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PubMed1988

Clinical features and outcome in patients with acute asthma presenting with hypercapnia.

To determine the clinical features and outcome of patients with hypercapnia from acute asthma, we examined 229 (62 men, 167 women) consecutive episodes of acute asthma over a 6-yr period. Sixty-one episodes were associated with hypercapnia at presentation (PaCO2 greater than 38 mm Hg). Men more commonly presented with hypercapnia: 31 of 62 (50%) men with acute asthma had hypercapnia compared with only 30 of 167 (18%) women (p less than 0.001). Patients with hypercapnia had a longer duration of chronic asthma and were more likely to be steroid-dependent. Hypercapnic patients had greater airway obstruction, respiratory rate, and pulsus paradoxus than did nonhypercapnic patients. Findings of a quiet chest on auscultation, inability to talk, and cyanosis also suggested the presence of hypercapnia. Five hypercapnic patients required mechanical ventilation, but hypercapnia did not prolong hospitalization. In nonventilated patients, hypercapnia resolved in a mean time of 5.9 h; 50% of hypercapnic episodes resolved by 4 h, and all resolved by 16 h. No patient presenting with normocapnia progressed to hypercapnia with therapy, and there were no deaths in either the hypercapnic group or the nonhypercapnic group. In patients with more than one admission, the PaCO2 of one episode correlated with the PaCO2 on a subsequent admission, suggesting a role for individual variation in ventilatory control. With appropriate medical therapy, most patients with hypercapnia from acute asthma have rapid reversibility, and mechanical ventilation usually can be avoided. However, these patients require close inhospital observation until it is certain that the acute asthmatic episode has resolved.

Acute Disease↗

PubMed1995

Cardiopulmonary effects of hypercapnia during controlled intermittent positive pressure ventilation in the horse.

The cardiopulmonary effects of eucapnia (arterial CO2 tension [PaCO2] 40.4 +/- 2.9 mm Hg, mean +/- SD), mild hypercapnia (PaCO2, 59.1 +/- 3.5 mm Hg), moderate hypercapnia (PaCO2, 82.6 +/- 4.9 mm Hg), and severe hypercapnia (PaCO2, 110.3 +/- 12.2 mm Hg) were studied in 8 horses during isoflurane anesthesia with volume controlled intermittent positive pressure ventilation (IPPV) and neuromuscular blockade. The sequence of changes in PaCO2 was randomized. Mild hypercapnia produced bradycardia resulting in a significant (P < 0.05) decrease in cardiac index (CI) and oxygen delivery (DO2), while hemoglobin concentration (Hb), the hematocrit (Hct), systolic blood pressure (SBP), mean blood pressure (MBP), systemic vascular resistance (SVR), and venous admixture (QS/QT) increased significantly. Moderate hypercapnia resulted in a significant rise in CI, stroke index (SI), SBP, MBP, mean pulmonary artery pressure (PAP), Hct, Hb, arterial oxygen content (CaO2), mixed venous oxygen content (CvO2), and DO2, with heart rate (HR) staying below eucapnic levels. Severe hypercapnia resulted in a marked rise in HR, CI, SI, SBP, PAP, Hct, Hb, CaO2, CvO2, and DO2. Systemic vascular resistance was significantly decreased, while MBP levels were not different from those during moderate hypercapnia. No cardiac arrhythmias were recorded with any of the ranges of PaCO2. Norepinephrine levels increased progressively with each increase in PaCO2, whereas plasma cortisol levels remained unchanged. It was concluded that hypercapnia in isoflurane-anesthetized horses elicits a biphasic cardiopulmonary response, with mild hypercapnia producing a fall in CI and DO2 despite an increase in MBP, while moderate and severe hypercapnia produce an augmentation of the cardiopulmonary performance and DO2.

Anesthetics, Inhalation↗

PubMed2004

Effects of withdrawal of phasic lung inflation during normocapnia and hypercapnia on the swallowing reflex in humans.

