Changes In Minute Ventilation Research Articles

Effects of chemical feedback on respiratory motor and ventilatory output during different modes of assisted mechanical ventilation.

The purpose of the study was to examine the effects of chemical feedback on respiratory motor and ventilatory output in conscious subjects ventilated on various modes of assisted mechanical ventilation. Seven subjects were connected to a ventilator and randomly ventilated on assist-volume control (AVC), pressure support (PS) or proportional assist ventilation (PAV). On each mode, the assist level was set to the highest comfortable level. Airway and oesophageal (Poes) pressures, tidal volume, respiratory frequency (fR) and end-tidal carbon dioxide tension (PET,CO2) were measured breath-by-breath. When the subjects were stable on each mode, the fraction of inspired carbon dioxide (FI,CO2) was increased stepwise, and changes in minute ventilation (V'E) and respiratory motor output, estimated by the pressure-time product of all the respiratory muscles per breath (PTPrm) and per minute (PTPminute), were observed. At zero FI,CO2, PTPminute/PET,CO2 did not differ between modes, while V'E/ PTPminute was significantly lower with PAV than that with PS and AVC. As a result V'E/PET,CO2 was significantly lower with PAV, preventing, unlike AVC and PS, a significant drop in PET,CO2. With PAV, independent of CO2, V'E/PTPminute remained constant, while it decreased significantly with increasing CO2 stimulus with PS and AVC. At high PET,CO2 respiratory effort was significantly lower with PAV than that with PS and AVC. In conclusion, the mode of mechanical ventilation modifies the effects of chemical feedback on respiratory motor and ventilatory output. At all carbon dioxide stimulus levels neuroventilatory coupling was better preserved with proportional assist ventilation than with pressure support and assist-volume control ventilation.

A low concentration of nitrous oxide reduces dyspnoea produced by a combination of hypercapnia and severe elastic load

We have measured how a low concentration of nitrous oxide affected respiratory sensation and ventilation. Severe dyspnoea was induced in nine normal subjects by a combination of hypercapnia and inspiratory elastic load (50 cm H2O litre-1). Subjects were asked to rate their sensation of respiratory discomfort using a visual analogue scale (VAS) while breathing either 20% nitrous oxide or 20% nitrogen gas mixture. We compared the effects of each gas mixture on respiratory sensation and ventilation using steady-state values of ventilatory variables and VAS scores obtained before, during and after inhalation of each gas mixture. Inhalation of 20% nitrous oxide reduced the sensation of respiratory discomfort from a median VAS score of 6.5 (range 5.0-8.1) before inhalation to 3.6 (2.4-5.9) during inhalation (P < 0.05). There was no significant change in minute ventilation but tidal volume increased during inhalation of 20% nitrogen did not alter VAS scores or ventilatory variables. We found that a low concentration of nitrous oxide greatly alleviated the intensity of dyspnoea without changing respiratory load compensation.

Electromyogram as an indicator of neuromuscular fatigue during incremental exercise.

This study analysed the changes in the electromyographic activity (EMG) of the vastus lateralis muscle (VL) during an incremental maximal oxygen uptake test on a treadmill. A breakpoint in the integrated electromyogram (iEMG)-velocity relationship has already been interpreted in two ways: either as a sign of neuromuscular fatigue or as an expression of the iEMG-velocity relationship characteristics. The aim of this study was to test a method of distinguishing fatigue effects from those due to increases in exercise power. Eight well-trained male runners took part in the study. They completed a running protocol consisting of 4-min stages of increments in power output. Between each stage (about 15 s after the start of a minute at rest), the subjects had to maintain a standard effort: a 10-s isometric leg extension contraction [50% isometric maximal voluntary contraction (IMVC)]. The EMG was recorded during the running and isometric protocols, a change in the EMG signal during the isometric exercise being considered as the sign of fatigue. The iEMG-velocity relationships were strongly fitted by a second-order polynomial function for data taken at both the start (r = 0.98) and the end (r = 0.98) of the stage. Based on the stability of the 50%IMVC-iEMG relationship noted between stages, the start-iEMG has been identified as expressing the iEMG-velocity relationship without fatigue. The stage after which end-iEMG increased significantly more steeply than start-iEMG was considered as the iEMG threshold and was simultaneous with the ventilatory equivalent for carbon dioxide threshold. The parallel changes of minute ventilation and iEMG would suggest the existence of common regulation stimuli linked either to effort intensity and/or to metabolic conditions. The fall in intracellular [K+] has been discussed as being one of the main factors in regulating ventilation.

