Changes In End-tidal CO2 Research Articles

Changes in cerebral hemodynamics during laparoscopic cholecystectomy

Laparoscopic surgery requires a series of procedures, including intraperitoneal CO2 insufflation, which can cause cardiovascular and hemogasanalytic modifications, potentially able to Impair cerebral perfusion. The aim of this study was to evaluate changes in cerebral blood flow velocity during laparoscopic cholecystectomy. Eighteen patients undergoing laparoscopic cholecystectomy were studied. Middle cerebral artery blood flow velocity was monitored using transcranial Doppler ultrasonography. Electrical bioimpedance was employed to measure cardiac output, stroke volume and to calculate derived parameters. End-tidal CO2, mean arterial blood pressure, end expiratory anesthetic concentration and 02 saturation were monitored non-invasively. Cerebral artery blood flow velocity increased significantly after CO2 insufflation (p < 0.05) and remained stable. The highest values were reached after CO2 desufflation. A significant reduction in stroke volume and cardiac output (p< 0.05) associated with increased vascular systemic resistances (p< 0.001) was observed soon after CO2 insufflation. The decrease in cardiac output and the increase in vascular systemic resistances remained significant throughout abdominal insufflation. Heart rate and mean arterial pressure remained substantially unchanged with the exception of a significant decrease (p< 0.001) before CO2 insufflation. There was no significant change in end-tidal CO2 during abdominal insufflation. These findings suggest that the cerebrovascular system can undergo adaptive changes during all phases of laparoscopic surgery. However, the extent of cardio- and cerebrovascular variation indicates the need for careful preliminary evaluation of cerebral hemodynamics in patients with vascular disorders before laparoscopic surgery. [Neurol Res 1999; 21: 658-660]

PARTIAL CO2 REBREATHING FICK TECHNIQUE FOR NONINVASIVE MEASUREMENT OF CARDIAC OUTPUT

Introduction: The noninvasive partial CO2 rebreathing technique uses a differential form of the Fick Equation tocalculate cardiac output (CO). The ratio of the change in end-tidal CO2 and CO2 excretion, in response to a brief period of rebreathing, gives a non-invasive estimate of the CO. [1,2] The method assumes that the difference between end-tidal and arterial CO2 content does not change during rebreathing. We have developed a partial CO2 rebreathing algorithm based on a two-compartment lung model, which minimizes error in estimation of CO when this assumption is not true. This model compensates for the changing end-tidal to arterial CO2 gradient during partial rebreathing. Methods: After IRB approval and patient consent the system was tested in seven patients (6 Male, 1 Female, Age 47-78 Years) undergoing cardiac surgery. End-tidal CO2 was measured using a mainstream CO2 analyzer and a disposable pneumotachograph (COSMO[registered sign], Novametrix Medical Systems, Wallingford, CT). CO2 production was calculated as the integral of the flow and CO2 signals over the entire breath. Actuation of a pneumatic valve under computer control resulted in breathing circuit changes, which increased airway dead space by 120 ml thereby causing partial rebreathing of exhaled gas. The valve was actuated for 50 seconds once every 3 minutes. Changes in CO2 excretion and etCO2 were used to calculate the partial CO2 rebreathing CO using the differential Fick equation. An average of three consecutive thermodilution cardiac output (TDco) measurements made during end expiration were compared with corresponding partial CO2 rebreathing cardiac output measurements. Measurements made during the first 45 minutes after bypass were discarded since thermal noise can make the TDco measurement unreliable [3]. Results: A total of 44 comparisons were made with CO ranging from 2.5 to 9.4 L/min. Regression analysis gives an r = 0.90 with a slope of 0.71 and an offset of 1.49 L/min. Bland-Altman analysis resulted in a bias of 0.07 L/min with a precision (1SD) of +/- 0.85 L/min. Discussion: The results suggest that partial CO2 rebreathing technique may be a clinically acceptable method for measurement of CO. Observed differences between the two techniques may have resulted from intrapulmonary shunts. The partial CO2 rebreathing system is completely automatic and can provide frequent, nearly continuous measurements of CO. (Figure 1)Figure 1