PURPOSE: This study was done to test the hypothesis that hypercapnia has a direct, inhibitory effect on swallowing. METHODS: We investigated changes in the frequency and timing of repeated swallows induced by continuous infusion of water into the pharynx before, during, and after transient airway occlusion at normocapnia and hypercapnia in 12 healthy volunteers. Hypercapnia was induced by adding a dead space. Ventilation was monitored using a pneumotachograph, and swallowing was identified by submental electromyogram. RESULTS: We found that hypercapnia decreased the frequency of swallows (8.2 +/- 3.7 vs 11.4 +/- 5.3 swallows.min-1 [mean +/- SD]: hypercapnia vs normocapnia; P < 0.05), together with a loss of the preponderant coupling of swallows with expiratory phase observed at normocapnia. We also found that the withdrawal of phasic lung inflation produced by airway occlusion at end-expiration suddenly increased the swallowing frequency, both at normocapnia (from 11.4 +/- 5.3 to 16.7 +/- 3.7 swallows.min-1; P < 0.01) and at hypercapnia (from 8.2 +/- 3.7 to 22.0 +/- 6.7 swallows.min-1; P < 0.01). Although the degree of increased swallowing frequency during airway occlusion was more prominent at hypercapnia than at normocapnia ( P < 0.05), the distribution of the timing of swallows in relation to the phase of the respiratory cycle during airway occlusion at hypercapnia was similar to that during airway occlusion at normocapnia. CONCLUSION: The results of our study strongly suggest that the attenuation of the swallowing reflex during hypercapnia is not due to the direct, inhibitory effect of CO2 on the swallowing center, but, rather, is due to the increased inhibitory influence of a lung-volume-related reflex.

Adult↗

PubMed1985

Indomethacin does not potentiate renovascular constriction during hypercapnia in unanesthetized rabbits.

The role of prostanoids in regulation of the renal circulation during hypercapnia was examined in unanesthetized rabbits. Renal blood flow (RBF) was determined with 15 micron radioactive microspheres during normocapnia (PaCO2 congruent to 30 mmHg) and hypercapnia (PaCO2 congruent to 60 mmHg), before and after intravenous administration of indomethacin (10 mg/kg) or vehicle (n = 6 for each group). Arterial blood pressure was not different among the 4 conditions in each group. RBF was 438 +/- 61 and 326 +/- 69 (P less than 0.05) ml/min per 100 g during normocapnia and hypercapnia, respectively, before indomethacin, and following administration of indomethacin, RBF was 426 +/- 59 ml/min per 100 g during normocapnia and 295 +/- 60 ml/min per 100 g during hypercapnia (P less than 0.05). In the vehicle group, RBF was 409 +/- 74 and 226 +/- 45 (P less than 0.05) ml/min per 100 g during normocapnia and hypercapnia, respectively, before vehicle; and following administration of vehicle, RBF was 371 +/- 46 ml/min per 100 g during normocapnia and 219 +/- 50 (P less than 0.05) ml/min per 100 g during hypercapnia. RBF during normocapnia was not affected by administration of indomethacin or vehicle. The successive responses to hypercapnia were not different within the indomethacin and vehicle groups, and the second responses to hypercapnia were not different between the two groups. These findings suggest that prostanoids do not contribute significantly to regulation of the renal circulation during normocapnia and hypercapnia in unanesthetized rabbits.

Animals↗

PubMed1997

Permissive hypercapnia with and without expiratory washout in patients with severe acute respiratory distress syndrome.

