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Seven Evidence-Based Practice Habits: Putting Some Sacred Cows Out to Pasture

Marianne Chulay is a consultant in clinical research and critical care nursing in Gainesville, Florida.

Elizabeth Bridges is an assistant professor at the University of Washington School of Nursing in Seattle and a clinical nurse researcher at the University of Washington Medical Center in Seattle.

Kathleen M. Vollman is a clinical nurse specialist, educator, and consultant at Advancing Nursing LLC in Northville, Michigan.

Richard Arbour is a critical care clinical nurse specialist at Albert Einstein Medical Center in Philadelphia, Pennsylvania.

To purchase reprints, contact The InnoVision Group, 101 Columbia, Aliso Viejo, CA 92656. Phone, (800) 899-1712 or (949) 362-2050 (ext 532); fax, (949) 362-2049; e-mail, reprints{at}aacn.org.

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To learn more about evidence-based therapy, read "Using Evidence and Process Improvement Strategies to Enhance Healthcare Outcomes for the Critically Ill: A Pilot Project," by Carol W. Hatler et al in the American Journal of Critical Care, 2006;15(5):549–555.[Abstract/Free Full Text] Available online at www.ajcconline.org.

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Financial Disclosures
None reported.

Corresponding author: Carol A. Rauen, RN, MS, CCNS, CCRN, PCCN, 14800 Fireside Dr., Silver Spring, MD 20905 (e-mail: carolrauen{at}starpower.net).

Critical care nurses find themselves in a unique situation. We have our feet deeply rooted in the art of nursing. Yet our hands and minds reach for the scientific basis that our highly technical, physiological, and pharmacological specialty requires. To base our practice on science, we must use research to answer questions, establish protocols, and promote critical thinking and decision making at the bedside. Doing so requires us to be willing and able to change practices, regardless of the tradition and commonly held beliefs, if validated, reliable, and useful evidence leads to such change. Nurses are at the forefront of evidence-based approaches.²

The Institute of Medicine defines evidence-based practice (EBP) as "the integration of best research, clinical expertise, and patient values in making decisions about the care of individualized patients."³ Research findings are a collection of facts. They become evidence when the findings are relevant and useful in particular clinical circumstances.⁴ Using research to guide clinical decision making is a shift in culture from basing decisions on opinion, past experiences, and precedents to basing decisions on science, research, and evidence.⁵ The Agency for Healthcare Research and Quality published Making Health Care Safer: A Critical Analysis of Patient Safety Practices.⁶ This document outlines 79 evidence-based practices and targets related to patient safety. The 11 recommendations with the strongest research support have a direct connection to critical care practice (Table 1).

Instillation of Normal Saline Before Endotracheal Suctioning: Helpful or Harmful?

Most hospital policies and procedures for management of artificial airways include instilling 5 to 10 mL of normal saline before endotracheal suctioning is done.⁷ This nursing and respiratory therapy routine was advocated as a way to improve oxygenation and removal of secretions by thinning thick secretions and stimulating coughing to assist with mobilization of secretions. Although instillation of normal saline is a long-practiced suctioning intervention, no research has ever documented the benefit of this practice, and some researchers have found the practice potentially harmful.

Effect on Oxygenation
In most experimental studies^8–13 on the effect of instillation of normal saline before endotracheal suctioning, oxygen saturation or PaO₂ was evaluated as the primary end point; in only a single study¹⁴ was mixed venous oxygenation evaluated. In these studies, oxygen saturation was significantly lower with instillation of saline than with no instillation of saline,^8–10 or the results of the 2 methods (saline vs no saline) did not differ.^11,12 In no studies to date did instillation of normal saline before suctioning improve oxygen saturation compared with suctioning without instillation of saline.

An interesting finding in studies^8–13 that showed decreases in oxygenation after instillation of saline before suctioning was that return to baseline oxygenation levels did not occur until at least 3 to 5 minutes after the suctioning procedure was finished. Although the decrease in oxygenation with instillation of normal saline may not be dramatic, it is far from a transient derangement.

Effect on Removal of Secretions
Several researchers^9,12,15,16 have attempted to determine if more secretions are removed with suctioning when normal saline is instilled than when suctioning is done without instillation of saline. By weighing the volume of secretions removed during suctioning, the researchers hoped to quantify differences between the 2 methods of suctioning. However, in all but a single study, researchers did not take into account the weight of the saline instilled in their calculations, creating a serious flaw in the experimental design of the study and negating the results. In the one, small study¹⁶ (N = 12) in which the weight of the saline was taken into account, serious flaws in the study design (lack of randomization of the interventions) make the results invalid.

Although an alleged benefit of instillation of saline is improvement in removal of secretions, to date no adequately reported scientific studies support that contention. This lack of research is no doubt partly due to the methodological issues associated with the measurement of secretion volumes in clinical studies, meriting further research to determine the best way to quantify removal of pulmonary secretions.¹⁷

Effect on Thinning Secretions
Although clinicians often believe that instillation of normal saline "thins" thick pulmonary secretions, no research has ever shown that this belief is correct. In fact, experts in airway humidification long ago pointed out the fallacy of this notion, because small-particle humidification, not administration of a fluid bolus, is required to achieve any semblance of incorporation of fluid into thick secretions.^18(p504) And even small-particle humidification falls short of actually "thinning" secretions noticeably. Experts^18–20 recommend systemic hydration to decrease the viscosity of pulmonary secretions, because thick secretions reflect dehydration of mucous glands. The topical application of a 5- or 10-mL bolus of normal saline to thick mucus will not lead to incorporation of the saline into the mucus.²¹

For clinicians who believe that normal saline thins secretions, try the following experiment to see for yourself what impact administration of a bolus of normal saline has on thick secretions.²² The next time you use suctioning, use a mucus trap to collect some of the thick secretions. Then, insert 5 to 10 mL of normal saline into the trap and observe how the saline remains separate from the mucus, even after vigorous shaking. Let the mixture sit a while to validate that even with exposure over time, the mucus and fluid remain separate from each other. If normal saline cannot thin thick secretions in a mucus trap with really vigorous shaking, it certainly cannot do it in a patient’s lungs.

