Decrease In Arterial PO2 Research Articles

Laser smoke effect on the bronchial system.

The photoresection of endobronchial tumors produces smoke which is partly inhaled by the patient as well as the surgical staff. In an animal study we investigated whether a single exposure or repetitive exposures to smoke might have harmful side effects on the airways. Eleven sheep were exposed to smoke produced by laser-vaporizing (6,500 J) sections of bronchial tissue (1 cm3) in a Plexiglas chamber. The smoke analysis revealed 0.92 mg/liter particles with a mean particle size of 0.54 micron. Carbon monoxide content was estimated as 0.04%. We measured the effects of one or three separate ten-minute exposures on airway resistance, gas exchange, and mucociliary clearance rate in the trachea. We found that the smoke inhalation resulted in a decrease of arterial PO2 with relatively little change in airway mechanics. Tracheal mucus velocity, a marker of lung mucociliary clearance, was significantly depressed in a dose-dependent manner with increasing smoke exposures. Results of bronchoalveolar lavages performed before and one day after the exposure showed that the smoke inhalation induced a severe inflammation with dramatic increases of inflammatory cells. The total number of cells per milliliter lavage return increased from 3.2 million to 25 million; percent neutrophils increased from 2.3 to 45.6% and percent macrophages decreased from 86 to 41%. These findings indicate that the side effects of smoke inhalation during intrabronchial laser surgery should not be neglected. The impairment of the defense mechanism of the lung combined with the inflammation as well as hypoxia might be fatal in compromised patients. Effective smoke removal devices should be developed to protect the patient as well as the surgeon.

Influences of exercise-stress and adrenaline upon intra- and extracellular acid-base status, electrolyte composition and respiratory properties of blood in tench (Tinca tinca) at different seasons.

Exercise-stress in tench resulted in severe acidosis in both the red cells and the extracellular fluid in vivo. These coincident pH decreases conformed to the in vitro pHi-pHe relationship for tench blood in the oxygenated state. The extracellular acidosis was primarily respiratory in winter and metabolic in spring and summer. This was due to more effective buffering of metabolic protons in winter by an elevation in [HCO3-] levels, rather than to differences in the lactic- and carbonic acid loads. A good correspondence was found between buffered metabolic protons and increases in [lactate]. There was no evidence for beta-adrenergic red cell swelling and associated red cell pH changes in tench both after exercise and adrenaline infusion. Arterial O2 transport was, however, improved in exercise by pronounced increases in PO2. This increase was not of adrenergic origin, as adrenaline alone caused a decrease in arterial PO2. Large increases in plasma potassium concentration and small elevations of chloride and calcium levels occurred in exercise. Hematocrit and blood [Hb] also increased, probably due to an adrenergic release of erythrocytes from the spleen, but these increases were small and appeared unimportant for blood O2 transport. Seasonal differences were found in exercise-induced changes in [lactate], in the magnitude of electrolyte and PO2 changes, as well as in resting values for pHe, pHi, [HCO3-], [Cl-] and [Ca++]. The origin and importance of these are discussed.

Time course of muscular blood metabolites during forearm rhythmic exercise in hypoxia.

O2 concentration, PO2, PCO2, pH, osmolarity, lactate (LA), and hemoglobin (Hb) concentrations in deep forearm venous blood were repeatedly measured during submaximal exercise of forearm muscles. Concentrations of arterial blood gases were determined at rest and during exercise. Experiments were conducted under normoxia and hypobaric hypoxia (PB = 465 Torr). In arterial blood, data obtained during exercise were the same as those obtained during rest under either normoxia or hypoxia. In venous muscular blood, PO2 and O2 concentration were lower at rest and during exercise in hypoxia. The muscular arteriovenous O2 difference during exercise in hypoxia was increased by no more than 10% compared with normoxia, which implied that muscular blood flow during exercise also increased by the same percentage, if we assume that exercise O2 consumption was not affected by hypoxia. Despite increased [LA], the magnitude of changes in PCO2 and pH in hypoxia were smaller than in normoxia during exercise and recovery; this finding is probably due to the increased blood buffer value induced by the greater amount of reduced Hb in hypoxia. Hence all the changes occurring in hypoxia showed that local metabolism was less affected than we expected from the decrease in arterial PO2. The rise in [Hb] that occurred during exercise was lower in hypoxia. Possible underlying mechanisms of the [Hb] rise during exercise are discussed.

