Changes In PETCO2 Research Articles

Changes in PETCO2 and pulmonary blood flow after bronchial occlusion in dogs.

The use of PETCO2 in detecting accidental bronchial intubation was investigated. The PETCO2 was measured in six mongrel dogs after occluding the left mainstem bronchus in three conditions; pentobarbital anaesthesia, 0.8% halothane insufflation together with pentobarbital anaesthesia, and simultaneous left pulmonary artery and bronchial airway occlusion with intravenous pentobarbital anaesthesia. An external flow probe measured left pulmonary artery blood flow. The PETCO2 decreased after bronchial occlusion during pentobarbital (35 +/- 3 vs 30 +/- 5 mmHg) and halothane-pentobarbital (30 +/- 6 vs 25 +/- 6 mmHg) conditions (P less than 0.05). However, within three minutes of bronchial occlusion, the values of PETCO2 had returned to their pre-occlusion values. After five minutes of bronchial occlusion pulmonary artery blood flow in the non-ventilated lung decreased (P less than 0.05) during pentobarbital (770 +/- 533 ml.min-1 vs 575 +/- 306 ml.min-1) and halothane-pentobarbital (495 +/- 127 ml.min-1 vs 387 +/- 178 ml.min-1) conditions. Simultaneous bronchial and pulmonary artery occlusion prevented any changes in PETCO2. It was concluded that accidental one-lung ventilation results in small and transient decreases in PETCO2. A redistribution of blood flow from the non-ventilated to ventilated lung occurs which restores PETCO2 to the original values observed with two-lung ventilation.

Can Changes in End-Tidal Pco2 Measure Changes in Cardiac Output?

In recent studies of cardiopulmonary resuscitation, an increase in end-tidal carbon dioxide tension (PETCO2) signifies an increase in cardiac output (QT) as spontaneous circulation resumes. We hypothesized that changes in QT might generally be measured by changes in PETCO2. In five pentobarbital-anesthetized dogs, we inflated percutaneously inserted vena cava balloons to impede venous return and to decrease QT (measured by pulmonary thermodulation). The PECTCO2 was measured at the airway opening by sidestream infrared capnometry. In 32 vena cava balloon inflation sequences during constant ventilation in five dogs, the percent decrease in PETCO2 directly correlated with the percent decrease in QT (slope = 0.73, R2 = 0.89, P less than 0.001). During decreased QT, reduced CO2 delivery to the lungs decreased alveolar PCO2 to cause part of the decrease in PETCO2. The remaining reduction in PETCO2 resulted from the increase in alveolar dead space (in turn due to lower pulmonary perfusion pressures during reduced QT), which diluted the CO2 from perfused alveolar spaces to further reduce PETCO2. During a sustained reduction in QT, increasing CO2 accumulation in the peripheral tissues and in venous blood began to restore CO2 delivery to the lung and PETCO2 toward baseline levels. Reciprocal changes occurred during increases in QT when the vena cava balloons were deflated. The linear relationship between changes in PETCO2 and QT in animals supports a decision to perform clinical studies necessary to determine whether a change in PETCO2 will be useful as a noninvasive, continuous monitor of a change in QT during anesthesia or intensive care.