Risks of Bacterial Contamination
In 2 studies,^23,24 researchers reported that instillation of normal saline may place the patient at risk for hospital-acquired pneumonia. Rutula et al²³ found that the rims of the individual-dose vials of normal saline were often contaminated with bacterial organisms just before insertion of the fluid into the endotracheal tube. On the basis of the type of bacterial organisms found on the rim, they hypothesized that the contamination of the vial had occurred when clinicians had "popped" the top off the vial with a thumb. Although the researchers²³ did not evaluate infection of patients, introduction of bacterial organisms because of contamination during administration of the fluid is certainly theoretically possible.

In a laboratory study²⁴ of endotracheal tubes that had recently been removed from patients in the intensive care unit (ICU), the amount of bacteria evacuated from the end of endotracheal tubes was 5 times greater when a bolus of normal saline was administered through the endotracheal tube before the suction catheter was introduced than when a suction catheter alone was passed through the endotracheal tube. The investigators²⁴ hypothesized that a similar high load of bacterial contamination of the pulmonary system might occur when normal saline is instilled into the endotracheal tube during suctioning. The instillation of normal saline may act as a vehicle to "wash" the bacteria that normally cling to the inner aspects of the artificial airway into the lung, potentially leading to infection. Hagler and Traver²⁴ did not evaluate clinical infection; however, they pointed out that instillation of saline before endotracheal suctioning may have some unintended outcomes.

Although the normal saline that is instilled should be sterile and without preservatives, isolated cases of outbreaks of bacterial pneumonia due to vials of normal saline contaminated during the manufacturing process have been reported.^25,26

Surveys of Nursing Practice
In several reports^7,27–29 since 1996, researchers have described how often nurses and respiratory therapists instill normal saline before endotracheal suctioning. In most of the studies,^7,27,29 25% to 33% of nurses routinely or frequently instilled normal saline before suctioning. Twice as many respiratory therapists as nurses instilled normal saline.^7,29 In a 1996 survey,²⁸ pediatric critical care nurses almost universally instilled normal saline before doing suctioning. Most of the hospitals surveyed indicated that instillation of normal saline before endotracheal suctioning was included in the hospital’s policy/ procedure for suctioning.⁷

EBP Recommendations
Resources for EBP recommendations are unanimous in their recommendation that instillation of normal saline should not be performed as a routine step with endotracheal suctioning. From reviews^19,20,30,31 of the literature on the topic to national guidelines^32–34 for EBP procedures, experts in airway management practices reiterate that despite some practitioners beliefs, no credible, scientific information supports the routine use of instillation of normal saline with endotracheal suctioning. In addition to the lack of any theoretical benefit, no studies have shown that instillation of normal saline is beneficial to patients, and some researchers have found it detrimental.

Verification of Proper Placement of Gastric and Postpyloric Tubes: What Is the Best Way?

Incidence of Inadvertent Pulmonary Placement
The incidence of inadvertent placement of gastric or postpyloric tubes into the lungs, instead of the gastrointestinal system, with blind insertion at the bedside is not clearly known. Most of the information about inadvertent placement has come from case reports.^35,36

According to 2 research studies done to determine the sensitivity and specificity of capnography for detecting inadvertent pulmonary placement of gastric and postpyloric tubes, the incidence of pulmonary placement was 11% (11 of 100 attempts) when verified by chest radiography³⁷ and 20% (4 of 20 attempts) when verified by carbon dioxide waveforms.³⁸ Even if the actual clinical incidence is lower than observed in these limited studies, the complications associated with a feeding tube placed in the lung can be lethal; thus, a 100% effective method for verifying proper location of such tubes is needed.

Methods of Detecting Inadvertent Pulmonary Placement
A variety of methods have been advocated to detect when a gastric or postpyloric tube has been introduced into the pulmonary system: auscultation during air insufflation through the tube, pH testing of aspirated fluid, visual inspection of aspirated fluid, detection of carbon dioxide in the tube, and radiographic tube verification.

Auscultation During Air Insufflation Through the Tube.
Auscultation over the gastric abdominal area during rapid insufflation of air into the distal end of a gastrointestinal tube is commonly performed after a tube is inserted. Research on air insufflation has never documented that this technique is accurate for identifying inadvertent intubation of the lungs. Numerous case reports of documented inadvertent pulmonary intubation despite auscultation over the gastric area of air during insufflation, though, have been published.^36,39,40 In the early 1990s, researchers found that air insufflation with auscultation over the gastric area could not be used to predict the inadvertent placement of a gastric tube into the lungs.³⁹ Because of the proximity of the lungs and stomach, it is not surprising that the sounds created by air insufflation through the tube could easily be transmitted to adjacent areas, causing clinicians to err in determining proper tube placement.

Testing the pH of Aspirated Fluid.
Another technique that has been advocated over the years to identify inadvertent pulmonary intubation with gastric tubes is measuring the pH of fluids aspirated immediately after tube placement.^41,42 It was hypothesized that because pulmonary secretions have an alkaline pH and gastric contents have an acidic pH, this simple bedside procedure could allow quick identification of tube location. Because a variety of situations can alter the pH of the gastric contents from acid to alkaline (drugs that change gastric pH, enteral feeding) and such situations are common in critically ill patients, the usefulness of this technique is limited. The outcome of pH testing is helpful only if the fluid tested is acidic, thus verifying gastric placement. If the fluid is alkaline, the gastric contents may be alkaline or the tube may be in the lung. Because of the lack of specificity of the pH technique and the numerous situations and conditions that lead to alkaline gastric contents, experts^36,43–45 no longer advocate the use of pH testing to verify tube location.

