Blood transfusion and oxygen consumption in surgical sepsis

OBJECTIVE: To evaluate the use of serum lactic acid values to predict flow-dependent increases in oxygen consumption (VO2) in response to increasing oxygen delivery (DO2) after blood transfusion in surgical sepsis. DESIGN: Prospective study. SETTING: Tertiary care, trauma center. PATIENTS: Twenty-one patients, postsurgical or posttrauma, judged septic by defined criteria. INTERVENTIONS: Serum lactic acid concentrations, DO2, and VO2 were measured before and after transfusion therapy. MEASUREMENTS AND MAIN RESULTS: Overall, the DO2 increased from 532 +/- 146 to 634 +/- 225 (SD) mL/min.m2 (p less than .001), and the VO2 increased from 145 +/- 39 to 160 +/- 56 mL/min.m2 (p = .02). These changes occurred with an Hgb increase from 9.3 +/- 1.1 to 10.7 +/- 1.5 g/dL (p less than .001). The patients were grouped by their pretransfusion serum lactic acid values. In those patients with normal (less than 1.6 mmol/dL) serum lactic acid (n = 10), DO2 increased from 560 +/- 113 to 676 +/- 178 mL/min.m2 (p less than .02), and VO2 increased from 150 +/- 25 to 183 +/- 46 mL/min.m2 (p less than .02). However, in the increased serum lactic acid group (n = 17), VO2 was not significantly changed after transfusion (143 +/- 46 to 146 +/- 58 mL/min.m2) despite increased DO2 (515 +/- 163 to 609 +/- 251 mL/min.m2, p less than .01). CONCLUSIONS: Blood transfusion can be used to augment DO2 and VO2 in septic surgical patients. Increased serum lactic acid values do not predict patients who will respond. The absence of lactic acidosis should not be used in this patient population to justify withholding blood transfusions to improve flow-dependent VO2. Patients who have increased lactate concentrations may have a peripheral oxygen utilization defect that prevents improvement in VO2 with increasing DO2.     

Circuit factors in the high cardiac output of sepsis

The increase of cardiac output (CO) in sepsis must be matched by an increase in venous return. Our goal was to determine which of the determinants of venous return are responsible in volume-loaded and nonvolume-loaded pigs with endotoxemia. The determinants include stressed volume, venous compliance (C_v), venous resistance (RVR) and right atrial pressure (Pra). We also tested the effect of the nitric oxide (NO) synthase inhibitor, N^ω-nitro- -arginine-methyl ester (L-NAME) after the hemodynamics with endotoxin stabilized.

Pigs were anesthetized and mechanically ventilated. We measured CO by thermodilution, mean circulatory filling pressure (MCFP) by inflating a balloon in the right atrium, blood volume by dye dilution, and C_v by rapid blood infusions. RVR was calculated from MCFP - Pra/CO). After baseline measurements, we infused 10 μg/(kg x h⁻¹) of Escherichia coli endotoxin. Eight animals also received 30 mL × kg⁻¹ of dextran over the 2 hours (volume treated), and seven did not (no volume). After 2 hours we injected 25 mg × kg⁻¹ of the NO synthase inhibitor, L-NAME, and repeated the measurements.

In volume-treated animals, CO increased from 3.9 ± 0.7 to 5.4 ± 0.8 L x min⁻¹ (P < .05), and blood pressure (BP) fell from 118 ± 9 to 76 ± 12 mmHg. MCFP rose, and there was no change in RVR or C_v, whereas capacitance increased (ie, right shift of pressure-volume curve). Cardiac function (ie, Starling curve) did not change. In no-volume animals, CO fell from 4.47 ± 0.64 to 2.50 ± 0.86 L × min⁻¹, BP from 114 ± 10 to 9 13 mmHg and MCFP fell. Systemic vascular resistance did not change. Cardiac function was markedly depressed, and the heart rate increased from 143 ± 13 to 203 ± 30 beats x min⁻¹. L-NAME restored BP in both groups but also increased RVR and depressed cardiac function.

