Indications and Contraindications

The only contraindications to careful measurement of RR are the scenarios of respiratory distress, apnea, and upper airway obstruction, which require immediate therapeutic intervention. RR and respiratory effort should be measured as soon as patient care demands allow.

The respiratory status of both adults and children plays a crucial role in determining the overall assessment of illness. Although it is a sensitive yet nonspecific indicator of respiratory dysfunction, the RR can also predict nonpulmonary morbidity. Several prehospital and hospital-based illness or injury severity scores feature the RR as a cardinal value. A prehospital RR of less than 10 or greater than 29 breaths/min is associated with major injury in 73% of children.³² Using tachypnea alone as a predictor of pulmonary pathology, infants with an RR higher than 60 are found to be hypoxic 80% of the time.³³ Pediatric studies have linked abnormal RRs to in-hospital mortality and the level of care required in the ED.^34,35 In a retrospective study exploring predictors of critical care admission for adult ED patients who were initially triaged as having low to moderate acuity, an abnormal RR at the first nursing assessment increased the odds of critical care admission by a factor of 1.66.³⁶ An RR higher than 25 breaths/min in prehospital trauma patients was associated with increased mortality.³⁷ Pre-arrest respiratory insufficiency (RR >36 breaths/min or pulse oximetry <90%) was an independent predictor of mortality (odds ratio [OR], 4.2) in patients with EMS-witnessed cardiac arrest.³⁸ Although some studies have associated abnormal RRs in adult ED patients with increased mortality,^39,40 a recent large prospective cohort study of adult patients found that an initial abnormal RR on triage in the ED was not an independent predictor of hospital mortality.⁴¹

Procedure

To measure RR (inspirations per minute), count the respirations when the patient is unaware that his or her breathing is being observed. Count for a full minute to most accurately determine the RR. The frequency of breathing is less regular than the pulse, and inaccurate measurement is more likely to occur if the count is taken for a shorter interval. An infant’s RR can easily be determined by observing or palpating the excursion of the chest or the abdominal wall.⁴² Infants should be observed for grunting respirations, which are produced by expiration against a partly closed glottis (an attempt to maintain positive airway pressure).

Interpretation

Physiology

Blood flowing into the aorta with each cardiac cycle initiates a pressure wave. Blood flows through the vasculature at approximately 0.5 m/sec, but pressure waves in the aorta move at 3 to 5 m/sec. Therefore, palpated peripheral pulses represent pressure waves, not blood flow.

Indications and Contraindications

Assessment of blood flow by palpation of the pulse can be used to gauge the presence of cardiac contractility and not just the electrical rhythm. Caution should be taken to not over-generalize the presence or strength of a pulse in predicting blood pressure. The necessity for repeated pulse evaluations is dictated by the clinical complaint and the status of the patient. Continuous monitoring is not routine but may be helpful when the clinical situation may predict significant variability in heart rate, as in the setting of sepsis.⁵⁰ An association between absence of a radial pulse or absence of both radial and femoral pulses and hypotension has been demonstrated in hypovolemic trauma patients. The variability in individual response prohibits the use of this parameter as an absolute gauge of blood pressure.⁵¹

No contraindications exist to assessment of the pulse rate, but keep in mind a few cautionary notes about examination of the carotid pulse. Avoid concurrent bilateral carotid artery palpation because this maneuver could endanger cerebral blood flow. Massage of the carotid sinus, found at the bifurcation of the external and internal carotid arteries at the level of the mandibular angle, may result in reflex slowing of the heart rate. To avoid inadvertent carotid sinus massage, palpate the carotid pulse at or below the level of the thyroid cartilage. In adults with atherosclerotic disease, there is a rare risk of precipitating a cerebrovascular event by vigorous palpation of the carotid artery. Minimize this risk by prior auscultation of the carotid artery. If a bruit is present, gently palpate the carotid pulse while avoiding vigorous palpation.

Procedure

Depending on the clinical scenario, pulses are palpable at numerous sites, although for convenience the radial pulse at the wrist is routinely used. Use the tips of the first and second fingers to palpate the pulse. The two advantages of this technique are that (1) the fingertips are quite sensitive, thereby enabling the pulse to be located easily and counted, and (2) the examiner’s own pulse may be erroneously counted if the thumb is used instead of the first and second fingers. Pulses are also easily palpated at the carotid, brachial, femoral, posterior tibial, and dorsalis pedis arteries. Palpate the pulse at the brachial artery to appreciate its contour and amplitude. Locate the pulse at the medial aspect of the elbow and note that it is more easily palpated when the elbow is held slightly flexed.⁵² Determine the pulse rate by counting for 1 minute, particularly if any abnormality is present. Common convention in the acute care setting is to count a regular pulse for 15 seconds and multiply the resulting number by 4 to determine the beats per minute.

In newborns, use direct heart auscultation and umbilical palpation as the methods of choice to determine the heart rate. Instantaneous changes in newborn heart rates are best indicated to the resuscitation team by the clinician tapping out each heartbeat.⁵³ In unstable children, palpate the central arteries, particularly the femoral and brachial pulses, instead of the more peripheral arteries. In a comparison of four methods of determining the heart rate in infants, listening at the apex of the heart was found to be more accurate than palpation of the brachial, carotid, or femoral pulses.⁵⁴ Of the sites for palpation of the heart rate, the femoral artery has proved most valuable, especially in hypotensive infants.⁵⁵

Interpretation

Physiology

Arterial blood pressure indicates the overall state of hemodynamic interaction between cardiac output and peripheral vascular resistance. Arterial blood pressure is the lateral pressure or force exerted by blood on the vessel wall. It indirectly measures perfusion, and blood flow equals the change in pressure divided by resistance. Because peripheral vascular resistance varies, a normal blood pressure does not confirm adequate perfusion.⁶² Mean arterial blood pressure (MAP) can be estimated by adding one third of the pulse pressure (i.e., the difference between systolic and diastolic blood pressure) to diastolic pressure or by using the following measure.⁶³

Indications and Contraindications

Patients with minor ambulatory complaints unrelated to the cardiovascular system may not necessarily need their blood pressure measured in the ED, but those with hemodynamic instability need frequent monitoring of blood pressure. In children there is a significant amount of variability regarding standard situations that require measurement of blood pressure. In general, the younger the patient, the less likely blood pressure will be measured.64,65 In newborns, infants, and even toddlers, capillary refill is sometimes substituted for standard blood pressure measurement, although viewing these tests as equivalent can lead to significant errors.

In low-flow states, Doppler measurement of blood pressure may be obtained rapidly. Repeated measurements will provide an evaluation of the adequacy of resuscitation in patients whose blood pressure cannot be auscultated by standard techniques and in those in whom intraarterial blood pressure measurements are either contraindicated or technically unobtainable.66,67 Placing a catheter for direct intraarterial measurement of blood pressure has a higher risk for complications, but it may be performed safely in the ED. In particular, direct measurement of arterial pressure during pulseless electrical rhythms may help discriminate between severe shock and otherwise nonresuscitatable status.⁶⁸ Alternative noninvasive devices for continuous blood pressure measurement (CBPM) have been introduced clinically, with varying success. One common method of CBPM uses finger cuffs equipped with infrared (IR) photoplethysmography and sophisticated technology for quantification of finger blood pressure levels. Finapres (Ohmeda, Madison, WI) was the first commercial product using this technique, and several newer products are on the market today. A number of commercial systems use an alternative method of arterial applanation tonometry to measure CBPM. Further study is needed for solid validation of devices using these techniques.^69,70

Relative contraindications to specific extremity blood pressure measurement include an arteriovenous fistula, ipsilateral mastectomy, axillary lymphadenopathy, lymphedema, and circumferential burns over the intended site of cuff application.

