Increases in coronary vein CO2 during cardiac resuscitation

1990 ◽  
Vol 68 (4) ◽  
pp. 1405-1408 ◽  
Author(s):  
C. V. Gudipati ◽  
M. H. Weil ◽  
R. J. Gazmuri ◽  
H. G. Deshmukh ◽  
J. Bisera ◽  
...  
Keyword(s):  
Spontaneous Circulation ◽  
Co2 Production ◽  
Acid Base ◽  
Coronary Vein ◽  
Arterial Pco2 ◽  
Control Value ◽  
Great Cardiac Vein ◽  
Aortic Blood ◽  
Highly Correlated ◽  
Mixed Venous

We investigated the aortic, mixed venous, and great cardiac vein acid-base changes in eight domestic pigs during cardiac arrest produced by ventricular fibrillation and during cardiopulmonary resuscitation (CPR). The great cardiac vein PCO2 increased from a control value of 52 +/- 2 to 132 +/- 28 (SD) Torr during CPR, whereas the arterial PCO2 was unchanged (39 +/- 4 vs. 38 +/- 4). The coronary venoarterial PCO2 gradient, therefore, increased remarkably from 13 +/- 2 to 94 +/- 29 Torr. The simultaneously measured great cardiac vein lactate concentrations increased from 0.24 +/- 0.06 to 7.3 +/- 2.34 mmol/l. Much more moderate increases in the lactate content of aortic blood from 0.64 +/- 0.25 to 2.56 +/- 0.27 mmol/l were observed. Increases in great cardiac vein PCO2 and lactate were highly correlated during CPR (r = 0.91). After successful CPR, the coronary venoarterial PCO2 gradient returned to normal levels within 2 min after restoration of spontaneous circulation. Lactate content was rapidly reduced and lactate extraction was reestablished within 30 min after CPR. These studies demonstrate marked but reversible acidosis predominantly as the result of myocardial CO2 production during CPR.

Ventilation and CSF ions during hypocapnic HCl and HNO3 acidosis in conscious rabbits

1983 ◽  
Vol 55 (6) ◽  
pp. 1748-1757 ◽  
Author(s):  
E. E. Nattie ◽  
G. F. Birchard
Keyword(s):  
Minute Ventilation ◽  
Respiratory Frequency ◽  
Co2 Production ◽  
Central Venous ◽  
Acid Base ◽  
Arterial Pco2 ◽  
Mean Values ◽  
Frequency Responses ◽  
Ionic Mechanisms ◽  
Conscious Rabbits

In conscious rabbits with preimplanted arterial, central venous, and cisterna magna catheters, we infused HNO3 or HCl to lower and maintain arterial PCO2, pH, and plasma HCO-3 at the same mean values in both groups over 9 h. The hypothesis was that greater entry into cerebrospinal fluid (CSF) of the strong anion NO-3 vs. Cl- would result in a greater decrease in CSF [HCO-3] in the HNO3 vs. the HCl experiment, even though the acid-base stress as measured by arterial PCO2 and plasma [HCO-3] was the same. The results did not support the hypothesis. With HCl acidosis, delta CSF [HCO-3] was equal to delta CSF [Cl-]. With HNO3 acidosis, delta CSF [HCO-3] was equal to delta CSF [NO-3] + delta CSF [Cl-], as both CSF Cl- and HCO-3 decreased with NO-3 entry into CSF. The change in CSF [HCO-3] appeared tightly linked to the PCO2 or the plasma [HCO-3], it did not depend on the type of acid used. The ionic mechanisms that determine the CSF [HCO-3] in metabolic acidosis appear able to utilize changes in the strong anions NO-3 and Cl- to bring about CSF acid-base regulation. The change in alveolar ventilation per unit CO2 production as reflected by the arterial PCO2 was the same in both groups, although the expired minute ventilation and respiratory frequency responses were diminished in the HNO3 vs. the HCl groups. In both groups with acidosis, tidal volume increased, whereas respiratory frequency decreased.

scholarly journals Ventilation and acid-base balance during graded activity in lizards

