Influence of cerebral activity in wakefulness on regulation of breathing

1961 ◽  
Vol 16 (1) ◽  
pp. 15-20 ◽  
Author(s):  
B. Raymond Fink
Keyword(s):  
Carbon Dioxide ◽  
Control Volume ◽  
Control Level ◽  
Periodic Breathing ◽  
Carbon Dioxide Tension ◽  
Respiratory Drive ◽  
Healthy Men ◽  
Cerebral Activity ◽  
Control Frequency ◽  
Regulation Of Breathing

Thirteen healthy men, unaware of the objectives of this study, underwent passive or active overventilation lowering the end-expiration carbon dioxide tension to 25 mm. Hg or below. At the end of the period of hyperventilation, rhythmic respiration continued uninterrupted at approximately the control frequency. The volume of ventilation was above control during the first minute of recovery and then stabilized at about two-thirds of the control volume; it continued at this level for over 10 minutes during which time the end-expiration PCO2 gradually rose toward the control level. No instance of periodic breathing occurred. The absence of overventilatory apnea in the waking condition contrasts with its easy elicitation during general anesthesia. It is concluded that cerebral activity associated with wakefulness is a component of the normal respiratory drive, and that carbon dioxide acts by augmenting the effects of this component. Submitted on June 27, 1960

scholarly journals Effect of Nitric Oxide Blockade by NG-Nitro-l-Arginine on Cerebral Blood Flow Response to Changes in Carbon Dioxide Tension

1992 ◽  
Vol 12 (6) ◽  
pp. 947-953 ◽  
Author(s):  
Qiong Wang ◽  
Olaf B. Paulson ◽  
Niels A. Lassen
Keyword(s):  
Nitric Oxide ◽  
Carbon Dioxide ◽  
Blood Pressure ◽  
Control Level ◽  
Inhibitory Effect ◽  
Carbon Dioxide Tension ◽  
Extracellular Acidosis ◽  
Flow Response ◽  
Arterial Blood ◽  
Oxide Synthase

The importance of nitric oxide (NO) for CBF variations associated with arterial carbon dioxide changes was investigated in halothane-anesthetized rats by using an inhibitor of nitric oxide synthase, NG-nitro-l-arginine (NOLAG). CBF was measured by intracarotid injection of 133Xe. In normocapnia, intracarotid infusion of 1.5, or 7.5, or 30 mg/kg NOLAG induced a dose-dependent increase of arterial blood pressure and a decrease of normocapnic CBF from 85 ± 10 to 78 ± 6, 64 ± 5, and 52 ± 5 ml 100g−1 min−1, respectively. This effect lasted for at least 2 h. Raising Paco2 from a control level of 40 to 68 mm Hg increased CBF to 230 ± 27 ml 100g−1 min−1, corresponding to a percentage CBF response (CO2 reactivity) of 3.7 ± 0.6%/mm Hg Paco2 in saline-treated rats. NOLAG attenuated this reactivity by 32, 49, and 51% at the three-dose levels. Hypercapnia combined with angiotensin to raise blood pressure to the same level as the highest dose of NOLAG did not affect the CBF response to hypercapnia. l-Arginine significantly prevented the effect of NOLAG on normocapnic CBF as well as blood pressure and also abolished its inhibitory effect on hypercapnic CBF. d-Arginine had no such effect. Decreasing Paco2 to 20 mm Hg reduced control CBF to 46 ± 3 ml 100g−1 min−1 with no further reduction after NOLAG. Furthermore, NOLAG did not change the percentage CBF response to an extracellular acidosis induced by acetazolamide (50 mg/kg). The results suggest that NO or a closely related compound is involved in the regulation of CBF in normocapnia and even more so in hypercapnia.

Clinical evaluation of an instrument to measure carbon dioxide tension at the oxygenator gas outlet in cardiopulmonary bypass

Perfusion ◽  
2006 ◽  
Vol 21 (1) ◽  
pp. 21-26 ◽  
Author(s):  
Frode Kristiansen ◽  
Jan Olav Høgetveit ◽  
Thore H Pedersen
Keyword(s):  
Carbon Dioxide ◽  
Cardiopulmonary Bypass ◽  
Venous Blood ◽  
Carbon Dioxide Tension ◽  
Circuit Board ◽  
Separate Analysis ◽  
Blood Gas ◽  
Arterial Blood ◽  
Gas Measurement ◽  
Venous Blood Gas

