Arteriovenous Oxygen Saturation Difference Research Articles

Acute hemodynamic effects of adjustable atrial septal defect closure in the lateral tunnel Fontan procedure

Objectives. This study evaluated the acute hemodynamic changes with atrial septal defect closure in thek postoperative period in patients undergoing the Fontan procedure.Background. The adjustable atrial septal defect is a modification of the Fontan procedure designed to improve cardiac output and reduce systemic venous hypertension during the postoperative period. Limited information is available on the effects of interatrial shunting on the physiology of direct cavopulmonary connection.Methods. In 11 patients (aged 9 months to 14.5 years), the atrial septal defect was closed 8 h to 4.6 days (mean 1.7 days) postoperatively. Indications for closure included mean right atrial pressure <15 mm Hg or arterial oxygen saturation <80%, or both.Results. Data presented are mean values ±1 SD. Mean right atrial pressure was 13.4 ± 3.0 mm Hg on admission to the intensive care unit, 10.0 ± 2.0 mm Hg (p = 0.02) immediately before closure and 11.4 ± 2.8 mm Hg (p = 0.02) after closure. There was a significant decrease in cardiac output, as calculated from arteriovenous oxygen saturation difference (26 ± 9%, p = 0.003), Doppler aortic flow (19 ± 9%, p = 0.0002) and ventricular volumes by two-dimensional echocardiography (20 ± 8%, p = 0.0001). Arterial oxygen saturation increased from 82 ± 5% to 94 ± 4% (p = 0.0001), and arteriovenous oxygen saturation difference increased from 25 ± 8% to 33 ± 9% (p = 0.0001). Systemic oxygen delivery decreased from 727 ± 354 to 655 ± 325 ml/min per m2(p = 0.02). One patient required reopening of the atrial septal defect.Conclusions. These data demonstrate that a controlled right to left atrial shunt improves cardiac output and systemic oxygen delivery and facilitates the postoperative management of patients after the Fontan procedure. Atrial septal defect closure increases systemic saturation to normal values and prevents potential systemic embolization but significantly decreases oxygen delivery and might limit exercise tolerance.

Periventricular white matter lucency and cerebral blood flow autoregulation in hypertensive patients.

The goal of this study was to elucidate the association between the development of periventricular white matter lucency and autoregulation of cerebral blood flow in hypertensive patients through the arteriovenous oxygen saturation difference method. We studied 51 hypertensive patients who had previously suffered from minor strokes (lacunar infarction, 43; deep basal minor hemorrhage, 8). Patients were divided into three groups based on the findings of periventricular white matter lucency. We measured the absolute value of resting cerebral blood flow using the argon inhalation method, and stepwise reduction of blood pressure was obtained with patients on a tilting table. Intracerebral venous blood sampling was accomplished by direct cannulation into the jugular vein up to the jugular bulb. We calculated several cerebral circulatory parameters, such as cerebrovascular resistance and cerebral oxygen consumption, and also delineated individual autoregulation curves. Cerebrovascular resistance was significantly greater in patients with severe periventricular white matter lucency than in patients without it (P < .05). Impaired autoregulation was also significantly more prevalent in patients with more severe periventricular lesions (P < .05). Multiple regression analysis revealed that the impaired autoregulation was significant and an independent determinant of the severity of such periventricular lesions (R = .34, P < .05). In conclusion, our findings indicated that hypertensive patients with severe periventricular white matter lucency were more likely to have impaired autoregulation of cerebral blood flow and suggest that stricter blood pressure control is required in such patients to prevent deterioration of the cerebral microcirculation.