BACKGROUND: Permissive hypercapnia is a ventilatory strategy aimed at avoiding lung volutrauma in patients with severe acute respiratory distress syndrome (ARDS). Expiratory washout (EWO) is a modality of tracheal gas insufflation that enhances carbon dioxide removal during mechanical ventilation by reducing dead space. The goal of this prospective study was to determine the efficacy of EWO in reducing the partial pressure of carbon dioxide (PaCO2) in patients with severe ARDS treated using permissive hypercapnia. METHODS: Seven critically ill patients with severe ARDS (lung injury severity score, 3.1 +/- 0.3) and no contraindications for permissive hypercapnia were studied. On the first day, hemodynamic and respiratory parameters were measured and the extent of lung hyperdensities was assessed using computed tomography. A positive end-expiratory pressure equal to the opening pressure identified on the pressure-volume curve was applied. Tidal volume was reduced until a plateau airway pressure of 25 cm H2O was reached. On the second day, after implementation of permissive hypercapnia, EWO was instituted at a flow of 15 l/min administered during the entire expiratory phase into the trachea through the proximal channel of an endotracheal tube using a ventilator equipped with a special flow generator. Cardiorespiratory parameters were studied under three conditions: permissive hypercapnia, permissive hypercapnia with EWO, and permissive hypercapnia. RESULTS: During permissive hypercapnia, EWO decreased PaCO2 from 76 +/- 4 mmHg to 53 +/- 3 mmHg (-30%; P < 0.0001), increased pH from 7.20 +/- 0.03 to 7.34 +/- 0.04 (P < 0.0001), and increased PaO2 from 205 +/- 28 to 296 +/- 38 mmHg (P < 0.05). The reduction in PaCO2 was accompanied by an increase in end-inspiratory plateau pressure from 26 +/- 1 to 32 +/- 2 cm H2O (P = 0.001). Expiratory washout also decreased cardiac index from 4.6 +/- 0.4 to 3.7 +/- 0.3 l.min-1.m-2 (P < 0.01), mean pulmonary arterial pressure from 28 +/- 2 to 25 +/- 2 mmHg (P < 0.01), and true pulmonary shunt from 47 +/- 2 to 36 +/- 3% (P < 0.01). CONCLUSIONS: Expiratory washout is an effective and easy-to-use ventilatory modality to reduce PaCO2 and increase pH during permissive hypercapnia. However, it significantly increases airway pressures and lung volume through expiratory flow limitation, reexposing some patients to a risk of lung volutrauma if the extrinsic positive end-expiratory pressure is not substantially reduced.

Acute Disease↗

PubMed1998

Acute hypercapnia increases the oxygen-carrying capacity of the blood in ventilated dogs.

OBJECTIVE: To test the hypothesis that PaCO2 levels generated during permissive hypercapnia may enhance arterial oxygenation, when ventilation is maintained. DESIGN: Prospective study. SETTING: Research laboratory in a hospital. SUBJECTS: One group of eight mongrel dogs (four male; four female). INTERVENTIONS: The dogs were anesthetized (30 mg/kg iv pentobarbital), intubated, and cannulated in one femoral artery and vein. While paralyzed with 0.1 mg/kg/hr iv vecouronium bromide, all subjects were ventilated with room air. Anesthesia was maintained, using 2 to 3 mg/kg/hr iv pentobarbital. Arterial hypercapnia at the levels generated during permissive hypercapnia was produced by stepwise increases in the dry, inspired Pco2 (PiCO2) (0, 30, 45, 60 and 75 torr [0, 4, 6, 8, and 10 kPa]; 15 mins each). MEASUREMENTS AND MAIN RESULTS: Blood gas profiles were determined at each level of hypercapnia. The minute volume was maintained at the baseline level during all exposures. Arterial hypercapnia produced gradual and significant increases in the hemoglobin concentration. These increases were approximately 6%, 7%, 11%, and 14% at PiCO2 of 30, 45, 60, and 75 torr (4, 6, 8, and 10 kPa), respectively (p < .05; repeated analysis of variance followed by Dunnett multiple comparisons test). In parallel, the oxygen content increased by approximately 6%, 7%, 11%, and 13%, respectively. During hypercapnic trials, the PaO2 remained at the normal range, whereas the dry, inspired PO2 (PiO2) was reduced from 150 to 138 torr (20 to 18.4 kPa). The average PaO2 at the highest investigated level of arterial hypercapnia was at a normal range. The hemoglobin concentration and oxygen content returned to baseline values 30 mins after hypercapnic trials. The PaCO2 and pH became normalized 15 mins after hypercapnic trials. Indirect evidence for a similar response to hypercapnia in humans is presented. CONCLUSIONS: Permissive hypercapnia due to inhaled CO2 increases oxygen-carrying capacity in dogs. The PaO2 remains at normal range even at a PiCO2 of 75 torr (10 kPa). The benefits of these effects during permissive hypercapnia, due to controlled hypoventilation, warrants investigation.

Acute Disease↗

PubMed1999

Acute graded hypercapnia increases collateral coronary blood flow in a swine model of chronic coronary artery obstruction.