Perceptual and Psychophysiological Responses of Non-smokers to a Range of Environmental Tobacco Smoke Concentrations

Abstract To estimate the perceptual, psychophysiological and cognitive impact of environmental tobacco smoke (ETS) on non-smokers, seventeen male never-smokers, ages 21–33, were exposed to five concentrations yielding mean ETS-respirable suspended particles (RSP) levels of 58, 113, 217, 368, and 765 μg/m3. During each 90-minute session, four smokers were seated behind a partition and smoked, when cued, to generate 70-minute exposures. For control exposures, smokers “puffed” on unlit cigarettes. Odor Strength, Annoyance, Overall Acceptance and Eye Irritation at the lowest level were significantly different from control values and the degree of change generally increased monotonically with ETS level. Fatigue was not affected by any ETS level. Odor Strength (rated highest of all attributes at all levels) at the 217 μg/m3 ETS-RSP level was 12.5% of the maximum odor intensity experienced prior to the study. No effect of ETS on information processing was observed. Psychological state and eye blink rate were affected at only the 765 μg/m3 ETS-RSP level. During times when the participants were not completing a questionnaire or test, all ETS levels resulted in a 5–8% decrease in respiratory rate, due largely to an increase in expiratory duration, but no change in minute ventilation. The breathing changes may represent a psychophysiological response mediated by the olfactory system. Non-smokers are aware of ETS at ETS-RSP concentrations as low as 58 μg/m3 (˜80-fold higher than the level typical of current U.S. workplace environments where smoking is permitted) but its sensory impact remains relatively small until ETS-RSP concentrations above 217 μg/m3 are encountered.

Determinants of effective ventilation during nasal intermittent positive pressure ventilation.

Our aim was to verify in healthy subjects submitted to nasal intermittent positive pressure ventilation (nIPPV) with a volumetric ventilator on controlled mode, whether changes in ventilator settings (delivered tidal volume (VT), respiratory frequency (fR) and inspiratory flow (V'I) could influence effective minute ventilation (V'E), thus allowing identification of the settings resulting in the highest V'E during nIPPV. We then compared these experimentally obtained "best" settings to those obtained retrospectively in a group of patients submitted to long-term nIPPV for clinical reasons. We studied 10 healthy subjects awake and asleep, and 33 patients with restrictive ventilatory disorders. Changes in delivered V'I (for a constant delivered VT and fR) led to significant changes in V'E. V'E was significantly higher when a given delivered V'E was obtained using higher fR and lower VT than when it was obtained using lower delivered fR and higher VT. Increases in fR generally resulted in increases in V'E. The "best" settings derived from these results were: VT: 13 mL.kg-1 of body weight; fR: 20 breaths.min-1 and V'I: 0.56-0.85 L.s-1. The corresponding average values found in the patient group were: delivered VT: 14 mL.kg-1; fR: 23 breaths.min-1 and delivered V'I: 0.51 L.s-1. Changes in minute ventilation resulting from modifications in ventilator settings can be attributed to the glottic response to mechanical influences. This leads to "ideal" settings quite different from the standard ones in intubated patients. Values derived from nasal intermittent positive pressure ventilation in healthy subjects seem to apply to patients submitted to long-term nasal intermittent positive pressure ventilation.

Laboratory evaluation of the I-NOvent nitric oxide delivery device

The "I-NOvent delivery system" (Ohmeda Inc., Madison, WI, USA) is a device designed to add nitric oxide to a ventilator breathing system so that the inspired nitric oxide concentration remains constant in spite of changes in minute ventilation. In a laboratory study the device maintained the inspired nitric oxide concentration delivered to a model lung in the range 10.2-10.7 parts per million (ppm) when set to deliver 10 ppm, and in the range 40.5-42 ppm when set to deliver 40 ppm, for tidal volumes of 500, 700 and 900 ml, ventilator rates of 10, 15 and 20 bpm, peak inspiratory flow rates of 30, 40 and 50 litre min-1, and square, sine and decelerating ramp flow waveforms.