Changes in vascular tone during endotoxemia are dependent on volume status. The increased cardiac output in volume-treated septic animals occurred because of an increase in stressed volume due to the volume given in combination with a dilated vasculature. L-NAME restored arterial tone but decreased CO because of a rise in RVR and decrease in cardiac function.     

Dependence of shunt on cardiac output in unilobar oleic acid edema

Objective

In acute respiratory failure, increased cardiac output ( \(\dot Q_t \) ) increase; shunt ( \({{\dot Q_s } \mathord{\left/ {\vphantom {{\dot Q_s } {\dot Q_t }}} \right. \kern-0em} {\dot Q_t }}\) ). We have tested if this is caused by: 1) a redistribution of blood flow towards edematous regions, or 2) a decrease of regional ventilation in the edematous region.

Design

Oleic acid edema was induced in the left lower lobe (LLL) of 11 pigs. \(\dot Q_t \) was varied with bleeding and infusion of blood and dextran. Blood flow to the LLL was measured at low and high \(\dot Q_t \) with electromagnetic low probes in 6 animals and with a gamma camera in 5. In the gamma camera pigs regional ventilation was also measured.

Measurements and results

\(\dot Q_t \) was increased by 45% (electromagnetic flow probes) and 73% (gamma camera). \({{\dot Q_s } \mathord{\left/ {\vphantom {{\dot Q_s } {\dot Q_t }}} \right. \kern-0em} {\dot Q_t }}\) increased from 24.9–31.3% (p<0.05) and from 17.6–28.8% (p<0.001) respectively. No change in fractional perfusion of LLL could be seen, neither with flow probes nor with gamma camera. A decrease in ventilation of LLL, 2.6%, was observed when Q_t was increased (p<0.05).

Conclusion

Theoretically a small decrease in ventilation can explain the increase in shunt, if regions with low ventilation/perfusion (VA/ \(\dot Q\) ) ratio are transformed to shunt. This is, however, unlikely since earlier studies have shown that blood flow is distributed either to regions with normal VA/ \(\dot Q\) ratio or to shunt regions. We conclude that the cardiac output dependent shunt is not caused by redistribution of blood flow between lobes or by decreased ventilation in the edematous region. We cannot exclude that blood flow is redistributed within the edematous lobe.     

Method for continuously measured oxygen consumption and cardiac output for use in critically ill patients

A method for continous measurements of oxygen consumption (VO2) and cardiac output is described. This relatively inexpensive system was found to be practical for monitoring critically ill patients over the past 5 years. Clinical studies illustrating its usefulness are presented.     

Different response of oxygen consumption and cardiac output to various endogenous and synthetic catecholamines in awake dogs

OBJECTIVE: To determine whether catecholamines with different adrenergic receptor affinities are characterized by individual relationships between cardiac output (Q) and oxygen consumption (VO2). DESIGN: Comparison of the dose-effect relationships and Q/VO2 relationships of four different catecholamines in the same awake dogs. SETTING: University research department of experimental anesthesiology. SUBJECTS: Ten trained, healthy dogs in the basal metabolic state with chronically implanted ultrasonic flow transducers around the pulmonary artery for the continuous measurement of cardiac output. INTERVENTIONS: Increasing doses of norepinephrine, epinephrine, dobutamine, or dopexamine were infused in a randomly varied sequence on separate days until VO2 and Q reached a maximum. MEASUREMENTS AND MAIN RESULTS: VO2 was measured by indirect calorimetry, and Q was measured via the pulmonary artery by ultrasonic flowmetry. In healthy dogs, catecholamines increased both VO2 and Q in a dose-dependent manner until a plateau was reached when VO2 had doubled and Q had quadrupled compared with baseline conditions. Regardless of the catecholamine, the resulting Q/VO2 relationships were linear up to the maximal effects, but their slopes (s) differed significantly between agents (p < .05, paired sign test) and increased approximately three-fold in the order norepinephrine (s = 34), epinephrine (s = 54), dobutamine (s = 86), and dopexamine (s = 105). Except for norepinephrine, the catecholamines also increased oxygen delivery more than VO2, so that O2 extraction decreased to 40% below baseline. CONCLUSIONS: Catecholamines are characterized by linear Q/VO2 relationships with drug-specific slopes. All agents (except norepinephrine) increased oxygen delivery more than oxygen demand. For the practice of catecholamine therapy, our experiments imply that synthetic agents such as dobutamine and particularly dopexamine may be preferred in the treatment of low cardiac output states because they increase Q with the least metabolic effects.     