OBJECTIVE: To evaluate the effect of acute hypercapnia on regional myocardial blood flow in a swine model of chronic, single-vessel coronary artery obstruction. Permissive hypercapnia is being used frequently in critical care settings. One possible detrimental effect of hypercapnia is the initiation of coronary "steal" in patients with coronary artery disease. The effects of hypercapnia on collateral coronary blood flow in the setting of coronary obstruction have not been defined. DESIGN: Prospective controlled experimental study. SETTING: Institutional animal research facility. SUBJECTS: Eight juvenile swine weighing 25-30 kg. INTERVENTIONS: Collateral coronary circulation was induced in eight piglets by banding the proximal left anterior descending coronary artery for 8-10 wks followed by total ligation. Graded hypercapnia (mean Paco2, 81 torr [10.80 kPa; Paco2 = 81 torr] and 127 torr [16.93 kPa; Paco2 = 127 torr]) was induced by increasing inspiratory carbon dioxide under isoflurane anesthesia (1 minimum alveolar concentration). MEASUREMENTS AND MAIN RESULTS: Animals were attached to instruments to measure pulmonary and systemic hemodynamics, regional myocardial blood flow, and cardiac output. Regional myocardial blood flow was determined using radiolabeled microspheres. Cardiac output, mean arterial pressure, and coronary perfusion pressure were unchanged at both levels of hypercapnia compared with baseline values. Heart rate was increased at Paco2 [HI] (p < .05). Regional blood flow was increased at both levels of hypercapnia in the collateral-dependent and normally perfused myocardium (p < .05; as high as 56% for subendocardium and as high as 106% for subepicardium at Paco2 [HI]). The intercoronary blood flow ratio remained unaltered. The transmural flow ratio was reduced at Paco2 [HI] (P < .05). During hypercapnia, regional lactate extraction remained unaltered, and regional oxygen extraction was unchanged or reduced despite the increase in oxygen consumption. CONCLUSIONS: In this swine model of chronic single-vessel coronary artery obstruction, acute hypercapnia does not induce coronary steal from collateral-dependent myocardium, but it does increase global coronary blood flow.

Animals↗

PubMed1996

Effects of hypoxia and hypercapnia on contact lens-induced corneal acidosis.

It has been assumed that contact lens wear (CLW) may induce stromal acidosis, which is a result of corneal hypoxia and the accumulation of CO2 (hypercapnia) at the tear-lens interface. However, it has not been directly shown whether hypoxia and hypercapnia are the only causes of CL-Induced corneal acidification. In this study, we provide preliminary data about the relative contributions of hypercapnia and hypoxia to CL-induced stromal acidification by monitoring pH while the cornea was exposed to a hyperbaric oxygen atmosphere. This paradigm minimized if not eliminated the pH effects of lens-induced hypoxia on all but one subject without altering the pH effect of hypercapnia. Seven subjects were fitted with hydrogel lenses; 5 with low O2 transmissibility (Dk/LO2 = 14.0 x 10(-9) (cm/s) (ml O2/[ml x mm Hg)]), and 2 with medium O2 transmissibility (Dk/LO2 = 17.2 x 10(-9) (cm/s) (ml O2/[ml x mm Hg])) lenses. After lens insertion, modified goggles were fitted to control the corneal environment by exposing 1 eye to 20%O2 and 80%N2 (air), and the contralateral eye to 80%O2 and 20%N2 (hyperbaric O2). Corneal thickness (CT) was measured before CL insertion and over 120 min of wear. We assumed that corneal hypoxia was present if CT increased during the test period. Stromal pH was measured using a slitlamp fluorophotometer before lens insertion and at 20-min intervals for a total of 80 min. After 80 min of wearing the low Dk/L lens under hyperbaric exposure, 4 of 5 subjects showed reduced pH (mean delta pH = 0.23 +/- 0.05) and no increase in CT, suggesting that only hypercapnia was contributing to acidosis. For the same lens, but with exposure to air, 4 of 5 subjects showed a larger drop in pH (mean delta pH = 0.62 +/- 0.48) compared to hyperbaric exposure and an increase in CT, indicating that both hypoxia and hypercapnia reduced pH. Subjects wearing the medium Dk/L lens showed a small but equal drop in pH under both air and hyperbaric conditions without changes in CT, suggesting that only hypercapnia was contributing to acidosis. These preliminary results suggest that both mechanisms contribute to the pH shift accompanying CLW and that the contribution of hypercapnia is approximately 30%. Finally, the effects of hypercapnia and hypoxia are dependent on individual metabolic requirements and the transmissibility of the lens to O2 and CO2.

Acidosis↗

PubMed1999

Multimodality monitoring during passive tilt and Valsalva maneuver under hypercapnia.

