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Ann Thorac Surg 1996;61:817-822
© 1996 The Society of Thoracic Surgeons

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Original Articles: Cardiovascular

The Gastrointestinal Tract: An Underestimated Organ as Demonstrated in an Experimental LVAD Pig Model

Centre de Recherches Chirurgicales, Centre National de Recherche Scientifique, Unité de Recherche Associée 1431, Centre Hospitalier Universitaire Henri Mondor, Créteil, France

Accepted for publication November 1, 1995.

	Abstract

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Background. Although hemodynamic stability and renal function are important and are monitored closely in patients with implanted left ventricular assist devices (LVAD), the gastrointestinal tract may be underestimated in the early postoperative period with regard to adequate perfusion. We investigated renal, intestinal, and whole body metabolic changes in response to variations in LVAD flow and inspired oxygen concentration (FiO₂).

Methods. Left ventricular assist devices were implanted in 10 adult pigs (weight, 55 ± 1.76 kg). Renal vein (RV), superior mesenteric vein (SMV), and pulmonary artery (PA) blood oxygen saturation and lactate concentration were measured and used as tissue perfusion markers. These measurements were made at baseline and after changes in LVAD flow or FiO₂.

Results. Oxygen saturation in the PA, SMV, and RV decreased significantly after a reduction in LVAD flow (p = 0.05), with a greater reduction in the SMV than in the PA and RV (p < 0.05 at LVAD flow 3.5 L/min; p < 0.01 at LVAD flow 2.0 and 1.0 L/min). The lactate concentration in the PA and SMV increased significantly (p < 0.01) with decreased flow, with a greater increase in the SMV than in the PA (p < 0.05), whereas it remained unchanged in the RV. Oxygen saturation in the PA, SMV, and RV decreased significantly after a reduction in FiO₂ (p < 0.05). Lactate concentration in the PA, SMV, and RV increased significantly at FiO₂ of 0.10 (p < 0.05). Lactate concentration in the PA and SMV was significantly higher than that in the RV at FiO₂ of 0.10 (p < 0.01).

Conclusions. The results show that the gastrointestinal tract is at high risk during low perfusion or low FiO₂, whereas the kidneys' metabolic function appears to be less disturbed. In clinical practice, this emphasizes the need to ensure adequate blood flow and respiratory function, especially after extubation, in patients with implanted LVAD. This might avoid intestinal ischemia and subsequent endotoxemia. Gastrointestinal tonometry may help in the assessment of intestinal perfusion.

	Introduction

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
The use of left ventricular assist devices (LVADs) has increased in patients with end-stage cardiac failure due to either acute (eg, postcardiotomy) or chronic (eg, dilated cardiomyopathy) cardiac decompensation [1–4]. These devices have so far been used as a temporary support for the circulation awaiting myocardial recovery after the acute insult or as a bridge to transplantation awaiting a suitable donor heart [1–11]. With the increase in demand for orthotopic heart transplantation and the shortage of donor hearts, there has been an increase in the last 2 decades in the frequency and length of time that these devices have been used.

There are a number of LVAD-related complications that can occur, including bleeding, thromboembolism, and infection [1–3, 9–14]. The incidence of infection in these very sick patients is a major concern for the clinician, as infection is often difficult to eradicate and is associated with increased morbidity and mortality [1–3, 9–14]. Infection still accounts for about one third of LVAD-related complications [11–3, 9–14] and was even as high as 73% in one report [11]. This high incidence of infection is related to a number of factors, including a large foreign body with percutaneous access, poor preoperative nutrition status [11, 14], postoperative bleeding [11–3, 9–14], prolonged respiratory support, prolonged use of the intravenous cannula, and more advanced patient age [1, 12–14]. Prevention of infection is thus a priority for clinicians managing these patients. Preventive techniques include strict operative management with regard to sterility, prevention of bleeding, careful tissue handling with minimal but adequate exposure, and use of prophylactic antibiotics. To prevent the complications associated with prolonged intensive care, in particular infection, it is often emphasized that extubation and withdrawal of the intravenous cannula should be performed as early as possible in the postoperative period to mobilize the patients and thus decrease intensive care–related morbidity.

