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J Takala

Publications and source records attributed to J Takala.

At least 163 records · Page 9Linked to original sources

Peripheral and liver tissue oxygen tensions in hemorrhagic shock.

BACKGROUND AND METHODS: Hepatic dysfunction after severe hemorrhagic shock is common and may be a consequence of visceral tissue hypoxia. Peripheral tissue PO2 has been suggested to correlate with the development of visceral hypoxia. To test the hypothesis that changes in peripheral tissue PO2 reflect changes in hepatic PO2, we measured subcutaneous PO2, transcutaneous PO2, transconjunctival PO2, and liver tissue PO2, and their relationship with changes in mean arterial blood pressure (MAP) and systemic oxygen transport (DO2), during progressive bleeding in pigs (n = 23). In addition to the tissue PO2, portal vein PO2 and circulating lactate concentrations were also measured in six of the animals. The animals were anesthetized and bled to an MAP of 50 mm Hg within 1 hr. RESULTS: After an induced 10% reduction of MAP, only the DO2 decreased significantly (p less than .05). After a 20% reduction of MAP, the DO2 decreased further and was associated with a significant (p less than .05) reduction of all peripheral tissue PO2 values. A significant (p less than .05) reduction of liver tissue PO2 was observed later during bleeding, after induction of a 30% reduction in MAP. In the subgroup with portal venous PO2 and lactate measurements, reductions of all peripheral tissue PO2 and portal venous PO2 values occurred after a 20% reduction (p less than .05) of MAP. An increase (p less than .05) in the portal venous lactate concentration was observed after a 50% reduction of MAP, and a decrease (p less than .05) in liver tissue PO2 was noted after a 60% reduction of MAP. CONCLUSIONS: Reductions of both peripheral and portal venous PO2 values occur early during hemorrhage. The liver tissue PO2, though initially low, appears to be better defended, suggesting either redistribution of splanchnic blood flow or adaptation in hepatic oxygen demand.

Animals↗

Does the anesthetic method influence the postoperative breathing pattern and gas exchange in hip surgery? A comparison between general and spinal anesthesia.

We studied the effects of elective hip surgery, performed under either spinal (SA, n = 10) or general anesthesia (GA, n = 10), on breathing pattern and gas exchange. Measurements were made with respiratory inductive plethysmograph and indirect calorimetry in two positions before and after surgery. The method of anesthesia had no effect on the severity of postoperative hypoxemia. Reduced arterial oxygenation (PaO2; P less than 0.001, SA from 12.5 +/- 2.37 kPa to 10.5 +/- 1.38 kPa, GA from 12.5 +/- 2.95 kPa to 10.5 +/- 1.75 kPa) despite increased alveolar ventilation (P less than 0.01; from 2.30 +/- 0.37 l/min to 2.39 +/- 0.43 l/min in SA, 2.27 +/- 0.56 l/min to 2.57 +/- 0.35 l/min in GA) and reduced arterial carbon dioxide partial pressure (PaCO2; SA from 5.20 +/- 0.22 kPa to 4.95 +/- 0.33 kPa, P less than 0.01, GA from 5.07 +/- 0.36 kPa to 4.72 +/- 0.41 kPa, P less than 0.05) indicated maldistribution of ventilation and perfusion. Changes in breathing pattern and gas exchange and differences between the groups were minimal. Minute ventilation, tidal volume and mean inspiratory flow remained unchanged in both groups. The contribution of rib cage to tidal volume increased postoperatively in the supine position (P less than 0.001; SA from 32.6% +/- 10.3 to 46.3% +/- 7.5, GA from 36.5 +/- 16.4 to 48.5% +/- 15.4). CO2 production, oxygen consumption and energy expenditure remained unchanged. The postoperative changes in breathing pattern are related to the operation, not to the type of anesthesia and do not explain the alterations in gas exchange.

Adult↗

Effect of tidal volume on gas exchange and oxygen transport in the adult respiratory distress syndrome.

