Acid-base balance during lactic acid infusion in the lizard Varanus salvator

Although reptiles rely heavily on anaerobic metabolism and lactic acid production during activity, little is known concerning their ventilatory response to the attendant metabolic acidosis. We measured arterial PCO2, H+ and lactate (L)ion concentrations, and the rates of CO2 (MCO2) and O2 (MO2) exchange in Varanus salvator (n = 9) during intravenous infusions of lactic acid (HL) or sodium lactate (NaL; 250 mM) at rest. Two protocols were used: (1) 15 min infusions of 0.42 ml/min at both 25 and 35 degrees C with measurements every 5 min; (2) 4.5 min infusions of 1.73 ml/min at 35 degrees C with measurements at 4.5 min. At 35 degrees C, control pH decreased from its value at 25 degrees C with a slope of -0.007/degrees C and PaCO2 increased. The results of HL infusion were: (1) [L]a increased, (2) MCO2 increased, (3) R (MCO2/MO2) increased, (4) pHa decreased, and (5) PaCO2 remained unchanged from control at both temperatures and at both infusion rates. The only significant changes in PaCO2 observed were following the termination of fast HL infusions, when PaCO2 decreased. In NaL infusions, only small changes were observed except in [L]a. The results indicate that: (1) delta pH/delta T in V. salvator is less than in other poikilothermic vertebrates, but consistent with other varanid lizards, (2) respiratory compensation is slight in response to acute metabolic acidosis in this species, and (3) ventilation follows changes in MCO2 rather closely, accounting for precise regulation of PaCO2 despite 4-fold increases in MCO2 elicited by bicarbonate buffering and increased metabolic rate.     

Acid-base balance in haemodialyzed patients

Metabolic acidosis is a known complication of chronic renal failure. Maintenance of the pH within the reference range is important for influencing manifestations of the uraemic syndrome and the mortality of haemodialyzed patients. Intermittent bicarbonate haemodialysis should ensure the acid-base balance within the reference range also during the interval between haemodialyzations. In a short-term prospective study 20 haemodialyzed patients with chronic glomerulonephritis and pyelonephritis were examined. The authors assessed indicators of the acid-base balance (pH, HCO3-, pCO2) at the time of two haemodialyses and during the interval between haemodialyses. The blood flow in the dialyzation monitor was 300 ml/min. and the flow of the dialyzation solution 500 ml/min. The bicarbonate concentration in the dialyzation solution was 34 mmol/l. The duration of haemodialysis was 4 hours three times per week. Bicarbonate haemodialysis with a bicarbonate concentration of 34 mmol/l in the dialyzation solution ensured also during the interval between dialyzations a pH in the reference range in patients with chronic renal failure.     

Acid-base balance of pleural liquid in dogs.

Acid-base balance and electrolyte concentrations were measured in dogs on small artificial hydrothoraces and in vitro on bicarbonate buffered Ringer solution on serosal and interstitial side of specimens of parietal pleura. Under steady conditions, pleural liquid PCO 2 was similar to and pH higher (delta = 0.022 +/- 0.006 SE) than that in mixed venous blood. Computed pleural liquid [HCO-3] was similar to that in venous plasma and hence less than that set by the Donnan effect, with which Na+ and Cl- approximately complied. In vitro, pH, [Na+], [Cl-], and computed [HCO-3] were significantly lower (delta = 0.030 +/- 0.004; -2.6 +/- 0.5; -1.2 +/- 0.5 and -1.7 +/- 0.2 meq/L, respectively) on the serosal than on interstitial side of pleural specimens, PCO2 being 42 mm Hg on both sides . HCO-3 and Na+ were not distributed according to transpleural potential (-0.4 +/- 0.1 mV on serosal side), suggesting an active transport of Na+ and HCO-3 from pleural liquid to blood. This, however, does not seem to add to the absorption pressure of plasma proteins in setting pleural liquid pressure.     

Physiology of breathing and respiratory control during sleep

Studies of respiratory control during sleep have revealed that multiple sites of central CO (2) chemosensitivity exist within the brainstem, and different chemosensory sites may function only during certain sleep states. In general, chemical control of respiratory function, related to both hypercapnia and hypoxia, appears to be blunted during sleep. The decline in respiratory activity during sleep is particularly marked in the muscles of the upper airway. A variety of neuromechanical factors originating in the lungs, chest wall, and upper airway also modify respiratory function during sleep. Cardiorespiratory function seems to be less stable during sleep, and arousal responses represent a final element in the control system that preserves cardiorespiratory function by terminating the sleep state and restoring more effective control mechanisms.     

