Mechanism of transient nocturnal hypoxemia in hypoxic chronic bronchitis and emphysema

1985 ◽  
Vol 59 (6) ◽  
pp. 1698-1703 ◽  
Author(s):  
J. R. Catterall ◽  
P. M. Calverley ◽  
W. MacNee ◽  
P. M. Warren ◽  
C. M. Shapiro ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Chronic Bronchitis ◽  
Rem Sleep ◽  
Normal Subjects ◽  
Arterial Pco2 ◽  
Content Difference ◽  
Nocturnal Hypoxemia ◽  
Voluntary Hypoventilation ◽  
Arterial Po2 ◽  
Mixed Venous

In five patients with hypoxic chronic bronchitis and emphysema we measured ear O2 saturation (SaO2), chest movement, oronasal airflow, arterial and mixed venous gas tensions, and cardiac output during nine hypoxemic episodes (HE; SaO2 falls greater than 10%) in rapid-eye-movement (REM) sleep and during preceding periods of stable oxygenation in non-REM sleep. All nine HE occurred with recurrent short episodes of reduced chest movement, none with sleep apnea. The arterial PO2 (PaO2) fell by 6.0 +/- 1.9 (SD) Torr during the HE (P less than 0.01), but mean arterial PCO2 (PaCO2) rose by only 1.4 +/- 2.4 Torr (P greater than 0.4). The arteriovenous O2 content difference fell by 0.64 +/- 0.43 ml/100 ml of blood during the HE (P less than 0.05), but there was no significant change in cardiac output. Changes observed in PaO2 and PaCO2 during HE were similar to those in four normal subjects during 90 s of voluntary hypoventilation, when PaO2 fell by 12.3 +/- 5.6 Torr (P less than 0.05), but mean PaCO2 rose by only 2.8 +/- 2.1 Torr (P greater than 0.4). We suggest that the transient hypoxemia which occurs during REM sleep in patients with chronic bronchitis and emphysema could be explained by hypoventilation during REM sleep but that the importance of changes in distribution of ventilation-perfusion ratios cannot be assessed by presently available techniques.

Effect of analyzer on determination of mixed venous PCO2 and cardiac output during exercise

1995 ◽  
Vol 79 (3) ◽  
pp. 1032-1038 ◽  
Author(s):  
L. Hornby ◽  
A. L. Coates ◽  
L. C. Lands
Keyword(s):  
Cardiac Output ◽  
Gas Mixture ◽  
Arterial Pco2 ◽  
Venous Pco2 ◽  
The Face ◽  
High O2 ◽  
Collision Broadening ◽  
Rebreathing Methods ◽  
Mixed Venous

Cardiac output (CO) during exercise can be determined noninvasively by using the indirect Fick CO2-rebreathing technique. CO2 measurements for this technique are usually performed with an infrared analyzer (IA) or mass spectrometer (MS). However, IA CO2 measurements are susceptible to underreading in the face of high O2 concentrations because of collision broadening. We compared an IA (Ametek model CD-3A) with a MS (Marquette model MGA-1100) to see the effect this would have on mixed venous PCO2 (PVCO2) and CO measurements. After calibration with room air and a gas mixture of 5% CO2–12% O2–83% N2, both devices were tested with three different gas mixtures of CO2 in O2. For each gas mixture, IA gave lower CO2 values than did the MS (4.1% CO2: IA, 3.85 +/- 0.01% and MS, 4.13 +/- 0.01%; 9.2% CO2: IA, 8.44 +/- 0.07% and MS, 9.19 +/- 0.01%; 13.8% CO2: IA, 12.57 +/- 0.15% and MS, 13.82 +/- 0.01%). Warming and humidifying the gases did not alter the results. The IA gave lower values than did the MS for eight other medical gases in lower concentrations of O2 (40–50%). Equilibrium and exponential rebreathing procedures were performed. Values determined by the IA were > 10% higher than those determined by the MS for both rebreathing methods. We conclude that all IAs must be checked for collision broadening if they are to be used in environments where the concentration of O2 is > 21%. If collision broadening is present, then either a special high O2-CO2 calibration curve must be constructed, or the IA should not be used for both arterial PCO2 and PVCO2 estimates because it may produce erroneously low PVCO2 values, with resultant overestimation of CO.