Equipment

Two types of blood pressure monitoring equipment are currently available and used in EDs: cuff-type and noninvasive waveform analysis.

Procedure

Obtain indirect blood pressure measurements at the patient’s bedside by palpation, auscultation, Doppler, or oscillometric methods. The technique is straightforward and accurate when the equipment is well maintained, calibrated, and used by clinicians who follow accepted standards. The patient may be lying or sitting, as long as the site of measurement is at the level of the right atrium and the arm is supported.66,74 Unless the arm is kept perpendicular to the body with the elbow resting on a desk, measurements will be 9 to 14 mm Hg higher, regardless of body position.^75,87 Allowing the arm to be parallel to the body when supine but supporting the arm perpendicular to the body when measuring blood pressure may create a pseudo-drop in blood pressure. These changes are thought to be dependent on the mechanical properties of the arteries themselves and not associated with hydrostatic pressure alone.⁸⁸

To palpate arterial blood pressure, inflate the cuff to 30 mm Hg above the level at which the palpable pulse disappears. Once properly inflated, palpate directly over the artery and deflate the cuff at a rate of 2 to 3 mm Hg/sec. Report the initial appearance of arterial pulsations as the palpable blood pressure. This practice, known as the Riva-Rocci palpatory technique, has shown mixed results in yielding accurate estimations of blood pressure. One study determined that the average underestimation of systolic blood pressure was 6 mm Hg.⁸⁹ Another operative study looking at the combination of palpated systolic blood pressure and observed visual return of continuous pulse oximetry reported an underestimation of 10 to 20 mm Hg.⁸⁵ The same technique is used with the Doppler device, but the palpated pulse is replaced with the Doppler auditory signal. Measurement of arterial pressure by palpation and Doppler yields only estimates of systolic blood pressure. The Doppler method is preferred when determining blood pressure in infants.⁸⁶

When auscultating blood pressure at the brachial artery, apply the blood pressure cuff about 2.5 cm above the antecubital fossa with the center of the bladder over the artery.⁷⁴ Apply the bell of the stethoscope directly over the brachial artery with as little pressure as possible.⁹⁰ Systolic arterial blood pressure is defined as the first appearance of faint, clear, tapping sounds that gradually increase in intensity (Korotkoff phase I). Diastolic blood pressure is defined as the point at which the sounds disappear (Korotkoff phase V).^74–91 In children, phase IV defines diastolic blood pressure (Fig. 1-2).⁷ Phase IV is marked by a distinct, abrupt muffling of sound when a soft, blowing quality is heard.

It is best to measure by auscultation over the brachial artery because of accepted standardization of the measured values. Alternative sites include the radial, popliteal, posterior tibial, or dorsalis pedis arteries, although any fully compressible extremity artery may be used. Studies evaluating direct and indirect blood pressure measurements have demonstrated good correlation between these methods.92,93

It may not be feasible to obtain upper extremity blood pressure measurements because of patient access issues, particularly those encountered in the prehospital setting. Forearm measurements may be obtained more easily and show fair correlation to standard upper extremity values (within 20 mm Hg in 86% of systolic measurements and 94% of diastolic measurements).⁹⁴ Alternatively, noninvasive finger blood pressure measurements have shown promise when compared with standard upper extremity readings. The overall discrepancy in an ED study was 0.1 mm Hg with a standard deviation of ±5.02 mm Hg when comparing finger blood pressure and invasive MAP via radial artery cannulation.⁹⁵

Novel noninvasive continuous finger cuff technology offers the benefit of uninterrupted monitoring and has the advantage over invasive techniques of being safer and immediately available. Noninvasive finger cuff measurements have shown reasonable correlation, even in critically ill populations in the ED.⁷⁰ Wrist blood pressure has shown to have good average accuracy in the surgical environment when compared with oscillometric devices. Patient comfort is reported to be greater with these devices. The typically stated contraindications to the acquisition of upper arm blood pressure (limitation after mastectomy, etc.) may not apply.⁹⁶

The accuracy of the palpatory, Doppler, and oscillometric methods has also been investigated.97–99 When phase I and V Korotkoff sounds are used, indirect methods typically underestimate systolic and diastolic pressure by several millimeters of mercury.^97–100 During shock, the palpatory and auscultatory methods underestimate simultaneous direct arterial pressure measurements.¹⁰¹ The flush method, in which return of color after deflation of the cuff is used to estimate blood pressure in infants, may underestimate systolic blood pressure by up to 40 mm Hg.¹⁰² This method is unreliable and not recommended.

Complications

Complications of indirect blood pressure measurements are minimal when the proper procedure is followed. Inadvertent prolonged application of an inflated blood pressure cuff may result in falsely elevated diastolic pressure and ischemia distal to the site of application.⁷⁶ Invasive blood pressure monitoring is associated with a number of potential problems (see Chapter 20).

Interpretation

Normal blood pressure increases with decreasing distance from the heart and aorta. Blood pressure tends to increase with age and is generally higher in males. Individual factors that influence blood pressure include body posture, emotional or painful stimuli, environmental influences, vasoactive foods or medications, and the state of muscular and cerebral activity. Exercise and sustained isometric muscular contraction increase blood pressure in proportion to the strength of the contraction. A normal diurnal pattern of blood pressure consists of an increase throughout the day with a significant, rapid decline during early, deep sleep.¹⁰³

Normal lower limits of systolic blood pressure in infants and children can be estimated by adding 2 times the age (in years) to 70 mm Hg. The 50th percentile for a child’s systolic arterial blood pressure from 1 to 10 years of age can be estimated by adding 2 times the age (in years) to 90 mm Hg. Children older than 2 years are considered hypotensive when systolic blood pressure is less than 80 mm Hg.¹⁰⁴ Children are able to maintain MAP until very late during shock.¹⁰⁵ The finding of a normal blood pressure in a child with signs of poor perfusion should not dissuade the clinician from appropriate treatment. Most adults are considered hypotensive if systolic blood pressure is lower than 90 mm Hg, but some individuals normally exhibit a systolic pressure in that range. In the elderly, the presence of normotension within defined or published limits may not be reassuring. When considering systolic blood pressure cutoffs for trauma patients, 85 mm Hg for patients aged 18 to 35, 96 mm Hg for patients aged 36 to 64, and 117 mm Hg for those older than 65 have been proposed as new standards for hypotension.²⁰ When accompanied by signs of shock, immediate treatment is indicated. In patients with shock, blood flow cannot be reliably inferred from heart rate and blood pressure values.^106,107

Principles of Doppler Ultrasound

Doppler ultrasound is based on the Doppler phenomenon. The frequency of sound waves varies depending on the speed of the sound transmitter in relation to the sound receiver. Doppler devices transmit a sound wave that is reflected by flowing erythrocytes, and the shift in frequency is detected. Frequency shift can be detected only for blood flow greater than 6 cm/sec.

