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PubMed1994

Intraluminal "balloonless" air tonometry: a new method for determination of gastrointestinal mucosal carbon dioxide tension.

OBJECTIVE: To determine if air introduced directly into the lumen of a hollow viscus can be used instead of fluid in a Silastic balloon to estimate gastrointestinal mucosal PCO2. DESIGN: Prospective, unblinded comparison of two methods of mucosal PCO2 measurement. SETTING: Animal surgery suite at a large, university-affiliated medical center. INTERVENTIONS: Standard, commercially available, tonometric catheters were positioned in the ileum (n = 4) or the stomach and ileum (n = 12) of anesthetized, immature Yorkshire swine. Using gas-tight purse-string sutures, plastic cannulas were inserted into the lumen of the stomach (n = 12) and the lumen of a 10-cm isolated segment of ileum (n = 16). Data were collected after equilibration periods of 30 or 60 mins. Before each equilibration period, the "air tonometers" (i.e., the lumens of the stomach and/or the isolated ileal segment) were lavaged with 200 mL (stomach) or 20 mL (ileum) of air. In group 1 (n = 4) and group 2 (n = 3), graded degrees of mesenteric hypoperfusion were achieved by mechanical mesenteric occlusion or pericardial tamponade, respectively. In group 3 (n = 8), graded degrees of respiratory acidosis were induced. At various intervals, PCO2 was determined simultaneously in arterial blood, gastric air, saline from the gastric tonometric balloon, ileal air, and saline from the ileal tonometric balloon. MEASUREMENTS AND MAIN RESULTS: In pigs with ischemia created by mesenteric vascular occlusion (group 1), there was a moderate correlation between PCO2 values in air samples from the ileal lumen and samples of saline from the standard tonometer (r2 = .61, p < .001). In pigs with mesenteric ischemia secondary to pericardial tamponade (group 2), air and saline tonometry were well-correlated in the stomach (r2 = .71, p < .001) and ileum (r2 = .83, p < .001). In pigs with normal mesenteric perfusion (group 3) and PaCO2 > 40 torr (5.3 kPa), PaCO2 correlated with ileal mucosal PCO2, determined using air (r2 = .93, p < .001) or saline (r2 = .91, p < .001) tonometry, or gastric mucosal PCO2, determined using air (r2 = 1.00, p < .001) or saline (r2 = .97, p < .001) tonometry. Values obtained by air tonometry were highly correlated with values obtained using standard saline tonometry in the stomach (r2 = .98, p < .001; bias = -5 +/- 5 torr [-0.65 +/- 0.65 kPa]) or ileum (r2 = .96, p < .001; bias = 1 +/- 9 torr [0.13 +/- 1.17 kPa]). CONCLUSIONS: a) Under stable hemodynamic and respiratory conditions, air tonometry (which, in theory, can be performed using a conventional nasogastric or nasoenteric feeding tube) estimates gastrointestinal mucosal PCO2 as accurately as standard saline tonometry in the stomach or ileum; b) respiratory acidosis leads to tissue hypercarbia, a phenomenon that must be considered when tonometry is used to guide therapy in the clinical setting; c) under stable, nonischemic conditions, gastric or intestinal tonometry can be used to estimate PaCO2.

Acidosis↗
PubMed1992

[Erythrocyte membrane band 3 protein and HCO3-/Cl- exchange function in cor pulmonale patients].

The changes of erythrocyte membrane band 3 protein, blood gases and electrolytes of intraerythrocyte and extra-erythrocyte were investigated in 3 groups: type I respiratory failure (group I, n = 36), type II respiratory failure (group II, n = 33) and control group (CG, n = 50). The distribution of band 3 protein was narrow and the staining intensity of band 3 protein was lower in the electrophotogram of group II. The relative composition of band 3 protein in group II was significantly lower than that in group I and CG (P less than 0.01). The intraerythrocyte HCO3- in group II was significantly higher than that in group I and CG (P less than 0.01), but the extra-erythrocyte Cl- in group II was significantly lower than that in group I and CG (P less than 0.01). These findings suggested that (1) The relative composition reduction of erythrocyte membrane band 3 protein and HCO3-/Cl- exchange restrain may be one of the reasons that aggravated CO2 retention and respiratory acidosis in cor pulmonale patients with type II respiratory failure. (2) Because there was hypochloremia in the most cor pulmonale patients with type II respiratory failure, it was necessary to supply them enough chloride in time, which could not only correct hypochloremia, but also accelerate the rate of HCO3-/Cl- exchange and promote to eliminate CO2.

