Corticosteroid therapy in intensive care unit patients with PCR-confirmed influenza A(H1N1) infection in Finland.

OBJECTIVE: To evaluate the incidence, treatment, and outcome of influenza A(H1N1) in Finnish intensive care units (ICUs) with special reference to corticosteroid treatment. METHODS: During the H1N1 outbreak in Finland between 11 October and 31 December 2009, we prospectively evaluated all consecutive ICU patients with high suspicion of or confirmed pandemic influenza A(H1N1) infection. We assessed severity of acute disease and daily organ dysfunction. Ventilatory support and other concomitant treatments were evaluated and recorded daily throughout the ICU stay. The primary outcome was hospital mortality. RESULTS: During the 3-month period altogether 132 ICU patients were tested polymerase chain reaction-positive for influenza A(H1N1). Of these patients, 78% needed non-invasive or invasive ventilatory support. The median (interquartile) length of ICU stay was 4 [2-12] days. Hospital mortality was 10 of 132 [8%, 95% confidence interval (CI) 3-12%]. Corticosteroids were administered to 72 (55%) patients, but rescue therapies except prone positioning were infrequently used. Simplified Acute Physiology Score II and Sequential Organ Failure Assessment scores in patients with and without corticosteroid treatment were 31 [24-36] and 6 [2-8] vs. 22 [5-30] and 3 [2-6], respectively. The crude hospital mortality was not different in patients with corticosteroid treatment compared to those without: 8 of 72 (11%, 95% CI 4-19%) vs. 2 of 60 (3%, 95% CI 0-8%) (P = 0.11). CONCLUSIONS: The majority of H1N1 patients in ICUs received ventilatory support. Corticosteroids were administered to more than half of the patients. Despite being more severely ill, patients given corticosteroids had comparable hospital outcome with patients not given corticosteroids.

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.

Community-acquired septic shock: early management and outcome in a nationwide study in Finland.

AIM: To determine how the early treatment guidelines were adopted, and what was the impact of early treatment on mortality in septic shock in Finland. METHODS: This study was a sub-analysis of a prospective observational investigation of severe sepsis and septic shock in Finland (Finnsepsis). All patients with severe sepsis over 4 months in 24 intensive care units were included in the Finnsepsis study. Patients with community-acquired septic shock, admitted directly from the emergency department to the intensive care unit, were included in the sub-study. The following treatment targets were evaluated: measurement of lactate during the first 6 h; analysis of blood culture before antibiotics; commencement of antibiotics within 3 h; attainment of a mean arterial pressure of > or =65 mmHg, central venous pressure of > or =8 mmHg and central venous oxygen saturation of > or =70% or mixed venous oxygen saturation of > or =65% during the first 6 h. RESULTS: Of the 92 patients who fulfilled the inclusion criteria, six reached all treatment targets and 33 reached four or more targets (group > or =4). The hospital mortality of group > or =4 was 24% (8/33), compared with 42% (25/59) for those who reached three or fewer targets (group < or =3) (P= 0.08). The 1-year mortality rates of group > or =4 and group < or =3 were 36% and 59% (P= 0.04), respectively. In logistic regression analysis, a delayed initiation of antimicrobials was associated with an unfavourable outcome (P= 0.04). CONCLUSIONS: Compliance with international guidelines for the early treatment of septic shock was poor in Finnish hospitals. A failure to diagnose early and to start appropriate treatment was reflected in the high mortality. The delayed start of antibiotics was the most important individual variable leading to a high mortality in this nationwide study.

Practical sources of error in measuring pulmonary artery occlusion pressure: a study in participants of a special intensivist training program of The Scandinavian Society of Anaesthesiology and Intensive Care Medicine (SSAI).