In occlusive cerebrovascular disease cerebral blood flow (CBF) autoregulation can be impaired and constant CBF during fluctuations in blood pressure (BP) cannot be guaranteed. Therefore, an assessment of cerebral autoregulation should consider not only responsiveness to CO2 or Diamox. Passive tilting (PT) and Valsalva maneuver (VM) are established tests for cardiovascular autoregulatory function by provoking BP changes. To develop a comprehensive test for vasomotor reactivity with a potential increase of sensitivity and specificity, the authors combined these maneuvers. Blood pressure, corrected to represent arterial pressure at the level of the circle of Willis, middle cerebral artery Doppler frequencies (DF), heart rate (HR) and endtidal partial pressure of CO2 (PtCO2) were measured continuously and noninvasively in 81 healthy subjects (19-74 years). Passive tilt and Valsalva maneuver were performed under normocapnia (mean, 39 + 4 mmHg CO2) and under hypercapnia (mean, 51 + 5 mm Hg CO2). Resting BP, HR, and DF increased significantly under hypercapnia. Under normocapnia and hypercapnia, PT induced only minor, nonsignificant changes in mean BP at the level of the circle of Willis compared to baseline (normocapnia: + 2 + 15 mm Hg; hypercapnia: -3 +/- 13 mm Hg). This corresponded with a nonsignificant decrease of the mean of DF (normocapnia: -4 +/- 11%; hypercapnia -6 +/- 12%). Orthostasis reduced pulsatility of BP by a predominantly diastolic increase of BP without significant changes in pulsatility of DF. Valsalva maneuver, with its characteristic rapid changes of BP due to elevated intrathoracic pressure, showed no significant BP differences in changes to baseline between normocapnic and hypercapnic conditions. Under both conditions the decrease in BP in phase II was accompanied by significantly increased pulsatility index ratio (PIDF/PIBP). Valsalva maneuver and PT as established tests in autonomic control of circulation provoked not only changes in time-mean of BP but also in pulsatility of BP. The significant increase in pulsatility ratio and decrease of the DF/BP ratio during normocapnia and hypercapnia indicated preserved CBF autoregulation within a wide range of CO2 partial pressures. Hypercapnia did not significantly influence the autoregulatory indices during VM and PT. Physiologically submaximally dilated cerebral arterioles can guarantee unchanged dynamics of cerebral autoregulation. Combined BP and MCA-DF assessment under hypercapnia enables investigating the effect of rapid changes of blood pressure on CO2-induced predilated cerebral arterioles. Assuming no interference of hypercapnia-induced vasodilation, VM, with its rapid, distinct changes in BP, seems especially to be adequate provocation for CBF autoregulation. This combined vasomotor reactivity might provide a more sensitive diagnostic tool to detect impaired cerebral autoregulation very early.

Adult↗

PubMed1996

Effects of hypercapnia on prostanoid and cAMP production by cerebral microvascular cell cultures.

In the newborn pig cerebral circulation, arteriolar dilation in response to hypercapnia requires the presence of intact endothelium and is accompanied by an indomethacin-sensitive increase in cortical adenosine 3',5'-cyclic monophosphate (cAMP). The effects of short-term hypercapnia on production of dilator prostanoids and cAMP were investigated using newborn pig cerebral microvascular smooth muscle cells and endothelial cells cultured both separately and in noncontact coculture. Microvascular smooth muscle cells respond to hypercapnia (pH 7.00 +/- 0.05 PCO2 75 +/- 3 mmHg) by a 1.3- to 1.7-fold increase in basal cAMP production that is not affected by indomethacin, whereas hypercapnia and 80 mM sodium propionate do not affect iloprost-stimulated cAMP production. Microvascular endothelial cells cultured on Millicel inserts respond to hypercapnia by a two- to fourfold increase in prostacyclin (as 6-keto-prostaglandin F1 alpha) and prostaglandin E2 production in both luminal and abluminal compartments. For noncontact coculture, Millicel inserts with endothelial cells (as hypercapnia-sensitive producers of prostanoids) were installed into cell culture dishes with aspirin-pretreated smooth muscle cells (as targets for endothelium-derived dilator prostanoids). Exposure of noncontact microvascular cell cocultures to hypercapnia results in a three- to fourfold stimulation of prostanoid and cAMP production. Therefore, short-term hypercapnia increases cAMP production by microvascular smooth muscle cells via 1) a direct (prostanoid independent) mechanism and 2) an endothelial-dependent pathway that involves prostanoids. Endothelium-produced prostanoid signals are necessary for a full increase in cAMP production by cerebral microvascular smooth muscle cells in response to hypercapnia.