Acidosis, Respiratory↗
PubMed1983

Regulation of CSF composition--blocking chloride-bicarbonate exchange.

The possibility that the increase in cerebrospinal fluid (CSF) [HCO-3] observed during respiratory acidosis could be the result of a decrease in CSF [Cl-] was studied by blocking a putative Cl--HCO-3 exchange transport system. Anesthetized dogs (pentobarbital 30 mg, iv) were given either 4,4'-diisothiocyano-2,2'-disulfonate stilbene (DIDS, 0.02 mumol/kg) or pyridoxal 5-phosphate (P-5-P, 4 mumol/kg) in the lateral cerebral ventricles and maintained either normocapnic (RA) or hypercapnic (5% CO2). CSF and arterial Pco2, pH, [Na+], [K+], [Ca2+], [Cl-], and [lactate] were determined. [HCO-3] was calculated. Samples were drawn before and 4 h after the drug was administered. In control dogs on RA no significant change was observed in any measured parameter after 4 h. Dogs receiving either DIDS or P-5-P and on RA had decreased CSF [Na+] of 2-4 meq/l and CSF [Cl-] of 6 meq/l. CSF [HCO-3] in DIDS dogs decreased approximately 5 meq/l. There was no significant change in CSF [HCO-3] in P dogs. After 4 h of 5% CO2, control dogs had decreased CSF [Cl-] of 3 meq/l and CSF [HCO-3] increased approximately 4 meq/l. Dogs receiving DIDS or P-5-P and breathing 5% CO2 for 4 h had decreased CSF [Cl-] of 6-9 meq/l and [HCO-3] increased of 7-9 meq/l. CSF [Na+] did not change during respiratory acidosis in any group. It was concluded the Cl- transport in CSF can be interfered with by use of blocking agents which inhibit Cl--HCO-3 exchange channels.

4,4'-Diisothiocyanostilbene-2,2'-Disulfonic Acid↗
PubMed1997

[A 85-year-old woman with one year history of convulsion, dementia, and consciousness disturbance].

We report a 85-year-old woman who died after one year history of convulsion, dementia, and consciousness disturbance. She was apparently well until January 6, 1995 when she was 85 year old; on that evening, she suddenly stated that some one was in her room and she became confused. A local MD gave her diazepam and she fell into sleep. At 3 o'clock in the following morning, she developed tonic-clonic convulsion in her right lower extremity which showed a march to her right upper extremity and the left lower extremity. She was admitted to our hospital. On admission, she was comatose with respiratory acidosis. She was intubated and placed on a ventilator. She was treated with intravenous phenytoin. She gradually gained consciousness and became alert. Respiration became normal. Her MRI revealed ventricular dilatation, fronto-parietal cortical atrophy, and a T1-low and T2-high signal intensity lesion in the left occipital lobe. She was discharged for out patient follow-up on February 4, 1995. Since then, she noted loss of memory and small step gait. A follow-up CT scan revealed a mass lesion which showed a ring-shaped enhancement in the left occipital lobe and was admitted again. On admission, she was alert but markedly demented. The optic fundi was unremarkable, but she appeared to have right homonymous hemianopsia. No motor weakness was noted. In Gd-DTPA enhanced MRI, the above tumor showed a ring enhancement. The diagnosis of glioblastoma was entertained, however, considering her age, she was treated with intravenous glycerol and intramuscular steroid. She was discharged for out-patient follow-up on July 15, 1995. Her gait disturbance had progressively become worse and she developed nausea and vomiting and was admitted again on October 2, 1995. On admission, she was somnolent and markedly demented. Brain stem responses were retained normally. She was unable to stand or walk. Deep tendon reflexes were slightly increased in the right upper extremity and the plantar response was extensor on the right. Her hospital course was complicated by respiratory tract infection and respiratory acidosis. She expired on November 2, 1995. The patient was discussed in a neurological CPC and the chief discussant arrived at the conclusion that she had a glioblastoma involving the left occipital lobe and the adjacent areas. Post-mortem examination revealed an infiltrating tumor in the left occipital lobe. On microscopic examination, the tumor was very cellular; nuclear atypism was marked and tumor cells undergoing mitosis were seen. In some areas, capillary proliferation was seen. Histologic characteristics were consistent with glioblastoma.

