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Query: UMLS:C0085383 (hypocapnia)
 1,697 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Respiration is a complex physiological system affecting a variety of physical processes that can act as a critical link between mind and body. This review discusses the evidence for dysregulated breathing playing a role in three clinical syndromes: panic disorder, functional cardiac disorder, and chronic pain. Recent technological advances allowing the ambulatory assessment of endtidal partial pressure of CO2 (PCO2) and respiratory patterns have opened up new avenues for investigation and treatment of these disorders. The latest evidence from laboratories indicates that subtle disturbances of breathing, such as tidal volume instability and sighing, contribute to the chronic hypocapnia often found in panic patients. Hypocapnia is also common in functional cardiac and chronic pain disorders, and studies indicate that it mediates some of their symptomatology. Consistent with the role of respiratory dysregulation in these disorders, initial evidence indicates efficacy of respiration-focused treatment.
Behav Modif 2001 Sep
PMID:Respiratory dysregulation in anxiety, functional cardiac, and pain disorders. Assessment, phenomenology, and treatment. 1153 Jul 14

The authors describe a new methodologically improved behavioral treatment for panic patients using respiratory biofeedback from a handheld capnometry device. The treatment rationale is based on the assumption that sustained hypocapnia resulting from hyperventilation is a key mechanism in the production and maintenance of panic. The brief 4-week biofeedback therapy is aimed at voluntarily increasing self-monitored end-tidal partial pressure of carbon dioxide (PCO2) and reducing respiratory rate and instability through breathing exercises in patients' environment. Preliminary results from 4 patients indicate that the therapy was successful in reducing panic symptoms and other psychological characteristics associated with panic disorder. Physiological data obtained from home training, 24-hour ambulatory monitoring pretherapy and posttherapy, and laboratory assessment at follow-up indicate that patients started out with low resting PCO2 levels, increased those levels during therapy, and maintained those levels at posttherapy and/or follow-up. Partial dissociation between PCO2 and respiratory rate questions whether respiratory rate should be the main focus of breathing training in panic disorder.
Behav Modif 2001 Sep
PMID:Respiratory biofeedback-assisted therapy in panic disorder. 1153 Jul 17

Winter athletes have an increased incidence of asthma, suggesting that repetitive hyperventilation with cold air may predispose individuals to airways disease. We used a canine model of exercise-induced hyperpnea to examine the effects of repeated hyperventilation with cool, dry air (i.e., dry air challenge [DAC]) on peripheral airway resistance (Rp), reactivity, and inflammation. Specific bronchi were exposed to a single DAC on five consecutive days. Rp and Delta Rp to aerosolized histamine, intravenous histamine, or hypocapnia were measured daily. Bronchoalveolar lavage fluid (BALF) was obtained on the fifth day. Rp increased from 0.70 +/- 0.08 to 1.13 +/- 0.22 cm H(2)O/ml/s (n = 25) 24 h after the first DAC, rose to 1.49 +/- 0.24 cm H(2)O/ml/s by Day 3, and remained elevated throughout the remainder of the protocol. Repeated DAC increased reactivity to hypocapnia and intravenous histamine. Intravenous salbutamol failed to reduce Rp as effectively in challenged airways (111% of Day 1 baseline) as in naive airways (54% of baseline). Repeated DAC caused increased BALF neutrophils, eosinophils, and sulfidopeptide leukotrienes. We conclude that repeated DAC causes peripheral airways inflammation, obstruction, hyperreactivity, and impaired beta-agonist-induced relaxation. This suggests that other mechanisms in addition to increased smooth muscle tone may contribute to the development of repetitive hyperventilation-induced bronchial obstruction and hyperreactivity.
Am J Respir Crit Care Med 2001 Sep 01
PMID:Repeated hyperventilation causes peripheral airways inflammation, hyperreactivity, and impaired bronchodilation in dogs. 1154 33

We describe a 74-year-old patient with dyspnoea and tachypnoea induced by chlorpromadinone acetate, a synthetic progesterone used to treat prostatic hyperplasia. The dyspnoea, tachypnoea and hypocapnia improved after discontinuing the chlorpromadinone acetate. It is important to recognize that synthetic progesterones can cause dyspnoea and hyperventilation.
Respirology 2001 Sep
PMID:Dyspnoea and hyperventilation induced by synthetic progesterone chlorpromadinone acetate for the treatment of prostatic hypertrophy. 1155 87