Accuracy of 30-minute indirect calorimetry studies in predicting 24-hour energy expenditure in mechanically ventilated, critically ill patients.

There is no consensus regarding the optimal duration of measurement or time of day to perform indirect calorimetry (IC). Energy expenditure (EE) varies at different times of day and with different activity levels. We sought to assess the variability of EE in mechanically ventilated patients over a 24-hour period and the accuracy of 30-minute IC studies in predicting the 24-hour energy expenditure (EE24). The study was a prospective comparison between the resting EE obtained by 30-minute measurement of IC and EE values obtained from 24-hour measurements. Tests were performed in the Medical Intensive Care Unit (MICU) of a tertiary care, university hospital. Oxygen consumption (VO2) and carbon dioxide production (VCO2) were measured for 24 hours in eight ventilated patients. Measurements were made every 3 minutes and used to calculate 30-minute and 24-hour oxygen consumption values. EE24 was calculated using the modified Weir equation. Each 30-minute interval was compared with the value obtained from the 24-hour measurement. Three hundred forty-one of 384 30-minute intervals remained for analysis. Average EE24 measured was 1490 +/- 486 kcal/d. Average EE24 predicted by extrapolation from 30-minute studies was 1501 +/- 503 kcal/d, with a mean difference of 0 +/- 209 kcal/d from the measured 24-hour values (range: -1068 to +585 kcal/d). Thirty-minute studies were within 20% of 24-hour measurements for 89% of intervals. The difference between 24-hour and 30-minute studies correlated with changes in minute ventilation (VE), heart rate, systolic blood pressure, and breath rate from their 24-hour means (p < .001). The mean error of EE estimate was greatest between 3 and 11 PM (p < .001). We conclude the following: (1) EE in MICU patients is variable; (2) 30-minute IC studies predict measured EE24 acceptably well for clinical purposes; and (3) accuracy is maximized if a 30-minute study is performed between 11 PM and 3 PM, and when Ve, heart rate, systolic blood pressure, and breath rate are near the day's average.

Attenuated oxygen sensifitivy after prenatal nicotine exposure-evidence for a dopaminergic mechanism. † 1797

Maternal smoking is associated with the sudden infant death syndrome. Exposure to nicotine or tobacco smoke impairs hypoxic defense mechanisms in young animals and human infants. Nicotine enhances the release of the neuromodulator dopamine (DA) in the brain. Increased DA content in the carotid bodies (CB), and in the brain stem (BS) attenuates the ventilatory responses to changes in FiO2. The study hypothesis was that antenatal nicotine exposure during the last trimester decreases ventilatory responses to changes in FiO2 through a dopaminergic mechanism in CB or BS. Subjects& Methods: Hyperoxic tests (change in minute ventilation (Vdot1) to FiO2 1.0 for 10 sec or 5 breaths) were performed in 3 groups of awake, 3-14 d old lambs: 8 controls (CTRL), 6 prenatally nicotine treated (PT) and 6 pre- and postnatally treated (PPT) by implanted minipumps. Hyperoxic tests were performed during infusion of a) saline, b) domperidone (domp), a DA2 receptor blocker in CB or c) SCH 23390, a DA1 receptor blocker in the BS.