Effects of NG‐nitro‐l‐arginine methyl ester on the cardiovascular system of the anaesthetized rabbit and on the cardiovascular response to thyrotropin‐releasing hormone

1. The effects of 300 mg kg-1 of the nitric oxide (NO) inhibitor NG-nitro-L-arginine methyl ester (L-NAME) on the regional blood flow, on the flow response to 1 mg kg-1 of thyrotropin-releasing hormone (TRH) and on cerebral blood flow autoregulation were studied in urethane anesthetized rabbits subjected to unilateral sectioning of the cervical sympathetic claim. The blood flow measurements were performed by the tracer microspheres method. 2. The cerebral arteriovenous difference in oxygen saturation (CAVOD) was measured before and after the administration of L-NAME and TRH in order to ascertain whether the effects on cerebral blood flow that were observed were secondary to changes in cerebral metabolism. 3. L-NAME caused a significant decrease in blood flow in several cerebral regions; CBFtot decreased to 72 +/- 4% of control (P < 0.001). An increase in blood pressure and a concurrent decrease in heart rate and cardiac output were noted. 4. In the eye, L-NAME caused a reduction in uveal blood flow which was more pronounced on the sympathetically intact side; in the retina the blood flow decreased to 50% of control on both sides. 5. The administration of TRH in animals pretreated with L-NAME caused a significant increase in blood pressure and cerebral blood flow. 6. In L-NAME-treated animals the CBF was not affected when the mean arterial blood pressure was increased by ligation of the abdominal aorta. 7. The CAVOD increased from 56.0 +/- 5.2 to 73.6 +/- 3.5%, 20 min after the administration of L-NAME. In animals given 1 mg kg-1 TRH after L-NAME the CAVOD decreased to 54.6 +/- 4.6%, 5 min after the injection of TRH.8. The results of the present study indicate that endogenous NO is involved in the regulation of regional blood flow and blood pressure in the anaesthetized rabbit. The reduction in cerebral blood flow that was caused by L-NAME was not due to a reduction in cerebral metabolism. An interaction between the NO synthesis/release/effect and the sympathetic nervous system was found in the uvea. There was no evidence for a major involvement of NO in the cardiovascular responses to TRH and autoregulation of cerebral blood flow was not abolished by L-NAME.

Forecasting of the Course and Outcome of Shock in Severe Mechanical Traumas

The ability to forecast the course and outcome of severe mechanical trauma would aid clinicians in making decisions concerning the treatment of patients. Multifactorial regression models, developed from data obtained from 933 patients with polytrauma and shock, have a high predictive value. A two-part data sheet was developed to give a rating system that predicts the duration of shock in patients that survive and the life span in patients that eventually die. Factors considered in developing the rating system include systemic hemodynamics, hematocrit number, blood density, arteriovenous difference in oxygen saturation, and rectocutaneous temperature gradient, among others.

Frequently repeated fick cardiac output measurements during anesthesia

A computer-based system was developed for monitoring cardiac output using the Fick principle during general anesthesia. The variables of the oxygen-consumption Fick equation were measured using the following system: oxygen uptake by an originally developed respiratory gas monitoring system, arteriovenous oxygen saturation difference by pulse and fiberoptic oximetry, and hemoglobin concentration by an in vitro oximeter. Fick cardiac output and systemic vascular resistance were calculated every 30 seconds. Fick cardiac output was compared with thermodilution cardiac output in 11 anesthetized patients. A total of 208 corresponding cardiac output measurements showed a range of 2 to 9 L.min-1. The correlation coefficient between the thermodilution and Fick cardiac outputs was 0.961, with a regression equation of Fick cardiac output = 1.058 thermodilution cardiac output - 0.359. The difference between the thermodilution and Fick cardiac outputs was 0.103 +/- 0.395. The Fick cardiac output was significantly lower than the thermodilution cardiac output, especially in the low flow range. We demonstrated that this new monitoring system was clinically feasible and sufficiently accurate, under the limited circumstances of our study. The integration of routinely used equipment has made possible a frequently repeatable method for estimating cardiac output in patients.