1981 ◽  
Vol 240 (1) ◽  
pp. R29-R37 ◽  
Author(s):  
G. S. Mitchell ◽  
T. T. Gleeson ◽  
A. F. Bennett
Keyword(s):  
Treadmill Exercise ◽  
Control Level ◽  
Hydrogen Ion ◽  
Co2 Production ◽  
Acid Base Balance ◽  
Acid Base ◽  
Lizard Species ◽  
Arterial Pco2 ◽  
Base Balance ◽  
Graded Activity

Arterial PCO2, hydrogen ion ([H+]a), and lactate ([L]a) concentrations, rates of metabolic CO2 production (VCO2) and O2 consumption (VO2), and effective alveolar ventilation (Veff) were determined in the lizards Varanus exanthematicus and Iguana iguana at rest and during steady-state treadmill exercise at 35 degrees C. In Varanus, VCO2 increased ninefold and VO2 sixfold without detectable rise in [L]a at running speeds below 1.0 to 1.5 km x h-1. In this range, Veff increased 12-fold resulting in decreased levels of PaCO2 and [H+]a. At higher speeds [L]a rose. Increments of 5 mM [L]a were accompanied by hyperventilation, reducing PaCO2 and thus maintaining [H+]a near its resting level. When [L]a increased further, [H+]a increased. Sustainable running speeds (0.3-0.5 km x h-1 and below) were often associated with increased VO2, VCO2, and [L]a in Iguana. Sixfold increases in VCO2 and 9-mM increments in [L]a were accompanied by sufficient increase in Veff (9-fold) to maintain [H+]a at or below its control level. When [L]a increased further, [H+]a increased. These results indicate that both lizard species maintain blood acid-base homeostasis rather effectively via ventilatory adjustments at moderate exercise intensities.

Effect of water immersion on cardiopulmonary physiology at high gravity (+Gz)

1986 ◽  
Vol 61 (5) ◽  
pp. 1686-1692 ◽  
Author(s):  
R. Arieli ◽  
U. Boutellier ◽  
L. E. Farhi
Keyword(s):  
Cardiac Output ◽  
Functional Residual Capacity ◽  
Water Immersion ◽  
Systemic Circulation ◽  
Co2 Production ◽  
Arterial Pco2 ◽  
Residual Capacity ◽  
Gravitational Influence ◽  
End Tidal ◽  
Mixed Venous

We compared the cardiopulmonary physiology of eight subjects exposed to 1, 2, and 3 Gz during immersion (35 degrees C) to the heart level with control dry rides. Immersion should almost cancel the effects of gravity on systemic circulation and should leave the lung alone to gravitational influence. During steady-state breathing we measured ventilation, O2 consumption (VO2), CO2 production, end-tidal PCO2 (PACO2), and heart frequency (fH). Using CO2 rebreathing techniques, we measured cardiac output, functional residual capacity, equivalent lung tissue volume, and mixed venous O2 content, and we calculated arterial PCO2 (PaCO2). As Gz increased, ventilation, fH, and VO2 rose markedly, and PACO2 and PaCO2 decreased greatly in dry ride, but during immersion these variables changed very little in the same direction. Functional residual capacity was lower during immersion and decreased in both the dry and immersed states as Gz increased, probably reflecting closure effects. Cardiac output decreased as Gz increased in dry rides and was elevated and unaffected by Gz during immersion. We conclude that most of the changes we observed during acceleration are due to the effect on the systemic circulation, rather than to the effect on the lung itself.

Respiratory, Ventilatory, Acid-Base and Ionoregulatory Physiology of the White Sucker Catostomus Commersoni: The Influence of Hyperoxia

1981 ◽  
Vol 91 (1) ◽  
pp. 239-254
Author(s):  
P. R. H. Wilkes ◽  
R. L. Walker ◽  
D. G. McDonald ◽  
C. M. Wood
Keyword(s):  
Rainbow Trout ◽  
Blood Gases ◽  
Catostomus Commersoni ◽  
Acid Base ◽  
Aortic Blood ◽  
Respiratory Parameters ◽  
Arterial Ph ◽  
O2 Extraction ◽  
Acid Base Status ◽  
Aortic Blood Pressure

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.

