Quantification of right-to-left shunt with 99mTc-labelled albumin macroaggregates and 100% oxygen in patients with hereditary haemorrhagic telangiectasia

2002 ◽  
Vol 102 (2) ◽  
pp. 127-134 ◽  
Author(s):  
Johannes J. MAGER ◽  
Pieter ZANEN ◽  
Fred VERZIJLBERGEN ◽  
Cornelius J.J. WESTERMANN ◽  
Tjeerd HAITJEMA ◽  
...  

Pulmonary arteriovenous malformations (PAVMs) are often associated with hereditary haemorrhagic telangiectasia (HHT). The quantification of right-to-left shunts in patients with PAVMs is important in diagnosis and follow up. Traditionally, this shunt is measured by the 100% oxygen method, in which the value for the arteriovenous difference in oxygen content, Cao2-Co2 (where Cao2 is the oxygen content of arterial blood and Co2 is the oxygen content of mixed venous blood) is estimated. Alternative methods consist of measurement of the systemic or renal uptake of 99mTc-labelled macroaggregates of albumin (MAA), which are trapped in pulmonary capillaries, but pass through PAVMs. We first measured Cao2-Co2 in 12 HHT patients before and after embolization of PAVMs. We obtained a mean value of 4.4ml/100ml, instead of the usual 5ml/100ml. Subsequently, we measured right-to-left shunt in 21 HHT patients using the 100% oxygen method and with two different methods involving 99mTc. We used the kidney-lung method (K/L method), in which it is assumed that the right kidney receives 10% of the cardiac output, and we also used a method with two tracers (HSA/MAA method): (1) 99mTc-labelled human serum albumin (HSA) (which passes through pulmonary capillaries) to measure the fraction of the cardiac output perfusing the kidneys, and (2) MAA to measure the shunt fraction. In 35 shunt measurements we evaluated this new technique and the K/L method, by comparing the results with those from the 100% oxygen method. There was poor agreement between the 100% oxygen method and the K/L method, with 95% limits of agreement for the shunt fraction of -15.2% to +15.2%. There was moderate agreement between the 100% oxygen method and the HSA/MAA method, with limits of agreement of -8.3% to +7.7%. We conclude that the different methods cannot replace each other, because the limits of agreement are too wide for clinical use.

2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo

The measurement of cardiac output was first proposed by Fick, who published his equation in 1870. Fick's calculation called for the measurement of the contents of oxygen or CO2 in pulmonary arterial and systemic arterial blood. These values could not be determined directly in human subjects until the acceptance of cardiac catheterization as a clinical procedure in 1940. In the meanwhile, several attempts were made to perfect respiratory methods for the indirect determination of blood-gas contents by respiratory techniques that yielded estimates of the mixed venous and pulmonary capillary gas pressures. The immediate uptake of nonresident gases can be used in a similar way to calculate cardiac output, with the added advantage that they are absent from the mixed venous blood. The fact that these procedures are safe and relatively nonintrusive makes them attractive to physiologists, pharmacologists, and sports scientists as well as to clinicians concerned with the physiopathology of the heart and lung. This paper outlines the development of these techniques, with a discussion of some of the ways in which they stimulated research into the transport of gases in the body through the alveolar membrane.


1963 ◽  
Vol 18 (5) ◽  
pp. 933-936 ◽  
Author(s):  
P. Harris ◽  
T. Bailey ◽  
M. Bateman ◽  
M. G. Fitzgerald ◽  
J. Gloster ◽  
...  

