Systemic Oxygen Consumption Research Articles

Spontaneous Ear Hemorrhage During Cardiac Surgery

A 79-year-old patient who underwent mitral valve replacement experienced prolonged elevated central venous pressure associated with poor venous return during a cardiopulmonary bypass. After the procedure, the patient was noted to have spontaneous bleeding from the left ear. Otolaryngologic examination in the operating room showed no trauma in the exterior auditory canal and suggested that the hemorrhage was related to a superior vena cava syndrome and anticoagulation during the cardiopulmonary bypass. Determinants and management considerations of poor venous return, including maintenance of cerebral perfusion pressure, are discussed.

Free Fatty Acids and Delayed Cerebral Ischemia After Subarachnoid Hemorrhage

The purpose of this study was to understand factors related to increases in serum free fatty acid (FFA) levels and association with delayed cerebral ischemia (DCI) after subarachnoid hemorrhage. We performed serial measurement of systemic oxygen consumption by indirect calorimetry and FFA levels by liquid chromatography/mass spectrometry in the first 14 days after ictus in 50 consecutive patients with subarachnoid hemorrhage. Multivariable generalized estimating equation models identified associations with FFA levels in the first 14 days after SAH and Cox proportional hazards model used to identified associations with time to DCI. There were 187 measurements in 50 patients with subarachnoid hemorrhage (mean age, 56±14 years old; 66% women) with a median Hunt-Hess score of 3. Adjusting for Hunt-Hess grade and daily caloric intake, n-6 and n-3 FFA levels were both associated with oxygen consumption and the modified Fisher score. Fourteen (28%) patients developed DCI on median postbleed Day 7. The modified Fisher score (P=0.01), mean n-6:n-3 FFA ratio (P=0.02), and mean oxygen consumption level (P=0.04) were higher in patients who developed DCI. In a Cox proportional hazards model, the mean n-6:n-3 FFA ratio (P<0.001), younger age (P=0.05), and modified Fisher scale (P=0.004) were associated with time to DCI. Injury severity and oxygen consumption hypermetabolism are associated with higher n-FFA levels and an increased n-6:n-3 FFA ratio is associated with DCI. This may indicate a role for interventions that modulate both oxygen consumption and FFA levels to reduce the occurrence of DCI.

The relationship between plasma concentrations of ionized calcium and magnesium with cardiac energetics and systemic oxygen transport in neonates after the Norwood procedure

We sought to determine the relationship between plasma calcium and magnesium concentrations with postoperative systemic hemodynamics and oxygen transport in neonates after the Norwood procedure. Postoperative systemic oxygen consumption was continuously measured using respiratory mass spectrometry for 72 hours in 17 neonates. Arterial, superior vena caval and pulmonary venous blood gases and pressures, plasma calcium, and lactate levels were measured at 2- to 4-hour intervals to calculate cardiac output, rate pressure product, cardiac power output, systemic oxygen delivery, and oxygen extraction ratio. Plasma magnesium levels were measured at 2- to 8-hour intervals. Plasma calcium levels decreased in the first 8 hours from 1.08±0.13 mmol/L to 0.98±0.08 mmol/L, followed by an increase to 1.10±0.26 mmol/L at 72 hours (P<.0001). Mg2þ change was significantly related to time after logarithmic transformation, rapidly decreasing from 1.62±0.25 mg/L to 0.90±0.15 mg/L in the first 40 hours and further decreasing slowly thereafter to 0.64±0.13 mg/L at 72 hours (P<.0001). Plasma magnesium levels had a significant positive correlation with cardiac output (P=.008) and cardiac power output (P=.01), and a negative correlation with heart rate (P=.05). Plasma magnesium levels correlated positively with systemic oxygen delivery and negatively with systemic oxygen consumption (P=.08 for both), resulting in significant negative correlations with oxygen extraction ratio (P=.04) and lactate levels (P=.05). For a given cardiac power output, plasma magnesium showed a significantly negative correlation with rate pressure product (P=.01). Plasma calcium levels showed the opposite trend, which was statistically insignificant except for lactate (P=.007). Plasma magnesium may exert favorable effects on myocardial energetics and systemic oxygen transport in neonates after the Norwood procedure, whereas plasma calcium may be harmful. Maintaining a relatively high level of plasma magnesium and a low level of plasma calcium may improve myocardial work efficiency and the balance of systemic and myocardial oxygen transport.