PARTIAL CO2 REBREATHING FICK TECHNIQUE FOR NONINVASIVE MEASUREMENT OF CARDIAC OUTPUT

Introduction: The noninvasive partial CO2 rebreathing technique uses a differential form of the Fick Equation tocalculate cardiac output (CO). The ratio of the change in end-tidal CO2 and CO2 excretion, in response to a brief period of rebreathing, gives a non-invasive estimate of the CO. [1,2] The method assumes that the difference between end-tidal and arterial CO2 content does not change during rebreathing. We have developed a partial CO2 rebreathing algorithm based on a two-compartment lung model, which minimizes error in estimation of CO when this assumption is not true. This model compensates for the changing end-tidal to arterial CO2 gradient during partial rebreathing. Methods: After IRB approval and patient consent the system was tested in seven patients (6 Male, 1 Female, Age 47-78 Years) undergoing cardiac surgery. End-tidal CO2 was measured using a mainstream CO2 analyzer and a disposable pneumotachograph (COSMO[registered sign], Novametrix Medical Systems, Wallingford, CT). CO2 production was calculated as the integral of the flow and CO2 signals over the entire breath. Actuation of a pneumatic valve under computer control resulted in breathing circuit changes, which increased airway dead space by 120 ml thereby causing partial rebreathing of exhaled gas. The valve was actuated for 50 seconds once every 3 minutes. Changes in CO2 excretion and etCO2 were used to calculate the partial CO2 rebreathing CO using the differential Fick equation. An average of three consecutive thermodilution cardiac output (TDco) measurements made during end expiration were compared with corresponding partial CO2 rebreathing cardiac output measurements. Measurements made during the first 45 minutes after bypass were discarded since thermal noise can make the TDco measurement unreliable [3]. Results: A total of 44 comparisons were made with CO ranging from 2.5 to 9.4 L/min. Regression analysis gives an r = 0.90 with a slope of 0.71 and an offset of 1.49 L/min. Bland-Altman analysis resulted in a bias of 0.07 L/min with a precision (1SD) of +/- 0.85 L/min. Discussion: The results suggest that partial CO2 rebreathing technique may be a clinically acceptable method for measurement of CO. Observed differences between the two techniques may have resulted from intrapulmonary shunts. The partial CO2 rebreathing system is completely automatic and can provide frequent, nearly continuous measurements of CO. (Figure 1)Figure 1

CO2 reactivity in patients after subarachnoid haemorrhage.

CO2 reactivity was tested in patients with transcranial Doppler sonography (TCD) and endtidal CO2 measurements after an average time interval of ten months after subarachnoid haemorrhage (SAH). After deliberately changing breathing there was a significant change in endtidal CO2 and in flow velocities in all three examination groups. Comparing 27 patients with SAH and 5 patients treated for incidental aneurysms and 20 patients without cerebrovascular disease there were no significant differences in CO2 reactivity. Furthermore, there were no right to left differences. In 12 patients with vasospasm, two of them treated by percutaneous transluminal angioplasty for delayed ischaemic deficits, CO2 reactivity was normal at the time of investigation. Furthermore, normal CO2 reactivity was found in patients after SAH and surgery for ruptured aneurysms regardless of the severity of the SAH.

Cardiopulmonary responses to intravenous infusion of soluble and relatively insoluble gases.

