A 28-year-old woman is admitted to your unit after sustaining multiple fractures, a blunt myocardial injury, and a retroperitoneal hematoma in a motor vehicle crash. Her blood pressure is 112/56 mmHg, her heart rate 122 bpm, and her skin pale and cool.

A 54-year-old man is transferred to your unit after undergoing elective hip replacement surgery. The post-anesthesia care unit nurse reports that the man lost approximately 900 mL of blood; he received two liters of crystalloid and two units of packed red blood cells. His blood pressure is 128/62 mmHg and heart rate 98 bpm with a urine output of less than 15 mL per hour.

What information can you as a nurse gather from clinical data to indicate the effectiveness of tissue perfusion in these patients? Is the information sufficient for an accurate assessment? Are these signs early or late changes in tissue perfusion? What interventions are appropriate — fluid, blood, vasopressors; all three; nothing? We now have technology to obtain early, accurate information to direct our practice and improve outcomes for patients — gastric tonometry.

In today’s healthcare arena, nurses who care for the very ill are acutely aware of the limited time available to accurately obtain patient information, assess this data, and actpromptly and effectively to best meet the needs of patients. Each year, more than 5 million patients are admitted to critical care units. Critical illness is not only pervasive, but expensive: Critical care services alone accounted for $180 billion in 2006.¹

A noninvasive means of monitoring the regional carbon dioxide level of the gastrointestinal (GI) tissue bed — gastric tonometry — serves as a sentinel and gives nurses early information about end-organ perfusion.²

Nurses use many therapies and medications to improve the perfusion and function of vital organs, such as the heart, lungs, brain, and kidneys. Gastric tonometry is a continuous bedside monitoring system that provides early warning of perfusion abnormalities, leaving ample time for appropriate interventions.^3,4 It can then evaluate the effects of the intervention by assessing perfusion of the gut mucosa, a tissue bed that is sensitive to ischemic events.

Oxygenation and perfusion

Nurses have traditionally used blood pressure, heart rate, urine output, and capillary refill to assess tissue perfusion.⁴ The assumption that justifies the use of these parameters is that as long as a patient has a normal blood pressure, a regular heart rate, an appropriate urine output, and pink, warm skin, all is well. Although this may be true, these indices are global measurements that only reflect general circulation to large tissue beds throughout the body, such as skeletal muscle and skin. These tissue beds may be slow to exhibit signs of severe perfusion defects.^3,4 For example, signs of hypoperfusion in hemorrhagic shock, such as cool temperature or mottling, do not occur until 30% of a person’s blood volume has been lost.^2,4

Another problem with traditional indices is that preexisting disease can obscure the meaning of their readings.⁴ For example, in the first patient scenario above, did the unconscious man have a low urine output because of diminished perfusion of his kidneys from an acute event or from preexisting renal disease? In this case, all problems need to be known to appropriately interpret the traditional indices and accurately assess perfusion.

A device frequently used today to evaluate perfusion is a pulmonary artery (PA) catheter. Although valuable information is collected through this technology, its invasiveness carries its own risks, such as infection, and its complexity requires educated operators to maintain the device and interpret data.²

Modern technology assesses perfusion by evaluating systemic tissue oxygenation (SO2). Adequate oxygenation is achieved when there is a balance between oxygen delivery (DO2) and oxygen consumption (VO2). DO2 relies on factors that affect the transport of O2, such as cardiac output, hemoglobin, and arterial oxygen saturation, while VO2 depends on factors that influence demands for energy, that is, activity, pain, fever, and sepsis.^3,5 Under normal conditions, the DO2 rises and falls to meet the O2 needs of the tissues, and aerobic metabolism is maintained.⁶

When diminished delivery or increased consumption disrupts the delicate balance of oxygenation, the body resorts to a less efficient process (anaerobic metabolism), to generate energy for cell function. Metabolism without oxygen results in the byproduct lactate, which causes cellular acidosis, impairing cellular function; and prolonged acidosis causes cellular death and subsequently organ failure.⁷ Traditional measurements of DO2 and VO2, although important in guiding care, reflect global perfusion and can miss early critical changes in regional perfusion. Gastric tonometry readings can alert nurses caring for critically ill patients when serious perfusion defects in regional tissue beds are occurring, even in the presence of normal vital signs and normal DO2 and VO2 readings.

The body’s canary

In 1856, Claude Bernard first suggested that there was a barrier in the gut that prevented the autodigestion of the stomach by its own acid. It became clear that this protective mucosal barrier relied on a highly vascular tissue bed for adequate oxygenation. Early researchers referred to the gut as the “canary” of the body. Like the canaries coal miners relied on as a harbinger of deteriorating air supplies and impending doom, changes in the gut, related to CO2 and pH, anticipate later alterations that may threaten a patient’s survival.^8,9

