Changes In Alveolar Ventilation Research Articles

Arterial P CO2 and lung ventilation in man exposed to 1-5% CO2 in the inspired gas.

Conflicting results have been published on the shape of the curve relating the change in lung ventilation to the change in alveolar or arterial PCO2 induced by increased inspired CO2 (the CO2 sensitivity). In this study eight human subjects with in-dwelling arterial cannulae were each exposed to five different levels of increased inspired CO2 (1-5%). Arterial PCO2 and ventilation were measured in the 7th minute of each period of CO2 exposure. Each CO2 exposure period was flanked by control periods in which similar measurements were carried out during air breathing. We found non-linear increases in both ventilation and arterial PCO2 with increasing levels of inspired CO2. When 5% CO2 in air was inspired the arterial PCO2 increased by about 15% of the inspired CO2 load. There was no significant non-linearity in the relation between change in alveolar ventilation (normalized to body surface) and change in arterial PCO2. The inter-individual variation in CO2 sensitivity was less when alveolar ventilation was normalized to the CO2 output rather than to body surface area. We conclude that the sensitivity to CO2 is close to constant within the range 0-5% CO2 in the inspired gas.

Determinants of alveolar ventilation during high-frequency transtracheal jet ventilation in dogs.

The effectiveness of transtracheal jet ventilation is a function of gas delivery pressure (drive pressure), duty cycle (insufflation time/total cycle time), and respiratory frequency. Nine dogs, anesthetized with sodium pentobarbital, were ventilated through a cricothyrotomy cannula using a controller that allowed separate setting of drive pressure, duty cycle, and frequency. PaO2 and PaCO2 were measured after achieving steady-state gas exchange at 15 to 22 different combinations of drive pressure, duty cycle, and frequency in each dog. There were slight increases in PaCO2 and larger decreases in PaO2 as frequency was increased from 10 to 200 cycle/min. Increases in drive pressure and duty cycle resulted in reduced PaCO2 and increased PaO2. Multiple linear regression showed good correlation between PaCO2 and drive pressure, duty cycle, and frequency. The distribution of air flow between alveolar and physiologic dead space, upper airway leakage, and entrainment was determined for each set of conditions. Changes in alveolar ventilation corresponding to the blood gas changes resulted from interaction of dead-space ventilation and upper airway leakage, which varied with breath duration. Decreases in leakage during short breaths tended to compensate for the increased fractional dead-space ventilation at high frequency, thus minimizing the effects of frequency changes on gas exchange.

Estimation of ventilatory response to carbon dioxide in newborn infants using skin surface blood gas electrodes

Using only skin surface blood gas measurements, we calculated the ventilatory response to inhaled carbon dioxide from changes in skin surface PCO2 (PSCO2). This new method is based on the fact that if CO2 elimination is nearly constant, the change in alveolar ventilation from one steady state level to another is inversely proportional to the change in PSCO2. From this we derived a ventilatory ratio (VR) for 0%, 2%, and 4% CO2 breathing. A ventilatory response slope is then calculated from the three VR values, and is similar to a standard CO2 response slope. We serially studied 20 infants (28 to 40 weeks gestation) 2 to 9 weeks of age. Ten infants had serious apnea, ten did not. The infants breathed each test gas for 8 to 10 minutes during quiet sleep with skin surface electrodes attached. Infants with apnea were studied before and after apneic spells resolved. We found that apneic infants had a significantly reduced VR slope compared with that in the nonapneic infants, regardless of age. When apnea disappeared, the ventilatory ratio slope always increased into the range measured in nonapneic infants. In nonapneic infants the ventilatory ratio slope significantly increased with postnatal age. We conclude that infants with serious apnea have a reduced ventilatory response to CO2 and that the resolution of apnea is associated with the development of a normal CO2 response.

Ventilation and CSF ions during hypocapnic HCl and HNO3 acidosis in conscious rabbits.