Diagnostic and Prognostic Significance of Hemodynamic and Respiratory Parameters in Venous Air Embolism

MULLER, H.; BRAHLER, A.; GERLACH, I.; GERLACH, H.; BECKER, W.; HEMPELMANN, G. Author Information

The role of lavage in preventing hemodynamic and blood-gas changes during cemented arthroplasty.

An experimental model was designed to investigate the role of meticulous intramedullary lavage in the prevention of the blood-gas and hemodynamic changes that have been documented to occur during cemented arthroplasty. Twenty-one adult mongrel dogs were divided into two groups. One group had the medullary canal thoroughly lavaged prior to insertion of the cement and prosthesis and the other group had no lavage. The results clearly showed that careful lavage can eliminate the significant decreases in arterial PO2 and increases in intrapulmonary shunt fraction and pulmonary artery pressure that were evident in the group that did not have lavage. Femoral medullary reaming was investigated and was shown not to compromise the dogs' cardiopulmonary status. During cemented arthroplasty, thorough lavage of a plugged medullary canal prior to insertion of the cement and prosthesis is a highly effective prophylactic measure in the elimination of gas-exchange and hemodynamic complications.

Gas exchange after pulmonary fat embolism in dogs

Gas exchange following moderately severe experimental pulmonary fat embolism was studied in nine dogs. A new method designed to describe the distribution of ventilation-perfusion ratios in the lung was applied before and after intravenous injection of homologous neutral fat. The dose of fat (0.75 ml/kg) was low enough to produce a small but significant decrease in arterial PO2 (mean change of 10 mm Hg) in the first 15 minutes after the embolism but high enough to result in the death of two of the four dogs that were allowed to survive the initial postembolism period. Pulmonary artery pressure and pulmonary vascular resistance both rose significantly within 5 minutes of the fat injection and remained elevated for the 2 hour experimental period. Immediately after the embolism there was an increase in the percentage of the total ventilation going to areas of the lung with ventilation-perfusion ratios between 10 and 100, which usually appeared as a discrete mode in the ventilation distribution. This mismatching of ventilation and perfusion partially resolved within 2 hours after the embolism, as indicated by the gradual disappearance of this population of gas exchanging units with relatively decreased blood flow. At no time within 2 hours after the embolism was there a significant increase in shunt or in ventilation to totally unperfused lung. The gas exchange pattern in the two dogs that subsequently died was indistinguishable from that of the other seven in the immediate postembolism period.

The Effect of Arterial-Blood PO2, PCO2, and pH on Diving Bradycardia in the Bullfrog Rana catesbeiana

Bullfrogs were submerged for 25 min in water at 25 C saturated with either O2, air, or N2. The heart rates of all three groups were not significantly different prior to submergence. The heart rate of the O2 group did not change during submergence while the air and N2 groups experienced significant bradycardia. In paired comparisons, only the O2 and N2 groups exhibited significantly different degrees of bradycardia. The extent of bradycardia, therefore, was correlated inversely with the O2 saturation of the water. Upon emergence, heart rates were elevated above the initial rates in all three groups. All three groups showed predive arterial PO2 (PaO2), PCO2 (PaCO2), and pH values that were not significantly different. All three groups underwent significant changes in all three blood parameters during submergence. In paired comparisons, the O2 and air groups and the O2 and N2 groups showed PaO2 values during submergence that were different and which related directly to levels of O2 in the water. No differences were observed among the three groups in either PaCO2 or arterial pH levels during the dive period. Bullfrogs breathing N2 exhibited an increase in heart rate, but PaO2 levels were not different from the group submerged in air at middive. It is concluded that a decrease in arterial PO2 coupled with inhibition of lung ventilation is correlated with development of diving bradycardia in the bullfrog.

Ventilation-perfusion inequality in asymptomatic asthma.

Ventilation-perfusion (Va/Q) inequality was measured by a multiple inert gas elimination method in 6 asymptomatic patients with asthma and in a seventh patient during a severe asthmatic episode. Measurements were made before and at 5-min intervals after administration of aerosolized isoproterenol. All patients had some residual airway obstruction as measured during forced expirations. All except one patient had clearly bimodal distributions of Va/Q ratios during all phases of the study, as confirmed by an extensive exploration of distributions compatible with each set of inert gas data. One mode lay within the normal range of Va/Q, but the other, containing 19.8 per cent of the cardiac output on the average, was centered on a Va/Q ratio of only 0.07. There was essentially no shunt. Five min after the administration of isoproterenol, the blood flow to the low Va/Q mode approximately doubled, accounting for the observed decrease in arterial PO2. Breathing 100 per cent O2 had little effect on the distribution. The presence of a bimodal distribution of Va/Q ratios without shunt suggests that collateral ventilation may be an important mechanism determining the distribution of Va/Q ratios and preventing the development of shunts. This study also showed that in some asymptomatic asthmatic patients, as many as one half of the lung units may lie behind completely closed airways and have very low but finite Va/Q ratios as a result of collateral ventilation.