The Effects of Changes in Ventilation and Cardiac Output on Expired Nitric Oxide

The measurement of nitric oxide (NO) in expired gas is being increasingly reported in disease states such as sepsis, heart failure, and asthma. However, the effects of changes in ventilatory and cardiac parameters on expired NO are not known. Therefore, we assessed the effects of changes in minute ventilation (VE), ventilatory pattern, and cardiac output on expired gas NO levels in five anesthetized, intubated pigs. The animals were mechanically ventilated at three settings for each of respiratory rate (12 to 14, 16 to 18, and 22 to 24/min) and tidal volume (10, 15, and 20 mL/kg) applied in random sequence, yielding nine ventilatory patterns and a range of VE (3.7+/-0.1 to 13.2+/-0.8 L/min). When VE was increased, expired NO concentration declined slightly (r=-0.40, p<0.01), but the rate of excretion of NO in expired gas increased significantly (r=0.60, p<0.01). In contrast, when cardiac output was increased progressively from 3.6+/-0.1 to 4.7+/-0.3 and 5.8+/-0.4 L/min (p<0.01) by volume loading during constant eucapneic ventilation, there was no change in expired NO. Changes in VE over a physiologic range significantly affect the measurement of NO in expired gas, whereas short-term changes in cardiac output do not. To facilitate comparison between studies, we suggest that the measurement of expired NO should be reported in conjunction with data on VE.

Tracheal Injury

Tracheal Injury

Age dependency of cerebral oxygenation assessed with near infrared spectroscopy

Near infrared spectroscopy (NIRS) is an optical technique that provides information on cerebral tissue oxygenation and hemodynamics on a continuous, direct, and noninvasive basis. It is used to determine cerebral blood volume (CBV) and cerebrovascular CO2 reactivity during normoxic hyper- and hypocapnia in a group of 28 healthy volunteers aged 20 to 83 years. The main focus is on to the age dependency of the measured variables. The influence of changes in minute ventilation during normocapnia on the cerebral oxygenation was also studied. The mean CBV (6SD) in age was, for 20 to 30 years, 2.1460.51 ml/100 g of brain tissue; for 45 to 50 years, 1.9260.40 ml/100 g; and for 70 to 83 years, 1.4760.55 ml/100 g. The CBV showed a significant decrease with advancing age. No influence was found for a change in minute ventilation on cerebral oxygenation. During hypercapnia cerebral blood flow (CBF) significantly increased in all age groups, with a factor of 1.3160.17 kPa−1, 1.6461.39 kPa−1, and 2.461.7 kPa−1, respectively, for the three age groups. The difference in change among the age groups was not statistically significant (p50.09). The trend seen was an increased change in CBF with advancing age. During hypocapnia, the CBF significantly decreased in all age groups, with a factor of 0.8960.08 kPa−1, 0.8960.04 kPa−1, and 0.8560.11 kPa−1, respectively. There was no significant difference among the age groups (p50.50).

The safety of digital mobile cellular telephones with minute ventilation rate adaptive pacemakers.

In vitro tests suggest that rate adaptive pacemakers using changes in transthoracic impedance to vary pacing rate may be affected by digital mobile telephones. Electromagnetic fields generated by digital mobile telephones (Global System for Mobile [GSM]) represent a potential source of electromagnetic interference (EMI) for the Telectronics META rate adaptive pacemakers, which use transthoracic impedance as a sensor to determine changes in minute ventilation. Sixteen implanted Telectronics META pulse generators were exposed to 25-W simulated GSM transmissions (900-MHz carrier pulsed at 2, 8, and 217 Hz with a pulse width of 0.6 ms) and the antenna of a 2-W digital mobile telephone (900-MHz, 217-Hz pulse, 0.6-ms pulse width). The 12 dual and four single chamber devices were programmed to maximum sensitivity and assessed in unipolar and bipolar settings and rate adaptive and nonrate adaptive modes. In all cases of EMI, testing was repeated at lower, more routinely set bipolar sensitivity levels. At maximum sensitivity, 11 of 16 devices displayed no evidence of EMI. Brief ventricular triggering occurred in 2, a brief pause in 1, a combination of both in 1, and a brief episode of pacemaker-mediated tachycardia in 1. With pulse generators programmed to more routine sensitivities, only one device displayed rare single beat ventricular triggering. No changes in minute ventilation rate adaptive pacing were observed. At maximum unipolar sensitivities, the META series of rate adaptive pacemakers are resistant to clinically important EMI from digital mobile telephones. Set at routine sensitivities, these devices perform reliably in the presence of digital mobile telephones.

