The Vital Signs, Part 2: Pulse

     The classic vital signs of blood pressure, pulse, respiration and temperature have been the backbone of EMS since its inception. Vital signs give prehospital care providers insight to what's going on inside our patients and let us evaluate their responses to our interventions. This multipart series takes a fresh look at these vital signs and what they actually tell us in terms of changing our prehospital treatment, predicting the severity of presenting problems and even predicting survival. This article examines the pulse.

     Pulse might seem to be the easiest of the vital signs to obtain. Evidence suggests otherwise. A 1996 study led by German physician Balthasar Eberle was among the first to conclude that recognition of pulselessness by rescuers with basic CPR training was time-consuming and inaccurate. In the study, even professional EMTs and paramedics scored poorly. In 10% of patients, an absent carotid pulse was not recognized as pulselessness, and in 45% a pulse was not identified despite the presence of a carotid pulse with a systolic pressure of 80 mmHg or more.¹ A more recent study found that only 40 of 105 healthcare students who'd completed at least BLS instruction could accurately find a carotid pulse on a computerized manikin within 10 seconds.² The American Heart Association, for its part, deleted the carotid pulse check from its 2000 CPR/ECC guidelines.

     One study in infants determined that heart rates assessed by auscultation and palpation tended to be inaccurate and underestimate the ECG heart rate by 14 and 22 beats a minute, respectively.³ Another study evaluated 28 nurses' ability to detect infants' cardiac activity. The nurses determined the infants' heart rates with five different techniques: palpation of brachial pulse, carotid pulse, femoral pulse and apical impulse, and auscultation of apical impulse with the naked ear. The authors determined that the direct auscultation technique was more rapid and accurate than any other technique to determine cardiac activity without instruments, and it was also superior to palpation of the brachial artery in cardiopulmonary resuscitation in infants.⁴ The most recent article on the subject evaluated the long-held position that the brachial artery is the best site to check for a pulse in the critical infant. Its authors concluded that femoral pulse palpation proved best for detecting heartbeat and counting heart rate in hypotensive infants.⁵

     Pulsus alternans is a cardiovascular phenomenon characterized by alternating strong and weak pulses during a sinus rhythm. No changes are apparent on ECGs. The mechanism of pulsus alternans is not entirely clear, though it is attributed to an alteration in the stroke volume with every other cardiac cycle and is typically seen in patients with advanced myocardial disease. The difference in the beats is best detected by palpating the femoral pulses rather than the brachial, radial or carotid pulses. In many cases, pulsus alternans is an ominous sign that suggests severe cardiac failure.

     Pulsus paradoxus is a physical sign of tremendous diagnostic and prognostic significance. Under normal conditions, arterial blood pressure fluctuates throughout the respiratory cycle, falling with inspiration and rising with expiration. The changes in the intrathoracic pressures during breathing are transmitted to the heart and great vessels. During inspiration the fall in the left ventricular stroke volume is reflected as a fall in the systolic blood pressure. The converse is true for expiration. During quiet respiration, the changes in the intrathoracic pressures and blood pressure are minor. The accepted upper limit for fall in systolic blood pressure with inspiration is 10 mmHg. The "paradox" refers to the fact that the heartbeat can be heard with a stethoscope, but no radial pulse is felt. This is due to an exaggeration of normal mechanisms mentioned above. Moreover, the clinical method of assessment of this "pulse" is by measurement of systolic blood pressure.⁶

     Pulsus paradoxus is an ominous sign in acute exacerbation of bronchial asthma, and a recent study concluded that physical assessment in a child with acute exacerbation of asthma should at least include accessory muscle use and pulsus paradoxus, since these best predict hypoxemia.⁷ The presence of pulsus paradoxus greater than 15 mmHg also predicted admission for further treatment or relapse and correlated with clinical score, peak expiratory flow rate and oxygen saturation. Pulsus paradoxus is another sign associated with pericardial effusion and cardiac tamponade.

