OBJECTIVES: To evaluate the base excess response during acute in vivo carbon dioxide changes. DESIGN: Secondary analysis of individual participant data from experimental studies. SETTING: Three experimental studies investigating the effect of acute in vivo respiratory derangements on acid-base variables. SUBJECTS: Eighty-nine (canine and human) carbon dioxide exposures. INTERVENTIONS: Arterial carbon dioxide titration through environmental chambers or mechanical ventilation. MEASUREMENTS AND MAIN RESULTS: For each subject, base excess was calculated using bicarbonate and pH using a fixed buffer power of 16.2. Analyses were performed using linear regression with arterial dioxide (predictor), base excess (outcome), and studies (interaction term). All studies show different baselines and slopes for base excess across carbon dioxide titrations methods. Individual subjects show substantial, and potentially clinically relevant, variations in base excess response across the hypercapnic range. Using a mathematical simulation of 10,000 buffer power coefficients we determined that a coefficient of 12.1 (95% CI, 9.1-15.1) instead of 16.2 facilitates a more conceptually appropriate in vivo base excess equation for general clinical application. CONCLUSIONS: In vivo changes in carbon dioxide leads to changes in base excess that may be clinically relevant for individual patients. A buffer power coefficient of 16.2 may not be appropriate in vivo and needs external validation in a range of clinical settings.

• MeSH
• acidobazická rovnováha * fyziologie   MeSH
• dospělí MeSH
• hyperkapnie patofyziologie   metabolismus   MeSH
• koncentrace vodíkových iontů MeSH
• lidé MeSH
• oxid uhličitý * metabolismus   MeSH
• poruchy acidobazické rovnováhy patofyziologie   metabolismus   MeSH
• psi MeSH
• umělé dýchání MeSH
• zvířata MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mužské pohlaví MeSH
• psi MeSH
• ženské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Pro Pickwickův syndrom bylo několik posledních dekád obdobím výrazného zájmu. Z nic nevypovídajícího popisného názvu je dnes logicky pojmenovaná klinicko-patologická jednotka – hypoventilační syndrom obézních. Je definován souběhem obezity (index tělesné hmotnosti [body mass index, BMI] ≥30 kg/m2), chronické denní hyperkapnie (parciální tlak oxidu uhličitého v arteriální krvi [paCO2] ≥45 mm Hg, tj. 6,0 kPa) a porušeným dýcháním během spánku ve smyslu hypoventilace. U 90 % pacientů se na porušeném dýchání ve spánku podílí syndrom obstrukční spánkové apnoe, u zbytku se jedná o prostou hypoventilaci. Změny v mechanice dýchání, porušené dýchání během spánku a alterace centrálního řízení dechu s leptinovou rezistencí jsou základními patofyziologickými mechanismy hypoventilačního syndromu obézních. Onemocnění má dosti příznačnou klinickou manifestaci. Dominuje chrápání, buzení se během noci s ranním pocitem únavy a nadměrnou celodenní spavostí. Nejdůležitějším krokem v diagnostice je na toto onemocnění vůbec pomyslet. Další vyšetřovací algoritmus není komplikovaný. Diagnóza de facto stojí na nativním odběru arteriálních krevních plynů s průkazem hyperkapnie a spánkové monitoraci, která doloží obstrukční spánkovou apnoi či hypoventilaci. Pokroků v oblasti terapie bylo bezpochyby učiněno nejvíce. Jedinou kauzální léčbou zůstává kontrolovaná redukce tělesné hmotnosti. Nejúčinnější je léčba přetlakem v dýchacích cestách. Zásadní rozdíly mezi léčbou trvalým přetlakem v dýchacích cestách a dvojúrovňovým přetlakem v dýchacích cestách při dlouhodobém užití a dobrá compliance nebyly prokázány. Výběr komfortní a dobře těsnící masky jsou základním kamenem pro dobrou adherenci k přetlakové terapii. Titrace je proces, kterým zjišťujeme optimální nastavení ventilátoru. Cílem je stanovit jednoúrovňový nebo dvouúrovňový přetlak, který eliminuje apnoi či hypopnoi a zajistí dostatečnou ventilaci i okysličení během spánku.