The effect of tidal volume (VT) on gas exchange and oxygen delivery (DO2) was studied in nine patients with adult respiratory distress syndrome (ARDS) and in 10 postoperative open-heart surgery patients (CABG). During controlled mechanical ventilation, VT was initially 10 to 12 ml/kg, followed by an increase and reduction of 25% (1.25 VT and 0.75 VT, respectively). In both groups of patients, dead space (VD) correlated strongly with VT (p < 0.001), while the VD/VT ratio was independent of VT. PaO2 tended to increase in CABG patients and decrease in ARDS patients at 1.25 VT. Arterial oxygen saturation (SaO2) did not change at 1.25 VT but decreased at 0.75 VT (p < 0.001) in the ARDS group. Venous admixture (QS/QT) decreased with 1.25 VT and increased with 0.75 VT (p < 0.001). A relatively larger increase in cardiac output compensated for the increased QS/QT and the reduced SaO2, resulting in significantly higher DO2 with 0.75 VT (p < 0.01). A lower VT resulted in improved balance between pulmonary gas exchange and whole body oxygen supply.

Blood Gas Analysis↗

Effects of PEEP on respiratory mechanics after open heart surgery.

Respiratory dysfunction, particularly atelectasis, is common after open heart surgery. Routine use of PEEP (5 to 10 cm H2O) in these patients has been advocated. We studied the effects of different levels of PEEP on respiratory mechanics in ten mechanically ventilated open heart surgery patients in the immediate postoperative period. PEEP was studied in increasing increments and decreasing decrements. This procedure was repeated three times. Flow, tidal volume, and airway pressure were measured. We used the rapid airway occlusion technique to determine static compliance of the respiratory system (Cst,rs) and intrinsic PEEP (PEEPi). The changes in end-expiratory lung volume (delta EELV) were measured with respiratory inductive plethysmography. Recruitment of lung units (Vrec) was estimated as the difference in lung volume between PEEP and zero end-expiratory (ZEEP) for the same static inflation pressure (15 cm H2O). We found that (1) Cst,rs at ZEEP was significantly reduced (60 +/- 2 ml/cm H2O); (2) while PEEP of 5 cm H2O did not cause significant recruitment, higher levels of PEEP (10 to 15 cm H2O) were effective; (3) Cst,rs, Vrec, and delta EELV were higher during stepwise PEEP decrease; (4) after the first and second stepwise PEEP increase-decrease run, there was a small persistent increase in EELV and Cst,rs at ZEEP. No further changes were found after the third run. We conclude that after open heart surgery, PEEP less than 10 cm H2O is not effective to reopen atelectatic lung units.

Aortic Valve↗

Evaluation of respiratory inductive plethysmography in the measurement of breathing pattern and PEEP-induced changes in lung volume.

STUDY OBJECTIVE: To assess the accuracy of the respiratory inductive plethysmography in the measurement of PEEP-induced changes in end-expiratory lung volume during mechanical ventilation and its accuracy and stability in the measurement of ventilation during controlled mechanical ventilation and spontaneous breathing. DESIGN: An open comparison between two methods using a criterion standard. Either a pneumotachometer (mechanically ventilated patients) or a spirometer (spontaneously breathing subjects) was used as the reference method. SETTING: Tertiary care center; a multidisciplinary intensive care unit and a metabolic research unit. PATIENTS: Six mechanically ventilated, paralyzed postoperative open heart surgery patients, six spontaneously breathing COPD patients, and eight healthy volunteers. INTERVENTIONS: Stepwise increases and reductions of PEEP from zero to 12 cm H2O during controlled mechanical ventilation; repeated validation of the calibration of the respiratory inductive plethysmography (RIP) in both mechanically ventilated and spontaneously breathing subjects. MEASUREMENTS AND RESULTS: The baseline drift of the RIP in vitro was 10 ml/150 min and in a ventilated model it was 20 ml/150 min. In mechanically ventilated patients, the mean error of the calibration after 150 min was within +/- 5 percent. Change in end-expiratory lung volume (EELV) during the stepwise increase of PEEP up to 12 cm H2O was 849 +/- 136 ml with the RIP and 809 +/- 125 ml with the pneumotachometer (PT), and during the stepwise reduction of PEEP it was 845 +/- 124 ml and 922 +/- 122, respectively (not significant [NS]. The mean difference between methods in the measurement of change in EELV was -6.6 +/- 3.5 percent during increasing and 6.6 +/- 6.7 percent during decreasing PEEP (NS). Both in mechanically ventilated and spontaneously breathing subjects, the difference between methods was significant for VT and VT/TI. The difference in VT was -2.2 +/- 0.2 percent during mechanical ventilation, -1.1 +/- 0.5 percent in spontaneously breathing COPD patients, and 2.9 +/- 0.4 percent in healthy volunteers (NS between groups). CONCLUSIONS: The RIP is sufficiently accurate for the measurement of PEEP-induced changes in EELV during controlled mechanical ventilation. The accuracy of tidal volume measurement is similar during mechanical ventilation and spontaneous breathing. The calibration of the RIP is stable enough for bedside monitoring of changes in lung volumes.

