Variation in cardiac output with acid-base changes in the anesthetized dog

1965 ◽  
Vol 20 (5) ◽  
pp. 948-953 ◽  
Author(s):  
S. A. Allan Carson ◽  
Gordon E. Chorley ◽  
F. Norman Hamilton ◽  
Do Chil Lee ◽  
Lucien E. Morris

Studies were performed in dogs anesthetized with pentobarbital, 30 mg/kg, and ventilated mechanically during succinylcholine apnea in order to ascertain the variation in cardiac output under various acid-base conditions. The findings were: 1) metabolic acidosis decreases cardiac output; 2) increasing respiratory acidosis in the absence of severe metabolic acidosis causes increase in cardiac output; 3) increasing respiratory acidosis in the presence of severe metabolic acidosis causes depression of cardiac output. The effect on cardiac output of changing arterial pH at steady PaCOCO2 is shown quantitatively. The relationship of PaCOCO2 to “pH adjusted” cardiac output is determined. From these data a nomogram is presented from which the combined effects of arterial pH and PaCOCO2 on cardiac output can be estimated. cardiac output and anesthesia; acid-base status and cardiac output; pH and cardiac output; PaCOCO2 and cardiac output Submitted on June 29, 1964

1982 ◽  
Vol 243 (4) ◽  
pp. F335-F341 ◽  
Author(s):  
M. S. Lucci ◽  
L. R. Pucacco ◽  
N. W. Carter ◽  
T. D. DuBose

Previous micropuncture studies utilizing indirect methods to estimate bicarbonate transport in the rat superficial distal tubule have indicated that the distal bicarbonate reabsorptive process normally operates well below the saturation level. Recent studies from our laboratory failed to demonstrate a spontaneous acid disequilibrium pH in this segment, implying that the bicarbonate reabsorptive rate was less than previously estimated. The purpose of the present experiments were 1) to measure the rate of absolute bicarbonate reabsorption by the rat superficial distal tubule while controlling bicarbonate delivery, and 2) to examine the effects of alterations in acid-base status on the rate of bicarbonate reabsorption. Five groups of rats in different states of acid-base balance were studied. No significant bicarbonate reabsorption was detected in the control hydropenic, combined respiratory acidosis-metabolic alkalosis, acute respiratory acidosis, or acute metabolic acidosis groups. In contrast, metabolic acidosis of 3 days duration resulted in a significant bicarbonate reabsorptive rate of 52.6 +/- 13.9 pmol . mm-1 . min-1. The observation of significant bicarbonate reabsorption in the distal tubule only during chronic metabolic acidosis of 3 days duration is compatible with adaptation of this normally low-capacity segment to chronic changes in systemic acid-base states.


2005 ◽  
Vol 63 (2b) ◽  
pp. 532-534 ◽  
Author(s):  
Jayme E. Burmeister ◽  
Rafael R. Pereira ◽  
Elisa M. Hartke ◽  
Michele Kreuz

Topiramate infrequently induces anion gap metabolic acidosis through carbonic anhydrase inhibition on the distal tubule of the nephron - a type 2 renal tubular acidosis. We report on a 40 years old woman previously healthy that developed significant asymptomatic metabolic acidosis during topiramate therapy at a dosage of 100mg/day for three months. Stopping medication was followed by normalization of the acid-base status within five weeks. This infrequent side effect appears unpredictable and should be given careful attention.


1983 ◽  
Vol 17 (2) ◽  
pp. 114-117 ◽  
Author(s):  
A. M. Carter

Neuroleptanalgesia was induced in late pregnancy in guineapigs with diazepam and fentanyl-fluanisone. Hypotension occurred, but the arterial acid-base status after 45-60 min was near normal. When repeated injections of fentanyl-fluanisone were given to maintain neuroleptanalgesia, the blood pressure fell further and severe metabolic acidosis developed. Placental blood flow determined with radioactive microspheres was much lower during maintained neuroleptanalgesia than in guineapigs anaesthetized with diazepam and pentobarbitone.


Blood ◽  
1983 ◽  
Vol 62 (4) ◽  
pp. 754-757 ◽  
Author(s):  
JT Prchal ◽  
WM Crist ◽  
M Roper ◽  
VP Wellner

Abstract The clinical and laboratory features of a 3-mo-old black male infant with glutathione (GSH) synthetase deficiency of the generalized type was evaluated. Partial albinism, brisk hemolytic anemia, recurrent febrile episodes, and mental retardation were noted. Also, severe recurrent metabolic acidosis and marked oxoprolinemia and oxoprolinuria were found in the proband but not in his first-degree relatives. The relationship of these disease manifestations to the underlying metabolic defect is discussed.


1981 ◽  
Vol 91 (1) ◽  
pp. 239-254
Author(s):  
P. R. H. Wilkes ◽  
R. L. Walker ◽  
D. G. McDonald ◽  
C. M. Wood

Blood gases, acid-base status, plasma ions, respiration, ventilation and cardiovascular function were measured in white suckers, using standard cannulation methods. Basic respiratory parameters under normoxia were compared to those in the active, pelagic rainbow trout and in other benthic teleosts. Sustained environmental hyperoxia (350–550 torr) increased arterial O2 (102–392 torr) and venous O2 (17–80 torr) tensions so that blood O2 transport occurred entirely via physical solution. Dorsal aortic blood pressure and heart rate fell, the latter due to an increase in vagal tone. Ventilation volume declined markedly (by 50%) due to a decrease in ventilatory stroke volume, but absolute O2 extraction rose so that O2 consumption was unaffected. While the preceding effects were stable with time, arterial and venous CO2 tensions approximately doubled within 4 h, and continued to increase gradually thereafter. This CO2 retention caused an acidosis (7.993–7.814) which was gradually compensated by an accumulation of plasma [HCO3−]. However, even after 72 h, arterial pH remained significantly depressed by 0.10 units. The gradual rise in plasma [HCO3−] was accompanied by a progressive fall in both [Na+] and [Cl−]; [K+] and [Ca2+] remained unchanged. The responses of the sucker to hyperoxia are compared to those of the rainbow trout.