Indications and Contraindications

Doppler ultrasound is commonly used in the ED for the measurement of blood pressure in low-flow states, evaluation of lower extremity peripheral perfusion, and assessment of fetal heart sounds after the first trimester of pregnancy. Doppler’s sensitivity allows detection of systolic blood pressure down to 30 mm Hg in the evaluation of a patient in shock. In a patient with peripheral vascular disease in whom there is concern about the adequacy of peripheral perfusion, the ankle-brachial index provides a rapid, reproducible, and standardized assessment.¹⁴⁵ Fetal heart sounds provide a baseline assessment of any pregnant patient with 12 weeks’ gestation or longer in the setting of abdominal trauma or fetal distress as a result of a complication of pregnancy. The use of Doppler ultrasound for the evaluation of deep venous thrombosis is a valuable tool, but specific training and experience are required to attain proficiency. Discussion of this topic is beyond the scope of this chapter.

Equipment

A nondirectional Doppler device has a probe that houses two piezoelectric crystals. One crystal transmits the signal and the other receives it. Reflected signals are converted to an electrical signal and fed to an output that transforms them to an audible sound.

Probes with a frequency of 2 to 5 MHz are best for detecting fetal heart sounds. Frequencies of 5 to 10 MHz are appropriate for limb arteries and veins. The probes should be monitored periodically for electrical damage and integrity of the crystals. The sphygmomanometers used in conjunction with the Doppler device should be calibrated periodically, as described in the section on evaluation of blood pressure.

Procedure

Place the Doppler probe against the skin with an acoustic gel used as an interface. The gel ensures optimal transmission and reception of the ultrasound signal and protects the crystals. In an emergency, water-soluble lubricant (e.g., Surgilube or K-Y jelly) may be substituted for commercial acoustic gel. Angle the probe at 45 degrees along the length of the vessel to optimize frequency shifts and signal amplitude.

To evaluate peripheral perfusion, place a sphygmomanometer cuff proximal to the arterial pulse and inflate it. Place the probe over the arterial pulse and slowly deflate the cuff. The pressure at which flow is first heard is the systolic pressure under the cuff.

In the evaluation of peripheral vascular disease, one may determine the ankle-brachial index. It is standard for this procedure to be performed in a formal vascular laboratory. However, an approximation of pressures can be determined in the ED (Fig. 1-4). Usually, only the ankle-brachial index is considered for ED purposes. Examine both brachial arteries at the medial aspect of the antecubital fossa. Angle the probe until the most satisfactory signal is obtained. Inflate the cuff and slowly deflate it until the systolic pulse is heard. Repeat the procedure for the posterior tibial and dorsalis pedis arteries of both lower extremities. This procedure may be done with oscillometric devices but lacks sensitivity in identifying disease.¹⁴⁶

In evaluating fetal heart tones, because of variable positioning of the fetus, an examination of several locations and angles over the uterus must be performed in search for the optimal signal. It is best to begin in the mid-suprapubic area and then explore the uterus via angulation of the probe. Once tones are located, move the probe along the abdomen to reach a position closer to the origin of the sound. Distinguish fetal heart tones from placental flow by differentiating the quality of the fetal heart tones, which will not match the maternal pulse. The placental flow and maternal pulse should be identical.

Interpretation

As noted earlier, in low-flow states, Doppler ultrasound can detect blood pressure as low as 30 mm Hg. Calculate the ankle-brachial index of each limb by dividing the higher systolic pressure of the posterior tibial or the dorsalis pedis artery of the limb by the higher of the systolic pressures in the brachial arteries. In normal individuals the index should be greater than 1.0 (Fig. 1-5). Patients with claudication have values between 0.6 and 0.8. Values lower than 0.5 indicate severe impairment and are consistent with rest pain or gangrene.¹⁴⁷ When the lower extremity has been amputated or injured, brachial-brachial indices can be used (i.e., comparison of systolic blood pressure in the injured or diseased upper extremity with the other extremity). Patients with ankle-brachial index values of 0.9 or lower have increased cardiovascular morbidity and mortality.¹⁴⁸ One study of 323 penetrating extremity wounds found that an ankle-brachial index (or brachial-brachial index) lower than 0.9 was 72.5% sensitive and 100% specific for vascular injuries.¹⁴⁹ Segmental lower extremity pressure measurements may help identify the level of the obstruction (Table 1-4).¹⁵⁰ Obese patients, diabetic patients, or those with calcified vessels that are not compressible may have abnormally high systolic pressure (e.g., 250 to 300 mm Hg) and indices that do not accurately reflect flow. Normal fetal heart tones should be between 120 and 140 beats/min. Fetal heart tones may be heard as early as the 12th week of gestation.

Physiologic Response to Hypovolemia

Acute blood loss or severe hypovolemia related to dehydration decreases venous return.¹⁵⁷ This can be seen with acute blood loss (usually greater than 20% of blood volume), severe burns, or prolonged vomiting or diarrhea that depletes body fluids. As a result, cardiac output falls and clinical manifestations of shock ensue. Several compensatory mechanisms are initiated by acute hypovolemia (Box 1-1). The dominant compensatory mechanism in shock is a reduction in carotid sinus baroreceptor inhibition of sympathetic outflow to the cardiovascular system. This increased sympathetic outflow results in several effects: (1) arteriolar vasoconstriction, which greatly increases peripheral vascular resistance; (2) constriction of venous capacitance vessels, which increases venous return to the heart; and (3) an increase in the heart rate and force of contraction, which helps maintain cardiac output despite significant loss of volume.¹⁵³

The value of sympathetic reflex compensation is illustrated by the fact that 30% to 40% of blood volume can be lost before death occurs. When sympathetic reflexes are absent, loss of only 15% to 20% of blood volume may cause death.¹⁵⁸ Increased sympathetic nerve activity results in the commonly recognized physical signs of shock, including pallor, cool clammy skin, rapid heart rate, muscle weakness, and venous constriction. An inadequate immediate compensatory response will result in dizziness, altered mental status, or loss of consciousness.¹⁵⁹ The central nervous system response to ischemia further stimulates the sympathetic nervous system after arterial pressure falls below 50 mm Hg.¹²⁸ Subsequent compensatory mechanisms that work to restore blood volume to a normal level include the release of angiotensin and antidiuretic hormone (vasopressin). This causes arteriolar vasoconstriction, conservation of salt and water by the kidneys, and a shift in fluid from the interstitium to the intravascular space.¹⁵⁹

Several investigators have examined the changes in blood pressure and pulse that occur in supine patients with blood loss.153,154,160 Collectively, these studies have shown variable individual hemodynamic responses to acute blood loss of up to 1 L. The frequent inability to detect significant loss of volume with supine vital signs and the observation that syncope frequently develops in patients with acute volume loss on rising led to investigation of the use of orthostatic vital signs to detect occult hypovolemia.