Effect of acute hyperventilation on the venous-arterial PCO2 difference

I read with great interest the article by Morel et al. [1], suggesting that acute changes in the arterial partial pressure of carbon dioxide (PaCO2) can affect the venous-arterial difference in carbon dioxide tension ([increment]CO2). Ten ventilated and hemodynamically stable patients were included after elective cardiac surgery. Hypocapnia was induced by increasing of respiratory rate. The authors found that a decrease of PaCO2 was associated with a significant increase in [increment]CO2. This was explained by the fact that acute hypocapnia resulted in systemic vasoconstriction, thus decreasing the elimination of the total CO2 produced by the peripheral tissues, and therefore increased the gap. However, as all patients were monitored with a pulmonary artery catheter (PAC), the authors should have shown if there were any increase in systemic vascular resistance to support their hypothesize. Furthermore, there is a possible another explanation of the increase of [increment]CO2 induced by the decrease in PaCO2. Indeed, acute respiratory alkalosis has been shown to increase systemic oxygen consumption and CO2 production [2,3]. Thus, for a given venous blood flow the increase of tissue CO2 production should increase the PCO2 gap.

Low central venous oxygen saturation is associated with increased mortality in critically ill dogs

To investigate relationships between central venous oxygen saturation (ScvO(2)) and survival to hospital discharge in dogs. Central venous oxygen saturation is an accessible measure of the balance between systemic oxygen delivery and consumption. Prospective observational cohort study, enrolling 126 client-owned dogs with central venous catheters. Central venous oxygen saturation was measured over the 24 hours following intensive care unit admission. Poor outcome was defined as death or euthanasia performed for moribund status. Regression analysis identified independent predictors of non-survival and physiologic parameters associated with central venous oxygen saturation. Area under the receiver operator curve analysis identified a cut-off point of central venous oxygen saturation, below which central venous oxygen saturation decrease was associated with increased mortality risk. Mortality risk was 30·9%. Low central venous oxygen saturation was associated with poor outcome (P<0·05). Area under the receiver operator curve analysis selected a central venous oxygen saturation of 68% as the point below which a fall in central venous oxygen saturation was associated with increased mortality risk. For each 10% drop in central venous oxygen saturation below 68%, odds of non-survival increased by 2·66 times (P=0·0002, 95% confidence interval of odds ratio=1·45 to 4·85). Central venous oxygen saturation was equivalent to lactate in predicting non-survival. Predictors of central venous oxygen saturation (packed cell volume, mean arterial blood pressure, fever, % arterial haemoglobin saturation as measured by pulse oximeter) were consistent with hypothesised physiologic mechanisms. Central venous oxygen saturation was a strong mortality predictor. Further work is needed to determine if therapy targeting central venous oxygen saturation can reduce mortality in canine intensive care unit patients.

Relationship Between C-Reactive Protein, Systemic Oxygen Consumption, and Delayed Cerebral Ischemia After Aneurysmal Subarachnoid Hemorrhage