This paper presents the clinical testing of a new capno-graph designed to measure the carbon dioxide tension at the oxygenator exhaust outlet in cardiopulmonary bypass (CPB). During CPB, there is a need for reliable, accurate and instant estimates of the arterial blood CO2 tension (PaCO2) in the patient. Currently, the standard practice for measuring PaCO2 involves the manual collection of intermittent blood samples, followed by a separate analysis performed by a blood gas analyser. Probes for inline blood gas measurement exist, but they are expensive and, thus, unsuitable for routine use. A well-known method is to measure PexCO2, ie, the partial pressure of CO2 in the exhaust gas output from the oxygenator and use this as an indirect estimate for PaCO2. Based on a commercially available CO2 sensor circuit board, a laminar flow capnograph was developed. A standard sample line with integrated water trap was connected to the oxygenator exhaust port. Fifty patients were divided into six different groups with respect to oxygenator type and temperature range. Both arterial and venous blood gas samples were drawn from the CPB circuit at various temperatures. Alfa-stat corrected pCO2 values were obtained by running a linear regression for each group based on the arterial temperature and then correcting the PexCO2 accordingly. The accuracy of the six groups was found to be (±SD): ±4.3, ±4.8, ±5.7, ±1.0, ±3.7 and ±2.1%. These results suggest that oxygenator exhaust capnography is a simple, inexpensive and reliable method of estimating the PaCO2 in both adult and pediatric patients at all relevant temperatures.

The Influence of Foetal Outcome of Maternal Carbon Dioxide Tension at Caesarean Section Under General Anaesthesia

1985 ◽  
Vol 5 (3) ◽  
pp. 113
Author(s):  
P. T. Cook ◽  
K. Bernstein ◽  
L. Gisselsson ◽  
L. Jacodsson ◽  
S. Ohrlander ◽  
...  
Keyword(s):  
Carbon Dioxide ◽  
Caesarean Section ◽  
General Anaesthesia ◽  
Carbon Dioxide Tension ◽  
Foetal Outcome

Breathing in brief exercise

1960 ◽  
Vol 15 (4) ◽  
pp. 583-588 ◽  
Author(s):  
F. N. Craig ◽  
E. G. Cummings
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Uptake ◽  
Respiratory Exchange Ratio ◽  
Metabolic Cost ◽  
Carbon Dioxide Tension ◽  
Minute Volume ◽  
Carbon Dioxide Output ◽  
Respiratory Minute Volume ◽  
Before And After

Two men ran for 20 or 60 seconds while inhaling air, oxygen or 4% carbon dioxide. Inspired respiratory minute volume was determined for each breath. Ventilation increased suddenly in the first breath with minimal changes in end-expiratory carbon dioxide tension and respiratory exchange ratio to a rate that remained constant for 20 seconds before increasing further. The rate of carbon dioxide output was uniform during the first 20 seconds. A 12% grade did not increase ventilation or oxygen uptake during runs of 20 seconds, but in the first minute of recovery, ventilation was 64% greater than after level runs. Inhalation of oxygen inhibited ventilation by 24% in the 20-second periods before and after the end of a 60-second run. Inhalation of carbon dioxide begun at rest produced increments in ventilation and end-expiratory carbon dioxide tension that varied little during running and recovery. In the 20-second runs ventilation varied with speed but appeared independent of ultimate metabolic cost. Submitted on January 21, 1960

Oxygen uptake, acid-base status, and performance with varied inspired oxygen fractions

1980 ◽  
Vol 49 (5) ◽  
pp. 863-868 ◽  
Author(s):  
R. P. Adams ◽  
H. G. Welch
Keyword(s):  
Carbon Dioxide ◽  
Oxygen Uptake ◽  
Bicycle Ergometer ◽  
Carbon Dioxide Tension ◽  
Limiting Factor ◽  
Vo2 Max ◽  
And Performance ◽  
Lactate Levels ◽  
Performance Times ◽  
Inspired Oxygen

Six subjects rode a bicycle ergometer on three occasions breathing 17, 21, or 60% oxygen. In addition to rest and recovery periods, each subject worked for 10 min at 55% of maximal oxygen uptake (VO2 max) and then to exhaustion at approximately 90% VO2 max. Performance time, inspired and expired gas fractions, ventilation, and arterialized venous oxygen tension (PO2), carbon dioxide tension (PCO2), lactate, and pH were measured. VO2, carbon dioxide output, [H+]a, and [HCO3-]a were calculated. Performance times were longer in hyperoxia than in normoxia or hypoxia. However, VO2 was not different at exhaustion in normoxia compared with hypoxia or hyperoxia. During exercise, hypoxia was associated with increased lactate levels and decreased [H+]a, PCO2, and [HCO3-]a. The opposite trends were generally associated with hyperoxia. At exhaustion, [H+]a was not different under any inspired oxygen fraction. These results support the contention that oxygen is not limiting for exercise of this intensity and duration. The results also suggest that [H+] is a possible limiting factor and that the effect of oxygen on performance is perhaps related to control of [H+].

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