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Anesth Analg 2008; 106:595-600
© 2008 International Anesthesia Research Society
doi: 10.1213/ane.0b013e31816064d2
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GENERAL ARTICLE

The Immediate and Sustained Effects of Volume Challenge on Regional Blood Flows in Pigs

Syed Z. Ali, MD*, Hendrik Bracht, MD{dagger}, Vladimir Krejci, MD*, Mario Beck{dagger}, Michael Stalder{dagger}, Luzius Hiltebrand, MD*, Jukka Takala, MD, PhD{dagger}, Sebastian Brandt, MD*, and Stephan M. Jakob, MD, PhD{dagger}

From the Departments of *Anesthesiology and {dagger}Intensive Care Medicine, University Hospital Bern, Inselspital, Bern, Switzerland.

Address correspondence to Stephan M. Jakob, MD, PhD, University Hospital Bern, Inselspital, CH-3010 Bern, Switzerland. Address e-mail to stephan.jakob{at}insel.ch.


   Abstract
Top
 Abstract
Introduction
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
BACKGROUND: The postoperative assessment of volume status is not straightforward because of concomitant changes in intravascular volume and vascular tone. Hypovolemia and blood flow redistribution may compromise the perfusion of the intraabdominal organs. We investigated the effects of a volume challenge in different intra- and extraabdominal vascular beds.

METHODS: Twelve pigs were studied 6 h after major intraabdominal surgery under general anesthesia when clinically normovolemic. Volume challenges consisted of 200 mL rapidly infused 6% hydroxyethyl starch. Systemic (continuous thermodilution) and regional (ultrasound Doppler) flows in carotid, renal, celiac trunk, hepatic, and superior mesenteric arteries and the portal vein were continuously measured. The acute and sustained effects of the challenge were compared with baseline.

RESULTS: Volume challenge produced a sustained increase of 22% ± 15% in cardiac output (P < 0.001). Blood flow increased by 10% ± 9% in the renal artery, by 22% ± 15% in the carotid artery, by 26% ± 15% in the superior mesenteric artery, and by 31% ± 20% in the portal vein (all P < 0.001). Blood flow increases in the celiac trunk (8% ± 13%) and the hepatic artery (7% ± 19%) were not significant. Increases in regional blood flow occurred early and were sustained. Mean arterial and central venous blood pressures increased early and decreased later (all P < 0.05).

CONCLUSIONS: A volume challenge in clinically euvolemic postoperative animals was associated with a sustained increase in blood flow to all vascular beds, although the increase in the celiac trunk and the hepatic artery was very modest and did not reach statistical significance. Whether improved postoperative organ perfusion is accompanied by a lower complication rate should be evaluated in further studies.


   Introduction
Top
 Abstract
 Introduction
METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 
Major organ systems are at risk of perioperative injury,1 which can be improved by increasing blood flow and oxygen delivery.2–5 Insufficient hepatosplanchnic and renal blood flow may contribute to the pathogenesis of organ dysfunction and failure.6–9 Signs of hypoperfusion of intraabdominal organs have been observed in sepsis,9 in hypovolemic shock10 and cardiogenic shock,11 and after cardiac surgery.12,13 It has been shown that perioperative plasma volume expansion reduces the incidence of gut mucosal hypoperfusion,12,14 and postoperative organ dysfunction. On the other hand, efforts to increase oxygen delivery to supranormal levels have increased morbidity and mortality in trauma patients.15 In some patients, fluid restriction has been recommended for minimizing blood loss and operation time.16,17

Whether increasing oxygen delivery in the postoperative period is associated with improved outcome has not been clearly defined. In this period, clinical estimation of volume status is complicated by continuing, and often occult, blood loss, capillary leak, changing vascular tone, and the effects of anesthetic and analgesic drugs. Additional volume administration in the postoperative period could be beneficial if it produces a sustained increase in the perfusion of intraabdominal and other organs.

The aim of this study was to assess the physiological effects of a volume challenge on hemodynamics and regional blood flow. We hypothesized that occult hypovolemia is present in the postoperative period, and that a volume challenge would produce a sustained increase in regional blood flow, particularly in the gut and kidney.