Subarachnoid hemorrhage (SAH) is known to result in elevated systemic oxygen consumption (Vo(2)) and increases in high-sensitivity C-reactive protein (hsCRP), although the relationship among hsCRP, Vo(2), and delayed cerebral ischemia (DCI) after SAH remains unknown. We hypothesized that hsCRP is directly associated with Vo(2) and that elevated Vo(2) is a predictor of DCI after SAH. Prospective serial assessments of Vo(2) and hsCRP over 4 prespecified time periods during the first 14 days after bleed in consecutive SAH patients admitted to a single academic medical center for a 2-year period. One hundred ten SAH patients met study criteria (mean age, 55±16 years; 62% women), with a median admission Hunt Hess grade of 3 (interquartile range, 2-4). In multivariate generalized estimating equation model of the first 14 days after bleed, Vo(2) was associated with younger age (P=0.01), male gender (P=0.01), and hsCRP levels (P=0.03). Twenty-four (22%) patients had DCI develop, with a median onset on day 7 after bleed (interquartile range, 5-11). The mean Vo(2) (291±65 mL/min versus 226±55 mL/min; P=0.003) was higher in DCI patients. In a multivariable Cox proportional hazards model, younger age (hazard ratio, 1.2 per 5 years; 95% CI, 1.1-1.3), a higher modified Fisher scale score (hazard ratio, 3.4 per 1-point increase; 95% CI, 1.7-6.9), and higher Vo(2) (HR, 1.2 per 50-mL/min increase; 95% CI, 1.1-1.3) were predictive of DCI. Systemic oxygen consumption is associated with hsCRP levels in the first 14 days after SAH and is an independent predictor of DCI.

The cerebral critical oxygen threshold of ventilated preterm lambs and the influence of antenatal inflammation

Perinatal inflammation is associated with adverse neurodevelopmental outcomes, which may be partly due to changes in the cerebral oxygen delivery/consumption relationship. We aimed to determine the critical oxygen delivery threshold of the brain of preterm, ventilated lambs and to determine whether the critical threshold is affected by exposure to inflammation in utero. Pregnant ewes received intra-amniotic injection of lipopolysaccharide or saline at 125 or 127 days of gestation. Pulmonary and systemic flow probes and catheters were surgically positioned in the fetus immediately before delivery at 129 days of gestation. After delivery, lambs were ventilated for 90 min using a positive end-expiratory pressure recruitment strategy. Cardio-respiratory variables and blood gases were measured regularly. Systemic and cerebral oxygen delivery, consumption (Fick), and extraction were calculated, and the relationship between cerebral delivery and consumption analyzed. Linear regression was used to define the transition or "critical" oxygen threshold as the point at which the slope of the oxygen delivery/consumption curve changed to be > 10°. Four subgroups were defined according to the calculated critical threshold. A total of 150 measurements were recorded in 18 lambs. Fetal cerebral oxygen consumption was increased by antenatal lipopolysaccharide (P < 0.05). The postnatal critical oxygen threshold was 3.6 ml·kg⁻¹·min⁻¹, corresponding to cerebral oxygen consumption of 0.73 ml·kg⁻¹·min⁻¹. High oxygen delivery and consumption were associated with increased pulmonary and carotid blood flow and systemic extraction compared with low oxygen delivery and consumption. No postnatal effect of antenatal inflammation was observed. Inflammation in utero increases fetal, but not postnatal, cerebral oxygen consumption. Adverse alterations to pulmonary blood flow can result in reduced cerebral blood flow, oxygen delivery, and consumption. Regardless of exposure to inflammation, there is a consistent postnatal relationship between cerebral oxygen delivery and consumption.

Dynamic changes of myocardial oxygen consumption at pacing increased heart rate – the first observation by the continuous measurement of systemic oxygen consumption

Objectives. To assess dynamic changes in myocardial oxygen consumption (myoVO2) during atrial pacing increased heart rate by continuous measurement of systemic oxygen consumption (sysVO2). Methods. Six mechanically ventilated pigs were atrially paced to increase heart rate from baseline 98 ± 9 to 120-140-160-180 bpm for 10 minutes at each stage, with 10 minute intervals without pacing between stages. sysVO2 was continuously measured with a respiratory mass spectrometer. Left anterior descending coronary arterial flow, aorta and coronary sinus blood gases were measured to calculate index of whole heart myoVO2. Results. sysVO2 peaked at the initiation of pacing in the first two to three minutes, followed by a decrease and subsequent stabilization. As heart rate increased, sysVO2 increased by 0.08 ± 0.06 ml/kg/min, 0.14 ± 0.05 ml/kg/min and 0.17 ± 0.10 ml/kg/min, representing a 1.2 ± 0.9%, 2.1 ± 0.7% and 3.0 ± 1.8% increase of sysVO2 respectively; myoVO2 increased by 0.16 ± 0.12 to 0.31 ± 0.14 to 0.36 ± 0.24 ml/100 g/min, representing a 11 ± 9%, 21 ± 9% and 26 ± 12% increase of myoVO2, respectively. The absolute and relative increases in sysVO2 were significantly correlated with the increases in myoVO2. Conclusions. On-line continuous sysVO2 monitoring by respiratory mass spectrometry allows non-invasive assessments of dynamic changes in myoVO2 in vivo. The mechanism for the peaked increase in sysVO2 at the initiation of pacing remains to be explored.