1976 ◽  
Vol 40 (6) ◽  
pp. 864-867 ◽  
Author(s):  
S. N. Koyal ◽  
B. J. Whipp ◽  
D. Huntsman ◽  
G. A. Bray ◽  
K. Wasserman

Ventilation and acid-base responses were studied at comparable levels of O2 uptake during cycle ergometer and treadmill exercise, to determine the extent to which the type of exercise affects these responses. Twenty male subjects performed 50-, 100-, and 150-W cycle ergometer exercise and three work rates of similar O2 uptake on a treadmill. At comparable oxygen uptakes, arterial lactate and VE were higher and arterial pH and bicarbonate were lower for cycle ergometer than treadmill exercise. These differences could be accounted for by the greater degree of metabolic acidosis during cycle ergometer work. The increment in VE over that predicted (from an extrapolation of the linear relationship of the VE-VO2 relationship for low work rates) was linearly related to the decrease in arterial bicarbonate; VE was increased by approximately 4 1/min for each meq/1 of bicarbonate decrease for both treadmill and cycle ergometry.


1986 ◽  
Vol 250 (5) ◽  
pp. G588-G593 ◽  
Author(s):  
J. D. Wagner ◽  
P. Kurtin ◽  
A. N. Charney

We previously reported that changes in ileal net Na absorption correlated with arterial pH, changes in net HCO3 secretion correlated with the plasma HCO3 concentration, and changes in net Cl absorption correlated with arterial CO2 partial pressure (PCO2) during the systemic acid-base disorders. To determine whether changes in intracellular pH (pHi) and HCO3 concentration [( HCO3]i) mediated these effects, we measured pHi and calculated [HCO3]i in the distal ileal mucosa of anesthetized, mechanically ventilated Sprague-Dawley rats using 5,5-[14C]dimethyloxazolidine-2,4,-dione and [3H]inulin. Rats were studied during normocapnia, acute respiratory acidosis, and alkalosis, and uncompensated and pH-compensated acute metabolic acidosis and alkalosis. When animals in all groups were considered, mucosal pHi was not altered, but there were strong correlations between mucosal [HCO3]i and both arterial PCO2 (r = 0.97) and [HCO3] (r = 0.61). When we considered the rates of ileal electrolyte transport that characterized these acid-base disorders [A. N. Charney and L.P. Haskell, Am. J. Physiol. 245 (Gastrointest. Liver Physiol. 8): G230-G235, 1983], we found strong correlations between mucosal [HCO3]i and both net Cl absorption (r = 0.88) and net HCO3 secretion (r = 0.82). These findings suggest that the systemic acid-base disorders do not affect ileal mucosal pHi but do alter mucosal [HCO3]i as a consequence of altered arterial PCO2 and [HCO3]. The effects of these disorders on ileal net Cl absorption and HCO3 secretion may be mediated by changes in [HCO3]i. Arterial pH does not appear to alter ileal Na absorption through changes in the mucosal acid-base milieu.


1977 ◽  
Vol 232 (1) ◽  
pp. R10-R17 ◽  
Author(s):  
R. G. DeLaney ◽  
S. Lahiri ◽  
R. Hamilton ◽  
P. Fishman

Upon entering into aestivation, Protopterus aethiopicus develops a respiratory acidosis. A slow compensatory increase in plasma bicarbonate suffices only to partially restore arterial pH toward normal. The cessation of water intake from the start of aestivation results in hemoconcentration and marked oliguria. The concentrations of most plasma constituents continue to increase progressively, and the electrolyte ratios change. The increase in urea concentration is disproportionately high for the degree of dehydration and constitutes an increasing fraction of total plasma osmolality. Acid-base and electrolyte balance do not reach a new equilibrium within 1 yr in the cocoon.


1981 ◽  
Vol 51 (2) ◽  
pp. 452-460 ◽  
Author(s):  
P. E. Bickler

The effects of constant and changing temperatures on blood acid-base status and pulmonary ventilation were studied in the eurythermal lizard Dipsosaurus dorsalis. Constant temperatures between 18 and 42 degrees C maintained for 24 h or more produced arterial pH changes of -0.0145 U X degrees C-1. Arterial CO2 tension (PCO2) increased from 9.9 to 32 Torr plasma [HCO-3] and total CO2 contents remained constant at near 19 and 22 mM, respectively. Under constant temperature conditions, ventilation-gas exchange ratios (VE/MCO2 and VE/MO2) were inversely related to temperature and can adequately explain the changes in arterial PCO2 and pH. During warming and cooling between 25 and 42 degrees C arterial pH, PCO2 [HCO-3], and respiratory exchange ratios (MCO2/MO2) were similar to steady-state values. Warming and cooling each took about 2 h. During the temperature changes, rapid changes in lung ventilation following steady-state patterns were seen. Blood relative alkalinity changed slightly with steady-state or changing body temperatures, whereas calculated charge on protein histidine imidazole was closely conserved. Cooling to 17-18 degrees C resulted in a transient respiratory acidosis correlated with a decline in the ratio VE/MCO2. After 12-24 h at 17-18 degrees C, pH, PCO2, and VE returned to steady-state values. The importance of thermal history of patterns of acid-base regulation in reptiles is discussed.


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