Effects of sleep-induced increases in upper airway resistance on ventilation

To determine the effects of the sleep-induced increases in upper airway resistance on ventilatory output, we studied five subjects who were habitual snorers but otherwise normal while awake (AW) and during non-rapid-eye-movement (NREM) sleep under the following conditions: 1) stage 2, low-resistance sleep (LRS); 2) stage 3-4, high-resistance sleep (HRS) (snoring); 3) with continuous positive airway pressure (CPAP); 4) CPAP + end-tidal CO2 partial pressure (PETCO2) mode isocapnic to LRS; and 5) CPAP + PETCO2 isocapnic to HRS. We measured ventilatory output via pneumotachograph in the nasal mask, PETCO2, esophageal pressure, inspiratory and expiratory resistance (RL,I and RL,E). Changes in PETCO2 were confirmed with PCO2 measurements in arterialized venous blood in all conditions in one subject. During wakefulness, pulmonary resistance (RL) remained constant throughout inspiration, whereas in stage 2 and especially in stage 3-4 NREM sleep, RL rose markedly throughout inspiration. Expired minute ventilation (VE) decreased by 12% in HRS, and PETCO2 increased in LRS (3.3 Torr) and HRS (4.9 Torr). CPAP decreased RL,I to AW levels and increased end-expiratory lung volume 0.25-0.93 liter. Tidal volume (VT) and mean inspiratory flow rate (VT/TI) increased significantly with CPAP. Inspiratory time (TI) shortened, and PETCO2 decreased 3.6 Torr but remained 1.3 Torr above AW. During CPAP (RL,I equal to AW), with PETCO2 returned to the level of LRS, VT/TI and VE were 83 and 52% higher than during LRS alone. Also on CPAP, with PETCO2 made equal to HRS, VT, VT/TI, and VE were 67, 112, and 67% higher than during HRS alone.(ABSTRACT TRUNCATED AT 250 WORDS)

End-tidal Carbon Dioxide in Critically ill Patients during Changes in Mechanical Ventilation

Values of end-tidal CO2 (PETCO2) approximate PaCO2 in spontaneous breathing normal subjects and in stable patients receiving mechanical ventilatory support (MVS). Because marked inequality of ventilation/perfusion ratios in critically ill patients might affect this correlation, we assessed changes of PETCO2 in predicting changes in PaCO2 (delta PaCO2) and changes in minute ventilation (delta Ve) in this patient population. Twenty consecutive intubated patients 38 to 89 yr of age (mean, 70 yr) with respiratory failure while receiving MVS with indwelling arterial lines were studied. Settings on the mechanical ventilator were varied for frequency and tidal volume, and after a minimum of 5 to 10 min equilibration, PaCO2 and PETCO2 were measured. Vt and Ve were recorded from the digital indicator of the pneumotachygraph within the mechanical ventilator and corrected for compression volume in the respirator circuit. A total of 116 simultaneous measurements were performed. PETCO2 correlated well with PaCO2 (r = 0.78, p less than 0.001). The 95% confidence interval for the mean difference in PaCO2-PETCO2 was 4.0 +/- 0.97 mm Hg. However, delta PETCO2 (measured from baseline) did not correlate as well with delta PaCO2 (r = 0.58, p = less than 0.001). In four patients, the trend in their PETCO2 during changes in mechanical ventilation were in the opposite direction from the trend in their PaCO2. Thus, many critically ill patients, who cannto be preidentified, have an inconstant PaCO2-PETCO2 gradient with changes of ventilation. Utilization of PETCO2 as a noninvasive monitoring substitute for trends in PaCO2 in critically ill patients may be misleading despite establishing an initial PaCO2-PETCO2 relationship.

Dynamic response of peripheral chemoreflex loop to changes in end-tidal CO2.

The dynamic ventilatory response of the peripheral chemoreflex loop after isoxic step changes in end-tidal PCO2 (PETCO2) (range 5-30 Torr) was studied in 12 alpha-chloralose-urethan-anesthetized cats. The technique of artificial brain stem perfusion allowed the response to be observed in isolation from the central chemoreflex loop. The data were fitted by an exponential with time delay. During normoxia the mean time constant and time delay (with SD) were 8.6 +/- 7.3 and 3.3 +/- 0.9 s, respectively (9 cats, 56 runs). During hypoxia [arterial PO2 (PaO2) approximately 60 Torr] these values were 6.0 +/- 4.5 and 2.9 +/- 0.9 s (6 cats, 38 runs). In 17 of the 94 runs an augmented breath occurred in the first three breaths after the stepwise increase in PETCO2. For these augmented breaths, tidal volume, inspiratory time, and expiratory time were not different from the next augmented breath occurring in the same run in the steady state. Neither a rate-sensitive component nor a central neural mechanism (central afterdischarge), with the property of maintaining an increased but slowly declining respiratory activity for some minutes after cessation of the PETCO2 challenge, was found. We conclude that the description of the ventilatory response of the peripheral chemoreflex loop to step changes in PETCO2 with a single exponential and time delay is adequate.