Effects of catecholamines on hepatic and skeletal muscle mitochondrial respiration after prolonged exposure to faecal peritonitis in pigs

Use of norepinephrine to increase blood pressure in septic animals has been associated with increased efficiency of hepatic mitochondrial respiration. The aim of this study was to evaluate whether the same effect could be reproduced in isolated hepatic mitochondria after prolonged in vivo exposure to faecal peritonitis. Eighteen pigs were randomized to 27 h of faecal peritonitis and to a control condition (n = 9 each group). At the end, hepatic mitochondria were isolated and incubated for one hour with either norepinephrine or placebo, with and without pretreatment with the specific receptor antagonists prazosin and yohimbine. Mitochondrial state 3 and state 4 respiration were measured for respiratory chain complexes I and II, and state 3 for complex IV using high-resolution respirometry, and respiratory control ratios were calculated. Additionally, skeletal muscle mitochondrial respiration was evaluated after incubation with norepinephrine and dobutamine with and without the respective antagonists (atenolol, propranolol and phentolamine for dobutamine). Faecal peritonitis was characterized by decreasing blood pressure and stroke volume, and maintained systemic oxygen consumption. Neither faecal peritonitis nor any of the drugs or drug combinations had measurable effects on hepatic or skeletal muscle mitochondrial respiration. Norepinephrine did not improve the efficiency of complex I- and complex II-dependent isolated hepatic mitochondrial respiration [respiratory control ratio (RCR) complex I: 5.6 ± 5.3 (placebo) vs. 5.4 ± 4.6 (norepinephrine) in controls and 2.7 ± 2.1 (placebo) vs. 2.9 ± 1.5 (norepinephrine) in septic animals; RCR complex II: 3.5 ± 2.0 (placebo) vs. 3.5 ± 1.8 (norepinephrine) in controls; 2.3 ± 1.6 (placebo) vs. 2.2 ± 1.1 (norepinephrine) in septic animals]. Prolonged faecal peritonitis did not affect either hepatic or skeletal muscle mitochondrial respiration. Subsequent incubation of isolated mitochondria with norepinephrine and dobutamine did not significantly influence their respiration.

Vasopressor Agents After Experimental Brain Death: Effects of Dopamine and Vasopressin on Vitality of the Small Gut

Background Both congenital and acquired short bowel syndrome frequently leads to the necessity for long-term parenteral nutrition, which in turn may lead to any of several complications or death. Transplantation of the small bowel from brain-dead organ donors has been successfully performed over the last years. However, systemic blood pressure and blood perfusion to the splanchnic area decrease rapidly after brain death, which comprises the vitality of the small bowel. Objective To evaluate the differences between dopamine and low-dose vasopressin on perfusion and vitality of the small bowel after brain death. Methods Fifteen pigs were randomized into 3 groups: vasopressin (n = 6), dopamine (n = 6), or control (n = 3). Brain death was induced via stepwise filling of an epidural balloon. When the hypotensive phase was achieved, vasopressin, maximum dose of 0.04 IU/kg/h, or dopamine, maximum dose of 20 μg/kg/min, was administered for 5 hours with the objective of increasing mean arterial blood pressure by 15 mm Hg. Results Target blood pressure was achieved in the vasopressin group but not the dopamine group. Vasopressin reduced cardiac output, superior mesenteric artery (SMA) blood flow and oxygen delivery, and systemic oxygen delivery and consumption, and increased oxygen extraction. Dopamine increased SMA blood flow, and had no effect on systemic oxygen delivery or consumption. Conclusions Vasopressin reversed hypotension but compromised both the systemic and SMA blood flow. Vasopressin was associated with inadequate oxygen delivery, estimated from decreased oxygen delivery and increased oxygen extraction. These adverse effects were not observed with dopamine.

