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Query: UMLS:C0020440 (hypercapnia)
7,939 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The effects of hypo-, normo- and hypercapnia on the variations in arterial oxygenation and their indices in critical patients with acute respiratory failure (ARF) receiving mechanical ventilation are studied. It is a prospective and randomized study carried out in multidisciplinary ICU. Fifteen ARF patients, intubated and mechanically ventilated, were studied within the first 48 h of evolution. Three stages were delimited: I) 30 min after the beginning of anaesthesia; II) 30 min after adding 30 cm of dead space (VD); III) 30 min after replacing the previous VD with VD of 60 cm. Ventilation parameters and FiO2 were kept stable. Stage I was characterized by respiratory alkalosis and stage II by normal acid-base balance with an increase in PaO2 (p < 0.01) and a decrease in intrapulmonary shunt (Qsp/Qt) (p < 0.001); the indices alveolar to arterial oxygen tension gradient [P(A-a)O2], respiratory index (R.I.) and estimated shunt (Est Shunt) also decreased significantly, whereas arterial to alveolar oxygen tension ratio (PaO2/PAO2) and arterial oxygen tension to inspired oxygen fraction ration (PaO2/FiO2) increased significantly. In stage III there was pure hypercapnic acidosis, with decreases in PAO2 (p < 0.001), P(A-a)O2 (p < 0.01) and R.I. (p < 0.05), while PaO2, Qsp/Qt, Est Shunt, PaO2/PAO2 and PaO2/FiO2 remained stable with respect to the previous situation. The observed PaO2 differs (p < 0.05) from the expected PaO2 in stage III. It is suggested that local or regional modifications of pulmonary perfusion are responsible for the observed variations. The P(A-a)O2 and R.I. indices do not make it possible to differentiate the causes of arterial hypoxemia in the presence of hypercapnia.
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PMID:The effect of hypo-, normo-, and hypercapnia induced by mechanical ventilation on intrapulmonary shunt. 780 Sep 19

Quantitative electroencephalography was assessed in 6 dogs anesthetized with 1.8% end-tidal halothane, under conditions of eucapnia, hypocapnia, and hypercapnia. Ventilation was controlled in each condition. Heart rate, arterial blood pressure, core body temperature, arterial pH, blood gas tensions, end-tidal CO2 tension, and end-tidal halothane concentration were monitored throughout the study. A 21-lead linked-ear montage was used for recording the EEG. Quantitative electroencephalographic data were stored on an optical disk for analysis at a later date. Values for absolute power of the EEG were determined for delta, theta, alpha, and beta frequencies. Hypocapnia was achieved by hyperventilation. Hypercapnia was achieved by titration of 5% CO2 to the inspired gas mixture. Hypercapnia was associated with an increase in the absolute power of the delta band. Hypocapnia caused an increase in the absolute power of delta, theta, and alpha frequencies. Quantitative electroencephalographic data appear to be altered by abnormalities in arterial carbon dioxide tension. Respiratory acidosis or alkalosis in halothane-anesthetized dogs may obscure or mimic electroencephalographic abnormalities caused by intracranial disease.
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PMID:Effects of altered arterial carbon dioxide tension on quantitative electroencephalography in halothane-anesthetized dogs. 801 90

We studied the effect of respiratory acidosis and respiratory alkalosis on acid-base composition and on microdissected renal adenosinetriphosphatase (ATPase) enzymes. Rats were subjected to hypercapnia or hypocapnia of 6, 24, and 72 h duration. After 6 h of hypercapnia, collecting tubule (CT) ATPases were not changed. At 24 h, plasma bicarbonate was 35 +/- 1 meq/l (P < 0.01) and CT H-ATPase and H-K-ATPase activities were 90% greater than controls (P < 0.01). By 72 h, plasma bicarbonate was 37 +/- 1 meq/l (P < 0.005 vs. control) and CT enzyme activity had increased even more, averaging approximately 130% of control (P < 0.05). Significant increases in enzyme activities were also observed in the proximal convoluted tubule and medullary thick ascending limb. Plasma aldosterone was three to four times that of control at all three time periods. In hormone-replete adrenalectomized rats, acid-base parameters and ATPase activities were the same as those seen in adrenal intact animals. After 6 h of hypocapnia, plasma bicarbonate was not significantly changed, but H-ATPase and Na-K-ATPase activities were decreased by 35% along the entire nephron (P < 0.05). H-K-ATPase activity in CT also decreased by 35%. At 24 h, plasma bicarbonate was 20.5 +/- 0.5 meq/l (P < 0.05 vs. control) and CT H-ATPase and H-K-ATPase activities were 60% less than control (P < 0.01). By 72 h, plasma bicarbonate was 18.5 +/- 0.5 meq/l (P < 0.05); however, only CT H-ATPase activity continued to fall, averaging 75% less than control (P < 0.005). Hypocapnia had no effect on plasma aldosterone or potassium. These results demonstrate that chronic, but not acute, respiratory acidosis stimulates activity of both renal proton ATPases. By contrast, both acute and chronic respiratory alkalosis decrease the two renal proton pumps. The stimulatory effect of hypercapnia and the inhibitory effect of hypocapnia on the renal ATPases appear to be potassium and aldosterone independent. Although the precise mechanisms for these results are not known, a direct effect of PCO2, pH, or changes in bicarbonate delivery may be involved.
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PMID:Effect of respiratory acidosis and respiratory alkalosis on renal transport enzymes. 809 53