BACKGROUND: Physiological data obtained with the pulmonary artery catheter (PAC) are susceptible to errors in measurement and interpretation. Little attention has been paid to the relevance of errors in hemodynamic measurements performed in the intensive care unit (ICU). The aim of this study was to assess the errors related to the technical aspects (zeroing and reference level) and actual measurement (curve interpretation) of the pulmonary artery occlusion pressure (PAOP). METHODS: Forty-seven participants in a special ICU training program and 22 ICU nurses were tested without pre-announcement. All participants had previously been exposed to the clinical use of the method. The first task was to set up a pressure measurement system for PAC (zeroing and reference level) and the second to measure the PAOP. RESULTS: The median difference from the reference mid-axillary zero level was - 3 cm (-8 to + 9 cm) for physicians and -1 cm (-5 to + 1 cm) for nurses. The median difference from the reference PAOP was 0 mmHg (-3 to 5 mmHg) for physicians and 1 mmHg (-1 to 15 mmHg) for nurses. When PAOP values were adjusted for the differences from the reference transducer level, the median differences from the reference PAOP values were 2 mmHg (-6 to 9 mmHg) for physicians and 2 mmHg (-6 to 16 mmHg) for nurses. CONCLUSIONS: Measurement of the PAOP is susceptible to substantial error as a result of practical mistakes. Comparison of results between ICUs or practitioners is therefore not possible.

The proportion of intensive care unit admissions related to alcohol use: a prospective cohort study.

BACKGROUND: Alcohol abuse is a risk factor for serious illnesses, and a history of chronic alcohol abuse adversely affects the outcome of critically ill patients. It is not known what proportion of intensive care unit (ICU) admissions is related to alcohol use. Therefore, we investigated the proportion of emergency admissions related to alcohol. METHODS: A prospective cohort study was conducted in a university hospital ICU. All adult patients (n = 893) who underwent emergency admission to our ICU during a period of 1 year were studied. RESULTS: The admitting physician determined whether there was a relationship between alcohol use and admission. ICU and hospital mortality and ICU length of stay (LOS) were recorded. The Therapeutic Intervention Scoring System (TISS) was used for ICU resource use estimation. There was a relationship between alcohol use and admission in 24% (215/893) of admissions and, in 156/893 admissions (17.5%), this seemed to be definite. ICU LOS was 1.2 days (0.7; 2.3) (median; interquartile range) for alcohol-related and 1.8 days (0.9; 3.6) for other admissions (P < 0.001). Patients with alcohol-related admissions consumed 17.8% of ICU patient-days and 18.7% of all accumulated TISS scores. ICU (8.8 vs. 10.5%, P = 0.603) and hospital (19.1 vs. 20.2%, P = 0.769) mortalities were no different between alcohol-related and other admissions. CONCLUSION: ICU admission is very often related to long-term chronic and/or occasional alcohol use.

Lack of effect of ranitidine on gastric luminal pH and mucosal PCO2 during the first day in the ICU.

BACKGROUND: Histamine(2) (H(2))-blocking agents can attenuate intragastric CO(2)-production by reducing gastric acid secretion and preventing the interaction between H(+) and bicarbonate. However, gastric acid production may be impaired in acute circulatory failure due to poor mucosal perfusion, and H(2)-blockade could further impair mucosal perfusion. METHODS: Forty patients with acute circulatory and/or respiratory failure, age 61 +/- 16 years (mean +/- SD), APACHE II score 21 +/- 7, and SOFA score 8 +/- 3, received randomly either ranitidine, 50 mg (R) or placebo (P) every 8 h. Gastric intraluminal pH (gpH; antimony probe with external reference electrode) and mucosal pCO(2) (prCO(2), semicontinuous air-tonometry) were measured during 24 h, and blood gases were taken at 6-h intervals. RESULTS: Gastric intraluminal pH was 4.3 +/- 2.4 in P and 5.1 +/- 1.6 in R (NS). Mean prCO(2) was 6.8 +/- 2.7 kPa in P and 7.4 +/- 2.1 kPa in R, and mucosal-arterial pCO(2) gradient (Delta pCO(2)) was 2.2 +/- 2.9 kPa and 2.4 +/- 2.4 kPa, respectively (NS). Within-patient variabilities of gpH and prCO(2) were not influenced by ranitidine. A posthoc analysis revealed that non-survival in R was associated with a low mucosal pHi after 24 h (P = 0.002). This was explained by a low arterial pH but not by differences in gpH or prCO(2). CONCLUSION: In acute respiratory and circulatory failure, H(2) blockade has an inconsistent impact on gpH and does not reduce variabilities of gpH or prCO(2).

Results and costs of intensive care in a tertiary university hospital from 1996-2000.

