Increase In Dead Space Research Articles

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.

What are the mechanisms producing increased ventilation in dead space studies in neonates?

In 21 studies on 15 infants an additional dead space tube produced a significant rise in end-tidal PCO2 and fall in end-tidal PO2, associated with a rise in minute ventilation (228 +/- 77 mL/kg/min at zero, 348 +/- 85 mL/kg/min at one, and 437 +/- 128 mL/kg/min at two anatomical dead spaces). The differences between end-inspiratory and end-expiratory PCO2 and PO2 did not change significantly, suggesting an increase in dead space, but not in alveolar ventilation. In a further 9 babies the rise in ventilation was unchanged when measurements were repeated in 30% oxygen (361 +/- 65 vs. 340 +/- 54 mL/kg/min at one anatomical dead space). Studies on 8 babies, with the added tube ventilated by a fan, showed that a mean 28% of the rise in minute ventilation was due to increased resistance. Although the response to tube breathing in neonates is complex, carbon dioxide appears to be the major factor producing increased ventilation.

気管口閉鎖前後の呼吸様式の変化 換気量，換気時間，血液ガスの検討

In the field of respiratory physiology, it seems interesting to evaluate the change of respiratory pattern as the results of alteration of the respiratory route before and after the closure of tracheostoma.Tracheostomized patients breathe without the upper airway such as the nose, the mouth and the larynx. When tracheostoma is closed, the patients are suddenly forced to breathe through the upper airway. As the result, an anatomical dead space, a respiratory resistance and a humidifying function are added to their airway abruptly. The purpose of this study was to examine the above-mentioned change of respiratory pattern before and after the closure of tracheostoma.The subjects were seven tracheostomized patients with normal lung function. Tidal volume, respiration time and blood gases were measured before and just after, 1 hour and 2 hours after the closure of tracheostoma.The results were as follows: 1) When tracheostoma was closed, tidal volume and respiration time increased and respiratory minutes volume tended to decrease gradually in the course of time. 2) While Pao2 did not change in the course of time before and after the closure of tracheostoma, Paco2 was increased slightly after the closure and the value continued in 2 hours almost constantly.These changes were statistically significant except for minutes volume.It is obvious that the anatomical dead space increases when the tracheostoma is closed. As the results, the efficiency of ventilation would decrease.Our results showed, however, Pao2 did not decrease after closing the tracheostoma. On the other hand, respiratory minutes volume tended to decrease, and Paco2 increased just after the closing it and the value continued constantly for two hours.These results confirm that the ventilatory efficiency would be improved sometimes after the closure of tracheostoma in spite of the increased dead space, suggesting that the humidifying function and the resistance of the upper airway play a significant role in the respiration.

Volumetric determination of adsorption of helium over some zeolites with a temperature-compensated, differential tensimeter having symmetrical design

Amounts of adsorption of helium over some zeolites were determined ranging from 77 to 673 K with a temperature-compensated, differential tensimeter having symmetrical design. The amount of adsorption of helium was determined by measuring an increase in apparent dead space between the sample adsorption cell containing the sample and the reference adsorption cell containing several glass rods on the assumption that the amount adsorbed of helium at 673 K was negligibly small, the temperature of the adsorption cells being changed after each determination. Discussion has been made of the errors caused by the adsorption of helium to the determination of the density of solids when helium is used as the dilatometric fluid, and the determination of the surface areas of solids based upon the adsorption of nitrogen with a conventional volumetric adsorption apparatus.

Increased alveolar deadspace after closure of cardiac septal defects: pulmonary air embolism or failure of homeostasis?

During surgery for closure of atrial or ventricular septal defects (ASD, VSD), we used a computerized on-line system to follow changes in the alveolar deadspace fraction. We observed a large increase in the alveolar deadspace immediately following septal defect closure. No increase had been observed post-cardio-pulmonary bypass in children operated upon because of aortic or pulmonary stenosis, or in adults undergoing myocardial revascularization. The increase in deadspace is probably a result of the lung's failure to adjust to the large decrease in pulmonary blood flow following septal defect closure. An alternative cause for the finding, that of pulmonary artery air embolism occurring intraoperatively, appears to be less likely.