Acute hyperosmolality in the Pekin duck results in an extracellular acidosis and hypercarbia without any stimulation of ventilation. The development of the extracellular acidosis is accompanied by the concurrent development of an intracellular alkalosis systemically which has been hypothesized to depress ventilation (Kasserra et al., J. Appl. Physiol., 1993). In order to investigate this apparent suppression of ventilation, the ventilatory response to various respiratory challenges (CO2, O2, K+) was studied both before (normosmotic) and after (hyperosmotic) hypertonic sucrose infusion. Increased plasma osmolality caused a significant drop in arterial pH of 0.06 +/- 0.01 units and a 4 Torr increase in PaCO2, yet did not stimulate any significant increase in ventilation despite a significant increase in oxygen consumption. Acute hyperosmolality increased the PaCO2 associated with resting ventilation, and decreased the magnitude of the ventilatory response to a given increase in PaCO2, compared with the response to the same ventilatory challenge in normosmotic animals. Acute hyperosmolality increased the ventilatory response to hypoxia and K+ compared with normosmotic animals. The opposite effect of hyperosmolality on the ventilatory responses to hypercapnia compared with hypoxia suggests that the mechanisms of chemoreception for hypercapnia and hypoxia are different. The depressed ventilatory response curve to increased PaCO2 and decreased arterial pH during hyperosmolality, both alone and during the hypercapnic challenge, suggests that the peripheral chemoreceptor response to pH and CO2 is suppressed. It is hypothesized that the suppression results from the intracellular alkalosis occurring during acute hyperosmolality.
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PMID:Hyperosmolality alters the ventilatory response to acute hypercapnia and hypoxia. 827 90

Uremic acidosis accompanies chronic renal failure in hemodialysis patients because of a retention of nonvolatile acids. Standard bicarbonate (39 mEq/L) and acetate (38 mEq/L) dialysates do not completely correct the acidosis. The acid-base and biochemical effect of a high-bicarbonate (42 mEq/L) dialysate was evaluated in 38 patients during high-efficiency and high-flux dialysis over 12 wk. All patients were dialyzed on standard bicarbonate dialysate before the study and for 8 wk after the study. In order to monitor potential excessive alkalosis, predialysis and postdialysis arterial blood gases were measured in seven patients who initially had a normal predialysis pH. Serum chemistries revealed no significant changes in predialysis BUN, calcium, ionized calcium, or phosphorus during the 12-wk study. There was no change in postdialysis ionized calcium or phosphorus. Predialysis and postdialysis serum total CO2 (STCO2) increased over the 12-wk study (P < 0.0001). By week 12, 75% of the hemodialysis patients had an STCO2 > 23 mEq/L and no patient had an STCO2 > 30 mEq/L predialysis. After the 8-wk washout, all chemistries were no different from prestudy concentrations. Predialysis blood gases in seven patients with normal predialysis HCO3 revealed a significant increase (P < 0.009) in PCO2 and HCO3 over the 12-wk study; predialysis pH and PO2 did not change. There was no significant change in postdialysis blood gases. It was concluded that: (1) a high-bicarbonate dialysate corrects predialysis acidosis in 75% of hemodialysis patients without causing progressive alkalemia, hypoxia, or hypercarbia; and (2) predialysis BUN, calcium, ionized calcium, and phosphorus are unaffected by high-bicarbonate dialysate.
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PMID:Normalization of uremic acidosis in hemodialysis patients with a high bicarbonate dialysate. 813 52

