Carbon Dioxide Tension In Patients Research Articles

Variability of Resting Carbon Dioxide Tension in Patients with Intracranial Steno-occlusive Disease.

Introduction Controlling the partial pressure of carbon dioxide (PaCO 2 ) is an important consideration in patients with intracranial steno-occlusive disease to avoid reductions in critical perfusion from vasoconstriction due to hypocapnia, or reductions in blood flow due to steal physiology during hypercapnia. However, the normal range for resting PCO 2 in this patient population is not known. Therefore, we investigated the variability in resting end-tidal PCO 2 (P ET CO 2 ) in patients with intracranial steno-occlusive disease and the impact of revascularization on resting P ET CO 2 in these patients. Setting and Design Tertiary care center, retrospective chart review Materials and Methods We collected resting P ET CO 2 values in adult patients with intracranial steno-occlusive disease who presented to our institution between January 2010 and June 2021. We also explored postrevascularization changes in resting P ET CO 2 in a subset of patients. Results Two hundred and twenty-seven patients were included [moyamoya vasculopathy ( n = 98) and intracranial atherosclerotic disease ( n = 129)]. In the whole cohort, mean ± standard deviation resting P ET CO 2 was 37.8 ± 3.9 mm Hg (range: 26-47). In patients with moyamoya vasculopathy and intracranial atherosclerotic disease, resting P ET CO 2 was 38.4 ± 3.6 mm Hg (range: 28-47) and 37.4 ± 4.1 mm Hg (range: 26-46), respectively. A trend was identified suggesting increasing resting P ET CO 2 after revascularization in patients with low preoperative resting P ET CO 2 (<38 mm Hg) and decreasing resting P ET CO 2 after revascularization in patients with high preoperative resting P ET CO 2 (>38 mm Hg). Conclusion This study demonstrates that resting P ET CO 2 in patients with intracranial steno-occlusive disease is highly variable. In some patients, there was a change in resting P ET CO 2 after a revascularization procedure.

Correlation of End-Tidal Carbon Dioxide Tension with Arterial Carbon Dioxide Tension in Patients with Respiratory Failure on Mechanical Ventilation

Background: Patients undergo mechanical ventilation need continuous evaluation of their respiratory condition. Monitoring of end-tidal carbon dioxide (ETCO2) as noninvasive measurement of arterial carbon dioxide (PaCO2) is a good tool for assessment and management of mechanically ventilated patients. Aim of the work: The aim of this work is to correlate expiratory end-tidal carbon dioxide tension with arterial carbon dioxide tension in patients with respiratory failure on mechanical ventilation and its significance. Patients and methods: This study was carried out on 50 patients on invasive mechanical ventilation with acute or acute on top of chronic respiratory failure admitted to respiratory I.C.U. at Bab El- Shaeria University Hospital, Studied patients had obtained two ABG samples one at the onset of mechanical ventilation(M.V.) and the second when the patient was on weaning mode of mechanical ventilation with continuous capnographic monitoring and reading record at the onset of ABG sampling. Results: The study include 31 males (62%),and 19 female (38%),24 patients (48%) had C.O.P.D, 9 patients (18%) had pneumonia, 8 patients (16%) had O.H.S, 7 patients (14%) had I.L.D and2 patients (4%) had acute severe asthma. The study shows no statistical significant difference between PaCO2 and ETCO2 at the onset of mechanical ventilation (74.78 ± 20.19 and67.5 ± 19.23) mmHg and on weaning mode (43.98 ± 8.07 and 42.2±7.2) mmHg. that PaCO2 measurements vary approximately 2-7 mmHg above ETCO2 values which mean good correlation between PaCO2 and ETCO2. Conclusion: - ETCO2 measurement provides an accurate estimation of PaCO2 in ventilation and weaning which may reduce the need for invasive, high coast monitoring and repeated arterial blood gas analyses.