Hepatosplanchnic Vasoregulation and Oxygen Consumption During Selective Aortic Blood Flow Reduction and Reperfusion

Several studies have shown that the distribution of cardiac output to the intra-abdominal organs may vary during low-flow states. In this study, we developed an experimental model to selectively reduce the abdominal aortic blood flow in order to assess the initial impact of selective hepatosplanchnic hypoperfusion on regional blood flow redistribution. Eight anesthetized and mechanically ventilated mongrel dogs were subjected to aortic blood flow reduction with an occluder in a stepwise manner by 50% and 100% for 45 min. After the ischemic period, the occluder was released, and animals were observed for an additional 45 min. Systemic hemodynamics were evaluated through a Swan-Ganz and arterial catheters, and gastrointestinal tract perfusion was evaluated by portal vein and hepatic arterial blood flows measurements (ultrasonic flowprobe). Intestinal O2-derived variables, intestinal mucosal (tonometric)-arterial and tonometric-(end-tidal-carbon-dioxide) gradients (Dt-apCO2 and Dt-EtpCO2) were also calculated. No significant changes in systemic and regional oxygen consumption were observed during the 50% reduction of aortic blood flow. On the other hand, both microregional pCO2 gradients (Dt-apCO2 e Dt-EtpCO2) showed a significant increase during this period. Aortic occlusion was associated with a marked reduction of systemic and regional oxygen delivery and consumption. During the reperfusion, no significant improvement in the tonometry-based pCO2 gradients was observed, in spite of the partial reestablishment of blood flow to the hepatosplanchnic territory. During selective intra-abdominal low-flow, a proportional reduction in the splanchnic and hepatic blood flows occurs. A selective reduction of approximately 50% in splanchnic oxygen delivery was not associated with significant changes in macroregional markers of hypoperfusion. In this situation, tonometry-based pCO2 gradients can be used for the assessment of hepatosplanchnic perfusion and histologic changes.

Utility Of Near Infrared Spectroscopy (nirs) Guided Tilt Table Testing.

Syncope is transient loss of consciousness. Neurocardiogenic syncope is the most common cause of syncope. Confirmation of the diagnosis of syncope is based on the head-up tilt table test. Near-infrared spectroscopy (NIRS) is a monitor of regional oxygenation and is helpful in predicting cerebral and renal ischemia. PURPOSE: Determine if multi-site NIRS monitoring will reveal differential desaturation patterns in the brain and renal vascular beds during postural stresses. METHODS: All patients (7-21 years old) scheduled to undergo tilt table testing were recruited. NIRS measurements were obtained at the forehead and above the left paravertebral level at the T10 to L1space. Tissue saturations (rSO2) were recorded at rest, during tilt test and throughout recovery. All data routinely obtained during tilt table testing (i.e. HR, BP) were included in the research database. RESULTS: 20 patients were recruited. Average age of the group was 12.9 years. 7 patients had a positive tilt table test. Patients with syncope had rSO2 trends distinctly different form non-fainters. In these patients, cerebral rSO2 shows a sudden abrupt decrease from hypo perfusion, which was followed by various progressive clinical symptoms. Cerebral rSO2 trend was paralleled by a dramatic increase in renal rSO2. These rSO2 trends are progressive until patient is returned to supine position with normalization of rSO2 thereafter. CONCLUSION: Multi-site NIRS guided tilt table testing revealed dramatic desaturation patterns in the vascular beds during postural gravitational stresses that preceded physiologic symptoms. These patterns underlie the systemic oxygen consumption to flow-coupling dynamics observed during syncope.