It is well known that the incidence of cardiac arrhythmia is particularly high in patients with chronic respiratory insufficiency (CRI). This study examines the prevalence, incidence and prognostic clinical importance of arrhythmia occurring during the course of CRI on the basis of data taken from the literature and the authors' personal experience using dynamic electrocardiographic diagnosis (24-hour Holter monitoring). The majority of arrhythmias observed in these patients appeared to take the form of premature ventricular and/or supraventricular beats and less frequently of atrial fibrillation and/or attacks of supraventricular paroxysmal tachycardia. Cardiac rhythm alterations were observed using Holter monitoring in 70-90% of patients. No cardiac rhythm disorder is specific to this pathological condition. The aim of this study was to formulate, as far as was possible, a rational therapeutic approach which took account of the electrogenesis of arrhythmic phenomena, variations in the type of arrhythmia and the hemodynamic conditions under which they occur. The etiopathogenesis of arrhythmias within the framework of CRI is relatively complex and probably multifactorial since there are a number of concomitant pathological conditions able to trigger off arrhythmogenic processes both inducing the onset of reflux circuits and enhancing cardiac automatism centres. Many studies correlate the presence of arrhythmia with hypoxemia, hypercapnia and both respiratory and metabolic alkalosis. Even the combined effect of hypoxia with respiratory acidosis and the integrity or otherwise of cardiac function (chronic pulmonary heart, right ventricular hypertrophy, ischemic cardiopathy) have a notable pro-arrhythmic effect. Hypokalemia induced by both respiratory alkalosis and by drugs used during the course of CRI (eg diuretics and/or steroids) may induce a marked dispersion of refractory periods of the various fibrocells thus encouraging the onset of arrhythmia. With regard to drugs, it has been observed that both digitalis and theophylline and beta-2 stimulants if frequently used during the course of CRI may possibly induce arrhythmia. It is therefore important to underline that they should be used with particular caution. As far as concerns the use of beta-2 adrenergic compounds, it is advised that they be administered using an aerosol rather than systemic route. Digitalis has limited indications; the molecules of the methylxanthine classes require careful pharmacological dose monitoring. Arrhythmic therapy should also be seen in terms of prophylaxis and the correction of predisposing and decisive factors such as hypoxemia, hypercapnia, hemoglobin and electrolyte levels, and alterations in blood pH following the obstruction of small airways.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:[Respiratory insufficiency and cardiac arrhythmia: the rationale of treatment]. 833 38

The purpose of the first study was to identify the relationship between reflex sympathetic nerve activity and plasma concentration of lidocaine. Lidocaine was infused in 4 different doses: 2 mg.kg-1 bolus + 100 micrograms.kg-1 x min-1, 3 mg.kg-1 bolus + 200 micrograms.kg-1 x min-1, 6 mg.kg-1 bolus + 400 micrograms.kg-1 x min-1 and 12 mg.kg-1 bolus + 800 micrograms.kg-1 x min-1. Baroreflex depressor and pressor tests using sodium nitroprusside (5-10 micrograms.kg-1) and phenylephrine (2-4 micrograms.kg-1) were performed before and at 10 min after the start of lidocaine infusion. Plasma lidocaine concentrations determined by HPLC revealed that its steady-state levels were maintained during the baroreflex tests. Baroreflex sensitivity was preserved at clinical concentrations of lidocaine (< 5 micrograms.ml-1). However, baroreflex was significantly attenuated when plasma lidocaine concentrations were above seizure levels (> 10 micrograms.ml-1). This result indicates that hemodynamic derangement observed in the lidocaine-induced CNS toxicity is, at least in part, due to the attenuated arterial baroreflex. In the second study, the author evaluated the effect of respiratory acidosis and alkalosis on the baroreflex with or without lidocaine infusion (2 mg.kg-1 + 100 micrograms.kg-1 x min-1). Respiratory acidosis (PaCO2: 65.6 +/- 3.4) enhanced the baroreflex significantly, but lidocaine infusion abolished this acidosis-induced enhancement. The author concludes that hypercarbia should be avoided in patients receiving intravenous lidocaine infusion.
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PMID:[Effect of intravenous lidocaine infusion on arterial baroreflex]. 851 40