   METHODS
Top
 Abstract
 Introduction
 METHODS
RESULTS
 DISCUSSION
 REFERENCES
 
This study was performed according to the National Institutes of Health guidelines for the use of experimental animals. The protocol was approved by the Animal Care Committee of the Canton of Berne, Switzerland. Twelve pigs of both sexes (37–42 kg) were deprived of food but not water 24 h before the experiments. Premedication with atropine 0.05 mg/kg IM, xylazine 2 mg/kg IM, and ketamine 20 mg/kg IM was followed by cannulation of an ear vein and IV administration of 5–15 mg/kg thiopental for endotracheal intubation. Anesthesia was maintained with thiopental (7 mg · kg–1 · h–1) and fentanyl (30 µg · kg–1 · h–1 until the end of surgery, 5 µg · kg–1 · h–1 thereafter). Neuromuscular relaxation was obtained by pancuronium 0.1 mg/kg bolus and maintained with 1 mg · kg–1 · h–1. The lungs were ventilated with a volume-controlled mode (Servo 900C, Siemens, Erlangen, Germany) with 5 cm H2O of positive end-expiratory pressure. The inspired oxygen fraction was adjusted from 40% to 60% to keep the arterial oxygen partial pressure between 100 and 150 mm Hg. Tidal volume was kept at 10 mL/kg and the minute ventilation was adjusted to maintain arterial carbon dioxide partial pressure between 34 and 41 mm Hg.

A pulmonary artery catheter (via the left internal jugular vein) and femoral artery catheter were inserted. A fluid-filled catheter was inserted into the carotid artery, and an ultrasound transit time flow probe (TransonicTM Systems, Ithaca, NY) was placed around the artery. A large-bore catheter for fluid administration was inserted into the femoral vein. The abdominal cavity was opened by a midline abdominal incision. A drainage catheter was inserted into the urinary bladder. The celiac trunk, superior mesenteric, hepatic, and renal arteries, and the portal vein were exposed. Ultrasound transit time flow probes (Transonic Systems) were placed around the vessels. During surgery, the animals received 8 mL · kg–1 · h–1 infusions of saline. Additional fluid was administered to maintain stable hemodynamics (pulmonary capillary wedge pressure, PCWP, at least 5 mm Hg, and urinary output >0.5 mL · kg–1 · h–1). Body temperature was kept between 38°C and 39°C using an operating table heater and warmed fluids when necessary. After surgery, the abdominal wall was reapproximated, although the fascia was not closed, and wet towels were placed on the abdomen to avoid dehydration.

Femoral, pulmonary arterial, and central venous, and PCWP were transduced, displayed on a multimodular monitor (S/5 Compact Critical Care Monitor, Datex-OhmedaTM, Helsinki, Finland), and recorded (see below). All pressure transducers were calibrated simultaneously and zeroed to the level of the heart. Continuous thermodilution cardiac output (L/min) was measured with the Vigilance® monitor (Baxter Healthcare Corporation, Edwards Critical Care Division, Irvine, CA). This monitor displays a moving average of the 10 latest 1-min values. Regional blood flow signals were displayed continuously on dual channel flowmeters (T206; Transonic System). Regional blood flows were recorded by ultrasound transit time flow probes (Transonic). Heart rate was measured using the electrocardiogram, which was continuously monitored. Stroke volume was calculated by dividing cardiac output by heart rate. Once the experiment was started, manipulation was avoided to minimize the possibility of probe displacement.

We clinically assessed euvolemic status based on the absence of the following: poor peripheral perfusion, cool pale extremities, tachycardia with low volume pulses, hypotension, and hemoconcentration. Additionally, we measured central venous pressure and PCWP, as well as hourly urine output. After 6 h of stabilization, in the absence of clinical signs of hypovolemia, the animals received a rapid volume challenge with 200 mL 6% hydroxyethyl starch (Voluven® 130/0.4) given over 2 min. Measurements were taken 4 min after the end of infusion. Continuous cardiac output and the various regional blood flow measurements were recorded at baseline (i.e., before the challenge), and at 4 (acute effect) and 20 (sustained effect) min after the volume challenge. Femoral arterial pressures and celiac trunk, superior mesenteric, hepatic, renal, and carotid arterial flows, as well as portal venous flow values, were collected at 20 Hz by WindaqTM 1.60 (Dataq Instruments Inc., Akron, OH). Carotid, pulmonary arterial, and central venous pressures, as well as airway flow and pressure, were recorded at 100 Hz by AcqKnowledgeTM, Version 3.7.0 (Biopac Systems, Inc., Goleta, CA). For each animal, mean values from all the collected blood flow and pressure values were obtained from the three time points and used for further calculations.

