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PubMed1996

A physical-chemical analysis of the acid-base response to chronic obstructive pulmonary disease.

The metabolic contributions to chronic acid-base changes were examined in the plasma of arterial blood in patients with chronic obstructive pulmonary disease (COPD) and chronic hypercapnia, by a quantitative physical-chemical analysis. Patients were stratified into three groups: group 1 (Paco2 less than 40 mmHg; 1 mmHg = 133.3 Pa), group 2 (Paco2 between 40 and 50 mmHg), and group 3 (Paco2 higher than 50 mmHg). With the development of hypercapnia (Paco2 from 38.2 +/- 1.6 to 53.8 +/- 0.6 mmHg) and hypoxemia (Pao2 from 73.6 +/- 2.5 to 62.1 +/- 2.1 mmHg), blood pH decreased slightly (from 7.405 +/- 0.007 to 7.372 +/- 0.009). The strong ion difference ([SID]) increased in the hypercapnic group (from 39.7 +/- 1.7 to 46.2 +/- 2.9 mequiv.L-1) parallel to the increase in [HCO3-] (from 23.8 +/- 0.5 to 30.8 +/- 0.8 mequiv.L-1). The change in [SID] was quantitatively similar to the [HCO3-] change, thus reflecting a metabolic compensation of chronic respiratory acidosis. [SID] increase was mainly accounted for by changes in the [Na+]/[Cl-] ratio due to a significant decrease in plasma [Cl-]. Other ions measured as well as the weak acid buffers ([ATOT]) remained constant. From the present results, we suggest the usefulness of the physical chemical approach in the characterization of acid-base disturbances due to chronic hypercapnia when water retention or protein depletion are expected further to hypochloremia, as can be the case in severe COPD patients.

Acid-Base Equilibrium↗
PubMed1981

Respiratory, circulatory and acid-base adjustments to hypercapnia in a strictly aquatic and predominantly skin-breathing urodele, Cryptobranchus alleganiensis.

Upon initial exposure to increased ambient CO2, Cryptobranchus is titrated along an in vivo buffer line whose slope is considerably reduced from that observed when whole blood samples are equilibrated in vitro. During this time, there is no apparent reduction in the PCO2 difference between arterial blood and inspired media (PaCO2 -PICO2), despite an increase in auxiliary respiratory activities (lung and buccopharyngeal ventilation). The development of this non-compensated respiratory acidosis in the skin-breathing salamander is reminiscent of the situation seen in gill-breathing fish where the control of the acid-base balance is achieved by means other than ventilation. The increased ventilatory activities in Cryptobranchus can be interpreted as a response to the effect that the acidotic conditions have on arterial oxygenation (i.e.: CO2 Bohr effect); as a result, PaO2 increases and appears to counteract the arterial hypoxaemia which would otherwise result. More prolonged hypercapnia leads to compensatory phase of acid-base adjustment whereby plasma bicarbonate increases along a gently rising PaCO2 line to a new steady state equilibrium. This compensatory stage is slow acting and offers little by way of restoring the arterial blood pH, at least over the 36-h CO2 exposure period studied. The recovery period in air-saturated conditions is very gradual with PaCO2 levels exhibiting an exponential pattern of decline. This, together with the PaCO2 -PICO2 observations above, lends support to an accumulating body of evidence which suggests that respiratory CO2 losses across the amphibian skin are passive or at best only poorly controlled.

Acid-Base Equilibrium↗
PubMed1999

Subarachnoid hemorrhage following permissive hypercapnia in a patient with severe acute asthma.