In conscious rabbits with preimplanted arterial, central venous, and cisterna magna catheters, we infused HNO3 or HCl to lower and maintain arterial PCO2, pH, and plasma HCO-3 at the same mean values in both groups over 9 h. The hypothesis was that greater entry into cerebrospinal fluid (CSF) of the strong anion NO-3 vs. Cl- would result in a greater decrease in CSF [HCO-3] in the HNO3 vs. the HCl experiment, even though the acid-base stress as measured by arterial PCO2 and plasma [HCO-3] was the same. The results did not support the hypothesis. With HCl acidosis, delta CSF [HCO-3] was equal to delta CSF [Cl-]. With HNO3 acidosis, delta CSF [HCO-3] was equal to delta CSF [NO-3] + delta CSF [Cl-], as both CSF Cl- and HCO-3 decreased with NO-3 entry into CSF. The change in CSF [HCO-3] appeared tightly linked to the PCO2 or the plasma [HCO-3], it did not depend on the type of acid used. The ionic mechanisms that determine the CSF [HCO-3] in metabolic acidosis appear able to utilize changes in the strong anions NO-3 and Cl- to bring about CSF acid-base regulation. The change in alveolar ventilation per unit CO2 production as reflected by the arterial PCO2 was the same in both groups, although the expired minute ventilation and respiratory frequency responses were diminished in the HNO3 vs. the HCl groups. In both groups with acidosis, tidal volume increased, whereas respiratory frequency decreased.

Physiology of the Kidney

This compact and frugally written soft-cover text has many appealing virtues. First, it represents the distillation of knowledge from a well-seasoned teacher of basic medical physiology. Second, it adds the judgment and disease-oriented approach of an experienced clinical nephrologist who is also well versed in fundamental aspects of renal function and pathophysiology. The two authors have provided their reading audience, primarily medical students and other physicians and scientists interested in reviewing the fundamentals of renal physiology, with an up-to-date, well-illustrated, and eminently readable volume. The well-chosen illustrations and line drawings supplement the textual material in a useful and instructive way. The acid-base sections might have been improved by incorporating the well-known nomograms for predicting the physiological adjustments in plasma bicarbonate concentration and pH that occur with acute and chronic changes in alveolar ventilation, as well as the changes in ventilation that are predicted following a primary disturbance in plasma bicarbonate

The use of ventilation and perfusion lung scans to document changes following experimental pulmonary embolism.

Ventilation and perfusion lung scans were used to further document haemodynamic and respiratory changes following experimental pulmonary embolism. Changes in alveolar ventilation were only slightly greater in embolised areas of lung compared to unembolised areas, and neither heparin nor isoprenaline made any appreciable difference to ventilation. Perfusion scans revealed that large amounts of blood can flow around a massive pulmonary embolus and most of the increase in pulmonary blood flow following isoprenaline occurred in the non-embolised areas of the lung.

The effect of mechanical vibration physiotherapy on arterial oxygenation in acutely ill patients with atelectasis or pneumonia.

The effect of mechanical chest vibration on arterial blood gases was studied in 10 patients requiring oxygen therapy who had acute lung disease and an abnormal chest roentgenogram. Eight patients were using mechanical ventilators. For the duration of the study, patients were seated or in a high semi-Fowlers position. No other pharmacologic or physical therapy was given during the study period, nor was there any change in the fraction of inspired oxygen or the respirator settings. The patients ranged from 23 to 89 yr of age. After control blood gas measurements were taken, each patient received 30 min of mechanical vibration to the thorax followed immediately by tracheal suction. Blood gases were re-examined 30 min and 1 h after completion of the physiotherapy. Results showed a significant increase in PO2 at 30 min and 1 h after completion of mechanical chest vibration with no change in PCO2 or pH. This study demonstrated that external mechanical vibration of the chest is a useful therapeutic modality in the management of hypoxemia in patients with atelectasis or pneumonia. This was reflected by the increase in PO2 with no change in alveolar ventilation. We presume the better matching of ventilation to perfusion accounted for our results.

Phlebotomy improves pulmonary gas exchange in chronic mountain polycythemia.

There is not unanimous agreement in the literature regarding the effects of bleeding on pulmonary gas exchange in polycythemic patients. Spirometry, alveolar arterial O2 and CO2 tension differences, PaO2 breathing 100% oxygen and carbon monoxide-diffusing capacity were measured before and after 1 week of chronic phlebotomy in 4 chronic mountain polycythemic patients. Studies were carried out at 3,700 m above sea level (PB = 491 mm Hg). Before phlebotomy, 2 patients showed abnormal spirometry and gas exchange. Only 1 patient had high PaCO2 and all of them showed low values of PaO2 breathing oxygen. Phlebotomy improved both spirometry and gas exchange. Improvement in arterial oxygen saturation and PaO2 could not be attributed to changes in alveolar ventilation, but rather to better distribution of VA/Qc ratios since physiological dead space decreased. Our results are similar to those reported in polycythemia vera patients. A significant correlation between the changes in PaO2 with phlebotomy and the control PaO2 have been found from 45 polycythemic patients with chronic obstructive pulmonary disease collected from the literature. It is concluded that excessive polycythemia worsened hypoxemia and that phlebotomy improved gas exchange.