Oxygen transport characterization of a human model of progressive hemorrhage

Background Hemorrhage continues to be a leading cause of death from trauma sustained both in combat and in the civilian setting. New models of hemorrhage may add value in both improving our understanding of the physiologic responses to severe bleeding and as platforms to develop and test new monitoring and therapeutic techniques. We examined changes in oxygen transport produced by central volume redistribution in humans using lower body negative pressure (LBNP) as a potential mimetic of hemorrhage. Methods and results In 20 healthy volunteers, systemic oxygen delivery and oxygen consumption, skeletal muscle oxygenation and oral mucosa perfusion were measured over increasing levels of LBNP to the point of hemodynamic decompensation. With sequential reductions in central blood volume, progressive reductions in oxygen delivery and tissue oxygenation and perfusion parameters were noted, while no changes were observed in systemic oxygen uptake or markers of anaerobic metabolism in the blood (e.g., lactate, base excess). While blood pressure decreased and heart rate increased during LBNP, these changes occurred later than the reductions in tissue oxygenation and perfusion. Conclusions These findings indicate that LBNP induces changes in oxygen transport consistent with the compensatory phase of hemorrhage, but that a frank state of shock (delivery-dependent oxygen consumption) does not occur. LBNP may therefore serve as a model to better understand a variety of compensatory physiological changes that occur during the pre-shock phase of hemorrhage in conscious humans. As such, LBNP may be a useful platform from which to develop and test new monitoring capabilities for identifying the need for intervention during the early phases of hemorrhage to prevent a patient's progression to overt shock.

Near Infrared Spectroscopy: Guided Tilt Table Testing for Syncope

Syncope is transient loss of consciousness. Neurocardiogenic syncope (NCS) is the most common cause of syncope. Head-up tilt-table test (HUTT) has been used to demonstrate physiologic events during graded orthostatic challenge in individuals with significant handicap from NCS. Near-infrared spectroscopy (NIRS) provides a noninvasive, continuous method to monitor trends of regional tissue oxygenation (rSO2). We hypothesize that multisite NIRS monitoring will show differential desaturation patterns in the brain and renal vascular beds during postural stresses. All patients age 7-21 years old scheduled to undergo HUTT were recruited. Two probes for NIRS monitoring were placed on the forehead and above the left paravertebral level at the T10 to L1 space. These leads were attached to the Somanetics monitor (Somanetics, Troy MI). Tissue saturations (rSO2) obtained at two sites were recorded at rest, during the test, and throughout a 5-min recovery period. All data routinely obtained in HUTT were included in the research study database. Thirteen patients were recruited. The average age was 12.9 years. Five patients had a positive tilt-table test. The patients with syncope had rSO2 trends distinctly different from the normal subjects. In these patients, cerebral rSO2 showed a sudden decreasing trend from hypoperfusion, soon followed by various clinical symptoms. The cerebral rSO2 trend, which showed a dramatic increase, was paralleled by renal rSO2. These rSO2 trends were progressive until the patient was brought back to the supine position, which resulted in the rSO2 in both beds returning to baseline. Multisite NIRS-guided HUTT shows differential trends in the different vascular beds during postural gravitational stresses, and these patterns underlie the systemic oxygen consumption to flow-coupling dynamics observed during syncope.

Another explanation for decreased oxygen consumption in lactic acidosis

In their recent paper, Protti and colleagues reported depressed oxygen consumption in patients with lactic acidosis due to biguanide intoxication and they suppose that the cause is inhibited mitochondrial respiration [1]. Another explanation for depressed oxygen consumption in these patients is also possible, however. If the blood pH is very low, glucose utilization is decreased [2] because the glycolytic enzyme phosphofructokinase is pH dependent - with decreasing pH, its activity is also decreasing [3]. Glucose utilization is an oxygen-consuming process: The consequence of decreased utilization of glucose is thus also decreased oxygen consumption. The patients reported by Protti and colleagues had on admission very low blood pH of 6.93 ± 0.20 and systemic oxygen consumption of 67 ± 28 ml/min/m2 [1]. Systemic oxygen consumption 'normalized within the next 48-72 hours' and 'Systemic O2 consumption was positively associated with arterial pH' (P < 0.001). According to Tables 2 and 3 [1], arterial pH reached normal values on days 2 to 3. Depressed oxygen consumption in patients reported by Protti and colleagues can thus be explained by their very low blood pH.

