Vital Signs, MAP, Shock Index, and Circulatory Shock
Zohair Al Aseri, FRCPC (EM & CCM)
Consultant of Emergency and Critical Care Medicine
King Saud University, King Khalid University Hospital
Departments of Emergency Medicine and ICU
Pearl: Using vital signs to diagnose shock is not always reliable. This article discusses how and when vital signs can be used in the
assessment of circulatory shock.
Presentation: A nursing home patient presents with worsening of her mental status. Even though she has had previous transient ischemic
attacks (TIAs), her caretakers report that she was fully oriented and alert and capable of communicating her needs and opinions. Now she
seems confused and unable to recognize family members. She is not febrile and, in fact, her temperature is 35.6 C. Her blood pressure is
110/40 and her heart rate is 120. Analysis of her urine shows too numerous to count (TNTC) white blood cells. While it is clear that this
patient has a urinary tract infection and an altered mental status, the diagnosis of septic shock is less obvious.
Discussion: Shock is an imbalance between oxygen delivery and demand that leads to tissue hypoxia regardless of the presence or
absence of hypotension.1 Shock can be broadly grouped into five main pathophysiologic categories: hypovolemic, distributive, cardiac,
obstructive, and cytotoxic (i.e., CO, cyanide).
The diagnosis and management of shock are among the most common challenges facing practitioners in emergency and critical care
medicine. Failure of end-organ cellular metabolism and eventually cardiac dysfunction are the features and the end result in the late stage of
all types of shock. In the early stage of shock, a surge in catecholamines and neural regulation maintains mean arterial pressure (MAP) at
the expense of decreased tissue perfusion.2 This explains why changes in vital signs are late findings in individuals in shock 3 and the
absence of hypotension despite evidence of tissue hypoperfusion.4
Although blood pressure (BP) is an easy and universal tool for monitoring patients developing shock, data are lacking that clarify the most
specific level in shock patients.1,5 A normal BP can be sustained despite loss of up to 30% of blood volume.
What about tachycardia in the diagnosis of shock? In the initial evaluation of trauma victims the sensitivity and specificity of tachycardia limit
its usefulness despite the fact that tachycardia is independently associated with hypotension. McGee et al. showed that only 1 in 5 patients
demonstrated postural pulse increments of ≥ 30/min or were unable to stand for vital signs because of severe dizziness after 450-630 mL of
blood loss.6
A systematic evaluation of physical findings in patients with hypovolemia indicates that a systolic BP < 95 mm Hg is not a sensitive measure
for ruling out moderate or significant blood loss.7 Furthermore, postural hypotension (a > 20-mm Hg decrease in systolic BP) has little
additional predictive value. Its sensitivity is only 9% in those younger than 65 years and 27% in those older than 65 years.
In data collected from 14,325 trauma patients aged 16-49 years presenting to a university-based trauma center, hypotension was present
only in 3.3%. Of the hypotensive patients, 35% (n = 169) were not tachycardic. Hypotensive patients with tachycardia had a higher mortality
rate compared with hypotensive patients who were not tachycardic (P = 0.003). Patients who are both hypotensive and tachycardic have an
associated increased mortality and warrant careful evaluation.8 Jeng et al. found that the average base deficit and blood lactate level were
abnormal despite normal vitals signs in patients with burns resuscitated to normal vital signs and urine output.9 Scalea et al. found that 80%
of 40 victims of blunt trauma with head injuries had elevated blood lactate levels despite normal vital signs and urine output.10 Hypertensive
subjects will need a higher MAP to ensure the same degree of blood flow.11
In the critically ill patient, noninvasive measurements of arterial pressure, regardless of the method used, must be interpreted with caution.