Carbon dioxide is the current gas of choice for pneumoperitoneum, but hemodynamic and acid-base effects secondary to its systemic absorption have been reported. Various studies have suggested inert gases as alternatives. We studied the cardiopulmonary responses to intravenous infusion of carbon dioxide, nitrous oxide, argon, helium, and nitrogen in anesthetized swine. The gas was infused into the femoral vein at a rate of 0.1 ml . kg-1 . min-1 for 30 min. The changes in end-tidal CO2, mean arterial pressure, hemodynamics, and arterial blood gases were compared to baseline values. No animals died during infusion of the soluble gases (CO2 and N2O). Three of the five pigs infused with nitrogen died suddenly at 20 and 30 min of infusion. The animals in the insoluble gas groups (Ar, He, N2) experienced clinical pulmonary gas embolism and severe acidemia, hypercapnea and tachycardia. Venous gas embolism is poorly tolerated when the gas is relatively insoluble. Insoluble gases should not be used for pneumoperitoneum when there is any risk of venous gas embolism.

The effects of inverse ratio ventilation on intracranial pressure: a preliminary report.

To determine the effects of pressure control inverse ratio ventilation [PC-IRV], as compared with volume controlled normal ratio ventilation [VC], on the intracranial pressure [ICP] of patients with severe head injury. A prospective study with unblinded intervention. The Intensive Therapy Unit of a base hospital. Nine cases of head injury requiring mechanical ventilation and intracranial pressure monitoring were studied. Patients were twice transferred from VC (1:E ratio 1:2) to PC-IRV (1:E ratio 2:1). Firstly, tidal volume was maintained at an equal value. Secondly, end tidal CO2 was maintained at an equal value. No other changes were made to ventilation, vasopressor therapy or ICP control. Measurements were taken of ICP, mean arterial pressure (MAP) end tidal CO2 and respiratory parameters. In the first observation, there were significant changes in peak inspiratory pressure (PIP), mean airway pressure (Paw) and intrinsic positive end expiratory pressure (PEEP) but not for ICP, end tidal CO2, MAP and cerebral perfusion pressure (CPP). The correlation between change in ICP and change in end tidal CO2 was r = -0.74. In the second observation there were significant changes in tidal volume, PIP, Paw and intrinsic PEEP but not for ICP, MAP and CPP. The correlation between the change in ICP and the change in Paw was insignificant. PC-IRV has a minimal net effect on ICP. Changes in ICP correlate more strongly with changes in CO2 than changes in Paw.

Glottic aperture and effective minute ventilation during nasal two-level positive pressure ventilation in spontaneous mode.

Our goal was to verify glottic behavior and its effects on effective minute ventilation during intermittent positive pressure ventilation applied at increasing inspiratory pressure levels through a nasal mask (nIPPV) using a two-level positive pressure ventilator (two-level IPPV) in spontaneous mode. Ten subjects were studied while awake. The spontaneous mode was used at three levels of inspiratory positive airway pressure (IPAP): 10, 15, and 20 cm H2O. The expiratory pressure was kept at 4 cm H2O. Records of spontaneous breathing without nIPPV were also performed. The glottis was continuously monitored through a fiberoptic bronchoscope. We measured, breath by breath, the widest inspiratory angle formed by the vocal cords at the anterior commissure, the corresponding tidal volume (with respiratory inductive plethysmography), the respiratory frequency and other indices. Our data during wakefulness show that inspiratory pressures of 10 and 15 cm H2O did not result in increases in effective minute ventilation with respect to spontaneous breathing. Only at 20 cm H2O of IPAP did effective minute ventilation increase. This was due essentially to a decrease in respiratory frequency with increasing pressures, offsetting increases in tidal volume at 10 and 15, but not at 20 cm H2O of inspiratory pressure. Changes in end-tidal CO2 suggest that alveolar ventilation increased due to the change in breathing pattern. Contrary to what we observed previously with either two-level IPPV used in the controlled mode, or nIPPV performed with volumetric ventilators, the glottis did not play any noticeable role in the control of effective minute ventilation.