Adult↗

Measurement of tissue oxygen tension: comparison between two subcutaneous oxygen tonometers.

We compared the 95% response time (95% RT) of two tissue oxygen tonometers under two sets of circumstances. We first evaluated the devices during normoxia, hyperoxia, and anoxia in vitro, using a transcutaneous PO2 electrode (PtcO2) as the reference. The responses to normoxia and to different grades of hyperoxia were examined in vivo in 8 healthy volunteers to assess the relationship between changes in subcutaneous PO2 and PtcO2, an estimate of arterial PO2 (PaO2). One subcutaneous method (ScA) used a technique based on a polarographic needle electrode in situ connected to an ammeter; the second method (ScB) was based on a blood gas analyzer system first described by Hunt (Lancet 164;2:1370). ScA and PtcO2 both responded to stepwise changes in ambient oxygen concentration (21-100%) in vitro within 10 seconds; the 95% RT of ScA was 1.39 +/- 0.5 to 2.39 +/- 0.8 minutes and that of PtcO2 was 0.32 +/- 0.1 to 0.49 +/- 0.1 minutes. ScB had a lag of 3 minutes, and the 95% RT was 6.75 +/- 0.5 to 8.2 +/- 0.8 minutes. In contrast to the results in vitro, the response of ScA to changes in FiO2 in vivo was delayed compared with the rapid response of PtcO2, reflecting the physiologic delay of tissue PO2 in response to increased PaO2. The time lag and the long 95% RT of ScB were even more evident in vivo. ScA reacted three to four times faster than ScB, both in vitro and in vivo, to changes in the oxygen environment. The in vitro 95% RT of ScA to changes in ambient oxygen varied from 2 to 3.5 minutes.(ABSTRACT TRUNCATED AT 250 WORDS)

Blood Gas Monitoring, Transcutaneous↗

Respiratory changes after open-heart surgery.

Breathing pattern was studied non-invasively in 20 coronary artery bypass surgery patients before the operation and post-operatively after weaning from mechanical ventilation. Post-operatively minute ventilation (VE), breathing frequency (Fr) and mean inspiratory flow (VT/TI) increased (28%, 42%, 27%; p less than 0.01, p less than 0.001, p less than 0.01, respectively), while tidal volume (VT) decreased (15%, p less than 0.025). CO2 production (VCO2) and oxygen consumption (VO2) increased postoperatively (p less than 0.001 for both), contributing to the increase in ventilatory demand. Reduced variation of VT and Fr (p less than 0.001, p less than 0.01, respectively) and number of sighs (p less than 0.001) were characteristic of the post-operative breathing pattern. Post-operatively an increase in the contribution of rib cage (%RC) to tidal volume in the supine position was observed suggesting reduced motion of the diaphragm. All patients had atelectasis, 17 had pleural fluid and only 6 normal vascularity post-operatively. The shallow breathing in combination with increased ventilatory demand, impaired gas exchange and the surgical trauma of the thorax predispose to postoperative respiratory complications.

Coronary Artery Bypass↗

Nitrogen and energy balance in septic and injured intensive care patients: response to parenteral nutrition.