Visual Inspection of Aspirated Fluid.
Visual inspection of the color of fluid aspirated from the tube has been advocated as a method to differentiate gastric fluid (green, dark yellow) from pulmonary fluid (white, light yellow). In the only study⁴⁶ in which visual inspection of fluid was evaluated as a way of determining gastric or pulmonary location of the tube, visual inspection was a poor predictor of tube location. Similar to gastric pH, the colors of gastric and pulmonary secretions are altered by a variety of conditions, making development of a standard difficult.

Presence of Carbon Dioxide in the Tube.
Most recently, in several small studies,^{37,38,47–51} investigators evaluated the use of devices to measure the presence of carbon dioxide in the tube as a way to determine if the lungs have been inadvertently entered. Because carbon dioxide is present only in exhaled pulmonary gases and not in the gastric contents, this technique may be helpful in differentiating between the 2 locations. In studies^{37,38,47–50} in which end-tidal carbon dioxide monitors or disposable, color-indicator carbon dioxide devices were connected to the gastrointestinal tube during insertion, detection of carbon dioxide with the devices allowed successful detection of gastric tubes that had been placed in the lungs. In all but a single study,⁵¹ no instances of false identification of pulmonary placement were noted.^{37,38,47–50} The results of these studies show promise for finding a bedside technique that allows accurately detection of inappropriate pulmonary intubation. Because of the consequences of missing an incorrect placement of a gastric tube, additional studies are need to validate carbon dioxide detection techniques in larger and more diverse populations of patients and in a variety of clinical situations. Of particular interest is the ability of multiple caregivers to correctly interpret the color indications displayed by the disposable carbon dioxide device and to determine if fluid obstruction in the gastrointestinal tube and/or contamination of the carbon dioxide indicator affects the accuracy of the device.

EBP Recommendations
At this time, national guidelines and expert opinion indicate that the best method for confirming the location of blindly inserted gastrointestinal tubes is chest radiography.^{36,43–45,52,53} The radiopaque marker on each tube makes radiographic detection of inadvertent pulmonary placement clear, because the tube marker is easily seen by a radiologist in the right or left main bronchus, structures easily discerned on a chest radiograph.

Use of radiography to validate placement of small-bore gastrointestinal tubes is a clinically common policy in many facilities because inadvertent pulmonary intubations are thought to be more common with this type of tube. However, in a study by Burns et al,⁵⁰ the incidence of pulmonary intubations did not differ between large- and small-bore gastric tubes. At this time, national guidelines recommend that proper placement of gastric tubes should be confirmed by radiographic means.

Accurate Measurements of Blood Pressure

In addition to the national guidelines⁵⁴ for blood pressure measurement, a growing body of evidence supports specific procedural techniques that will improve the accuracy and reliability of noninvasive and invasive measurement of arterial blood pressure.⁵⁵

How Do You Pick the Correct Cuff Size?
The American Heart Association recommendations for correct sizes of blood pressure cuffs are summarized in Table 2. Selection of the appropriate cuff size is important because a cuff that is too small yields an overestimation of blood pressure and a cuff that is too large yields an underestimation of blood pressure.⁵⁶

View larger version (39K): [in this window] [in a new window]   Figure 1 Correct positioning of the arm for blood pressure measurements in the sitting, supine (0° backrest elevation), and supine with backrest positions. The arm should be supported and at the level of the heart (midsternum). Reprinted from AACN Practice Alert,55 with permission.

The challenge with measuring blood pressure in patients who are morbidly obese is finding an appropriately sized cuff, although new cuffs are being developed that have long length but normal width. For every 5-cm increase in arm circumference (starting at 35 cm), use of a standard cuff leads to an overestimation of systolic blood pressure by 3 to 5 mm Hg and diastolic blood pressure by 1 to 3 mm Hg compared with an appropriately sized large cuff.⁷⁴ To size the cuff correctly, measure the circumference of the patient’s arm midway between the elbow and the wrist. Cuff size should be similar to that specified in the guidelines for upper arm circumference (Table 2). The cuff should be centered between the elbow and wrist, and the arm should be supported at the level of the heart.^60–64

Can You Use an Automatic (Oscillometric) Cuff to Measure Blood Pressure in Patients With Atrial Fibrillation?
No evidence-based guidelines are available for noninvasive measurement of blood pressure in patients with arrhythmias. Current recommendations based on the American Heart Association consensus⁵⁴ for auscultated blood pressure in patients with arrhythmias are (1) measure the blood pressure 3 times and use the mean value, and (2) in patients with severe bradycardia, slow deflation of the cuff (target in bradycardia, 2 to 3 mm Hg per pulse) to prevent underestimation of systolic blood pressure and overestimation of diastolic blood pressure. A potential limitation of the use of oscillometric measurement of blood pressure in patients with marked arrhythmias is that with this method the maximal oscillation (mean arterial pressure) is detected and the systolic and diastolic blood pressures are estimated. In patients with atrial fibrillation or frequent ectopy, the beat-to-beat variability of stroke volume and the height of the oscillation may preclude the accurate measurement of the mean arterial pressure and thus the systolic and diastolic blood pressures. Conversely, auscultated systolic blood pressure may be overestimated or underestimated on the basis of selection of the first Korotkoff sound. In a comparison⁷⁵ of 3 sets of auscultated and oscillometric measurements of blood pressure in patients with rate-controlled atrial fibrillation, the mean (standard deviation) measurements of blood pressure for each method were as follows: systolic, manual: 126 (18) mm Hg, oscillometric: 131 (12) mm Hg; diastolic, manual: 72 (15) mm Hg, oscillometric: 73 (15) mm Hg. These findings suggest that the methods are interchangeable. Because the algorithms for different oscillometric blood pressure machines vary, the results of a single study cannot be generalized to other monitors.⁷⁶ If a patient is using an oscillometric cuff at home, the results should be validated by using auscultation. The accuracy of oscillometric measurements of blood pressure in patients with unstable atrial fibrillation has not been evaluated.

