Significant Changes In PCO2 Research Articles

Noninvasive High-Frequency Oscillatory Ventilation: A Retrospective Chart Review.

This study aimed to review the feasibility of nasal high-frequency oscillatory ventilation (NHFOV) in preventing reintubation in preterm infants. This is a retrospective cohort study of all premature newborn infants placed on NHFOV in a single-center neonatal intensive care unit. Twenty-seven patients (birth weight: 765 ± 186 g, gestational age: 28 ± 2 weeks) were commenced on NHFOV on 32 occasions. NHFOV was used immediately postextubation as the primary mode of noninvasive ventilation (NIV; prophylaxis) in 10 of 32 occasions and as "rescue" (failure of NCPAP or biphasic CPAP) in 22 of 32 occasions. Treatment with NHFOV was successful in 22 occasions (69%) while on 10 occasions (31%) reintubation was required within 72 hours. In the rescue group, there was significant reduction in the mean (standard deviation [SD]) number of apneas (0.9 ± 1.07 vs. 0.3 ± 0.29, p < 0.005), but there were no significant changes in the PCO2 level (52 [ ± 9.8] vs. 52 [ ± 8.6] mm Hg, p = 0.8), or the FiO2 requirement (0.39 ± 0.19 vs. 0.33 ± 0.10, p = 0.055) before and after commencing NHFOV, respectively. The use of NHFOV is feasible as a prophylactic or rescue mode of NIV following extubation and was associated with decrease in the number of apneas without significant changes in PCO2 or oxygen requirements. A well-designed randomized control trial is needed to determine the indications, clinical outcomes, and safety of this treatment modality. · NHFOV is a new and evolving mode of noninvasive ventilation.. · The use of NHFOV is feasible as a prophylactic or rescue mode of noninvasive ventilation.. · A well-designed randomized control is needed to evaluate the efficacy and safety of NHFOV safe..

The carboxytherapy opportunities in surgery

The carbon dioxide of the body is the most important natural regulator of respiration, blood circulation, metabolism, electrolyte balance, nervous system excitability, smooth muscle tonus. Carboxytherapy is based on the use of carbon dioxide. It is an effective and safe method of many diseases’ treatment due to its rich pharmacodynamics. Inhalation of CO2 is used in resuscitation and anesthesiology practice. Another area of CO2 application in surgery is intra‑abdominal insufflation for all endoscopic laparoscopic procedures. Carbon dioxide is quickly absorbed by the mucous membrane of the gastrointestinal tract, which causes an increased interest in its use as an insufflation agent for all endoscopic procedures. In addition, CO2 has antispasmodic, analgesic, anti‑inflammatory and antiseptic effects, which is important for these diagnostic measures. CO2 insufflation during a colonoscopy causes less post‑procedure pain and distension of the intestine without significant changes in pCO2 compared to air one. An additional mechanism for pain reducing after the CO2 procedure may be the vasodilating effect of CO2 and its spasmolytic action on the wall in the enlarged part of the colon. For the past 50 years, CO2 has been used in cardiothoracic surgery to remove air from the surgical area, which reduces the air embolism probabily during heart surgery. Recently, heated and hydrated CO2 insufflation is used as a method to reduce the infections rate at the surgery site in an open wound. A carbon dioxide laser has physical, biological and surgical properties valuable for the surgeon. Carbon dioxide is also used as an alternative diagnostic contrast agent. Therefore, CO2 due to its antibacterial, antihypoxic, antispasmodic, analgesic, anti‑inflammatory, antioxidant properties and the side effects absence is an important component of therapeutic and diagnostic procedures in surgery, anesthesiology, gynecology, dermatology and other fields of medicine.

Inadequacy of Pulse Oximetry in the Catheterization Laboratory. An Exploratory Study Monitoring Respiratory Status Using Arterial Blood Gases during Cardiac Catheterization with Conscious Sedation

Benzodiazepines and opioids are commonly used for conscious sedation (CS) in cardiac catheterization laboratory (CCL) patients. Both drugs are known to predispose to hypoxemia, apnea and decreased responsiveness to PCO2, resulting in decreased arterial pH and PO2, as well as increased PCO2. We want to determine the effects of CS on arterial blood gas (ABG) in CCL patient, and identify if pulse oximetry monitoring is adequate. We enrolled 18 subjects undergoing elective catheterization. Measurement of ABGs at one-minute intervals was done from the moment of arterial access until case end. The results of ABGs were not available to the clinician who administered sedation. Relationships of pH, PCO2, PaO2 and SaO2 were studied by plotting time series graphs. Significant changes were defined as pH <7.30, SaO2 < 90, and PCO2 > 50 mmHg. No significant change in pH, PCO2, PaO2 and SaO2 was noted in 4/18 (22%) subjects. A significant drop in SaO2 was noted in 4/18 (22%). A significant change in PCO2 and/or pH was noted in 10/18 (55%) cases. Among the 16 (16/18) subjects receiving supplemental oxygen, 7 (7/18, 39%) had no drop in SaO2, but developed respiratory acidosis. At the end of the case, 5/18 (28%) subjects had respiratory acidosis with normal PaO2. Significant hypercarbia and acidosis occurred frequently in this small study during CS in patients undergoing cardiac catheterization. Relying on pulse oximetry alone especially with patients on supplemental oxygen may lead to failure in detecting respiratory acidosis in a significant number of patients.