Relationship between cardiac output and mixed venous-arterial Pco2 gradient in sodium bicarbonate-treated dogs

Resuscitation ◽  
1995 ◽  
Vol 29 (3) ◽  
pp. 266
Author(s):  
K Okamoto ◽  
H Kishi ◽  
H Choi ◽  
M Kurose ◽  
T Sato ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Sodium Bicarbonate ◽  
Arterial Pco2 ◽  
Mixed Venous

Circulatory response to arterial hyperoxia

1979 ◽  
Vol 46 (5) ◽  
pp. 973-977 ◽  
Author(s):  
Y. Cassuto ◽  
L. E. Farhi
Keyword(s):  
Cardiac Output ◽  
Lactic Acidosis ◽  
The Other ◽  
O2 Uptake ◽  
Right Heart ◽  
Arterial Pco2 ◽  
Circulatory Response ◽  
Systemic Artery ◽  
The Right ◽  
Arterial Po2

We have studied the circulatory response to 100% O2 at 1 and 3 atm, using unanesthetized rabbits in which a systemic artery and the right heart had been cannulated previously. One group of animals served as controls; the other was infused with a flurocarbon emulsion that boosted blood O2 solubility to approximately 5 ml.100 ml-1.atm-1. Exposure to hyperoxia caused an identical sustained rise in arterial PO2 in both groups. O2 uptake was measured during normobaric exposure to 100% O2 and was found to be the same as in control conditions. There was an immediate rise in right heart PO2, more marked in infused animals, but this increase was only temporary, and PO2 dropped, while the right heart-arterial PCO2 difference rose, indicating a gradual fall in cardiac output. This readjustment occurred at a faster rate in the infused animals, a difference that led us to conclude that the peripheral response to hyperoxia is influenced by factors other than arterial PO2. The pronounced decrease in cardiac output seen in infused rabbits was accompanied by lactic acidosis, implying that some of the animals' tissues were becoming hypoxic in the presence of arterial hyperoxia.

scholarly journals Oxygen transfer during aerobic exercise in a varanid lizardVaranus mertensiis limited by the circulation

2002 ◽  
Vol 205 (17) ◽  
pp. 2725-2736 ◽  
Author(s):  
Peter Frappell ◽  
Tim Schultz ◽  
Keith Christian
Keyword(s):  
Cardiac Output ◽  
Oxygen Transfer ◽  
Maximal Exercise ◽  
Saturation Curve ◽  
Direct Proportion ◽  
Content Difference ◽  
Air Convection ◽  
Hemoglobin Saturation ◽  
Rate Of Oxygen Consumption ◽  
Arterial Po2

SUMMARYOxygen transfer during sustained maximal exercise while locomoting on a treadmill at 0.33 m s-1 was examined in a varanid lizard Varanus mertensi at 35 °C. The rate of oxygen consumption(V̇O2) increased with locomotion from 3.49±0.75 (mean ± S.D.) to 14.0±4.0 ml O2 kg-1 min-1. Ventilation(V̇E) increased, aided by increases in both tidal volume and frequency, in direct proportion to V̇O2. The air convection requirement(V̇E/V̇O2=27)was therefore maintained, together with arterial PaCO2 and PaO2. The alveolar—arterial PO2 difference(PAO2—PaO2)also remained unchanged during exercise from its value at rest, which was approximately 20 mmHg. Pulmonary diffusion for carbon monoxide(0.116±0.027 ml kg-1 min-1 mmHg-1) was double the value previously reported in V. exanthematicus and remained unchanged with exercise. Furthermore, exercise was associated with an increase in the arterial—venous O2 content difference(CaO2—CvO2),which was assisted by a marked Bohr shift in the hemoglobin saturation curve and further unloading of venous O2. During exercise the increase in cardiac output (Q̇tot) did not match the increase in V̇O2, such that the blood convection requirement(Q̇tot/V̇O2)decreased from the pre-exercise value of approximately 35 to 16 during exercise. Together, the results suggest that ventilation and O2transfer across the lung are adequate to meet the aerobic needs of V. mertensi during exercise, but the decrease in the blood convection requirement in the presence of a large arterial—venous O2content difference suggests that a limit in the transport of O2 is imposed by the circulation.