Effect of respiratory apparatus on timing and depth of breathing in man

The effects of breathing of (1) nose-clips, with and without mouthpieces, (2) tube breathing with incremental dead spaces upt to 600 ml, and (3) a Venturi mask with a high air inflow reducing the effective dead space to zero were measured with respiratory inductance plethysmography. The effective dead spaces of the lengths of tubing were 25% smaller than their water-displacement volumes. The principal response to the increase in dead space was an increase Vt without any change in frequency or timing. The increase in V̇e 16% greater than the ventilation of the effective dead space. The facemask with a high flow of air did not affect the pattern of breathing. External devices alone (nose-clips, mouthpieces) by themselves brought about a significant increase in Vt (10%, P<0.05). The increase in DS with the change from nasal to oral breathing may have contributed to the accompanying increase in Vt; the fall in frequency with the nose-clip alone might have been caused by stimulation of receptors in the trigeminal area.

Inspiratory airway CO2 loading in the pony.

To determine if CO2-sensitive airway receptors are important in the control of breathing, CO2 was preferentially loaded into the respiratory airways in conscious ponies. The technique involved adding small amounts of 100% CO2 to either the latter one-third or latter two-thirds of the inspiratory air in an attempt to raise CO2 concentrations in the airway dead space independent of the arterial blood. Arterial blood gas tensions (PCO2 and PO2) and pH, as well as respiratory output (minute volume, tidal volume, and respiratory rate), were measured in a series of 20 experiments on 5 awake ponies. Elevation of airway CO2 to approximately 12% by addition of CO2 to the latter portion of the inspiratory tidal volume did not alter either ventilation or arterial blood gases. When CO2 was added earlier in the inspiratory phase to fill more of the airway dead space, a small but significant increase in minute volume (2.1 l X min-1 X m-2) and tidal volume (0.1 l X m-2) was accompanied by an increase in arterial PCO2, arterial PO2, and a fall in pH (0.96 Torr, 10.5 Torr, 0.007 units, respectively). A second series of 12 experiments on 6 awake ponies using radiolabeled 14CO2 determined that the increases in breathing were minimal when compared with the large increase that occurred when these animals inhaled 6% 14CO2 (12.7 l X min-1 X m-2). Also, stimulation of systemic arterial or central nervous system chemoreceptors cannot be eliminated from the response since significant amounts of 14CO2 were present in the arterial blood when this marker gas was added to the latter two-thirds of the inspiratory tidal volume. The results, therefore, provide no evidence for CO2-sensitive airway receptors that can increase breathing when stimulated during the latter part of the inspiratory cycle.

The Pall Ultipor Breathing Circuit Filter???An Efficient Heat and Moisture Exchanger

The Pall bacterial filter was tested as a potential heat and moisture exchanger on a model patient, placed on a circle absorber system, and clinically. The laboratory study was conducted during mechanical ventilation at a V of 6 L/min with fresh gas inflows of 1, 3 and 6 L/min. The model patient introduced carbon dioxide into the circuitry at a rate of 200 ml/min. The resistance of the filter was tested before and after each experiment. With all fresh gas inflows , absolute humidity increased from around 19 mg H2O/L at the start of experimentation to about 27 mg H2O/L within 30 min. Maximum humidities reached were 28 +/- 0.7 mg H2O/L, 27.6 +/- 0.5 mg H2O/L, and 27.7 +/- 0.5 mg H2O/L within 3 hr, with fresh gas inflows of 1, 3, and 6 L/min, respectively. Variations in inspired humidity were also assessed at minute volumes of 4 and 5 L/min with fresh gas inflows of 6 and 3 L/min. Increases in percent dead space were negligible when the filter was inserted between the model patients (assumed to weigh between 70-40 kg) and the circuit. There was no statistically significant increase in pressure with gas flows of 50 L/min when the instrument was dry (0.02 +/- 0.001 cm H2O/L X min-1) or when it was wet (0.02 +/- 0.002 cm H2O/L X min-1). The clinical study was conducted on ten adult anesthetized patients breathing through the bacterial filter and ten controls. The loss of body temperature was 0.2 degrees C when the filter was used and 1.5 degrees C when the filter was not used. Arterial blood gas tensions were within normal limits when the bacterial filter was used as a humidifier.

