Skip to Main Content

++

SOURCE

+

Sources: MacLaren R, Mueller SW, Dasta JF. Use of vasopressors and inotropes in the pharmacotherapy of shock. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=146057724. Erstad BL. Hypovolemic shock. In: DiPiro JT, Talbert RL, Yee GC, Matzke GR, Wells BG, Posey LM, eds. Pharmacotherapy: A Pathophysiologic Approach. 10th ed. New York, NY: McGraw-Hill; 2017. http://accesspharmacy.mhmedical.com/content.aspx?bookid=1861&sectionid=134126763. Both accessed May 9, 2017.

++

DEFINITION

++

  • Acute, generalized state of inadequate perfusion of critical organs associated with systolic blood pressure (SBP) <90 mm Hg or reduction of at least 40 mm Hg from baseline with perfusion abnormalities despite adequate fluid resuscitation.

++

ETIOLOGY

++

  • Intravascular volume deficit (hypovolemic shock)

    • Blood loss due to:

      • Trauma.

      • Surgery.

      • Hemorrhage.

    • Plasma loss due to fluid sequestration or loss.

    • Dehydration.

      • Excessive insensible fluid loss.

      • Diuretic overuse.

      • Severe vomiting or diarrhea.

  • Myocardial pump failure (cardiogenic shock)

  • Peripheral vasodilation (septic, anaphylactic, neurogenic shock)

++

PATHOPHYSIOLOGY

++

  • Fall in blood pressure (BP) compensated by increased sympathetic outflow, activation of renin–angiotensin system, and other humoral factors that stimulate peripheral vasoconstriction.

  • Vasoconstriction redistributes blood away from skin, skeletal muscles, kidneys, and GI tract toward vital organs (eg, heart and brain) to maintain oxygenation, nutrition, and organ function.

  • Metabolic lactic acidosis develops from tissue ischemia and causes vasodilation, further exacerbating impaired cardiovascular function.

++

EPIDEMIOLOGY

++

  • Incidence unknown.

  • More than 100,000 deaths in the United States each year due to injuries that often involve bleeding.

++

RISK FACTORS

++

  • Surgery.

  • Trauma.

  • Hemorrhage.

  • Infection.

  • Heart failure.

  • Burns.

  • Dehydration.

  • Anaphylaxis.

++

CLINICAL PRESENTATION

++
SIGNS AND SYMPTOMS
++

  • Hypovolemic shock:

    • Thirst.

    • Anxiousness.

    • Weakness.

    • Lightheadedness.

    • Dizziness.

    • Reduced urine output.

    • Dark yellow-colored urine.

  • Signs of volume loss:

    • Tachycardia (>120 beats/min)

    • Tachypnea (>30 breaths/min)

    • Hypotension (SBP < 90 mm Hg)

    • Mental status changes or unconsciousness.

    • Agitation.

    • Normal or low body temperature with cold extremities.

    • Decreased capillary refill.

  • Reduced cardiac index (CI < 2.2 L/min/m2)

++

DIAGNOSIS

++
MEANS OF CONFIRMATION AND DIAGNOSIS
++

  • Use noninvasive and invasive monitoring (Table 1), medical history, clinical presentation, and laboratory findings to confirm diagnosis and identify underlying cause.

++
LABORATORY TESTS
++

  • Elevated serum sodium and chloride with acute volume depletion.

  • Increased blood urea nitrogen (BUN): serum creatinine ratio with dehydration.

  • Increased serum creatinine with renal dysfunction.

  • Metabolic acidosis with elevated base deficit and lactate concentrations and decreased bicarbonate and pH

  • Normal complete blood cell count (CBC) in absence of infection.

  • Reduced red cell count, hemoglobin, and hematocrit in hemorrhagic shock.

  • Elevated serum transaminase levels with hepatic dysfunction.

++

Reduced urine output (<0.5–1 mL/kg/h)

++
Table Graphic Jump Location
TABLE 1.aHemodynamic and Oxygen (O2)-Transport Monitoring Parameters

Pop-up div Successfully Displayed

This div only appears when the trigger link is hovered over. Otherwise it is hidden from view.