Recent experimental and clinical data demonstrate that both hypocapnia and hypercapnia during the neonatal period may result in beneficial or adverse consequences. Multiple retrospective studies report a strong association between PaCO2 levels less than 25 to 30 mm Hg and an increased incidence of cystic PVL and CP in preterm infants. Prolonged exposure to PaCO2 values less than 25 to 30 mm Hg is also associated with hearing loss in term and near-term infants. A low tidal volume strategy combined with permissive hypercapnia is potentially a strategy that could prevent lung injury. Clearly, more randomized, controlled trials are needed before this latter strategy or that of permissive hypercapnia can be recommended routinely for preterm, near-term, or term gestation infants with respiratory disorders.
Clin Perinatol 2001 Sep
PMID:Hypocapnia and hypercapnia in respiratory management of newborn infants. 1157 Jan 52

Air hunger (uncomfortable urge to breathe) is a component of dyspnea (shortness of breath). Three human H(2)(15)O positron emission tomography (PET) studies have identified activation of phylogenetically ancient structures in limbic and paralimbic regions during dyspnea. Other studies have shown activation of these structures during other sensations that alert the organism to urgent homeostatic imbalance: pain, thirst, and hunger for food. We employed blood oxygen level dependent (BOLD) functional magnetic resonance imaging (fMRI) to examine activation during air hunger. fMRI conferred several advantages over PET: enhanced signal-to-noise, greater spatial resolution, and lack of ionizing radiation, enabling a greater number of trials in each subject. Six healthy men and women were mechanically ventilated at 12-14 breaths/min. The primary experiment was conducted at mean end-tidal PCO(2) of 41 Torr. Moderate to severe air hunger was evoked during 42-s epochs of lower tidal volume (mean = 0.75 L). Subjects described the sensation as "like breath-hold," "urge to breathe," and "starved for air." In the baseline condition, air hunger was consistently relieved by epochs of higher tidal volume (mean = 1.47 L). A control experiment in the same subjects under a background of mild hypocapnia (mean end-tidal PCO(2) = 33 Torr) employed similar tidal volumes but did not evoke air hunger, controlling for stimulus variables not related to dyspnea. During each experiment, we maintained constant end-tidal PCO(2) and PO(2) to avoid systematic changes in global cerebral blood flow. Whole-brain images were acquired every 5 s (T2*, 56 slices, voxel resolution 3 x 3 x 3 mm). Activations associated with air hunger were determined using voxel-based interaction analysis of covariance that compared data between primary and control experiments (SPM99). We detected activations not seen in the earlier PET study using a similar air hunger stimulus (Banzett et al. 2000). Limbic and paralimbic loci activated in the present study were within anterior insula (seen in all 3 published studies of dyspnea), anterior cingulate, operculum, cerebellum, amygdala, thalamus, and basal ganglia. Elements of frontoparietal attentional networks were also identified. The consistency of anterior insular activation across subjects in this study and across published studies suggests that the insula is essential to dyspnea perception, although present data suggest that the insula acts in concert with a larger neural network.
J Neurophysiol 2002 Sep
PMID:BOLD fMRI identifies limbic, paralimbic, and cerebellar activation during air hunger. 1220 70

The effect of the basal cerebral blood flow (CBF) on both the magnitude and dynamics of the functional hemodynamic response in humans has not been fully investigated. Thus, the hemodynamic response to visual stimulation was measured using blood oxygenation level-dependent (BOLD) functional magnetic resonance imaging (fMRI) in human subjects in a 7-T magnetic field under different basal conditions: hypocapnia, normocapnia, and hypercapnia. Hypercapnia was induced by inhalation of a 5% carbon dioxide gas mixture and hypocapnia was produced by hyperventilation. As the fMRI baseline signal increased linearly with expired CO2 from hypocapnic to hypercapnic levels, the magnitude of the BOLD response to visual stimulation decreased linearly. Measures of the dynamics of the visually evoked BOLD response (onset time, full-width-at-half-maximum, and time-to-peak) increased linearly with the basal fMRI signal and the end-tidal CO2 level. The basal CBF level, modulated by the arterial partial pressure of CO2, significantly affects both the magnitude and dynamics of the BOLD response induced by neural activity. These results suggest that caution should be exercised when comparing stimulus-induced fMRI responses under different physiologic or pharmacologic states.
J Cereb Blood Flow Metab 2002 Sep
PMID:Effect of basal conditions on the magnitude and dynamics of the blood oxygenation level-dependent fMRI response. 1221 10