Animals↗

PubMed1986

Protection of the blood-brain barrier by hypercapnia during acute hypertension.

The purpose of this study was to examine effects of hypercapnia on susceptibility of the blood-brain barrier to disruption during acute hypertension. Two methods were used to test the hypothesis that cerebral vasodilatation during hypercapnia increases disruption of the blood-brain barrier. First, permeability of the blood-brain barrier was measured in anesthetized cats with 125I-labeled serum albumin. Severe hypertension markedly increased permeability of the blood-brain barrier during normocapnia, but not during hypercapnia. The protective effect of hypercapnia was not dependent on sympathetic nerves. Second, in anesthetized rats, permeability of the barrier was quantitated by clearance of fluorescent dextran. Disruption of the blood-brain barrier during hypertension was decreased by hypercapnia. Because disruption of the blood-brain barrier occurred primarily in pial venules, we also measured pial venular diameter and pressure (with a servo-null method). Acute hypertension increased pial venular pressure and diameter in normocapnic rats. Hypercapnia alone increased pial venular pressure and pial venular diameter, and acute hypertension during hypercapnia further increased venular pressure. The magnitude of increase in pial venular pressure during acute hypertension was significantly less in hypercapnic than in normocapnic rats. We conclude that hypercapnia protects the blood-brain barrier. Possible mechanisms of this effect include attenuation of the incremental increase in pial venular pressure by hypercapnia or a direct effect on the blood-brain barrier not related to venous pressure.

Acute Disease↗

PubMed2005

Transition from acute to chronic hypercapnia in patients with periodic breathing: predictions from a computer model.

Acute hypercapnia may develop during periodic breathing from an imbalance between abnormal ventilatory patterns during apnea and/or hypopnea and compensatory ventilatory response in the interevent periods. However, transition of this acute hypercapnia into chronic sustained hypercapnia during wakefulness remains unexplained. We hypothesized that respiratory-renal interactions would play a critical role in this transition. Because this transition cannot be readily addressed clinically, we modified a previously published model of whole-body CO2 kinetics by adding respiratory control and renal bicarbonate kinetics. We enforced a pattern of 8 h of periodic breathing (sleep) and 16 h of regular ventilation (wakefulness) repeated for 20 days. Interventions included varying the initial awake respiratory CO2 response and varying the rate of renal bicarbonate excretion within the physiological range. The results showed that acute hypercapnia during periodic breathing could transition into chronic sustained hypercapnia during wakefulness. Although acute hypercapnia could be attributed to periodic breathing alone, transition from acute to chronic hypercapnia required either slowing of renal bicarbonate kinetics, reduction of ventilatory CO2 responsiveness, or both. Thus the model showed that the interaction between the time constant for bicarbonate excretion and respiratory control results in both failure of bicarbonate concentration to fully normalize before the next period of sleep and persistence of hypercapnia through blunting of ventilatory drive. These respiratory-renal interactions create a cumulative effect over subsequent periods of sleep that eventually results in a self-perpetuating state of chronic hypercapnia.

Acute Disease↗

PubMedDate not supplied

Cardiovascular responses of goat fetuses to hypercapnia during extrauterine incubation using extracorporeal membrane oxygenation.

The purpose of this study was to assess the effects of changes in fetal PaCO2 on circulatory functions without maternal influences. In 5 goat fetuses that were incubated using an extrauterine incubation system with arteriovenous extracorporeal membrane oxygenation, fetal carotid arterial blood flow, heart rate, mean blood pressure, and serum catecholamine levels were determined under the conditions of several grades of hypercapnia without hypoxemia. The hypercapnia was induced gradually by decreasing the flow of gas to the membrane oxygenator located on the extracorporeal circulation system. Fetal arterial CO2 tension increased significantly, from 36.2 +/- 1.1 mm Hg (means +/- SE) to 82.9 +/- 6.5 mm Hg, and the pH decreased significantly, from 7.410 +/- 0.012 to 7.121 +/- 0.028, due to the hypercapnia. In all cases, the fetal carotid arterial blood flow increased significantly (from 42.2 +/- 6.2 to 52.4 +/- 6.2 ml/min). Although a slight increase was observed in the heart rate at the mild hypercapnia stage, severe hypercapnia induced bradycardia in all cases. The mean arterial pressure and rate of extracorporeal circulation were unchanged during hypercapnia. We found that cerebral blood flow increased due to hypercapnia's direct effect on the vascular system, but the response of the peripheral chemoreceptor to hypercapnia seemed to be attenuated in chronic stimulation because bradycardia was induced in chronic hypercapnia.