We studied energy and nitrogen balance in 50 intensive care patients with sepsis (n = 18) or multiple trauma (n = 32). Most patients were mechanically ventilated during the study. Within 72h of admission the patients were randomised to receive one of 5 infusion regimens for 48h (group n = 9-11). The control group received hypocaloric glucose, two groups received 1.5g/kg/day of amino-acids, either with hypocaloric glucose on both days or with energy adjusted to pre-nutrition REE on the second day. The fourth group received 0.6g/kg/day of amino-acids and energy at REE, and the fifth group a high nitrogen (18g/day) regimen with a stepwise increase in energy intake from day 1 to day 2. Baseline REE was 118 +/- 18.9% of predicted. No significant differences in REE were observed between the diagnostic groups, treatments or measurements performed during mechanical or spontaneous ventilation. Nitrogen balance in the control group was -250.3 +/- 83.3 mg/kg on day 1 and 218.6 +/- 95.3 mg/kg on day 2. Nitrogen balance remained negative in all groups throughout the study (range of group means-218.6 to -48.5 mg/kg/day). Increasing energy intake equal to prenutrition REE at an amino-acid dosage of 1.5g/kg/day decreased the negative nitrogen balance by 66%. Further increase in energy balance had only a marginal effect on nitrogen balance.

Journal Article↗

Peripheral tissue energy metabolism during recovery from hypothermia after cardiopulmonary bypass: effect of amino-acid infusions.

We studied the effects of amino-acid administration on the leg exchange of energy substrates and amino-acids during recovery from hypothermia after open heart surgery. Glucose (G, n = 5), glucose and conventional amino-acids (CA, n = 5) or glucose and branched chain amino-acids (BC, n = 5) were infused during recovery from hypothermia after open heart surgery. The leg exchange of energy substrates and amino-acids were measured after arrival at the intensive care unit, after rewarming, and 2h and 4h after rewarming during increasing amino-acid intake. Despite a normal stress response to surgery, reflected by increased energy expenditure and increased concentrations of insulin and catabolic hormones, amino-acids had no effect on the leg exchange of branched chain amino-acids, glutamine, alanine and energy substrates. This suggests that the transport of amino-acids and energy substrates into the cell are impaired after hypothermic cardiopulmonary bypass and intracellular substrates are utilised for the increased demand for energy during rewarming.

Journal Article↗

Nitrogen and energy balance in depleted patients undergoing major gastrointestinal surgery: response to TPN.

We studied energy and nitrogen balance during pre- and post-operative parental nutrition in 16 malnourished patients undergoing major abdominal surgery due to suspected gastrointestinal malignancy. The response to amino-acids alone (1.5g/kg; group AA) and energy alone (energy intake equal to pre-nutrition energy expenditure; group REE) was studied during the first day of pre- and post-operative nutrition. On the second day of parental nutrition both groups received amino-acids (1.5g/kg) and non-protein energy equal to pre-nutrition energy expenditure. Energy expenditure (EE) was increased both pre- and post-operatively (EE 112 +/- 15 and 121 +/- 14% of predicted, respectively). Nitrogen balance in group REE was more positive than in group AA on pre-operative day 2 (81.1 +/- 35.8 vs. 17.8 +/- 60.5 mg/kg; p < 0.05). N balance was better pre- than post-operatively on day 2 in both groups (17.8 +/- 60.5 vs. -49.6 +/- 49.2 mg/kg; group AA and 81.1 +/- 35.8 vs. 7.8 +/- 82.6 mg/kg; group REE; p < 0.05). Pre-operatively, administration of energy alone reduced EE (1489 +/- 301 vs. 1403 +/- 312 kcal/day; p < 0.05). We conclude that: 1) The patients were hypermetabolic both pre- and post-operatively. 2) Surgical trauma had a minor effect on EE. 3) Good nitrogen retention could be obtained both pre- and post-operatively at close to zero energy balance. 4) EE increased during the infusion of amino-acids more post-operatively than pre-operatively; non-protein energy at EE had no thermogenic effect. 5) Priming with energy improved nitrogen balance on the following day.

Journal Article↗

Effect of food restriction on tissue carnitine concentration in rats.