Aged↗
PubMed2000

[Significance of respiratory compensation in acidosis in calves].

The respiratory component PvCO2 of acid-base-status was observed in n = 36 calves (age: x +/- s = 8.7 +/- 5.0 d) with neonatal diarrhea and an acidosis (venous blood-pH: < 7.30; x +/- s = 7.08 +/- 0.15). In n = 10 (28%) calves with a severe metabolic acidosis (pH: x +/- s = 7.03 +/- 0.12; BE: x +/- s = -22.1 +/- 5.3 mmol/l) the PvCO2 was decreased < 5.3 kPa (x +/- s = 4.5 +/- 0.5 kPa) and showed a distinct respiratory compensation. A PvCO2 between 5.3-6.7 kPa (x +/- s = 6.0 +/- 0.4 kPa) was observed in n = 16 (44%) acidotic calves (pH: x +/- s = 7.11 +/- 0.13; BE: x +/- s = -15.2 +/- 7.4 mmol/l). These n = 26 (72%) calves showed a simple metabolic acidosis which is well known for calves with neonatal diarrhea. The remaining n = 10 (28%) calves showed an increase of the PvCO2 > 6.7 kPa (x +/- s = 8.0 +/- 1.5 kPa). These animals had a mixed respiratory-metabolic acidosis (pH: x +/- s = 7.08 +/- 0.20; BE: x +/- s = -13.9 +/- 10.3 mmol/l), as the decrease of the pH could not be determined by the decreased metabolic component HCO3- of acid-base-status alone. Calves which died during hospitalization and calves with a PvCO2 > 6.7 kPa tended to be younger and showed partially significant lower values for the parameters of oxygen-supply PvO2 and SvO2. Lactate was significantly higher in dying calves but not in calves with a mixed acidosis which on the other hand were more dehydrated. The functional capacity of respiratory compensation of acidotic disorders in the calves studied promised to be almost the same as in dog and man. One reason for the failure of respiratory compensation in some calves could be a more severe hypovolemia. With the use of "venous hypoxemia" (decrease PvO2 and decrease SvO2) the detection of tissue hypoxia was easier than with lactate concentration.

Acidosis↗
PubMed1989

Basolateral membrane H-OH-HCO3 transport in the proximal tubule.

This review focuses on the basolateral membrane mechanisms of H-OH-HCO3 transport in the proximal tubule. The mechanism that has the greatest transport capacity and mediates most of transepithelial H-HCO3 transport is the electrogenic, Na-3HCO3 cotransporter. This transporter has been extensively characterized in the salamander, rat, and rabbit proximal tubule, and has now been found in a number of other epithelia that effect transepithelial NaHCO3 transport. Transporter rate is sensitive to intra- and extracellular [Na], intra- and extracellular [HCO3]/pH, and cell voltage. Adaptations in transporter activity have been demonstrated in chronic metabolic acidosis and alkalosis, chronic respiratory acidosis and alkalosis, and chronic hyperfiltration. In addition to the Na-3HCO3 cotransporter, the basolateral membrane possesses both Na-dependent and -independent Cl-HCO3 exchangers, a H leak, and in the S3 proximal tubule an Na-H antiporter. The role of these H-OH-HCO3 transport mechanisms in transcellular HCO3 and Cl absorption and pHi defense is discussed.