Animals↗

PubMed1990

Peripheral chemoreceptor control of fetal renin responses to hypoxia and hypercapnia.

The renin response to hypoxia in late gestation fetal sheep has been well characterized. However, the renin response to asphyxia--the combination of hypoxia and hypercapnia--has not been extensively studied. The purpose of this study was to determine 1) the interaction of hypoxia and hypercapnia in the control of renin secretion in late gestation fetal sheep and 2) the role of peripheral arterial chemoreceptors therein. Chronically catheterized fetal sheep (intact or sinoaortic denervated) were exposed to hypoxia and/or hypercapnia for 30 minutes. Hypercapnia alone had no effect on plasma renin activity or aldosterone but did result in a significant increase in angiotensin II. Hypercapnia combined with hypoxia resulted in a significant increase in renin activity, angiotensin II, and aldosterone. Sinoaortic denervation attenuated the renin and angiotensin II responses to hypercapnia plus hypoxia. The increase in renin and angiotensin II in response to hypercapnia with or without concomitant hypoxia strongly correlated with the magnitude of the decrease in arterial pH in intact fetuses only. Hypoxia alone and in concert with hypercapnia increased mean arterial pressure and decreased heart rate in intact but not sinoaortic denervated fetuses. We conclude that 1) hypercapnia more potently increases plasma renin activity than does hypoxia in late gestation fetal sheep, 2) arterial pH may be the relevant signal perceived by the peripheral arterial chemoreceptors for the control of the renin-angiotensin system during asphyxia, and 3) the cardiovascular response to hypoxia is mediated, in part, by peripheral arterial chemoreceptors.

Aldosterone↗

PubMed1994

Cerebral vasodilation during hypercapnia. Role of glibenclamide-sensitive potassium channels and nitric oxide.

BACKGROUND AND PURPOSE: The purpose of these experiments was to examine mechanisms by which hypercapnia produces vasodilatation in brain. We examined the hypothesis that dilatation of cerebral arterioles during hypercapnia is dependent on activation of ATP-sensitive potassium channels and formation of nitric oxide. METHODS: Diameters of cerebral arterioles were measured using a closed cranial window in anesthetized rabbits. Changes in diameter of arterioles were measured in response to topical application of acetylcholine and sodium nitroprusside and during two levels of systemic hypercapnia. RESULTS: Increasing arterial PCO2 from 32 +/- 1 mm Hg (mean +/- SE) to 54 +/- 1 and 66 +/- 1 mm Hg dilated cerebral arterioles by 25 +/- 3% and 38 +/- 5%, respectively, from a control diameter of 93 +/- 3 microns. The response to the low level of hypercapnia was attenuated (25 +/- 3% versus 16 +/- 4%, P < .05) by glibenclamide (1 mumol/L), an inhibitor of ATP-sensitive potassium channels. Vasodilatation in response to the high level of hypercapnia was not affected by glibenclamide. Increases in arteriolar diameter in response to sodium nitroprusside were not inhibited by glibenclamide. NG-nitro-L-arginine (300 mumol/L), an inhibitor of nitric oxide synthase, completely inhibited dilatation of cerebral arterioles in response to the low level of hypercapnia and inhibited vasodilatation during the high level of hypercapnia by 66%. CONCLUSIONS: Thus, activation of glibenclamide-sensitive potassium channels may contribute to dilatation of cerebral arterioles during hypercapnia. Cerebral vasodilatation during hypercapnia is dependent in large part on production of nitric oxide.

Acetylcholine↗

PubMed2004

Bench-to-bedside review: Permissive hypercapnia.