Carbon dioxide gas embolism in the experimental animal

Accidental vascular placement of Veress needle or cannula during laparoscopic insufflation with carbon dioxide gas (CO2) may cause a fatal gas embolism. Deliberate CO2 injection into the vena cava of dogs did not define a safe flow rate or pressure to prevent mortality. We studied incremental increase in pressure at the same maximum rate of gas flow (corresponding to 2.5 L/mm in a 70-kg man, the maximum flow rate possible with a Veress needle) to define the pressure at which pigs did not reversibly tolerate intravenous CO2 insufflation. The right iliac vein was cannulated and CO2 was insufflated at the maximum flow rate but at three pressures, 15, 20, and 25 mm Hg. During each cycle CO2 was insufflated until the elapse of 30 seconds or a change in end tidal CO2 by 50%. Five of the six animals tolerated intravenous CO2 at 15 mm Hg pressure. In one animal, during insufflation at 15 mm Hg the flow rate was accidentally set at twice the standard level, which resulted in immediate and fatal CO2 embolism. During insufflation at 20 mm Hg four pigs died, the last one during insufflation at 25 mm Hg. Transient insufflation of CO2 at low pressure (15 mm Hg) is well tolerated because pressure in the venous system may limit gas flow. However, a decrease in end tidal CO2 should alert the anesthesiologist to stop insufflation immediately. This will allow recovery. When insufflating pressures are in the middle (20 mm Hg) or high range (25 mm Hg), CO2 embolism can be fatal despite its early recognition.

Dynamics of Carbon Dioxide Elimination Following Ventilator Resetting*

Carbon dioxide elimination (VCO2) at steady state corresponds to the metabolic rate. A change in tidal ventilation will lead to a transient response in VCO2 if other determinants of VCO2 are constant. This principle may be applied in the critical care unit to reset ventilators. To define and characterize the transient response of VCO2 to a well-defined change in ventilation. Forty-four patients in stable condition receiving volume-controlled mechanical ventilation had trend recordings of ventilator pressures, flow, volumes, VCO2, and end-tidal CO2 (ETCO2) for 20 min. At time t0, the minute ventilation was either increased (n = 22) or decreased (n = 22) by 10% after which these parameters were monitored over 30 min. Blood gas values were measured 5 and 20 min after the change in ventilation and the dead space fractions were computed using the single breath-CO2 test. The first ten breaths (till t1) after a change in ventilation were excluded. The time constant (tau) of the relative change in VCO2 (delta VCO2) was calculated by fitting exponential regressions to delta VCO2 for periods up to 20 min after t1. The delta VCO2 at t1 was proportional to the relative change in tidal volume (delta VT). The proportionality decreased gradually during 20 min. The proportionality of the relative change in ETCO2 (delta ETCO2) or PaCO2 (delta PaCO2) with delta VT was minimal at t1 and increased during the 20 min. tau increased progressively when calculated over longer periods (p < 0.001). tau was similar in the groups with increased and decreased ventilation up to 5 min, after which it was longer in the group with decreased ventilation (p < 0.05). The delta PaCO2 after 20 min correlated best with delta VCO2 at t1 (r = -0.8) and with delta ETCO2 at the end of 20 min (r = 0.8). Noninvasively monitored VCO2 provides an instantaneous indication of the change in alveolar ventilation in well-sedated, mechanically ventilated patients in stable condition without significant cardiopulmonary disease.

Morning reduction of cerebral vasomotor reactivity

We measured cerebral vasomotor reactivity during normoventilation, hyperventilation (hypocapnia), and breathing of 6% CO2 (hypercapnia) in 20 normal subjects during the hours of 6 to 8 AM, 1 to 3 PM, and 7 to 9 PM. Cerebral vasomotor reactivity was calculated, using transcranial Doppler, as percent change in the mean blood flow velocity of the middle cerebral artery per mm Hg change in end-tidal CO2 during hypocapnia and hypercapnia. Vasomotor reactivity during hypercapnia was lower in the morning (1.72 +/- 0.66 %/mm Hg) than in the afternoon (2.34 +/- 0.74 %/mm Hg, p < 0.01) and evening (2.31 +/- 0.56 %/mm Hg, p < 0.001). Vasomotor reactivity during hypocapnia did not vary significantly during the three periods (2.34 +/- 0.59 %/mm Hg in the morning, 2.43 +/- 0.51 %/mm Hg in the afternoon, and 2.26 +/- 0.52 %/mm Hg in the evening). This reduced morning response to hypercapnia suggests diminished vasodilator reserve during this period, and may be related to the increased stroke risk during the morning hours.