Clarification of Kinetic Terminology

P.S.A. Glass, M.B., Ch.B., F.F.A. (S.A.); Associate Professor, S.T. Howell, MD; Associate in Anesthesia, Department of Anesthesia, Duke University Medical Center, Durham, North Carolina 27710.In Reply:--We appreciate the suggestions of Overdyk and Roy and agree that the essential point of our manuscript was to validate the context-sensitive half-time (CSHT) predicted by the pharmacokinetics previously programmed into our Computer Assisted Continuous Infusion device. This was done, and the modeled CSHT from our measured data was not significantly different from CSHT calculated from historical pharmacokinetic parameters. For alfentanil, the “historical CSHT” was published previously and is reported in the first paragraph of the discussion section as 59.4 min. The measured alfentanil CSHT was reported in Table 3 as 51.9+/-12.3 min (mean+/-SD) and represents a validation of the “historical” calculation of CSHT. The same is true for remifentanil. In hindsight, we may have presented confusing nomenclature by using the terms “modeled” and “measured” CSHT (Table 3). These terms would probably have been better called “measured CSHT: entire data” and “measured CSHT: terminal data”, respectively, to indicate that they both represent measured CSHTs, but that each was based on different parts of the same data set. We used the exponential functions simply because one cannot directly measure the precise time for a 50% decrease in concentration with intermittent (discrete) blood samples. Instead, one has to develop a continuous function, fit to the data, from which the time to a 50% decrease can be interpolated accurately.As Overdyk and Roy correctly observe, the essential point is that no matter how the measured CSHT was calculated, it should (and does) confirm the previously published a priori expectation of CSHT. We appreciate the opportunity to clarify this portion of the article.As for their concern of the pharmacodynamic CSHT regarding the “usually … sigmoidal relationship between effect site concentration and the effect,” we simply re-state that we have reasonable assurance that we were measuring ventilation effects over the middle range of the sigmoidal curve, where the change in effect site concentration and effect is nearly linear. Therefore, we do not require a sigmoidal curve to define our change in minute ventilation because we did not seek to measure a 50% change in minute ventilation from maximal effect (Emax) to no effect (E0), but rather a 50% change in the measured effect over the linear portion of the curve, as exhibited in our study population.(Accepted for publication May 14, 1996.)P.S.A. Glass, M.B., Ch.B., F.F.A. (S.A.); Associate Professor, S.T. Howell, MD; Associate in Anesthesia, Department of Anesthesia, Duke University Medical Center, Durham, North Carolina 27710.

Decreased Carbon Dioxide Sensitivity in Infants of Substance-Abusing Mothers

To determine whether there is a demonstrable abnormality in control of breathing in infants of substance-abusing mothers during the first few days of life. We enrolled 12 drug-free control infants and 12 infants of substance abusing mothers (ISAMs). These infants experienced otherwise uncomplicated term pregnancies and deliveries. The infants were assigned to a group based on the results of maternal histories and maternal and infant urine toxicology screens. Studies were performed during quiet sleep during the first few days of life. We measured heart rate, oxygen saturations via a pulse oximeter, end-tidal carbon dioxide (ET-CO2) level, respiratory rate, tidal volume, and airflow. The chemoreceptor response was assessed by measuring minute ventilation and the ET-CO2 level after 5 minutes of breathing either room air or 4% carbon dioxide. The gestational ages by obstetrical dating and examination of the infants were not different, although birth weights and birth lengths were lower in the group of ISAMs. Other demographic data were not different, and there were no differences in the infants' median ages at the time of study or in maternal use of tobacco and alcohol. The two groups had comparable baseline (room air) ET-CO2 levels, respiratory rates, tidal volumes, and minute ventilation. When compared with the group of ISAMs, the drug-free group had markedly increased tidal volume and minute ventilation on exposure to 4% carbon dioxide. These increases accounted for the difference in sensitivity to carbon dioxide, calculated as the change in minute ventilation per unit change in ET-CO2 (milliliters per kg/min per mm Hg). The sensitivity to carbon dioxide of control infants was 48.66 +/- 7.14 (mean +/- SE), whereas that of ISAMs was 16.28 +/- 3.14. These data suggest that ISAMs are relatively insensitive to challenge by carbon dioxide during the first few days of life. We speculate that this reflects an impairment of the chemoreceptor response.