Effect of atropine on alveolar gas mixing in man.

1. Atropine is known to diminish bronchomotor tone. In order to investigate the acute effect of atropine on respiration and alveolar gas mixing, a dose of 2.4 mg was given intravenously. 2. Ten normal male volunteers were each studied three times with a nitrogen washout method, once before administration of atropine and then 20 min and 60 min thereafter. 3. After the administration of atropine there was a reduction in tidal volume, a slight increase in frequency of respiration and an increase in series dead space. The tidal mixing volume showed a fall of 25%. In spite of the reduced alveolar dead space the effective mixing volume fell by 29%. Multi-breath alveolar mixing efficiency fell by 3.5%. 4. Multi-breath alveolar mixing efficiency was found to be less with smaller tidal mixing volumes, a fall of 518 ml in the latter causing a reduction of 17.2% in mixing efficiency. 5. A reduction of 100 ml in tidal volume in normal subjects was associated with a decrease of 6.9% in alveolar mixing efficiency. In the subjects receiving atropine tidal volume reduced by 96 ml, but the observed fall in alveolar mixing efficiency was only 3.5%, This suggests an improvement in alveolar mixing of 3.4% due to the administration of atropine. Despite this small improvement, the mixing efficiency is still only 66%. The residual inefficiency of 34% cannot therefore be explained on the basis of bronchomotor tone.

Effects of PEEP and tolazoline infusion on respiratory and inert gas exchange in experimental meconium aspiration

Meconium aspiration syndrome often produces respiratory failure in the neonate. We utilized the multiple inert gas elimination technique to study the effects on respiratory and inert gas exchange of the application of positive end expiratory pressure or continuous infusion of tolazoline HCl. The application of PEEP, with the optimal level of PEEP defined for each animal, produced a decrease in AaDO2 and pulmonary shunt, without an increase in blood flow to low VA/Q areas, or an increase in dead space. Tolazoline infusion, at 2 mg/kg/hour, had no apparent effect on AaDO2 or shunt, or magnitude of low VA/Q regions. Tolazoline therapy was associated with an increase in heart rate and a decrease in systemic blood pressure. We conclude that immediate postaspiration application of PEEP, but not of tolazoline, will diminish pulmonary shunt without creating low VA/Q areas, and therefore will improve gas exchange in MAS.

Management of Contaminated Bone Grafts

Using an experimental animal model, the infection rate of contaminated bone grafts after irrigation with either normal saline, povidone-iodine, or a cefazolin solution was evaluated. Mechanical cleansing appears to be the important factor in preventing infection in these grafts, since all the solutions showed almost equal effectiveness. As the amount of bulk and dead space increases, particularly in Pseudomonas infections, povidone-iodine might be slightly superior, although this difference was not statistically significant.

Ventilation during prolonged hypercapnia in the rat.

Awake rats, with chronically implanted arterial catheters and abdominal thermistors, were continuously exposed to 5 or 7% CO2 in air in an environmental chamber for up to 3 wk. To obtain measurements, rats were transferred to a body plethysmograph flushed with the same CO2 mixture, and, after stabilization, O2 consumption (Vo2), ventilation (VE), and arterial blood gases (ABG) were determined. After 2-h exposure, VE, tidal volume/inspiratory time (VT/TI), and VO2 were significantly increased. Thereafter, VE and VT/TI fell gradually with time, the largest decrease occurring within the 1st day of exposure. The increase in VO2 was maintained up to 3 days and then declined. ABG revealed extensive metabolic compensation for respiratory acidosis within 3-7 days. delta(VT/TI) correlated well with delta VE and delta [HCO3]a (P less than 0.05). It is likely that the gradual return toward normal pHa reduces ventilatory drive (VT/TI), which in turn lowers VE. Estimated alveolar ventilation did not decrease consistently with time in parallel with VE, suggesting that the early ventilatory overshoot might also be due to an increase in dead space.