Global trends of pCO2 across the Cretaceous–Paleogene boundary supported by the first Southern Hemisphere stomatal proxy-based pCO2 reconstruction

Reliable reconstructions of atmospheric carbon dioxide concentrations (pCO2) are required at higher resolution than currently available to help resolve the relationship between mass extinctions and changes in palaeo-pCO2 levels. Such reconstructions are needed: 1, at a high temporal resolution for constraining the pre- and post-extinction atmospheres; and 2, at a sufficient spatial resolution to constrain potential inter-hemispheric differences. Here we estimate pCO2 based on fossil Lauraceae leaf cuticle specimens derived from three localities with strata spanning the latest Cretaceous to the mid-Paleocene, including a new Cretaceous–Paleogene boundary (K–Pg) locality, in New Zealand. We use two independent methods of stomatal density-based pCO2 reconstructions; a transfer function calibrated using herbarium material and the stomatal ratio method, producing three calibration sets. Our results based on the mean values of each of the three calibration methods indicate pCO2 ranging between ca. 460 and 650ppm during the latest Cretaceous, falling precipitously to average values between ca. 360 and 430ppm across the K–Pg boundary, and further to ca. 305–320ppm in the mid-Paleocene. A ‘spike’ of extremely high pCO2 at the K–Pg could not be confirmed, but our results are, nonetheless, consistent with previously published pCO2 records from the Northern Hemisphere, and show that stomatal density worldwide was responding to significant changes in pCO2 across the K–Pg.

Time to Steady State after Changes in FIO2 in Patients with COPD

Background: International guidelines recommend that when changing FIO2 in patients with COPD receiving Long-Term Oxygen Therapy (LTOT), 30 minutes should be waited for steady state before measurement of arterial blood gasses. This study evaluates whether 30 minutes is really necessary, as a smaller duration might improve the logistics of care, potentially reducing the time spent by patients at the out-patient clinic. Methods: 12 patients with severe to very severe COPD according to the GOLD guidelines were included. Patients had a median FEV1% of 23% of the predicted value (range 15–64%), median FEV1/FVC 0.43 (range 0.26–0.63), and chronic respiratory failure necessitating LTOT, 1–4 liters/minute, minimum 16 hours/day. Following a FIO2 reduction (wash out), arterial blood gases were measured at 0, 1, 2, 4, 8, 12, 17, 22, 32 and 34 minutes. FIO2 was then increased to baseline levels (wash in) and blood gasses measured at 0, 1, 2, 4, 8, 12, 17, 22, 32, and 34 minutes. Data were analyzed to examine the dynamics of arterial PO2 and saturation (SO2) wash out and wash in by calculating the time constants, tau (ô), and to evaluate the time required to reach values which might be considered clinically stable, defined as PO2 within 0.5 kPa and SO2 within 1% of equilibrium values. Results: For arterial PO2 values of time constants were about 3 minutes and similar for both wash out and wash in. A median of 5 minutes was required to reach clinically stable values of PO2 in both wash out and wash in, with 7–8 minutes sufficient in 75% of patients, and in the worst case 14 minutes. For SO2, values of the time constant were 4.5 and 1.4 minutes for wash out and wash in, respectively. The time required to reach clinically stable values was different in the two phases. For wash out the median time was 7.4 minutes, and in the worst case 15.6 minutes. For wash in the median time was 2.6 minutes and in worst case 6.8 minutes. No significant changes in PCO2 or pH were seen during FIO2 changes. Discussion/Conclusion: This study shows that oxygen equilibration relevant for clinical interpretation requires only 10 minutes following an increase and 16 minutes following a decrease in FIO2. over the range studied.

Oxygen as a regulator of tissue perfusion.