The gut or splanchnic circulation is the largest regional blood collection in the body. The spleen, liver, intestine, pancreas, gall bladder, and omentum constitute the splanchnic organs.² The splanchnic circulation contains 20% to 25% of the systemic blood volume and receives 25% (1,500 mL/min) of the cardiac output. The splanchnic circulation is thought to be an optimal monitor for detecting early signs of tissue ischemia and the development of shock. When global perfusion is compromised, blood flow to the splanchnic viscera decreases to a greater extent than does perfusion to the body as a whole. Its early susceptibility to hypoperfusion and responsiveness to even subtle perfusion deficits can detect deterioration in physiologic functioning long before it is revealed by more global indicators, such as blood pressure and heart rate.¹⁰ Thus monitoring of regional CO2 levels, particularly within the splanchnic circulation may indirectly provide information regarding adequacy of tissue oxygenation.^11,12

Two anatomical characteristics of this blood supply predispose the gut mucosa to hypoxia early on during stress, making it an effective early indicator of the adequacy of blood flow to other vital tissue beds. First, the blood supply of the gut flows in a countercurrent matrix from the arterial to the venous beds. During low-flow or ischemic episodes, the matrix works against the gut’s best interest, shunting blood to other organs and leaving large areas of the gut hypoperfused. Blood flow from the arterioles has difficulty making the “hairpin” turns through the matrix, leaving the mucosal bed hypoperfused. Second, the narrow tips of the villi — tiny projections that line the inside of the intestinal mucosa — are particularly susceptible to ischemia.^13,14 While the matrix and villi are well-suited for the absorption of solutes, they fare poorly during periods of hypoxia. Thus, ischemic changes become evident in the gut before they appear in other organs.

The impact of neural and hormonal factors on splanchnic blood flow also makes the gut a useful monitor of ischemia. For example, because sympathetic nerve fibers innervate the gut, circulatory shock or adrenergic “fight or flight” stimulation triggers the release of norepinephrine shunting blood away from the gut.^13-15 Other hormones, such as angiotension II or vasopressin, can cause severe splanchnic vasoconstriction and further compromise flow before other areas of the body are affected.^15,16

Gastric tonometry

Tonometry is defined as the measurement of the tension or pressure of an entity, such as intravascular tension or blood pressure. In gas exchange physiology, tonometry refers to the equalization of partial pressures between a fluid, such as blood or saline, and a gas. The technique relies on bringing the fluid and gas components in close contact so that over time, their partial pressures will be similar. Tonometers have been described in the literature as early as 1926.¹⁷ It was not until 1959 that two Hungarian physicians actually employed the technology of gastric tonometry to adjust the ventilators of children who were paralyzed by polio.^8,18

In a hypoperfused gut, ischemia increases hydrogen ion production, lactate formation, and the accumulation of carbon dioxide (CO2).¹⁹ Carbon dioxide produced as a result of cellular activity should move from an area of higher partial pressure (gastric mucosa) to an area of lower partial pressure (gastric lumen).¹¹ Because CO2 diffuses freely across tissue and cell membranes,¹⁸ the partial pressure of CO2 (PgCO2) in the stomach approximates the PCO2 of the gut mucosa. Gastric tonometry detects increasing levels of CO2 in the stomach as blood flow diminishes and acidosis develops.

The technique for measuring stomach PCO2 uses a gastric tonometer — a modified nasogastric (NG) tube with a gas-permeable silicone balloon. The gastric tonometer looks like any other 16Fr- or 18Fr-NG tube: It has a lumen with a distal opening that allows decompression of the stomach or the instillation of medications or fluid. However, a secondary lumen is tipped with a gas-permeable silicone balloon.

The balloon is filled with 2.5 mL of normal saline that equalizes with the CO2 in the gastric lumen after 30 minutes to 90 minutes of equilibration time. After that, the saline-filled balloon will theoretically have the same PCO2 as the mucosal membrane of the stomach. Sampling requires removal of 1 mL of deadspace saline then with a different syringe aspiration of the remainder 1.5 mL. The latter will be the tonometric sample.^2,11 At the same time an arterial blood sample is obtained to determine the amount of bicarbonate ion (HCO3) present. Both of these values are entered into a modified Henderson-Hasselbach equation to calculate the intramucosal pH.^20-22 This method is based on the assumption that: (1) CO2 diffuses freely, (2) PCO2 in the luminal fluid equilibrates with mucosal PCO2, and (3) arterial bicarbonate concentration equals the gut mucosal bicarbonate. During low-flow states there is more time for CO2 to equilibrate, causing an increase in PgCO2.²³ As a result, splanchnic tissues become hypoxic and result in less efficient anaerobic metabolism, producing more CO2, increased PgCO2, and subsequent decreased pHi. Normal values are similar to normal serum levels: PgCO2 is 35 mmHg to 45 mmHg and pHi is 7.35 to 7.45.^{11, 20-24, 26}

A normal pHi — greater than 7.35 — indicates adequate tissue oxygenation. A pHi value of less than 7.35 for extended periods of time indicates tissue hypoxia and subsequent acidosis. Trending the PgCO2 value also monitors tissue perfusion. A PgCO2 value that rises above 45 indicates hypoperfused tissue beds.^24-26

The PCO2 gap is another measurement that can be used to monitor tissue perfusion and may be more accurate than pHi alone.^15,27 The PCO2 gap is the difference between PgCO2 and the patient’s PaCO2 (P [g-a] CO2) and it may be the preferred method for evaluating perfusion because —