The Effect of Pressure Controlled Ventilation on Pulmonary Mechanics in Prone Patients Undergoing Elective Spine Surgeries: Comparative Study with Volume Controlled Ventilation

Abstract Background: As patients turned into prone position expe-rienced more decrease in lung compliance than those on supine position, this prospective, randomized study was designed to compare the effect of PCV and volume-controlled ventilation (VCV) on lung mechanics and heamodynamics in the prone position using the Wilson frame during elective lumbar spine surgery.Patients and Methods: Sixty patients scheduled for elective lumbar spine surgery were randomly allocated to receive mechanical ventilation using either the VCV (n=30) or PCV (n=30) mode. Respiratory variables (peak airway pressure, mean airway pressure, shunt fraction, alveolar-arterial oxygen gradient). Dynamic compliance (Cdyn) of the respiratory system was calculated as VT/ (Ppeak-PEEP). The alveolar dead space-to-tidal volume ratio (VD/VT) will be estimated using the Hardman and Aitkenhead equation: VD/VT=1. 135– (PaCO2-ETCO2)/(PaCO2-0. 005). Results: The Ppeak in the PCV group was lower than that in the VCV group throughout the study period (p-value=0.961 and 0. 0.109 at supine position and prone position, respectively) and was increased at prone position compared with supine position in both groups. Cdyn was decreased from supine to prone position in both groups. However, the Cdyn in the PCV group was higher than that in the VCV group during the study period however it is only statistically significant after 1.5 and 2hrs. The arterial oxygen tension was comparable between the 2 groups during the study period.Conclusions: PCV provides lower Ppeak compared with VCV when the ventilator is set to deliver the same tidal volume and variable respiratory rate to maintain a constant end-tidal carbon dioxide tension in patients undergoing pos-terior lumbar spine surgery in the prone position using the Wilson frame.

The Effect of Pressure-controlled Ventilation on Pulmonary Mechanics in the Prone Position During Posterior Lumbar Spine Surgery

When an anesthetized patient is turned to the prone position using the Wilson frame, dynamic compliance (Cdyn) decreases and peak airway pressure (Ppeak) increases. As pressure-controlled ventilation (PCV) decreases the Ppeak, this prospective, randomized study was designed to compare the effect of PCV and volume-controlled ventilation (VCV) on lung mechanics in the prone position using the Wilson frame during posterior lumbar spine surgery. Forty patients scheduled for posterior lumbar spine surgery were randomly allocated to receive mechanical ventilation using either the VCV (n=20) or PCV (n=20) mode. Respiratory variables (including Ppeak and Cdyn) and oxygenation parameters were recorded at the supine position (Tsupine) and 30 minutes after prone positioning (Tprone). During the study period, tidal volume, minute volume, end-tidal carbon dioxide tension, and positive end-expiratory pressure were comparable between the 2 groups. The Ppeak in the PCV group was lower than that in the VCV group throughout the study period (P=0.007 and 0.003 at Tsupine and Tprone, respectively) and was increased at Tprone compared with Tsupine in both groups. Cdyn was decreased from Tsupine to Tprone in both groups. However, the Cdyn in the PCV group was higher than that in the VCV group during the study period. The arterial oxygen tension was comparable between the 2 groups during the study period. PCV provides lower Ppeak compared with VCV when the ventilator is set to deliver the same tidal volume and variable respiratory rate to maintain a constant end-tidal carbon dioxide tension in patients undergoing posterior lumbar spine surgery in the prone position using the Wilson frame.

Relation between urinary bicarbonate concentration and carbon dioxide tension in patients with proximal or distal renal tubular acidosis.

