faced with insurmountable ventilatory limitation. Even in health, submissive hypercapnia ensues during CO2 breathing/rebreathing when the inhaled CO2 renders normocapnia difficult to restore even with maximal respiratory effort, hence the respiratory controller's 'ain't fresh, so won't breathe' modus operandi. This 'wisdom of the body' with a principled decision to tolerate hypercapnia when faced with prohibitive ventilatory or gas exchange limitations rather than striving for untenable normocapnia at all costs is analogous to the notion of permissive hypercapnia in critical care, a clinical strategy to minimize the risks of ventilator-induced lung injury in patients receiving mechanical ventilation.

Respiratory determinants of diurnal hypercapnia in obesity hypoventilation syndrome. What does weight have to do with it?

RATIONALE: Among morbidly obese individuals, obstructive sleep apnea (OSA) is highly prevalent, with up to 20% suffering from hypoventilation syndrome. An increased diurnal PaCO2, the signature of obesity hypoventilation syndrome (OHS), implies diminished global ventilation, hence the term hypoventilation. OBJECTIVES: We hypothesized that hypercapnic patients with OSA have lower Ve than eucapnic patients with OSA. METHODS: In this prospective study we recorded respiratory variables to determine the pathophysiological mechanisms of steady-state diurnal hypercapnia of 12 consecutive hypercapnic and 20 consecutive eucapnic patients with OSA, matched for apnea-hypopnea index. Patients with any known causes of hypercapnia were not included. MEASUREMENTS AND MAIN RESULTS: Comparing hypercapnic to eucapnic patients, the mean value (±SD) for PaCO2 (52 ± 5 vs. 40 ± 3 mm Hg) was significantly higher, and the mean PaO2 (59 ± 8 vs. 75 ± 10 mm Hg) was significantly lower, in the hypercapnic patients. Surprisingly, the mean values for [Formula: see text]e (12.2 ± 3.0 vs. 11.6 ± 2.0 L/min), alveolar ventilation, breathing rate, [Formula: see text]t, and dead space did not differ significantly. However, hypercapnic patients had a significantly greater CO2 production (336 ± 79 vs. 278 ± 58 ml/min), which was the main reason for hypercapnia. When adjusted for body surface area, the mean values for CO2 production were similar between the two groups. CONCLUSIONS: These data emphasize the importance of weight loss, which could potentially reverse hypercapnic OSA to eucapnic OSA, hypothetically even in the absence of improvement in apnea-hypopnea index. In addition, reversal of hypercapnia should also improve oxygenation, both during sleep and while awake, minimizing hypoxia-induced organ dysfunction of OHS.