Microcapnometry: A Noninvasive Method for Monitoring Arterial CO2Tension in Conscious Rats

Characterizing disorders in the control of pulmonary ventilation requires measuring changes in both ventilatory parameters and the partial pressure of arterial CO2. Although the conscious rat has been used as a model for evaluating the effects of drugs, environmental agents, and disease on the control of pulmonary ventilation, obtaining samples of arterial blood for CO2 analysis by needle puncture or arterial catheterization during ventilatory measurements is not practical in the conscious rat and has limited the use of this model. The objective of this study was to develop a noninvasive method for monitoring arterial CO2 tension in conscious rats during ventilatory measurements using end-tidal CO2 measurements. Progressive increases in end-tidal CO2 (125–400% of baseline) caused by progressive decreases in pulmonary ventilation (75–25% of baseline) following intravenous doses of the opioid analgesic morphine were measured in conscious rats using this noninvasive method. Changes in end-tidal CO2 were comp...

End-tidal CO2 changes under constant cardiac output during cardiopulmonary resuscitation.

To evaluate a) whether end-tidal CO2 values change under constant cardiac output during cardiopulmonary resuscitation (CPR), and b) what factors are responsible for the change. A cohort study. University research laboratory. Nine mongrel dogs. Ventricular fibrillation was electrically induced. After 2 mins, open-chest cardiac massage was initiated to maintain cardiac output at 0.2 L/min (23% of baseline cardiac output) by the measurement of blood flow with an electromagnetic flow probe on the ascending aorta. The cardiac massage was kept constant until 50 mins after the induction of ventricular fibrillation. Before and during ventricular fibrillation, end-tidal CO2, minute volume of alveolar ventilation, and CO2 excretion were continuously monitored. Blood gases and oxygen saturation values were also measured in arterial and the mixed venous blood samples. CO2 content was calculated. After induction of ventricular fibrillation, end-tidal CO2 decreased and thereafter continued to increase until the end of the experiment. Two mechanisms may have contributed to the early reduction in end-tidal CO2. One mechanism is a further decrease in CO2 excretion compared with the reduction in alveolar ventilation and the other is an increase in alveolar deadspace (estimated from the increase in the difference between PaCO2 and end-tidal CO2). The subsequent increase in end-tidal CO2 was mainly due to a change in CO2 excretion. There are two hypotheses concerning the subsequent increase in CO2 excretion: the increase in pulmonary capillary blood flow (estimated from the change in the arteriovenous CO2 content gradient) and the increase in CO2 production itself. End-tidal CO2 changes under constant cardiac output during CPR. When end-tidal CO2 is used to estimate the effectiveness of the cardiac massage, this type of change must be recognized.

Changes in End Tidal CO2 before and After Release of Tourniquet

In 24 healthy adult patients having orthopedic surgical procedures requiring the use of a tourniquet under general anesthesia with controlled mechanieal ventilation, we have deter- mined ehanges in end tidal CO₂(PetCO₂) and arterial blood gas values before and after release of tourniquet. After deflation of tourniguet, PETCO and PaCO₂ increased significantly with the maximal elevation occuring within two minutes. The pH level decreased significantly and maximally within three minutes. There was statistically significant linear correlation between PCO and PaCO2 Sugesting prediction of the PaCO₂, level by monitoring the PetCO₂ level. On these findings, hyperventilation may be indicated to facilitate the return of PaCO₂ and pH to baseline just before and for several minutes after tourniquet release, especially in patients with increased intracranial pressure. In conclusion, we recommend noninvasive monitoring of the PetCO₂ level instead of invasive measure-ment of the PaCO₂ level.