In this article, we describe a case of a subarachnoid hemorrhage (SAH) in an acute severe asthma patient following mechanical hypoventilation. A 49-year-old man was admitted to an Intensive Care Unit with an acute exacerbation of asthma. After 3 days of mechanical ventilation (hypercapnia and normoxaemia), it was noted that his right pupil was fixed, dilated, and unreactive to light. Computed tomography (CT) scan showed localized SAH within the basilar cisterns and diffuse cerebral swelling. On the fourth day, a new CT scan showed hemorrhage resorption and a cerebral swelling decrease. In the following days, the patient's condition continued improving with no detectable neurological deficits. A review of similar published reports showed that all patients performed respiratory acidosis, normoxaemia, and hypercapnia. The most frequent neurological sign was mydriasis, and all subjects showed cerebral edema. Since normoxaemic hypercapnia has been associated with absence, or less cerebral edema, we considered additional factors to explain cerebral edema and intracranial hypertension causes. Thus, intrathoracic pressures due to patient's efforts by forcibly exhaling, or during mechanical ventilation, would further increase intracranial pressure by limiting cerebral venous drainage. This case emphasizes the fact that patients with acute severe asthma who have developed profoundly hypercarbic without hypoxia before or during mechanical ventilation, may have raised critical intracranial pressure.

Acute Disease↗
PubMed2000

Metabolic component of intestinal PCO(2) during dysoxia.

The adequacy of intestinal perfusion during shock and resuscitation might be estimated from intestinal tissue acid-base balance. We examined this idea from the perspective of conventional blood acid-base physicochemistry. As the O(2) supply diminishes with failing blood flow, tissue acid-base changes are first "respiratory, " with CO(2) coming from combustion of fuel and stagnating in the decreasing blood flow. When the O(2) supply decreases to critical, the changes become "metabolic" due to lactic acid. In blood, the respiratory vs. metabolic distinction is conventionally made using the buffer base principle, in which buffer base is the sum of HCO(3)(-) and noncarbonate buffer anion (A(-)). During purely respiratory acidosis, buffer base stays constant because HCO(3)(-) cannot buffer its own progenitor, carbonic acid, so that the rise of HCO(3)(-) equals the fall of A(-). During anaerobic "metabolism," however, lactate's H(+) is buffered by both A(-) and HCO(3)(-), causing buffer base to decrease. We quantified the partitioning of lactate's H(+) between HCO(3)(-) and A(-) buffer in anoxic intestine by compressing intestinal segments of anesthetized swine into a steel pipe and measuring PCO(2) and lactate at 5- to 10-min intervals. Their rises followed first-order kinetics, yielding k = 0. 031 min(-1) and half time = approximately 22 min. PCO(2) vs. lactate relations were linear. Over 3 h, lactate increased by 31 +/- 3 mmol/l tissue fluid (mM) and PCO(2) by approximately 17 mM, meaning that one-half of lactate's H(+) was buffered by tissue HCO(3)(-) and one-half by A(-). The data were consistent with a lumped pK(a) value near 6.1 and total A(-) concentration of approximately 30 mmol/kg. We conclude that the respiratory vs. metabolic distinction could be made in tissue by estimating tissue buffer base from measured pH and PCO(2).

Acid-Base Equilibrium↗
PubMed1998

Pulmonary vagal innervation is required to establish adequate alveolar ventilation in the newborn lamb.

To investigate the effects of bilateral intrathoracic vagotomy on the establishment of continuous breathing and effective gas exchange at birth, we studied 8 chronically instrumented, unanesthetized, sham-operated and 14 vagotomized newborn lambs after a spontaneous, unassisted vaginal delivery. Fetal lambs were instrumented in utero to record sleep states, diaphragmatic electromyogram, blood pressure, arterial pH, and blood-gas tensions. Six of eight sham-operated lambs established effective gas exchange within 10 min of birth, whereas 12 of 14 vagotomized animals developed respiratory acidosis and hypoxemia (P = 0.008). Breathing frequency in vagotomized newborns was significantly lower during the entire postnatal period compared with sham-operated newborns. Vagotomized subjects also remained hypothermic during the entire postnatal period (P < 0.05). Bronchoalveolar lavage indicated an increased minimum surface tension, whereas lung histology showed perivascular edema and partial atelectasis in the vagotomized group. We conclude that stimulation of breathing and effective gas exchange are critically dependent on intact vagal nerves during the transition from fetal to neonatal life.

Animals↗
PubMed1978

[Haemodynamic data, blood gas measurements and coagulation disorders in acute respiratory failure of patients with chronic lung disease (author's transl)].