Hemodynamic and ventilatory effects of skin-cooling in cattle.

Cooling the skin of cattle at an ambient temperature of 25 degrees C decreased cardiac output and increased systemic and pulmonary vascular resistances. Minute ventilation was reduced by about 50%. There was no change in alveolar ventilation as measured by arterial blood gases. These results indicate that thermoregulatory ventilation has significant cardiopulmonary effects in cattle at normal laboratory temperatures.

Transient respiratory responses to step-changes in airflow resistance in anesthetized cats

Breath by breath responses to on and off step-changes in inspiratory airflow resistance were investigated in intact anesthetized cats to differentiate the neural and chemical components of the response. Examination of the changes in alveolar ventilation, inspiratory duration, inspiratory work, diaphragm electromyogram, and blood gases established the characteristics of the transient responses. The neural component reflected in the first loaded breath is a prolongation of the inspiratory phase. This prolongation of the inspiratory phase resulted in an increase in work without changes in rate of work or rate of diaphragm activity. The secondary chemical component, manifested in subsequent breaths, consisted of gradual increases in rates of inspiratory work and diaphragm activity supplementing the increase in work accomplished by the neural component alone. The neural component and the chemical component combine to minimize the effect of mechanical loading on ventilation.

PULMONARY CLEARANCE OF ANAESTHETIC AGENTS A Theoretical Study

The pulmonary clearance of anaesthetic agents (Cl) represents a useful index of their elimination from the lungs. Its value depends on pulmonary blood flow (), alveolar ventilation (VA), and anaesthetic blood solubility (λ) according to equation: Cl = (VAQ)/(VA+λQ). When the alveolar ventilation and pulmonary blood flow are constant the pulmonary clearance of the anaesthetic depends on its blood solubility. In this case the lower the blood solubility is, the higher the value of pulmonary clearance becomes. For each anaesthetic agent a change in alveolar ventilation or in pulmonary blood flow will produce a change in pulmonary clearance which in its turn depends on anaesthetic blood solubility. When λ = (VA/Q)2 a change in alveolar ventilation or in pulmonary blood flow will affect the pulmonary clearance to the same extent. When the anaesthetic blood solubility value is higher than (VA/Q)2, its pulmonary clearance is predominantly affected by alveolar ventilation, and when anaesthetic blood solubility is lower than (VA/Q)2 its pulmonary clearance is predominantly dependent on pulmonary blood flow. Changes in pulmonary clearance produced by changes in alveolar ventilation (/VA) are larger with halothane, nitrous oxide and cyclopropane than with agents of greater blood-gas solubility at all VA/Q ratios in the range 0.5—2.0.

The effect of added expiratory obstruction on gas exchange in chronic airways obstruction

Ventilation and arterial blood gases were measured in ten patients with severe chronic airways obstruction with and without added expiratory obstruction. Added obstruction resulted in a statistically significant decrease in minute ventilation, tidal volume and respiratory frequency. There were no significant changes in alveolar ventilation, arterial blood gases or estimated venous admixture. Oxygen consumption tended to decrease but this was not statistically significant. There was a uniform decrease in physiological dead space indicating some improvement in ventilation perfusion relationships in the lung. The results are compared to those reported during pursed lips breathing.

Cardiopulmonary effects of continuous pressure breathing in hypothermic dogs.