Should We Compare the Arterial Blood Pressure With the Cuff Pressure to Ensure That the Arterial Pressure Is Accurate?
The practice of using oscillometric brachial pressure to determine if an arterial pressure monitoring system is accurate and to decide whether to monitor the arterial pressure or the cuff pressure is not evidence based. The following factors should be considered when evaluating this practice. First, the aortic, brachial, and radial measurements of blood pressure are not the same. As a blood pressure wave moves into the peripheral vasculature, it is modified with an increase in systolic blood pressure and a decrease in diastolic blood pressure, whereas the mean arterial pressure is relatively unchanged. Generally, more central (aortic, femoral, brachial) measurements of systolic blood pressure are lower than radial measurements of systolic blood pressure by 7 to 14 mm Hg and are similar to or higher than diastolic blood pressure by 1 to 9 mm Hg, whereas the mean arterial pressure is unchanged.^70,77 Second, the differences in systolic blood pressure change with aging (radial approximately the same as aortic systolic blood pressure),^78,79 vasoconstriction (radial brachial and femoral),^80–83 and vasodilatation (femoral approximately the same as radial; aortic = radial).^84,85 In addition to evaluating an absolute pressure, monitoring for trends or changes in blood pressure over time to guide clinical decisions is equally important. Finally, the more important clinical questions are whether the blood pressure is adequate, if a given method accurately reflects central blood pressure, and whether the technical aspects of the method have been optimized.

What Steps Will Improve the Dynamic Response Characteristics of the Invasive Arterial Pressure Monitoring System?
Arterial pressure monitoring systems, particularly those with blood reservoirs, tend to be underdamped, which may lead to an overestimation of systolic pressure and an underestimation of diastolic pressure.^86,87 A validated evidence-based protocol for preparation for an invasive catheter is presented in Table 3.⁸⁸ Two points to note in this protocol are (1) an increased emphasis on avoiding formation of microbubbles, including completely filling the drip chamber and using minimal pressure during initial flushing of the catheter, and (2) the use of the rocket flush⁸⁹ (ie, vigorously flushing the system with 10 mL of flush solution through the proximal port to remove any hidden microbubbles). The rocket flush should never be performed when the catheter is in place in a patient because of the risk of retrograde air embolization. When this protocol (minus the fast flush) was used, 59% of pressure systems with a blood reservoir had adequate dynamic response characteristics and 41% were underdamped. The addition of the fast flush markedly improved the systems (92% adequate/ optimal and 8% underdamped).⁸⁸ Validated, evidence-based algorithms^87,90 are also available to optimize a system once it is in use in a patient.

Electrocardiographic (ECG) monitoring is performed for 3 primary reasons: detection of arrhythmia and conduction disturbance, monitoring of the ST segment, and monitoring of the QT interval.

Telemetry
Are 3-Lead Systems Equivalent to 5-Lead Systems for Monitoring Wide-Complex Tachycardia?
For a 3-lead system, a modified chest lead (MCL-1 or MCL-6) should be used instead of lead II for the differential diagnosis of wide-complex tachycardia.^91,92 Use of an MCL requires the following modifications in lead placement: right arm electrode on left shoulder, left arm electrode at V₁ position, left leg electrode at V₆ position. After repositioning the leads, for MCL-1, select lead I, and for MCL-6, select lead II. However, the 3-lead system is not as accurate as 5-lead system for the differential diagnosis of aberrancy vs ectopy. The V₁ criteria for the differential diagnosis of wide-complex tachycardia cannot be applied to MCL-1. For example, in a study by Drew and Scheinman,⁹³ the QRS morphology in MCL-1 differed from that in V₁ in 40% of cases (supraventricular tachycardia with aberrancy vs ventricular tachycardia), and use of MCL-1 resulted in 20% misdiagnosis compared with use of V₁.

Which Leads Are Most Sensitive and Specific for Differentiating Ventricular Ectopy From Aberrancy?
Leads V₁ and V₆ provide the most diagnostic clues for the differentiation of wide-complex tachycardia (Figure 2). Monitoring a lead (III or II) that allows evaluation of the relationship between the P wave and the QRS complex may also aid in the differential diagnosis^93,95 (Table 4). Despite the utility of V₁ for monitoring arrhythmia, it is not sensitive for TP baseline monitoring the ST segment or QT interval.^98,99

View larger version (62K): [in this window] [in a new window]   Figure 2 ST-segment deviation is defined as greater than 1- to 2-mm change in the ST segment from the patient’s baseline measured 0.06 seconds (60 ms) after the J point.a a Based on information from Drew et al.94

View larger version (25K): [in this window] [in a new window]   Figure 3 Measurement of QT interval.

QT-Interval Monitoring
How Should the QT Interval Be Measured?
Most of the recommendations for QT-interval monitoring are based on expert opinion.^95,103 The QT interval, which represents the duration of electrical activation (depolarization) and recovery (repolarization), is measured from the start of the QRS complex to the point where the T wave returns to the TP baseline (Figure 3). One suggestion to aid in identifying this point is to draw a tangent along the steepest part of the downslope of the T wave; the end of the QT interval is where this line intersects the TP baseline. If a U wave is present, the QT interval is measured from the onset of the QRS complex to the lowest point between the T and the U wave (Figure 4); however, if the U wave is large and merges with the T wave, it should be included in the measurement.¹⁰³ Lead II may provide the best separation between the T and the U waves. If a biphasic T wave is present, the point of the final return of the T wave to baseline should be used. No consensus has been reached on how to measure the QT interval during atrial fibrillation. One suggestion is to take the QTc from the shortest and longest R-R intervals and average the 2 values.¹⁰⁴ The same lead should be used for serial measurements.