24 subjects with chronic obstructive pulmonary disease were investigated in the course of acute respiratory failure defined by hypoxaemia, hypercapnia and respiratory acidosis. Haemodynamic data of right heart catheterization and coagulation tests were particularly studied. 12 of these subjects had right heart failure defined by a rise of right ventricular end-diastolic pressure above 10 Torr. Coagulation tests brought evidence of consumption coagulopathy in 8 patients, 7 of whom had right heart failure. Data suggest a significant correlation between right heart failure and coagulation disorders in patients with acute exacerbation of chronic obstructive pulmonary disease. These disturbances, accompanied by reduction of pulmonary vascular area, could be in part related to the presence of microthrombi in pulmonary arterial vessels.

Aged↗
PubMed1990

[Classification of respiratory insufficiency in pulmonary tuberculosis].

605 patients with different forms of pulmonary tuberculosis were examined. Blood gases and acid-base condition (ABC) were studied. In 22.2 per cent of the patients, hypoxemia was lacking with normal ABC and no respiratory failure (RF); in 36.6 per cent, hypoxemia was not accompanied by ABC changes and hence was caused by circulatory disturbances; in 15.6 per cent, it was combined with respiratory alcoholism; and in 6.8 per cent, with respiratory acidosis. The rest of the cases found to have metabolic disturbances of the ABC. Thus, hypoxemia is observed both with chronic forms of tuberculosis and with infiltrative/focal one, i.e. it follows a subacute course. In case of pulmonary tuberculosis, it is recommended to isolate subacute RF with PaO2 of 68.3 +/- 0.56 mm Hg, chronic RF of the 1-st phase with PaO2 of 71.8 +/- 0.7 mm Hg and chronic RF of the 2-nd phase with PaO2 of 64.2 +/- 0.88 mm Hg and accompanied by chronic cor pulmonale. In this case it seems necessary to find the basic mechanism of RF which is important for the treatment purposes.

Humans↗
PubMed2002

Negative-pressure ventilation: is there still a role?

Negative-pressure ventilation (NPV) was the primary mode of assisted ventilation for patients with acute respiratory failure until the Copenhagen polio epidemic in the 1950s, when, because there was insufficient equipment, it was necessary to ventilate patients continually by hand via an endotracheal tube. Thereafter, positive-pressure ventilation was used routinely. Since it was also observed that patients with obstructive sleep apnoea could be treated noninvasively with positive pressure via a nasal mask, noninvasive positive-pressure ventilation (NPPV) has become the most widely used noninvasive mode of ventilation. However, NPV still has a role in the treatment of certain patients. In particular, it has been used to good effect in patients with severe respiratory acidosis or an impaired level of consciousness, patients that to date have been excluded from all prospective controlled trials of NPPV. NPV may be used in those who cannot tolerate a facial mask because of facial deformity, claustrophobia or excessive airway secretion. NPV has also been used successfully in small children, and beneficial effects on the cardiopulmonary circulation maybe a particular advantage in children undergoing complex cardiac reconstructive surgery. This review is divided into two parts: the first is concerned with the use of negative-pressure ventilation in the short term, and the second with its use in the long term.

Acute Disease↗
PubMed1993

Hypoxia, arterial pH and theophylline disposition.

