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<< Symptomatic Hypotension: ED Stabilization And The Emerging Role Of Sonography

Epidemiology

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Epidemiology

Epidemiology

 While it is difficult to determine with accuracy the incidences of hypotension in a general population or even in a select population of ED or hospitalized patients, studies have examined data on critically ill patients and effects of hypotension on outcome.

The duration of hypotension after trauma, sepsis, anaphylaxis, and cardiogenic sources are critical determinants of morbidity, prognosis, and survival in these groups of hypotensive patients.3

Jones et al performed a secondary analysis of data accrued from a randomized, controlled trial of rapid versus delayed bedside goal-directed ultrasound of patients with symptomatic, non-traumatic shock. In this study, hypotension was defined as an initial ED systolic blood pressure reading of less than 100 mmHg. Shock was defined by the presence of hypotension with one or more predetermined signs or symptoms. The hospital mortality of the 190 ED shock patients in this study was 15%. Adverse hospital outcomes included organ failure, the need for intensive care admission, and in-hospital mortality. Fifty percent of the patients with a SBP < 80 mmHg had an adverse hospital outcome. Forty percent of the patients with an adverse outcome had blood pressure readings that were consistently below 100 mmHg for more than 60 minutes.13

The one month mortality rate after the onset of hypovolemic shock is dependent on the underlying cause and the patient's co-morbidities. A 2002 study by Moore et al of ED patients with atraumatic hypotension (defined as a SBP < 100 mmHg) showed an in-hospital mortality rate of 18%.4 In a recently released prospective cohort study by Jones et al, ED patients with a SBP < 80 mmHg had a six-fold increased incidence of in-hospital death. Patients with a SBP < 100 mmHg for more than 60 minutes had nearly three times the incidence of in-hospital death.14 Within one month of the diagnosis of septic shock, the overall mortality rate can be as high as 40%. Mortality for cardiogenic shock can be as high as 60%.15,16 

Use of the presence of hypotension alone as a predictor of ED patient mortality is incomplete and risks ignoring the importance of the associated clinical context. In certain well-defined disease entities (such as aortic dissection and cardiac failure), hypotension is associated with sicker patients; thus, there are higher mortality rates of 50-80%.17 Hypotension in patients with end-stage renal disease (ESRD) and/or atherosclerotic cardiovascular disease is also associated with higher mortality rates. Consequently, rapid identification of the etiology of the hypotensive state has a potentially critical impact on the patient's short and long term clinical outcome.

Hypotension In Trauma 

The ATLS protocols support the practice of using hypotension as only a late marker of shock because of its low sensitivity. Prior to 1989, ATLS guidelines taught that the absence or presence of the carotid, femoral, and radial pulses could be correlated to systolic blood pressures. When compared to invasively obtained arterial blood pressure measurements, however, it was discovered that the correlations previously made were overestimations.19 ATLS no longer teaches pulse and SBP correlations in the context of clinical decision making.

The National Trauma Data Bank (n = 115,830), where hemorrhagic shock was the main cause of hypotension, reports that SBP correlates with serum base deficits (considered to be a marker of circulatory shock). The mean and median SBP decreased to less that 90 mmHg when the base deficits were worse than -20.20 The Data Bank supports the conclusion that SBP is a late marker for mortality and that, in the setting of hemorrhagic shock, SBP should not be used as a primary decision point in choosing which patient should receive resuscitation efforts. Patients with hypotension and significant base deficits had a mortality rate of 65%.

Publication Information
Authors

Anthony J. Weekes; Ryan J. Zapata; Antonio Napolitano

Publication Date

November 1, 2007

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