View larger version (15K): [in this window] [in a new window]   Figure 4 Measurement of QT interval when a U wave is present.

Debate is increasing about the use of the Bazett formula, because it results in an underestimation of the QTc at low heart rates and overestimations of it at high heart rates.^106,107

A normal QTc is less than 0.46 seconds in women and less than 0.45 seconds in men. An abnormal QTc for women is greater than 0.48 seconds and for men is greater than 0.47 seconds. A QTc greater than 0.5 seconds is considered an increased risk for torsades de pointes, although torsades de pointes may also develop in patients with a QTc less than 0.5 seconds.¹⁰³ There is no QTc below which a patient is considered free of risk for arrhythmias.¹⁰⁴

Can Bedside Monitoring Replace the 12-Lead ECG for the Diagnosis of Prolonged QTc?
12-Lead ECG is the standard for the diagnosis of prolonged QT interval, and it cannot be replaced by bedside monitoring. The QT interval should be measured manually from the same lead, and the corrected value should be averaged over 3 to 5 beats.¹⁰³ The QTc should be measured before the start of proar-rhythmic therapy, at the time of the anticipated peak plasma level of the drug, after a change in drug dosage, and every 8 to 12 hours or more often if the QTc is prolonged.^98,108

Bedside monitoring may be useful in detecting changes in the QTc and determining if an additional 12-lead ECG should be obtained. In a study¹⁰⁹ in which QTc measurements from a 12-lead ECG were compared with those from a bedside monitor (leads I/II), with a cutoff of 0.46 seconds, the monitor QTc agreed with the 12-lead ECG in 72%. However, in 26%, the QTc from the bedside monitor was greater than 0.46 seconds, whereas the 12-lead QTc was within normal limits; and in 2%, the 12-lead QTc was longer than 0.46 seconds, whereas the bedside monitor was within normal limits (bedside QTc sensitivity 50%, specificity 92%). This high specificity and low sensitivity means that episodes of prolonged QTc will not generally be missed when a bedside ECG is used; however, prolonged QTc may be overdiagnosed. The diagnosis of prolonged QTc made on the basis of values on the bedside monitor should be confirmed with a 12-lead ECG.

What Leads Should Be Used for QT-Segment Monitoring?
A 12-lead ECG should be used to determine which lead to choose for bedside monitoring of the QT interval. The lead with the most well-defined T wave (usually lead II)⁹⁸ may have the clearest signal, particularly if a biphasic T wave or a U wave is present. On a 12-lead ECG, the anteroseptal leads generally have the longest QT,^109,110 and in the study by Sadanaga et al,¹¹¹ the leads with the highest sensitivity for detecting QT prolongation were V₃ (94%), V₄ (81%), II (66%), and V₂ (63%).

Does Lead Placement Really Make a Difference?
Attention to correct lead placement is imperative (Table 5). The most commonly misplaced leads are V₁, V₂, and V₆.^113,114 The displacement of V₁ (from the fourth to the third intercostal space) can cause false ST-segment changes⁹⁷ and morphological QRS changes that may lead to a misdiagnosis of myocardial infarction, right or left bundle branch block, or left ventricular hypertrophy.^115,116 The recent American Heart Association guidelines¹¹² also recommend that V₅ and V₆ be positioned parallel to V₄ rather than in the fifth intercostal space (Table 5).

"Teach us to live that we may dread unnecessary time in bed. Get people up and we may save our patients from an early grave"¹¹⁷ In a 1947 article published in the British Medical Journal, Dr R. A. J. Asher made that statement. However, recognizing the science of positioning as a part of treatment in caring for acute and critically ill patients has taken a long time. For many years, nurses have recognized that positioning prevents skin breakdown, mobilizes secretions, and provides comfort. They have not, however, identified the effects that different types of positioning strategies have on pulmonary gas exchange, outcomes of weaning from ventilatory support, and prevention of deconditioning in survivors of intensive care.

The importance of positioning as a priority of practice is challenged in an environment based on high technology. In a study¹¹⁸ of positioning of critically ill patients during an 8-hour period, only 2.70% of patients had a change in position every 2 hours, and 49.5% never moved during an 8-hour period. Immobility is a problem, and the solution rests in increasing awareness of the importance of positioning on short- and long-term outcomes for patients.

Impact of Immobility
Immobility is a major factor in the development of atelectasis, ventilator-associated pneumonia (VAP), and functional limitations that linger long after a patient is discharged from the ICU and hospital.^118–120 Most critical care patients spend most of their time supine, and supine positioning is an independent risk factor for mortality in patients receiving mechanical ventilation.^121,122 Krishnagopalan et al¹¹⁸ found that during an 8-hour time frame, less than 3% of critically ill patients were turned every 2 hours (the standard). Close to 50% of patients during that same period had no change in body position.¹¹⁸ What effect does the stationary supine position have on lung physiology? Anzueto et al¹²³ examined the impact of turning every 2 hours on the lungs of healthy adult baboons receiving mechanical ventilation. By study conclusion at 11 days, pathological examination of the lungs of baboons turned every 2 hours showed areas of bronchiolitis, and 5 of the 7 animals had surrounding bronchopneumonia.

Mobility Strategies
Positioning therapies have been targeted to meet specific pulmonary abnormalities. Researchers^124–128 have shown conclusively that if a patient experiences a consolidated type pneumonia in one lung, then positioning with the good lung down will result in better oxygenation. Despite mechanical restriction in the downward position, the healthy lung has an adequate number of functioning alveoli to match gravity-dependent perfusion and thus promote effective gas exchange. For patients with bilateral lung disease, the best position is selected on the basis of the severity of the patient’s lung disease and critical illness. For many patients, turning every 2 hours is not enough to preserve the oxygenating ability of the lungs or to prevent pneumonia.^128,129 When the risk for complications of immobility are high, the use of rotational therapy is often considered.