Data are presented as mean ± sd. Baseline values were compared with values at 4 and 20 min using ANOVA for repeated measurements. When the ANOVA was found significant, Wilcoxon's signed rank test was used to compare the 4-min values to baseline and 20-min values, with Bonferroni correction for multiple comparisons. For all statistical analyses, we used the SPSS software (SPSSTM 12 for Windows, SPSS Inc., Chicago, IL). A P value of <0.05 was considered significant.


   RESULTS
Top
 Abstract
 Introduction
 METHODS
 RESULTS
DISCUSSION
 REFERENCES
 
Systemic hemodynamics, fluid status, hemoglobin, and blood gases only varied within a few percent during the 6-h stabilization period before volume challenge. The results of the volume challenge are shown in Table 1. Central venous pressure increased from 4.6 ± 2.0 mm Hg (baseline) to 6.3 ± 2.2 mm Hg (at 4 min, P < 0.001), and then decreased at 20 min to 5.6 ± 2.2 mm Hg (P < 0.05). Stroke volume increased from 30 ± 6 mL at baseline to 39 ± 7 mL at 20 min (P < 0.001). Cardiac output increased from 83 ± 16 mL · kg–1 · min–1 at baseline to 100 ± 19 mL · kg–1 · min–1 at 20 min (P < 0.05). Mean arterial blood pressure increased from 62 ± 5 mm Hg (baseline) to 76 ± 11 mm Hg (at 4 min, P < 0.001), and then decreased after 20 min to 68 ± 8 mm Hg (P = 0.003).


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  		Table 1. Systemic Hemodynamics

 

Regional blood flows at baseline were as follows: carotid artery: 4.4 ± 1.2 mL · kg–1 · min–1; renal artery: 4.5 ± 1.7 mL · kg–1 · min–1; portal vein: 15.8 ± 6.2 mL · kg–1 · min–1; celiac trunk: 6.5 ± 2.3 mL · kg–1 · min–1; hepatic artery: 2.3 ± 0.9 mL · kg–1 · min–1; and superior mesenteric artery: 15.1 ± 6.0 mL · kg–1 · min–1. Relative changes in regional blood flows are shown in Figure 1. Although the flows became slightly higher in celiac trunk and hepatic arteries after the volume challenge, this increase was not statistically significant. Regional vascular resistance varied after the volume challenge, as shown in Table 2. The percentage increases in flows in superior mesenteric, renal, and splenic arteries, and portal vein were similar at 4 and at 20 min, with high interindividual variability.


Figure 137
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  		Figure 1. Changes in regional blood flows at baseline (100%) and at 4 min (acute effects) and 20 min (sustained effects) after fluid challenge. Values are means ± sd. *Wilcoxon's signed rank test, compared with baseline, P < 0.05.

 

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  		Table 2. Regional Vascular Resistance

 


   DISCUSSION
Top
 Abstract
 Introduction
 METHODS
 RESULTS
 DISCUSSION
REFERENCES
 
Correcting and preventing hypovolemia and increasing systemic blood flow with fluid therapy and vasoactive drugs are the basis for restoring and preserving regional perfusion. The main finding of this study was the very modest increase in celiac trunk and hepatic artery blood flow after volume challenge, which was quite different from the large increase in mesenteric and carotid blood flow. The lack of increase in celiac trunk and hepatic arterial blood flow, and the blunted response of renal blood flow to volume challenge indicate a heterogeneous response to volume expansion, and suggest that the liver and the kidney may be at greater risk for hypoperfusion.

We have previously observed that during isolated reduction and partial restoration of abdominal aortic blood flow, intraabdominal regional blood flows changed in parallel with aortic blood flow, without redistribution.18 The lack of increase in celiac trunk and hepatic artery blood flow in the present study suggests a different vasoregulation in the liver and in the extrahepatic vasculature supplied by the celiac trunk when compared with the other regions. A reduced hepatic arterial buffer response has been observed in low flow states,19 in mesenteric ischemia,20 and in sepsis.21 It is conceivable that major abdominal surgery and prolonged anesthesia may also alter hepatic and celiac trunk blood flow control. We have gradually increased the length of the stabilization period in our pilot experiments from 60 min to 6 h, due mainly to postoperative changes in regional splanchnic blood flows.