Abnormal breathing during sleep and chemical control of breathing during wakefulness in patients with sleep apnea syndrome

The possible role of ventilatory control in relation to sleep apnea has not yet been clarified. We investigated the relationship between awake ventilatory drives to hypoxia and hypercapnia and sleep-disordered breathing in 21 subjects with sleep apnea syndrome. The awake hypoxic ventilatory drive, which was evaluated by occlusion pressure responses, was inversely correlated with the magnitude of maximal oxygen desaturation during sleep as well as the ratio of duration with more than 4 and 10% oxygen desaturation to total sleep time. On the other hand, the awake hypercapnic ventilatory drive was not correlated with these parameters of sleep desaturation. Apnea index and duration were not correlated with the degree of hypoxic or hypercapnic ventilatory drive, respectively. Our study concluded that sleep desaturation is better correlated with hypoxic ventilatory drive than with hypercapnic ventilatory drive in patients with sleep apnea syndrome. These results are different from the results obtained in the patients with COPD in our previous study.     

Electrocardiogram-derived respiration in screening of sleep-disordered breathing

Methods for assessment of sleep-disordered breathing (SDB), including sleep apnea, range from a simple questionnaire to complex multichannel polysomnography. Inexpensive and efficient electrocardiogram (ECG)–based solutions could potentially fill the gap and provide a new SDB screening tool. In addition to the heart rate variability (HRV)–based SDB screening method that we reported a year ago, we have developed a novel method based on ECG-derived respiration (EDR). This method derives the respiratory waveform by (a) measuring peak-to-trough QRS amplitude in a single-channel ECG, (b) removing outlier introduced by noise and artifacts, (c) interpolating the derived values, and (d) filtering values within the respiration rates of 5 and 25 cycles per minute. Each 30 seconds of the respiratory waveform is then classified as normal, SDB, or indeterminate epoch. The previously reported HRV-based method, applied at the same time, is based on power spectrum of heart rate over a sliding 6-minute time window to classify the middle 30-second epoch. We then combined the EDR- and HRV-based techniques to optimize the classification of each epoch. The combined method further improved the accuracy of SDB screening in an independent test database with annotated SDB epochs. The development database was from PhysioNet (n = 25 polysomnograms). The test database was from Sleep Health Centers in Boston (n = 1907 polysomnogram) where the SDB epochs (n = 1 538 222 epochs) were scored using American Academy of Sleep Medicine criteria. The first test was to classify every epoch in the evaluation data set. The combined EDR and HRV method classified 78% of the epochs as either normal or SDB and 22% as indeterminate, with a total accuracy of 88% for scored epochs (not indeterminate). The second test was to evaluate the SDB status for each patient. The algorithm correctly classified 71% of patients with either moderate-to-severe SDB or mild-to-no SDB. We believe that the ECG-based methods provide an efficient and inexpensive tool for SDB screening in both home and hospital settings and make SDB screening feasible in large populations.     

Acid-base state and intermittent breathing in the torpid bat, Eptesicus fuscus.

The effects of intermittent breathing on acid-base state and blood gases were characterized in the torpid bat, Eptesicus fuscus, during steady-state torpor between body temperatures (Tb) of 5 and 37 degrees C. Arterial blood samples were taken from indwelling catheters without disturbing the torpid state. Arterial pH (pHa) of samples taken without knowledge of ventilatory state rose by 0.15 units from 37 to 5 degrees C with a delta pHa/delta Tb slope over this range of -0.0055 U/degrees C. However, at and below Tb = 20 degrees C, Eptesicus fuscus breathes intermittently with typical apneic periods of 40-150 min and 4-12 min at 10 and 20 degrees C, respectively. Samples taken at the end of a ventilatory bout and near the end of an apneic period at Tb = 20 degrees C revealed cyclic changes in pH (from 7.49 +/- 0.02 to 7.34 +/- 0.01), PO2 (from 96.6 +/- 3.4 to 30.8 +/- 3.9 Torr), and PCO2 (28.2 +/- 1.4 to 45.9 +/- 1.5 Torr). Between 10 and 37 degrees C, end-ventilatory pHa varied inversely with temperature with a delta pHa/delta T slope of -0.011 U/degrees C. Because intermittent breathing is common to many animals during hibernation, these results demonstrate the importance of coordinating blood sampling with ventilatory state for a reliable interpretation of acid-base regulation under these conditions.     