Animals↗
PubMed1977

An analysis of changes in blood pH following exhausting activity in the starry flounder, Platichthys stellatus.

Exhausting activity results in a marked and immediate drop in blood pH which gradually returns to normal over the following 6h. The acidosis is caused largely by elevated Pco2 levels, which vary inversely with pH. Blood lactate concentration increases slowly, reaching a maximum at 2--4h post-exercise, and contributes significantly to the acidosis only late in the recovery period. The slow time course of lactic acid release into the blood permits temporal separation of the peak metabolic acidosis from the peak respiratory acidosis. Evidence is presented that a metabolic acid other than lactic also makes a modest contribution to the pH depression during the recovery period.

Acid-Base Equilibrium↗
PubMed1982

Long-term submergence at 3 degrees C of the turtle Chrysemys picta bellii in normoxic and severely hypoxic water. III. Effects of changes in ambient PO2 and subsequent air breathing.

Western Painted Turtles, Chrysemys picta bellii (N = 5), were maintained submerged and apneic for 90 days: days 0-21 in severely hypoxic water (PO2 = 0-5 mmHg), days 22-43 in aerated water (PO2 approximately 160 mmHg), and days 44-90 again in hypoxic water. From day 90 onward, the water was aerated and the turtles were allowed access to the air; water and air temperatures were maintained at 3 degrees C. Arterial blood samples were taken periodically and analysed for PO2, PCO2, pH, [Na+], [K+] [Cl-], [lactate-], [glucose] and haematocrit. Plasma [HCO3-] was calculated for all samples and total plasma calcium was measured on samples from two animals. Each exposure to low PO2 water caused progressive lactic acidosis and a transient respiratory acidosis with an accompanying fall in plasma [Cl-] and rise in plasma [K+] and [calcium]. During the intervening period in aerated water, blood pH recovered significantly (from 7.33 to 7.74 in 7 days), due primarily to a fall in PCO2 (from 23.5 to 10.6 mmHg), while [lactate-] remained unchanged (at about 50 mM), and [HCO-3] rose slightly. Plasma [K+] promptly returned to nearly normal values. When permitted to breathe on day 90, the three surviving turtles rapidly restored pH to normal by pronounced hyperventilation (PCO2 less than 5 mmHg). Metabolic acidosis, however, disappeared slowly with a t1/2 for [lactate-] and [HCO-3] restoration of about 2 weeks. We conclude that a wintering turtle can stabilize or even slightly improve its acid-base and ionic status by moving from an anoxic environment to well-oxygenated water. Further improvements can be gained by breathing air, but recovery proceeds at a very slow rate if the animal remains at 3 degrees C.

Acclimatization↗
PubMed1980

The role of pH and the lack of a requirement for hydorgencarbonate in the regulation of hepatic glutamine metabolism.

The rate of net glutamine degradation in non-recirculating perfused rat liver was estimated by the release of urea, ammonia and alanine in steady states of operation of glutaminase. Corrected for a slight intracellular accumulation of glutamate, accounting for 7% of the flux at 5mM glutamine, the estimated glutaminase activity agrees well with measurements of glutamine removal described in the literature for recirculating perfusion experiments. Glutaminase activity was decreased when the perfusate pH was lowered (i) by infusion of hydrochloric acid, (ii) by increasing the CO2 concentration, or (iii) by decreasing the hydrogencarbonate concentration. Conversely, it was increased when the perfusate pH was increased by infusion of sodium hydroxide or by increasing the hydrogencarbonate concentration. However, glutaminase activity did not depend on medium hydrogencarbonate. When the hydrogencarbonate buffer system was replaced by DMO or by Hepes equilibrated with O2 (no CO2 present), there was practically no change in the observed rates. These results, obtained in an iso-pH system, are in contrast to recent suggestions of a role of hydrogencarbonate in the regulation of glutamine metabolism based on results from incubations of isolated mitochondria or hepatocytes. It is concluded that the conservation of glutamine by the inhibition of hepatic glutaminase, which provides glutamine for the pH regulation by renal glutaminase, can be increased not only in metabolic acidosis but also in respiratory acidosis associated with high hydrogencarbonate concentration.