Physiologic Response to Changes in Posture

When an individual assumes the upright posture, complex homeostatic mechanisms compensate for the effects of gravity on the circulation to maintain cerebral perfusion with minimal change in vital signs. These responses include (1) baroreceptor-mediated arteriolar vasoconstriction, (2) venous constriction and increased muscle tone in the legs and the abdomen to augment venous return, (3) sympathetic-mediated inotropic and chronotropic effects on the heart, and (4) activation of the renin-angiotensin-aldosterone system.¹⁵⁹ These compensatory mechanisms preserve cerebral perfusion in the upright position with minimal changes in vital signs. When a normal subject stands, the pulse increases by an average of 13 beats/min, systolic blood pressure falls slightly or does not change, and diastolic pressure rises slightly or does not change.¹⁶⁰ In patients with vasodepressor syncope, the normal compensatory reflexes that preserve cerebral perfusion with changes in posture are altered. The normally increased sympathetic tone on standing is paradoxically inhibited, and an exaggerated enhancement of parasympathetic activity (bradycardia) occurs and can lead to syncope.¹⁵⁴

Few data exist regarding the true effect of acute blood loss on postural vital signs, and this parameter varies greatly among individuals experiencing hypovolemia. One study of 23 young adult volunteers from whom 500 to 1200 mL of blood was withdrawn found no reliable change in postural blood pressure, but a consistent postural increase in pulse of 35% to 40% was noted after 500-mL blood loss.¹⁶¹ Of the six subjects from whom approximately 1000 mL of blood was withdrawn, only two were able to tolerate standing, and each had a postural increase in pulse of greater than 30 beats/min. The other four subjects experienced severe symptoms on standing, followed by marked bradycardia and syncope if they were not allowed to lie down.

Following phlebotomy of 450 to 1000 mL of blood from healthy volunteers, the criterion of an increase in pulse of 30 beats/min or the presence of severe symptoms (syncope or near-syncope) during a supine-to-standing test accurately distinguished between 1000-mL blood loss and no blood loss. The sensitivity and specificity of using the aforementioned criteria for detecting 1000-mL blood loss (Box 1-2) were both 98%, for an accuracy of 96% (2% false-negative results and 2% false-positive results). The investigators were unable to consistently detect blood loss of 500 mL with these criteria, though.¹⁶² In a similar study, the change in heart rate with postural changes after 500-mL phlebotomy was more discriminatory for blood loss than were changes in blood pressure or a change in the bioimpedance-based stroke index. Of note, these authors found that a change in heart rate of 30 beats/min or greater was 13.2% sensitive and 99.5% specific for 500-mL blood loss and that a change in heart rate of 20 beats/min or greater was 44.7% sensitive and 95.4% specific. The finding of a significant rise in pulse, though insensitive for 500-mL blood loss, was relatively specific in these healthy adult blood donors.¹⁶¹ In the most recent meta-analysis of orthostatic vital signs, the authors concluded that a large postural pulse change (>30 beats/min) or severe postural dizziness precluding the completion of vital sign measurements is required to clinically diagnose hypovolemia secondary to acute blood loss. The analysis demonstrated that orthostatic vital signs are often absent after moderate amounts of blood loss, thus significantly limiting the test’s sensitivity (22%) in this scenario.¹⁶² A consensus statement defined orthostatic hypotension as a reduction in systolic blood pressure of at least 20 mm Hg or a reduction in diastolic blood pressure of at least 10 mm Hg within 3 minutes of standing but appropriately reinforces that this is a physical finding rather than a disease process.¹⁵⁹

Variables Affecting Orthostatic Vital Signs

Many conditions affect the compensatory mechanisms that allow patients to assume the upright posture (Box 1-3).¹⁵⁸ Most of the conditions that affect postural blood pressure regulation involve a pathologic condition that affects the sympathetic nervous system. Orthostatic hypotension caused by autonomic insufficiency is not usually accompanied by tachycardia, but the orthostatic hypotension produced by acute volume depletion is commonly accompanied by a pronounced reflex tachycardia. Even in normal subjects, passive tilting generates a high incidence of orthostatic syncope.¹⁶³

Because of decreased vasomotor tone, limited chronotropic response, and other factors, the elderly have a higher incidence of orthostatic hypotension leading to syncope and fall-related injuries.¹⁶⁴ Carotid sinus hypersensitivity may play a greater role than orthostasis in geriatric syncope.¹⁶⁵ Note that drugs that antagonize the normal autonomic compensatory mechanisms can also produce orthostatic changes. These changes can be severe enough to produce frank syncope, especially in the elderly. A study of patients with syncope seen in an ED found that orthostatic hypotension was considered to be the cause of the syncope in 24% and that the largest proportion of these cases were drug related. Patients with orthostatic hypotension as the cause of syncope were older, had more comorbid conditions, and were found to be more frequently taking antihypertensive medications.¹⁶⁶ Advanced patient age is an independent risk factor for orthostatic blood pressure changes but does not appear to have a direct correlation to the presence of chronic cardiovascular disease, disability, or body mass index.¹⁶⁷

Patients with hypertension may also have abnormal vasomotor responses to tilt testing and demonstrate more instability.¹⁶⁸ Chronic anemia patients, who exhibit compensated blood volume, seem to have the same postural response as normal subjects do.¹⁶⁹ Ethanol ingestion exaggerates postural pulse changes and mimics the hemodynamic changes seen with acute blood loss.¹⁷⁰

The utility of orthostatic vital signs in children has been questioned. Healthy adolescents had changes in heart rate of 21.5 ± 21.2 beats/min and variable changes in systolic blood pressure (+19 to −17 mm Hg) after 2 minutes of standing.¹⁷¹ A study comparing mildly dehydrated children with normal children found a significant difference in the orthostatic rise in pulse, but no difference in orthostatic blood pressure. The investigators concluded that an orthostatic increase in pulse of greater than 25 beats/min constitutes a positive tilt test and less than 20 beats/min constitutes a negative test (sensitivity of 75%, specificity of 95%, and predictive value of 92% when using near-syncope or an increase in heart rate greater than 25 beats/min).¹⁷²

Another complicating factor in interpreting orthostatic vital signs is the development of paradoxical bradycardia in the presence of blood loss. Bradycardia in the face of hemorrhage has generally been considered a preterminal finding of irreversible shock, but bradycardia has been documented in hypovolemic, yet conscious trauma patients as well. It has been reported that when orthostatic syncope occurs, it is accompanied by hypotension and often bradycardia.149,151 Many central nervous system factors can contribute to vagally mediated syncope in ED patients with acute traumatic blood loss, including pain, the sight of blood, anxiety, and nausea. This paradoxical bradycardia may be more frequently associated with rapid and massive bleeding. Patients with more gradual blood loss tend to have a more typical tachycardic response. When the patient’s clinical findings are consistent with loss of volume or shock, the clinician should not allow the absence of tachycardia to change the assessment.

Indications and Contraindications

When the volume status of a patient is assessed with use of orthostatic vital signs, several points should be remembered. Many factors influence orthostatic blood pressure, including age, preexisting medical conditions, medications, and autonomic dysfunction (see Box 1-3). Data relating the effect of blood loss to orthostatic vital signs are limited to phlebotomized healthy volunteers. Great care must be used when extrapolating these data to patients with anemia, dehydration, or painful trauma. The clinician must consider the patient’s clinical condition coupled with the orthostatic vital signs when evaluating a patient for volume depletion.