Halothane affects ventilatory afterdischarge in humans

In awake humans, when ventilatory stimulation is suddenly removed, the subsequent change in minute ventilation (which remains at higher levels for longer times than expected from the dynamics of the chemoreceptors) is termed ventilatory after discharge. In this study we investigated the effects of subanaesthetic concentrations of halothane on afterdischarge. The ventilatory pattern after sudden termination of brief periods (90-180 s) of isocapnic hypoxia (PE'cO2 approximately 0.1 kPa above initial resting values; PE'O2 6.5 kPa) by normoxia (PE'O2 14 kPa) was determined in healthy volunteers. Six subjects underwent 13 studies without halothane (control) and six others 10 studies during inhalation of 0.22% halothane. Isocapnic hypoxia caused a mean increase in ventilation of 10.8 (SD 2.4) litre min-1 in the control and 4.2 (2.4) litre min-1 in the halothane studies (P < 0.01). The transition to normoxia caused a slow ventilatory decay in the control and a fast decay in the halothane groups: the interval that occurred between the "last hypoxic" breath and the time required for ventilation to return to 110% of baseline was 60.7 (23) s for the control and 12.3 (6.0) s for the halothane studies (P < 0.05). Taking into consideration the different factors that determine the pattern of breathing immediately after termination of a brief period of hypoxia by normoxia (PE'O2 waveform, transport delay time between lungs and carotid bodies, time constant of the peripheral chemoreflex loop and afterdischarge), the faster ventilatory decay observed with halothane is probably related to suppression of afterdischarge.(ABSTRACT TRUNCATED AT 250 WORDS)

Tidal volume and respiratory rate changes during CO 2 rebreathing after lung transplantation

To evaluate the contribution of the respiratory pattern to the ventilatory response after lung transplantation, we studied the changes in minute ventilation, tidal volume, and respiratory rate during CO 2 rebreathing in 14 patients with severe obstructive pulmonary disease, and compared them with 10 normal subjects. Seven patients underwent a bilateral lung transplantation and 7 patients had single-lung transplantation. Single-lung transplant recipients increased their respiratory rate by the last postoperative test compared with either preoperative or initial test periods (0.38 ± 0.13 versus 0.027 ± 0.24 or 0.12 ± 0.08 breaths · min −1 · mm Hg −1; P < 0.005). Bilateral lung transplant recipients showed a diminished ability to augment their respiratory rate by the last postoperative test compared with either preoperative or initial test periods (0.13 ± 0.23 versus 0.54 ± 0.25 or 0.25 ± 0.29 breaths · min −1 · mm Hg −1; p < 0.06). The restored ventilatory response by the fourth postoperative week was due to a statistically significant increase in tidal volume for both single and bilateral lung transplant recipients. This study demonstrates that when lung transplant recipients have an appropriate ventilatory response to CO 2 rebreathing, single-lung transplant recipients have a respiratory pattern similar to normal; whereas the bilateral lung transplant recipients show the effects of total pulmonary denervation. We conclude that the preserved ventilatory response in lung transplant recipients is composed of a respiratory pattern that is influenced by the presence or absence of vagal inputs.

Effect of ventilation on acid-base balance and oxygenation in low blood-flow states