The last few decades have been a period of considerable interest for Pickwick syndrome. From a nondescriptive name, the clinicopathological entity - obesity hypoventilation syndrome - is now logically named. It is defined by the combination of obesity (body mass index [BMI] ≥30 kg/m2), chronic daytime hypercapnia (partial pressure of carbon dioxide in arterial blood [paCO2] ≥ 45 mm Hg, i.e. 6.0 kPa) and impaired breathing during sleep in the sense of hypoventilation. In 90% of patients, obstructive sleep apnoea syndrome is involved in sleep-disordered breathing; the remainder have simple hypoventilation. Changes in breathing mechanics, impaired breathing during sleep and alteration of central control of breathing with leptin resistance are the underlying pathophysiological mechanisms of obesity. hypoventilation syndrome. The disease has a rather characteristic clinical manifestation. It is dominated by snoring, waking during the night with morning fatigue and excessive daytime sleepiness. The most important step in diagnosis is to think about the disease at all. The further investigative algorithm is not complicated. The diagnosis is based on native arterial blood gas sampling with evidence of hypercapnia and sleep monitoring to document obstructive sleep apnoea or hypoventilation. Advances in therapy have undoubtedly been made. Controlled weight reduction remains the only causal treatment. The most effective treatment is positive airway pressure. No major differences have been demonstrated between continuous positive airway pressure and bilevel positive airway pressure therapy in long-term use and good compliance. The choice of a comfortable and well-sealing mask is the cornerstone for good adherence to positive pressure therapy. Titration is the process by which we determine the optimal ventilator settings. The goal is to establish a single or dual level positive pressure that eliminates apnea or hypopnea and ensures adequate ventilation and oxygenation during sleep.

• MeSH
• hyperkapnie etiologie   patofyziologie   terapie   MeSH
• hypoventilační syndrom při obezitě * etiologie   patofyziologie   terapie   MeSH
• lidé MeSH
• obezita komplikace   terapie   MeSH
• obstrukční spánková apnoe etiologie   patofyziologie   terapie   MeSH
• Check Tag
• lidé MeSH
• Publikační typ
• práce podpořená grantem MeSH
• přehledy MeSH

Domácí neinvazivní ventilace je desítky let zavedená metoda léčby chronické hyperkapnické respirační insuficience. Její efektivita je podložena řadou klinických studií a prevalence užití celosvětově i v České republice narůstá. Článek nabízí stručný souhrn patofyziologie hyperkapnické respirační insuficience a její léčby v tuzemských podmínkách.

Domiciliary non-invasive ventilation has been an established method of treating chronic hypercapnic respiratory insufficiency for decades. Its effectiveness is based on a number of clinical studies and the prevalence of use worldwide and in the Czech Republic is increasing. The article offers a brief summary of the pathophysiology of hypercapnic respiratory insufficiency and its treatment.

• MeSH
• chronická obstrukční plicní nemoc terapie   MeSH
• hyperkapnie etiologie   patofyziologie   terapie   MeSH
• hypoventilační syndrom při obezitě terapie   MeSH
• lidé MeSH
• masky MeSH
• neinvazivní ventilace * metody   MeSH
• respirační acidóza etiologie   patofyziologie   prevence a kontrola   MeSH
• respirační insuficience * etiologie   patofyziologie   terapie   MeSH
• služby domácí péče MeSH
• Check Tag
• lidé MeSH

Breathing impairments, such as an alteration in breathing pattern, dyspnoea, and sleep apnoea, are common health deficits recognised in Parkinson's disease (PD). The mechanism that underlies these disturbances, however, remains unclear. We investigated the effect of the unilateral damage to the rat nigrostriatal pathway on the central ventilatory response to hypercapnia, evoked by administering 6-hydroxydopamine (6-OHDA) into the right medial forebrain bundle (MFB). The respiratory experiments were carried out in conscious animals in the plethysmography chamber. The ventilatory parameters were studied in normocapnic and hyperoxic hypercapnia before and 14 days after the neurotoxin injection. Lesion with the 6-OHDA produced an increased tidal volume during normoxia. The magnified response of tidal volume and a decrease of breathing frequency to hypercapnia were observed in comparison to the pre-lesion and sham controls. Changes in both respiratory parameters resulted in an increase of minute ventilation of the response to CO(2) by 28% in comparison to the pre-lesion state at 60 s. Our results demonstrate that rats with implemented unilateral PD model presented an altered respiratory pattern most often during a ventilatory response to hypercapnia. Preserved noradrenaline and specific changes in dopamine and serotonin characteristic for this model could be responsible for the pattern of breathing observed during hypercapnia.