Oscillometric devices can underestimate systolic BP by as much as 6-19% and can overestimate diastolic BP by as much as 5-27%.12,13,14
Noninvasive measurements of arterial pressure become less reliable in patients who have marked hypovolemia or abnormal cardiac
function.4
In cardiogenic shock with ST elevation myocardial infarction (MI), the recommended systolic BP is 100 mm Hg, but strong evidence for this
recommendation is lacking.15 Mean arterial pressure (MAP) calculated as MAP = BPdias + 1/3 (BPsys - BPdias) is less affected by wave
reflection, characteristics of the hemodynamic monitoring system, and small-vessel vasoconstriction than is systolic BP. Furthermore, it is
more accurate in patients who have low-flow states. As a general rule, a MAP < 60 mm Hg always should be considered pathologic.16 A MAP
of 65 mm Hg is sufficient in most patients in septic shock.11,17,18
All these limitations make blood pressure, MAP, and heart rate changes inadequate indices alone for detecting tissue hypoxia and
hypoperfusion.19,20
Shock index (SI) (calculated as heart rate/systolic BP; normal range, 0.5-0.7) may be useful to evaluate acute critical illness in the
emergency department. In a prospective study of 275 consecutive adults who presented for urgent medical care, Rady found that with
apparently stable vital signs, an abnormal elevation of the SI to > 0.9 was associated with an illness that was treated immediately, admission
to the hospital, and intensive therapy on admission.20 Other studies have confirmed the usefulness of the shock index as an indicator of
clinical instability.21,22,23
References:
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Stern SA, Dronen SC, Birrer P, et al. Effect of blood pressure on hemorrhage volume and survival in a near-fatal hemorrhage
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Jeng JC, Lee K, Jablonski K, Jordan MH. Serum lactate and base deficit suggest inadequate resuscitation of patients with burn
injuries: Application of a point-of-care laboratory instrument. J Burn Care Rehabil 1997;18:402-405.
Scalea TM, Maltz S, Yelon J, et al. Resuscitation of multiple trauma and head injury: Role of crystalloid fluids and inotropes. Crit
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Ledoux D, Astiz ME, Carpati CM, et al. Effects of perfusion pressure on tissue perfusion in septic shock. Crit Care Med
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Umana E, Ahmed W, Fraley MA, et al. Comparison of oscillometric and intraarterial systolic and diastolic blood pressures in lean,
overweight, and obese patients. Angiology 2006;57:41-45.
Araghi A, Bander JJ, Guzman JA. Arterial blood pressure monitoring in overweight critically ill patient: Invasive or noninvasive?
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Bur A, Hirschl MM, Herkner H, et al. Accuracy of oscillometric blood pressure measurement according to the relation between
cuff size and upper-arm circumference in critically ill patients. Crit Care Med 2000;28:371-376.
Halperin JL, Hiratzka LF, Hunt SA, et al. Guidelines for management of patients with ST elevation myocardial infarction: A report
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1999 Guidelines for the Management of patients with acute myocardial infarction). J Am Coll Cardiol 2004;44:E1-E211.
Pinsky MR, Payen D. Functional hemodynamic monitoring. Crit Care 2005;9:566-572.
Bourgoin A, Leone M, Delmas A, et al. Increasing mean arterial pressure in patients with septic shock: Effects on oxygen
variables and renal function. Crit Care Med 2005;33:780-786.
Rivers E, Nguyen B, Havstad S, et al. Early goal-directed therapy in the treatment of severe sepsis and septic shock. N Engl J
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Wo CCJ, Shoemaker WC, Appel PL, et al. Unreliability of blood pressure and heart rate to evaluate cardiac output in emergency
resuscitation and critical illness. Crit Care Med 1993l; 21:218-223.
Rady MY, Smithline H, Blake H, et al. A comparison of the shock index and conventional vital signs to identify acute critical illness
in the emergency department. Ann Emerg Med 1994; 24:685-690.
Birkhahn RH, Gaeta TJ, Bei R, et al. Shock index in the first trimester of pregnancy and its relationship to ruptured ectopic
pregnancy.Acad Emerg Med. 2002;9:115-9.
Birkhahn RH, Gaeta TJ, Terry D, et al. Shock indexin diagnosing early acute hypovolemia.Am J Emerg Med. 2005;23:323-6.
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patients.Eur J Obstet Gynecol Reprod Biol. 20061;126:99-103. Epub 2005 Oct 24.
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