# Situation: A 48-year-old woman developed acute tubular necrosis after 7 days of intravenous gentamicin for a complicated abdominal infection; the gentamicin has been stopped. She has no history of heart or kidney disease and is now in the oliguric phase of acute kidney injury. On day 4, she is alert, with deep, rapid respirations of 28/min and an oxygen saturation (SpO2) of 97% on room air. Her arterial blood gas (ABG) shows pH 7.29, PaCO2 (partial pressure of arterial carbon dioxide) 30 mmHg, and HCO3− (bicarbonate) 14 mEq/L. Which action is appropriate for her breathing pattern?

> source: MyMerci (mymerci.kr)  
> url: https://mymerci.kr/pages/nclex_q.php?qn_id=629814  
> language: ko  
> subject: Nursing Practice III — Care of Clients with Problems in Surgery, Oxygenation, Fluid and Electrolytes, Infectious, Inflammatory and Immunologic Response, Cellular Aberrations

## 문제

Situation: A 48-year-old woman developed acute tubular necrosis after 7 days of intravenous gentamicin for a complicated abdominal infection; the gentamicin has been stopped. She has no history of heart or kidney disease and is now in the oliguric phase of acute kidney injury.

On day 4, she is alert, with deep, rapid respirations of 28/min and an oxygen saturation (SpO2) of 97% on room air. Her arterial blood gas (ABG) shows pH 7.29, PaCO2 (partial pressure of arterial carbon dioxide) 30 mmHg, and HCO3− (bicarbonate) 14 mEq/L. Which action is appropriate for her breathing pattern?

## 보기

1. Coach her to breathe slowly through pursed lips
2. Give oxygen by nonrebreather mask at 15 L/min
3. Have her rebreathe into a paper bag for a while
4. Allow the pattern and monitor her closely **✔ 정답**

**정답: 4**

## 해설

Her ABG shows metabolic acidosis (low pH and low HCO3−) because the failing kidneys cannot excrete acid, and her deep, rapid (Kussmaul) breathing is the lungs' compensation, blowing off carbon dioxide to limit the fall in pH. The nurse should not try to slow it; care is directed at the cause, while respiratory status, potassium, and cardiac rhythm are monitored.

## 심화 해설

Why the breathing pattern is compensatory, not a problem to suppress

The ABG reveals a primary metabolic acidosis: the pH is 7.29, the HCO3− is 14 mEq/L, and the PaCO2 is 30 mmHg. In acute tubular necrosis, the injured tubules lose their ability to excrete the daily acid load and to regenerate bicarbonate, so hydrogen ions accumulate and bicarbonate falls. The low pH then stimulates central and peripheral chemoreceptors, driving the respiratory center to increase both the depth and rate of ventilation. This is Kussmaul breathing, and its purpose is to blow off carbon dioxide. Because CO2 is an acid in solution, lowering PaCO2 from the usual 40 mmHg toward 30 mmHg reduces the acid burden and partially buffers the fall in pH. The deep, rapid breathing is therefore a protective compensation, not a primary respiratory disorder, and suppressing it would worsen the acidosis.

The SpO2 of 97% on room air confirms that oxygenation is adequate. Kussmaul respirations in metabolic acidosis are driven by acid–base chemoreceptors, not by hypoxemia, so there is no indication for supplemental oxygen. A nonrebreather mask at 15 L/min would treat a problem the patient does not have and would not correct the underlying acid–base disturbance.

Watch out! A paper bag is used for hyperventilation caused by anxiety or respiratory alkalosis, where rebreathing CO2 raises PaCO2 back toward normal. In metabolic acidosis, the low PaCO2 is the body’s attempt to compensate; making the patient rebreathe CO2 would drive the pH even lower and can precipitate dangerous arrhythmias or altered mental status.

Key point! Pursed-lip breathing slows expiration and is useful for obstructive lung disease or panic-related hyperventilation. Here, slowing the respiratory rate would reduce CO2 elimination, allowing PaCO2 to rise and pH to fall further. The nurse should not coach the patient to breathe slowly.

Clinical reasoning for the oliguric phase of acute kidney injury

During the oliguric phase, urine output falls below 400 mL/day, and the kidneys cannot clear fixed acids, potassium, or fluid. The metabolic acidosis seen here is expected. The respiratory system compensates within minutes to hours, which is why the PaCO2 is low on day 4. Management targets the cause of the acidosis—the acute kidney injury itself—while the nurse monitors for complications of both the acidosis and the compensatory breathing.

Because acidosis shifts potassium out of cells, hyperkalemia is a major threat during oliguric AKI. The nurse should monitor the ECG for peaked T waves, widened QRS, or arrhythmias, and check serum potassium. Respiratory muscle fatigue can also occur if Kussmaul breathing is prolonged, so ongoing assessment of respiratory effort, mental status, and ABG trends is essential. If the acidosis worsens or the patient becomes unable to sustain the increased work of breathing, renal replacement therapy may be indicated, but in this alert patient with an SpO2 of 97%, the appropriate action is to allow the compensatory pattern and monitor closely.

| Intervention | Rationale in metabolic acidosis | Appropriate here? |
| --- | --- | --- |
| Pursed-lip breathing | Slows expiration, raises PaCO2, lowers pH further | No |
| Nonrebreather mask 15 L/min | Treats hypoxemia; SpO2 is 97% on room air | No |
| Paper bag rebreathing | Raises PaCO2; intended for respiratory alkalosis, not metabolic acidosis | No |
| Allow Kussmaul breathing and monitor | Preserves respiratory compensation while treating the AKI and watching potassium and cardiac rhythm | Yes |

The respiratory pattern is a sign that the lungs are working to limit the acid–base disturbance; the nurse’s role is to support that compensation, not to interrupt it. In the oliguric phase of acute tubular necrosis, the priority is close monitoring of respiratory status, serum potassium, and cardiac rhythm while definitive treatment of the kidney injury proceeds.

## 임상 시나리오

Kussmaul Breathing in Metabolic AcidosisProtect the compensation, treat the cause
In acute tubular necrosis, the kidneys cannot excrete acid, producing a primary metabolic acidosis with low pH and low HCO3-. The deep, rapid Kussmaul breathing lowers PaCO2 to partially correct the pH and must not be suppressed.

Assess respiratory status, potassium, and cardiac rhythm closely. Direct treatment at the underlying cause of the acidosis, not at the breathing pattern.

CautionDo not give oxygen for a normal SpO2 97% or have the patient rebreathe CO2; both are inappropriate and may worsen the acid-base disturbance.

## 핵심 개념

- **Kussmaul breathing** — Deep, rapid respirations that compensate for metabolic acidosis by blowing off CO2.
- **Metabolic acidosis** — Low pH with low HCO3- caused by acid accumulation or bicarbonate loss.
- **Acute tubular necrosis** — Kidney injury from ischemic or nephrotoxic damage to tubular cells, causing loss of acid excretion.
- **Compensation** — Physiologic response that partially corrects an acid-base disturbance, e.g., hyperventilation lowering PaCO2 in metabolic acidosis.
- **Anion gap** — Calculated difference between measured cations and anions, used to classify metabolic acidosis.

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