To investigate how minute ventilation affects the partial pressure of end-tidal CO2 and arterial and mixed venous pH, PCO2, PO2, and the concentration of bicarbonate during low blood-flow states. We tested the null hypothesis that acid-base conditions during low rates of blood flow are not significantly different when minute ventilation is doubled or halved.Prospective, experimental, animal study.University hospital laboratory.Domestic swine.We studied ten anesthetized and mechanically ventilated swine (weight, 43 to 102 kg) in a new model of controlled systemic and pulmonary blood flow in which each animal was maintained on ventricular assist devices. After electrical induction of ventricular fibrillation, ventricular assist device blood flow was decreased in steps. At each decrease, control minute ventilation, two times the control minute ventilation (hyperventilation), and one-half the control minute ventilation (hypoventilation) were administered; each ventilatory change was maintained for 6 mins.Aortic, pulmonary arterial and central venous pressures, ventricular assist device blood flow, and end-tidal CO2 were recorded continuously. Acid-base conditions were studied at three different mean blood flow rates: 49%, 30%, and 12% of baseline prearrest cardiac index. Arterial pH and PaO2 and mixed venous pH varied directly (p < .003) with minute ventilation, while PaCO2 and mixed venous PCO2, and end-tidal CO2 varied inversely (p < .0001) with minute ventilation. Mixed venous PO2 was not significantly related to minute ventilation (p = .6). PaCO2 and arterial bicarbonate; mixed venous pH, mixed venous PO2, and mixed venous bicarbonate, and end-tidal CO2 varied directly (p < .001) with blood flow, while mixed venous PCO2 varied inversely with blood flow (p < .05). Arterial pH was not significantly related to blood flow (p = .3). When minute ventilation changed from hyperventilation to hypoventilation at a mean blood flow rate of 49%, mean arterial pH decreased 0.22 +/- 0.06 (p < .05), mean PaCO2 increased 28 +/- 6 torr (3.7 +/- 0.8 kPa) (p < .05), and mean PaO2 decreased 99 +/- 77 torr (13.2 +/- 10 kPa); mean mixed venous pH decreased 0.11 +/- 0.02, mean mixed venous PCO2 increased 16 +/- 2.2 torr (2.1 +/- 0.3 kPa) (p < .05), and mean mixed venous PO2 did not change; mean end-tidal CO2 increased 18 +/- 2 torr (2.4 +/- 0.3 kPa) (p < .05). The effect of changes in minute ventilation on blood gases and end-tidal CO2 was similar for mean blood flow rates of 30% and 12% of baseline cardiac index.During low rates of blood flow similar to those rates found in shock and cardiopulmonary resuscitation, alterations in minute ventilation significantly influenced end-tidal CO2 and both arterial and mixed venous pH and PCO2. These findings may have clinical importance in improving the treatment of shock and cardiac arrest.

Effect of ventilation on acid-base balance and oxygenation in low blood-flow states

To investigate how minute ventilation affects the partial pressure of end-tidal CO2 and arterial and mixed venous pH, PCO2, PO2, and the concentration of bicarbonate during low blood-flow states. We tested the null hypothesis that acid-base conditions during low rates of blood flow are not significantly different when minute ventilation is doubled or halved. Prospective, experimental, animal study. University hospital laboratory. Domestic swine. We studied ten anesthetized and mechanically ventilated swine (weight, 43 to 102 kg) in a new model of controlled systemic and pulmonary blood flow in which each animal was maintained on ventricular assist devices. After electrical induction of ventricular fibrillation, ventricular assist device blood flow was decreased in steps. At each decrease, control minute ventilation, two times the control minute ventilation (hyperventilation), and one-half the control minute ventilation (hypoventilation) were administered; each ventilatory change was maintained for 6 mins. Aortic, pulmonary arterial and central venous pressures, ventricular assist device blood flow, and end-tidal CO2 were recorded continuously. Acid-base conditions were studied at three different mean blood flow rates: 49%, 30%, and 12% of baseline prearrest cardiac index. Arterial pH and PaO2 and mixed venous pH varied directly (p < .003) with minute ventilation, while PaCO2 and mixed venous PCO2, and end-tidal CO2 varied inversely (p < .0001) with minute ventilation. Mixed venous PO2 was not significantly related to minute ventilation (p = .6). PaCO2 and arterial bicarbonate; mixed venous pH, mixed venous PO2, and mixed venous bicarbonate, and end-tidal CO2 varied directly (p < .001) with blood flow, while mixed venous PCO2 varied inversely with blood flow (p < .05). Arterial pH was not significantly related to blood flow (p = .3). When minute ventilation changed from hyperventilation to hypoventilation at a mean blood flow rate of 49%, mean arterial pH decreased 0.22 +/- 0.06 (p < .05), mean PaCO2 increased 28 +/- 6 torr (3.7 +/- 0.8 kPa) (p < .05), and mean PaO2 decreased 99 +/- 77 torr (13.2 +/- 10 kPa); mean mixed venous pH decreased 0.11 +/- 0.02, mean mixed venous PCO2 increased 16 +/- 2.2 torr (2.1 +/- 0.3 kPa) (p < .05), and mean mixed venous PO2 did not change; mean end-tidal CO2 increased 18 +/- 2 torr (2.4 +/- 0.3 kPa) (p < .05). The effect of changes in minute ventilation on blood gases and end-tidal CO2 was similar for mean blood flow rates of 30% and 12% of baseline cardiac index. During low rates of blood flow similar to those rates found in shock and cardiopulmonary resuscitation, alterations in minute ventilation significantly influenced end-tidal CO2 and both arterial and mixed venous pH and PCO2. These findings may have clinical importance in improving the treatment of shock and cardiac arrest.