Anatomical dead space and airway resistance after glycopyrrolate or atropine premedication.

The effects of atropine and glycopyrrolate on anatomical dead space, one and three second forced expiratory volume, maximal expiratory flow rate, and total forced expiratory volume were determined in ten healthy volunteers. Using Fowler's single breath nitrogen analyzing technique, atropine was found to increase dead space by 19.2 per cent at one hour, declining to 11.02 per cent at four hours. Glycopyrrolate increased dead space by 21.57 per cent at one hour, 29.28 per cent at two hours, and 26.65 per cent at four hours. When compared to the effects of saline control injection, the dead space increases are significant. The difference between glycopyrrolate and atropine is significant only at four hours. Increases in maximal expiratory flow rate induced by atropine and glycopyrrolate were significant at one-half hour, while atropine alone induced a significant increase in one second forced expiratory volume. Three second forced expiratory volume and total forced expiratory volume were not significantly altered.

Blood Carbon Dioxide Tension Changes During Hysteroscopy

During hysteroscopy the uterus may be distended with carbon dioxide (CO2), nitrous oxide (N2O), or Hyskon (a high molecular weight dextran). An initial study in 27 patients (group 1) using arterialized venous blood samples demonstrated rises in carbon dioxide tension (PCO2) when N2O was insufflated by using a laparoscopy insufflating device--a constant-pressure, variable-volume gas source. Cardiovascular collapse occurred in one patient in this group, most probably as a result of macropulmonary emboli of N2O. The rise in PCO2 is accounted for by an increase in physiologic dead space. In another 24 patients (group 2) the gaseous media were introduced by using a constant-volume, variable-pressure gas source; this resulted in minimal changes in arterial PCO2. The choice of whether a gaseous or liquid distending medium is used for hysteroscopy is governed by the state of the endometrium. If a gaseous medium is indicated, then CO2 is preferable to N2O and should be introduced with a constant-volume, variable-pressure gas source.

Gas exchange abnormalities produced by venous gas emboli

Bubbles of either He, N 2 or SF 6 were infused intravenously into anesthetized dogs at a rate of 0.2 ml/kg/min. Alterations in pulmonary gas exchange were quantitated by the inert gas elimination method during control, steady state infusion and resolution phases. The hypoxemia produced was predominantly due to regions of low V̇ a/Q̇ rather than pure shunt, and the increase in physiological dead space was due to the addition of high V̇ a/Q̇ regions than ‘pure’ dead space. The V̇ a/Q̇ distribution returned to normal within 30 minutes of stopping the He or N 2 bubbles, but remained abnormal for longer periods with SF 6 bubbles. The net elimination of insoluble gases (such as He or N 2) was only slightly impaired by bubble emboli, provided the cardiac output remained constant. Early pulmonary edema from bubble embolization was documented by increased wet weight/dry weight ratio, but the increased lung water was not apparent on histological examination. This form of pulmonary embolus is unique in that there is a constant fraction of the vasculature blocked although any given region with embolus is undergoing continuous resorption of the bubble. This produced a partial obstruction of the affected gas exchange units which manifests as regions of high V̇ a/Q̇ rather than pure dead space.

HYPERTONIC MANNITOL IN THE THERAPY OF THE ACUTE RESPIRATORY DISTRESS SYNDROME

Increased pulmonary artery pressure, an increase in pulmonary vascular resistance and an increase in physiologic dead space are consistent findings in patients with post-traumatic respiratory distress. Since mannitol has been shown to decrease renal vascular resistance following trauma, the effect of a bolus injection of 100 ml of 25% solution of this drug on pulmonary hemodynamics and physiologic dead space was investigated in 11 patients who had suffered multiple trauma. Five minutes after the injection, pulmonary vascular resistance fell (p less than .01), cardiac index increased (p less than .001) and physiologic dead space decreased (p less than .05). In contrast, the administration of 40 mg of furosemide produced no significant change in any of these parameters. Mannitol rapidly equilibrates in the extracellular space and exerts an osmotic effect across cell membranes. We postulate that the beneficial response to mannitol on the pulmonary vascular resistance and the improved perfusion of ventilated regions of the lung is due to a reduction in cell swelling and is not explainable by its diuretic effect. Improvement in the distribution of perfusion of pulmonary blood flow by mannitol may be a useful aid in the treatment of the post-traumatic form of the respiratory distress syndrome.