Orthostatic vital signs can be considered an adjunct for the evaluation of any patient with known or suspected loss of blood volume or a history of syncope. Contraindications to orthostatic measures include supine hypotension, the clinical syndrome of shock, severely altered mental status, the setting of possible spinal injuries, and lower extremity or pelvic fractures.

The use of medications that block the normal vasomotor and chronotropic response to orthostatic tests is also a contraindication to using this test for the assessment of volume status. However, when the patient’s volume status is believed to be adequate and the clinician seeks to determine whether specific medications may have affected the patient’s ability to respond to postural changes, the test may be useful. In these situations the primary finding may be the feeling of near-syncope with little or no change in vital signs.

Orthostatic vital signs are often used to assess a patient’s response to therapy. In patients receiving intravenous rehydration therapy, serial orthostatic vital signs are widely used to judge the end point of therapy before release. In one study, individual orthostatic vital sign response to saline infusion in women with hyperemesis gravidarum was associated with other measures of rehydration, including weight gain and decreased urine specific gravity.¹⁷³ Although the individual improvement in orthostatic vital signs in response to rehydration was of clinical value, the initial orthostatic vital signs were considered insufficient as the sole indicator of clinical dehydration in this population.

Technique

To obtain orthostatic vital signs, record the blood pressure and pulse after the patient has been in the supine position for 2 to 3 minutes (see Box 1-2). Allow the patient to rest quietly and do not perform any painful or invasive procedures during the test.

Next, ask the patient to stand and be prepared to assist if severe symptoms or syncope develop. A supine-to-standing test is more accurate than a supine-to-sitting one. If severe symptoms develop on standing, defined as syncope or extreme dizziness requiring the patient to lie down, the test is considered positive and should be terminated. If not symptomatic, allow the patient to stand for 1 minute and then record the blood pressure and pulse. A 1-minute interval resulted in the greatest difference between control and 1000-mL phlebotomy groups in one study.¹⁶²

A number of studies have been conducted on normotensive, normovolemic patients to assess end points for orthostatic vital sign parameters. Such studies have included sitting-to-standing methods and varying rates of postural changes,¹⁷⁴ including lying times of 5 to 10 minutes and standing times of 0 to 2 minutes.¹⁷⁵ Arm position may affect postural changes in blood pressure and should be held constant to accurately assess orthostatic change.¹⁷⁶ Complications include syncope with resulting falls and injuries.

Interpretation

The most sensitive criteria for orthostasis is tachycardia or symptoms of cerebral hypoperfusion (e.g., near-syncope). Although changes in blood pressure may be seen, they are too variable to be an indicator of loss of blood volume. Specific population-based thresholds for changes in pulse rate and blood pressure have some value in identifying patients at high risk for significant loss of blood volume, but great individual variability limits the use of this technique as a screening test. That is, a loss of 500 mL, and occasionally more, may be associated with a negative orthostatic vital sign assessment.165,177 The use of serial measurements to ascertain the response to therapy of patients considered to be at risk for loss of volume appears to have clinical utility.¹⁷⁸

In the setting of suspected blood loss, if the patient has a rise in pulse of 30 beats/min or manifests severe symptoms and other complicating factors have been excluded, blood loss is highly likely (2% false-positive rate). The presence of a negative test indicates only that acute blood loss of 1000 mL is unlikely (2% false-negative rate) and that blood loss of 500 mL cannot be excluded (43% to 87% false-negative rate).162,165–177,179 Orthostatic changes in the shock index were no more sensitive than established tilt test criteria in discriminating normal individuals from those with moderate acute blood loss (450 mL).¹⁷⁸

Criteria for significant orthostatic changes in blood pressure cannot be definitively set for the following reasons: (1) large variability in postural blood pressure has been found in the adult ED population180–185; (2) the results of studies using passive tilt tables cannot be extrapolated to the bedside use of orthostatic vital signs; (3) studies using healthy patients with acute blood loss may not reflect the orthostatic changes seen in the elderly or those with chronic bleeding, dehydration, and other medical problems; and (4) many studies of orthostatic changes never used a criterion standard in their determinations.

In summary, orthostatic vital sign testing in common in the ED, but in reality, this procedure has limited proven value, and clinical interpretation of orthostatic changes in blood pressure and pulse varies widely. Although this intervention may occasionally yield information not obtained through other means, the authors do not consider orthostatic blood pressure testing a standard of care in the evaluation of ED patients.

Indications and Contraindications

CRT should not be determined from a dependent extremity, from a recently burned or injured extremity, or at the site of an infection or acute injury. Because CRT can be used without additional equipment and takes only a few seconds to perform, it can be a useful bedside assessment of perfusion and dehydration when used in conjunction with other objective signs of the adequacy of perfusion. It should not be considered accurate as a stand-alone tool. Capillary refill is not an appropriate alternative to measuring blood pressure in pediatric patients.

Procedure

The preferred sites for determining CRT are the nail bed, the thenar surface of the palm, and the heel. Alternative sites may have different CRTs, and the current standards are best developed for capillary refill determined at the nail bed.¹⁸⁶ Regardless of the site chosen, position the extremity at about the level of the right atrium. The minimum pressure necessary to produce blanching yields the most reproducible values. Release the nail bed and begin timing with a stopwatch or simply by counting out “one-thousand-one, one-thousand-two” for an approximation of the interval. Stop the clock when the nail bed becomes pink again. Interobserver reliability has been shown to be moderate, with kappa values less of than 0.5 in the evaluation of both adults and children.^182,183

Interpretation

The normal CRT increases with age and is slightly longer in female patients. It is further increased by degrees of dehydration or hypoperfusion. Hypothermia, hyponatremia, congestive heart failure, malnutrition, and edema all increase CRT. Environmental conditions such as ambient air temperature can falsely alter capillary refill.¹⁸² Fever alone did not appear to prolong or shorten CRT in children,¹⁸³ but a study of healthy adults found a 5% decrease in CRT for each degree Celsius rise in patient temperature.^187,188

The main difficulty in interpreting CRT is that normal values in healthy patients fall into a wide range. In 30 normal infants 2 to 24 months of age, mean CRT was 0.8 ± 0.3 second. Measurements obtained from the nail bed were more reproducible than those from the heel. Combined results from four studies evaluating capillary refill revealed a pooled sensitivity of 0.60 (95% confidence interval [CI], 0.29 to 0.91) and a specificity of 0.85 (95% CI, 0.72 to 0.98) for detecting 5% dehydration in children.¹⁸⁹ The presence of a 2-second or longer delay in CRT when combined with any two or more of the findings of absent tears, dry mucous membranes, or ill general appearance predicted clinical dehydration (>5% deficit in body weight) in children (1 month to 5 years of age) with 87% sensitivity and 82% specificity.^190–192

Frequent monitoring of capillary refill may be useful in assessing responses to rapid fluid resuscitation in children. A normal CRT of 2 seconds or less has recently been shown to correlate with superior vena cava oxygen saturation (Svco₂) of 70% or higher in critically ill children.186,192 The role of serial CRT measurements for assessing the response to rehydration in adults is unknown, but it does not appear to be useful for assessing acute loss of blood volume. Lima and colleagues¹⁹³ studied the prognostic value of the subjective assessment of peripheral perfusion in critically ill patients following initial resuscitation. When an abnormal CRT was defined as greater than 4.5 seconds, coupled with extremity coolness, these parameters identified patients who had been hemodynamically stabilized but continued to have more severe organ dysfunction and higher lactate levels. In adults, CRT was found to be less sensitive and less specific than orthostatic vital signs in detecting 450-mL blood loss during blood donation.¹⁶¹

In summary, assessment of CRT is a common technique used in the ED, but in reality this procedure has limited proven value, clinical interpretation is very subjective, and use varies widely. Although this intervention may occasionally yield information not obtained through other means, predominantly in children, the authors do not consider such testing an absolute standard of care in the evaluation of ED patients.