Kinetic therapy/table-based rotation and continuous lateral rotation therapy reduce the incidence of VAP and atelectasis.^129–135 The results of studies^134,135 on the contribution of rotational therapy to reducing duration of ventilatory support and length of stay in the ICU are conflicting. In most studies, patients were rotated more than 18 hours a day to achieve maximum benefit and the therapy was started as early as possible. Researchers have not yet determined whether the degree or the frequency of rotation is the crucial factor. Ahrens et al¹³⁴ randomized 234 medical-surgical trauma patients to receive rotation therapy or standard care and measured the impact on VAP, lobar atelectasis, and length of stay. Rotational therapy resulted in a significant reduction in the occurrence of VAP and lobar atelectasis but had no effect on length of stay.¹³⁴ Four systematic reviews^{129,136–138} of the literature on rotational therapy have indicated similar results. In the most recent review,¹³⁸ regardless of the rotational degree achieved, the proportion of patients with VAP was significantly lower for the rotation groups than for the control groups (P<.001; Figure 5).

View larger version (64K): [in this window] [in a new window]   Figure 5 Meta-analysis of pneumonia (with subgroups of prophylaxis and treatment for respiratory dysfunction): rotation versus control. Abbreviation: CI, confidence interval. Reprinted from Goldhill et al.138 with permission.

Progressive Mobility: Combating Deconditioning
Once a patient’s hemodynamic status allows forms of mobilization, every attempt should be made to progressively mobilize the patient to dangle the legs, sit in a chair, bear weight, and walk to decrease the severe muscle wasting that occurs in critically ill patients.¹²¹ Hemodynamic instability is due to spending prolonged periods in a stationary position or the establishment of a "gravitational equilibrium."¹⁴⁵ The physical deconditioning and challenges with hemodynamic instability that occur with bed rest can be dealt with by using a stepwise mobility progression program (Figure 6). Once a patient’s cardiovascular system is stable when the head of bed is higher than 30°, a progressive mobility program can be started. The goal is to progress in a stepwise fashion by increasing the height of the head of the bed, followed by placing the legs in a dependent position. If this change is tolerated, dangling of the legs and then weight bearing should begin as soon as possible. The next step is supported ambulation. The mobility program can be performed safely while the patient is intubated and receiving mechanical ventilation.¹⁵¹ One group¹⁵² who used the bed-chair position 3 times a day for patients who met the criteria for mobilization reported a decrease in ICU length of stay and occurrence of VAP.

View larger version (58K): [in this window] [in a new window]   Figure 6 Suggested algorithm for positioning critically ill patients. Reprinted from Ahrens et al.150 with permission from ADVANCING NURSING LLC.

EBP Recommendations
EBP practice recommendations for positioning are as follows:

• If a patient experiences consolidated pneumonia in one lung, positioning with the good lung down will result in better oxygenation.
  
• Progressive mobilization to dangling legs, standing, and walking are safe for intubated patients.
  
• Patients breathe better and experience improved oxygenation with higher elevations of the head of the bed if their hemodynamic status is such that they can tolerate the elevation.
  
• For many critically ill patients, turning every 2 hours is not enough to preserve the oxygenating ability of the lungs or to prevent health care–acquired pneumonia.
  
• Kinetic and continuous lateral rotation therapy reduces the risk of VAP in patients receiving mechanical ventilation. Optimal benefit depends on early placement and more than 18 hours of rotation per day. Research has not yet determined whether the degree or the frequency of rotation is the crucial factor.
  
• Prone positioning improves oxygenation but has not yet been shown to affect mortality.
  
• Use of the prone position should be considered after conventional strategies for lung recruitment have been tried unsuccessfully.
  

The Glasgow Coma Scale in Neurological Assessment

For decades, the level of consciousness has been deservedly described as the most sensitive and the earliest indicator of progression in intracranial abnormalities such as intracranial hypertension.^153,154 Since its introduction in 1974, the Glasgow Coma Scale (GCS)¹⁵⁵ has been used in many clinical areas to assess and document consciousness and responsiveness. The GCS is used to assign a numerical value to a set of responses in 3 spheres: eye opening, motor responses, and verbal responses (Table 6).

Even with these limitations, the GCS is used extensively, and the GCS score is incorporated into many critical care documentation records, trauma and emergency medicine documentation systems, and other clinical scoring systems. Additional limitations exist in each of the 3 spheres assessed by the GCS (Table 7). In patients with these limitations, the GCS score may provide inaccurate data on consciousness, motor function, and arousal.

The effectiveness of the GCS depends on the ability of a patient to respond and interact with a clinician. Optimal neurological assessment will indicate clinical states that interfere with and limit the efficacy of the GCS. Deep sedation/ analgesia produces a drug-induced depression of consciousness, arousal, and cognitive ability, making the GCS ineffective. In this setting, a sedation assessment tool may be highly appropriate. Neuromuscular blockade, in a dose-related manner, produces skeletal muscle relaxation in which a patient may potentially be awake but appears to be poorly responsive solely because of drug effects on neuromuscular transmission, not brain function. In each instance, optimal evaluation of the central nervous system is facilitated by using electrophysiological monitoring.

Predictive Value of GCS Scores
In clinical practice, the GCS score is used for multiple purposes, including guiding therapeutic decisions, predicting outcomes, and evaluating patients after they have ingested a toxin¹⁵⁹ (Table 8).