• MeSH
• fasciculus telencephali medialis účinky léků   fyziologie   MeSH
• hyperkapnie patofyziologie   MeSH
• krysa rodu rattus MeSH
• oxidopamin toxicita   MeSH
• parkinsonské poruchy chemicky indukované   patofyziologie   MeSH
• plicní ventilace účinky léků   fyziologie   MeSH
• potkani Wistar MeSH
• sympatolytika toxicita   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH

Background: Respiratory parameters are important predictors of prognosis in the COPD population. Global Initiative for Obstructive Lung Disease (GOLD) 2017 Update resulted in a vertical shift of patients across COPD categories, with category B being the most populous and clinically heterogeneous. The aim of our study was to investigate whether respiratory parameters might be associated with increased all-cause mortality within GOLD category B patients. Methods: The data were extracted from the Czech Multicentre Research Database, a prospective, noninterventional multicenter study of COPD patients. Kaplan-Meier survival analyses were performed at different levels of respiratory parameters (partial pressure of oxygen in arterial blood [PaO2], partial pressure of arterial carbon dioxide [PaCO2] and greatest decrease of basal peripheral capillary oxygen saturation during 6-minute walking test [6-MWT]). Univariate analyses using the Cox proportional hazard model and multivariate analyses were used to identify risk factors for mortality in hypoxemic and hypercapnic individuals with COPD. Results: All-cause mortality in the cohort at 3 years of prospective follow-up reached 18.4%. Chronic hypoxemia (PaO2 <7.3 kPa), hypercapnia (PaCO2 >7.0 kPa) and oxygen desaturation during the 6-MWT were predictors of long-term mortality in COPD patients with forced expiratory volume in 1 second ≤60% for the overall cohort and for GOLD B category patients. Univariate analyses confirmed the association among decreased oxemia (<7.3 kPa), increased capnemia (>7.0 kPa), oxygen desaturation during 6-MWT and mortality in the studied groups of COPD subjects. Multivariate analysis identified PaO2 <7.3 kPa as a strong independent risk factor for mortality. Conclusion: Survival analyses showed significantly increased all-cause mortality in hypoxemic and hypercapnic GOLD B subjects. More important, PaO2 <7.3 kPa was the strongest risk factor, especially in category B patients. In contrast, the majority of the tested respiratory parameters did not show a difference in mortality in the GOLD category D cohort.

• MeSH
• analýza krevních plynů MeSH
• chronická obstrukční plicní nemoc diagnóza   mortalita   patofyziologie   terapie   MeSH
• databáze faktografické MeSH
• dýchání * MeSH
• hyperkapnie diagnóza   mortalita   patofyziologie   terapie   MeSH
• hypoxie diagnóza   mortalita   patofyziologie   terapie   MeSH
• Kaplanův-Meierův odhad MeSH
• komorbidita MeSH
• lidé středního věku MeSH
• lidé MeSH
• multivariační analýza MeSH
• plíce patofyziologie   MeSH
• prediktivní hodnota testů MeSH
• prognóza MeSH
• proporcionální rizikové modely MeSH
• rizikové faktory MeSH
• senioři MeSH
• stupeň závažnosti nemoci MeSH
• test chůzí MeSH
• usilovný výdechový objem MeSH
• Check Tag
• lidé středního věku MeSH
• lidé MeSH
• mužské pohlaví MeSH
• senioři MeSH
• ženské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• multicentrická studie MeSH
• práce podpořená grantem MeSH
• Geografické názvy
• Česká republika MeSH

During breathing experiments in avalanche snow, measurement of CO2 is often conducted in order to monitor the volunteers or as an endpoint of the trials. From the measured CO2 curves, monitors calculate end-tidal CO2 concentrations (EtCO2). The aim of the study is to investigate, whether Datex-Ohmeda S/5 anesthesia monitor evaluates EtCO2 and other parameters of breathing gas correctly, otherwise to characterize the occurrence of the error and to find out a possible cause of error. Data from a real experiment aimed at investigation of work of breathing into snow in the presence and absence of an artificial air pocket were used to study precision of the monitor. The data were evaluated in Matlab environment. The analysis found that the average error of EtCO2 evaluation occurred in 39% and in 30 % of the total experimental time of breathing with and without the air pocket respectively (range from 13% to 93% of time). Breathing experiments with simulated snow were conducted in order to find the cause of the error. The error occurs immediately after a significant increase of CO2 in the breathing circuit as a consequence of expired gas rebreathing and is independent on other breathing parameters related to a change in breathing pattern. The experiment confirmed that a newer model CARESCAPE B650 monitor is prone to this error as well. The last experiment conducted with a standard anesthesia machine but with removed CO2 absorbing soda lime confirmed, that the error occurs even in a standard clinical setup, which might cause a wrong diagnoses or might harm a volunteer or a patient.