TRH‐Induced blood flow and mean arterial pressure changes in the rabbit are not dependent on the anaesthetic used

1. The effects of thyrotropin releasing hormone (TRH) on regional cerebral blood flow were studied in rabbits anaesthetized with pentobarbitone or ketamine. The blood flow was determined with the labelled microsphere method before and after the i.v. administration of either 50 micrograms kg-1 or 2 mg kg-1 TRH. 2. In order to measure the cerebral O2 consumption the arteriovenous difference in oxygen saturation in the brain (CAVOD) was measured before and after the administration of 2 mg kg-1 TRH. 3. In animals under pentobarbitone anaesthesia 50 micrograms kg-1 TRH elicited an increase in mean arterial blood pressure (MAP) of about 1 kPa and 2 mg kg-1 TRH elevated the MAP by about 2 kPa. With ketamine as the anaesthetic the corresponding values were 0.5 kPa and 7 kPa, respectively. TRH induced significant vasoconstriction in several peripheral tissues. 4. The total cerebral blood flow (CBFtot) increased from 54 +/- 4 to 78 +/- 5 g min-1 100 g-1 after the administration of 50 micrograms kg-1 TRH in pentobarbitone-anaesthetized animals. An even greater effect was elicited by 2 mg kg-1 TRH, from 48 +/- 6 to 113 +/- 19 g min-1 100 g-1. In ketamine-anaesthetized rabbits, 50 micrograms kg-1 TRH tended to enhance the CBFtot and 2 mg kg-1 increased it from 71 +/- 6 to 141 +/- 19 g min-1 100 g-1. 5. In animals anaesthetized with pentobarbitone, the CAVOD decreased from 47.3 +/- 1.7% to 35.1 +/- 2.2% at 3 min after TRH delivery, and then gradually increased to the control level. In animals under ketamine anaesthesia the CAVOD decreased from 63.3 + 2.0% to 45.2 + 7.4% after the administration of 2 mg kg'- TRH. 6. It is concluded that TRH elicits cerebral vasodilatation in excess of that required by the change in cerebral metabolism which may have taken place. The pattern of responses was similar to that produced in rabbits under urethane anaesthesia.

A pitfall in the measurement of arterial blood pressure in the ischaemic limb during elevation

In order to evaluate if elevation of the ischaemic limb above heart level is an alternative to the conventionally applied method with external counterpressure for estimation of skin perfusion pressure, femoral and popliteal artery pressures were measured directly in eight patients with occlusion of the superficial femoral artery. The measurements were done in the horizontal position and during elevation of the calf above heart level. During elevation relative blood flow, measured by arterio-venous oxygen saturation differences, decreased compared with the horizontal position. In contrast the popliteal arterial pressure decreased only by 20% of the value expected from the degree of elevation of the calf above the level of the heart. Thus, it could be calculated that calf vascular resistance increased two- to three-fold on average during elevation. Four patients were reexamined with the venous pressure kept at 10 mmHg during elevation. In these patients, the increase in vascular resistance was significantly less compared with the situation in which venous pressure was 0 mmHg during elevation. The arterial pressure still did not decrease. It is concluded that perfusion pressure in the ischaemic lower extremity cannot be determined non-invasively by elevation of the extremity, probably due to collapse of segments of the vascular bed increasing the vascular resistance considerably.

Effects of supine and lateral positions on cardiac output and intracardiac pressures: an experimental study.

Hemodynamic measurements in human subjects and in experimental animals are generally made in the supine position; not much attention is paid to potential beneficial or harmful effects of right or left lateral positions on cardiac output or other hemodynamic variables. To evaluate the potential influence of such positional changes on cardiac performance, we measured cardiac output and left and right ventricular pressures (with micromanometer catheters) in anesthetized experimental animals (eight dogs and nine pigs) in the supine, right lateral, and left lateral positions. Cardiac output increased from supine to left lateral (mean +/- SD, 2.6 +/- 0.9 to 3.1 +/- 1.0 liters/min; p less than .001) and from supine to right lateral positions (2.6 +/- 0.9 to 3.1 +/- 1.1 liters/min; p less than .001). There was an associated decrease in arteriovenous oxygen saturation difference from supine to left lateral position (31 +/- 8% to 24 +/- 4%; p less than .001) and from supine to right lateral position (32 +/- 9% to 25 +/- 6%; p less than .001). Left ventricular systolic and end-diastolic pressures increased from supine to left lateral (128 +/- 17/9 +/- 2 to 147 +/- 19/16 +/- 4 mm Hg; both p less than .001) and from supine to right lateral positions (128 +/- 19/9 +/- 2 to 141 +/- 16/16 +/- 7 mm Hg; p less than .01 and p less than .001, respectively).(ABSTRACT TRUNCATED AT 250 WORDS)

Thyrotropin-releasing hormone (TRH) causes sympathetic activation and cerebral vasodilation in the rabbit.