Effect of epinephrine on the ability of end-tidal carbon dioxide readings to predict initial resuscitation from cardiac arrest.

To determine if the administration of epinephrine changes the partial pressure of end-tidal CO2 during cardiac arrest, as previously reported. Such a change could diminish the demonstrated ability of end-tidal CO2 measurements to predict resuscitation from cardiac arrest. The partial pressures of end-tidal CO2 of adult cardiac arrest patients who received i.v. epinephrine in doses from 1 to 15 mg were monitored throughout arrest. Emergency department of a university hospital. Adults (n = 64) in cardiac arrest with a mean age of 70 +/- 12 yrs, of whom 35 were males and 15 had a mean time of return of spontaneous circulation of 6.5 +/- 11 hrs. End-tidal CO2 (in torr) was analyzed on arrival, before the first dose of epinephrine, and 4 mins after epinephrine was administered in varying doses chosen by the supervising physician. The end-tidal CO2 decreased an average of 0.3 torr (0.04 kPa) after epinephrine was administered. Patients with a return of pulse had a decrease of -2 torr (-0.3 kPa) vs. an increase of 0.3 torr (0.04 kPa) for those patients with no return of pulse (p = .07). In 33% of patients, there was no change; in 28%, the partial pressure of end-tidal CO2 increased, and in 39%, it decreased. There was no correlation between the change in end-tidal CO2 after epinephrine and whether or not patients regained a pulse (r2 = .08, p = .07), although a decrease in end-tidal CO2 was most often associated with return of pulse. At a threshold of 10 torr (1.3 kPa), the first end-tidal CO2 had a positive predictive value for return of pulse of 50% and a negative predictive value of 82%. Just before epinephrine administration, the positive predictive value was 71% and the negative predictive value was 83%; 4 mins after epinephrine administration, the positive predictive value was 64% and the negative predictive value was 86%. A decrease in end-tidal CO2 after epinephrine had a positive predictive value of 53% and a negative predictive value of 92%. End-tidal CO2 readings predicted resuscitation most accurately when taken after initial stabilization and before administration of epinephrine. Although epinephrine administration may decrease end-tidal CO2 tensions in cardiac arrest, it does so unpredictably in individual patients, and it does not eliminate the predictive value of this measurement.

Desflurane Is a Trigger of Malignant Hyperthermia in Susceptible Swine

Desflurane (difluoromethyl 1-fluoro 2,2,2-trifluoroethyl ether: CF2-H-O-CFH-CF3) is a potent inhalation anesthetic agent being investigated for possible clinical use. The authors examined the effects of this agent on normal swine and those from a special breeding program that were considered purebred for susceptibility to malignant hyperthermia (MH). Animals were exposed to 1 or 2 MAC or both doses of desflurane and observed for changes in end-tidal CO2, arterial blood gases, lactate, catecholamines, core temperature, blood pressure, and heart rate. All normal swine tolerated exposure to desflurane without clinical signs of MH, but significant changes in heart rate and blood pressure were noted. In contrast, of six MH susceptible swine tested, two had unequivocal MH reactions to deflurane, defined by significant increases of end-tidal CO2 (greater than 50 mmHg), an increase in PaCO2 (greater than 70 mmHg), a decrease in blood pH (less than 7.30), an increase in blood lactate concentration, and an increase in core temperature. Two other susceptible swine showed equivocal signs of MH but not until desflurane had been administered for 40-60 min. Finally, two other susceptible swine showed no signs of MH after 60 min of exposure to 2 MAC desflurane. These latter four animals all developed episodes of MH immediately after intravenous succinylcholine (2 mg/kg). The increased PaCO2, blood lactate concentrations, and temperature, and the decrease in pH induced by desflurane, were successfully treated with dantrolene and supportive measures. All surviving animals were biopsied 1 to 2 weeks after the exposure to desflurane for in vitro contracture testing to confirm MH susceptibility.(ABSTRACT TRUNCATED AT 250 WORDS)

Is Distal Sampling of End-tidal CO2Necessary in Small Subjects?