A Rate Responsive Pacemaker that Physiologically Reduces Pacing Rates at Rest

Current rate responsive pacemakers incorporate sensors such as minute ventilation (MV) for adapting to changing patient conditions during exercise and periods of exertion. However, for sleep and/or rest periods, the only pacemakers currently on the market that slow the pacing rate utilize an internal timer to determine a decrease in pacing rate. It would be advantageous if the pacing rate could be automatically lowered during periods of sleep or rest. This study utilized a rate responsive sensor, MV, to track the patient's sleeping and resting periods and to decrease the pacing rate at such times. A total of eight patients implanted with Sentri 1210 single chamber MV sensor pacemakers were studied. A sleep rate (SR) of 45 beats/min was selected. A sleep rate response function, which indicated the relationship between changes in MV and corresponding heart rate, was initially set at a value of 16 and continually and automatically updated in a 3-month study. Adaptation was based on the premise that 3 hours per day should be spent at the SR. The average decrease in pacing rates from onset to 3 month for the eight patients was 12.4% +/- 5.3%. Correspondingly, the histograms of the lowest datalog histogram (40-59 beats/min) increased from 0% to 15.4% +/- 0.9% of paced beats. Correlation between the patients' 24-hour diary and Holter recordings showed that the pacing rates during sleep were consistently lower than when the patients were awake and active. This was also the case with a patient whose nocturnal and daily routine was intentionally altered.(ABSTRACT TRUNCATED AT 250 WORDS)

The Measurement of Thoraco-abdominal Asynchrony in Infants With Severe Laryngotracheobronchitis

Retractions of the lower ribcage (chest wall distortion [CWD]) during inspiration are frequently observed with moderate to severe respiratory disease in the infant. Laryngotracheobronchitis (LTB) results in a reversible partial airway obstruction with severe CWD. We wished to measure the motion of the chest wall during distortion to determine the changes in minute ventilation (VE) and to evaluate this clinical sign as a means of assessing disease severity. The respiratory inductance plethysmograph was used to determine the distortion of the lower chest wall, and distortion was correlated with VE, measured at the mouth, in six infants with severe LTB and ventilatory failure. As the conditions of these infants improved, the CWD decreased with decreasing transcutaneous carbon dioxide tension (tcPCO2), VE increased from 0.27 +/- 0.12 L.min-1 x kg-1 at a tcPCO2 of 64 mm Hg to 0.64 +/- 0.06 L.min-1 x kg-1 when the tcPCO2 had fallen to 28 mm Hg. Over the same change in tcPCO2, the tidal volume (VT) increased from 4.8 +/- 0.5 ml.kg-1 to 15.7 +/- 1.4 ml.kg-1. In the most severe disease state, the excursion of the chest wall (as an inductance) was -14 +/- 3 mV in severe obstruction, but increased to 75 mV +/- 4 mV with resolution of the illness. The timing and vector of movement of the abdomen and chest wall were expressed as a Lissajous figure, which is measured as a phase angle. The severity of the disease process, as determined by tcPCO2 was directly related to the phase relationship, and thus reflected both VE and VT. The severity of the CWD may be assessed rapidly by the use of Lissajous figures.