Physiology

Under normal conditions, the temperature of deep central body tissues (i.e., core temperature) remains at 37°C ± 0.6°C (98.6°F ± 1.08°F).¹⁹⁹ Core body temperature can be maintained within a narrow range while environmental temperature varies from as much as 13°C to 60°C (55°F to 140°F),¹⁹⁹ but surface temperature rises and falls with the environmental and other influences. Mean oral temperature is 36.8°C ± 0.4°C (98.2°F ± 0.7°F).²⁰⁰ Maintenance of normal body temperature requires a balance of heat production and heat loss. Heat loss occurs by radiation, conduction, and evaporation. Approximately 60%, 18%, and 22% of heat loss, respectively, occurs by these methods. Heat loss is increased by wind, water, and lack of insulation (e.g., clothing). Sweating, vasodilation, and decreased heat production serve to decrease temperature. Piloerection, vasoconstriction, and increased heat production serve to increase body temperature. Heat production is increased by shivering, fat catabolism, and increased thyroid hormone production.

Temperature is controlled by feedback mechanisms operating through the preoptic area of the hypothalamus. Heat-sensitive neurons in this area increase their rate of firing during experimental heating. Receptors in the skin, spinal cord, abdominal viscera, and central veins primarily detect cold and provide feedback to the hypothalamus that signals an increase in heat production. Stimuli that change core body temperature result in reflex changes in mechanisms that increase either heat loss or heat production.197–206

Indications and Contraindications

Clinicians generally measure body temperature to determine whether it is outside the normal range and as an indication of pathologic conditions that can affect core body temperature. Measurement of actual core body temperature requires the placement of invasive monitors, such as an esophageal or pulmonary artery probe. Clinicians commonly use estimates of core body temperatures to conveniently and safely assess abnormalities in core temperature. All noncore body sites and methods have inherent limitations in accuracy, and clinicians have come to accept these shortcomings in assessing most patients.

Measurement of oral temperature requires a cooperative adult or child. Patients who are uncooperative, hemodynamically unstable, septic, or in respiratory distress (with an RR >20 beats/min) require a method of measuring temperature other than the traditional oral route.²⁰¹ This group includes children younger than 5 years and patients who are intubated. Recent ingestion of hot or cold beverages can alter oral temperature readings for 5 to 30 minutes and can falsely elevate a normal temperature or mask a fever.²⁰²

Special techniques of measuring core body temperature may be indicated in certain patients (e.g., those with profound hypothermia, frostbite, or hyperthermia). Measurement of core body temperature is indicated in these individuals because it accurately measures the effects of treatment. This is the group of patients who will benefit the most from continuous temperature measurements.²⁰³

Measurement Sites

Procedure

Begin the temperature measurement by selecting the body site. Consider the accuracy of using a certain site to reflect core temperature, the sensitivity of the site to changes in temperature, the convenience, the time required, the safety, and the availability of the site.²³⁰ Insert the temperature probe and allow the probe to equilibrate with the temperature of the local body tissues.

Proper placement of the temperature probes significantly influences the results of oral, rectal, esophageal, and vascular temperature.231–233 Obtain sublingual oral temperatures in either the right or the left posterior sublingual pocket with the mouth closed.²³⁴ Though anxiety-producing for parents, biting and breaking a mercury thermometer is generally inconsequential with regard to ingestion of either glass or mercury. Obtain a rectal temperature with the patient in the left or right lateral decubitus position and advance the probe gently to a depth of 3 to 5 cm to ensure accurate, atraumatic results.²³⁵ Complications associated with rectal temperature measurements are extremely rare but include rectal perforation, pneumoperitoneum, bacteremia, dysrhythmias, and syncope.²³⁶ Falsely low but supranormal rectal temperature measurements may be seen during shock.²³⁷ Rectal temperature may also lag behind changes in core temperature.

An esophageal catheter or pulmonary artery probe can be placed for measurement of core body temperature, but these techniques are not used in the ED.

Though not commonly used, measurement of the temperature of a freshly voided urine specimen can validate measurement of temperature at other body sites.²³⁸ Urinary bladder temperature measurement has been demonstrated to be similar to pulmonary artery catheter temperature.²³⁹

Digital electronic probes are commonly used for the measurement of oral temperature in ambulatory patients.²³⁶ Electronic methods of temperature measurement are based on the thermocouple principle. Modern electronic thermometers signal once extrapolation of the temperature-time curve occurs. Current in vitro standards call for an accuracy of ±0.1°C (±0.18°F) over the range of 37°C to 39°C (98.6°F to 102.2°F). Disadvantages include factors that affect clinical accuracy and sensitivity. Disposable single-use oral thermometers are now available and are as reliable as mercury or TM thermometers.²³⁴ In the pediatric population, pacifier thermometers record supralingual readings in infants. The average time needed to record a reading with a pacifier thermometer is 3 minutes and 23 seconds, thus making its application in emergency medicine limited, although its sensitivity (72%) and specificity (98%) rival that of alternative methods.²⁴⁰ Various IR ear thermometers are available commercially with varying operating temperature ranges, features, and reported accuracy.²⁴¹ Complications associated with axillary, oral, ear IR, and liquid crystal thermometers are rare or unreported. TM perforation and pain have been reported as complications of placement of the thermistor probe in the auditory canal.

Interpretation

Normal values for body temperature are affected by the following variables: (1) site and methods used for measurement, (2) perfusion, (3) environmental exposure, (4) pregnancy, (5) activity level, and (6) time of day. Clinicians must interpret body temperature with knowledge of the range of normal values at the intended site of measurement. Although core body temperature remains nearly constant (37.0°C ± 0.6°C or 98.6°F ± 0.18°F), surface temperature rises and falls with changes in ambient temperature, exercise, and time of day. The definition of fever varies by the site of measurement and is defined by a temperature greater than 2 standard deviations above the mean. Fever has been defined as an oral temperature of 37.8°C or higher (100.0°F),²³⁵ a rectal temperature of 38.0°C or higher (100.4°F),²⁴² or an IR ear temperature of 37.6°C or higher (99.6°F).²³⁵ Based on measurement of temperatures in normal, healthy infants, it is recommended that fever be defined as a rectal temperature of 38°C or higher in infants younger than 30 days, 38.1°C or higher in infants 30 to 60 days (1 to 2 months), and 38.2°C or higher in infants 60 to 90 days old (2 to 3 months).²⁴³ Hypothermia has been defined as a core body temperature lower than 35°C (<95°F), and hyperthermia has been defined as a core body temperature higher than 41°C (>105.8°F) with accompanying symptoms and signs.^207,244 A useful nomogram and formulas for conversion of centigrade to Fahrenheit are provided in Figure 1-6.