The authors compared PaCO2 with end-tidal CO2 (ETCO2) sampled at multiple sites along the endotracheal tube (ETT) in seven anesthetized rabbits (weight, 2.7-3.6 kg) to determine the most convenient, yet accurate, sampling location. Comparisons were made during spontaneous and controlled ventilation with fresh gas flows (FGF) of two and ten times the minute ventilation using a Mapleson D circuit. An Engstrom Eliza analyzer with a continuous sampling rate of 100 ml/min was used to measure ETCO2. A 0.75-mm ID polyethylene tube inserted in the side of the ETT sampled ETCO2 at the distal tip and at the 6-, 12-, and 15-cm marks on the ETT. ETCO2 was also measured at the standard proximal connector. The differences (P less than 0.05) between PaCO2 and ETCO2 at the distal, 6-, 12-, and 15-cm marks were 2.9 +/- 0.4, 3.1 +/- 0.4, 3.6 +/- 0.4, and 4.6 +/- 0.5 mmHg (mean +/- SEM), respectively, and did not change with FGF or mode of ventilation. The difference between PaCO2 and ETCO2 measured at the proximal connector was always large but significantly (P less than 0.05) greater during spontaneous than controlled ventilation (24.2 +/- 1.5 versus 15.0 +/- 1.4 mmHg) and at higher FGF (19.4 +/- 1.3 versus 16.8 +/- 1.6 mmHg). The differences (P less than 0.05) between ETCO2 at the distal tip and ETCO2 at the 6-, 12-, and 15-cm marks were 0.24 +/- 0.07, 0.73 +/- 0.11, and, 1.77 +/- 0.20 mmHg, respectively. This demonstrates that the change in ETCO2 between the distal tip and the 12-cm mark on the ETT is less than 1 mmHg, and that this clinically insignificant difference is independent of FGF and mode of ventilation. The 12 cm-mark is outside of the mouth on a newborn, and sampling ETCO2 at that point, which may be accomplished simply by inserting a small needle in the side of the ETT, may be the most appropriate sampling location.

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.

Effects of the dopamine antagonists haloperidol and domperidone on the normoxic ventilatory response to CO2 in cats

We investigated the effects of the dopamine antagonists haloperidol and domperidone on the ventilatory response following square-wave changes in end-tidal CO2 during normoxia in chloralose-urethane anaesthetized cats. In 7 cats these responses were measured before (control, 28 runs) and after the administration of 1 mg/kg haloperidol i.v. (26 runs) and in 8 other cats before (39 runs) and after 0.5 mg/kg domperidone i.v. (34 runs). Each response was separated into a slow central and a fast peripheral part by fitting two exponential functions to the measured ventilation. These functions have as parameters a CO2 sensitivity, a time constant, a time delay and an apnoeic threshold B (extrapolated PETCO2 of the steady-state response curve at zero ventilation). Haloperidol significantly diminished the peripheral (Sp) and the central (Sc) ventilatory sensitivity to CO2 and the B-value (P less than 0.001). The ratio Sp/Sc, the time constants and the time delays were not significantly changed. Domperidone only diminished the B-value significantly (P less than 0.001). Since domperidone does not readily cross the blood-brain barrier, its effect was a CO2 independent increase of the ventilation mediated by the peripheral chemoreceptors. Haloperidol exhibited, besides the peripheral stimulatory effect a depressant central effect due to an action on the central integrative structures, resulting in a proportional decrease of Sp and Sc.

Venous air embolism, hypotension, and end-tidal nitrogen.

