Use these parameters to adequately assess tissue perfusion,as traditional monitoring may not tell the full story.
After a prolonged and stressful resuscitation, your staff members are congratulating each other on restoring the patient's vital signs and reversing life-threatening shock. The patient's blood pressure (BP) is higher than 90 mm Hg, his heart rate is just under 120 beats/minute, and a bit of concentrated urine is trickling down the indwelling urinary catheter to the drainage pouch. Do these encouraging clinical physiologic parameters indicate that the patient is out of the shock state? Not necessarily.
For shock to be reversed, perfusion and oxygenation must be reestablished at the cellular level. Knowing whether or not this has occurred can be a challenge, even for the most experienced critical care nurses.
Why traditional monitoring falls short
In compensated, or Phase I, shock, compensatory responses triggered by the sympathetic nervous system help maintain vital signs. The heart rate is mildly elevated, the BP remains within normal limits with a slightly narrowed pulse pressure, and the urine output decreases slightly-all of which can cause clinicians to prematurely cease resuscitation efforts. Changes in vital signs become alarming during uncompensated, or Phase II, shock: The heart rate increases above 110 beats/minute, BP falls noticeably, and urine output decreases further.
Here's why these preliminary clinical assessment parameters can be misleading.
[white diamond suit]Heart rate may not adequately reflect the patient's degree of compromise. Geriatric patients may be unable to mount a tachycardic response to shock and their cardiac medications can interfere with heart rate. Pain, anxiety, and hyperthermia can further elevate heart rate.
[white diamond suit]Blood pressure is a function of cardiac output (CO) and systemic vascular resistance (SVR) rather than tissue perfusion itself. The usual resuscitation target of a systolic pressure of 90 mm Hg may be well below a patient's usual baseline. Use of vasopressors can easily augment the SVR to achieve a "normal" BP, but this vasoconstriction exacerbates the tissue perfusion deficit. Similarly, the catecholamine response to stressors, including cold, agitation, head injury, and pain, aggravates cellular hypoxia while maintaining a normal BP.
[white diamond suit]Urine output is unreliable as a resuscitation guide. Patients who are elderly, hypothermic, or who have renal dysfunction can't concentrate urine normally, resulting in falsely high urine outputs that may not accurately represent intravascular volume status.Critically ill and injured patients can be oliguric for many reasons, including urinary system obstructions, acute tubular necrosis, and medication-induced nephrotoxicity, all of which may coexist with shock. Also, the renal system is one of the first systems compromised and one of the last to regain perfusion during shock, suggesting that urine output serves as a useful guide only for limited times during resuscitation.
[white diamond suit]Body temperature is unreliable since temperature regulation is significantly impaired by shock. Staff members may not be able to accurately gauge how much of their patient's hypothermia is due to exposure and how much is due to refractory shock. Vasoconstriction and decreased CO resulting from hypothermia increase SVR, which raises BP regardless of actual intravascular volume.Further, hypothermia gives hemoglobin an increased affinity for oxygen. As a result, hemoglobin may be well saturated with oxygen, but hypothermia may prevent it from releasing oxygen to the tissues, causing cellular hypoxia despite normal vital signs.
[white diamond suit]Hemodynamic monitoring via pulmonary artery (PA) catheters can provide more informative data, but also has limitations. Determining adequate preload in critically ill or injured patients with complications is a challenge because central venous pressure (CVP) and pulmonary artery wedge pressure (PAWP) values are greatly influenced by many factors, including cardiac function. These numbers reflect how much pressure is exerted on fluid in the cardiopulmonary structures but not the actual volume present.Consequently, a patient with seemingly adequate cardiac filling pressures may actually be hypovolemic. Systemic vascular resistance, a derived parameter based on calculations using BP and heart rate data, may not accurately reflect volume status for reasons described earlier.