The effect of feeding different amounts of a standard laboratory pellet diet on tissue carnitine concentration was studied in four groups of rats. Group I was fed ad libitum, whereas food intake was restricted to 25, 20, and 15g protein/kg body weight/day in group II, III, and IV, respectively. The intake of food, protein, energy and carnitine was constant and adjusted to actual body weight in groups 2-4. Six weeks food restriction had no effect on muscle carnitine. Restricted diet caused lowered concentrations of carnitine in serum (group I, fed ad libitum, total 95.0 +/- 13.8, free 80.2 +/- 2.7; group II total 78.4 +/- 8.4, free 56.9 +/- 4.7; group III total 81.7 +/- 8.8, free 66.0 +/- 8.8; and group IV total 73.8 +/- 8.7, free 59.5 +/- 7.6 micromol/l) and urinary carnitine excretion (group I, total 7.1 +/- 3.3, free 6.3 +/- 3.1; group II, total 2.5 +/- 0.7, free 2.2 +/- 0.7; group III, total 1.9 +/- 0.8, free 1.6 +/- 0.8; and group IV, total 1.3 +/- 0.4 free 1.1 +/- 0.3 micromol/day). In contrast, the liver carnitine tended to increase when dietary intake was reduced (group I total 1.1 +/- 0.1, free 1.0 +/- 0.1; group II total 1.5 +/- 0.2, free 1.4 +/- 0.2; group III total 1.3 +/- 0.1, free 1.1 +/- 0.1; and group IV total 1.5 +/- 0.2, free 1.4 +/- 0.2 micromol/g dry wt). The highest liver carnitine concentrations were observed during the lowest dietary intake when also the serum and urine carnitine were lowest. We conclude that the amount of food intake has a direct impact on carnitine concentrations in the liver, serum, and urine while muscle carnitine concentration remains relatively stable despite wide variations in food intake.

Journal Article↗

Experimental carnitine depletion in rats.

We studied tissue carnitine concentrations after long-term peroral feeding with carnitine-free parenteral nutrient solutions in rats. Group I (n = 22) was fed perorally for 6 weeks with the carnitine free experimental diet. The control group (group II, n = 22) was pair-fed a standard laboratory pellet diet containing carnitine 60 nmol/g. The carnitine free experimental diet caused approximately 50% depletion of carnitine in serum, muscle, and liver while the concentrations in the pair-fed rats were normal. The free and total carnitine concentrations in serum were 25.5 +/- 7.8 and 32.9 +/- 9.3 micromol/l (group I), and 69.3 +/- 13.7 and 84.1 +/- 16.5 micromol/l (group II, p < 0.001), in muscle 2.1 +/- 0.3 and 2.3 +/- 0.4 micromol/g dry weight (group I), and 3.8 +/- 0.6 and 4.3 +/- 0.8 micromol/g dry weight (group II, p < 0.001), and in liver 0.5 +/- 0.1 and 0.6 +/- 0.1 micromol/g dry weight (group I), and 1.2 +/- 0.1 and 1.3 +/- 0.1 micromol/g dry weight (group II p < 0.001). Daily supplementation of the experimental liquid diet with I-carnitine caused normal tissue carnitine concentrations, indicating the exclusion of dietary carnitine as the cause of carnitine depletion. We conclude that in rats carnitine depletion in serum, muscle, and liver can be induced by prolonged peroral feeding with carnitine free diet.

Journal Article↗

Changes in whole body and tissue oxygen consumption during recovery from hypothermia: effect of amino acid infusion.