Patients who receive LVAD implantation are often unstable hemodynamically. They may have multiple systemic problems including end-organ dysfunction and metabolic derangement. If there is any compromise in the flow of blood to an organ, there may be deleterious consequences. One of the organs that can be affected is the gastrointestinal tract (GIT). Decreased splanchnic blood flow will result in GI ischemia and subsequently endotoxemia because of the decreased ability of the gut mucosa to act as a barrier against translocation of intraluminal pathogens [15–21].

In this experiment, we investigated the effects of reducing the inspired oxygen concentration (FiO₂) or systemic blood flow on renal, intestinal, and whole body metabolic responses in pigs implanted with an LVAD. Venous blood saturation and blood lactate concentration were used as tissue perfusion markers [22–24].

	Material and Methods

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Operative Procedures
Ten pigs (weight, 55 ± 1.76 kg; range, 48 to 64 kg) were used. All animals received humane care in compliance with the ``Principles of Laboratory Animal Care'' formulated by the National Society for Medical Research and the ``Guide for the Care and Use of Laboratory Animals'' published by the National Institutes of Health (NIH publication 85-23, revised 1985).

All pigs were anesthetized with intravenous pentobarbitone (30 mg/kg), mechanically ventilated through an endotracheal tube, and maintained with 1% to 2% halothane and 40% oxygen. An arterial catheter was inserted in the right carotid artery for continuous measurement of arterial blood pressure and for measurements of arterial oxygen saturation (SO₂) and lactate concentration. A pulmonary artery (PA) catheter (Swan-Ganz thermodilution; Baxter, Irvine, CA) was inserted in the right jugular vein to measure right cardiac output, PA SO₂, lactate concentration, and right atrial and pulmonary arterial pressures.

Through a left thoracotomy, we excised the fifth and sixth ribs and exposed and prepared the descending aorta for anastomoses of the outflow graft from the LVAD. The pericardium was opened through a longitudinal incision, and a pursestring suture was inserted in the wall of the left atrium in preparation for insertion of the inflow cannula. A long paramedian incision was then performed on the abdomen, and through a retroperitoneal approach, the superior mesenteric and left renal arteries were located and mobilized. The superior mesenteric vein (SMV) and renal vein (RV) were located, and each vein was cannulated to obtain blood samples later in the procedure.

After intravenous heparin administration (300 U/kg), the outflow tract from the pump was anastomosed end to side to the descending aorta. The tip of the inflow cannula was inserted into the left atrium through the previously created pursestring suture. The pneumatically driven artificial heart (Nippon Zeon Co Ltd, Tokyo, Japan) was connected to the inflow and outflow tubes, and the pump was placed extracorporeally on the chest. Care was taken to exclude air from all parts of the circuit.

Experimental Protocol
Baseline hemodynamic indices and blood samples for later analysis were taken with the pump circuit clamped. The pump was then started, aiming to reach a flow of 3.5 L/min. To study the influence of changing LVAD flow on the rest of the body, we decided to clamp the ascending aorta at this stage. Thus, all systemic blood flow was dependent on the LVAD flow, with no contribution from the left ventricle. At a constant LVAD flow (3.5 L/min), the FiO₂ was varied in the latter part of the experiment.

CHANGING THE FLOW OF THE PUMP.
The LVAD flow was reduced from 3.5 to 2.0 to 1.0 L/min sequentially. The FiO₂ was maintained at 0.40 and the body temperature was kept at 36°C. Changing the LVAD flow was achieved by changing the systolic and diastolic pressures of the console and changing the pump rate. To achieve 1.0 L/min flow, partial clamping of the inflow cannula was required.

CHANGING THE INSPIRED OXYGEN CONCENTRATION.
The FiO₂ was reduced from 0.80 to 0.40 to 0.10 sequentially with the ascending aorta clamped. The LVAD flow was kept at 3.5 L/min and the body temperature was at 36°C. Changing the FiO₂ was achieved by reducing the flow of oxygen in the ventilator. To obtain 0.10 FiO₂, we added NO₂ gas.