Theophylline is a bronchodilator used extensively in the management of obstructive pulmonary disease. Factors implicated in altered theophylline clearance include smoking, age, concomitant drug intake, liver disease and left ventricular heart failure. However, evidence now suggests that theophylline clearance may be altered by changes in severity of the pulmonary obstruction, hypoxia and variation in arterial pH. The in vitro disposition of theophylline has been evaluated in isolated rat livers and mouse hepatocytes. In vivo studies have assessed the metabolism of theophylline under hypoxia in rats, rabbits and dogs. In isolated mouse hepatocytes and rat livers, low oxygen concentrations resulted in higher theophylline concentrations, a longer elimination half-life and a decrease in the production of the metabolite 1,3-dimethyl uric acid, suggesting impaired metabolism of theophylline. In rabbits, hypoxia, hypercapnia and respiratory acidosis decreased total body clearance and increased plasma theophylline concentrations. On the other hand, experiments involving dogs showed no significant changes in theophylline concentrations or pharmacokinetic parameters with hypoxia. At present, animal studies remain inconclusive. This can be attributed to the use of different animal models and variations in study methodology, including the extent and duration of hypoxia and acidaemia, concurrent acid-base disorders such as hypercapnia, as well as the severity of pulmonary obstruction. Human studies assessing alterations in theophylline disposition secondary to the hypoxia present in pulmonary disease are few and include mostly case reports and observational studies. There is evidence suggesting decreased theophylline clearance and protein binding during acute illness and some consensus can be achieved using case reports and controlled studies. There is additional evidence that drug clearance decreases with age and that elderly patients may have a decreased theophylline clearance at baseline. However, the most obvious markers appear to be the severity of pulmonary disease and the rate of change in the patient's condition. Caution should be exercised when administering theophylline to elderly patients with chronic obstructive pulmonary disease presenting with acute exacerbations of a concomitant respiratory illness, as these patients appear to be most likely to exhibit altered theophylline metabolism. Therefore, they would be at increased risk for toxicity should conventional dosages be used during an acute respiratory event.

Acid-Base Imbalance↗
PubMed1992

Effectiveness of pressure support ventilation for mechanical ventilatory support in patients with status asthmaticus.

We compared the effects of pressure support ventilation (PSV) with those of assist control ventilation (ACV) on breathing patterns and blood gas exchange in six patients with status asthmaticus. Both PSV and ACV delivered adequate minute ventilation (PSV: 7.5 +/- 1.4 l/min/m2, ACV: 7.3 +/- 1.3 l/min/m2) to correct respiratory acidosis (pH = 7.33 +/- 0.12 during both PSV and ACV) and prevent hypoxia. Peak airway pressure during PSV was significantly lower with the same tidal volume than that during ACV (PSV: 30 +/- 10 cmH2O (2.9 +/- 1.0 kPa), ACV: 50 +/- 13 cmH2O (4.9 +/- 1.3 kPa)). The lower airway pressure during PSV was due to persistent inspiratory muscle activity. The oxygen cost of breathing estimated by oxygen consumption was equivalent in both modes. We conclude that PSV is effective in supplying tidal volumes adequate to improve hypercarbia at markedly lower airway pressures than ACV.

Adolescent↗
PubMed1993

Cerebral metabolic studies in vivo by combined 1H/31P and 1H/13C NMR spectroscopic methods.

Intracellular pH and ammonium ion concentration are potent modulators of cerebral amino acid metabolism. Furthermore, intracellular acidosis and hyperammonemia accompany conditions such as ischemic encephalopathy and seizures and may contribute to the pathological sequelae observed. In vivo NMR spectroscopy permits multiple, non-destructive measurements of important cerebral metabolic intermediates in the same animal. We describe here the use of 1H, and 31P NMR spectroscopy to investigate the effects of acute changes in intracellular pH and ammonium ions on cerebral glutamate, glutamine, and lactate levels in vivo. We then show how 1H NMR can be used to indirectly follow the flow of 13C label from [1-13C] glucose into the cerebral glutamate pool, allowing us to measure cerebral TCA activity in normal and chronically hyperammonemic rats. Male Sprague-Dawley rats (160-210 gm), fasted 24-hours, were tracheotomized, paralyzed and ventilated on 30% O2/70% N2O. NMR spectroscopy was performed at a field strength of 8.4 Tesla using a Bruker AM-360 wide bore spectrometer. An elliptical surface-coil (8 x 12 mm) was double-tuned to either the 1H and 31P or 1H and 13C frequencies. After retraction of extracranial tissues, the coil was positioned over the skull 2 mm posterior to the bregma. Tail arteries and veins were cannulated allowing periodic measurements of PO2, pCO2, pH and glucose in arterial blood and intravenous infusions. Respiratory acidosis was induced in rats by the addition of CO2 to the ventilation gas mixture. Arterial pCO2 increased within 5 min from a pre-hypercarbic value of 36.4 +/- 6.1 mm Hg to 200-220 mm Hg and was maintained at this level for over 1 hour. Hypercarbia led to rapid cerebral acidification. Intracellular pH decreased from 7.18 +/- 0.08 (pre-hypercarbic period) to 6.68 +/- 0.06 (n = 4) at 10 min and remained stable throughout the NMR observation period. Glutamate decreased to 53 +/- 4% of control after 60 min of hypercarbia, while glutamine increased to 126 +/- 7% of control. Acute hyperammonemia was produced by a programmed intravenous infusion of 250 mM ammonium acetate, which rapidly raised and maintained the concentration of ammonium ions in the blood at approximately 500 microM. Shortly after the start of the infusion (10-20 min), the levels of glutamine and lactate rose continuously throughout the experiment, reaching levels of 170 +/- 25% and 260 +/- 60% of control, respectively (n = 12) after 50 min. Glutamate decreased during the same time interval to 80 +/- 4% of control (n = 12).(ABSTRACT TRUNCATED AT 400 WORDS)