     Preliminary data suggests the character of the radial pulse alone is a significant vital sign and may be an acceptable method for initial rapid evaluation of trauma patients. This simple method may be enough to triage trauma patients in field conditions with limited instrumentation. These results indicated that systolic blood pressures taken at the scene were a mean of 26 mmHg lower in those patients with radial pulses described as "weak" (102 vs. 128 mmHg). Mortality increased with weak pulse character such that rates were 3% for the normal-pulse-character group and 29% for the weak-pulse-character group.⁸ An Army Institute of Surgical Research team led by Col. John Holcomb, MD, FACS, concluded that predicting the need for a life-supporting intervention could have been achieved from the Glasgow Coma Score motor and verbal components and radial pulse character without noninvasive automated blood pressure monitors, end-tidal carbon dioxide monitors, heart rate and respiratory rate or pulse oximetry.⁹

• There is evidence that a femoral pulse is a better indicator than a brachial pulse for evaluating an infant's cardiac status.
• Pulsus paradoxus should be looked for in every asthmatic patient.
• Tachycardia is not a reliable indicator of hypotension or shock, especially with abdominal trauma/internal bleeding.
• Postural/orthostatic vital sign changes are not reliable.
• Growing evidence supports shock index (heart rate divided by systolic blood pressure) as a more reliable indicator of blood loss and severity than pulse or BP.

     A primary teaching in EMT courses is that tachycardia is an indicator of shock, especially as a relatively early sign. Recent research calls even this doctrine into question. A 2003 study concluded that tachycardia is not a reliable sign of hypotension after trauma and that absence of tachycardia should not reassure the clinician about the absence of significant blood loss after trauma. Over a 10-year period, 35% of hypotensive trauma patients were not tachycardic. Tachycardia was present in 39% of patients with systolic blood pressures greater than or equal to 120 mmHg. Hypotensive patients with tachycardia had a higher mortality (15%) compared with hypotensive patients who were not tachycardic.¹⁰ A 1989 article found that half of studied patients who were hypotensive following penetrating abdominal trauma were not tachycardic.¹¹ Sixteen years later a study found that following penetrating abdominal trauma, vital signs and hemodynamic "stability" did not reliably exclude significant hemorrhage, including 11% of patients with 750–1,500 ml of blood loss, and 7% with 1,500 ml or more.¹² Studies have also challenged the concept that tachycardia is a reliable indicator of shock in patients with hemoperitoneum; one found that ruptured ectopic pregnancy patients with normal vital signs had a 20% chance of having lost greater than 40% of their blood volume.^13,14 Also note that millions of people in the United States take prescription beta blocker therapy, which impairs or prevents their ability to increase their heart rate to compensate for hypovolemia, as in a GI bleed.

     Although EMTs are commonly taught to use orthostatic (postural) changes in blood pressure and pulse as an indication of hypovolemia, there is debate as to what indicates a significant postural change, as well as the proper technique for determining it. Many factors influence postural blood pressures, including age, pre-existing medical conditions (including pregnancy), the use of medications and nervous system dysfunction. No data supports the use of postural changes in pulse and blood pressure for the elderly or pediatric populations.^15–17 One study found the test to be positive in 43% of emergency room patients with no history or suspicion of trauma or blood or fluid loss.¹⁸ There is also debate in the prehospital field as to whether the test is to go from supine to standing, supine to sitting or sitting to standing. And protocols vary as to how long to wait before taking the comparison set of vital signs.

     Some authorities have identified the criterion for positive vital sign changes as a pulse increase of greater than 30 beats per minute from the previous position without consideration for blood pressure, while others cite an increase of 20 beats per minute or decrease of 20 mmHg in systolic blood pressure. Others simply look for the reproduction of signs/symptoms of shock or cerebral hypoperfusion as a positive test without looking at any numbers whatsoever. A "20-10-20" rule has been cited that refers to the expected decrease in systolic BP (up to 20 mmHg), a rise in diastolic BP of 10 mmHg and an increase in heart rate by 20 bpm with change in position.¹⁹ Another study cited a "20-10-10" rule, only this time with a heart rate increase of more than 20 beats per minute with a systolic BP decrease of more than 10 mmHg, or a diastolic blood pressure decrease of more than 10 mmHg.