OBJECTIVE: To study the effects of amino acids on whole body and peripheral energy metabolism during recovery from post-operative hypothermia. DESIGN: Clinical study using three randomly assigned patient groups. SETTING: ICU of a university hospital. PATIENTS: Nineteen elective coronary bypass operation patients. INTERVENTIONS: Postoperatively, either glucose alone, glucose and a conventional amino acid solution, or glucose and a branch-chain amino acid enriched solution was infused. After ICU arrival (period 1) both conventional amino acid solution and branch-chain amino acid enriched solution groups received 0.15 g/kg-day of nitrogen as a conventional amino acid mixture (20% branch-chain amino acids). After rewarming (period 2), both groups received 0.18 g of nitrogen/kg-day for 2 hrs (branch-chain amino acid content 20% in the conventional amino acid solution and 35% in the branch-chain amino acid enriched solution), and for the following 2 hrs (period 3), 0.22 g of nitrogen/kg-day (branch-chain amino acid content 20% in the conventional amino acid solution and 50% in the branch-chain amino acid enriched solution). MEASUREMENTS AND MAIN RESULTS: Whole body oxygen consumption (VO2) increased during period 1 and continued to increase during period 2 (baseline, 133 +/- 20 mL/min.m2; period 1, 152 +/- 12 mL/min.m2; period 2, 158 +/- 21 mL/min.m2; period 3, 153 +/- 15 mL/min.m2; p less than .05, period 1 vs. baseline). VO2 in the leg increased during period 1 but remained constant thereafter (baseline, 16 +/- 8 mL/min.m2; period 1, 26 +/- 14 mL/min.m2; period 2, 23 +/- 6 mL/min.m2; period 3, 24 +/- 10 mL/min.m2; p less than .05, period 1 vs. baseline). Amino acid infusions had no thermogenic effect. A two-phase redistribution of VO2 and leg VO2 suggested increased visceral VO2 after rewarming. CONCLUSION: The amino acid infusions had no effect on the leg uptake of glucose, ketone bodies, and pyruvate and the leg release of lactate, free fatty acids, and triglycerides, which remained constant during the study.

Adult↗

Septic shock and multiple organ failure.

OBJECTIVE: To assess the frequency and mortality rates of septic shock in ICU patients and the clinical course of multiple organ failure associated with septic shock. DESIGN: Retrospective case survey. SETTING: Tertiary care center. PATIENTS: During a 2-yr period, 2,469 consecutive intensive care patients were studied regarding the frequency and hospital mortality rates of septic shock. A subset of 1,311 patients was further analyzed for the occurrence of organ system failures within 48 hrs of the onset of septic shock and again 4 to 7 days later. MEASUREMENTS AND MAIN RESULTS: The frequency rate of septic shock was 1.9% (n = 48), with a mortality rate of 72.9% (n = 35) in patients with septic shock. Deaths due to septic shock represented 14.6% of all deaths in the ICU during the study period. Eighteen patients died within 72 hrs of the onset of septic shock. Refractory hypotension was the cause of death in 15 of these 18 patients. Beyond 72 hrs, multiple organ failure accounted for eight of 17 deaths. The mean +/- SD number of organ systems failing at 48 hrs was 3.3 +/- 1.3 in survivors and 4.0 +/- 1.1 in nonsurvivors, and at 4 to 7 days was 2.1 +/- 1.5 in survivors and 4.0 +/- 1.5 in nonsurvivors (p less than .05). None of the specific organ system failures had prognostic value. The number of organ system failures was not related to the duration of hypotension, but had a weak correlation (r2 = .26, p less than .05) with the duration of vasoactive treatment at 4 to 7 days. The prolonged need for norepinephrine therapy was associated with an increased occurrence of renal failure. Thirty (62.5%) patients had positive blood cultures and a mortality rate similar to the mortality rate of patients with negative blood cultures. Patients with negative blood cultures died more often with hypotension (p less than .02). CONCLUSIONS: Septic shock is a major cause of death in intensive care patients. Refractory hypotension is a main cause of early deaths. Later on, multiple organ failure becomes the primary clinical problem and cause of mortality.

Adult↗

Measurement of alveolar ventilation and changes in deadspace by indirect calorimetry during mechanical ventilation: a laboratory and clinical validation.