1204 DECREASED ARTERIAL OXYGEN TENSION ACCOMPANYING ASYNCHRONOUS CHEST WALL MOVEMENT IN ACTIVE SLEEP

In the neonate a decrease in lung volume accompanies the asynchronous(paradoxical)chest wall movement seen during active sleep. We sought to determine whether this would result in a decrease in arterial PO2 in view of the higher incidence of apnea in active as compared to quiet sleep. 10 healthy term infants were studied at a mean age of 39 hours(range 15-56 hrs) during both active (A.S.)and quiet sleep(Q.S.).We monitored transcutaneous PO2 continuously and recorded the timing and synchrony of chest wall movement during the respiratory cycle by means of mercury strain gauges placed over the upper chest wall and abdomen.Sleep state was determined from observation of body movement, respiratory variation,and electro-oculograms. Strikingly in all 10 infants PO2 was consistently lower and more variable during A.S.(see table). During A.S. the upper chest wall moved asynchronously with respect to the abdomen 80% of the time.This never occurred during Q.S. These findings reveal a marked instability of arterial PO2 accompanying asynchronous movement of the upper chest wall in the healthy term neonate during A.S. The lower and more variable PO2 may be due to regional ventilation/perfusion inequalities. Apneic episodes (>5 sec)occurred in 5 of the infants,only during A.S.These findings may have important implications in our understanding of the higher incidence of apnea during A.S. in both preterm and term infants.

Effects of sublingual nitroglycerin on resting pulmonary gas exchange and hemodynamics in man.

Simultaneous hemodynamic, ventilation and blood gas measurements were performed in 19 males during cardiac catheterization for evaluation of chest pain syndrome before and 3 to 5 min after 0.4 mg sublingual nitroglycerin. Pulmonary arterial pressures and total pulmonary vascular resistance fell (P less than 0.001 for both), and mean systemic arterial pressure decreased (P less than 0.05). However, peripheral vascular resistance, cardiac output, and mixed venous PO2 did not change. Total and tidal ventilation, PCO2, pH, and base excess remained unchanged. However, the arterial PO2 decreased from a mean of 80 +/- 3 (SEM) to 72 +/- 2 mm Hg (P less than 0.001) and mean venous admixture increased from 8.8 +/- 1% to 12.6 +/- 1.5% (P less than 0.001). The alveolar arterial PO2 difference increased (P less than 0.001) and the dead space tidal volume ratio rose (P less than 0.05). We conclude that the decrease in arterial PO2 following sublingual nitroglycerin is caused by redistribution of pulmonary blood flow with imbalance in ventilation-perfusion relationships or shunting.

Introductory remarks: oxygen linked response of carotid chemoreceptors.

Recognition of oxygen in the animal organism is a fundamental phenomenon in biology. There are various examples of physiologic responses to small changes in oxygen pressure in the range of normal PO2 at sea level. We have already had glimpses of these chemoreception functions in the previous sessions of the symposium. In mammals the outstanding examples are provided by the microscopic organs along the aortic and carotid arteries known as peripheral arterial chemoreceptors. Their oxygen reception function is well seen in the stimulation of breathing due to hypoxia. It is well known that a decrease in arterial PO2 results in an increase in breathing if the nervous connections of the receptors with central nervous system are intact. This is shown in figure 1. After denervation of these receptors a similar intensity of hypoxia results in decreases of ventilation. Thus decreases in alveolar and arterial PO2 show simultaneous dual effects on ventilation: the net effect in intact animal being stimulation of ventilation. Regardless of the mechanisms involved these results clearly demonstrate oxygen sensitive property in more than one system.

Blood Parameters in Leucocytozoon smithi Infected Poults Fed Clopidol

Poults naturally infected with L. smithi demonstrated a significant (P < 0.01) decrease in arterial PO2 (mm. Hg) during the second and third weeks after exposure to black fly bites. Poults fed Clopidol (0.0125%) during the exposure period and subsequent experimental periods showed very little parasitemia and no significant reduction in arterial PO2.