Alanine↗
PubMed1992

[Abnormalities in acid-base balance in the elderly].

Physiological decline in the ability to adjust acid-base balance and increase the incidence of diseases with aging, modifies pathophysiological and clinical features of acid-base disturbance in the elderly. Regulation of pH ultimately depends on the kidney and lung, however, the ability of the two organs is decreased with physiological aging. Moreover, the elderly are more prone to suffer from renal insufficiency and/or chronic obstructive pulmonary disease. Furthermore, medication with various drugs, such as diuretics, often affect the acid-base balance in the elderly. This paper describes the characteristics of the abnormalities in acid-base balance in the elderly, including metabolic acidosis and alkalosis, and respiratory acidosis and alkalosis.

Acid-Base Imbalance↗
PubMed1980

Effects of changes in acid-base balance on neuromuscular blockade produced by ORG-NC 45.

The effects of acute acid-base changes on the neuromuscular blocking action of ORG NC 45 (a monoquaternary homologue of pancuronium) were measured in 10 cats, utilizing a constant infusion technique. Partial NC 45 blockade was antagonized slightly in the tibialis, soleus, and diaphragm during respiratory alkalosis (pH 7.53; PaCO2 1.9 kPa), whereas metabolic alkalosis (pH 7.64; Paco2 3.5 kPa) produced significant antagonism of NC 45 block in those muscles. Respiratory acidosis (pH 6.98; Paco2 10.3 kPa) and metabolic acidosis (p H 7.13; PaCO2 4.9 kPa) significantly potentiated partial NC 45 blocks in the tibialis, soleus, and diaphragm (except in the diaphragm during metabolic acidosis). Cumulative dose responses studied in six cats showed that the NC 45 dosage required to produce 85--95% tibialis block was slightly greater than controls during respiratory and metabolic alkalosis. Conversely, significantly less NC 45 was needed to produce the same degree of block during respiratory and metabolic acidosis. In vitro studies in rat hemidiaphragms likewise showed minimal NC 45 block antagonism when pH was raised to 7.68, and significant potentiation under acidotic conditions (pH 7.05). These actions are attributed in part to an increased rate of NC 45 metabolism by alkaline hydrolysis in alkalotic states and greater molecular stability during acidosis. Possible clinical implications are discussed.

Acidosis↗
PubMed1989

Therapy of acute bronchospasm. Complicated by lactic acidosis and hypokalemia.

Hypokalemia and lactic acidosis developed following correction of respiratory acidosis in a 5-year-old child who presented with respiratory failure secondary to severe asthma and treated with theophylline, inhaled albuterol, and parenteral methylprednisolone. Calculation of the "anion gap" that provided the clue to presence of lactic acidosis was confirmed by the measurement of serum lactate level.

Acidosis, Lactic↗
PubMed1975

Influence of hematocrit, blood gas tensions, and pH on pressure-flow relations in the isolated canine lung.

An isolated perfused canine lung preparation in which determinants of vascular caliber could be individually controlled was developed. The relation of pulmonary arterial (Pa), venous (PV), and alveolar (PA) pressures was such that Pa greater than PA greater than PV throughout the whole lung. The addition of isoprenaline to the perfusate abolished vascular reactivity. Once stability was reached, vascular cross-sectional area remained acceptably constant for 2.25 hours as judged by normalized conductance. The influence of perfusate hematocrit, blood gas tensions, and pH on pressure-flow relations was then studied in 15 isolated canine lungs. The hematocrit-vascular conductance relation was derived at constant perfusion pressure. Conductance varied linearly with hematocrit over a range of 16.5 to 89.5%. Mean pulmonary arterial blood gas tensions were: PO2 = 121 mm Hg, PCO2 = 28 mm Hg, and pH = 7.46. Acute respiratory acidosis (PO2 = 30 mm Hg, PCO2 = 81 mm Hg, pH = 7.17) and lactic acidosis and hypoxemia (PO2 = 32 mm Hg, PCO2 = 21 mm Hg, pH = 6.96) did not significantly alter this relation. Transformation of the conductance-hematocrit data indicated that hematocrit was the most important determinant of relative apparent viscosity of the blood. Both acute respiratory and lactic acidosis failed to significantly increase relative viscosity within the range of hematocrit usually found in secondary polycythemia.