[white diamond suit]Right ventricular end-diastolic volume index (or RVEDVI; normal range, 60 to 100 ml/min/m2) may be a better indicator of preload than CVP or PAWP. This parameter is measured using a PA catheter with the ability to measure right heart ejection fraction. Cardiac index (CI) and stroke volume index often improve when RVEDVI is greater than 100 ml/min/m2. Right ventricular end diastolic volume index is probably not a resuscitation end point but a value that tells the caregiver when giving additional volume will improve CI (rather than giving inotropes).
Staff should exercise caution when interpreting RVEDVI. Following a bolus of intravenous (I.V.) fluids, RVEDVI, CVP, PAWP, and CI should all increase proportionately. However, when fluid is infused into a noncompliant heart, the stiff right ventricle doesn't stretch to accommodate the extra fluid, and increased hydrostatic forces push the fluid into the pulmonary capillary beds. The RVEDVI remains low while the PAWP increases dramatically.
The merits of global parameters
Global and organ-specific parameters help staff assess end products of anaerobic metabolism to determine if complete resuscitation has been achieveRd. Because many variables influence global indexes, they're more valuable as trended values than as isolated figures.
[white diamond suit]Oxygen delivery index (DO2I; normal range, 500 to 600 ml/min/m2) is determined by CO, hemoglobin saturation, and the ability of the lungs to load oxygen onto the hemoglobin. When a patient exhibits a low DO2I (less than 500 ml/min/m2), staff must decide which of these three factors has been most affected and treat it accordingly. Frequently, aberrations in all three components coexist in a patient.
[white diamond suit]Oxygen consumption index (VO2I; normal, 125 ml/min/m2) can increase four to five times the normal level in a critically ill patient. Causes of increased VO2I include tachycardia, pain, agitation, seizures, shivering, posturing, increased work of breathing, and fever. Interventions to return high VO2I to within normal limits include analgesia, sedation, paralysis, antiepileptics, mechanical ventilation, and antipyretics.In late shock, oxygen use significantly drops as cells are compromised and VO2I values fall below 100 ml/min/m2. A normal ratio between oxygen delivery and consumption is 4:1; the tissues receive four times more oxygen than they actually use. In times of severe physiologic stress, however, this ratio shrinks to 2:1 or worse, suggesting anaerobic metabolism and pending cell death.
[white diamond suit]Mixed venous oxygen saturation (SvO2) monitoring continuously and indirectly reflects how much oxygen was consumed by the tissues. In a patient that requires resuscitation, this value will be abnormally low because of inadequate oxygen delivery or excessive oxygen demand by the tissues, or both. Normal values for SvO2 are between 65% and 80%; values less than 50% indicate anaerobic metabolism. Poor SvO2 measurements strongly correlate with poor DO2I and a poor patient outcome. A low SvO2 tells caregivers that the patient is still in shock but doesn't indicate whether the source of the inadequate oxygenation is poor CO, low hemoglobin, or inadequate pulmonary function.
[white diamond suit]Serum lactate provides an indirect way of assessing oxygen debt and the imbalance between oxygen delivery and consumption in the tissue beds. Normal lactate values are less than 2 mmol/liter; values higher than 15 mmol/liter are associated with high mortality. Time to normalization is a critical consideration. Patient survival rates approach 100% if lactate returns to normal within 24 hours; the rate drops to 14% if lactate isn't normalized within 48 hours. Following the trend of lactate levels is more informative than a single value. If lactate trends downward, then shock is reversing. If lactate continues to climb, then the source of shock still exists.
[white diamond suit]Base deficit, like lactate, is another approximation of overall tissue hypoperfusion. Base deficit reflects the amount of base solution needed to bring 1 liter of acidotic blood to a pH of 7.4. The more acidotic the patient, the greater the base deficit. Easily determined from arterial blood gas results, a base deficit of -2 to -5 is mild hypoperfusion, -6 to -15 is moderate hypoperfusion, and greater than -15 is severe hypoperfusion. The patient who has normal vital signs in the presence of a high base deficit requires persistent scrutiny for the source of shock. This value, too, should be monitored as a trend, rather than an isolated parameter.