Acid-base balance in a canine model of cardiac arrest

Our study was performed to determine the pattern of arterial, venous, and cerebral spinal fluid (CSF) acidosis in a canine model of cardiac arrest and resuscitation; and the effect of bicarbonate treatment on arterial, venous, and CSF acidosis. Animals were instrumented to sample arterial blood, mixed venous blood, and CSF through a cisternal catheter. Following six minutes of ventricular fibrillation, manual CPR efforts were begun and continued for 30 minutes of cardiac arrest. Arterial, mixed venous, and CS fluids were sampled at baseline, six, 12, 18, 24, 27, and 30 minutes. Ten experimental dogs received sodium bicarbonate (2 mEq/kg) at 20 minutes of cardiac arrest, while ten animals in the control group received no alkali treatment. The experimental group showed a significantly higher arterial (7.79 +/- 0.20 vs 7.46 +/- 0.16 at 30 minutes) and venous pH (7.34 +/- 0.12 vs 7.19 +/- 0.10 at 24 minutes) following bicarbonate administration. This higher pH occurred despite a concomitant increase in arterial (31 +/- 10 vs 19 +/- 9 mm Hg at 27 minutes; 31 +/- 9 vs 10 +/- 8 at 30 minutes) and venous (104 +/- 30 vs 63 +/- 10 mm Hg at 24 minutes) pCO2. CSF analysis showed a gradually worsening acidosis. However, CSF pH (7.12 +/- 0.14 vs 7.16 +/- 0.23 at 30 minutes) and pCO2 were not significantly changed by the administration of bicarbonate.     

Mechanics and gas distribution in normal and obstructed lungs during tidal breathing

Quantitative characteristics of the dynamic mechanical and gas distribution behavior in 6 normal subjects and 5 subjects with COPD were compared during tidal breathing. Transpulmonary pressure, total lung volume, flow, and N2 fraction at the mouth were measured while N2 was washed out from the lung. The washouts were performed at several frequencies and lung volumes. As an index of nonuniform mechanical behavior, we calculated the frequency variation in dynamic pulmonary compliance (CLdyn). Based on a moment analysis of the multibreath N2 washout, we calculated a mean dilution number (MDN) as an index of the inhomogeneity of alveolar gas distribution and mixing. At FRC or above FRC the CLdyn decreased much more with frequency for the COPD subjects than for the normal subjects. The MDN was also much greater in the presence of COPD. However, the frequency dependence of the MDN was small for both the normal and COPD subjects and uncorrelated with the frequency dependence of CLdyn. Because the multibreath N2 washout and the frequency dependence of CLdyn reflect different aspects of ventilation inhomogeneity, these two responses are unique.     

Extracellular and intracellular acid-base effects of submergence anoxia and nitrogen breathing in turtles

We compared extracellular and intracellular acid-base state in turtles (Chrysemys picta bellii) subjected to anoxic submergence to turtles made anoxic by N2-breathing. Measurements made on control animals and on animals after 1, 2, 4, or 6 h of anoxia included blood pH, PO2, PCO2, and lactate as well as liver, heart, skeletal muscle, and brain pHi (using DMO equilibration), lactate, and glycogen concentrations. We hypothesized that the anaerobic metabolic rate of submerged turtles would be depressed by the more severe extra- and intracellular acidosis, and that this would be indicated by reduced lactate accumulation and glycogen depletion. Submerged turtles became extremely acidemic due to a combined metabolic and respiratory acidosis and had significantly lower arterial pH than N2-breathing animals (6.98 and 7.34, respectively, after 6 h). In spite of this disparity in pHa, 6 h pHi values for liver, heart, and brain were similar. Likewise, our data on glycogen depletion and lactate accumulation at h 6 in these tissues suggest no dramatic differences in anaerobic metabolic rate. While skeletal muscle pHi was somewhat lower at h 6 in the submerged group (6.73 vs 6.91 for N2-breathers), we observed no differences in either glycogen depletion or lactate accumulation in this tissue between our two treatments. Thus, at h 6, in spite of a 0.37 pH unit difference in pHa and a nearly 70 mm Hg difference in arterial and presumably cytosolic PCO2, pHi and tissue lactate and glycogen concentrations were similar. These results can be explained if the in vivo intracellular buffer values (beta) of turtle tissues are very high. We conclude that extracellular acid-base state is not necessarily reflected intracellularly in vivo in turtles and care must be taken in extrapolating from one compartment to another when attempting to make inferences about metabolic depression or acid-base regulation in this species.     

麻醉患者的血气变化和酸碱失衡

麻醉患者由于疾病、麻醉、手术以及术中出血和输血、输液的影响，很容易出现血气变化和酸碱失衡，而发生在麻醉中和麻醉恢复期间的心跳骤停约有60％与低氧血症和高碳酸血症有关。血气分析能全面了解患者的呼吸功能，及时发现和准确诊断低氧血症和高碳酸血症，为正确处理麻醉患者所出现的血气变化和酸碱失衡提供依据，从而避免因此引起的麻醉意外的发生，保证病人在麻醉和手术中的安全，减少术中和术后的并发症。