BACKGROUND: Costs of intensive care may be 20% of all hospital costs. Population aging likely increases the demand for intensive care services, while health care has financial limitations. Therefore data about outcome and costs of intensive care are needed. We studied changes in patient characteristics, outcome, intensity of care and costs of intensive care in a tertiary university hospital in Finland. METHODS: We analyzed retrospectively data of patients admitted to the ICU between 1 January 1996 and 31 December 2000 using the patient data management system. Postoperative and ICU patients were analyzed separately. Data included age, Apache II score, cause of intensive care admission, length and intensity of ICU care. ICU, hospital and 6-month mortality were analyzed. Intensity of care was assessed by TISS points and the annual costs of intensive care were evaluated. RESULTS: The number of ICU admissions from 1996-2000 was 11,323. The proportions of ICU and postoperative patients were 39% and 61%, respectively. The mean age of the patients did not change. The mean Apache II score increased over time both in the ICU and postoperative patients. There was no change in crude hospital mortality. Total ICU costs decreased from 8,660,000 euros (in 1997) to 7,480,000 euros (in 2000). In the ICU patients, the costs of hospital survival decreased towards the end of the study period. CONCLUSIONS: We treated more severely ill patients with unchanged outcome but at lower costs towards the end of the study period. Costs of intensive care are not necessarily increasing.

Myocardial function and haemodynamics in extensive burn trauma: evaluation by clinical signs, invasive monitoring, echocardiography and cytokine concentrations. A prospective clinical study.

BACKGROUND: The objectives of this study were to (1). describe the haemodynamic profile of patients with extensive burns during the early fluid resuscitation phase, (2). evaluate myocardial performance by invasive monitoring and echocardiography and (3). analyze the relations between serum cytokine (IL-6, IL-8, TNF) and natriuretic peptide (ANP, BNP) concentrations and myocardial function in these patients. METHODS: Prospective, clinical study in a tertiary care burn centre. Invasive haemodynamic measurements including a pulmonary artery catheter, echocardiography, blood samples for cytokine and atriopeptide analyses. The follow-up time was up to 72 h postinjury. RESULTS: According to echocardiography, patients were hypovolaemic despite aggressive (median 7,9 ml kg(-1) h(-1), range 3.3-11.7) fluid resuscitation and adequate urine output (median 0.9 ml kg(-1) h(-1), range 0.46-1.35) during the first day postinjury. There were no consistent findings of hyperlactatemia, metabolic acidosis or low mixed venous oxygen saturations. Daily highest and lowest values of cardiac index and stroke volume index increased and the lowest and highest values of systemic vascular resistance decreased. Cardiac performance (stroke volume index) improved during the study period even though there were no initial signs of myocardial depression in echocardiography. Three patients received a dobutamine infusion based on clinical judgement. There was no consistent association between haemodynamic changes and plasma cytokine concentrations. CONCLUSION: Persisting hypovolaemia is evident in the resuscitation phase of extensive burns despite aggressive fluid therapy and the lack of classic signs of hypoperfusion. Cardiac performance improves during the first days after extensive burn injury without association with plasma cytokine profile.

High-dose thiopental in the treatment of refractory status epilepticus in intensive care unit.

The authors studied prospectively the effects of thiopental anesthesia on seizure control, hemodynamics, and the course of intensive care in 10 patients with refractory status epilepticus. Clinical and electrophysiological seizures were terminated in every patient. Hemodynamically, thiopental was well tolerated, but slow recovery from anesthesia prolonged the need for intensive care.

Gastric tonometry after subarachnoid hemorrhage.