Research and Alternatives to the GCS
Because of the limitations of the GCS, research into alternative neurological assessment tools is ongoing. One tool, the Full Outline of UnResponsiveness (Table 9), has been studied in multiple clinical settings by members of several disciplines, including critical care/neuroscience nurses, neurology residents, and neurointensivists.¹⁶³ The tool is easy to use and has good interrater agreement between experienced and novice nurses from the neuroscience ICU and other nurses.¹⁶⁴ Moreover, it adds brain stem and respiratory assessment and provides additional information beyond that provided by the GCS.^163,164 It can assist in detecting disorders such as uncal herniation and locked-in syndrome¹⁶⁴ and in predicting inhospital mortality.^163,164

Management of Intracranial Hypertension

Intracranial pressure is the total pressure produced within the skull by cerebrospinal fluid, blood, and brain.^{153,168–170} In order to maintain stable intracranial pressure, an increase in volume of one component must be balanced by a decrease in volume of one or both of the other components.^153,168,169 Selective manipulation of these components is a mainstay of therapy for intracranial hypertension, and in attempts to improve patients’ outcomes, each component is the subject of ongoing research.

Modulation of Volume of Cerebrospinal Fluid: Intraventricular Drain
Drainage of cerebrospinal fluid is a hallmark of aggressive management of intracranial hypertension and is indicated for sustained elevations of intracranial pressure greater than 20 mm Hg.¹⁷¹ Further indications include depressed level of consciousness such as a GCS score of 8 or lower.^170,172 Drainage of cerebrospinal fluid improves management of intracranial pressure and cerebral perfusion pressure (CPP) as well as clinical and neurological outcomes, particularly for younger patients in whom coordinated, mechanism-based management is used, with interventions tailored more specifically to the underlying pathophysiological changes.¹⁷³ An example is drainage of cerebrospinal fluid in the management of hydrocephalus due to subarachnoid hemorrhage. Drainage of cerebrospinal fluid will remain a mainstay of therapy after traumatic brain injury¹⁷³ and after other clinical states such as hydrocephalus after subarachnoid hemorrhage. Such drainage may have predictable effects in decreasing intracranial pressure and increasing CPP when done in a controlled, protocol-directed manner.¹⁷⁴ In patients with intracranial hypertension, initially refractory elevations of intracranial pressure, drainage of cerebrospinal fluid was effective and was associated with improved functional outcome and lower mortality 6 months after injury.¹⁷⁵ Drainage of cerebrospinal fluid also is not associated with marked risks to other body systems as is drug-induced coma or hypothermia.¹⁷⁶ Available evidence strongly supports drainage of cerebrospinal fluid as an effective monitoring and therapeutic technique.

Modulation of Brain Volume: Mannitol and Hypertonic Saline
Modulating brain volume (80% of intracranial volume) is a focus for aggressive intervention. Osmotherapy with an agent such as mannitol to reduce brain volume works by 2 mechanisms. First, agents such as mannitol produce an osmotic gradient that draws water out from otherwise swollen brain tissue. Second, agents such as mannitol reduce blood viscosity and hematocrit and augment cerebral blood flow.^{168,170,176–178}

Mannitol has been used extensively as an osmotic diuretic for many years.¹⁶⁸ It can be administered as a bolus or as an infusion.^168,170 Recent studies^170,175 suggest earlier use of high-dose mannitol (eg, 1.4 g/kg) may be more effective than standard-dose therapy in improving intracranial pressure and outcomes. Bolus dosing of mannitol is generally more effective than continuous infusion.¹⁶⁸ Limitations of mannitol include hyperosmolality and volume loss from osmotic diuresis. Also, with longer duration such as several days of therapy, rebound elevation of intracranial pressure may occur.¹⁷⁸

Hypertonic saline, an osmotic agent with a concentration of sodium chloride that exceeds that of physiological saline (0.9%),^178,179 has more recently been studied and used to manage intracranial hypertension. Concentrations of hypertonic saline used to manage intracranial hypertension include 2%, 3%, 5%, 7%, 7.5%, and 23%.^178,179 In addition to reducing intracranial pressure, hypertonic saline augments hemodynamic stability¹⁷⁹ and intravascular volume.^168,170,177 In some studies and some patients, hypertonic saline has been more effective than mannitol for treatment of elevated intracranial pressure. When mannitol and hypertonic saline were compared in patients who had brain swelling and intracranial hypertension after ischemic stroke, hypertonic saline was more effective in reducing intracranial pressure and supporting CPP.¹⁷⁷ Hypertonic saline is also effective in managing intracranial pressure in patients refractory to mannitol, including patients who have had brain trauma and ischemic stroke.^177,178 Optimal concentration, volume, bolus vs infusion dosing, and timing/duration of therapy with hypertonic saline and targeted clinical state have not yet been determined. Hypertonic saline may be most effective with patient-specific titration of therapy, including volume, dosing interval, and concentration targeted to specific clinical goals, including CPP, intracranial pressure, and other monitored parameters.

Metabolic Suppression: Therapeutic Hypothermia
Therapeutic hypothermia is the controlled depression of body temperature to 36°C or lower.¹⁶⁹ Goals of therapeutic hypothermia include controlling refractory elevations of intracranial pressure and modulating effects of secondary brain injury.¹⁶⁹ Multiple factors are associated with secondary brain injury, including release of excitatory neurotransmitters, calcium release, hyperemia, inflammatory response, brain edema, and intracranial hypertension.^169,180 Many of these consequences are temperature dependent and potential targets for therapeutic hypothermia.^169,180 Therapeutic hypothermia improves neurological outcomes after cardiac arrest.^181,182 Therapeutic hypothermia is also effective in controlling dangerous refractory elevations of intracranial pressure.