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.

Estimation of the Resting Reflex Hypoxic Drive to Respiration in Patients with Diffuse Pulmonary Infiltration

1976 ◽  
Vol 50 (2) ◽  
pp. 109-114 ◽  
Author(s):  
R. A. Stockley ◽  
K. D. Lee
Keyword(s):  
Chronic Bronchitis ◽  
Respiratory Drive ◽  
Breath Tests ◽  
Arterial Pco2 ◽  
Pulmonary Infiltration ◽  
Arterial Po2

1. Oxygen breath tests were performed in nine patients with diffuse pulmonary infiltration whose resting arterial Po2 (Pa,o2) ranged from 8·9 kPa to 11·8 kPa. The inspired air was suddenly replaced with oxygen for 30 s and the percentage fall in ventilation over the last 10 s was measured. 2. Pa,o2 rose rapidly and exceeded 16 kPa within 20 s in each patient. 3. The ventilation fell significantly in seven of the nine patients. It is concluded that these seven patients had a demonstrable reflex hypoxic respiratory drive at rest. This tended to be greatest in patients with the lowest Pa,o2. The percentage falls in ventilation observed were similar to those previously reported at comparable Pa,o2 levels in patients with chronic bronchitis. 4. The resting arterial Pco2 (Pa,co2) ranged from 50 to 5·8 kPa. It did not change by more than 0·3 kPa during the oxygen breath tests in any patient.

Ventilatory control during exercise in calves with artificial hearts

1990 ◽  
Vol 68 (6) ◽  
pp. 2604-2611 ◽  
Author(s):  
A. Huszczuk ◽  
B. J. Whipp ◽  
T. D. Adams ◽  
A. G. Fisher ◽  
R. O. Crapo ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Treadmill Exercise ◽  
Ventilatory Control ◽  
Arterial Pco2 ◽  
Ventilatory Responses ◽  
Output Increase ◽  
Exercise Hyperpnea ◽  
Artificial Hearts ◽  
Arterial Po2

To determine the role of cardiac reflexes in mediating exercise hyperpnea, we investigated ventilatory responses to treadmill exercise in seven calves with artificial hearts and seven controls. In both groups, the ventilatory responses were adequate for the metabolic demands of the exercise; this resulted in regulation of arterial PCO2 and pH despite the absence of cardiac output increase in the implanted group. In this group, there was a small but significant reduction of arterial PO2 by 4 +/- 3 Torr and a rise of blood lactate by 1.1 +/- 1 mmol/l. When cardiac output was experimentally increased in the implanted calves to a level commensurate with that spontaneously occurring in the control calves, ventilation was not affected. However, experimental reductions of cardiac output led to an immediate augmentation of exercise hyperpnea by 4.56 +/- 4.3 l/min and a further significant lactate increase of 1.2 +/- 1.22 mmol/l that was associated with a significant decrease in the exercise O2 consumption (0.32 +/- 0.13 l/min). These observations indicate that neither cardiac nor hemodynamic effects of increased cardiac output constitute an obligatory cause of exercise hyperpnea in the calf.

Evaluation of a method for estimating cardiac output from a single breath in humans

1982 ◽  
Vol 53 (4) ◽  
pp. 1034-1038 ◽  
Author(s):  
H. Chen ◽  
N. P. Silverton ◽  
R. Hainsworth
Keyword(s):  
Cardiac Output ◽  
Normal Subjects ◽  
Random Errors ◽  
Tolerance Limits ◽  
Mean Values ◽  
Single Breath ◽  
Significant Difference ◽  
Venous Pco2 ◽  
Mixed Venous ◽  
Single Breath Method

We have modified the single-breath method of Kim et al. (J. Appl. Physiol. 21: 1338–1344, 1966) for estimating cardiac output and arterial and mixed venous carbon dioxide tensions (PCO2). We assessed this using 30 normal subjects and 23 cardiac patients. The procedure was performed satisfactorily in all but two patients. The random errors, from 60 pairs of estimates of cardiac output in normal subjects and 50 pairs in patients, were +/- 12.8 and +/- 19.6% (95% tolerance limits; i.e., coefficient of variation multiplied by 2 for n greater than 50). The systematic error was assessed in 15 patients from comparisons with results obtained by the direct Fick method. There was no significant difference except in two patients with large intracardiac shunts. Mean values of cardiac output by single-breath and direct Fick estimates were 3.80 and 3.83 l/min. Arterial and mixed venous PCO2 were estimated by the single-breath method with random errors of +/- 1.5 and +/- 1.4 Torr, respectively, and no significant systematic errors. We conclude that our modification of the single-breath method is reliable in humans at rest, although the procedures for delivering the breath and processing the data are of critical importance.