Acidosis↗
PubMedDate not supplied

Myocardial contractility recovery during hypercapnic acidosis: its dissociation from recovery in pHi by ryanodine.

Myocardial contractility falls quickly during respiratory acidosis but if acidosis is maintained a slow gradual return towards control state is detected. In cat papillary muscle, changes in developed tension (DT) during isometric contractions (pacing rate 0.2 Hz) and intracellular pH (pHi) were continuously monitored before and during hypercapnia to study the contribution of pHi recovery to the recovery of contractility. On exposure to hypercapnia (extracellular pH [pHo] = 6.90) DT fell to 50.33 +/- 2.20% of control and pHi decreased from 7.21 +/- 0.05 to 6.90 +/- 0.02. After 30 mins of hypercapnia DT recovered to 64.66 +/- 4.05% of control, but no significant recovery in pHi was detected. Intracellular sodium concentration slowly rose to 61.05 +/- 23.79% over basal level 10 mins after the onset of hypercapnia and it remained elevated for 10 mins before gradually returning to control levels. When pHo was kept at 7.40 during hypercapnia by increasing sodium bicarbonate concentration, DT recovered to 79.11 +/- 6.94% of control after 30 mins of hypercapnia, while a significant recovery of pHi (0.12 +/- 0.02 pH units) was detected. Low extracellular sodium concentration diminished contractility recovery during hypercapnia without changing the initial decrease in DT. 5-[N-ethyl-N-isopropyl] amiloride (EIPA) (5 microM) increased the initial fall in DT to 34.33 +/- 8.68% of control and abolished the recovery. Sarcoplasmic reticulum (SR) inhibition by ryanodine (0.5 microM) markedly reduced the recovery of contractility without altering the recovery in pHi.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis, Respiratory↗
PubMed1992

Contraction and intracellular Ca2+, Na+, and H+ during acidosis in rat ventricular myocytes.

We have investigated the effect of a CO2-induced (respiratory) acidosis on contraction and on intracellular Ca2+, Na+, and pH (measured using the fluorescent dyes fura-2, sodium-binding benzofuran isophthalate, and 2',7'-bis(carboxyethyl)-5,6-carboxyfluorescein, respectively) in ventricular myocytes isolated from rat hearts. Initial exposure to acidosis led to a rapid decrease in intracellular pH that was accompanied by an abrupt decline in contractility. There were no consistent changes of intracellular Na+ or Ca2+ during this period. The rapid decline of contractility was followed by a slower partial recovery, which was accompanied by increases in intracellular Na+, systolic and diastolic Ca2+, and an increase in the Ca2+ content of the sarcoplasmic reticulum (estimated using caffeine). Intracellular pH did not change during this slow recovery. The slow rise of intracellular Na+ and the recovery of the twitch were blocked by the Na(+)-H+ exchange inhibitor amiloride. The sarcoplasmic reticulum inhibitor ryanodine blocked the recovery of the twitch but had no effect on the rise of intracellular Na+ induced during acidosis. It is concluded that a major cause of the initial decline of the twitch during acidosis is a decrease in the response of the contractile proteins to Ca2+ due to the decrease of intracellular pH. The subsequent slow recovery of the twitch is due to the decrease of intracellular pH activating the Na(+)-H+ exchange mechanism. This elevates intracellular Na+ and presumably, via the Na(+)-Ca2+ exchange mechanism, intracellular Ca2+. This in turn may lead to increased Ca2+ loading of, and hence release from, the sarcoplasmic reticulum, and it is this that underlies the partial recovery of contraction during acidosis in this preparation.

Acidosis↗
PubMed1992

Critical role of bicarbonate in calcium release from bone.