We used extracorporeal perfusion of the vascularly isolated carotid sinus region to determine the effects of specific carotid body chemoreceptor hypocapnia-alkalosis on ventilatory control in the unanesthetized dog. Eight female dogs were studied during wakefulness, non-rapid-eye-movement (NREM) sleep, and rapid eye movement (REM) sleep. Carotid body perfusions lasted from 1 to 2 min, and each trial was preceded by a 1-min control period. Two levels of carotid body hypocapnia were employed, approximately 7 and 14 Torr below eupneic levels in a given dog. We found that 1) During wakefulness and NREM sleep, carotid body hypocapnia caused reduced tidal volume (VT) but not apnea or expiratory time prolongation. 2) The inhibition of ventilation in response to carotid body hypocapnia was graded below normocapnia, showing the highest sensitivity at carotid body PCO2 near 7 Torr below eupneic values. Inhibition reached a maximum near 14 Torr below the eupneic level; VT, inspiratory minute ventilation (VI), and VT-to-inspiratory time ratio fell 31, 23, and 27% in wakefulness and 30, 23, and 30% in NREM sleep. 3) Reductions in ventilation in response to carotid body hypocapnia are lessened but still persist throughout perfusion (up to at least 130 s) despite significant systemic hypercapnia. 4) During REM sleep, carotid body hypocapnia had no consistent inhibitory effect on ventilation until carotid body PCO2 was reduced to values near 14 Torr below the eupneic level, at which point ventilation was similar to wakefulness and NREM. 5) Moderate carotid body hypocapnia was as effective as carotid body hyperoxia in reducing VT and VI. We conclude that carotid body hypocapnia-alkalosis can significantly inhibit eupneic VT and ventilation during wakefulness and NREM sleep and, if the hypocapnia is severe enough, during REM sleep.
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PMID:Ventilatory effects of specific carotid body hypocapnia in dogs during wakefulness and sleep. 856 4

Acute hyperosmolality results in an extracellular dilution acidosis and hypercarbia that does not stimulate ventilatory compensation. The osmotic stress is also associated with shifts in water and electrolyte balance and an increase in intracellular pH. The alkaline intracellular pH was hypothesized to have a role in preventing a normal respiratory response to the extracellular acidosis and hypercarbia. Therefore, this study examined the effect of ion-exchange blockade on intra- and extracellular pH and ventilation during acute hyperosmolality in the Pekin duck (Anas platyrhynchos) by using 31P-nuclear magnetic resonance spectroscopy. Both 4,4'-diisothiocyanostilbene-2,2'-disulfonic acid (DIDS) and amiloride inhibited the development of the intracellular alkalosis that normally develops in muscle during acute hyperosmolality. Instead, exposure to hyperosmotic stress during ion-exchange blockade resulted in a significant acidosis both intracellularly and extracellularly. Arterial pH decreased 0.10 +/- 0.04 pH unit with a sucrose infusion after either blocker, and intracellular pH decreased 0.11 +/- 0.06 and 0.16 +/- 0.04 pH units with a sucrose infusion after DIDS and amiloride, respectively. Ventilation increased 79 +/- 28 and 122 +/- 100%, respectively, during acute hyperosmolality after ion-exchange blockade with either DIDS or amiloride. The results suggest that intracellular pH may play a role in the ventilatory response to acid-base perturbations. The data also indicate that both Cl-/HCO3- and Na+/H+ exchanges are involved in the development of the intracellular alkalosis during hyperosmotically induced extracellular acidosis.
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PMID:Dilution acidosis: evidence for a role of intracellular pH in the control of ventilation. 872 70

With the use of isolated perfused rabbit lungs (n = 152), roles of endothelium-derived relaxing factor (EDRF) in pulmonary vascular responses to hypocapnia and hypercapnia were studied. Lungs were ventilated with a gas mixture containing 1, 5, or 10% CO2 and 21% O2, adjusting the perfusate pH to 7.8, 7.4, or 7.1, respectively. Methemoglobin (MetHb), hemoglobin (Hb), methylene blue (MB), and L-argininosuccinic acid (L-ASA) were used as modulators of EDRF. To eliminate augmented shear stress, we used papaverine during hypercapnia. As a measure of EDRF, we spectrophotometrically examined nitric oxide (NO) metabolites in the perfusate. Hypocapnia and hypercapnia evoked, respectively, unsustainable vasodilatation and vasoconstriction. Hb, MB, and L-ASA, but not MetHb, produced an increase in baseline pulmonary arterial pressure (Ppa). These agents also exacerbated vasoconstriction during hypercapnia. Hypercapnia and hypocapnia caused an increase and decrease, respectively, in EDRF production. L-ASA suppressed EDRF production in hypercapnic lungs. Papaverine did not suppress EDRF production under hypercapnia. In conclusion, 1) the effects of pH on pulmonary circulation are transient, 2) the increase in Ppa caused by hypercapnia is modulated by EDRF, and 3) the pulmonary EDRF genesis is activated by hypercapnic acidosis but suppressed by hypocapnic alkalosis.
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PMID:Endothelial modulation of pH-dependent pressor response in isolated perfused rabbit lungs. 876 59


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