The concentrations of lactic acid, pyruvic acid, glucose, and free fatty acids have been measured simultaneously in the blood from the pulmonary and brachial arteries at rest and during exercise in a group of patients with acquired heart disease. The arteriovenous differences in the concentration of lactate, pyruvate, and free fatty acid were such as could be attributed to chance. The average concentration of glucose was slightly but significantly higher in the brachial arterial blood than in the mixed venous blood. cardiac output; lung metabolism; exercise Submitted on January 15, 1963


1956 ◽  
Vol 185 (3) ◽  
pp. 483-486 ◽  
Author(s):  
Shirley H. Brind ◽  
Joseph R. Bianchine ◽  
Matthew N. Levy

Changes in cardiac output, mean arterial blood pressure, hematocrit ratio, and arterial and venous oxygen content resulting from bilateral carotid occlusion were investigated. Cardiac output exhibited no significant alteration during endosinusal hypotension, and the systemic hypertension engendered was attributed to an increase in vasomotor tone. Arterial and venous oxygen content, as well as hematocrit ratio, increased significantly during the period of carotid occlusion. This increase was ascribed to splenic contraction evoked by carotid occlusion, since no comparable augmentation was observed when the splenic circulation was temporarily interrupted.


1965 ◽  
Vol 20 (4) ◽  
pp. 763-766 ◽  
Author(s):  
K. Klausen

The cardiac output during rest and work was determined by a CO2 rebreathing method as suggested by Defares. The partial pressure of CO2 in the mixed venous blood (PvCOCO2) was calculated from the rise of the CO2 percent in a Grollman bag during rebreathing. In the rest experiments the partial pressure of CO2 in arterial blood (PaCOCO2) was obtained from analysis of alveolar samples taken by the Haldane-Priestley direct sampling method. In the work experiments the PaCOCO2 was calculated using the Bohr formula and a dead space estimated from Asmussen and Nielsen's data. The metabolic rate including both O2 uptake and CO2 output was determined by the Douglas bag method. In each experiment the acetylene method as described by Christensen was applied after the CO2 rebreathing method. The values obtained by the two methods were almost identical, the standard deviation for all experiments being ±7.3%, and were of the same magnitude as those obtained by others with the dye-dilution or direct Fick method both during rest and work. cardiac output at rest and work; arterial Pco2 and venous Pco2 at rest and work; stroke volume at rest and work Submitted on November 25, 1964


2010 ◽  
Vol 55 (No. 9) ◽  
pp. 445-456 ◽  
Author(s):  
M. Patschova ◽  
R. Kabes ◽  
S. Krisova

This research aimed to determine the effect of aerosolized salbutamol administration on systemic and pulmonary hemodynamic, pulmonary mechanics and oxygen balance in healthy horses during general anaesthesia. Six healthy Thoroughbreds (body weight range 471&ndash;587 kg) underwent two general anaesthesias in dorsal recumbency with and without aerosolized salbutamol administration in randomized order with a one month washout period. The anaesthesia was induced by 1.1 mg/kg of xylazine, 0.02 mg/kg of diazepam and 2.2 mg/kg of ketamine, maintained with isoflurane in oxygen and air and horses were mechanically ventilated. Measurement of arterial and pulmonary arterial blood pressures, cardiac output and arterial and mixed venous blood gas analysis was carried out. Spirometry was performed using a Horse-lite. After achieving a steady state, baseline (T<sub>0</sub>) values of cardiac output, systemic and pulmonary arterial blood pressures, heart rate, dynamic compliance, airway resistance and arterial and mixed venous blood gas values and pH were recorded in both groups. In the S-group (salbutamol), 2 &micro;g/kg of aerosolized salbutamol were administered synchronously with inspirium into the tracheal tube. In both groups data were recorded at 15, 30, 45 and 60 min (T<sub>15</sub>, T<sub>30</sub>, T<sub>45</sub>, T<sub>60</sub>) after the baseline. PaO<sub>2</sub>/FiO<sub>2</sub> ratio, oxygen consumption (VO<sub>2</sub>), oxygen delivery (DO<sub>2</sub>), pulmonary shunt values were calculated. Data were tested for normality and compared within each group: T<sub>0</sub> value with T<sub>15</sub>, T<sub>30</sub>, T<sub>45</sub>, T<sub>60</sub> values using Wilcoxon's test with Bonferoni correction (significance level 0.0125). For each time point, comparisons were made between the S- and C-groups (control) using Wilcoxon's test. In the S-group, there was a significant increase in values (mean &plusmn; SD) of cardiac output (l/min), T<sub>0</sub> (38 &plusmn; 7), a peak at T<sub>15</sub> (64 &plusmn; 25.5), significantly higher values persisted throughout the period of anaesthesia; heart rate (beats/min), T<sub>0</sub> (32 &plusmn; 2), T<sub>15</sub> (40 &plusmn; 6), T<sub>30</sub> (38 &plusmn; 5); DO<sub>2</sub> (l/min), T<sub>0</sub> (5.8 &plusmn; 0.8), a peak at T<sub>15</sub> (9.6 &plusmn; 3.2), significantly higher values persisted until the end of anaesthesia and VO<sub>2</sub> (l/min), T<sub>0</sub> (1.1 &plusmn; 0.5), T<sub>30</sub> (1.6 &plusmn; 0.7) and T<sub>45</sub> (1.8 &plusmn; 0.5). In the C-group, there was a significant decrease in values of PaO<sub>2</sub>/FiO<sub>2</sub> ratio from T<sub>0</sub> (176 &plusmn; 67) to a minimum at T<sub>60</sub> (114 &plusmn; 36) and in DO<sub>2</sub> from T<sub>0</sub> (6 &plusmn; 2.3) to a minimum at T<sub>60</sub> (4.3 &plusmn; 1.2). A comparison of the S- and C-groups did not reveal any difference in the baseline data. Subsequently, significantly higher values of cardiac output, heart rate, DO<sub>2</sub>, and the PaO<sub>2</sub>/FiO<sub>2 </sub>ratio were found in the S-group compared to the C-group. Pulmonary arterial blood pressure was significantly lower in the S-group. Aerosolized salbutamol administration in healthy horses during general anaesthesia caused hemodynamic changes which resulted in an elevation of oxygen delivery. It can have a positive effect on arterial oxygenation, but the effect varies between individuals.