Effect of 30% Oxygen on Local Matching of Perfusion and Ventilation in Chronic Airways Obstruction

1977 ◽  
Vol 53 (4) ◽  
pp. 387-395 ◽  
Author(s):  
Noemi M. Eiser ◽  
Hazel A. Jones ◽  
J. M. B. Hughes
Keyword(s):  
Chronic Bronchitis ◽  
Minute Ventilation ◽  
Normal Subjects ◽  
Systematic Change ◽  
Lung Field ◽  
Arterial Pco2 ◽  
Oxygen Breathing ◽  
Airways Obstruction ◽  
Hypoxic Vasoconstriction ◽  
Change In The Mean

1. Sixteen patients with chronic bronchitis and airways obstruction were given radioactive nitrogen (13N) by intravenous injection and by inhalation, while breathing air and after 10–20 min breathing 30% oxygen. The clearance of 13N from four zones of each patient's whole lung field was monitored. 2. The 13N clearance of each region in these patients with chronic bronchitis was much slower than in normal subjects. Oxygen breathing produced a significant delay in the clearance of intravenously administered 13N in 23 zones in 10 patients but no systematic change in clearance after inhaled 13N. 3. With inhalation of 30% oxygen there was no significant change in the mean minute ventilation, tidal volume or arterial Pco2. 4. The results suggest that local hypoxic vasoconstriction is present in some patients on breathing air and that this is relieved by 30% oxygen, resulting in a diversion of local blood flow from well-ventilated to more poorly ventilated areas. The fall in V̇A/Q̇ on 30% oxygen is insufficient to increase arterial Pco2.

Peripheral circulatory responses to 96 h of hypoxia in conscious sinoaortic-denervated sheep

1986 ◽  
Vol 250 (5) ◽  
pp. R868-R874
Author(s):  
J. A. Krasney ◽  
K. Miki ◽  
K. McAndrews ◽  
G. Hajduczok ◽  
D. Curran-Everett
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Pressure ◽  
Coronary Flow ◽  
Systemic Arterial Pressure ◽  
Arterial Pco2 ◽  
Blood Flows ◽  
Pulmonary Arterial ◽  
Conscious Sheep ◽  
Arterial Po2

Conscious sheep exposed to 4 days of eucapnic hypoxia (arterial PO2 40 Torr, arterial PCO2 33 Torr) respond with sustained increases in heart rate, cardiac output, and coronary, cerebral, and respiratory muscle blood flows (Respir. Physiol. 59: 197-211, 1985). In the present investigation, seven adult ewes were studied during similar levels of hypoxia (arterial PO2 40 Torr, 4 days) after chronic section of the carotid sinus and aortic depressor nerves to determine the contribution of the arterial chemoreceptors to these responses. Ventilation and arterial PCO2 did not change, indicating that ventilatory acclimation did not occur. O2 consumption decreased by 24%. Cardiac output (thermodilution) increased by 12% for only 24 h, heart rate increased by 44-69% above normoxic levels for only 72 h, and stroke volume was unchanged. Systemic arterial pressure was unchanged, whereas pulmonary arterial pressure rose by 56%. Coronary flow (radio-labeled microspheres) increased from 155 +/- 50.4 (SE) to 299 +/- 81 ml X min-1 X 100 g-1 at 24 h and then declined to normoxic levels by 96 h. Cerebral flow rose from 62 +/- 6.5 to between 85 +/- 14.4 and 124 +/- 43.5 ml X min-1 X 100 g-1 for 96 h. These results indicate that the arterial chemoreflexes or reflexes secondary to increased ventilation are responsible for the continued elevation of heart rate, cardiac output, and coronary flow during eucapnic hypoxia.

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