After 5 minutes of stabilization following the change in flow of the LVAD or in FiO₂, measurements were taken. After each change, the flow of the LVAD was returned to 3.5 L/min and the FiO₂ was returned to 0.40.

Hemodynamic Measurements
The pigs were evaluated by monitoring the electrocardiogram; pressure measurements in the right atrium, PA, and aorta (Hewlett-Packard 7758B system; Hewlett-Packard France S.A., Evry, France); flow in the mesenteric and left renal arteries (Micron MU-1001-B; Micron Instruments, Inc, CA); and right cardiac output (Swan-Ganz thermodilution, Baxter).

Measurement of Oxygen Saturation
Oxygen saturation was measured in the carotid artery, PA, SMV, and left RV (1306 pH/Blood Gas Analyzer; Instrumentation Laboratory, R. Delhomme, France).

Measurement of Lactate Concentration
Lactate concentration was measured in the carotid artery, PA, SMV, and left RV. The lactate concentration in the PA, the SMV, or the left RV minus the lactate concentration in the carotid artery was taken as the lactate concentration in the body, GIT, or kidney, respectively.

Statistical Analysis
Results are given as mean ± standard error of the mean. Comparisons were done by paired t test, and p < 0.05 was considered significant.

	Results

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
The average weight of the 10 pigs was 55 ± 1.76 kg. The baseline mean heart rate was 105 ± 2.9 beats/min, and mean pressure in the aorta was 83.3 ± 5.7 mm Hg. The mean cardiac output before clamping was 5.74 ± 0.2 L/min; therefore, LVAD flows of 3.5, 2.0, and 1.0 L/min represent about 60%, 30%, and 20%, respectively, of the resting cardiac output. The arterial SO₂ was greater than 99% during the baseline measurements.

Changing the Flow of the Left Ventricular Assist Device
Table 1 shows the hemodynamic changes with alterations of the LVAD flow. As can be seen, the mean aortic pressure and heart rate decreased significantly when the LVAD flow was reduced to 1.0 L/min. Right cardiac output decreased significantly when the LVAD flow was reduced to 2.0 and to 1.0 L/min.

Oxygen saturations in the PA, left RV, and SMV decreased significantly after the reduction in FiO₂, with the greatest reduction in the SMV (Table 5).

	Comment

Top Footnotes Abstract Introduction Material and Methods Results Comment References

It is often perceived that early extubation and mobilization are important to prevent pulmonary and indwelling catheter infection [1, 12–14]. Although these are desirable, they may not be suitable, especially in patients with borderline hemodynamic indices or gas exchange.

In this experiment, we attempted to mimick the clinical situation of LVAD-dependent circulation in a pig. By changing either the FiO₂ or LVAD pump flow, we studied the metabolic effects of such changes on the GIT, kidney, and whole body. This may have similarity to the clinical situation when attempting to wean the patient from the respiratory pump or inotropic support.

Changing the Flow of the Left Ventricular Assist Device
Our results show that SO₂ in the PA, left RV, and SMV decreased significantly after a reduction in LVAD flow, with the greatest reduction measured in the SMV (see Table 2). In addition, lactate concentrations in the PA and SMV increased significantly with the reduction of LVAD flow to 1.0 L/min. Lactate concentration was greater in the SMV than in the PA, but remained unchanged in the RV (see Table 3). Finally, blood flow in the superior mesenteric and left renal arteries decreased significantly when the LVAD was reduced to 2.0 and 1.0 L/min (see Table 4).

Renal blood flow accounts for about 20% of cardiac output in the human [25, 26]. This is required because the kidney has an important excretory function, thus maintaining blood homeostasis. Despite this large blood flow to the kidneys, the renal metabolic requirements are low [27]. In fact, it has been demonstrated that the oxygen consumption of the kidney is about 4.6 mL• min^-1•100 g^-1 in the human [25], which is consistent with our results. Although the SO₂ in the RV and the blood flow in the renal artery decreased significantly after a reduction in LVAD flow, the lactate concentration in the RV remained unchanged, which confirms the low metabolic requirements of the kidneys. Thus, it appears that the kidneys may be able to tolerate an LVAD flow as low as 1.0 L/min.