The most sensitive method of venous air embolism (VAE) detection in clinical use is the precordial Doppler detector. Because the Doppler detector may provide false-positive and false-negative data, many clinicians rely on end-tidal gas measurements for verification of VAE in the operating room. End-tidal nitrogen (ETN2) increases soon after experimental VAE are small enough to cause minimal changes in blood pressure; however, decreases in end-tidal CO2 (ETCO2) are more sensitive. A large VAE causes hemodynamic instability, and the effect of low cardiac output on ETN2 has not been evaluated. This study was done to compare the changes in ETN2 and ETCO2 during large bolus and infusion VAE. Five mongrel dogs were anesthetized, intubated, and ventilated (FIO2 1.0, PaCO2 38 +/- 4 (SD) mm Hg). The animals were studied in the supine position; anesthesia and paralysis were maintained with a constant infusion of thiamylal and pancuronium. Maintenance fluids were administered at 5 ml kg-1 h-1. Mean arterial and pulmonary arterial pressures (PAP) and ETN2 and ETCO2 were displayed on a strip chart recorder. The dogs underwent both bolus and infusion VAE in separate experiments 10 to 14 days apart. The air emboli were given in random order by automated syringe over 1 minute (infusion) (1 to 2.5 ml kg-1 min-1) or by hand injection over 5 seconds (bolus) (1 to 2.5 ml kg-1). Changes in precordial Doppler sounds occurred in all animals at all doses. The peak increase in PAP and decrease in ETCO2 were significant after all air doses. ETN2 changes were biphasic. The peak increase was significant after all air doses; the peak decrease was significant in 37 of 40 bolus and infusion VAE episodes, occurred within 1 to 3 minutes, and lasted 20 to 30 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Venous air embolism, hypotension, and end-tidal nitrogen

The most sensitive method of venous air embolism (VAE) detection in clinical use is the precordial Doppler detector. Because the Doppler detector may provide false-positive and false-negative data, many clinicians rely on end-tidal gas measurements for verification of VAE in the operating room. End-tidal nitrogen (ETN2) increases soon after experimental VAE are small enough to cause minimal changes in blood pressure; however, decreases in end-tidal CO2 (ETCO2) are more sensitive. A large VAE causes hemodynamic instability, and the effect of low cardiac output on ETN2 has not been evaluated. This study was done to compare the changes in ETN2 and ETCO2 during large bolus and infusion VAE. Five mongrel dogs were anesthetized, intubated, and ventilated (FIO2 1.0, PaCO2 38 ± 4 (SD) mm Hg). The animals were studied in the supine position; anesthesia and paralysis were maintained with a constant infusion of thiamylal and pancuronium. Maintenance fluids were administered at 5 ml kg-1 h-1. Mean arterial and pulmonary arterial pressures (PAP) and ETN2 and ETCO2 were displayed on a strip chart recorder. The dogs underwent both bolus and infusion VAE in separate experiments 10 to 14 days apart. The air emboli were given in random order by automated syringe over 1 minute (infusion) (1 to 2.5 ml kg-1 min -1) or by hand injection over 5 seconds (bolus) (1 to 2.5 ml kg-1). Changes in precordial Doppler sounds occurred in all animals at all doses. The peak increase in PAP and decrease in ETCO2 were significant after all air doses. ETN2 changes were biphasic. The peak increase was significant after all air doses; the peak decrease was significant in 37 of 40 bolus and infusion VAE episodes, occurred within 1 to 3 minutes, and lasted 20 to 30 minutes. During bolus VAE, ETN2 increased earlier than ETCO2 decreased at all doses. During infusion VAE, 1 ml kg-1 min-1, ETN2 increased earlier than ETCO2 decreased; however, both changed simultaneously after higher infusion doses. It is concluded that ETN2 and PAP increase earlier than ETCO2 decreases after large bolus VAE; however, changes are simultaneous after large infusion emboli. The delayed and protracted depression of ETN2 may confuse VAE diagnosis unless air is aspirated from a central catheter. In addition, other causes of decreased ETCO2 and increased ETN2 must be excluded for accurate diagnosis of VAE. (Neurosurgery 21:378-382, 1987)