Temperature probes that depend on transfer of heat energy from local tissues to the probe require a period of equilibration and reliable tissue contact at the intended body site. Acceptable equilibration times for mercury-in-glass thermometers in oral, rectal, and axillary sites are 7, 3, and 10 minutes, respectively. Used in a predictive mode, electronic digital thermometers generally require 30 seconds for oral or rectal temperature equilibration. The predictive mode uses temperature changes versus time to predict an equilibration temperature.

Normal ranges and suggested febrile thresholds for common body sites and methods should be considered in the interpretation of temperature values (Table 1-5). Interpretation of temperature measurements during clinical assessment must consider the use of antipyretics, level of activity, pregnancy, environmental exposure, and patient age. Body temperature is increased during sustained exercise, pregnancy, and the luteal phase of the menstrual cycle. Temperature also increases in the late afternoon because of diurnal variation. Body temperature is generally reduced with advanced age, and age may have an impact on the magnitude of fever. Axillary temperatures have low sensitivity but a high specificity for fever. Axillary temperatures should not be used to screen for fever.

Oral temperature measurements are affected by the ingestion of hot or cold liquids,²¹⁸ tachypnea,²⁴⁵ and cold ambient air.²⁴⁶ Before taking an oral temperature, the examiner should inquire about these features and possibly delay taking the temperature. A 2.7°C (4.9°F) reduction in oral temperature measurement was found when the probe was placed under the tip of the tongue instead of under the posterior sublingual pocket.²³⁴ Given the extrapolation that occurs with rapidly reading thermocouple devices and IR detectors, it is not surprising that the sensitivity of these devices for detection of fever is only 86% to 88%.²⁴⁷ Many clinicians have adopted the adage that when an elevated temperature is suspected or crucial in decision making but not evident with an oral thermocouple probe or IR TM thermometer, measurement with a mercury-in-glass thermometer is indicated.

When rapid changes in body temperature occur, oral and TM temperature measurements appear to be more reliable than rectal temperature. In 20 adults examined during open heart surgery, oral temperatures showed a better correlation with blood temperature during rapid cooling and rewarming.²⁴⁰

Infrequently, ED patients require constant monitoring of temperature (e.g., in cases of profound hypothermia or hyperthermia). This can usually be performed by using a bladder or esophageal probe attached to a potentiometer. Patients with indwelling central venous or pulmonary arterial catheters may have electronic thermistors inserted into the central circulation to measure core body temperature. As noted earlier, rectal temperature measurements are less desirable for monitoring patients undergoing rapid changes in core temperature. Periodic IR TM temperature monitoring may represent one useful option in a hypothermic patient.²⁴⁸

Interpretation of ear IR temperatures requires knowledge of the mode of thermometer operation and ambient temperature. Occlusion of the ear canal by cerumen may produce a falsely low reading.²⁴⁹ Most IR ear thermometers have different modes that allow users to predict the equivalent temperature at other body sites. IR ear thermometers appear to be moderately sensitive for fever.²⁵⁰ If these devices are used, the clinician must be aware of the potential for a falsely low temperature. When in doubt, the measurement should be repeated with a more standard method.

Patients, parents, and caregivers often misinterpret the significance of a fever, and the term “fever phobia” has been coined to describe the ubiquitous and unsubstantiated fear that fever, by itself, is harmful or has diagnostic or prognostic significance.¹⁹⁷ Some of the highest fevers are the result of benign viral infections. Fever has been demonstrated to increase the body’s immune response, thus making aggressive fever reduction counterproductive. Most individuals, especially children, feel better when a high fever is lowered. However, uninitiated medical personnel may contribute to the incidence of fever phobia. Routine administration of antipyretics in the ED for any fever, regardless of the degree of discomfort, has fueled unwarranted concern and may result in potentially harmful interventions, unnecessary testing and treatments, avoidable side effects of medications, and additional patient anxiety. Mandatory medical evaluation for any fever, the use of alcohol sponge baths, waking a sleeping child to administer antipyretics, alternating ibuprofen with acetaminophen, around-the-clock use of antipyretics, and misconceptions about fever causing brain damage are some of the myths that are still extant in some EDs and throughout the general population. An ED protocol stating that any child be afebrile or demonstrate a significant decrease in hyperpyrexia or even have a temperature reading repeated before discharge has no scientific validity.

Background

For centuries, the goal of physicians has been alleviation of pain. Albert Schweitzer called pain “the most terrible of all the lords of mankind,” and appropriately, one of the goals of modern medicine has been to understand and accurately assess pain in the hope of designing better methods to treat it. A paradigm shift has occurred in which pain is viewed as a mechanism to provide a mechanical warning of actual or potential damage to cells and tissues in a specific area.

There is no question that at least temporary pain relief is one intervention that any clinician can usually accomplish with relative ease, but the concept of using pain as “the fifth vital sign” has not met with universal agreement.²⁵¹ Literal interpretation of this concept can be fraught with problems, and because of the subjective nature of pain, measurement and interpretation are, by nature, imprecise. Initiatives mandating documentation of pain as the fifth vital sign have not been associated with improvement in pain management.²⁵² A prospective, multicenter study evaluating the current state of ED pain management practices concluded that there is high pain intensity as demonstrated by intense pain on arrival (median rating, 8 of 10) and suboptimal pain management practices, with assessment of pain occurring in 83%, 40% receiving no analgesics, lengthy delays in analgesic administration, and a large proportion of patients reporting moderate to severe pain at discharge (74%).²⁵³ Assuming weight-based dosing for acute pain management, analgesic regimens did not conform to the recommended regimens in a study of ED patients.²⁵⁴ Simply mandating the recording of a triage pain score has been shown to improve time to initial analgesic treatment.²⁵⁵

Pain can cause sympathetically mediated changes in vital signs. With regard to the quantitative effect of pain, it is well established that standard vital signs (pulse, respiration, blood pressure) do not meaningfully correlate with the level of perceived pain, even in patients with substantial pain, regardless of age, gender, or diagnosis.²⁵⁶ A recent retrospective study of patients with confirmed painful diagnoses showed no clinically significant associations between self-reported triage pain scores and heart rate, blood pressure, or RR.²⁵⁷ Contentions that the judicious use of analgesics will obscure a clinical condition or otherwise adversely affect clinical care are antiquated, unscientific, and inhumane. In short, pain control facilitates the overall ED encounter for both the patient and clinician.

Two types of pain are of concern to ED clinicians. Acute pain is defined as the normal predicted physiologic response to a noxious chemical or thermal stimulus. It is generally time limited. Chronic pain is defined as persistent or episodic pain of a duration or intensity that adversely affects the function or well-being of the patient. Pain of either variety is the most common chief complaint of more than 50% of ED patients, with the figure approaching 75% in some studies.²⁵⁸ Special focus should be placed on pain based on goals of the Joint Commission on Accreditation of Healthcare Organizations (JCAHO), which mandates that all hospitals develop comprehensive programs for the measurement, treatment, and documentation of pain.²⁵⁹

Reliably quantifying pain should be the goal of ED clinicians and is an appropriate step in the triage process. The discrete cognitive process that signals the sensation of pain is inherently influenced by culture, personality, experiences, and the patient’s underlying emotional state. The ideal pain measurement continues to depend on methods that can use or control for subjective experience.