At 1.0 L/min LVAD flow, the lowest SO₂ (32.6% ± 3.2%) and the highest arterial minus venous SO₂ difference (65.4% ± 3.5%) were measured in the SMV. At this flow, the highest lactate concentration was also measured (0.81 ± 0.2 mmol) in the SMV. In their report, Robison and colleagues [24] indicated that anaerobic metabolism was demonstrated by a rise in the arterial lactate concentration greater than 1.0 mmol/L and a reduction of SO₂ to less than 40% (the actual lactate concentration was different from our results because they used the arterial lactate concentration in their experiment). Our results indicate that at this low flow status, the GIT shows signs of anaerobic metabolism, which thus indicates GI ischemia. The metabolic indices of the kidney suggest that they are able to tolerate this status better over this short period of time.

Oxygen saturation and lactate concentration in the PA reflect total body metabolic function, which includes the brain, heart, liver, skin, muscle, kidney, and GIT. Several authors have demonstrated that SO₂ and lactate concentration in the PA are useful as markers of tissue perfusion [2222–24]. From our results, it appears that the lactate concentration and SO₂ in the PA were better than those in the SMV but worse than those in the RV. This is a reflection of the venous blood return from all the organs mixing in the right atrium and consequently the PA. Therefore, PA lactate concentration and SO₂ do not specifically point to an organ that may have an increased risk of malperfusion relative to another organ, despite the reports that indicate that both may reflect adequate tissue perfusion, as we have demonstrated from our results.

Finally, blood flow in the superior mesenteric and left renal arteries decreased significantly when the LVAD flow was reduced to 2.0 and 1.0 L/min. There was no significant difference in the reduction in blood flow between the renal and superior mesenteric arteries (see Table 4). This validates our assumption that the reduced systemic blood flow (due to the reduction in LVAD flow) is similar in the renal and GI large-vessel beds. However, the GI metabolic indices at these low flow states indicate that the GIT is more susceptible to ischemia, which suggests a problem of the small-vessel mucosal blood supply.

The GIT can compensate somewhat for this low blood flow. Granger and Norris [21] demonstrated that a 64% fall in mean aortic pressure results in only a 40% fall in intestinal blood flow, attributed to a decrease in intestinal vascular resistance. However, our results showed that even at 50% reduction in mean aortic pressure, there was a significant decrease in large-vessel blood supply to the GIT.

Changing the Inspired Oxygen Fraction
Our results show that SO₂ in the PA, left RV, and SMV decreased significantly after a reduction in the FiO₂, with a greater decrease in the SMV than in the PA and left RV (see Table 5). Lactate concentrations in the PA and SMV increased significantly when the FiO₂ was reduced to 0.10, with a greater increase in the PA than in the SMV (no statistically significant difference), whereas it remained almost unchanged in the RV (see Table 6). Blood flow in the two arteries did not change with alterations of FiO₂ (see Table 7).

Although the SO₂ in the RV decreased significantly after a reduction in the FiO₂, this was only down to 61.6% ± 4.4% at an FiO₂ of 0.10. The lactate concentration did not increase significantly. We therefore assume that this reduction in the FiO₂ was within an acceptable range. This confirms our previous statement that despite the high blood flow to the kidneys (20% of cardiac output), the oxygen consumption (4.6 mL•min^-1•100 g^-1 in the human) is low [25, 26]. It therefore appears that the kidney may be able to tolerate low FiO₂, even as low as 0.10.

As discussed previously, SO₂ in the SMV showed a greater reduction than in the PA at low FiO₂. At 0.10 FiO₂, the SO₂ in the PA and SMV were almost the same value. In addition, lactate concentrations in the PA and SMV increased significantly at 0.10 FiO₂. Therefore, at low FiO₂, there is an increase in anaerobic metabolism in the GIT and the rest of the body, although the kidneys appear to tolerate this better. The implication of this is that hypoxia after LVAD implantation will cause substantial ischemia in various organs, including the GIT. This will be discussed later.