• MeSH
• dospělí MeSH
• dýchání MeSH
• hyperkapnie * patofyziologie   MeSH
• laviny MeSH
• lidé MeSH
• mladý dospělý MeSH
• oxid uhličitý analýza   MeSH
• sníh MeSH
• výzkum MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mladý dospělý MeSH
• mužské pohlaví MeSH
• Publikační typ
• práce podpořená grantem MeSH

This study was undertaken to determine pattern sensitivity of phrenic nerve plasticity in respect to different respiratory challenges. We compared long-term effects of intermittent and continuous hypercapnic and hypoxic stimuli, and combined intermittent hypercapnia and hypoxia on phrenic nerve plasticity. Adult, male, urethane-anesthetized, vagotomized, paralyzed, mechanically ventilated Sprague-Dawley rats were exposed to: acute intermittent hypercapnia (AIHc or AIHc(O2)), acute intermittent hypoxia (AIH), combined intermittent hypercapnia and hypoxia (AIHcH), continuous hypercapnia (CHc), or continuous hypoxia (CH). Peak phrenic nerve activity (pPNA) and burst frequency were analyzed during baseline (T0), hypercapnia or hypoxia exposures, at 15, 30, and 60 min (T60) after the end of the stimulus. Exposure to acute intermittent hypercapnia elicited decrease of phrenic nerve frequency from 44.25+/-4.06 at T0 to 35.29+/-5.21 at T60, (P=0.038, AIHc) and from 45.5+/-2.62 to 37.17+/-3.68 breaths/min (P=0.049, AIHc(O2)), i.e. frequency phrenic long term depression was induced. Exposure to AIH elicited increase of pPNA at T60 by 141.0+/-28.2 % compared to baseline (P=0.015), i.e. phrenic long-term facilitation was induced. Exposure to AIHcH, CHc, or CH protocols failed to induce long-term plasticity of the phrenic nerve. Thus, we conclude that intermittency of the hypercapnic or hypoxic stimuli is needed to evoke phrenic nerve plasticity.

• MeSH
• dlouhodobá potenciace fyziologie   MeSH
• hyperkapnie patofyziologie   MeSH
• hypoxie patofyziologie   MeSH
• krysa rodu rattus MeSH
• nervus phrenicus fyziologie   MeSH
• neuroplasticita fyziologie   MeSH
• periodicita * MeSH
• potkani Sprague-Dawley MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH

Presence of an air pocket and its size play an important role in survival of victims buried in the avalanche snow. Even small air pockets facilitate breathing. We hypothesize that the size of the air pocket significantly affects the airflow resistance and work of breathing. The aims of the study are (1) to investigate the effect of the presence of an air pocket on gas exchange and work of breathing in subjects breathing into the simulated avalanche snow and (2) to test whether it is possible to breathe with no air pocket. The prospective interventional double-blinded study involved 12 male volunteers, from which 10 completed the whole protocol. Each volunteer underwent two phases of the experiment in a random order: phase "AP"--breathing into the snow with a one-liter air pocket, and phase "NP"--breathing into the snow with no air pocket. Physiological parameters, fractions of oxygen and carbon dioxide in the airways and work of breathing expressed as pressure-time product were recorded continuously. The main finding of the study is that it is possible to breath in the avalanche snow even with no air pocket (0 L volume), but breathing under this condition is associated with significantly increased work of breathing. The significant differences were initially observed for end-tidal values of the respiratory gases (EtO2 and EtCO2) and peripheral oxygen saturation (SpO2) between AP and NP phases, whereas significant differences in inspiratory fractions occurred much later (for FIO2) or never (for FICO2). The limiting factor in no air pocket conditions is excessive increase in work of breathing that induces increase in metabolism accompanied by higher oxygen consumption and carbon dioxide production. The presence of even a small air pocket reduces significantly the work of breathing.

