Measurements of Cardiac Output and Management of Blood Transfusions During Burn Surgery—An Observational Prospective Study

2020 ◽  
Author(s):  
Jakob Skúlason Stefansson ◽  
Rasmus Christensen ◽  
Camilla Ikast Ottosen ◽  
Lars Simon Rasmussen
Keyword(s):  
Cardiac Output ◽  
Primary Outcome ◽  
Field Measurements ◽  
Blood Transfusions ◽  
Arterial Line ◽  
Arterial Blood ◽  
Perioperative Monitoring ◽  
Burn Surgery ◽  
Baseline Values ◽  
Perioperative Blood Transfusion

Abstract Burn surgery can cause extensive bleeding, which lead to perioperative blood transfusions. The purpose of this study was to investigate whether blood transfusions during burn surgery, guided by standard monitoring with inspection of the operative field, measurements of blood pressure, heart rate, hourly diuresis, and concentrations of hemoglobin and lactate could sustain the preoperative cardiac output (CO) till end of surgery. We investigated 15 patients ≥18 years of age scheduled for burn surgery, where the perioperative monitoring included an arterial line. After induction of anesthesia and before start of surgery, we measured baseline values of CO with the minimally invasive LiDCOrapid, mean arterial pressure, and concentrations of hemoglobin and lactate in arterial blood. We measured these values every 30 minutes through surgery. The primary outcome was change in CO from baseline till end of surgery. Secondary outcomes included the change in concentrations of hemoglobin and lactate from baseline till end of surgery. We found no statistically significant change in CO from baseline till end of surgery (6.6 [±2.4] liters/min; 7.2 [±3.2] liters/min; P = .26). We found a statistically significant decrease in concentration of hemoglobin (7.2 [±0.8] mmol/liter; 6.2 [±0.9] mmol/liter; P = .0002), and a statistically significant increase in concentration of lactate (1.3 [±0.5] mmol/liter; 1.7 [±1] mmol/liter; P = .02). The perioperative blood transfusion guided by standard monitoring seemed to sustain CO from baseline till end of surgery; however, further research is needed to confirm this.

IN SITU AND PILOT ORGAN PERFUSION TECHNIQUES FOR THE STUDY OF METABOLIC DYNAMICS

1972 ◽  
Vol 68 (2_Supplb) ◽  
pp. S9-S25 ◽  
Author(s):  
John Urquhart ◽  
Nancy Keller
Keyword(s):  
Cardiac Output ◽  
Large Fraction ◽  
Experimental Studies ◽  
Test Substance ◽  
Organ Perfusion ◽  
Systemic Blood ◽  
Experimental Control ◽  
Arterial Blood ◽  
Vascular Connections

ABSTRACT Two techniques for organ perfusion with blood are described which provide a basis for exploring metabolic or endocrine dynamics. The technique of in situ perfusion with autogenous arterial blood is suitable for glands or small organs which receive a small fraction of the animal's cardiac output; thus, test stimulatory or inhibitory substances can be added to the perfusing blood and undergo sufficient dilution in systemic blood after passage through the perfused organ so that recirculation does not compromise experimental control over test substance concentration in the perfusate. Experimental studies with the in situ perfused adrenal are described. The second technique, termed the pilot organ method, is suitable for organs which receive a large fraction of the cardiac output, such as the liver. Vascular connections are made between the circulation of an intact, anaesthetized large (> 30 kg) dog and the liver of a small (< 3 kg) dog. The small dog's liver (pilot liver) is excised and floated in a bath of canine ascites, and its venous effluent is continuously returned to the large dog. Test substances are infused into either the hepatic artery or portal vein of the pilot liver, but the small size of the pilot liver and its blood flow in relation to the large dog minimize recirculation effects. A number of functional parameters of the pilot liver are described.

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

HAEMODYNAMIC CHANGES AND ADRENAL FUNCTION IN MAN DURING INDUCED HYPOGLYCAEMIA

1963 ◽  
Vol 44 (3) ◽  
pp. 430-442 ◽  
Author(s):  
B. Arner ◽  
P. Hedner ◽  
T. Karlefors ◽  
H. Westling
Keyword(s):  
Blood Pressure ◽  
Cardiac Output ◽  
Mean Arterial Blood Pressure ◽  
Peripheral Vascular ◽  
Adrenocortical Activity ◽  
Arterial Blood ◽  
Haemodynamic Changes ◽  
The Mean ◽  
Temporary Rise ◽  
Catechol Amines

ABSTRACT Observations were made on healthy volunteers during insulin induced hypoglycaemia (10 cases) and infusion of adrenaline (3 cases) or cortisol (1 case). In all cases a rise in the cardiac output was registered during insulin hypoglycaemia. The mean arterial blood pressure was relatively unchanged and the calculated peripheral vascular resistance decreased in all cases. A temporary rise in plasma corticosteroids was observed. After infusion of adrenaline similar circulatory changes were observed but no rise in plasma corticosteroids was found. Infusion of cortisol caused an increased plasma corticosteroid level but no circulatory changes. It is concluded that liberation of catechol amines and increased adrenocortical activity following hypoglycaemia are not necessarily interdependent.