We have so far shown that the GIT was the most susceptible organ at low LVAD flow or low FiO₂ in our experimental study. In addition, although the kidney appeared to tolerate low blood flow or hypoxia because of its lower metabolic demands, other organs may be at risk, especially in hypoxic situations, as demonstrated by the PA lactate concentration and SO₂.

Our study has several clinical implications. Patients who require LVAD support often have been in a low blood flow state for a few days. This is reflected in poor urine output, which can progress to acute renal failure. We have demonstrated that the kidneys can tolerate low oxygenation and blood flow. Thus, acute renal failure per se is not a contraindication to the use of mechanical assist devices, a conclusion supported by clinical experience [28]. Renal function may improve after restoration of adequate blood flow and oxygenation with an appropriate mechanical assist device. Artificial renal support may be required for a time until the return of adequate kidney function.

Over recent years, the importance of the GIT has been more widely recognized with regard to patients in shock or in an intensive care setting [29, 30]. In addition, cardiopulmonary bypass (CPB) is associated with a 0.58% to 2% incidence of GI-related complications, such as gastric erosions and ulcers, esophagitis, duodenal ulcers, cholecystitis, pancreatitis, and colitis [31].

Cardiopulmonary bypass has been shown to be associated with an increased risk of endotoxemia [32] due to CPB-induced gut mucosal hypoperfusion [33]. In addition, endotoxemia has been implicated in irreversible decreases in systemic vascular resistance after use of the Jarvik artificial heart [34]. The mechanism of endotoxemia is thought to be bacterial translocation across the gut mucosal barrier [35]. The combination of CPB-induced mucosal hypoperfusion and the results from our experiment indicating GI ischemia with LVAD-supported circulation, albeit under low flow or hypoxic conditions, supports our policy of implanting an LVAD without CPB if possible [36]. Thus, in those very sick patients receiving LVAD support, the GIT appears to be at risk from conditions of low flow (eg, when attempting to wean from the assist device) or hypoxia (eg, after extubation). Careful monitoring by measuring the PA lactate concentration or SO₂, combined with the usual indices of adequate perfusion such as hourly urine output and continuous invasive hemodynamic monitoring, may not indicate the occurrence of intestinal ischemia.

Gastric and colonic tonometry has been used in monitoring GI perfusion. The principle of this technique is simple [37]. A balloon-filled catheter is introduced in the lumen of the viscus (stomach or colon) to measure intraluminal partial pressure of carbon dioxide, which is a measure of mucosal partial pressure of carbon dioxide. It is then possible to calculate the mucosal pH, which provides a simple index of mucosal blood flow. Gastric or colonic tonometry has been used and validated in the context of CPB [33, 38], although some reports have suggested that gastric tonometry does not reflect changes in splanchnic blood flow and oxygen delivery [39]. This may reflect heterogeneous or inadequate blood flow distribution within the spanchnic regions. Tonometry can thus be a further noninvasive and simple tool for the management of patients with LVAD.

In conclusion, our data show that the GIT is at more risk than can be appreciated from the usual indices of tissue perfusion in an LVAD-supported circulation. The kidneys appear to tolerate these conditions better. We are following this experiment with a further study to evaluate the incidence of endotoxemia under these conditions of hypoxemia and low perfusion.

	Footnotes

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 
Address reprint requests to Dr Loisance, Centre de Recherches Chirurgicales Henri Mondor, Faculte de Medecine-CHU Henri Mondor, 8, Rue du General Sarrail, 94010 Creteil, France.

	References

Top Footnotes Abstract Introduction Material and Methods Results Comment References

 

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This Article Abstract Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Add to Personal Folders Download to citation manager Author home page(s): Philippe H. Deleuze Daniel Y. Loisance Permission Requests Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Miyama, M. Articles by Loisance, D. Y. Search for Related Content PubMed PubMed Citation Articles by Miyama, M. Articles by Loisance, D. Y.