Differences between estimates and measured Pa CO 2 during rest and exercise in older subjects

1997 ◽  
Vol 83 (1) ◽  
pp. 312-316 ◽  
Author(s):  
J. S. Williams ◽  
T. G. Babb
Keyword(s):  
Good Accuracy ◽  
Maximal Exercise ◽  
Ventilatory Threshold ◽  
Correlation Coefficients ◽  
Blood Gases ◽  
Arterial Blood ◽  
Older Subjects ◽  
Mean Differences ◽  
End Tidal ◽  
Rest And Exercise

Williams, J. S., and T. G. Babb. Differences between estimates and measured [Formula: see text] during rest and exercise in older subjects. J. Appl. Physiol. 83(1): 312–316, 1997.—Arterial[Formula: see text]([Formula: see text]) has been estimated during exercise with good accuracy in younger individuals by using the Jones equation (PJ co 2) ( J. Appl. Physiol. 47: 954–960, 1979). The purpose of this project was to determine the utility of estimating [Formula: see text] from end-tidal[Formula: see text]([Formula: see text]) or PJ co 2at rest, ventilatory threshold (V˙Th), and maximal exercise (Max) in older subjects.[Formula: see text] was determined from respired gases simultaneously (MGA 1100) with arterial blood gases (radial arterial catheter) in 12 older and 11 younger subjects at rest and during exercise. Mean differences were analyzed with paired t-tests, and relationships between the estimated [Formula: see text] values and the actual values of [Formula: see text] were determined with correlation coefficients. In the older subjects,[Formula: see text] was not significantly different from [Formula: see text] at rest (−1.2 ± 4.3 Torr), V˙Th (0.4 ± 2.5), or Max (−0.8 ± 2.7), and the two were significantly ( P < 0.05) correlated atV˙th ( r = 0.84) and Max ( r = 0.87) but not at rest ( r = 0.47). PJ co 2was similar to [Formula: see text] at rest (−1.0 ± 3.9) and V˙th (−1.3 ± 2.3) but significantly lower at Max (−3.0 ± 2.6), and the two were significantly correlated at V˙th ( r = 0.86) and Max ( r = 0.80) but not at rest ( r = 0.54).[Formula: see text] was significantly higher than [Formula: see text] during exercise in the younger subjects but similar to [Formula: see text] at rest. PJ co 2was similar to [Formula: see text] at rest andV˙th but significantly lower at Max in younger subjects. In conclusion, our data demonstrate that[Formula: see text] during exercise is better estimated by [Formula: see text] than by PJ co 2in older subjects, contrary to what is observed in younger subjects. This appears to be related to the finding that[Formula: see text] does not exceed[Formula: see text] during exercise in older subjects, as occurs in the younger subjects. However,[Formula: see text] at rest is best estimated by PJ co 2in both younger and older subjects.

scholarly journals Can peripheral venous blood gases replace arterial blood gases in emergency department patients?

CJEM ◽  
2002 ◽  
Vol 4 (01) ◽  
pp. 7-15 ◽  
Author(s):  
Louise C.F. Rang ◽  
Heather E. Murray ◽  
George A. Wells ◽  
Cameron K. MacGougan
Keyword(s):  
Venous Blood ◽  
Correlation Coefficients ◽  
Blood Gases ◽  
Blood Gas ◽  
Emergency Physicians ◽  
Peripheral Venous Blood ◽  
Arterial Blood ◽  
The Mean ◽  
Mean Differences ◽  
Venous Blood Gas

ABSTRACTObjective:To determine if peripheral venous blood gas values for pH, partial pressure of carbon dioxide (PCO2) and the resultant calculated bicarbonate (HCO3) predict arterial values accurately enough to replace them in a clinical setting.Methods:This prospective observational study was performed in a university tertiary care emergency department from June to December 1998. Patients requiring arterial blood gas analysis were enrolled and underwent simultaneous venous blood gas sampling. The following data were prospectively recorded: age, sex, presenting complaint, vital signs, oxygen saturation, sample times, number of attempts and indication for testing. Correlation coefficients and mean differences with 95% confidence intervals (CIs) were calculated for pH,PCO2and HCO3. A survey of 45 academic emergency physicians was performed to determine the minimal clinically important difference for each variable.Results:The 218 subjects ranged in age from 15 to 90 (mean 60.4) years. The 2 blood samples were drawn within 10 minutes of each other for 205 (96%) of the 214 patients for whom data on timing were available. Pearson’s product–moment correlation coefficients between arterial and venous values were as follows: pH, 0.913;PCO2, 0.921; and HCO3, 0.953. The mean differences (and 95% CIs) between arterial and venous samples were as follows: pH, 0.036 (0.030–0.042);PCO2, 6.0 (5.0–7.0) mm Hg; and HCO3, 1.5 (1.3–1.7) mEq/L. The mean differences (± 2 standard deviations) were greater than the minimum clinically important differences identified in the survey.Conclusions:Arterial and venous blood gas samples were strongly correlated, and there were only small differences between them. A survey of emergency physicians suggested that the differences are too large to allow for interchangeability of results; however, venous values may be valid if used in conjunction with a correction factor or for trending purposes.