Enteral Nutrition and Cardiovascular Failure: From Myths to Clinical Practice

Cardiovascular failure and low flow states may arise in very different conditions from both cardiac and noncardiac causes. Systemic hemodynamic failure inevitably alters splanchnic blood flow but in an unpredictable way. Prolonged low splanchnic blood flow causes intestinal ischemia, increased mucosal permeability, endotoxemia, and distant organ failure. Mortality associated with intestinal ischemia is high. Why would enteral nutrition (EN) be desirable in these complex patients when parenteral nutrition could easily cover energy and substrate requirements? Metabolic, immune, and practical reasons justify the use of EN. In addition, continuous enteral feeding minimizes systemic and myocardial oxygen consumption in patients with congestive heart failure. Further, early feeding in critically ill mechanically ventilated patients has been shown to reduce mortality, particularly in the sickest patients. In a series of cardiac surgery patients with compromised hemodynamics, absorption has been maintained, and 1000-1200 kcal/d could be delivered by enteral feeding. Therefore, early EN in stabilized patients should be attempted, and can be carried out safely under close clinical monitoring, looking for signs of incipient intestinal ischemia. Energy delivery and balance should be monitored, and combined feeding considered when enteral feeds cannot be advanced to target within 4-6 days.

Diurnal Increase In Muscle Power Is Not Sustained For Repeated Sprints.

Maximal muscle power during a cycling sprint is know to be higher in the afternoon than in the morning. This diurnal variation still exists after an active warm-up but disappears if maximal sprints have to be repeated, suggesting a higher fatigability in the afternoon. PURPOSE: To investigate if the higher power decrement observed in the afternoon is the due to higher fatigability. METHODS: 8 subjects randomly performed a repeated-sprint test [10 x (6 s of maximal cycling sprint + 30 s of rest)] on three occasions [8-10 am, 5-7 pm and 5-7 pm but with a submaximal initial power for the 2 first sprints]. Muscle power, oxygen consumption, muscle oxygenation and muscle electrical activity were recorded. RESULTS: Power production was significantly higher for sprints 1, 2 and 3 in the afternoon as compared to the morning (e.g. 21.2 ±1 vs 23.3 ±1 W.Kg-1 for sprint 1 in the morning and afternoon respectively, P < 0.01). However, power decrement throughout the repetition of sprint was also higher in the afternoon and there were no differences during the five final sprints (e.g. 19.7 ±1 vs 20.4 ±1 W.Kg-1 for sprint 10 in the morning and afternoon respectively). When controlling for the diurnal difference between the two first sprints, subject were still able to produce higher muscle power in the afternoon than in the morning for sprints 3 to 6 (all P < 0.05) and power didn't decrease (e.g., 20.7 ±1 vs 20.5 ±1 W.Kg-1 for sprint 1 vs sprint 10). Both the muscle deoxygenation ([HHb]) and the systemic oxygen consumption increased during the exercise (P < 0.05), but without effect of time of day. The RMS activity of the Vastus Lateralis decreased during the exercise (P < 0.05), but without effect of time-of-day. CONCLUSIONS: Maximal initial power was higher in the afternoon than the morning and power decrement was higher in the afternoon if the sprints are to be repeated. In addition: 1) if the initial power production is matched in the afternoon with the morning value, there were no power decrement with repeated sprints; and 2) systemic oxygen consumption, muscle deoxygenation and muscle electrical activity were sensitive to fatigue but without effect of time-of-day. Collectively, these data showed that fatigability is not higher in the afternoon but that the beneficial effect of time-of day on muscle power is not sustained for repeated sprints.