Determination of cardiac output with a modified Fick method using estimated instead of measured oxygen consumption

Cardiac output (CO) was determined with a modification of the Fick method using estimated, instead of measured, oxygen consumption values. This avoids several possible sources of error in connection with air sampling and oxygen content analysis, thus a relaxed, steady state is obtained more easily. Using the thermodilution technique a good correlation with CO values was found (r = 0.92, p less than 0.001). We conclude that the modified Fick method is simple, accurate and offers reproducible CO estimates in the majority of patients.     

The International Sepsis Forum's frontiers in sepsis: High cardiac output should be maintained in severe sepsis

Despite a usually normal or high cardiac output, severe sepsis is associated with inadequate tissue oxygenation, leading to organ failure and death. Some authors have suggested that raising cardiac output and oxygen delivery to predetermined supranormal values may be associated with improved survival. While this may be of benefit in certain patients, bringing all patients to similar, supranormal values, is simplistic. It is much preferable to titrate therapy according to the needs of each individual patient. A combination of variables should be used for this purpose, in addition to a careful clinical evaluation, including not only cardiac output but also the mixed venous oxygen saturation and the blood lactate concentrations. The concept is to assess the adequacy of the cardiac output in patients with severe sepsis, enabling management strategies aimed at optimizing cardiac output to be tailored to the individual patient.     

Continuous cardiac output and mixed venous oxygen saturation monitoring

Continuous assessment of cardiac output and Svo₂ in the critically ill may be helpful in both the monitoring variations in the patient's cardiovascular state and in determining the efficacy of therapy.

Commercially available continuous cardiac output (CCO) monitoring systems are based on the pulsed warm thermodilution technique. In vitro validation studies have demonstrated that this method provides higher accuracy and greater resistance to thermal noise than standard bolus thermodilution techniques. Numerous clinical studies comparing bolus with continuous thermodilution techniques have shown this technique similarly accurate to track each other and to have negligible bias between them. The comparison between continuous thermal and other cardiac output methods also demonstrates good precision of the continuous thermal technique.

Accuracy of continuous oximetry monitoring using reflectance oximetry via fiberoptics has been assessed both in vitro and in vivo. Most of the studies testing agreement between continuous Svo₂ measurements and pulmonary arterial blood samples measured by standard oximetry have shown good correlation. Continuous Svo₂ monitoring is often used in the management of critically ill patients. The most recently designed pulmonary artery catheters are now able to simultaneously measure either Svo₂ and CCO or Svo₂ and right ventricular ejection fraction. This ability to view simultaneous trends of Svo₂ and right ventricular performance parameters will probably allow the clinician to graphically see the impact of volume loading or inotropic therapy over time, as well as the influence of multiple factors, including right ventricular dysfunction, on Svo₂. However, the cost-effectiveness of new pulmonary artery catheters application remains still questionable because no established utility or therapeutic guidelines are available.     

The International Sepsis Forum's frontiers in sepsis: high cardiac output should not be maintained in severe sepsis

Abnormal oxygen utilisation is one of the features of septic shock. Some studies have observed that patients that survive septic shock tend to have higher cardiac output and oxygen delivery compared to those that do not. It has been proposed that higher than normal (or "supra-normal") levels of cardiac output and oxygen deliver should be the goal in the management of septic shock. However, randomised controlled trials have not been able to validate that such a goal provides a mortality or morbidity advantage. In this commentary we discuss the various reasons put forward by the proponents of this strategy and review the available evidence.     