Role of tracheal and bronchial circulation in respiratory heat exchange

1985 ◽  
Vol 58 (1) ◽  
pp. 217-222 ◽  
Author(s):  
E. M. Baile ◽  
R. W. Dahlby ◽  
B. R. Wiggs ◽  
P. D. Pare
Keyword(s):  
Blood Flow ◽  
Blood Gases ◽  
Lung Parenchyma ◽  
Arterial Blood ◽  
Respiratory Heat Loss ◽  
Reference Flow ◽  
Pulmonary Arterial ◽  
End Tidal ◽  
Humidified Air

Due to their anatomic configuration, the vessels supplying the central airways may be ideally suited for regulation of respiratory heat loss. We have measured blood flow to the trachea, bronchi, and lung parenchyma in 10 anesthetized supine open-chest dogs. They were hyperventilated (frequency, 40; tidal volume 30–35 ml/kg) for 30 min or 1) warm humidified air, 2) cold (-20 degrees C dry air, and 3) warm humidified air. End-tidal CO2 was kept constant by adding CO2 to the inspired ventilator line. Five minutes before the end of each period of hyperventilation, measurements of vascular pressures (pulmonary arterial, left atrial, and systemic), cardiac output (CO), arterial blood gases, and inspired, expired, and tracheal gas temperatures were made. Then, using a modification of the reference flow technique, 113Sn-, 153Gd-, and 103Ru-labeled microspheres were injected into the left atrium to make separate measurements of airway blood flow at each intervention. After the last measurements had been made, the dogs were killed and the lungs, including the trachea, were excised. Blood flow to the trachea, bronchi, and lung parenchyma was calculated. Results showed that there was no change in parenchymal blood flow, but there was an increase in tracheal and bronchial blood flow in all dogs (P less than 0.01) from 4.48 +/- 0.69 ml/min (0.22 +/- 0.01% CO) during warm air hyperventilation to 7.06 +/- 0.97 ml/min (0.37 +/- 0.05% CO) during cold air hyperventilation.

scholarly journals Measuring the human ventilatory and cerebral blood flow response to CO2: a technical consideration for the end-tidal-to-arterial gas gradient

2016 ◽  
Vol 120 (2) ◽  
pp. 282-296 ◽  
Author(s):  
Michael M. Tymko ◽  
Ryan L. Hoiland ◽  
Tomas Kuca ◽  
Lindsey M. Boulet ◽  
Joshua C. Tremblay ◽  
...  
Keyword(s):  
Blood Flow ◽  
Minute Ventilation ◽  
Linear Regression Analysis ◽  
Blood Gases ◽  
Prediction Equation ◽  
Flow Response ◽  
Arterial Blood ◽  
Reactivity Test ◽  
End Tidal ◽  
Gas Gradients