[white diamond suit]Arteriovenous carbon dioxide gradient (AVpCO2), or the difference between arterial and mixed venous pCO2 levels, reflects the degree and duration of hypoperfusion and is an excellent indicator of severe hypovolemia. A gap greater than 11 mm Hg suggests significant compromise. Studies in trauma patients show that the AVpCO2 gap widens early in acute blood loss and can be detected even before elevations in organic acids are detected via lactate and base deficit measurements. It appears to be sensitive over a wide range of CI values. Resuscitation with I.V. fluids restores CI and, therefore, tissue perfusion, narrowing the AVpCO2 gap to less than 10 mm Hg. This parameter is measured using a pulmonary artery or centralvenous catheter.
Valuing organ-specific parameters
Blood flow isn't evenly distributed to all tissue beds and, even if global markers are within normal limits, inadequate tissue perfusion may persist in some regions. But three new technologic advances can help staff assess resuscitation in specific tissue beds.
[white diamond suit]Gastric tonometry assesses gastric mucosal pH (pH i) as a marker of the adequacy of gastrointestinal (GI) tract resuscitation. Even small decreases in circulating volume can significantly compromise gut perfusion. Obtain gastric mucosal pH by using a nasogastric tube with a saline-filled, gas permeable, silicone balloon at the tip. Carbon dioxide emitted from the gastric cells diffuses across the balloon membrane and equilibrates with the saline within 90 minutes. The measured pCO2 is then mathematically converted to a pH value: A pH less than 7.35 suggests mucosal anaerobic metabolism.Several studies have shown that mortality increases in patients who can't normalize their pH i despite resuscitation, even when their lactate and base deficit levels don't indicate hypoperfusion. Also, the longer pH i takes to normalize, the greater the patient's risk of multiple organ failure. Note that gastric acids can create an artificially low pH i; additionally, tube feedings must be interrupted for 30 minutes before measuring pH i, a shortcoming of this technology.
[white diamond suit]Sublingual capnometry has shown promise in early studies as an accurate estimate of the severity of shock. This relatively simple, noninvasive technology provides immediate and continuous information about tissue perfusion of the proximal GI tract, suggesting its potential as an early triage and resuscitation tool. Staff members place a microelectrode CO2 probe under the patient's tongue with the sensor facing the sublingual mucosa.Patients must be able to tolerate placement of the device and not toy with it by using their tongue or by biting down on the sensor or its connecting cables. Endotracheal tubes and orogastric tubes don't appear to affect the accuracy of the results, but severe oral trauma or swelling may cause erroneous readings.
[white diamond suit]Near-infrared spectroscopy is the most recent technology to show promise as a guide in resuscitation. Although gastric tonometry and sublingual capnometry can reveal adequacy of oxygen delivery and severity of hypoperfusion, they can't identify the point at which cells no longer use the oxygen made available to them-key information in a successful resuscitation. Detecting failed oxygen uptake and restoring proper use remain the final challenges in minimizing morbidity and mortality.Minimally invasive, continuous near-infrared spectroscopy measures intracellular oxygen levels, quantifies intracellular function, and identifies other conditions that might affect intracellular work. The technology assesses the absorption of infrared light by saturated hemoglobin molecules and cytochrome-aa3. Light waves are passed through tissue between two probes placed 6 mm apart on skeletal muscle, deltoid muscle, or GI tissue. Oxidized cytochrome-aa3 reflects red light; nonoxidized cytochrome-aa3 doesn't. This technology can alert staff to organ-specific hypoxia before significant compromise has occurred and can indicate when resuscitation efforts are succeeding. Although it doesn't function as a stand-alone tool, near-infrared spectroscopy's value has led researchers to explore its use in a variety of patient populations.
Watching the big picture
Don't let your staff be lulled into a false sense of security when their patient's vital signs and basic hemodynamic parameters have been restored to normal values during resuscitation. The technologies described in this article provide staff with a more complete set of tools for assessing resuscitation efforts. The best way to determine if a patient is fully resuscitated is to critically evaluate multiple assessment parameters.
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