THE EFFECT OF ANAESTHETIC AGENTS ON PRIMARY CORTICAL EVOKED RESPONSES

(1) The effect of increasing dosage of ethyl carbamate (urethane), trichloroethylene and pentobarbitone anaesthesia is to decrease die amplitude, increase the latency and produce a more stereotyped response, recorded from the short latency receiving area of the cerebral cortex to electrical or mechanical limb stimulation in both chronic and acute animals. (2) The extent of the short latency receiving area (defined as that from which responses with the shortest latency +12.5% of this latency could be obtained) increased in extent from the lightly to the deeply anaesthetized state. (3) The only consistent non-nervous change produced by these anaesthetic agents was a decrease in arterial Po2 as the anaesthetic depth was increased. (4) That cerebral hypoxia was not the cause of the changes seen in the evoked response was shown by the fact that the effect of the anaesthetic agents was the same in animals respiring 95% O2, 5% CO2 or in animals artificially respired. (5) It is concluded that the anaesthetic agents exert their effects on a central nervous structure. (6) Animals with cerebral oedema appear to be anaesthetic resistant. No change in the evoked cortical response was seen in any animal which showed the slightest signs of cerebral oedema.

Effect of age on development of cor pulmonale in nonhuman primates following pyrrolizidine alkaloid intoxication

Two groups of Macaca arctoides monkeys, 4 wk and 15 mo of age, were given four injections of the pyrrolizidine alkaloid, monocrotaline, over a 6-mo period. During the terminal month or two of life, the younger monkeys experienced an increase in hemoglobin, hematocrit, red cell mass, and arterial pCO2, and a decrease in arterial pO2 and pH. Increases in right heart and pulmonary artery pressures were suggestive of changes in the pulmonary vasculature. At necropsy, there was bilateral myocardial hypertrophy and right heart dilatation. The lungs were firm and failed to collapse readily when exposed to atmospheric pressure. Microscopically, there was a decided thickening of the pulmonary arterial walls and reduction in, or obliteration of, the luminal dimensions of the vessels. The right ventricular myocardium was edematous, the endocardium fibrotic, and the arterial vessels disrupted. In contrast to the young monkeys, the older animals developed ascites, distended abdominal veins and an increase in portal venous pressure. The livers were firm, small and granular on gross inspection. There was widespread venous occlusion of the hepatic venous system from the centrilobular to the large hepatic veins. Dilated, blood-filled sinuses were obvious in areas closely associated with the occluded vessels. This variation in response of infant and older monkeys is attributed to the difference in the hepatic microsomal enzyme activity and the metabolites produced from the biotransformation of monocrotaline.

PHYSIOLOGY FOR PEDIATRICIANS ASSESSMENT OF HYPOXIA IN THE NEWBORN SUGGESTIONS FOR A PRACTICAL APPROACH

Routine measurements of arterial Po2, Pco2, oxygen saturation of hemoglobin, P50, hemoglobin content allow a more accurate approach in the treatment of hypoxia in the neonate. Based upon these routinely available determinations and upon the clinical evaluation of the peripheral circulation, four types of hypoxia can be distinguished: (1) Hypoxia with hypoxemia due to a decrease in arterial Po2. (2) Hypoxia with hypoxemia due to a decrease in blood oxygen content without decrease in arterial Po2. (3) Hypoxia with normoxemia due to a decrease in peripheral blood flow. (4) Hypoxia with normoxemia due to an increase in the hemoglobin-oxygen affinity. Hyaline membrane disease represents a possible combination of these four different mechanisms.

Physiological alterations in increased pulmonary blood flow with and without pulmonary hypertension.

Alterations in pulmonary function and in hemodynamics were studied in dogs with high pulmonary blood flow resulting from systemic pulmonary artery shunts. In order to facilitate elevation in pulmonary artery pressure, the vascular bed was reduced in some cases by obstructing branches of the pulmonary artery with Teflon clips or by lobectomy. Results in 30 control dogs and in 30 animals that survived 5–36 months (average 16) following creation of shunts indicated that pulmonary function was not significantly altered by increased pulmonary blood flow until pulmonary artery hypertension developed. When systolic pulmonary artery pressure exceeded 40 mm Hg, there was a decrease in arterial Po2, an increase in venous admixture percentage of cardiac output, and an increase in the A-a O2 difference during three levels of O2 breathing, indicating both abnormal venous admixture and abnormal diffusion. Possible explanations for these findings are presented. Evidence in one dog suggests that these alterations are reversible. Submitted on August 10, 1960