OBJECTIVE: To evaluate splanchnic tissue perfusion, assessed by gastric tonometry, in patients with subarachnoid hemorrhage (SAH) and to study the effect of treatment, either surgical or endovascular, and the severity of initial SAH on splanchnic tissue perfusion. DESIGN: Prospective observational substudy, part of a randomised controlled trial of early treatment of ruptured intracranial aneurysms. SETTING: Intensive care unit (ICU) of a university hospital. PATIENTS: A consecutive sample of 26 patients [13 surgical (7/6 Hunt & Hess Grade I-II/H & H Gr IV-V) and 13 endovascular (3/10 H & H Gr I-II/H & H Gr IV-V)] out of 56 SAH patients randomly assigned to either endovascular or surgical treatment during the substudy period between 1 May 1995 and 31 August 1996. All patients were treated within 72 h after SAH. MEASUREMENTS AND RESULTS: After treatment of a ruptured aneurysm, hemodynamics and gastric intramucosal pCO2 were measured during the first 4 h and between 6 h and 12 h after aneurysm treatment. In the whole sample, neither the gastric intramucosal-arterial pCO2 difference (pCO2 gap) (1.5+/-1.9 kPa and 1.7+/-1.2 kPa, NS) nor gastric intramucosal pH (7.28+/-0.12 and 7.29+/-0.08, NS) changed during the study. There were no differences in pCO2 gap or gastric intramucosal pH between treatment groups or Hunt & Hess grade groups during the study period. CONCLUSIONS: Splanchnic tissue perfusion may be insufficient even though there is no systemic hemodynamic disturbance in patients after SAH. Neither the therapeutic treatment nor pre-treatment Hunt & Hess grade is associated with a specific pattern of pCO2 gap.

Gastric mucosal end-tidal PCO2 difference as a continuous indicator of splanchnic perfusion.

Gastric mucosal and arterial blood PCO2 must be known to assess mucosal perfusion by means of gastric tonometry. As end-tidal PCO2 (PE'CO2) is a function of arterial PCO2, the gradient between PE'CO2 and gastric mucosal PCO2 may reflect mucosal perfusion. We studied the agreement between two methods to monitor gut perfusion. We measured the difference between gastric mucosal PCO2 (air tonometry) and PE'CO2 (= DPCO2gas) and the difference between gastric mucosal PCO2 (saline tonometry) and arterial blood PCO2 (= DPCO2sal) in 20 patients with or without lung injury. DPCO2gas was greater than DPCO2sal but changes in DPCO2gas reflected changes in DPCO2sal. The bias between DPCO2gas and DPCO2sal was 0.85 kPa and precision 1.25 kPa. The disagreement between DPCO2gas and DPCO2sal increased with increasing dead space. We propose that the disagreement between the two methods studied may not be clinically important and that DPCO2gas may be a method for continuous estimation of splanchnic perfusion.

Ranitidine or dobutamine alone or combined has no effect on gastric intramucosal-arterial PCO(2) difference after cardiac surgery.

OBJECTIVE: To test the hypothesis that ranitidine, either alone or in combination with dobutamine, modifies the gastric intramucosal-arterial PCO(2) difference. DESIGN: Full factorial design (double-blinded for ranitidine). SETTING: Intensive Care Unit of a university hospital. PATIENTS: Sixty-four haemodynamically stable coronary artery bypass surgery patients. INTERVENTIONS: Ranitidine (150 mg preoperatively per os and 50 mg intravenously postoperatively) and dobutamine (4 micro g. kg(-1). min(-1) for 3 h postoperatively) were administered in four randomised groups of patients: preoperative and postoperative ranitidine, either alone (n = 15) or in combination with dobutamine (n = 17), dobutamine alone (n = 15) or neither ranitidine nor dobutamine (n = 17). MEASUREMENTS AND RESULTS: Gastric intramucosal-arterial PCO(2) difference was measured during the first 5 postoperative hours. No differences in the postoperative pattern of gastric intramucosal-arterial PCO(2) difference were found among the groups. CONCLUSIONS: Ranitidine and dobutamine have no effect on the gastric tonometry results on intramucosal-arterial PCO(2) difference after uncomplicated cardiac surgery. Hence, the routine use of H(2)-antagonists for gastrointestinal tonometry is not warranted. Our results must be limited to results obtained by tonometry; they do not allow any conclusions on the effects of these drugs on splanchnic blood flow or its distribution.

The Haldane effect--an alternative explanation for increasing gastric mucosal PCO2 gradients?