In patients with hepatic failure, neurophysiological changes such as brain edema, cerebral hyperemia, loss of autoregulation, and intracranial hypertension are, among others, risk factors for poor clinical and neurological outcomes.¹⁸³ Of particular concern are elevations in intracranial pressure exceeding 30 to 50 mm Hg, which are associated with severe hepatic failure.^183,184 Mortality due to intracranial hypertension in patients with acute liver failure is approximately 20%.¹⁸⁴ Mild to moderate therapeutic hypothermia with core temperature approximately 32°C to 34°C is safe and effective for controlling elevations in intracranial pressure refractory to other therapies in the ICU immediately before and during liver transplantation.^183–185

One review¹⁸⁶ of multiple studies concluded that therapeutic hypothermia after traumatic brain injury was effective in reducing intracranial pressure and may reduce risks of mortality and poor neurological outcome. Multiple aspects of therapeutic hypothermia have been researched, such as duration of therapy. Long-term therapy (5 days vs 2 days) was associated with improved outcomes such as control of intracranial pressure.¹⁸⁷ In children, preliminary data from a study¹⁸⁸ of 48 patients suggested that therapeutic hypothermia is most likely safe, effective for control of intracranial pressure, and associated with a potential trend toward improved functional outcomes 3 to 6 months after injury. In a study¹⁸⁹ of patients with severe head injury, patients treated with hypothermia had significant higher CPP than did patients in the normothermic and hyperthermic subgroups. In another investigation,¹⁹⁰ optimal body temperature for reducing intracranial hypertension in patients with severe brain injury was between 35.0°C and 35.5°C.

Therapeutic hypothermia potentially can have marked effects on multiple body systems. Risks include coagulopathy, cardiovascular instability, and increased risk of infection.^183,191,192 Optimal use of therapeutic hypothermia may ultimately be best when titrated as a patient-specific and mechanism-based therapy to desired core and brain temperature. Best practices for duration of therapy, rate of temperature decrease and rewarming, and target temperature as well as optimal selection of patients are not yet determined. Therapeutic hypothermia may be used as an option on an individual basis for refractory intracranial hypertension. The currently available evidence does not support routine use of therapeutic hypothermia after traumatic brain injury.

Modulating Cerebral Blood Volume: Controlled Hyperventilation
Decreasing arterial carbon dioxide levels via controlled hyperventilation has long been used to control intracranial pressure by reducing cerebral blood flow. Hyperventilation reduces elevated intracranial pressure but risks ischemic injury.¹⁹³ Reduction in intracranial pressure is also transient for a given degree of hypocapnia.^193,194 Because of the risks of brain ischemia, particularly during the first 24 hours after brain trauma, when cerebral blood flow is already compromised, prolonged hyperventilation (PaCO₂ 25–30 mm Hg) for more than a few hours pending optimal use of definitive therapy for control of intracranial pressure may cause global or localized cerebral ischemia.¹⁹⁴ Reductions in cerebral blood flow may last longer than reductions in intracranial pressure during controlled hyperventilation.¹⁹³ Effects of controlled hypocapnia in reducing intracranial pressure are well established,^194,195 but the risks associated with this treatment include brain ischemia and poor outcomes. Because of its effects on cerebral hemodynamics, blood flow, and ischemic risk, long-term use of hyperventilation is not supported by the available evidence.^193–195 The use of hyperventilation in patients with traumatic brain injury best supported by the evidence is in management of acute elevations in intracranial pressure pending aggressive use of definitive therapies specific to the cause of the elevation,^193,194 such as optimal use of osmotic or metabolic suppression therapies. Longer term application of hyperventilation may have a role when cerebral metabolic parameters such as brain tissue oxygenation are monitored, permitting real-time titration of therapy to a patient-specific metabolic state.^194,196

Summary

Many of the studies used to develop the EBP recommendations described here were nursing research. Nurses asked questions about practice and, using the scientific process, undertook the challenge to find the answers. Once evidence is discovered, it is left to nurses at the bedside to implement the appropriate change. Sometimes the change actually makes practice easier. For example, not icing cardiac output solution was easy to implement and saved nursing time but it took almost a decade before it became common practice. It is estimated that 30% to 40% of patients do not receive care consistent with the current scientific evidence.⁵ In a self-review of use of EBP in their unit during a 1-year period, IIan et al¹⁹⁷ found that they implemented their own approved protocols only 50% of the time. Ironically, they discovered that it was the "sickest patients" who were least likely to receive commonly recommended best practices. Pravikoff et al¹⁹⁸ examined nurses’ perceptions about readiness for EBP implementation and found that, after lack of time, the second highest barrier was a "lack of value for research in practice." Larrabee et al¹⁹⁹ found that a nurse’s "attitude" about research was a key factor as to whether the nurse was likely to be supportive of EBP changes. Plost and Nelson²⁰⁰ implemented 9 EBP protocols in their 35-bed ICU, and after 3 years, they found that the use of protocols simplified processes, standardized care, facilitated patients’ safety, and reduced costs.

Two major challenges are before us. We must continue to answer clinical questions with research, and we must implement the EBP recommendations that will assist us in providing best practice. As noted by Titler et al,²⁰¹ "Although education is necessary to change practice, alone it is not sufficient." If it took only posting an article in the bathroom or a poster in the back room to change practice, this article would not have been necessary. It will take the dedication of advanced practice and bedside nurses to evaluate their own practice and the needs of their patients and a continued vigilance to ask, Are we doing what is best for our patients with the current evidence available to us?

"The most cost-effective opportunity to improve the quality of care will not come from discovering new therapies, but from discovering how to deliver therapies that are known to be effective."⁵

PRIME POINTS

• About 30% to 40% of patients do not receive care consistent with current scientific evidence.
  
• Are we doing what is best for our patients with the current evidence available to us?
  
• Do not instill normal saline (physiological salt solution) before endotracheal suctioning.
  
• Use chest radiography to confirm correct placement of nasogastric tubes.
  
• Attention to correct placement of electrocardiography leads is imperative.
  

Acknowledgments

We thank the American Association of Critical-Care Nurses, Linda Bell, Nancy Munro, and the entire Advance Practice Work Group for their insight to pull the group together to present this information at the 2007 National Teaching Institute as an Expert Panel on Evidence-Based Practice.

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