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Difficulty: HardPhysiological Adaptation

A client is admitted to the intensive care unit with severe sepsis secondary to a perforated viscus. The nurse has just completed administering a prescribed initial intravenous fluid bolus of 30 mL/kg of 0.9% sodium chloride. A subsequent reassessment reveals a blood pressure of 82/46 mmHg, a heart rate of 126 beats/minute, a respiratory rate of 28 breaths/minute, and a urine output of 15 mL over the past hour. Arterial blood gas results demonstrate a pH of 7.27, PaCO2PaCO_2 of 30 mmHg, PaO2PaO_2 of 82 mmHg, and HCO3−HCO_3^- of 14 mEq/L. Based on these findings, which of the following is the priority nursing action?

  1. Initiate a prescribed continuous intravenous infusion of norepinephrine.Answer
  2. B
    Administer a prescribed intravenous dose of sodium bicarbonate.
  3. C
    Infuse a second 30 mL/kg bolus of isotonic crystalloids.
  4. D
    Prepare the client for immediate endotracheal intubation and mechanical ventilation.

Answer

The correct action is to initiate a prescribed continuous intravenous infusion of norepinephrine.
The client is exhibiting signs of fluid-refractory septic shock, evidenced by profound hypotension that persists after standard initial fluid resuscitation (30 mL/kg bolus). In this phase of shock, the profound systemic vasodilation must be counteracted with a vasopressor. Norepinephrine is the first-line vasopressor used to increase systemic vascular resistance, restore a mean arterial pressure of at least 65 mmHg, and improve tissue perfusion to reverse the ongoing lactic acidosis.

Step-by-Step Solution

1
Analyze the hemodynamic response to the initial fluid resuscitation.
The client's blood pressure remains critically low (82/46 mmHg) despite receiving the standard 30 mL/kg fluid bolus.
This identifies the transition from fluid-responsive shock to fluid-refractory vasodilatory shock.
2
Interpret the arterial blood gas values in the context of the client's vital signs.
The ABG shows partially compensated metabolic acidosis (low pH, low HCO3−HCO_3^-) with a compensatory respiratory alkalosis (tachypnea leading to low PaCO2PaCO_2). The PaO2PaO_2 is adequate.
This confirms that the tachypnea is a compensatory mechanism for lactic acidosis caused by hypoperfusion, rather than acute respiratory failure.
3
Determine the highest priority clinical intervention based on current guidelines.
Vasopressor support (norepinephrine) must be initiated immediately.
In fluid-refractory septic shock, vasopressors are the primary intervention to increase mean arterial pressure, restore organ perfusion, and halt the progression of lactic acidosis.

Key Concept

Fluid-Refractory Septic Shock and Hemodynamic Support
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Topics

Physiological Adaptation

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