When venous oxygen saturation increases as a result of increased blood flow, changes in venous blood PCO2 and carbon dioxide content may differ because of the Haldane effect. The Haldane effect may also explain increases in gastric mucosal-arterial PCO2 gradient despite major increases in splanchnic blood flow. We re-analysed data from 22 patients after cardiac surgery who were randomized to receive either dobutamine or placebo, and a separate group of patients who received dobutamine for low cardiac output (n = 6). Three different values of gastric mucosal oxygen extraction at baseline were assumed (0.3, 0.5 and 0.7). In nine of 14 patients with both increasing splanchnic blood flow and mucosal-arterial PCO2 gradient, an equal increase in mucosal and total splanchnic blood flow, oxygen consumption and carbon dioxide production together with the Haldane effect would have caused an increase in mucosal-arterial PCO2 gradients from a mean value of 0.53 (SD 0.88) kPa at baseline to 0.68-0.82 (0.89-0.90) kPa (P < 0.01). In the remaining patients, disproportionate changes in flow and metabolism must have been involved in addition to the Haldane effect. We conclude that whenever major changes in mucosal tissue oxygen extraction are likely to occur, an increase in the mucosal-arterial PCO2 gradient may be explained in part or completely by the Haldane effect, and may therefore not reflect worsening perfusion.

Angiotensin converting enzyme inhibition has no effect on blood pressure and splanchnic perfusion after cardiac surgery.

PURPOSE: The purpose of this study was to study the effect of the angiotensin-converting enzyme inhibitor, enalaprilat, on blood pressure and splanchnic perfusion after cardiac surgery. MATERIALS AND METHODS: Sixteen patients were studied after coronary artery bypass grafting. After admission to the intensive care unit, a 30-minute baseline measurement of systemic hemodynamics, oxygen transport, and gastric tonometry was performed. In 6 of 10 patients receiving enalaprilat and in each of 6 control patients, regional (splanchnic and leg) blood flows were measured also. After the baseline measurement period, 10 patients received a 0.5 mg bolus of enalaprilat and thereafter an incremental infusion of enalaprilat up to a total dose of 10 mg (mean 8.3; range 4 to 10 mg) was continued to reduce the mean arterial pressure (MAP) to 70 to 80 mm Hg. A 30-minute measurement period was repeated 2 to 3 hours after the first measurement period. In the control group, the second measurement was performed at corresponding time points. RESULTS: Though MAP decreased in the enalaprilat group (enalaprilat 99 +/- 14 mm Hg v 89 +/- 21 mm Hg, P < .05; control 95 +/- 13 mm Hg v82 +/- 10 mm Hg, P = NS) in only 4 of 10 patients was the targeted MAP reduction achieved. No significant changes were observed either in systemic or regional blood flows. Systemic, pulmonary, and femoral vascular resistance indices decreased significantly in both groups. Gastric-arterial PCO2 difference did not change in either groups. Angiotensin-converting enzyme activity decreased in the enalaprilat group (10.0 +/- 2.3 v 1.3 +/- 0.3 U x l(-1), P < .01), but plasma renin and endothelin-1 concentrations did not change in either group. CONCLUSIONS: The effect of enalaprilat on blood pressure was poor and it had no beneficial effects on splanchnic circulation. Renin-angiotensin activation is not a major factor in hypertension and splanchnic perfusion after cardiac surgery.

Epidural analgesia with bupivacaine does not improve splanchnic tissue perfusion after aortic reconstruction surgery.

Inadequate splanchnic tissue perfusion is relatively common during and after aortic surgery. We hypothesized that vasodilation caused by thoracic epidural analgesia improves splanchnic blood flow and tissue perfusion after aortic surgery. In this prospective, randomized, controlled study, we studied 20 patients undergoing elective aortic-femoral or aortic-iliac reconstruction surgery. Gastric and sigmoid colon mucosal PCO2 and pH were measured during surgery. An epidural bolus of bupivacaine 40 mg followed by infusion of 15 mg h-1 was started after operation in 10 patients. After operation, splanchnic blood flow and gastric and sigmoid colon mucosal PCO2 and pH were measured before and 2 h after the start of epidural analgesia. During surgery, the gastric mucosal-arterial PCO2 difference remained stable, whereas the sigmoid mucosal-arterial PCO2 difference increased during aortic clamping but returned to pre-clamping values after declamping. After operation, epidural analgesia had no effect on gastric or sigmoid mucosal-arterial PCO2 differences or on splanchnic blood flow.

Venoarterial CO2 gradient after cardiac surgery: relation to systemic and regional perfusion and oxygen transport.