Central venous oxygen saturation monitoring

It has been established that mixed venous oxygen saturation (Svo2) reflects the balance between systemic oxygen delivery and consumption. Literature indicates that it is a valuable clinical indicator and has good prognostic value early in patient course. This article aims to establish the usefulness of Svo2 as a clinical indicator. A secondary aim was to determine whether central venous oxygen saturation (Scvo2) and Svo2 are interchangeable. Of particular relevance to cardiac nurses is the link between decreased Svo2 and cardiac failure in patients with myocardial infarction, and with decline in myocardial function, clinical shock and arrhythmias. While absolute values Scvo2 and Svo2 are not interchangeable, Scvo2 and Svo2 are equivalent in terms of clinical course. Additionally, Scvo2 monitoring is a safer and less costly alternative to Svo2 monitoring. It can be concluded that continuous Scvo2 monitoring should potentially be undertaken in patients at risk of haemodynamic instability.

Systemic and microcirculatory responses to progressive hemorrhage

To compare systemic hemodynamics with microcirculatory changes at different vascular beds during progressive hemorrhage. University-based research laboratory. Twelve anesthetized, mechanically ventilated sheep. Sheep were randomly assigned to HEMORRHAGE or CONTROL group. In the HEMORRHAGE group (n = 8), three stepwise bleedings of 5 ml/kg at 30-min intervals were performed to add up 15 ml/kg. In the CONTROL group (n = 4), sheep had the same surgical preparation but were not bled. Progressive bleeding decreased cardiac output, and superior mesenteric artery blood flow, and systemic and intestinal oxygen transports from the first step of bleeding whereas systemic and intestinal oxygen consumption remained unchanged. Mean arterial blood pressure, arterial pH and base excess, and intramucosal-arterial PCO(2) were only significantly modified in the last step of bleeding. Arterial lactate increased and sublingual, and intestinal serosal and mucosal capillary microvascular flow indexes and red blood cell velocities progressively decreased after the first step of bleeding (3.0 +/- 0.1 vs. 2.3 +/- 0.4, 3.2 +/- 0.2 vs. 2.4 +/- 0.6, 3.0 +/- 0.0 vs. 2.0 +/- 0.2, and 1,082 +/- 29 vs. 977 +/- 79, 1,042 +/- 24 vs. 953 +/- 60, 287 +/- 65 vs. 262 +/- 16 mum/s; P < 0.05 for all). Alterations in sublingual, intestinal microcirculation, and arterial lactate simultaneously arose from the first step of bleeding. The microcirculatory changes were identified either by semi-quantitative flow index or by quantitative red blood cell velocity measurements.

Hemodynamics and metabolic studies on septic shock in patients with acute liver failure

Backgrounds Acute liver failure is often accompanied by hyperdynamic circulation, which is also a characteristic of septic shock. Pre-existing acute liver failure may worsen the hemodynamic impairment and prognosis in sepsis. Aims To evaluate the hemodynamic and metabolic characteristics and clinical outcomes of septic shock in patients with acute liver failure. Methods Twenty patients with acute liver failure and 19 patients without preexisting liver disease were evaluated. Systemic hemodynamics, arterial and mixed vein blood gases, arterial lactate levels, plasma renin activity, and plasma aldosterone levels were checked during the early phase of septic shock. Results In acute liver failure group, cardiac index (4.92 ± 1.13 vs 3.69 ± 1.06 L/min per square meter, P < .001) and oxygen delivery (604.7 ± 139.7 vs 485.4 ± 137.3 mL/min per square meter, P = .011) were significantly higher than those without preexisting liver diseases, while systemic vascular resistance index (1041.2 ± 503.3 vs 1409 ± 505.25 dyne·s/cm 5·m 2), oxygen consumption (119.1 ± 29.2 vs 162.4 ± 49.4 mL/min per square meter) and oxygen extraction ratio (20% ± 6% vs. 32% ± 8%) were significantly higher in the latter group. Furthermore, the patients with acute liver failure had higher arterial lactate ( P = .026), plasma renin activity ( P = .03), plasma aldosterone levels ( P < .001), and intensive care unit as well as hospital mortality rates ( P = .005, and 0.02 respectively). Conclusions In patients with acute liver failure, septic shock was characterized by an accentuated hyperdynamic circulation, hyperlactatemia and an augmented renin-angiotensin-aldosterone system activity. Pre-existing liver failure has a significant impact on the disease severity of septic shock and portends a grave prognosis.