The effects of TRH on regional blood flow were studied in rabbits under urethane anesthesia. Four types of experiments were performed with the following results. (1) I.v. injection of 2 mg/kg b.w. TRH in animals with unilateral cervical sympathotomy caused a rise in mean arterial blood pressure from 10.0 +/- 0.5 to 13.3 +/- 0.5 kPa. Total cerebral blood flow, measured with labeled microspheres, increased from 75 +/- 5 to 126 +/- 16 g/min/100 g tissue on the intact side. There was a similar increase on the side with sympathotomy. The greatest increase, about 70%, was observed in cortical gray matter, caudate nucleus and thalamic region. There were marked reductions in blood flows in the spleen, gastric mucosa, skin and skeletal muscle. Mydriasis occurred on the side with an intact sympathetic supply. (2) I.v. infusion of 0.06 mg/kg b.w. per min TRH in animals with unilateral cervical sympathotomy and stabilized blood pressure increased total cerebral blood flow from 84 +/- 10 to 139 +/- 7 g/min/100 g. Blood flows to the masseter muscle, submandibular gland and facial skin but not to the eye or tongue were markedly reduced on the side with an intact sympathetic supply while little or no effect was observed on the side with sympathotomy. (3) Unilateral peripheral stimulation of the sympathetic chain at 1 Hz after bilateral sympathotomy caused a reduction in blood flows in the tongue, masseter muscle, submandibular gland and facial skin in animals with stabilized blood pressure. No potentiation of the stimulation effect was observed during TRH infusion. (4) The arteriovenous difference in oxygen saturation in the brain decreased from 39.1 +/- 2.8 to 26.4 +/- 3.7% after i.v. injection of 2 mg/kg b.w. TRH. The results indicate that TRH caused cerebral vasodilation in excess of that required by possible changes in cerebral metabolism. The vasoconstriction in the head region and the mydriasis was caused mainly by an increase in the activity of the cervical sympathetic nerves.

Some aspects of the oxygen transport in patients with chronic obstructive lung diseases and respiratory insufficiency.

45 patients with chronic obstructive lung disease and chronic respiratory insufficiency were studied. The investigation of these hypoxemic patients concerned the compensating mechanisms in the oxygen transport. The study was performed at rest, during exercise and after 100% oxygen breathing. Normal values for the calculated oxygen consumption (VO2) and cardiac output (Q) were found. Low values of arterial oxygen pressure (PaO2) were compensated by a decrease of the venous oxygen pressure (PvO2) normalizing the arteriovenous oxygen saturation difference (Sa-v). In patients with very low values of PaO2 a further decrease of PvO2 was not established. In these patients, Sa-v became smaller and an increase of the hemoglobin concentration resulted as a compensating mechanism. During exercise, a shift to the right of the oxygen dissociation curve took place as an added compensation.

Oxygen analyses of chicken embryo blood

According to data obtained previously on the blood gas tensions and the oxygen dissociation curve of chicken embryos, the arteriovenous oxygen saturation difference in the allantoic circulation has been conjectured fairly large. In order to confirm this conjecture as well as to check the validity of the in vitro dissociation curve, both the blood oxygen capacity and content in allantoic artery and vein were measured. The in vivo O 2 saturation measured here resulted in a similar value to that estimated from the dissociation curve. The O 2 content in allantoic vein ranges from about 7 to 11.5 vol % during the 10th to the 18th days of incubation and that in artery is pronouncedly low in a range of 1 to 2.5 vol%, suggesting that the blood flow rate through the body tissues is fairly larger than that through the gas exchange capillary plexus. Then, the distribution of blood flow was estimated from the analyzed data based on a model of blood circulation and some assumptions. In connection with this estimation, the diffusing capacity for deoxygenation in the tissues was speculated to be much larger than that for oxygenation in the chorioallantoic capillaries.