The difference in CO2 tension between venous and arterial blood (delta PCO2) increases in low-flow states. Therefore, delta PCO2 has been suggested as an additional variable in the monitoring of perfusion. We measured CO2 tensions in arterial, mixed venous, hepatic venous, and femoral venous blood in 42 postoperative cardiac surgery patients. Splanchnic and leg blood flow was measured with dye dilution. Forty-three preoperative abdominal surgery patients served as controls. Systemic and femoral delta PCO2 was increased in cardiac patients, whereas there was no difference in splanchnic delta PCO2 between the groups. In cardiac patients, systemic delta PCO2 correlated well with both splanchnic and femoral delta PCO2 (r2 = .74 and r2 = .56, respectively). Femoral delta PCO2 was higher than splanchnic delta PCO2 (1.27 +/- .44 kPa versus .66 +/- .41; p < .001) after cardiac surgery, but not in the control group. The correlation between delta PCO2 and respective blood flow was weak in the whole body, the splanchnic region, and the leg. When splanchnic blood flow was low, systemic and splanchnic delta PCO2 varied widely. In the cardiac patients with an increased systemic delta PCO2 (> .93 kPa), systemic and regional blood flow was low, but there were no differences in systemic or regional oxygen consumption or lactate levels. After cardiac surgery, high systemic delta PCO2 is associated with marginal systemic and regional perfusion. The adequacy of regional blood flow cannot be assessed on the basis of the systemic delta PCO2.

Lactate metabolism and regional lactate exchange after cardiac surgery.

Tissue perfusion is at risk during cardiac surgery and in the immediate postoperative period. The association of low blood flow with metabolic acidosis and accumulation of lactate perioperatively has been well established. With the improvements in cardiopulmonary bypass and overall hemodynamic management, severe peri- and postoperative hypoperfusion has become rare. Despite the rarity of severe postoperative complications, several lines of evidence suggest that episodes of less severe hypoperfusion and borderline tissue oxygenation are relatively common, although generally well tolerated. Measurement of blood lactate levels is widely used to assess the adequacy of tissue perfusion. The interpretation of elevated blood lactate levels is limited by several confounding variables. Acute changes in acid-base balance, interorgan substrate flux, peripheral and visceral tissue perfusion, and hepatic lactate uptake will all influence blood lactate levels and may occur during and after cardiac surgery. Peri- and postoperative hyperlactatemia are rare occurrences and their presence may indicate inadequate tissue perfusion. Based on regional blood flow and lactate exchange measurements, we suggest that hyperlactatemia after cardiac surgery is a sign of inadequate or marginal tissue perfusion of the hepatosplanchnic region, as well as other tissues. In this article we briefly review: a) the normal physiology of lactate metabolism and the various causes of hyperlactatemia; b) studies on lactate levels during and after cardiac surgery; c) the evidence of insufficient or marginal tissue perfusion peri- and postoperatively; and d) the pathophysiology of postoperative increases in blood lactate based on regional lactate kinetics.

Sodium nitroprusside after cardiac surgery: systemic and splanchnic blood flow and oxygen transport.

BACKGROUND: Vasoactive drugs may interfere with splanchnic blood flow and tissue oxygenation. Sodium nitroprusside (SNP) is widely used in the treatment of postoperative hypertension after cardiac surgery, but the effects of SNP and other vasodilators on splanchnic blood flow have not been well documented. METHODS: The effects of SNP on systemic blood flow, oxygen transport and gastric intramucosal pH (pHi) were studied in 12 patients with arterial hypertension after coronary artery bypass grafting. In 9 of these patients, the effect on regional (splanchnic and leg) blood flow and oxygen transport was also measured. Hemodynamic and regional blood flow responses were measured before and during SNP infusion (mean 2.8 +/- 1.7 micrograms/kg/min, range 0.6-6.3 micrograms/kg/min), when the goal of the vasodilator treatment, mean arterial pressure 70-80 mmHg, had been reached. RESULTS: SNP increased splanchnic (0.65 +/- 0.22 vs. 0.87 +/- 0.37 L.min-1.m-2, P < 0.01) and femoral blood flow (0.15 +/- 0.04 vs. 0.21 +/- 0.06 L.min-1.m-2, P < 0.05) in parallel with cardiac index (2.6 +/- 0.6 vs. 3.3 +/- 0.7 L.min-1.m-2, P < 0.01). Fractional regional blood flows did not change. Mean gastric intramucosal pH decreased slightly (7.40 +/- 0.07 vs. 7.37 +/- 0.06, P < 0.05). Both systemic (420 +/- 85 vs. 495 +/- 90 mL.min-1.m-2, P < 0.05) and femoral oxygen delivery (25 +/- 5 vs. 32 +/- 10 mL.min-1.m-2, P < 0.05) increased, but neither systemic nor regional oxygen consumption changed. CONCLUSIONS: These results suggest that vasoregulation is well preserved during treatment of early postoperative hypertension with SNP, and that SNP has no adverse effects on splanchnic tissue oxygenation.