Procedure/Interpretation

Although JCAHO has required organizations to assess the nature and intensity of pain in all patients, there is no perfect measurement tool suitable for the wide variety of patients and clinical settings experienced in EDs. Pain is a complex, subjective, multifaceted, personal experience that is difficult to easily quantify in all individuals. The perfect pain assessment tool for the ED setting would be simple and rapid to administer while providing a precise, reliable, and valid measure of pain regardless of a patient’s age, cultural background, and cognitive or physical impairments. Although numerous instruments to measure acute pain have been proposed, none meets all the criteria necessary to satisfy this definition. Regardless of the instrument chosen to measure pain, the primary focus should be to allow patients to personally report their pain and to rate it from a personal viewpoint. It is widely accepted that health professionals cannot rate pain intensity as accurately as patients themselves.260,261 Even though a patient’s reporting of pain intensity can be frustrating to the clinician, a patient’s self- report of the pain is considered the gold standard for the initial assessment of pain and tracking of a response to interventions. Such patient reporting is not necessarily a gold standard to mandate specific interventions.²⁶²

Multiple unidimensional acute pain measurement instruments have been published, and many have been independently validated. These tools are limited to quantifying pain severity only and may overlook the other multidimensional aspects of an individual’s pain experience. Common unidimensional pain instruments include the verbal rating scale (VRS), numerical rating scale (NRS), visual analog scale (VAS), and graphic rating scales (Fig. 1-7). A systematic review recently evaluated a variety of graphic scales in pediatric patients and supported use of the Faces Pain Scale (FPS), the Faces Pain Scale-Revised (FPS-R), the Oucher Pain Scale, and the Wong-Baker Faces Pain Rating Scale (WBFPRS).²⁶³ Clinicians need to be aware of the possibility of misinterpreted application of self-reported pain intensity measurement tools that use facial expression.²⁶⁴ The VRS is administered by asking the patient to rate the severity of the pain by using a set of descriptors such as “none,” “mild,” “moderate,” or “severe.” These tests are rapid and easy to use but may be less responsive to changes in severity of pain because of the small number of categories.²⁶⁵ Language and cultural barriers can also limit effectiveness. In the prehospital setting, the verbal NRS appears to be the most appropriate pain measure to administer to adult patients. It is practical and valid. The Oucher scale or the FPS is suitable to assess pain in children.²⁶⁶

The NRS consists of numbers on a line, and patients are asked to score their pain after explanation of the scale.²⁶⁷ For example, 1 means no pain and 10 means the worst pain ever experienced. The NRS has been validated for verbal administration but may be difficult to use in cognitively impaired patients, who may have difficulty translating pain into numbers.²⁶²

Probably the most used pain scale in the ED is the 1 to 10 VAS. The VAS uses a 10-cm line bounded on each end by perpendicular stops and descriptors. Zero equates to no pain, and 10 equates to the worst pain ever experienced. The initial score is not as important as change during treatment. Generally, a change in VAS scores has been shown to be valid and reliable if self-completion is appropriate.²⁶⁸ There is wide variability in this technique, and at least a 13- to 30-mm (1.3- to 3-cm) change on the scale is required to validate clinically relevant worsening or relief.²⁶² Low completion rates may be seen in patients with visual or cognitive impairment. In one ED study, failure rates with the VAS were 15% versus 0% with the NRS.²⁶⁹ Graphic rating scales are useful for patients with limited cognitive and expressive ability, especially children. They may also be helpful to overcome language or cultural differences. In an ED survey, the WBFPRS was the most common (81.7% of responding facilities) pain measurement tool used for pediatric pain assessment.²⁶⁷ The FPS-R was developed to overcome potential cultural differences in how patients perceive tears or the act of smiling.

Multidimensional pain measurement tools attempt to provide more insight by incorporating affective, sensory, and cognitive aspects of the pain experience into the measurement process. Multidimensional measurement tools require more time to administer and are mostly impractical for routine use in the ED. One exception may be the short-form McGill Pain Questionnaire (SF-MPQ), which is reported to take only 2 to 5 minutes to complete.²⁷⁰ The SF-MPQ has been shown to be reliable and valid,²⁶⁷ but little study has been performed in the ED setting. These tools may be difficult to administer in patients with hearing or visual difficulty and in those with limited cognitive ability, such as children or the elderly.

Overview of Visual Analog Pain Scales

The patient’s use of the commonly applied 1 to 10 VAS, though perhaps helpful to monitor progress of pain control or lack thereof, often overestimates the level of pain from the clinician’s standpoint. Conversely, it may underestimate the pain in certain stoic individuals or certain cultural groups. A rating of 10 was designed to indicate the “worst pain ever experienced,” but this level is commonly chosen by patients with problems clearly of a minor nature. A rating of 10 may be patients’ understanding of their level of pain and be used to describe the worst pain that they have personally experienced. This rating does not mandate a specific pain reduction approach and is better driven by clinician evaluation and consideration of the entire scenario. It is not uncommon for patients to rate their pain a 12 on a scale of 1 to 10 in an attempt to emphasize their personal experience, anxiety, or fear of receiving inadequate analgesia. It may be a patient’s perception that a higher rating will expedite treatment, prompt higher doses of narcotics, or otherwise engender more compassionate care. A common erroneous tactic or subterfuge of litigation proceedings is to incriminate a clinician’s diagnosis, treatment, or disposition based on the patient’s rendition of the pain scale. Many benign kidney stones rightly garner a pain rating of 10, but some aortic dissections are totally painless, hardly rendering any pain report equal to the seriousness of the medical condition.

Overall Goal of Pain Relief

The goal of EP pain management is to adequately relieve or control pain without compromising diagnosis, treatment plans, or the safety of the patient and population. The ideal objective is to totally relieve pain (0 on the pain scale). This goal is difficult to consistently achieve in the complex ED milieu. It is best accomplished by combining clinician experience, real-time clinical judgment, repeated evaluation, and discussion with the patient and family. Concerns about the abuse potential of addictive pharmaceuticals often weigh into the decision-making process for emergency physicians, and universal prescriptive reporting services can be used to assist in patient care and safe prescribing practices.270,271 Strict adherence to protocols, patient self-reporting on any pain scale, or reliance on a dogmatic approach to relief of a patient’s pain can be fraught with peril. It is best to treat the patient, not the pain scale.

In summary, although the routine use of patient-reported pain scales may facilitate the administration of analgesics and be somewhat useful in trending response to analgesia, experienced clinicians and the authors view such pain scales with skepticism. With certainly, the vagaries and vicissitudes of pain in the ED do not allow one to scientifically conclude that any specific pain scale has any diagnostic or prognostic value. Pain scales are best used to raise awareness that pain—and prudent efforts to relieve it—should be aggressively addressed in the ED.

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