     One study evaluating postural vital signs found that the supine-to-standing test accurately distinguished 1,000 cc blood loss from no blood loss, and that when evaluating adults with suspected blood loss, the most helpful physical findings are either severe postural dizziness (preventing measurement of upright vital signs) or a postural pulse increment of 30 or more bpm.²⁰ The University of Washington's Steven McGee, MD, found that supine hypotension and tachycardia are frequently absent even after up to 1,150 ml of blood loss, and that the finding of mild postural dizziness has no proven value.²¹

     A test in which there is no clear standard for technique or expected results is obviously of limited use.

     Shock index is the heart rate divided by the systolic blood pressure. A systolic blood pressure of 110 with a heart rate of 90, for instance, gives a shock index of 0.82. A normal value for the shock index has been identified as between 0.5–0.7. Elevations in shock index have been identified as more sensitive than either heart rate or systolic blood pressure alone for detecting early hypovolemia.²² A shock index greater than 0.9 has been associated with greater rates of hospital admission and intensive therapy.²³ An orthostatic change in the shock index is also indicative of moderate hypovolemia.²⁴ Elevated SI has been studied as an early indicator of ruptured ectopic pregnancy; in one study an SI over 0.85 made this diagnosis 15 times more likely.²⁵ Since 40%–50% of ectopic pregnancies are misdiagnosed on initial visits to emergency departments, an additional diagnostic sign is important. SI also correlates best with actual quantity of hemorrhage, not just its diagnosis.²⁶ Note that these studies were performed on adults, and the shock index has not been verified as accurate in pediatrics, although studies are forthcoming. Prehospital providers may wish to do a quick SI conversion and confer with medical control, especially on decisions regarding transport to a specialty center, prolonged transport, calling for additional or higher-level resources, or in the case of the "stable" patient who wishes to RMA.

     A few points deserve reinforcement. One set of correctly done vital signs is important, but a series of repeated measurements is invaluable to determining your patient's true condition. Most studies of these areas are conducted in controlled environments, not, say, inside an overturned vehicle at 3 a.m. Nonetheless, prehospital providers have an obligation to understand the tests they're performing and the results they produce.

     In addition, many of the problems we see in determining vital signs come with pediatric patients. Training officers and medical directors should take this into account and make sure their providers are competent in determining the statuses of their pediatric patients.

     Next month: Respirations

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13. Snyder HS. Lack of a tachycardic response to hypotension with ruptured ectopic pregnancy. Am J Emerg Med 8(1):23–6, Jan 1990.

14. Hick JL, Rodgerson JD, Heegaard WG, Sterner S. Vital signs fail to correlate with hemoperitoneum from ruptured ectopic pregnancy. Am J Emerg Med 19(6):488–91, Oct 2001.

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21. McGee S, Abernethy WB III, Simel DL. The rational clinical examination: Is this patient hypovolemic? JAMA 281(11):1,022–9, Mar 17, 1999.

22. Birkhahn RH, Gaeta TJ, Terry D, Bove JJ, Tloczkowski J. Shock index in diagnosing early acute hypovolemia. Am J Emerg Med 23(3):323–6, May 2005.

23. Rady MY, Smithline HA, Blake H, Nowak R, Rivers E. A comparison of the shock index and conventional vital signs to identify acute, critical illness in the emergency department. Ann Emerg Med 24(4):685–90, Oct 1994.

24. Witting MD, Smithline HA. Orthostatic change in shock index: Comparison with traditional tilt test definitions. Acad Emerg Med 3(10):926–31, Oct 1996.

25. Birkhahn RH, Gaeta TJ, Van Deusen SK, Tloczkowski J. The ability of traditional vital signs and shock index to identify ruptured ectopic pregnancy. Am J Obst Gyn 189(5):1,293–6, Nov 2003.

26. Birkhahn RH, Gaeta TJ, Bei R, Bove JJ. Shock index in the first trimester of pregnancy and its relationship to ruptured ectopic pregnancy. Acad Emerg Med 9(2):115–9, Feb 2002.

     Rob Curran, DC, EMT, is a human anatomy and physiology instructor at CUNY-Brooklyn College, adjunct faculty in the Physical Therapy, Physician Assistant and Nursing programs at SUNY-Downstate, and New York State Coordinator for the President's Council on Physical Fitness and Sports.