Continuous pressure breathing was studied in hypothermic anesthetized dogs. Alveolar ventilation decreased during continuous positive-pressure breathing and increased during continuous negative-pressure breathing. The changes in alveolar ventilation were due to changes in respiratory rate as well as in respiratory dead space. Cardiac output fell significantly during continuous positive-pressure breathing due to a reduction in heart rate and stroke volume. During continuous negative-pressure breathing cardiac output was only slightly greater than during control as a result of a fall in heart rate and an increase in stroke volume. Oxygen consumption was reduced to 60% of control during continuous positive-pressure breathing of 16 cm H2O but was 25% greater than control during continuous negative-pressure breathing. Qualitatively, CO2 production changed as did O2 consumption but was different quantitatively during continuous negative-pressure breathing indicating hyperventilation due to increased respiratory rate. Mean pulmonary artery pressures and pulmonary resistance varied directly with the applied intratracheal pressure. The results indicate that the hypothermic animal can tolerate an imposed stress such as continuous pressure breathing and can increase its oxygen consumption during continuous negative-pressure breathing as does the normothermic animal. hypothermia; respiratory dead space; metabolic rate; cardiac output Submitted on December 8, 1964

TRACHEOSTOMY AND RESPIRATORY DEAD SPACE IN EMPHYSEMA.

Acute experimentation to judge the effects of reduction of dead space with tracheostomy breathing was performed on four subjects with lower airway obstruction (bronchitis and emphysema) and on two subjects with upper airway obstruction (carcinoma of the larynx and tracheal stenosis). With tracheostomy breathing, the reduction in dead space led to a decrease in minute ventilation except in the two patients with upper airway obstruction. Alveolar ventilation decreased except when alveolar hypoventilation was present to start with. There was no change or an increase in Pacoco2 and H+ in the subjects with lower airway obstruction and small increases in arterial oxygen saturation and Paoo2 occurred. A decrease in Pacoco2 and H+ occurred in one of two patients with upper airway obstruction. Reduction of dead space per se with tracheostomy breathing brings about small changes in alveolar ventilation and gas exchange in the lungs of patients with chronic bronchitis and emphysema. Note:(With the Technical Assistance of Roy Engstrom, Mabel Pearson, and Tom Purcell) physiological dead space and tracheostomy; arterial blood gases with tracheostomy breathing; tracheostomy versus mouth breathing; emphysema and tracheostomy breathing Submitted on February 11, 1963

THE SEPARATE AND COMBINED RESPIRATORY EFFECTS OF CHLORPROMAZINE AND MEPERIDINE IN NORMAL MEN CONTROLLED AT 46 MM HG ALVEOLAR PCO2

A method for artificially controlling alveolar pCO2 was used to study the time course of changes in respiratory rate, depth and minute volume after intramuscular administration of physiological saline solution (2 ml), chlorpromazine hydrochloride (25 mg/70 kg), meperidine hydrochloride (100 mg/70 kg) and of meperidine together with chlorpromazine in the stated doses. The method employed provided magnification of drug-induced respiratory alterations by preventing the physiological readjustments in alveolar pCO2 normally associated with changes in alveolar ventilation. The results obtained indicated (a) the time course of a consistent and prominent respiratory depression by meperidine, (b) that chlorpromazine alone produces no consistent respiratory depression but that it may tend to improve tolerance to elevated pCO2, and (c) that administration of chlorpromazine with meperidine causes respiratory depression greater in degree and duration than produced by meperidine alone. The data obtained are discussed with regard to mechanisms of the observed chlorpromazine-meperidine interaction.

An alveolar carbon dioxide tension control system: its use to magnify respiratory depression by meperidine.

A system was devised combining means of a) automatic sampling of end-tidal gas, b) rapid analysis of samples gas for Co2 concentration and c) manual or automatic modification of per cent Co2 in succeeding inspirations to permit maintenance of alveolar pCo2 at desired levels above the Co2 tension natural for a particular experimental situation. By imposing a fixed, elevated alveolar pCo2 upon a subject, effects of drugs or physiological stresses upon Co2-sensitive functions can be evaluated, unmasked by the compensatory alterations of alveolar and arterial pCo2 which normally result from changes in alveolar ventilation or metabolism. Validation of alveolar pCo2 control in 16 normal subjects, using arterial pCo2 as a reference standard, revealed no significant difference between the imposed end-tidal pCo2 and the pCo2 of arterial blood. Use of the pCo2 control system to evaluate the dynamics of meperidine effect on respiration in normal men indicated sufficient magnification of the effect of meperidine on respiratory minute volume to permit use of the method for comparative studies of rate of onset, time of peak effect and rate of disappearance of the action of meperidine on respiration. Submitted on July 9, 1959