Acid-Base Equilibrium↗
PubMed1989

Chronological relationships between mediator release and changes in airway dynamics during an ascaris response in sensitive cynomolgus monkeys.

Recently identified Ascaris suum sensitive cynomolgus monkeys were further characterized to determine if a chronologic relationship existed between mediator release and onset of bronchoconstriction. In these anesthetized Ascaris-sensitive monkeys, aerosol antigen challenge of each animal produced rapid and severe bronchoconstriction, as determined by decreases in dynamic lung compliance (-80.2 +/- 4.1%) and airway conductance (-64.5 +/- 13.8%). Maximum changes were achieved within 5 min following exposure and remained substantially altered throughout the 30 min observation period. However, changes in pulmonary function related to duration of onset and maximum change seemed to have some correlation with each animals' sensitivity to the antigen. Comparison of pre- and post-challenge blood gas profiles, showed a progressive formation of respiratory acidosis through decreases in arterial blood pH, partial pressure of O2 (pO2), O2 saturation (sO2) and an increase in partial pressure of CO2 (pCO2). When arterial blood plasma was assayed by RIA for mediators of anaphylaxis, large increases in 5-hydroxyeicostetraenoi acid (5-HETE), leukotriene B4 (LTB4) and histamine were observed. No amount of prostaglandin F2-alpha (PGF2 alpha) or thromboxane A2 were detected. Two of the three monkeys also produced detectable amounts of leukotriene C4 (LTC4). Therefore, in Ascaris-sensitive monkeys, histamine is the predominate mediator released and is probably responsible for at least the early part (5-10 min) of the observed bronchoconstriction. However, mediators from the lipoxygenase pathway may also be playing a role in the antigen-induced bronchoconstriction, especially beyond the 10 min period following anaphylaxis.

Animals↗
PubMed1995

Phenyl isocyanate-induced asthma in rats following a 2-week exposure period.

This study was conducted to assess the toxic effects of repeated inhalation exposures to phenyl isocyanate vapor in male Wistar rats. Rats were exposed to design concentrations of 0, 1, 4, 7, or 10 mg/m3 phenyl isocyanate air for 2 weeks (6 hr/day, 5 days/week). The rats were assessed for normal toxicologic parameters, and pulmonary function tests, blood gas measurements, and analysis of bronchoalveolar lavage fluid (BALF) parameters were utilized shortly after exposures as well as 2 months postexposure. The results indicated that rats exposed to 7 and 10 mg/m3 experienced decreased body weights, hypoactivity, hypothermia, signs of respiratory tract irritation, delayed onset of mortality, and changes in organ weights. In addition, pulmonary function tests demonstrated decreased forced expiratory flow rates and quasistatic lung compliance. Arterial blood gases showed an arterial hypoxemia and changes consistent with a pronounced venous-admixture-like perfusion, suggesting severe mismatch of the ventilation/perfusion relationship. Delayed onset of mortality appeared to be associated with respiratory acidosis and hypoxemia. Biochemical and cellular components in BALF complemented the results of the functional alterations. Remarkable changes were indicated by increased activities of the BALF parameters, gamma-GPT, protein, and sialic acid. Histopathological findings provided evidence of increased secretory cell activity and a concentration-dependent increase in goblet cell hyperplasia at concentrations of 4 mg/m3 and above. In rats exposed to 7 mg/m3 further findings consisted of intraluminal inflammation of airways, hypertrophia of bronchial smooth muscle, epithelial desquamation, and eosinophilia of the airways. A complete regression of morphological lesions was not found in the animals exposed to 4 mg/m3 and above at the 2-month postexposure time period. In conclusion, the damage to the airways comprise most of the features characteristic of chronic airway inflammation or asthma.