UEDA, H. Relation between Urinary Bicarbonate Concentration and Carbon Dioxide Tension in Patients with Proximal or Distal Renal Tubular Acidosis. Tohoku J. exp. Med., 1981, 133 (1), 21-32 The relation of urinary bicarbonate concentration (UHCO3-) to the difference between urinary pCO2 and arterial blood pCO2 (U-BpCO2) has not yet been clearly elucidated either in normal subjects or in patients with distal renal tubular acidosis (distal RTA). Nor are there any reports dealing with the relation between UHCO3- and U-BpCO2 in patients with hypokalemia or with proximal renal tubular acidosis (proximal RTA). In the present study, with the objective of analyzing the differences in the production of urinary pCO2 in different groups of patients with hypokalemia, those with distal RTA and those with proximal RTA, we loaded these patients and control subjects with sodium bicarbonate, and studied the changes in the relations between UHCO3- and U-BpCO2. The following results were obtained: (1) (a) When UHCO3- was higher than 130mEq/liter: Normal subjects had a positive correlation between UHCO3- and U-BpCO2 (p 0.7). In the patients with distal RTA, U-BpCO2 was lower than that in the control (p<0.005). (2) In the patients with hypokalemia, after the loading of potassium chloride, U-BpCO2 tended to rise compared on the same level of UHCO3-. (3) In the control subjects loaded with a large dose of phosphate, the values of U-BpCO2 compared on the same levelof UHCO3- were not distinctive compared with those in other control subjects, when UHCO3- was over 130mEq/liter. These results suggest that in the patient with proximal RTA, an increase in bicarbonate load in the distal tubule is likely to augment the formation of carbonic acid, raising the value of U-BpCO2. The fact that in the patients with distal RTA U-BpCO2 was lower than that in the control subjects seems to be attributed not only to the low value of UHCO3- due to potassium deficiency but also to the impairment of secretion of hydrogen ion in the distal tubule.

Acid-base response to acute carbon dioxide changes in chronic obstructive pulmonary disease.

The influence of the chronic arterial carbon dioxide tension on the acid-base response to acute change in arterial carbon dioxide tension was studied in patients with chronic obstructive pulmonary disease. Acute changes in arterial carbon dioxide tension were produced experimentally by having the patients breathe various mixtures of carbon dioxide in air and by hyperventilation. Acute changes in arterial carbon dioxide tension occurred clinically during oxygen-induced hypoventilation, followed by ventilator therapy. The acute acid-base response was expressed as the ratio of change in arterial hydrogen ion concentration to change in arterial carbon dioxide tension. This ratio was inversely and linearly related to chronic values of arterial carbon dioxide tension and plasma bicarbonate concentration. The more efficient buffering of acute changes in carbon dioxide tension in patients with chronic obstructive pulmonary disease with hypercapnia was attributed both to high chronic bicarbonate concentrations and...

Arterial oxygen and carbon-dioxide tension in patients with acute myocardial infarction.

Over a 2-year period, 450 cases of acute myocardial infarction were treated in a coronary care unit. Arterial PO2 and PCO2, were routinely determined on the day of admission. In

Measurement of alveolar carbon dioxide tension at maximal expiration as an estimate of arterial carbon dioxide tension in patients with airway obstruction.

Arterial and alveolar carbon dioxide tension at end-tidal and maximal expiration were measured simultaneously in 104 patients with chronic obstructive respiratory disease. Regardless of the degree of abnormality of distribution of ventilation, there was a consistent relationship between arterial and maximal expiratory carbon dioxide tension. Therefore, close approximation of arterial carbon dioxide tension was obtained from the measurement of carbon dioxide tension at maximal expiration by rapid infrared carbon dioxide analysis. An infrared carbon dioxide analyzer might be used at the bedside or in the laboratory for frequent monitoring of arterial carbon dioxide tension without repeated arterial punctures.

MAXIMAL DILATATION OF CEREBRAL VESSELS.

It has been repeatedly observed that the cerebral vascular response to an increase in arterial carbon dioxide tension, as induced by inhalation of 5% to 7% carbon dioxide in normal subjects, produces a 50% to 75% increase in overall cerebral blood flow. 1 On the other hand, a reduction below normal levels of the arterial carbon dioxide tension, as with passive or active hyperventilation, 2,3 causes as much as a 50% reduction in cerebral blood flow. It has also been appreciated that the magnitude of these changes may show a marked individual variability, particularly as regards the effects of increased arterial carbon dioxide tension in patients with cerebral vascular disease. 4,5 In this study, data are presented which suggest that the response to alterations in arterial carbon dioxide tension in patients with cerebral vascular disease may be conditioned by the resting state of the cerebral vessels. Method The subjects of

Physiologic factors in the treatment of chronic hypertrophic pulmonary emphysema.

Excerpt The difficulties involved in the treatment of chronic pulmonary emphysema have recently been emphasized, especially the undesirable reactions that may follow the administration of oxygen in...