Cardiopulmonary bypass (CPB) is one of the major tools of cardiac surgery. However, no clear data are available for the ideal value of sweep gas flow to oxygenator during CPB. The aim of this study was to determine the best value for sweep gas flow during CPB. Thirty patients undergoing isolated CABG were randomly and equally allocated into three groups. Sweep gas flow to oxygenator was kept at 1.35 l/min/m2 in group 1, 1.60 l/min/m2 in group 2, and 2.0 l/min/m2 in group 3. All patients were operated on under the same anaesthetic regime and surgical techniques. Samples for blood gas analysis were collected at T1: before CPB; T2: 5 min after the initiation of CPB; T3: just before rewarning; and T4: at the end of rewarming. Five minutes after the initiation of CPB (T2), pCO2 decreased significantly in groups 2 and 3 compared to group 1 (p < 0.02). With the addition of hypothermia (T3), the changes in the pH and pCO2 became more profound and, in this period, the levels in group 3 patients outranged the physiologic limits, with pCO2 and pH values being 28 +/- 3 mmHg and 7.50 +/- 0.04, respectively. At the end of the rewarming period (T4), in spite of increased carbon dioxide production, pCO2 values were below the physiologic limits in groups 2 and 3. We conclude that sweep gas flow to the oxygenator should be kept between 1.35 and 1.60 l/min/m2 during CPB to avoid hypocapnia, which results in alkalosis and has hazardous effects on lung mechanics, cerebral blood flow, and the cardiovascular system.
Perfusion 2002 Sep
PMID:Adjustment of sweep gas flow during cardiopulmonary bypass. 1224 39

During acclimatization to the hypoxia of altitude, the cerebral circulation is exposed to arterial hypoxia and hypocapnia, two stimuli with opposing influences on cerebral blood flow (CBF). In order to understand the resultant changes in CBF, this study examined the responses of CBF during a period of constant mild hypoxia both with and without concomitant regulation of arterial P(CO2). Nine subjects were each exposed to two protocols in a purpose-built chamber: (1) 48 h of isocapnic hypoxia (Protocol I), where end-tidal P(O2) (P(ET,O2)) was held at 60 Torr and end-tidal P(CO2) (P(ET,CO2)) at the subject's resting value prior to experimentation; and (2) 48 h of poikilocapnic hypoxia (Protocol P), where P(ET,O2) was held at 60 Torr and P(ET,CO2) was uncontrolled. Transcranial Doppler ultrasound was used to assess CBF. At 24 h intervals during and after the hypoxic exposure CBF was measured and the sensitivity of CBF to acute variations in P(O2) and P(CO2) was determined. During Protocol P, P(ET,CO2) decreased by 13% (P < 0.001) and CBF decreased by 6% (P < 0.05), whereas during Protocol I, P(ET,CO2) and CBF remained unchanged. The sensitivity of CBF to acute variations in P(O2) and P(CO2) increased by 103% (P < 0.001) and 28% (P < 0.01), respectively, over the 48 h period of hypoxia. These changes did not differ between protocols. In conclusion, CBF decreases during mild poikilocapnic hypoxia, indicating that there is a predominant effect on CBF of the associated arterial hypocapnia. This fall occurs despite increases in the sensitivity of CBF to acute variations in P(O2)/P(CO2) arising directly from the hypoxic exposure.
Exp Physiol 2002 Sep
PMID:Changes in cerebral blood flow during and after 48 h of both isocapnic and poikilocapnic hypoxia in humans. 1248 38

We investigated the effect of baroreflex-induced sympathetic activation, produced by lower body negative pressure (LBNP) at -40 mmHg, on cerebrovascular responsiveness to hyper- and hypocapnia in healthy humans. Transcranial Doppler ultrasound was used to measure blood flow velocity (CFV) in the middle cerebral artery during variations in end-tidal carbon dioxide pressure (PET,CO2) of +10, +5, 0, -5, and -10 mmHg relative to eupnoea. The slopes of the linear relationships between PET,CO2 and CFV were computed separately for hyper- and hypocapnia during the LBNP and no-LBNP conditions. LBNP decreased pulse pressure, but did not change mean arterial pressure. LBNP evoked an increase in ventilation that resulted in a 9 +/- 2 mmHg decrease in PET,CO2, which was corrected by CO2 supplementation of the inspired air. LBNP did not affect cerebrovascular CO2 response slopes during steady-state hypercapnia (3.14 +/- 0.24 vs. 2.96 +/- 0.26 cm s-1 mmHg-1) or hypocapnia (1.31 +/- 0.18 vs. 1.32 +/- 0.19 cm s-1 mmHg-1), or the CFV responses to voluntary apnoea (+51 +/- 19 vs. +50 +/- 18 %). Thus, cerebrovascular CO2 responsiveness was not altered by baroreflex-induced sympathetic activation. Our data challenge the concept that sympathetic activation restrains cerebrovascular responses to alterations in CO2 pressure.
J Physiol 2003 Sep 01
PMID:Baroreflex-induced sympathetic activation does not alter cerebrovascular CO2 responsiveness in humans. 1286 71


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