Our aim was to quantify the end-tidal-to-arterial gas gradients for O2 (PET-PaO2) and CO2 (Pa-PETCO2) during a CO2 reactivity test to determine their influence on the cerebrovascular (CVR) and ventilatory (HCVR) response in subjects with (PFO+, n = 8) and without (PFO−, n = 7) a patent foramen ovale (PFO). We hypothesized that 1) the Pa-PETCO2 would be greater in hypoxia compared with normoxia, 2) the Pa-PETCO2 would be similar, whereas the PET-PaO2 gradient would be greater in those with a PFO, 3) the HCVR and CVR would be underestimated when plotted against PETCO2 compared with PaCO2, and 4) previously derived prediction algorithms will accurately target PaCO2. PETCO2 was controlled by dynamic end-tidal forcing in steady-state steps of −8, −4, 0, +4, and +8 mmHg from baseline in normoxia and hypoxia. Minute ventilation (V̇E), internal carotid artery blood flow (Q̇ICA), middle cerebral artery blood velocity (MCAv), and temperature corrected end-tidal and arterial blood gases were measured throughout experimentation. HCVR and CVR were calculated using linear regression analysis by indexing V̇E and relative changes in Q̇ICA, and MCAv against PETCO2, predicted PaCO2, and measured PaCO2. The Pa-PETCO2 was similar between hypoxia and normoxia and PFO+ and PFO−. The PET-PaO2 was greater in PFO+ by 2.1 mmHg during normoxia ( P = 0.003). HCVR and CVR plotted against PETCO2 underestimated HCVR and CVR indexed against PaCO2 in normoxia and hypoxia. Our PaCO2 prediction equation modestly improved estimates of HCVR and CVR. In summary, care must be taken when indexing reactivity measures to PETCO2 compared with PaCO2.

Abstract 10355: Physiologic Effect of Repeated Epinephrine Doses During Cardiopulmonary Resuscitation: A Randomized Porcine Study

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Bjarne Madsen Härdig ◽  
Michael Götberg ◽  
Malin Rundgren ◽  
Matthias Götberg ◽  
David Zughaft ◽  
...  
Keyword(s):  
Systolic Pressure ◽  
Blood Gases ◽  
Brain Perfusion ◽  
Saline Control ◽  
Control Group ◽  
Arterial Blood ◽  
Pressure Peak ◽  
Blood Pressures ◽  
Lactate Levels ◽  
End Tidal

Objectives and Method: This porcine study was designed to explore the effect of repetitive epinephrine (EPI) doses on physiologic parameters during CPR. Thirty-six adult pigs were randomized to four injections of: EPI 0.02 mg/kg/dose, EPI 0.03 mg/kg/dose or saline control, given during 15 minutes of CPR. The effect on systolic, diastolic and mean arterial blood pressures (ABP), cerebral perfusion pressure (CePP), end tidal carbon dioxide (ETCO2), SpO2, cerebral tissue oximetry (SctO2), were analyzed immediately prior to each injection and at peak arterial systolic pressure. Arterial blood gases was analyzed after the baseline and after 15 min. Result: Prior to and following 4 minutes of baseline chest compressions without drug administration, there were no significant differences between the three groups. In the group given a 0.02 mg/kg/dose, there were increases in all ABP’s and CePP at the first 3 pressure peaks; at the 4th only mean ABP was increased. Decreased ETCO2 following peak 1 and beyond was seen. SctO2 and SpO2 were lowered following injection 2 and beyond. In the group given a 0.03 mg/kg/dose, all ABP’s and CePP increased at the first 3 pressure peaks. Lower ETCO2 was seen at peak 1 and beyond. SctO2 and SpO2 were lower following injection 2 and beyond. In the saline control group the systolic ABP was significantly lower at pressure peak 1 and beyond, no other parameter changed significantly compared to baseline. In the two EPI groups, pH and Base Excess were lower and lactate levels higher compared to baseline as well as compared to control. Conclusion: Repetitive EPI doses increased ABP’s and CePP, but this did not translate into better organ or brain perfusion.

Simple contrivance “clamps” end-tidal P CO 2 and P O 2 despite rapid changes in ventilation

2000 ◽  
Vol 88 (5) ◽  
pp. 1597-1600 ◽  
Author(s):  
Robert B. Banzett ◽  
Ronald T. Garcia ◽  
Shakeeb H. Moosavi
Keyword(s):  
Gas Flow ◽  
Blood Gases ◽  
Alveolar Ventilation ◽  
Functional Brain Imaging ◽  
Feedback Systems ◽  
Significant Delay ◽  
Arterial Blood ◽  
Rapid Changes ◽  
The Face ◽  
End Tidal

The device described in this study uses functionally variable dead space to keep effective alveolar ventilation constant. It is capable of maintaining end-tidal[Formula: see text] and[Formula: see text] within ±1 Torr of the set value in the face of increases in breathing above the baseline level. The set level of end-tidal [Formula: see text] or[Formula: see text] can be independently varied by altering the concentration in fresh gas flow. The device comprises a tee at the mouthpiece, with one inlet providing a limited supply of fresh gas flow and the other providing reinspired alveolar gas when ventilation exceeds fresh gas flow. Because the device does not depend on measurement and correction of end-tidal or arterial gas levels, the response of the device is essentially instantaneous, avoiding the instability of negative feedback systems having significant delay. This contrivance provides a simple means of holding arterial blood gases constant in the face of spontaneous changes in breathing (above a minimum alveolar ventilation), which is useful in respiratory experiments, as well as in functional brain imaging where blood gas changes can confound interpretation by influencing cerebral blood flow.