Effects of asphyxia on renal function in the newborn piglet.

This investigation was undertaken to determine the nature of acute alterations in renal function following the production of hypoxemia, hypercarbia, and acidosis in newborn piglets 6-96 hr of age. After completion of the surgical procedure piglets were allowed to recover from the effects of anesthesia. When respiratory dead space was increased arterial oxygen tension decreased whereas arterial carbon dioxide tension and hydrogen ion concentration increased. There was little change in glomerular filtration rate. Total renal blood flow decreased and renal vascular resistance increased significantly (504 +/- 78 mm Hg/liter/mm/m2 to 1422 +/- 504). There was no change in distribution of intrarenal blood flow. Sodium excretion and urinary flow rate demonstrated significant parallel increases following the increase in dead space. Plasma renin concentration increased from 67 to 110 ng/ml.

Lung function in alpha-1-antitrypsin deficient sisters

Two sisters were found to be homozygous for alpha-1-antitrypsin deficiency. One was disabled by breathlessness and had advanced clinical and radiological emphysema which was confirmed on lung function testing. The other, of similar age and smoking history, was symptom-free with a normal chest radiograph. She had a slightly increased airways resistance, a reduced gas transfer, a bilaterally reduced apex-base perfusion gradient and a small but generalized increase in physiological dead space in all zones. The minor pulmonary and vascular abnormalities present in the younger sibling suggest that we are witnessing early changes in the evolution of the panacinar emphysema characteristic of alpha-1-antitrypsin deficiency. The reason for the different rates of progress of the disease in these two sisters is not understood.

Hypertonic Mannitol in the Therapy of the Acute Respiratory Distress Syndrome

Increased pulmonary artery pressure, an increase in pulmonary vascular resistance and an increase in physiologic dead space are consistent findings in patients with post-traumatic respiratory distress. Since mannitol has been shown to decrease renal vascular resistance following trauma, the effect of a bolus injection of 100 ml of 25% solution of this drug on pulmonary hemodynamics and physiologic dead space was investigated in 11 patients who had suffered multiple trauma. Five minutes after the injection, pulmonary vascular resistance fell (p less than .01), cardiac index increased (p less than .001) and physiologic dead space decreased (p less than .05). In contrast, the administration of 40 mg of furosemide produced no significant change in any of these parameters. Mannitol rapidly equilibrates in the extracellular space and exerts an osmotic effect across cell membranes. We postulate that the beneficial response to mannitol on the pulmonary vascular resistance and the improved perfusion of ventilated regions of the lung is due to a reduction in cell swelling and is not explainable by its diuretic effect. Improvement in the distribution of perfusion of pulmonary blood flow by mannitol may be a useful aid in the treatment of the post-traumatic form of the respiratory distress syndrome.

Effects of temperature on respiration and acid-base balance in a monitor lizard

Ventilation, gas exchange, blood gas tensions and arterial pH were measured simultaneously in monitor lizards,Varanus exanthematicus. In contrast to previously studied poikilotherms, the arterial pH is independent of body temperature within the normally encountered temperature range (Fig. 1). This exception to the relative alkalinity concept (Rahn, 1966) is correlated with the finding thatV. exanthematicus maintains a constant ratio of ventilation to oxygen uptake (and CO2 production) at different temperatures (Fig. 3). The increase in arterial $$P_{{\text{CO}}_{\text{2}} }$$ (Fig. 1) is related to an increase in physiological dead space; i.e., alveolar ventilation increases less with temperature than total ventilation (Fig. 4). This may result from the increased frequency of breathing which results in a reduced breath holding time (Fig. 2). Varanid lizards have a higher oxygen requirement than other reptiles. This is reflected in the control of ventilation, the specialized lung morphology, the high arterial saturation due to low intracardiac shunting, pH regulation and other mammal-like features ofVaranus.