Respiratory measurements of cardiac output: from elegant idea to useful test

2004 ◽  
Vol 96 (2) ◽  
pp. 428-437 ◽  
Author(s):  
Gabriel Laszlo
Keyword(s):  
Cardiac Output ◽  
Human Subjects ◽  
Venous Blood ◽  
The Body ◽  
Mixed Venous Blood ◽  
Indirect Determination ◽  
Arterial Blood ◽  
Pulmonary Capillary ◽  
Pulmonary Arterial ◽  
Mixed Venous

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.

Dexmedetomidine Attenuates the Microcirculatory Derangements Evoked by Experimental Sepsis

2015 ◽  
Vol 122 (3) ◽  
pp. 619-630 ◽  
Author(s):  
Marcos L. Miranda ◽  
Michelle M. Balarini ◽  
Eliete Bouskela
Keyword(s):  
Blood Gases ◽  
Capillary Density ◽  
Sepsis Syndrome ◽  
In Vivo Studies ◽  
Experimental Sepsis ◽  
Leukocyte Rolling ◽  
Capillary Perfusion ◽  
Arterial Blood ◽  
Baseline Values

Abstract Background: Dexmedetomidine, an α-2 adrenergic receptor agonist, has already been used in septic patients although few studies have examined its effects on microcirculatory dysfunction, which may play an important role in perpetuating sepsis syndrome. Therefore, the authors have designed a controlled experimental study to characterize the microcirculatory effects of dexmedetomidine in an endotoxemia rodent model that allows in vivo studies of microcirculation. Methods: After skinfold chamber implantation, 49 golden Syrian hamsters were randomly allocated in five groups: (1) control animals; (2) nonendotoxemic animals treated with saline; (3) nonendotoxemic animals treated with dexmedetomidine (5.0 μg kg−1 h−1); (4) endotoxemic (lipopolysaccharide 1.0 mg/kg) animals treated with saline; and (5) endotoxemic animals treated with dexmedetomidine. Intravital microscopy of skinfold chamber preparations allowed quantitative analysis of microvascular variables and venular leukocyte rolling and adhesion. Mean arterial blood pressure, heart rate, arterial blood gases, and lactate concentrations were also documented. Results: Lipopolysaccharide administration increased leukocyte rolling and adhesion and decreased capillary perfusion. Dexmedetomidine significantly attenuated these responses: compared with endotoxemic animals treated with saline, those treated with dexmedetomidine had less leukocyte rolling (11.8 ± 7.2% vs. 24.3 ± 15.0%; P &lt; 0.05) and adhesion (237 ± 185 vs. 510 ± 363; P &lt; 0.05) and greater functional capillary density (57.4 ± 11.2% of baseline values vs. 45.9 ± 11.2%; P &lt; 0.05) and erythrocyte velocity (68.7 ± 17.6% of baseline values vs. 54.4 ± 14.8%; P &lt; 0.05) at the end of the experiment. Conclusions: Dexmedetomidine decreased lipopolysaccharide-induced leukocyte–endothelial interactions in the hamster skinfold chamber microcirculation. This was accompanied by a significant attenuation of capillary perfusion deficits, suggesting that dexmedetomidine yields beneficial effects on endotoxemic animals’ microcirculation.

The relative roles of external and internal CO2versusH+ in eliciting the cardiorespiratory responses ofSalmo salarandSqualus acanthiasto hypercarbia

2001 ◽  
Vol 204 (22) ◽  
pp. 3963-3971 ◽  
Author(s):  
S. F. Perry ◽  
J. E. McKendry
Keyword(s):  
Cardiac Output ◽  
Sea Water ◽  
Buccal Cavity ◽  
Respiratory Acidosis ◽  
Systemic Resistance ◽  
Measured Variable ◽  
Cardiorespiratory Responses ◽  
Arterial Blood ◽  
Water Ph ◽  
Stimulation Of

