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INTRODUCTION

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  • Shock is an acute state of inadequate perfusion of critical organs that can lead to death if therapy is not optimal. Shock is defined as systolic blood pressure (SBP) less than 90 mm Hg or reduction of at least 40 mm Hg from baseline with perfusion abnormalities despite adequate fluid resuscitation.

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PATHOPHYSIOLOGY

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  • Shock results in failure of the circulatory system to deliver sufficient oxygen (O2) to tissues despite normal or reduced O2 consumption. Shock may be caused by intravascular volume deficit (hypovolemic shock), myocardial pump failure (cardiogenic shock), or peripheral vasodilation (septic, anaphylactic, or neurogenic shock).

  • Hypovolemic shock is characterized by acute intravascular volume deficiency due to external losses or internal redistribution of extracellular water. It can be precipitated by hemorrhage; burns; trauma; surgery; intestinal obstruction; and dehydration from considerable insensible fluid loss, overaggressive diuretic administration, and severe vomiting or diarrhea. Relative hypovolemia leading to hypovolemic shock occurs during significant vasodilation, which accompanies anaphylaxis, sepsis, and neurogenic shock.

  • Fall in blood pressure (BP) is compensated by increased sympathetic outflow, activation of the renin–angiotensin system, and other factors that stimulate peripheral vasoconstriction. Compensatory vasoconstriction redistributes blood away from skin, skeletal muscles, kidneys, and gastrointestinal (GI) tract toward vital organs (eg, heart and brain) in attempt to maintain oxygenation, nutrition, and organ function.

  • Severe lactic acidosis often develops secondary to tissue ischemia and causes localized vasodilation, which further exacerbates the impaired cardiovascular state.

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CLINICAL PRESENTATION

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  • Patients with hypovolemic shock may have thirst, anxiousness, weakness, lightheadedness, dizziness, scanty urine output, and dark yellow urine.

  • Signs of more severe volume loss include tachycardia (>120 beats/min), tachypnea (>30 breaths/min), hypotension (SBP <90 mm Hg), mental status changes or unconsciousness, agitation, and normal or low body temperature (in the absence of infection) with cold extremities and decreased capillary refill.

  • Serum sodium and chloride concentrations are usually high with acute volume depletion. The blood urea nitrogen (BUN):creatinine ratio may be elevated initially, but the creatinine increases with renal dysfunction. Metabolic acidosis results in elevated base deficit and lactate concentrations with decreased bicarbonate and pH.

  • Complete blood cell count (CBC) is normal in absence of infection. In hemorrhagic shock, the red cell count, hemoglobin, and hematocrit will decrease.

  • Urine output is decreased to less than 0.5 to 1 mL/h. With more severe volume depletion, dysfunction of other organs may be reflected in laboratory testing (eg, elevated serum transaminases levels with hepatic dysfunction).

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DIAGNOSIS AND MONITORING

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  • Noninvasive and invasive monitoring (Table 12–1) and evaluation of medical history, clinical presentation, and laboratory findings are important in establishing the diagnosis and assessing mechanisms responsible for shock. Findings include hypotension (SBP <90 mm Hg), depressed cardiac index (CI <2.2 L/min/m2), tachycardia (heart rate >100 beats/min), and low urine output (<20 mL/h).

  • Pulmonary artery (Swan–Ganz) catheter can be used to determine central venous pressure (CVP), pulmonary artery pressure (PAP), cardiac output (CO), and pulmonary artery occlusion pressure (PAOP).

  • Renal function can be assessed grossly by hourly measurements of urine output, but estimation of creatinine clearance based on isolated serum creatinine values may be inaccurate. ...

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