Despite the lack of clinically evident hypovolemia, surgery and the associated intravascular volume shifts might have activated the renin–angiotensin system.22,23 Renal hypoperfusion secondary to occult hypovolemia in the perioperative period can trigger a decrease in renal blood flow secondary to increased renal vascular (afferent) resistance. The increase in efferent resistance is mediated by angiotensin II, thus maintaining the glomerular filtration rate. This may well explain the blunted response of renal arterial blood flow to volume challenge.

Changes in regional blood flows in response to changes in cardiac output can be highly variable and related to the underlying clinical condition. In acute hypovolemia in awake subjects, hepatosplanchnic perfusion decreases and remains reduced despite correction of hypovolemia.10,24 In contrast, parallel changes in cardiac output and regional mesenteric blood flow have been observed in various experimental models of low perfusion.25,26

Although in the postoperative period the animals remained stable, our animal model differed from the real physiological situation in certain aspects. The abdominal wall was not totally closed after surgery, as the invasive monitoring of major vessels continued. This required continuous general anesthesia instead of postoperative sedation. The abdominal wall was reapproximated, although the fascia not closed, after surgery, and wet towels were placed on the abdomen to avoid dehydration. This continual perioperative stress after an otherwise uncomplicated surgery also differed from clinical situations.

In the present study, changes in cardiac output were delayed in comparison with changes in regional blood flows. This finding is most likely related to the technique used to measure cardiac output, where the computation of cardiac output includes a delay of several minutes.27 We considered the possibility of continuous measurement to outweigh the disadvantage of the delay in this setting. The relative increase in splanchnic blood flows in the acute phase should therefore be considered, and not their fraction of cardiac output. Nevertheless, the proportional increase in cardiac output at 20 min and the sustained increase in the regional flows, except the celiac trunk and hepatic arterial flows, indicates that the superior mesenteric artery and carotid artery flows increased in parallel with cardiac output. In contrast, the increased systemic flow induced by volume challenge resulted in smaller increase in renal artery flow and only trivial changes in celiac trunk and hepatic artery flow despite an increased mean arterial blood pressure. This implies increased resistance in these vascular beds.

As noted earlier, our study demonstrated that, under clinically euvolemic conditions in the postoperative period, distribution of fluid after a volume challenge favored specific organs, such as the brain, gut, and kidney. Among these organs, interestingly, the vascular resistance decreased only in superior mesenteric and carotid vessels. It also increased in the celiac trunk and hepatic artery. Potential mechanisms involved in cardiovascular system changes in this setting include activation of the sympathetic nervous system, acute baroreceptor actions, viscosity changes, fluid and blood flow redistribution, cytokine and histamine release, and the effects of general anesthesia. Mechanical ventilation during general anesthesia may alter hemodynamics and fluid requirements by increasing intrathoracic pressure. However, standard ventilator settings along with established fluid therapies help maintain the intravascular volume, eventually stabilizing over a certain period. In one study, Connolly et al. showed that isoflurane, but not mechanical ventilation, decreased urinary excretion and increased interstitial fluid volume.28 We did not include any inhaled anesthetics in our study and do not know whether our thiopental/fentanyl anesthetic might have altered organ response to a fluid challenge.

We conclude that the physiological effects of volume challenge under hemodynamically stable perioperative conditions favor certain regional blood flows. Immediate and sustained increases in flows were seen in the carotid, renal, and superior mesenteric arteries, and in the portal vein. There were trivial increases in the celiac trunk and hepatic arterial blood flows, which did not reach statistical significance. It is not known whether the improved postoperative organ perfusion observed in this study might reduce the incidence of perioperative organ injury.


   Footnotes
 
Accepted for publication October 16, 2007.

Supported by grant 3200BO/102268 from the Swiss National Fund.

Dr. Jukka Takala, Section Editor for Critical Care and Trauma, was recused from all editorial decisions related to this manuscript.

Reprints will not be available from the author.


   REFERENCES
Top
 Abstract
 Introduction
 METHODS
 RESULTS
 DISCUSSION
 REFERENCES
 

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Lippincott, Williams & Wilkins Anesthesia & Analgesia® is published for the International Anesthesia Research Society® by Lippincott Williams & Wilkins and Stanford University Libraries' HighWire Press®. Copyright 2008 by the International Anesthesia Research Society. Online ISSN: 1526-7598   Print ISSN: 0003-2999 HighWire Press