Cardiac output, oxygen consumption and renal blood flow in essential hypertension

Cardiac output, oxygen consumption, total blood volume and mean circulatory transit time were investigated at rest in men with sustained essential hypertension in comparison with normal subjects of the same age and sex. In normal subjects and in patients with hypertension, oxygen consumption was positively correlated to cardiac output. In hypertensives, the slope of the curve was significantly shallower with an increase in arteriovenous oxygen difference. Oxygen consumption in both populations was negatively correlated with mean circulatory transit time but not with total blood volume. In normal subjects, mean circulatory transit time and arteriovenous oxygen difference were positively correlated. The correlation was not significant in hypertensive patients. The study suggests important abnormalities in the transport and cost of energy in erythrocytes of patients with sustained essential hypertension.     

Influence of cardiac output level on oxygen exchange in chronic obstructive pulmonary disease patients

STUDY OBJECTIVES: In the course of chronic obstructive pulmonary disease (COPD), pulmonary gas exchange deteriorates as a result of ventilation/perfusion inequalities and hypoxaemia. The aim of the present study was to evaluate the influence of cardiac output (CO) level observed at rest in COPD patients on interaction between central and peripheral O(2) exchange. METHODS: One hundred and nine patients with advanced but stable COPD were analysed in a retrospective study by the multiple inert gas elimination technique. As a function of CO, simulations were conducted to evaluate the respective part of PvO(2) and VA/Q inequalities on the degree of hypoxaemia. MEASUREMENTS AND RESULTS: PaO(2) was linked (i) to cardiac index (CI), (ii) to mean VA/Q ratio of blood flow distribution and (iii) to PvO(2), but PvO(2) was not correlated with CO. By comparing two groups with CI above and below the mean value of the series respectively, a significant difference was identified in PaO(2) (57 +/- 9 mmHg in the high CI group versus 63 +/- 10 mmHg in the low CI group, P<0.05) because of higher VA/Q inequalities in the high CI group. Comparing two other groups with values of PvO(2) above and below the mean value of the series respectively, a significant difference was identified in PaO(2): (mean +/- SD was 65 +/- 8 in high PvO(2) group versus 56 +/- 9 mmHg, P<0.001) but with no difference in either CI or perfusion distribution. Analysis of the cumulated effects of PvO(2) and CI values, indicated that high CI and low PvO(2) gave rise to the lowest PaO(2) (53 +/- 8 mmHg), with the highest PaO(2) (68 +/- 8 mmHg) being found in the low CI and normal PvO(2) group. CONCLUSIONS: We concluded that in COPD patients, PaO(2) appeared to be maintained better when peripheral gas exchange coped with tissue demand without an increase in CO. Conversely, when the physiological increase in CO could not maintain adequate tissue gas exchange, PaO(2) continued to fall due to the cumulative effects of increasing CO on VA/Q inequalities and low PvO(2).     

Influence of output capacitor, electrode and pulse width on power consumption in cardiac pacing.

Three different types of unipolar endocardial electrodes--47 in all--were compared in regard to power consumption at stimulation threshold with six different output capacitors and seven pulse widths. Fifteen were conventional large surface electrodes (area 47 mm2); 18 were conventional small surface electrodes (area 6 mm2), and 14 had a specially designed tip with a large area but small active surface of 8 mm2. Pulse widths ranged from 0.15 to 2.0 msec and output capacitors from 1.0 to 22.0 microFarads. All in all about 2,000 measurements were performed. The average current drain to the pacemaker output stage was measured and power consumption was calculated for each electrode--pulse width--output capacitor combination. In all combinations, the two small surface electrodes consumed approximately the same amount of power and, in both cases, significantly less than the larger one. With regard to power economy at stimulation threshold, the pulse width of choice was about 0.5 msec and, furthermore, power consumption decreased with increasing capacitor size. The optimal combination was a small surface electrode, an output capacitor of 22 microF and a pulse width of 0.5 msec.     

Non-invasive cardiac output and oxygen delivery measurement in an infant with critical anemia

Objective

To assess the combination of a non-invasive blood oxygen content (CaO₂) monitor and a non-invasive cardiac output (CO) monitor to continuously measure oxygen delivery (DO₂; DO₂ = CaO₂ × CO).

Methods

DO₂ was assessed during blood transfusions in an infant with acute hemolytic anemia following admission (~48 h). CaO₂ was measured by Pulse Co-Oximetry, which also provides estimates of hemoglobin (Hgb) concentration and percent oxygen saturation. CO was measured by Electrical Velocimetry, which also provides an estimate of stroke volume (SV). Lactate levels, an indirect measure of adequate DO₂, were assessed during the initial 8 h following admission.