1979 ◽  
Vol 57 (5) ◽  
pp. 385-388 ◽  
Author(s):  
R. D. Latimer ◽  
G. Laszlo

1. The left lower lobe of the lungs of six anaesthetized dogs were isolated by the introduction of a bronchial cannula at thoracotomy. Catheters were introduced into the main pulmonary artery and a vein draining the isolated lobe. 2. Blood-gas pressures and pH were measured across the isolated lobe and compared with gas pressures in alveolar samples from the lobe. 3. When the isolated lobe was allowed to reach gaseous equilibrium with pulmonary arterial blood for 30 min, there was no significant difference between alveolar and pulmonary venous Pco2. Mean values of whole-blood base excess were similar in pulmonary arterial and pulmonary venous blood. 4. After injection of 20 ml of 8·4% sodium bicarbonate solution into a peripheral vein, Pco2, pH and plasma bicarbonate concentrations rose in the mixed venous blood. There was no change of whole-blood base excess across the lung, indicating that HCO−3, as distinct from dissolved CO2, did not enter lung tissue in measurable amounts. 5. No systematic alveolar—pulmonary venous Pco2 differences were demonstrated in this preparation other than those explicable by maldistribution of lobar blood flow.


1985 ◽  
Vol 59 (2) ◽  
pp. 376-383 ◽  
Author(s):  
P. D. Wagner ◽  
C. M. Smith ◽  
N. J. Davies ◽  
R. D. McEvoy ◽  
G. E. Gale

Estimation of ventilation-perfusion (VA/Q) inequality by the multiple inert gas elimination technique requires knowledge of arterial, mixed venous, and mixed expired concentrations of six gases. Until now, arterial concentrations have been directly measured and mixed venous levels either measured or calculated by mass balance if cardiac output was known. Because potential applications of the method involve measurements over several days, we wished to determine whether inert gas levels in peripheral venous blood ever reached those in arterial blood, thus providing an essentially noninvasive approach to measuring VA/Q mismatch that could be frequently repeated. In 10 outpatients with chronic obstructive pulmonary disease, we compared radial artery (Pa) and peripheral vein (Pven) levels of the six gases over a 90-min period of infusion of the gases into a contralateral forearm vein. We found Pven reached 90% of Pa by approximately 50 min and 95% of Pa by 90 min. More importantly, the coefficient of variation at 50 min was approximately 10% and at 90 min 5%, demonstrating acceptable intersubject agreement by 90 min. Since cardiac output is not available without arterial access, we also examined the consequences of assuming values for this variable in calculating mixed venous levels. We conclude that VA/Q features of considerable clinical interest can be reliably identified by this essentially noninvasive approach under resting conditions stable over a period of 1.5 h.