Administration, Inhalation↗
PubMedDate not supplied

[Respiratory involvement secondary to crotalid ophidian bite (Crotalus durissus)].

Three patients presented respiratory abnormalities following Crotalus durissus snakebite. These abnormalities appeared in the first 48 h after the snake bite and consisted of dyspnea, tachypnea, use of accessory muscles of respiration (cases 1 and 2) and flaring of the nostrils (case 2). Cases 1 and 2 developed acute respiratory failure. Case 2, 24 h after the snakebite presented difficult breathing and periods of apnea. He was intubated in the emergency room and transferred to the intensive case unit where he arrive with spontaneous breathing. His respiratory pattern worsened and measurement of arterial pH and blood gases showed metabolic and respiratory acidosis with partial carbon dioxide pressure increasing from 40 to 50.3 mmHg compatible with acute ventilatory failure. Both patients needed mechanical ventilation. Weaning from the ventilator was accomplished after 33 days in case 1 and after 15 days in case 2. Both patients also presented acute renal failure treated with peritoneal dialysis with full recovery of the renal function. Measurements of forced vital capacity (FVC) and forced expiratory volume in the first second (FEV 1.0) was carried out 58 hours after the snakebite in case 3. Both FVC and FEV 1.0 were reduced in relation to the predicted values (60 and 67% respectively) but the ratio FEV 1.0/FVC was in the normal range. These findings were compatible with a restrictive pattern of ventilatory failure. Serial measurements showed progressive increase of both FVC and FEV 1.0 reaching 72 and 79% of the predicted values, respectively, in the 10th day after the snakebite.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1991

A case of chronic mountain sickness diagnosed by routine pulmonary function tests.

In summary, this is a patient who presented with respiratory acidosis and cor pulmonale. The major diagnostic challenge was in differentiating primary cardiopulmonary disease from a central abnormality of ventilatory drive. The arterial blood gases showed a normal A-a gradient suggesting hypoventilation as the etiology of his hypoxemia. Pulmonary function testing showed air trapping, but a relatively normal FEV1/FVC and airways resistance. The literature suggests that most altitude natives have depressed hypoxemic and hypercapnic drives with a distinct subset demonstrating a profoundly depressed drive to ventilation. This latter group has been labeled as having chronic mountain sickness or Monge's disease. As one might expect, ventilatory control during sleep is also abnormal in these patients with CMS. Our patient indeed showed typical frequent severe desaturations with hypopnea. The diagnosis of CMS in our patient was made with routine arterial blood gases and standard pulmonary function tests. Additional tests of ventilatory responsiveness to oxygen and carbon dioxide could have been performed, but are not necessary to make the diagnosis.

Altitude Sickness↗
PubMed2001

Beat-to-beat changes in stroke volume precede the general circulatory effects of mechanical ventilation: a case report.