Calcium release from cultured bone is pH dependent; net calcium flux (JCa) from bone increases with decreasing pH. At a similar decrement in pH there is greater JCa when acidosis is produced by a low medium bicarbonate concentration ([HCO3-]), a model of metabolic acidosis (Met), compared with an increased medium PCO2, a model of respiratory acidosis (Resp). To separate the role of [HCO3-] from that of pH in inducing JCa we cultured calvariae for 3 h under three different neutral (pH approximately 7.4) isohydric environments [control (Ctl), fully compensated Met (C-Met), or fully compensated Resp (C-Resp)] and two different acid (pH approximately 7.1) isohydric environments (Met or Resp). During neutral pH (Ctl, C-Met, and C-Resp) there was JCa from bone during C-Met (decreased [HCO3-]), no net flux during Ctl (normal [HCO3-]), and JCa into bone during C-Resp (increased [HCO3-]); and JCa was correlated inversely with [HCO3-] (r = -0.824, n = 36, P less than 0.001). During acid pH there was greater JCa from bone during Met (decreased [HCO3-]) than during Resp (normal [HCO3-]); and JCa was again correlated inversely with [HCO3-] (r = -0.848, n = 22, P less than 0.001). JCa from bone during Met and Resp was greater than C-Met and C-Resp, respectively. The addition of the osteoclastic inhibitor salmon calcitonin did not alter the relative JCa results. Thus at a constant pH the magnitude of JCa from cultured neonatal mouse calvariae appears dependent on the [HCO3-]; the lower the [HCO3-], the greater the calcium efflux.(ABSTRACT TRUNCATED AT 250 WORDS)

Acidosis↗
PubMed1993

Acute haemodynamic effect of sodium bicarbonate in canine respiratory or metabolic acidosis.

This study has examined the acute haemodynamic effects of 7% sodium bicarbonate solution 1 mmol kg-1 (1.2 ml kg-1) administered into the right atrium over 5 s in 25 anaesthetized dogs allocated randomly to respiratory (arterial pH (pHa) 7.18, PaCO2 10.1 kPa (n = 8)) or metabolic acidosis (pHa 7.27, base deficit -9.0 mmol litre-1 (n = 7)) or metabolic neutrality (pHa 7.39 (n = 10)). The pHa and PaCO2 in the respiratory acidosis group differed from those in the two other groups (P < 0.01). One dog with respiratory acidosis developed progressive circulatory depression and cardiac arrest 6 min after injection of sodium bicarbonate. In the remaining seven dogs with respiratory acidosis, administration of sodium bicarbonate 1 mmol kg-1 produced transient decreases in mean arterial pressure, right ventricular dP/dt, and pulmonary blood flow, with increased right atrial pressure, followed by a gradual return of these variables to the baseline. The magnitude of reduction in pulmonary blood flow after sodium bicarbonate was greater in dogs with respiratory acidosis (P < 0.05) compared with the changes in the two other groups. The haemodynamic depression after bicarbonate was pronounced during respiratory acidosis and this may be attributed to a smaller pHa in the respiratory acidosis group, further reduction of intracellular pH, or both. It is suggested that when metabolic acidosis is corrected, bicarbonate should be administered with caution in the presence of respiratory acidosis.

Acid-Base Equilibrium↗
PubMed2007

Extracorporeal carbon dioxide removal using the Novalung in a patient with intracranial bleeding.

A neurosurgical patient who required repeated surgery for intracranial haematoma developed acute respiratory distress syndrome. Raised intracranial pressure proved difficult to manage whilst attempting to maintain optimal gas exchange. The resultant arterial partial pressure of carbon dioxide remained unacceptably high, and treatment by extracorporeal carbon dioxide removal was started. A pumpless arteriovenous interventional lung assist device (Novalung) was connected from the right femoral artery to left femoral vein and reduced the arterial carbon dioxide, corrected the respiratory acidosis and enabled control of the intracranial pressure. Subsequently the requirements for both respiratory and cardiovascular support were reduced. The patient made a complete neurological recovery.

Acidosis, Respiratory↗