# A nurse is caring for a patient with chronic heart failure who has been receiving IV furosemide for the past 48 hours. The patient's urine output has decreased to 15 mL/hr over the last 4 hours despite continued diuretic therapy, and the patient appears more dyspneic with new bilateral lower extremity edema since morning assessment. Which nursing intervention should be the priority?

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## 문제

A nurse is caring for a patient with chronic heart failure who has been receiving IV furosemide for the past 48 hours. The patient's urine output has decreased to 15 mL/hr over the last 4 hours despite continued diuretic therapy, and the patient appears more dyspneic with new bilateral lower extremity edema since morning assessment. Which nursing intervention should be the priority?

## 보기

1. Increase the IV furosemide infusion rate as ordered
2. Assess for signs of cardiorenal syndrome and notify the physician immediately **✔ 정답**
3. Encourage increased fluid intake to improve kidney perfusion
4. Position the patient in Trendelenburg position to improve venous return

**정답: 2**

## 해설

Decreased urine output (15 mL/hr) with worsening dyspnea and edema despite diuretic therapy suggests cardiorenal syndrome. The priority is to assess for this and notify the physician immediately for treatment modification. Other interventions could worsen the condition.

## 심화 해설

Clinical Scenario Analysis

The patient exhibits a classic and dangerous clinical trajectory. Despite 48 hours of IV furosemide, the urine output has plummeted to 15 mL/hr, which is a critical threshold indicating severe oliguria. The simultaneous worsening of dyspnea and the new onset of bilateral lower extremity edema signal that congestion is intensifying. This combination of worsening congestion and declining renal function in the setting of aggressive diuretic therapy is the hallmark of diuretic resistance within the context of cardiorenal syndrome (CRS) [1].

Pathophysiology of the Priority

The priority is to recognize that this is not simply a case of insufficient diuretic dosing but a complex, maladaptive physiological state. The underlying problem is a vicious cycle: the failing heart's reduced cardiac output leads to renal hypoperfusion, which activates the renin-angiotensin-aldosterone system and sympathetic nervous system. This neurohormonal activation causes profound sodium and water retention, worsening congestion. This congestion, in turn, increases renal venous pressure, creating a state of "renal congestion syndrome" that further impairs kidney function and blunts the response to diuretics [4]. Simply escalating the diuretic dose, as suggested in option 1, often fails to address this underlying pathophysiology and can be counterproductive by further activating neurohormonal pathways and causing electrolyte disturbances that exacerbate diuretic resistance [2]. The emerging evidence points to a multi-ionic disturbance, where chloride depletion, not just sodium handling, is a key determinant of diuretic responsiveness, and this complex imbalance cannot be corrected by simply giving more furosemide [2].

Why the Correct Answer is the Priority

Option 2, assessing for signs of cardiorenal syndrome and notifying the physician immediately, is the priority because it focuses on recognizing a dangerous syndrome that requires a multi-faceted treatment strategy beyond simple dose adjustment. The patient's presentation—worsening renal function (oliguria) in the face of escalating congestion (dyspnea, new edema) despite loop diuretic therapy—is a clinical red flag for CRS with diuretic resistance [1]. This condition is strongly associated with prolonged hospitalization and adverse outcomes, and its management requires a phenotype-tailored approach that may include fluid restriction, combination diuretic therapy targeting different nephron segments, or ultrafiltration, none of which are independent nursing actions [1]. The nurse's critical role is prompt recognition and communication to facilitate a change in the medical plan. Encouraging fluid intake (option 3) is contraindicated as it would directly worsen the patient's primary problem of fluid overload and congestion . Placing a dyspneic patient with heart failure in the Trendelenburg position (option 4) is dangerous, as it would increase preload and pulmonary venous congestion, further compromising respiratory status.References (research sources)

- [1]Diuretic resistance in cardiorenal syndrome: mechanisms, monitoring and phenotype-tailored management.Research articleAletras G, Bachlitzanaki M, Stratinaki M, Foukarakis E, Petrakis I, Pantazis Y, Hamilos M, Stylianou K. (2025) · DOI: 10.3389/fcvm.2025.1731305

- [2]Chloride at the spotlight-but not alone: towards a multi-ionic diuretic strategy.Research articleMontomoli M, Gil Martins Roxo MI, González-Rico M, Núñez J, Núñez-Marín G, Uriarte BA, De La Espriella R, Puchades MJ, Górriz JL. (2026) · DOI: 10.1093/ckj/sfag119

- [4]Renal congestion syndrome in critically ill patients: a neglected mechanism of acute kidney injury - A narrative review.Research articleOrieux A, Boyer A, Lautrette A, Klouche K, Bitker L, KIRST (Kidney Intensive care Research South Team) collaborative group. (2026) · DOI: 10.1016/j.aicoj.2026.100083

## 임상 시나리오

Diuretic Resistance & Cardiorenal SyndromeRecognizing the Vicious Cycle in Worsening Heart Failure
A critical sign of cardiorenal syndrome is worsening congestion (dyspnea, edema) despite aggressive diuresis, coupled with a drop in urine output to less than 0.5 mL/kg/hr (oliguria). This indicates the treatment is failing.

The pathophysiology is a vicious cycle: low cardiac output causes renal hypoperfusion, activating neurohormonal systems. This leads to sodium/water retention, increasing renal venous pressure (renal congestion), which further impairs kidney function and blunts diuretic response.

CautionDo not simply increase the diuretic dose as a first response. This can worsen electrolyte imbalances and neurohormonal activation. The priority is to recognize the syndrome and notify the physician for a multimodal strategy (e.g., combination diuretics, inotropes, fluid removal).

## 핵심 개념

- **Cardiorenal Syndrome (CRS)** — A complex pathophysiological disorder of the heart and kidneys where acute or chronic dysfunction in one organ induces acute or chronic dysfunction in the other.
- **Diuretic Resistance** — A failure to achieve therapeutically desired reduction in edema or congestion despite an adequate dose of a diuretic, often due to neurohormonal activation and renal hypoperfusion.
- **Oliguria** — Urine output less than 400 mL per day or less than 0.5 mL/kg/hr; a critical sign of acute kidney injury or severe renal hypoperfusion.
- **Renal Congestion Syndrome** — A state where increased central venous pressure is transmitted back to the renal veins, impairing renal blood flow and glomerular filtration rate.

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