• MeSH
• asfyxie patofyziologie   prevence a kontrola   MeSH
• dechová práce fyziologie   MeSH
• dechový objem fyziologie   MeSH
• dospělí MeSH
• dvojitá slepá metoda MeSH
• hyperkapnie patofyziologie   MeSH
• hypoxie patofyziologie   MeSH
• inspirační rezervní objem fyziologie   MeSH
• katastrofy * MeSH
• klinické křížové studie MeSH
• kyslík fyziologie   MeSH
• laviny * MeSH
• lidé MeSH
• monitorování fyziologických funkcí MeSH
• oxid uhličitý fyziologie   MeSH
• sníh MeSH
• zdraví dobrovolníci pro lékařské studie MeSH
• Check Tag
• dospělí MeSH
• lidé MeSH
• mužské pohlaví MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH
• randomizované kontrolované studie MeSH

• MeSH
• dítě * MeSH
• hyperkapnie diagnóza   etiologie   patofyziologie   prevence a kontrola   terapie   MeSH
• hypoxie diagnóza   etiologie   patofyziologie   prevence a kontrola   terapie   MeSH
• imunoanalýza metody   využití   MeSH
• klinické zkoušky jako téma MeSH
• kojenec MeSH
• lidé MeSH
• plicní ventilace MeSH
• předškolní dítě MeSH
• respirační insuficience * diagnóza   etiologie   klasifikace   patofyziologie   prevence a kontrola   terapie   MeSH
• umělé dýchání * kontraindikace   ošetřování   škodlivé účinky   MeSH
• ventilace umělá s výdechovým přetlakem klasifikace   kontraindikace   metody   přístrojové vybavení   škodlivé účinky   využití   MeSH
• Check Tag
• dítě * MeSH
• kojenec MeSH
• lidé MeSH
• předškolní dítě MeSH
• Publikační typ
• práce podpořená grantem MeSH

Chronic hypoxia causes oxidative injury of pulmonary vessels and attenuates their reactivity to different stimuli. When combined with hypercapnia, biochemical markers of this injury are reduced but the effect of concomitant hypoxia and hypercapnia on vascular reactivity is not fully understood. This study was therefore designed to test whether hypercapnia can prevent also the hypoxia-induced loss of reactivity of pulmonary vessels. The reactivity of vessels from rats exposed either to hypoxia or hypoxia combined with hypercapnia was tested using a small vessel myograph (M 500A, Linton, Norfolk, GB). The second and third intrapulmonary branches of pulmonary arteries were isolated under a dissecting microscope from lungs of 8 control rats (group N), 6 rats exposed to hypoxia for 5 days (isobaric, 10 % O(2), group H) and 7 rats exposed to hypoxia combined with hypercapnia for 5 days (10 % O(2), 5 % CO(2), group H+CO(2)). The transmural pressure was set by automatic normalization to 30 mm Hg. The vessel size did not vary among the groups. After stabilization we challenged the vessels twice with KCl (80 mM) and once with PGF(2alpha) (0.1 mM). There were no significant differences in KCl induced contractions among the groups. The responses to PGF(2alpha) were expressed as a ratio to the maximal tension obtained by the exposure to 80 mM KCl. Contractions induced by PGF(2alpha) were markedly reduced in group H (0.07+/-0.02) and in group H+CO(2) (0.26+/-0.03) in comparison with group N (0.83+/-0.07). The vessels of group H responded to PGF(2alpha) less than those of group H+CO(2). However we observed the attenuated reactivity also in group H+CO(2) in comparison with N. Hypercapnia therefore partially blunted the hypoxia-induced loss of reactivity in pulmonary arteries. This finding supports the hypothesis that hypercapnia significantly alters the nature of lung injury induced by chronic hypoxia.

• MeSH
• arteria pulmonalis účinky léků   patofyziologie   MeSH
• časové faktory MeSH
• chronická nemoc MeSH
• hyperkapnie patofyziologie   MeSH
• hypoxie patofyziologie   MeSH
• krysa rodu rattus MeSH
• modely nemocí na zvířatech MeSH
• potkani Wistar MeSH
• vazokonstrikce * účinky léků   MeSH
• vazokonstriktory farmakologie   MeSH
• zvířata MeSH
• Check Tag
• krysa rodu rattus MeSH
• mužské pohlaví MeSH
• zvířata MeSH
• Publikační typ
• časopisecké články MeSH
• práce podpořená grantem MeSH