Results

Incremental blood transfusions during the first 36 h increased Hgb from 2.7 to 9.5 g/dL during which time heart rate (HR) normalized from 156 to 115 beats/min. Lactate levels decreased from 20 to 0.8 mmol/L in the first 7 h. Non-invasive Hgb and CaO₂ measurements were well correlated with invasive Hgb and CaO₂ measures (r ² = 0.88; P = 0.019; r ² = 0.86; P = 0.0074, respectively). CO decreased from 2.47 ± 0.06 to 1.28 ± 0.02 L/min and SV decreased from 15.9 ± 0.4 to 11.1 ± 0.2 mL/beat. Mean arterial blood pressure was stable throughout the admission with systemic vascular resistance increasing from 407.6 ± 15.2 to 887.7 ± 30.1 dynes-s/cm⁵. DO₂ was estimated to increase from 120.2 ± 18.9 to 182.4 ± 5.6 mL O₂/min.

Conclusions

Non-invasive contin- uous CO and CaO₂ monitors are shown in this single case to provide continuous DO₂ measurement. The ability to assess DO₂ may improve hemodynamic monitoring during goal directed therapies.     

Continuous Fick cardiac output compared to thermodilution cardiac output

A system has been developed to monitor continuously the components of the oxygen Fick equation: oxygen consumption by a gas exchange analyzer and arteriovenous oxygen difference by pulse and fiberoptic oximetry. A computer-based system was developed which calculates cardiac output and other variables every 20 sec. Continuous Fick (CF) cardiac output was compared to thermodilution (TD) cardiac output in 21 ventilated post-cardiac surgery patients. A total of 237 simultaneous cardiac output measurements had a range between 2 and 11 L/min. The correlation between CF and TD cardiac outputs was r = .86, with an equation of TD cardiac output = 0.92 CF cardiac output + 1.16. There was a significant (p less than .001) difference between the two methods of cardiac output estimation. The CF method was consistently lower than TD; this difference was greater at lower flows. CF cardiac output measurement is practical; it offers distinct advantages in viewing cardiac output together with oxygen demand and oxygen extraction.     

Effect of flecainide on cardiac output

The effect of intravenous flecainide (2 mg/kg) on cardiac output was evaluated by a dye dilution method in six healthy nonsmokers. The study was of a double-blind, crossover, placebo-controlled, randomized, and balanced design. Cardiac output, heart rate, and stroke volume were measured 0, 10, 30, 60, 90, 120, 150, 180, and 240 minutes after the beginning of the flecainide infusion. Flecainide reduced cardiac output and stroke volume during the first 90 minutes and heart rate increased during the first 30 minutes after flecainide. Visual analog scales for alertness and dry mouth were determined 0, 10, 60, and 240 minutes after dosing. Alertness was reduced 60 minutes after flecainide, but there was no increase in dryness of the mouth.     

氧供耗平衡导向温度管理在小儿心脏手术中的应用

目的研究氧供耗平衡导向温度管理在小儿心脏手术的应用。方法选择该院2013年10月至2017年9月115例心脏手术患儿作为研究对象,将采取氧供耗平衡导向温度管理的55例患儿设为管理组,60例进行常规管理的患儿设为常规组。比较两组的心脏复跳情况、手术情况、不同时段的氧供耗平衡、温度管理、术后情况。结果常规组心脏自动复跳率76.67%(46/60),显著低于管理组心脏自动复跳率89.09%(49/55),差异有统计学意义(均P<0.05)。两组循环时间、体循环最大流量、主动脉阻断时间、手术时间、苏醒时间、机械通气时间比较,差异均无统计学意义(P>0.05)。两组T0的VO2、SpO2、SvO2,T1、T2的SpO2比较,差异均无统计学意义(均P>0.05);常规组T1、T2的VO2显著高于管理组,T1、T2的SvO2显著低于管理组,差异均有统计学意义(均P<0.01)。常规组Tn最低温、Tr最低温显著低于管理组,Tn最高温、Tr最高温显著高于管理组,差异均有统计学意义(均P<0.01);两组累计降温时间、累计复温时间比较,差异均无统计学意义(均P>0.05)。常规组住院时间(9.52±1.56)d,与管理组住院时间(9.78±1.58)d比较,差异无统计学意义(P>0.05)。常规组病死率5.00%,与管理组病死率3.64%比较,差异无统计学意义(P>0.05)。结论氧供耗平衡导向温度管理可在常规管理的基础上,提高患儿心脏自动复跳率,稳定围手术期的体温与组织灌注及耗氧水平,提高小儿心脏手术的安全性。     