scholarly journals Ventilatory response to exercise in subjects breathing CO2 or HeO2

1997 ◽  
Vol 82 (3) ◽  
pp. 746-754 ◽  
Author(s):  
T. G. Babb
Keyword(s):  
Maximal Exercise ◽  
Respiratory Mechanics ◽  
Ventilatory Threshold ◽  
Ventilatory Response ◽  
Minute Ventilation ◽  
Normal Lung ◽  
Normal Lung Function ◽  
Older Subjects ◽  
Breathing Room ◽  
Response To Exercise

Babb, T. G. Ventilatory response to exercise in subjects breathing CO2 or HeO2. J. Appl. Physiol. 82(3): 746–754, 1997.—To investigate the effects of mechanical ventilatory limitation on the ventilatory response to exercise, eight older subjects with normal lung function were studied. Each subject performed graded cycle ergometry to exhaustion once while breathing room air; once while breathing 3% CO2-21% O2-balance N2; and once while breathing HeO2 (79% He and 21% O2). Minute ventilation (V˙e) and respiratory mechanics were measured continuously during each 1-min increment in work rate (10 or 20 W). Data were analyzed at rest, at ventilatory threshold (VTh), and at maximal exercise. When the subjects were breathing 3% CO2, there was an increase ( P < 0.001) inV˙e at rest and at VTh but not during maximal exercise. When the subjects were breathing HeO2,V˙e was increased ( P < 0.05) only during maximal exercise (24 ± 11%). The ventilatory response to exercise below VTh was greater only when the subjects were breathing 3% CO2( P < 0.05). Above VTh, the ventilatory response when the subjects were breathing HeO2 was greater than when breathing 3% CO2( P < 0.01). Flow limitation, as percent of tidal volume, during maximal exercise was greater ( P < 0.01) when the subjects were breathing CO2 (22 ± 12%) than when breathing room air (12 ± 9%) or when breathing HeO2 (10 ± 7%) ( n = 7). End-expiratory lung volume during maximal exercise was lower when the subjects were breathing HeO2 than when breathing room air or when breathing CO2( P < 0.01). These data indicate that older subjects have little reserve for accommodating an increase in ventilatory demand and suggest that mechanical ventilatory constraints influence both the magnitude of V˙eduring maximal exercise and the regulation ofV˙e and respiratory mechanics during heavy-to-maximal exercise.

Role of the carotid body in hyperpnea of moderate exercise in goats

1982 ◽  
Vol 52 (5) ◽  
pp. 1216-1222 ◽  
Author(s):  
G. E. Bisgard ◽  
H. V. Forster ◽  
J. Mesina ◽  
R. G. Sarazin
Keyword(s):  
Metabolic Rate ◽  
Carotid Body ◽  
Blood Gases ◽  
Co2 Production ◽  
Sham Operation ◽  
Positive Interaction ◽  
Arterial Blood ◽  
Before And After ◽  
Response To Exercise ◽  
Rest And Exercise

In the present study the ventilatory response to exercise was measured in goats before and after carotid body excision (CBE) (n = 7) or sham operation (n = 1). Nine-minute periods of moderate treadmill walking were carried out under three conditions: 4.8 kph, 0% grade during normoxia and hypoxia (arterial O2 tension approximately 43 Torr) and 4.8 kph, 5% grade during normoxia. Ventilatory variables, metabolic rate, and arterial blood acid-base and blood gases were measured at 30-s intervals for the first 3 min and again during the 6th and 9th min of exercise. In normal goats during exercise in normoxia, ventilation changed in proportion to changes in metabolic rate resulting in arterial CO2 tension (PaCO2) and arterial pH (pHa) homeostasis throughout exercise. CBE resulted in nearly equivalent hypoventilation during steady-state rest and exercise (delta PaCO2 approximately equal to 5--7 Torr) during normoxia and loss of the positive interaction between hypoxia and exercise. There was also a significant disruption of PaCO2-pHa homeostasis during the first 30 s of exercise after CBE when PaCO2 was 3 Torr below rest and pHa was 0.03 units above rest. Our data indicate: 1) that the carotid chemoreceptors may contribute a similar proportional drive to breathe during rest and exercise; 2) that transient hyperventilation at the onset of exercise after CBE may indicate an important neural drive to breathe that is normally damped by intact peripheral chemoreceptors; and 3) that the mechanism linking ventilation to CO2 production remains intact after CBE.