Effect of nasogastric suction and ranitidine on the calculated gastric intramucosal pH.

OBJECTIVE: To study the effect of nasogastric suction and ranitidine on the determination of gastric intramucosal pH (pHi). DESIGN: Prospective study. SETTING: Clinical research unit at a university hospital intensive care department. SUBJECTS: 12 healthy volunteers. INTERVENTIONS: After a 2-h measurement control period a tonometer was connected to nasogastric suction for 2 h, and thereafter ranitidine was given intravenously and gastric pHi measured. MEASUREMENTS AND RESULTS: During each 2-h measurement period gastric PCO2, gastric pHi, and pH gap were determined every 30 min. Luminal pH was measured after insertion of tonometer and at the end of each study period. Neither nasogastric suction nor ranitidine had an effect on the coefficient of variation for either gastric PCO2 or pHi. Compared to control and nasogastric suction periods, after ranitidine mean gastric pHi was higher (control 7.22 +/- 0.08; nasogastric suction 7.23 +/- 0.07; after ranitidine 7.31 +/- 0.06, p < 0.001) mean gastric PCO2 lower (control 6.4 +/- 1.3; nasogastric suction 6.5 +/- 1.3; after ranitidine 5.3 +/- 0.9, p < 0.001) and pH gap lower (control 0.18 +/- 0.08; nasogastric suction 0.17 +/- 0.05; after ranitidine 0.09 +/- 0.06, p < 0.01). Luminal pH increased after ranitidine in each subject. CONCLUSIONS: H2 blockers have no effect on the reproducibility of gastric pHi measurements, but the use of H2 blockers modifies the normal values for gastric pHi in healthy subjects.

Dobutamine-induced dissociation between changes in splanchnic blood flow and gastric intramucosal pH after cardiac surgery.

Gastric intramucosal acidosis, a sign of splanchnic tissue hypoxia, is common after cardiac surgery. We tested the hypothesis that an increase in splanchnic blood flow induced by dobutamine improves splanchnic tissue oxygenation after cardiac surgery. We measured changes in gastric intramucosal pH, splanchnic blood flow and oxygen transport in response to increased systemic flow induced by dobutamine (mean 4.4 (range 3.0-7.0) micrograms kg-1 min-1) after coronary artery bypass. We studied 22 stable postoperative patients who were allocated randomly to receive dobutamine (n = 11) or to serve as controls (n = 11). Dobutamine was given also to a separate group with a low cardiac index after operation (n = 6). The end-point was to increase cardiac index by at least 25% and to exceed 2 litre min-1 m-2. Dobutamine consistently increased mean splanchnic blood flow (control 0.6 (SD 0.2) vs 0.7 (0.2) litre min-1 m-2 (P < 0.05); normal cardiac output and dobutamine 0.7 (0.2) vs 1.1 (0.4) litre min-1 m-2 (P < 0.01); low cardiac output and dobutamine 0.4 (0.1) vs 0.7 (0.1) litre min-1 m-2 (P < 0.05)) and oxygen delivery (control 102 (29) vs 111 (28) ml min-1 m-2 (ns); normal cardiac output and dobutamine 106 (27) vs 156 (47) ml min-1 m-2 (P < 0.01); low cardiac output and dobutamine 75 (21) vs 110 (26) ml min-1 m-2 (P < 0.05)) but had no effect on splanchnic oxygen consumption (control 44 (10) vs 49 (10) ml min-1 m-2 (ns); normal cardiac output and dobutamine 45 (12) vs 51 (17) ml min-1 m-2 (ns); low cardiac output and dobutamine 37 (9) vs 40 (9) ml min-1 m-2 (ns)).(ABSTRACT TRUNCATED AT 250 WORDS)