1. An increase in the veno-arterial PCO2 gradient reflects tissue hypoperfusion more accurately than pHi alone.
2. The arterial bicarbonate level is assumed to be equal to the intra-mucosal bicarbonate level when the pHi is calculated using the Henderson-Hasselbach equation; but hypoperfusion may cause a discrepancy between these levels.
3. The systemic arterial bicarbonate used to calculate pHi is influenced by factors other than tissue hypoperfusion, such as, renal failure.²²

A normal PCO2 gap is less than 10 mmHg in normal physiologic states. A widening gap reflects compromised blood flow to the splanchnic bed; and a gap exceeding 20 mmHg indicates severe hypoperfusion and the need for aggressive intervention.²²

Whether pHi, PgCO2, and/or PCO2 gap are used to monitor perfusion the nurse should observe trends in the values rather than focusing on single measurements. When an abnormal value occurs, the nurse needs to evaluate the influence of pathophysiology, such as renal failure; activities such as operator error, presence of enteral feedings, tube migration, aggressive gastric suctioning; or administration of pharmacological agents, such as H2 blockers or vasopressors that could affect accuracy of measurements.^11,16,28

Gastric tonometry using the dual specimen technique (NG saline and arterial blood samples) can be labor-intensive. It also requires a high degree of accuracy in sample drawing, timing, flushing, and calculation. A mistake at any step could produce a measurement that misdirects therapy.²⁴ The newer technique obtains pHi by inserting a balloonless fiberoptic CO2 probe that provides bedside monitoring of end-tidal CO2 (EtCO2), pHi, and actual PgCO2 levels. Measurements are calculated automatically and digitally displayed at 10-minute intervals.^3,22,29 Semicontinuous sampling of PgCO2 using has also been developed using air as a tonometer medium. Both the Tonocap TC-200™ and Tonometery Module, M-TONO are devices that allow for monitoring of intramucosal CO2 air. Data show good correlation between air and saline tonometry with less operator error.¹¹

In the third patient scenario, the patient’s vital signs are relatively normal. However, gastric tonometry readings — pHi of 7.27 and PgCO2 of 49 — reveal perfusion deficits from blood loss in the OR. After more packed red cells and IV fluids, his pHi and PgCO2 normalize.

Managing the tube, nursing the patient

Catheters used for gastric tonometry are no more invasive or uncomfortable than conventional NG tubes. Nurses may insert them, but placement needs radiographic confirmation to be certain that the catheter sits in the stomach.²⁶ After initial setup and calibration, the monitor automatically displays readings at predetermined intervals.

Nurses who use gastric tonometry to monitor their patients must be certain that the values are accurate. Any aspects of care that can alter readings should be monitored and evaluated. For example, enteral feedings can lower the pHi, elevate the PgCO2 and thus widen the PCO2 gap, making it difficult to determine if the drop is due to mucosal ischemia or the feedings.^24,28 Postpyloric enteral feeding eliminates this problem. It has also been observed that CO2 variability tends to decrease after 24 hours of continuous enteral feeding. However it is still recommended to withhold enteral nutrition for a minimum of one hour prior to sampling.¹¹ Conflicting evidence does exist as to whether this timeframe is absolutely important to obtain accurate readings.²³

The acid environment of the stomach can also elevate PCO2 in the gastric lumen, confusing the etiology of the pHi measurements. It has been recommended that patients monitored by gastric tonometry receive H2 blocker therapy, such as ranitidine (Zantac) or cimetidine (Tagamet) to control bicarbonate buffering of hydrogen ions.² The need to suppress gastric acid secretion remains an area of uncertainty and evidence is conflicting.^11,27 Aggressive suctioning of gastric contents may falsely lower the PCO2, subsequently elevate the pHi, and alter the PCO2 gap. Therefore, gastric decompression should be by gravity. If low-intermittent suction is needed though, then it should be discontinued 30 minutes before obtaining a reading.^30,31 Patients with renal failure or metabolic acidosis can alter tonometric readings due to inherent decreased plasma bicarbonate levels.²⁸ Despite the various problems discussed, monitoring gastric pHi has proved to be of prognostic value in a wide variety of critically ill patients.¹⁰ Clearly a sustained PgCO2 gap is suggestive of splanchnic hypoperfusion and worse clinical outcome.²⁸

Nurses play an important role in monitoring the effects of disease and medical therapy on the delicate balance between oxygen delivery and consumption. Gastric tonometry represents yet another innovative bedside diagnostic tool that can provide early information about decreased tissue perfusion. Nurses caring for these patients can also monitor how nursing interventions affect oxygen consumption. For instance, if turning a patient causes an increase in PCO2 and a decrease in pHi, the nurse would know that this patient needs a period of time to recover before instituting other care. Gastric tonometry can more effectively direct the therapeutic use of fluid, blood, or vasopressor therapies, improving the quality of care and patient outcomes.^16,32

Evidence is accumulating that this technique can aid in fluid resuscitation across the continuum of care.^14,19 There is also promising data suggesting that gastric tonometry can facilitate early diagnosis of abdominal compartment syndrome in those patients at risk for this life-threatening complication.³³