OBJECTIVE: To validate the assessment of changes in alveolar ventilation and deadspace by indirect calorimetry. DESIGN: An open comparison of two methods using a criterion standard. METHODS: Simultaneous measurement of minute ventilation with a metabolic monitor and a pneumotachometer during controlled and synchronized intermittent mandatory ventilation in intensive care patients (n = 14). Measurement of a change in alveolar ventilation with three different tidal volume values in a single-compartment lung model using an added external deadspace. Alveolar ventilation and deadspace/tidal volume were calculated from Bohr's equation using end-tidal PCO2 for the alveolar PCO2 value. RESULTS: The mean differences between minute ventilation measured by a metabolic monitor and minute ventilation measured by a pneumotachometer during controlled and synchronized intermittent mandatory ventilation were -0.04 +/- 0.61 (SD) L and 0.01 +/- 0.85 L, respectively. No significant difference was observed between measurements at the endotracheal tube and the expiratory port of the ventilator. In studies using the lung model, the external deadspace represented 6% to 19% of the three tidal volume measurements. The mean difference between the actual and measured deadspace was 3 +/- 9 mL (8.2 +/- 4.7%), with a slightly, but not significantly, lower precision at the high tidal volume. CONCLUSIONS: Changes in alveolar ventilation and deadspace can be accurately measured by combined use of indirect calorimetry and end-tidal CO2 analysis.

Calorimetry, Indirect↗

Effect of vasoactive treatment on the relationship between mixed venous and regional oxygen saturation.

OBJECTIVE: To evaluate the relationship between the mixed venous (SvO2), hepatic, and femoral venous oxygen saturations before and during sympathomimetic drug infusions. DESIGN: Case series. SETTING: Tertiary care center. PATIENTS: Twenty-four ICU patients: postoperative open-heart surgery patients (n = 12), patients with septic shock (n = 8), and patients with acute respiratory failure (n = 4). INTERVENTIONS: In postoperative open-heart surgery patients and patients with respiratory failure, cardiac output was increased by at least 25% following therapy with either dobutamine or dopamine. Patients with septic shock were treated with either dopamine or norepinephrine to correct hypotension. MEASUREMENTS AND MAIN RESULTS: Vasoactive drug infusions increased cardiac index and oxygen delivery by 34% and oxygen consumption by 8%. SvO2 increased (62.6 +/- 6.7% vs. 69.5 +/- 6.0%, p less than .001). Although cardiac index was the most important determinant of SvO2, the correlation between cardiac index and SvO2 was weak (r2 = .32). The hepatic and femoral venous saturations also increased (49.0 +/- 12.1% vs. 59.4 +/- 9.8%, p less than .01, and 51.9 +/- 16.6% vs. 63.4 +/- 9.8%, p less than .001, respectively) in response to vasoactive treatment. The mean gradient between SvO2 and hepatic venous saturation was 11.9 +/- 8.7% and was independent of the clinical condition and baseline SvO2. The hepatic venous oxygen saturation increased in parallel with SvO2 regardless of the initial SvO2 value. CONCLUSIONS: The individual values of SvO2 have no predictive value concerning regional oxygen transport. The parallel increase in SvO2 and hepatic venous oxygen saturation suggests that the vasoactive treatment did not compromise splanchnic oxygenation.

Acute Disease↗

Hypermetabolism after coronary artery bypass.

We measured the changes in energy expenditure in the early postoperative phase after coronary artery bypass operations and the ventilatory response to the increased demand for respiratory gas exchange. Breathing pattern and gas exchange were measured noninvasively by respiratory inductive plethysmography and indirect calorimetry with a canopy. Eighteen patients were studied after weaning from mechanical ventilation. Energy expenditure increased by 18.3%, which is comparable to the response to major injury. Carbon dioxide production increased from 162 +/- 20 to 195 +/- 36 ml/min in the supine position (p less than 0.001), and similar changes were observed in the half-sitting position. Arterial carbon dioxide tension increased marginally (37.5 +/- 2.96 mm Hg preoperatively versus 39.7 +/- 4.87 mm Hg postoperatively; p less than 0.05), while oxygen tension decreased from 89.9 +/- 17.3 mm Hg to 62.9 +/- 13.4 mm Hg (p less than 0.001). Minute ventilation increased by 34% in the supine position (p less than 0.01) and by 28% in the half-sitting position (p less than 0.05), while tidal volume remained unchanged. We conclude that coronary artery bypass operations induce hypermetabolism and substantially increase ventilation and risk of arterial hypoxemia during the phase of compromised cardiovascular reserves.

Calorimetry, Indirect↗