Effect of systemic acid-base disorders on ileal intracellular pH and ion transport

1986 ◽  
Vol 250 (5) ◽  
pp. G588-G593 ◽  
Author(s):  
J. D. Wagner ◽  
P. Kurtin ◽  
A. N. Charney
Keyword(s):  
Intracellular Ph ◽  
Respiratory Acidosis ◽  
Strong Correlations ◽  
Sprague Dawley ◽  
Acid Base ◽  
Ileal Mucosa ◽  
Arterial Pco2 ◽  
Co2 Partial Pressure ◽  
Arterial Ph ◽  
Acute Metabolic Acidosis

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.

Influence of changes in cardiac output on the acid-base status of arterial and mixed venous blood

1987 ◽  
Vol 410 (3) ◽  
pp. 257-262 ◽  
Author(s):  
Y. L. Hoogeveen ◽  
J. P. Zock ◽  
P. Rispens ◽  
W. G. Zijlstra
Keyword(s):  
Cardiac Output ◽  
Venous Blood ◽  
Mixed Venous Blood ◽  
Acid Base ◽  
Acid Base Status ◽  
Mixed Venous

Ventilatory and blood acid-base adjustments to a decrease in body temperature from 30 to 10YC in black racer snakes Coluber constrictor

1996 ◽  
Vol 199 (4) ◽  
pp. 815-823
Author(s):  
J Stinner ◽  
M Grguric ◽  
S Beaty
Keyword(s):  
Steady State ◽  
Body Temperature ◽  
Minute Ventilation ◽  
Co2 Production ◽  
Bicarbonate Concentration ◽  
Acid Base ◽  
Slow Increase ◽  
Coluber Constrictor ◽  
Steady State Levels ◽  
Time Required

There is increasing evidence that many amphibian and reptilian species use relatively slow ion-exchange mechanisms in addition to ventilation to adjust pH as body temperature changes. Large changes in blood bicarbonate concentration with changes in temperature have previously been reported for the snake Coluber constrictor. The purpose of the present study was to determine the ventilatory and pH adjustments associated with the increase in CO2 stores when the snakes are cooled. Body temperature was lowered from 30 to 10 °C within 4 h, at which time measurements of inspired minute ventilation (V.air), O2 consumption (VO2) and CO2 production (V.CO2) were started and continued for 56 h. The decrease in temperature produced a transient fall in the respiratory exchange ratio (V.CO2/VO2) to 0.2-0.3 and a steady-state value of 0.65±0.14 (mean ± s.d., N=7) was not achieved until about 35 h. There were concomitant transient reductions in V.air and V.air/V.O2. However, V.air/V.CO2 initially increased, with a corresponding reduction in arterial PCO2 (PaCO2) and increase in arterial pH. By 35 h, V.air/V.CO2 had decreased and PaCO2 had increased to steady-state levels, but pH decreased very little because of a gradual increase in bicarbonate concentration. We conclude that the drop in temperature imposed a metabolic acidosis for approximately 35 h because of the time required to increase bicarbonate concentration, and that the acidosis was compensated for by an elevated V.air/V.CO2. Steady-state breathing and acid-base status were not achieved until the relatively slow increase in CO2 stores had been completed.

Ventilatory control during exercise with peripheral chemoreceptor stimulation: hypoxia vs. domperidone

1989 ◽  
Vol 67 (6) ◽  
pp. 2438-2446 ◽  
Author(s):  
S. L. Schaefer ◽  
G. S. Mitchell
Keyword(s):  
Dopamine D2 Receptor ◽  
D2 Receptor ◽  
Whole Body ◽  
Co2 Production ◽  
Peripheral Chemoreceptor ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Response To Exercise ◽  
Dopamine D2 Receptor Antagonist ◽  
Made In