SUMMARYFish breathing hypercarbic water encounter externally elevated PCO2 and proton levels ([H+]) and experience an associated internal respiratory acidosis, an elevation of blood PCO2 and [H+]. The objective of the present study was to assess the potential relative contributions of CO2versus H+ in promoting the cardiorespiratory responses of dogfish (Squalus acanthias) and Atlantic salmon (Salmo salar) to hypercarbia and to evaluate the relative contributions of externally versus internally oriented receptors in dogfish.In dogfish, the preferential stimulation of externally oriented branchial chemoreceptors using bolus injections (50 ml kg–1) of CO2-enriched (4 % CO2) sea water into the buccal cavity caused marked cardiorespiratory responses including bradycardia (–4.1±0.9 min–1), a reduction in cardiac output (–3.2±0.6 ml min–1 kg–1), an increase in systemic vascular resistance (+0.3±0.2 mmHg ml min–1 kg–1), arterial hypotension (–1.6±0.2 mmHg) and an increase in breathing amplitude (+0.3±0.09 mmHg) (means ± s.e.m., N=9–11). Similar injections of CO2-free sea water acidified to the corresponding pH of the hypercarbic water (pH 6.3) did not significantly affect any of the measured cardiorespiratory variables (when compared with control injections). To preferentially stimulate putative internal CO2/H+ chemoreceptors, hypercarbic saline (4 % CO2) was injected (2 ml kg–1) into the caudal vein. Apart from an increase in arterial blood pressure caused by volume loading, internally injected CO2 was without effect on any measured variable.In salmon, injection of hypercarbic water into the buccal cavity caused a bradycardia (–13.9±3.8 min–1), a decrease in cardiac output (–5.3±1.2 ml min–1 kg–1), an increase in systemic resistance (0.33±0.08 mmHg ml min–1 kg–1) and increases in breathing frequency (9.7±2.2 min–1) and amplitude (1.2±0.2 mmHg) (means ± s.e.m., N=8–12). Apart from a small increase in breathing amplitude (0.4±0.1 mmHg), these cardiorespiratory responses were not observed after injection of acidified water.These results demonstrate that, in dogfish and salmon, the external chemoreceptors linked to the initiation of cardiorespiratory responses during hypercarbia are predominantly stimulated by the increase in water PCO2 rather than by the accompanying decrease in water pH. Furthermore, in dogfish, the cardiorespiratory responses to hypercarbia are probably exclusively derived from the stimulation of external CO2 chemoreceptors, with no apparent contribution from internally oriented receptors.

Pulmonary gas exchange during exercise in women: effects of exercise type and work increment

2000 ◽  
Vol 89 (2) ◽  
pp. 721-730 ◽  
Author(s):  
Susan R. Hopkins ◽  
Rebecca C. Barker ◽  
Tom D. Brutsaert ◽  
Timothy P. Gavin ◽  
Pauline Entin ◽  
...  
Keyword(s):  
Cardiac Output ◽  
Gas Exchange ◽  
Blood Gases ◽  
Random Order ◽  
Pulmonary Gas Exchange ◽  
Male Athletes ◽  
Prediction Limit ◽  
Fast Running ◽  
Arterial Blood ◽  
Exercise Induced

Exercise-induced arterial hypoxemia (EIAH) has been reported in male athletes, particularly during fast-increment treadmill exercise protocols. Recent reports suggest a higher incidence in women. We hypothesized that 1-min incremental (fast) running (R) protocols would result in a lower arterial Po 2 (PaO2 ) than 5-min increment protocols (slow) or cycling exercise (C) and that women would experience greater EIAH than previously reported for men. Arterial blood gases, cardiac output, and metabolic data were obtained in 17 active women [mean maximal O2 uptake (V˙o 2 max) = 51 ml · kg−1 · min−1]. They were studied in random order (C or R), with a fastV˙o 2 max protocol. After recovery, the women performed 5 min of exercise at 30, 60, and 90% ofV˙o 2 max (slow). One week later, the other exercise mode (R or C) was similarly studied. There were no significant differences in V˙o 2 maxbetween R and C. Pulmonary gas exchange was similar at rest, 30%, and 60% of V˙o 2 max. At 90% ofV˙o 2 max, PaO2 was lower during R (mean ± SE = 94 ± 2 Torr) than during C (105 ± 2 Torr, P < 0.0001), as was ventilation (85.2 ± 3.8 vs. 98.2 ± 4.4 l/min btps, P < 0.0001) and cardiac output (19.1 ± 0.6 vs. 21.1 ± 1.0 l/min, P < 0.001). Arterial Pco 2 (32.0 ± 0.5 vs. 30.0 ± 0.6 Torr, P < 0.001) and alveolar-arterial O2 difference (A-aDo 2; 22 ± 2 vs. 16 ± 2 Torr, P < 0.0001) were greater during R. PaO2 and A-aDo 2 were similar between slow and fast. Nadir PaO2 was ≤80 Torr in four women (24%) but only during fast-R. In all subjects, PaO2 atV˙o 2 max was greater than the lower 95% prediction limit calculated from available data in men ( n = 72 C and 38 R) for both R and C. These data suggest intrinsic differences in gas exchange between R and C, due to differences in ventilation and also efficiency of gas exchange. The PaO2 responses to R and C exercise in our 17 subjects do not differ significantly from those previously observed in men.

Estimation of ventilation-perfusion inequality by inert gas elimination without arterial sampling

1985 ◽  
Vol 59 (2) ◽  
pp. 376-383 ◽  
Author(s):  
P. D. Wagner ◽  
C. M. Smith ◽  
N. J. Davies ◽  
R. D. McEvoy ◽  
G. E. Gale
Keyword(s):  
Cardiac Output ◽  
Venous Blood ◽  
Inert Gas ◽  
Chronic Obstructive ◽  
Obstructive Pulmonary Disease ◽  
Arterial Access ◽  
Arterial Blood ◽  
Potential Applications ◽  
Clinical Interest ◽  
Mixed Venous

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.

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