Optimization of oxygen transport in mechanically ventilated newborns using oximetry and pulsed Doppler-derived cardiac output

In respiratory distress syndrome (RDS), PEEP improves arterial oxygenation but may impair cardiac output. The effects of PEEP on gas exchange and hemodynamics were studied in 12 mechanically ventilated newborns in the acute phase of RDS. Stepwise increase in PEEP resulted in both a) a progressive increase in PaO2 and transcutaneous oxyhemoglobin saturation, and b) a depression of pulsed Doppler-measured cardiac output that was statistically significant at 9 cm H2O PEEP. Thus, averaged systemic oxygen delivery (DO2) was maintained with improved arterial oxygenation up to 6 cm H2O PEEP. Further increase in PEEP induced a significant fall in DO2. No variation was observed in heart rate and mean arterial pressure. The combined use of oximetry and pulsed Doppler echocardiography enables noninvasive optimization of mechanical ventilation and PEEP during the clinical course.     

Effects of diltiazem on oxygen delivery and consumption after asphyxial cardiac arrest and resuscitation.

BACKGROUND AND METHODS: Calcium-channel blockers may attenuate vasospasm after transient ischemia and improve organ blood flow after resuscitation. Our aim was to assess the effect of diltiazem on systemic oxygen delivery and consumption, hemodynamics, electroencephalogram (EEG), and organ blood flow after restoration of spontaneous circulation. After a 3-min period of asphyxial cardiac arrest, 14 pigs (20 to 27 kg) were randomly allocated to treatment with either diltiazem (0.1 mg/kg bolus followed by an iv infusion of 0.025 mg/min/kg over 120 mins) or placebo, given at 5 mins after successful resuscitation. Organ blood flow was measured using tracer microspheres 120 mins after resumption of spontaneous circulation. RESULTS: Median systemic oxygen delivery index values at 30, 60, and 120 mins after restoration of spontaneous circulation were 18.2 mL/min/kg (range 14.8 to 20.7), 16.8 mL/min/kg (13.2 to 20.8), and 19.6 mL/min/kg (16.9 to 21.0), respectively, in the diltiazem group and 13.1 mL/min/kg (11.2 to 14.6), 11.9 mL/min/kg (10.3 to 13.3), and 14.7 mL/min/kg (11.4 to 17.2), respectively, in the control group (p less than .05 for all three comparisons). At the same points in time, median systemic oxygen consumption indices were 3.2 mL/min/kg (range 2.2 to 3.7), 2.1 mL/min/kg (1.9 to 3.0), and 2.6 mL/min/kg (1.8 to 3.8) in the diltiazem group and 2.8 mL/min/kg (2.1 to 4.0), 2.7 mL/min/kg (1.7 to 4.3), and 2.3 mL/min/kg (1.6 to 3.8) in the placebo group (NS). Diltiazem enhanced the postarrest recovery of EEG total power. Right and left cerebral blood flow 120 mins after restoration of spontaneous circulation was significantly (p less than .01) higher in the diltiazem group in comparison with the control group. CONCLUSIONS: Diltiazem causes an increase in systemic oxygen delivery index by promoting vasodilation, but it does not change systemic oxygen consumption index in comparison to placebo treatment. It may be that an impairment in local autoregulation and/or in oxidative metabolism at the cellular or subcellular level was the reason why diltiazem did not improve these derangements. The observed increase in cerebral blood flow and in EEG recovery may be beneficial to the brain after a period of asphyxia.