Aortic body chemoreceptor responses to changes in PCO2 and PO2 in the cat

1979 ◽  
Vol 47 (4) ◽  
pp. 858-866 ◽  
Author(s):  
S. Lahiri ◽  
E. Mulligan ◽  
T. Nishino ◽  
A. Mokashi
Keyword(s):  
Carbon Dioxide ◽  
Discharge Rate ◽  
Arterial Oxygen Tension ◽  
Blood Gases ◽  
Carbon Dioxide Tension ◽  
Steady States ◽  
Arterial Oxygen ◽  
Arterial Blood ◽  
Discharge Rates ◽  
End Tidal

Responses of aortic chemoreceptor afferents to a range of arterial carbon dioxide tension (Paco2) changes at various levels of arterial oxygen tension (Pao2) were investigated in 18 cats anesthetized with alpha-chloralose and maintained at 38 degrees C. Aortic chemoreceptor activity, end-tidal oxygen pressure, end-tidal carbon dioxide pressure, and arterial blood pressure were continuously monitored. Arterial blood gases were measured in steady states. Single or a few clearly identifiable afferents were studied during changes and steady states of Pao2 and Paco2. All the aortic chemoreceptor afferent discharge rates increased with Paco2 increases from hypercapnia (10–15 Torr) to normocapnia and moderate hypercapnia (30–50 Torr) and with Pao2 decreases from above 400 to 30 Torr. Hypoxia augmented the response to Paco2 most effectively in the range of 10–40 Torr. At any Pao2, the discharge rate reached a plateau with sufficient intensity of hypercapnia. The Paco2 stimulus threshold at a Pao2 of 440 Torr was about 15 Torr, and at a Pao2 of 60 Torr it was 10 Torr. In the transition from hypocapnia to hypercapnia, responses increased gradually, usually without an overshoot. The steady-state responses to Paco2 of the majority of aortic chemoreceptors resembled those of carotid chemoreceptors. The responses of both receptors can be attributed to the same basic type of mechanism.

Comparison of Epidural and Systemic Tramadol for Analgesia Following Ovariohysterectomy

2012 ◽  
Vol 48 (5) ◽  
pp. 310-319 ◽  
Author(s):  
Sandra Mastrocinque ◽  
Tatiana F. Almeida ◽  
Angélica C. Tatarunas ◽  
Viviani H. Imagawa ◽  
Denise A. Otsuki ◽  
...  
Keyword(s):  
Postoperative Analgesia ◽  
Blood Gases ◽  
Arterial Blood Gases ◽  
Anesthetic Induction ◽  
Time Points ◽  
Analgesic Effects ◽  
Pain Scores ◽  
Arterial Blood ◽  
Baseline Values ◽  
End Tidal

The objective of the study was to compare epidural and systemic tramadol for postoperative analgesia in bitches undergoing ovariohysterectomy. Twenty animals, randomly divided into two groups, received either epidural (EPI) or intramuscular (IM) tramadol (2 mg/kg) 30 min before anesthetic induction. Analgesia, sedation, cardiorespiratory parameters, end-tidal isoflurane, blood catecholamines and cortisol, and arterial blood gases were measured at different time points up to 24 hr after agent administration. There were no differences between the two groups regarding cardiorespiratory parameters, end-tidal isoflurane, and pain scores. Two dogs in the IM and one in the EPI group required supplemental analgesia. Cortisol was increased (P&lt;0.05) at 120 min (3.59 μg/dL and 3.27μg/dL in the IM and EPI groups, respectively) and 240 min (2.45 μg/dL and 2.54μg/dL in the IM and EPI groups, respectively) compared to baseline. Norepinephrine was also increased (P&lt;0.05) at 120 min in both groups compared to baseline values. Epinephrine values were higher (P&lt;0.05) in the IM group compared with the EPI group at 50 min, 120 min, and 1,440 min after tramadol administration. Epidural tramadol is a safe analgesic, but does not appear to have improved analgesic effects compared with IM administration.

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