Fatty acid and prostaglandin composition of left ventricular myocardium from dexamethasone-treated dogs with severe low output syndrome (LOS)

The effects of dexamethasone (DEX) administration on the left ventricular myocardial content of fatty acids and prostaglandins E 1, E 2 and F 2α were studied. Following a complete right and left cardiac catheterization, either DEX (8 mg/kg) or an equivalent volume of its vehicle was given intravenously 30 minutes prior to low output syndrome (LOS induction, and supplemental doses of DEX (4 mg/kg) or vehicle administered at 15 and 75 minutes post-LOS induction. Low output syndrome was induced by intravenous administration of a myocardial depressor protein (MDP) which has been isolated from the venom of the Western diamondback rattlesnake, Crotalus atrox . Neither DEX nor its vehicle had a significant effect during the entire experiment, that is, in the normal or low cardiac output state in most of the hemodynamic parameters investigated. The three hour mortality rate for the DEX-treated animals was 22% (n=10) while that of the control group was 41% (n=26) indicating that the beneficial effects of this corticosteroid are not really apparent from hemodynamic evaluation alone. Since DEX only had a significant post-LOS induction effect in maintaining a lower left ventricular end-diastolic and pulmonary capillary wedge pressures, a higher arterio-venous oxygen saturation difference, and a more efficient contractile state of myocardial fibers (V max), an indirect correlation to coronary arterial blood flow at the subcellular level was sought. To this effect, prostaglandins and specific lipid classes of left ventricular myocardium (LVM) from control and LOS animals receiving either vehicle or DEX were analyzed. Low output state induction alone raised myocardial PG levels above those of sham-catheterized animals; on the other hand, dexamethasone induced a significant decrease in the three prostaglandins studied when administered to control (no LOS) animals. In the presence of LOS, however, dexamethasone overrode in part the increase in PGE 1 and PGE 2 brought about by LOS while in the case of PGE 2α the LOS effect was totally prevented and its concentration was not significantly higher than in control animals receiving dexamethasone. LOS induction led to an increase in myristic and arachidonic acids and a decrease in palmitic and linolenic acids. Dexamethasone administration to control animals increased the concentration of stearic acid above all the other groups but decreased the concentration of linolenic acid when compared to DEX-treated animals with LOS or sham-catheterized animals. There were no significant differences in the total myocardial lipid among the four groups of animals studied. It is suggested that the potentially beneficial effects of corticosteroid administration to animals with low output syndrome are related to their effects on fatty acid and prostaglandin content of myocardium.

Respiratory exchanges and acid-base balance during perfusion of ex vivo isolated pancreas.

We used the technique of ex vivo isolated pancreas, perfused with whole heparinized blood. The organ was stimulated by secretin (G.I.H. Stockolm, 0.1-5.0 clinic units/hr), and/or carbamylcholine (100-200 mug/hr). Oxygen consumption was increased under stimulation. This increase was a function of the dose of secretin and also of the bicarbonate output in the juice. Oxygen uptake increased further when carbamylcholine was super-imposed on secretin. This extra increase was independent of hemodynamic conditions of the organ perfusion. Arteriovenous difference in oxygen saturation did not increase when the gland was stimulated. It tended to decrease when the stimulation resulted in a marked vasodilatation. Thus, oxygen needs seemed to be neither the limiting factor of the response to a given stimulation nor the triggering mechanism of functional vasodilatation. Values of pCO2 were spread over a wide range from one experiment to another. However, it could be observed that CO2 efflux into the vein decreased under stimulation by secretin; in most experiments, CO2 efflux was even replaced by an apparent consumption of CO2 during the perfusion of the stimulated gland. Furthermore, arteriovenous pH difference increased following secretin stimulation. This increase was dose-related to secretin. These facts are discussed under the background of theories recently proposed for bicarbonate secretion.