1987 ◽  
Vol 410 (3) ◽  
pp. 257-262 ◽  
Author(s):  
Y. L. Hoogeveen ◽  
J. P. Zock ◽  
P. Rispens ◽  
W. G. Zijlstra

1970 ◽  
Vol 39 (3) ◽  
pp. 349-365 ◽  
Author(s):  
H. E. Berry ◽  
J. G. Collier ◽  
J. R. Vane

1. Circulating kinins were detected and continuously assayed during hypotension due to haemorrhage in dogs, using the blood-bathed organ technique and isolated strips of cat jejunum as the assay tissue. 2. In arterial blood kinin concentrations of 1–5 ng/ml were attained after a hypotension of 35–65 mmHg had been maintained for 10–190 min. When portal venous blood was simultaneously assayed kinins appeared earlier and in concentrations 1–2 ng/ml higher than in arterial blood. No differences in time course of kinin generation or in concentration were found when mixed venous blood and arterial blood were compared. In those instances in which the blood pressure was restored to normal by returning the shed blood, kinin formation stopped. 3. Kinin generation was due to the presence in the circulation of a kinin-forming enzyme, such as kallikrein. When kallikrein was infused into the portal vein, it was partially inactivated by the liver. 4. Prolonged intravenous infusions of kallikrein (20–60 mu kg−1 min−1) generated kinins in the circulation in concentrations (1–5 ng/ml) which were well maintained throughout the infusion, demonstrating that kinin generation is not limited by depletion of the precursor kininogen; nevertheless, the effects of kallikrein infusions on the blood pressure and central venous pressure waned. 5. It is concluded that in hypotension due to haemorrhage, an active kallikrein appears in the portal circulation. Delay in the appearance of kallikrein in the systemic circulation may be due to the kallikrein inactivating mechanism of the liver. This inactivating mechanism may fail during shock. Kinins are generated in amounts sufficient to have a substantial effect on the circulation and an influence on the course of events in shock.


1972 ◽  
Vol 56 (3) ◽  
pp. 657-666
Author(s):  
DAVID R. JONES ◽  
GEORGE F. HOLETON

1. Cardiac ouput, ventilatory minute volume and gaseous exchange at both tissues and lungs have been recorded in restrained unanaesthetized ducks exposed to simulated high altitudes. 2. A comparison between two species of duck showed that despite a significantly lower heart rate in resting Muscovy ducks, cardiac output, on a weight basis, was the same as in White Pekin ducks. Respiratory frequency and tidal volumes differed in the two species although their minute volumes were in the same range. 3. Ducks responded to reduction in oxygen tension of arterial blood (Pa, o2) by increases in cardiac output and ventilatory minute volume, both being significantly above control (normal Pa, o2 at rest) when Pa, o2 was in the range 54.5-63 mmHg. At all levels of hypoxia ducks were able to remove about 30% of the oxygen from the ventilated air. 4. When Pa, o2 was 38 mmHg the Po2, difference between arterial and venous blood had decreased by 20.5 mmHg from control. Pa,co2, and Pvco2 fell during hypoxia and arterial and venous pH rose. 5. The rate of oxygen uptake (V· o2) fell markedly at the lowest level of hypoxia but V· co2, remained constant so that R.Q. rose from 0.76 at control at 1.12 at Pa, o2 of 38 mmHg. 6. It is concluded that there are many basic similarities between the cardiovascular and respiratory responses of ducks and mammals when exposed to simulated high altitude.


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