Comparison of Arterial-End-Tidal PCO2 Difference and Dead Space/Tidal Volume Ratio in Respiratory Failure

End-tidal CO2 monitors are used to estimate arterial CO2 pressure (PaCO2), but appropriate use of this noninvasive method of assessing blood gases is unclear. In patients with lung disease, the end-tidal CO2 pressure (PETCO2) can differ from PaCO2 because of ventilation-perfusion (VA/Q) mismatching, and changes in PETCO2 may be seen with corresponding increase, decrease, or no change in PaCO2 depending on what happens to VA/Q mismatching. We compared the difference between PETCO2 and PaCO2 in 17 patients undergoing mechanical ventilation. Large differences were found between PaCO2 and PETCO2 in individual patients; P(a-et)CO2 correlated closely with VD/VT. Our studies confirm that PetCO2 is a poor estimate of PaCO2 in patients with respiratory failure. However, the P(a-et)CO2 may be the most appropriate use for end-tidal PCO2 monitoring. In addition, we found that the end-tidal CO2 monitor may be easily adapted for expedient measurement of VD/VT.

Alveolar gas pressure changes with resistive loads in man.

Respiratory responses to a single breath during which a resistive load was applied were studied in 8 conscious subjects. There was an increase in inspiratory time (TI), an increase in end-tidal PCO2 (PETCO2) and a decrease in end-tidal PO2 (PETO2) on the resisted breath. 12 subjects were given a single inspiration of a mixture of air containing increased CO2 and reduced O2. This gas mixture induced changes in PETCO2 and PETO2 approximately double those seen with the resistive loads. There was no change in tidal volume (VT), TI or expiratory time during the first breath. During the following breath there was a small increase in TI and VT. The results indicate that although resistive loading may cause changes in PETCO2 and PETO2, these changes are unlikely to contribute to the respiratory responses during the first loaded breath.

An assessment of overall "gain" of the O2-feedback control system with and without external dead space breathing.

Overall gain of the O2-ventilation feedback control system (GO2) was determined in 9 male and one female healthy subjects. GO2 progressively increased with decreasing end-tidal PO2 (PETO2). This value did not exceed the overall gain of the CO2-ventilation feedback system (GCO2) even at a PETO2 level of 40 mmHg, suggesting that hypoxic stimulation did not become predominant in the present experimental condition. With addition of 250 ml of external dead space, PETO2 decrement (delta PETO2 X actual) was experimentally observed. The delta PETO2 X actual thus obtained was found to be in good agreement with the PETO2 decrement deduced from GO2 (delta PETO2 X expected). This result was similar to that found in the PETCO2 change previously seen in normoxia.

Adaptive response of carotid body chemoreceptors to CO 2

Carotid body chemoreceptor responses to sudden changes in pETCO2 (end-tidal tracheal CO2 partial pressure) and paCO2 (arterial CO2 partial pressure) from one stable state to another at a constant level of PETO2 (end-tidal tracheal O2 partial pressure) and paO2 (arterial O2 partial pressure) were studied in 18 anesthetized cats. Chemoreceptor activity was recorded from single or pauci-fiber filaments of a cut sinus nerve. During a hypercapnic stimulus by CO2 inhalation the discharge rate rapidly increased to a peak and then adapted to a lower level in 20-30 s showing an overshoot in the response. Likewise, withdrawal of the hypercapnic stimulus was followed by an undershoot in chemoreceptor activity. Hypoxia decreased the latency of the response and increased the overshoot and stable state responses to hypercapnia. The responses to step paCO2 increases by blood perfusion were qualitatively similar but the latency and time to peak amplitude were shorter and the peak amplitude was larger at any given perfusate pO2. The stable state responses to a given paCO2 achieved by CO2 inhalation or by blood perfusion were similar. The transient overshoot and undershoot in the activity produced by the increase and decrease in paCO2 were blocked by acetazolamide, a carbonic anhydrase inhibitor. The results are best explained by postulating that in the carotid body tissue, H+ is generated from CO2 in one compartment in the presence of carbonic anhydrase and is transported to another containing the receptor site in a pO2 dependent way--a high pO2 attenuating and a low pO2 augmenting it.