Related Column: Continuing Along with End Points
An air medical transport team is called to the intensive care unit of a local referring center for a 27-year-old male brought to the emergency department after a high-speed rollover motor vehicle crash. The patient sustained a closed head injury and an open-book pelvic fracture. The crash occurred two hours prior to the team’s arrival at the referring center. He is still in spinal precautions, intubated, and has a pelvic binder in place.
Prior to the crew’s arrival on the unit, the patient had received four units of type-specific packed red blood cells (PRBCs) and six liters of crystalloid. He is restless and fighting mechanical ventilation. Blood pressure is 100/56. The monitor is showing a sinus rhythm at 104 beats per minute. Peripheral pulses are palpable and the patient’s skin is warm, dry and pale. His oxygen saturation is 96 percent on 1.0 fiO2. There is approximately 100 ml of amber urine in the patient’s urimeter.
While serum potassium level is slightly elevated at 5.5 mEq/liter, electrolytes are relatively normal. Hemoglobin and hematocrit are 12 gm/dl and 35 percent, respectively. Serum and urine toxicology screens are negative and the most recent arterial blood gas (ABG) includes a pH of 7.21, a PCO2 of 38 mmHg, a PO2 of 120 mmHg, and bicarbonate of 16 mEq/liter.
With a mean arterial pressure (MAP) of 71mmHg and an oxygen saturation of 96 percent, the patient appears to be stable from a hemodynamic perspective. Is this an accurate assessment? Is further resuscitation required? How do we know?
Determining Adequacy of Resuscitation
The patient in the above scenario is obviously suffering from hypovolemic shock. The point of contention is whether or not adequate resuscitation has occurred. Regardless of the type of shock involved, adequate resuscitation is dependant upon the maintenance of aerobic cellular metabolism. In order for this to occur, adequate blood flow needs to be delivered to the tissues and oxygen delivery must meet or exceed tissue requirements. This is where traditional hemodynamic parameters such as blood pressure, heart rate, mental status and urine output fail in terms of determining ongoing tissue hypoperfusion and hypoxia.1
Resuscitation Endpoints
Parameters that more accurately assess the adequacy of perfusion and oxygenation at the cellular level should be used to evaluate the effects of treatment, especially in the setting of shock. Some of these parameters are easily accessible to the air medical transport provider either at the bedside or in transit. Others require specialized equipment and training. While there is still debate with respect to the most appropriate endpoints for evaluating the effectiveness of resuscitation, some examples of values which accurately estimate “global” tissue oxygenation include:1,2
- Serum Base Deficit
- Serum Lactate
- Central Venous Oxygen Saturation (ScVO2)
- Mixed Venous Oxygen Saturation (SVO2)
- Calculation of Oxygen Content (CaO2), Delivery (DO2) and Consumption (VO2)
Additionally, the use of capnography and esophageal dopplers have been suggested to have merit in assessing tissue perfusion.
Practically Speaking
Looking at our trauma patient in the above case, three parameters were utilized in helping to guide resuscitative efforts: serum lactate, base deficit and capnography. As previously mentioned, standard or “traditional” hemodynamic parameters fail to adequately reflect the degree of physiologic derangement in this trauma patient at the cellular level. While there are limitations to these global endpoints, they can be used to determine the need for further intervention including fluid resuscitation with blood and crystalloid, as well as surgery.
Serum Lactate
Lactic acid is produced as a result of anaerobic metabolism, which is common in shock states where oxygen demand exceeds supply secondary to tissue hypoperfusion. Several studies have demonstrated the direct correlation between patient mortality and time taken to reach normalization of lactate levels.2 Trending lactate levels has been utilized as a method to steer treatment at the bedside. Several air medical programs have reported success with point-of-care testing to measure lactate levels and base deficits, such as the “i-stat©” device from Abbott (http://www.abbottpointofcare.com/istat/). Normal lactate levels range from 0.5-2.2 mmol/L.
Base Deficit
Base deficit is a decrease in the total concentration of bicarbonate, or buffer (normal range is -2 to 2 mEq/liter). It is measured during a blood gas analysis. An elevated base deficit during resuscitation can indicate inadequate oxygen delivery to tissues. It is often more readily available for analysis than serum lactate levels.1 Caution is warranted when using base deficit as the sole indicator of oxygen debt as other therapies and clinical conditions can affect this value (e.g., alcohol or cocaine use, administration of bicarbonate or diabetic ketoacidosis).1 This value has been used to guide fluid resuscitation in actual and relative hypovolemic shock states.
Capnography
Traditional end-tidal CO2 monitoring may be a valuable tool for providing an indication of perfusion. Changes in ETCO2 with no change in ventilatory status (i.e. minute volume) is a direct reflection of cardiac output and blood flow through the lungs.3 Decreased cardiac output secondary to hypovolemic shock will cause an alteration in the amount of CO2 delivered back to the lungs. This results in a lower end-tidal CO2 (ETCO2) reading. Clinicians often confuse this with a change in the patient’s ventilatory status rather than a change in perfusion. Being mindful of this concept can assist the clinician in utilizing capnography to its full potential.
Conclusion
Endpoint values are important indicators for determining adequacy of initial and ongoing resuscitation. Endpoints are essential to guide stabilization efforts and help the air medical transport provider decide the needs for further intervention. They can be measured and utilized at the bedside as well as during transport, along with traditional parameters. Resuscitation endpoints should be used to determine the overall clinical picture of any critically ill patient in shock. Next month we will look at additional endpoints useful for management of patients in shock.
References
1. Goodrich C. Endpoints of Resuscitation: What should we be monitoring? AACN Advanced Critical Care 17(3); 2006. pp. 306-316.
2. Napolitano LM. Resuscitation Endpoints in Trauma. Transfusion Alternatives in Transfusion Medicine 6(4); March 2005. pp. 6-14.
3. Jin X and Weill MH et. al. End-tidal Carbon Dioxide as a Noninvasive Indicator of Cardiac Index during Circulatory Shock. Critical Care Medicine 28(7); July 2000. pp. 2415-2419.