Current protective lung ventilation strategies commonly involve hypercapnia. This approach has resulted in an increase in the clinical acceptability of elevated carbon dioxide tension, with hypoventilation and hypercapnia 'permitted' in order to avoid the deleterious effects of high lung stretch. Advances in our understanding of the biology of hypercapnia have prompted consideration of the potential for hypercapnia to play an active role in the pathogenesis of inflammation and tissue injury. In fact, hypercapnia may protect against lung and systemic organ injury independently of ventilator strategy. However, there are no clinical data evaluating the direct effects of hypercapnia per se in acute lung injury. This article reviews the current clinical status of permissive hypercapnia, discusses insights gained to date from basic scientific studies of hypercapnia and acidosis, identifies key unresolved concerns regarding hypercapnia, and considers the potential clinical implications for the management of patients with acute lung injury.

Acidosis↗

PubMed1995

Effect of acute hypercapnia on alpha atrial natriuretic peptide, renin, angiotensin II, aldosterone, and vasopressin plasma levels in patients with COPD.

Disturbances in hormonal systems involved in sodium and water homeostasis are common during respiratory insufficiency. To investigate the role of hypercapnia, we designed a study to examine the hormonal response to acute hypercapnia induced at constant cardiac filling pressures and without hypoxemia. Seven sedated patients with COPD receiving mechanical ventilation were studied during five successive periods. Hemodynamics, arterial blood gases, and plasma hormone levels (atrial natriuretic peptide, renin, angiotensin II, aldosterone, vasopressin) were measured three times during 60 min of acute hypercapnia (52 +/- 5 mm Hg) and at control periods, before (36 +/- 4 mm Hg) and after (42 +/- 3 mm Hg) acute hypercapnia. During acute hypercapnia, mean pulmonary arterial pressure and cardiac output were increased without variation of other measured cardiorespiratory data and hormonal levels when compared with control values. After acute hypercapnia, cardiorespiratory variables returned to control values without variations of hormonal levels. Our results show that moderate acute hypercapnia does not significantly influence the hormonal levels when cardiac filling pressures and sympathetic tone remain stable. We suggest that changes in those plasma hormones involved in salt and water homeostasis during acute hypercapnia are secondary to hemodynamic changes induced by acute respiratory failure and not to acute hypercapnia per se.

Aged↗

PubMed2005

Daytime hypercapnia in adult patients with obstructive sleep apnea syndrome in France, before initiating nocturnal nasal continuous positive airway pressure therapy.

CONTEXT: Daytime hypercapnia in patients with obstructive sleep apnea syndrome (OSAS) has a highly variable prevalence in the published studies, and is usually thought to be the consequence of an associated disease, COPD, or severe obesity. STUDY OBJECTIVES: To assess the prevalence of daytime hypercapnia in a very large population of adult patients with OSAS, free of associated COPD, and with a wide range of body mass index (BMI), and to evaluate the relationship between daytime hypercapnia and the severity of obesity and obesity-related impairment in lung function. DESIGN: Retrospective analysis of prospectively collected data. METHODS: The database of the observatory of a national nonprofit network for home treatment of patients with chronic respiratory insufficiency (Association Nationale pour le Traitement a Domicile de l'Insuffisance Respiratoire Chronique) was used. Collected data at treatment initiation were age, apnea-hypopnea index, BMI, FEV(1), vital capacity (VC), and arterial blood gases. The study included 1,141 adult patients with OSAS treated in France with nocturnal nasal continuous positive airway pressure (CPAP), FEV(1) >/= 80% predicted, FEV(1)/VC >/= 70%, and absence of restrictive respiratory disease other than related to obesity. RESULTS: The prevalence of daytime hypercapnia (Paco(2) >/= 45 mm Hg) before initiating CPAP therapy was 11% in the whole study population. The prevalence of daytime hypercapnia was 7.2% (27 of 377 patients) with BMI < 30, 9.8% (58 of 590 patients) with BMI from 30 to 40, and 23.6% (41 of 174 patients) with BMI > 40. Patients with daytime hypercapnia had significantly higher BMI values and significantly lower VC, FEV(1), and Pao(2) values than the normocapnic patients. Stepwise multiple regression showed that Pao(2), BMI, and either VC or FEV(1) were the best predictors of hypercapnia, but these variables explained only 9% of the variance in Paco(2) levels. CONCLUSION: Daytime hypercapnia was observed in > 1 of 10 patients with OSAS needing CPAP therapy and free of COPD, and was related to the severity of obesity and obesity-related impairment in lung function. However, other mechanisms than obesity are probably involved in the pathogenesis of daytime hypercapnia in OSAS.

Adult↗