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Difficulty: HardReduction of Risk Potential

A 68-year-old client is admitted with a small bowel obstruction and has been receiving continuous nasogastric (NG) tube wall suctioning for the past 48 hours. The nurse notes the client has become increasingly irritable, with a respiratory rate of 11 breaths/min and shallow chest expansion. Arterial blood gas (ABG) results are: pH 7.54, PaCO2 49 mm Hg, HCO3- 35 mEq/L, and PaO2 85 mm Hg. Based on these findings, which action is the priority for the nurse to implement to reduce the risk of an impending complication?

  1. A
    Encourage the client to use an incentive spirometer to increase alveolar ventilation and decrease the elevated carbon dioxide levels.
  2. B
    Instruct the client to breathe into a paper bag to facilitate the rebreathing of exhaled carbon dioxide.
  3. C
    Assess for a narrowing pulse pressure and cold, clammy extremities as early indicators of hypovolemic shock.
  4. Obtain a 12-lead electrocardiogram (ECG) and evaluate the client for a positive Chvostek's sign.Answer

Answer

The correct priority action is to obtain a 12-lead electrocardiogram (ECG) and evaluate the client for a positive Chvostek's sign.
The client is experiencing partially compensated metabolic alkalosis (pH > 7.45, elevated HCO3-, and elevated PaCO2 as the lungs hypoventilate to retain acid). This is a direct complication of prolonged NG tube suctioning, which severely depletes gastric acid. Severe metabolic alkalosis causes extracellular potassium to shift into cells (resulting in hypokalemia) and increases calcium binding to albumin (resulting in symptomatic hypocalcemia). The nurse must prioritize assessing for these life-threatening electrolyte imbalances by obtaining an ECG (to detect hypokalemia-induced arrhythmias) and checking for Chvostek's sign (facial nerve hyperirritability indicating hypocalcemia).

Step-by-Step Solution

1
Analyze the ABG results to determine the primary acid-base imbalance.
A pH of 7.54 indicates alkalemia; an HCO3- of 35 mEq/L indicates a metabolic origin.
Establishing the primary physiological disruption is the first step in clinical judgment.
2
Identify the compensatory mechanism in progress.
The elevated PaCO2 of 49 mm Hg and a respiratory rate of 11 breaths/min indicate respiratory compensation via acid (CO2) retention.
Recognizing compensation prevents the nurse from inappropriately intervening to 'fix' a necessary physiological response.
3
Connect the client's medical treatment to the physiological state.
Continuous NG tube suctioning removes gastric hydrochloric acid, which directly causes the metabolic alkalosis.
Understanding the etiology helps anticipate the specific systemic complications that will follow.
4
Anticipate the downstream physiological complications of this specific imbalance.
Severe metabolic alkalosis causes extracellular potassium to shift into cells (hypokalemia) and increases calcium binding to albumin (hypocalcemia).
These electrolyte shifts are the primary mechanisms that cause immediate life-threatening events.
5
Select the nursing action that directly assesses or mitigates these high-risk complications.
Obtaining an ECG checks for hypokalemia-induced arrhythmias, and testing for Chvostek's sign checks for hypocalcemia-induced tetany.
This directly reduces the risk of sudden cardiac or neuromuscular decompensation.

Key Concept

Identifying the life-threatening systemic complications (hypokalemia and hypocalcemia) of metabolic alkalosis resulting from excessive gastric acid loss.
Estimated Time:1m 30s
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Topics

Reduction of Risk Potential

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