BACKGROUND: The haemodynamic as well as the ventilatory consequences of mechanical ventilation can be harmful in critically ill neonates. Newly developed ventilatory lung protective strategies are not always available immediately and in an acute situation the haemodynamic changes caused by mechanical ventilation can affect the oxygen delivery considerably. We report the case of a male neonate who was treated with conventional pressure-controlled mechanical ventilation because of respiratory distress and progressive respiratory acidosis resulting from meconium aspiration. Because of poor arterial oxygenation despite 100% inspired oxygen and increased ventilator settings, echocardiography was performed to exclude central haemodynamic reasons for low oxygen delivery. METHOD: Doppler echocardiography was used for the measurement of stroke volume and cardiac output. Pulse oximetry and aortic blood pressure were monitored continuously. RESULTS: Echocardiography revealed no cardiac malformations or signs of persistent fetal circulation. When inspiratory pressures and duration were increased, beat-to-beat variation in stroke volume preceded decay in cardiac output. Stroke volume variations and oxygen saturation values guided ventilator settings until extracorporal membrane oxygenation could be arranged for. After recovery and discharge 4 weeks later the boy is progressing normally. CONCLUSION: Because oxygen delivery is dependent on both blood flow and arterial oxygen content, measurement of cardiac output as well as left heart oxygen saturation is a useful guide to optimizing oxygen delivery. This case report demonstrates how Doppler echocardiographic monitoring of beat-to-beat changes in stroke volume can be used to detect early negative haemodynamic effects of increased mechanical ventilation settings before cardiac output is affected.

Cardiac Output↗
PubMed2000

Apparent diffusion limitations for CO(2) excretion in rainbow trout are relieved by injections of carbonic anhydrase.

Experiments were performed in vivo to elucidate the underlying mechanism(s) of apparent diffusion limitations for CO(2) excretion in rainbow trout (Oncorhynchus mykiss). Ligation of two gill arches and the associated expected reduction in gill surface area of 30% caused pronounced respiratory acidosis as indicated by elevated arterial blood P(CO(2)) (Pa(CO(2))) and reduced arterial blood pH. Under conditions of normoxia, arterial blood P(O(2)) (Pa(O(2))) was not significantly (statistically) reduced. However, during hypoxia (water P(O(2))=70-80 mmHg), the apparent trend for reduced Pa(O(2)) values became statistically significant in fish with 15% surface area reduction. To determine whether the elevated Pa(CO(2)) in fish with reduced surface area (30%) reflected true diffusion limitations or chemical equilibrium limitations imposed by the relatively slow rate of red blood cell Cl(-)/HCO(3)(-) exchange, fish were injected with carbonic anhydrase (CA) to permit catalysis of HCO(3)(-) dehydration within the plasma. Injection of CA caused a lowering of Pa(CO(2)) by 0.87+/-0.32 mmHg within 120 min and thus essentially eliminated the increase in Pa(CO(2)) (1.04+/-0.33 mmHg) that was caused by the reduction in surface area. These results clearly demonstrate that the elevation in Pa(CO(2)) evoked by gill surface area reduction is a consequence of chemical equilibrium limitations rather than true diffusion limitations, per se.

Animals↗
PubMed1998

Transcutaneous PCO2 monitoring during laparoscopic cholecystectomy in pregnancy.

PURPOSE: Respiratory acidosis during carbon dioxide (CO2) insufflation has been suggested as a cause of spontaneous abortion and preterm labour following laparoscopic cholecystectomy during pregnancy. Capnography may not be adequate as a guide to adjust pulmonary ventilation during laparoscopic surgery and hence arterial carbon dioxide (PaCO2) monitoring has been recommended. We report the feasibility and benefits of transcutaneous carbon dioxide monitoring (PtcCO2) as an approach to optimise ventilation during laparoscopic surgery in pregnancy. METHOD: A healthy parturient received general anaesthesia for laparoscopic cholecystectomy. Pulmonary ventilation was adjusted to maintain end-tidal carbon dioxide (conventional PETCO2) at 32 mmHg during CO2 insufflation. A PtcCO2 monitor was used to trend PaCO2 throughout the procedure. Mechanical ventilation was interrupted every five minutes to obtain an end-tidal PCO2 value at large tidal volume (squeeze PETCO2). RESULTS: The PtcCO2 increased from 39 mmHg before induction to 45 mmHg after CO2 insufflation. This corresponds to an estimated maximum PaCO2 of 39-40 mmHg during insufflation. The PtcCO2 gradually returned to pre-induction baseline values one hour after the termination of CO2 insufflation. Squeeze PETCO2 values approximated PtcCO2 more closely than did conventional PETCO2 values (P < 0.01). CONCLUSION: Continuous PtcCO2 measurements as well as squeeze PETCO2 may be of clinical value in trending and preventing hypercarbia during laparoscopic surgery.

Adult↗