Tissue perfusion is regulated so that the supply of blood, and in particular the supply of oxygen, can always match the demand of each organ or tissue. Regulation is conducted through the functioning of smooth muscle cells which spiral around the median layers of arteries and arterioles. For cerebral blood vasculature, the bed is innervated by sympathetic (noradrenaline producing) nerves to mediate constriction, and by parasympathetic (acetylcholine producing) nerves to mediate dilation. It is known that cyclic nucleotides also act in the regulation of tissue perfusion, and that cyclic GMP is a mediator of blood vessel relaxation induced by drugs such as nitroglycerine and by agents that function through the stimulation of release of EDRF (now known to be nitric oxide,NO). Thus NO is also a potent vasodilator. Additionally other regulators are involved in the control of perfusion of particular organs or tissues. For example there are a number of peptides present within the nerve fibre network which serves the cerebrovascular bed1 and which are thought to input into cerebral blood flow. All of these regulators are known to be under the direct control of blood pCO2 and blood pH, and so at first sight it might seem unnecessary for oxygen to directly and independently regulate arteriole dilation and contraction. However there are a number of situations where changes in blood pH and pCO2 are not matched by physiologically proportionate changes in blood pO2 (for example during a metabolic acidosis). Additionally, significant changes in pCO2 or pH can be systemic or partly so, suggesting that pH and pCO2 effects can spill from one organ to another. Problems could be expected to arise downstream under such a chain of command, which could have particularly undesirable effects where organs are perfused primarily or significantly by venous blood. It is also known that there are systems in the body which require a different (generally higher) blood pressure for optimum performance, for example the kidneys and lungs. Thus there is a need for input into the regulation of blood perfusion at the level of the individual organ or system.1

Ventilatory and arousal responses to hypoxia and hypercapnia in a canine model of obstructive sleep apnea.

We have previously described a canine model of obstructive sleep apnea (OSA) in which sleep-wake state is monitored continuously by a computer that produces tracheal occlusion when sleep occurs. Our aim was to assess the effects of long-term application of this model on resting ventilation and on the ventilatory and arousal responses to hypercapnia and hypoxia. Five dogs were maintained on the model for 15.5 +/- 1.7 (mean +/- SE) wk, with a mean apnea index of 57.5 +/- 4.5 occlusions/h of sleep. Resting ventilation and the ventilatory and arousal responses to progressive hypoxic and hypercapnic rebreathing were assessed during wakefulness (W) and both slow-wave (SWS) and rapid-eye-movement (REM) sleep at baseline prior to intervention, at the end of the OSA phase, and following a 1 to 3-mo recovery period. During the period of OSA there were small changes in respiratory timing at rest, but no significant changes in PCO2 or SaO2. As compared with baseline, the ventilatory response to hypoxia during OSA was strikingly reduced during W, and significantly although less markedly reduced during SWS and REM. The reduction was due to a decreased breathing frequency response to hypoxia. In addition, during OSA there was a significant decrease from baseline in SaO2 at arousal during hypoxic rebreathing in both SWS and REM. All responses returned to normal during recovery. In contrast to hypoxia, hypercapnic ventilatory responses during OSA were slightly increased over their baseline values both in W and SWS, owing to a leftward shift of the ventilation-versus-PCO2 relationship. During recovery, these responses reverted partly to baseline for W and reverted completely to baseline for SWS. There were no significant changes in arousal PCO2 during hypercapnic rebreathing in either SWS or REM across the pre-OSA baseline, OSA, and post-OSA recovery periods. We conclude that long-term application of the OSA model is associated with a selective, reversible decrease in ventilatory and arousal responses to hypoxia.

Importance of correct handling of samples for the results of blood gas analysis.

The importance of correct handling of samples for blood gas analysis was studied in 100 patients. Sixty minutes storage in iced water lowered pH by 0.02 pH-units. Storage at room temperature caused considerable changes in PCO2 and PO2 (+0.45 kPa and -1.05 kPa). Air bubbles in the syringes increased PO2 if not expelled within 30 s. Thirty minutes storage with air trapped inside the syringe caused an increase in PO2 of 1.8 kPa and a decrease in PCO2 of 0.16 kPa. The use of plastic syringes induced significant changes in PCO2 and PO2, of which the latter (+1.0 kPa) may be clinically significant. The findings indicate that sample collection and storage must be guarded by strict rules in order to avoid false results.

Arterial blood gas tensions, hydrogen ion, and electroencephalogram during sleep in patients with chronic ventilatory failure.

We have studied arterial PO2, PCO2, and hydrogen ion and electroencephalogram during sleep in 10 patients with stable severe chronic respiratory failure. As a group the patients slept badly. Sleep was associated with a worsening of hypoxia and no significant change in PCO2 and H+. Two patients were restudied, receiving oxygen therapy overnight. Both had improved sleep but one, who had an intact hypoxic drive to breathing, developed marked hypercapnia and acidosis when his PO2 was restored to normal during sleep; the other, who had no hypoxic drive to breathing, developed no more hypercapnia or acidosis during sleep when breathing oxygen than when breathing air. Oxygen therapy may improve sleep disturbance in these patients, but its effect on the drive to breathing during sleep should be considered if severe hypercapnia and acidosis are to be avoided.