The contribution of the shivering hind leg to the metabolic response to cold of the young ox (Bos taurus).

1. Total oxygen consumption (totalVO2), leg blood flow (legQV) and leg oxygen uptake (legVO2) were measured in young steers each exposed to thermoneutral and moderately cold environments on the same day. 2. Cold sufficient to double resting totalVO2 caused a 3 to 6-fold increase in legQVa 11/2 to 4-fold increase in leg arteriovenous oxygen saturation difference (SO2 A-EIV) and a small but significant elevation in haemoglobin concentration, resulting in a 5 to 24-fold increase in legVO2. This represented a 3 to 12-fold increase in the contribution of the hind leg to totalVO2. 3. These results were unaffected by whether thermoneutrality preceded cold orvice versa. 4. TotalVO2 was significantly correlated with legQV, legVO2 and SO2 A-EIV in both environments. Regression analysis showed that during cold exposure legVO2 varied with legQV, rather than SO2 A-EIV. 5. The metabolic response to cold of the hind leg is attributed to shivering skeletal muscle, and is shown to contribute substantially (15% per leg) to the response of the whole animal.

Oxygen cost of sodium reabsorption in proximal and distal parts of the nephron.

The relationship between changes in tubular sodium reabsorption and changes in renal oxygen consumption (Na/O2) was determined in dogs made anemic, as the arteriovenous difference in oxygen saturation was more than doubled by antecedent bleeding. Tubular sodium reabsorption was reduced by 45 ± 3%, and oxygen consumption by 36 ± 4% after blocking distal sodium transport with ethacrynic acid and chlorothiazide. On the basis of these data it could be calculated that 34 ± 5 Eq Na+ were transported in the distal nephron per/mol O2 consumed. Similar Na/O2 ratios were obtained by reducing proximal sodium reabsorption by lowering glomerular filtration rate after blocking distal sodium reabsorption. During infusion of chlorothiazide and ethacrynic acid, oxygen consumption was not further decreased by reduction of net proximal sodium reabsorption with mannitol infusion. This observation supports the hypothesis that energy-dependent sodium reabsorption in the proximal tubules is not reduced during mannitol diuresis....

Measurement of central venous oxygen saturation in patients with myocarial infarction.

Central venous oxygen saturation (CVSO 2 ) was measured in 31 patients with myocardial infarction. CVSO 2 correlated well with the patients' clinical course. In those patients not in heart failure, mean ± sem for CVSO 2 was 70 ± 1%. When heart failure was present, CVSO 2 averaged 56 ± 1%. When both heart failure and shock were present, CVSO 2 averaged 43 ± 1%. In nine patients, serial determinations of arterial oxygen saturation and CVSO 2 were made. In 22 of 26 instances, either a fall in CVSO 2 was accompanied by an increase in the arteriovenous oxygen saturation difference or an increase in CVSO 2 was accompanied by a decrease in arteriovenous oxygen saturation difference. Serial measurements of CVSO 2 appear to be a useful method of monitoring changes in myocardial function in patients with myocardial infarction.

Relations among activity, blood flow, and vascular state in skeletal muscle

The relation between stimulus interval and performance of skeletal muscle was investigated under conditions of controlled and spontaneous blood flow. Vascular resistance, arteriovenous oxygen saturation difference, oxygen consumption, and peak isometric tension and blood flow were used as indices of muscle performance. In all cases vascular resistance decreased while oxygen consumption increased as the stimulus interval was shortened. The relative contributions of alteration flow (where permitted) and alteration of arteriovenous oxygen difference to changes in oxygen consumption were assessed. The latter proved to be the more important contributor. The apparent oxygen cost per unit of tension change rate decreased to a nearly steady level as the stimulus interval shortened. Changes in these variables brought about by intra-arterial infusion of acetylcholine or d-tubocurarine were shown. The results illustrate some features of the myovascular interaction which occurs during muscular activity. A model of the blood flow-oxygen consumption relation, based on considerations of oxygen extraction, is presented.