Hypoxia potentiates the ventilatory response to exercise, eliciting a greater decrease in arterial PCO2 (PaCO2) from rest to exercise than in normoxia. The mechanism of this hypoxia-exercise interaction requires intact carotid chemoreceptors. To determine whether carotid chemoreceptor stimulation alone is sufficient to elicit the mechanism without whole body hypoxia, ventilatory responses to treadmill exercise were compared in goats during hyperoxic control conditions, moderate hypoxia (PaO2 = 38-44 Torr), and peripheral chemoreceptor stimulation with the peripheral dopamine D2-receptor antagonist, domperidone (Dom; 0.5 mg/kg iv). Measurements with Dom were made in both hyperoxia (Dom) and hypoxia (Dom/hypoxia). Finally, ventilatory responses to inspired CO2 at rest were compared in each experimental condition because enhanced CO2 chemoreception might be expected to blunt the PaCO2 decrease during exercise. At rest, PaCO2 decreased from control with Dom (-5.0 +/- 0.9 Torr), hypoxia (-4.1 +/- 0.5 Torr), and Dom/hypoxia (-11.1 +/- 1.2 Torr). The PaCO2 decrease from rest to exercise was not significantly different between control (-1.7 +/- 0.6 Torr) and Dom (-1.4 +/- 0.8 Torr) but was significantly greater in hypoxia (-4.3 +/- 0.7 Torr) and Dom/hypoxia (-3.5 +/- 0.9 Torr). The slope of the ventilation vs. CO2 production relationship in exercise increased with Dom (16%), hypoxia (18%), and Dom/hypoxia (68%). Ventilatory responses to inspired CO2 at rest increased from control to Dom (236%) and Dom/hypoxia (295%) and increased in four of five goats in hypoxia (mean 317%).(ABSTRACT TRUNCATED AT 250 WORDS)

Effect of acetazolamide on gas exchange and acid-base control after maximal exercise

1992 ◽  
Vol 72 (1) ◽  
pp. 278-287 ◽  
Author(s):  
J. M. Kowalchuk ◽  
G. J. Heigenhauser ◽  
J. R. Sutton ◽  
N. L. Jones
Keyword(s):  
Carbonic Anhydrase ◽  
Muscle Power ◽  
Inorganic Ions ◽  
Carbonic Anhydrase Activity ◽  
Co2 Production ◽  
Acid Base ◽  
Carbonic Anhydrase Inhibition ◽  
Severe Exercise ◽  
Arterial Plasma ◽  
End Tidal

To investigate the interactions between the systems that contribute to acid-base homeostasis after severe exercise, we studied the effects of carbonic anhydrase inhibition on exchange of strong ions and CO2 in six subjects after 30 s of maximal isokinetic cycling exercise. Each subject exercised on two randomly assigned occasions, a control (CON) condition and 30 min after intravenous injection of 1,000 mg acetazolamide (ACZ) to inhibit blood carbonic anhydrase activity. Leg muscle power output was similar in the two conditions; peak O2 uptake (VO2) after exercise was lower in ACZ (2,119 +/- 274 ml/min) than in CON (2,687 +/- 113, P less than 0.05); peak CO2 production (VCO2) was also lower (2,197 +/- 241 in ACZ vs. 3,237 +/- 87 in CON, P less than 0.05) and was accompanied by an increase in the recovery half-time from 1.7 min in CON to 2.3 min in ACZ. Whereas end-tidal PCO2 was lower in ACZ than in CON, arterial PCO2 (PaCO2) was higher, and a large negative end-tidal-to-arterial difference (less than or equal to 20 Torr) was present in ACZ on recovery. In ACZ, postexercise increases in arterial plasma [Na+] and [K+] were greater but [La-] was lower. Arteriovenous differences across the forearm showed a greater uptake of La- and Cl- in CON than in ACZ. Carbonic anhydrase inhibition with ACZ, in addition to impairing equilibration of the CO2 system to the acid-base challenge of exercise, was accompanied by changes in equilibration of strong inorganic ions. A lowered plasma [La-] was not accompanied by greater uptake of La- by inactive muscle.

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