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The Cardiorenal Syndrome is commonly encountered, and frequently misunderstood. Join the CardioNerds team as we discuss the complex interplay between the heart and kidneys with Dr. Elliott Miller (Assistant Professor of Medicine at Yale University School of Medicine and Associate Medical Director of the Cardiac Intensive Care Unit of Yale New Haven Hospital), and Dr. Nayan Arora (Clinical Assistant Professor of Medicine and Nephrologist at the University of Washington Medical Center). We are hosted by FIT lead Dr. Matthew Delfiner (Cardiology Fellow at Temple University), Cardiac Critical Care Series Co-Chairs Dr. Mark Belkin (AHFTC faculty at University of Chicago) and Dr. Karan Desai (Cardiologist at Johns Hopkins Hospital), and CardioNerds Co-Found Dr. Dan Ambinder. In this episode we discuss the definition and pathophysiology of the cardiorenal syndrome, explore strategies for initial diuresis and diuretic resistance, and management of the common heart failure medications in this setting. Show notes were developed by Dr. Matthew Delfiner. Audio editing by CardioNerds Academy Intern, student doctor Akiva Rosenzveig.

The CardioNerds Cardiac Critical Care Series is a multi-institutional collaboration made possible by contributions of stellar fellow leads and expert faculty from several programs, led by series co-chairs, Dr. Mark Belkin, Dr. Eunice Dugan, Dr. Karan Desai, and Dr. Yoav Karpenshif.

Enjoy this Circulation 2022 Paths to Discovery article to learn about the CardioNerds story, mission, and values.

Pearls • Notes • References • Production Team

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Pearls and Quotes – Management of Cardiorenal Syndrome in the CICU

1. Cardiorenal syndrome (CRS) represents a range of clinical entities in which there is both heart and kidney dysfunction, and can be driven by one, or both, of the organs.
2. CRS is caused by reduced renal perfusion, elevated renal congestion, or a combination of the two. Treatment therefore focuses on increasing perfusion, by optimizing cardiac output and mean arterial pressure, and reducing congestion through diuresis.
3. Patients should be monitored for an adequate response to the initial diuretic dose within 2 hours of administration. If the response is inadequate, the loop diuretic dose should be doubled.
4. Diuretic resistance can be managed via sequential nephron blockade, most commonly with thiazide diuretics, but also with amiloride, high-dose spironolactone, or acetazolamide, as these target different regions of the nephron.
5. In cases of refractory diuretic resistance, hypertonic saline can be considered with the help of an experienced clinician.
6. Continuation or cessation of renin-angiotensin-aldosterone system (RAAS) inhibitors in the setting of CRS should be made on a case-by-case basis.

Show notes – Management of Cardiorenal Syndrome in the CICU

1. Cardiorenal syndrome (CRS) is a collection of signs/symptoms that indicate injury to both the heart and kidneys. Organ dysfunction in one can drive dysfunction in the other. Cardiorenal syndrome can be categorized as:

• Type 1 – Acute heart failure causing acute kidney injury
• Type 2 – Chronic heart failure causing chronic kidney injury
• Type 3 – Acute kidney injury causing acute heart failure
• Type 4 – Chronic kidney injury causing chronic heart failure
• Type 5 – Co-development of heart and kidney injury by another systemic process.

These categories can be helpful for education, discussion, and research purposes, but they do not usually enter clinical practice on a regular basis since different categories of cardiorenal syndrome are not necessarily treated differently.

2. CRS is caused by either reduced renal perfusion, elevated renal congestion, or a combination of the two. When dealing with CRS, note that:

• CRS can be caused by poor kidney perfusion, though is mostly driven by low renal perfusion pressure.
• Renal perfusion pressure is the gradient between renal arteries and renal veins, which can be approximated by mean arterial pressure (MAP) minus central venous pressure (CVP)
• CRS can therefore be treated by reducing CVP (i.e. with diuresis) or increasing MAP or cardiac output

3. Renal decongestion is achieved primarily through diuresis.

• For diuretic “naïve” patients, furosemide 40 mg IV is a reasonable starting dose
• For patients already on diuretics prior to admission, increasing their home dose by 2.5x (administered intravenously) usually achieves an adequate initial response
• Patients should be reassessed 1-2 hours after their initial diuretics dose. If the patient has not made 200 mL of urine, the loop diuretic dose should be doubled.
• Diuretic dose and urine output have a logarithmic relationship, meaning doubling the dose does not double the urine output. Once you reach a certain dose threshold, you won’t necessarily increase the quantity of diuresis, but rather you will increase the duration of diuresis.

4. It is okay if creatinine rises with diuresis, to a degree.

• Creatinine elevation with decongestion is more a sign of hemoconcentration and is paradoxically associated with better outcomes.
• However, if the creatinine rises by more than 30-50% and you are not seeing clinical evidence of decongestion, then that is likely a poor prognostic sign.

5. There are multiple ways to manage diuretic resistance.

• Diuretic resistance is often due to a variety of mechanisms including increased sodium reabsorption and hypertrophy of the distal convoluted tubule. Sequential nephron blockade can be considered, most commonly with a thiazide diuretic in addition to a loop diuretic, after the loop diuretic dose is sufficiently optimized.
• Patients with diuretic resistance may also have increased sodium reabsorption in the proximal tubule, so acetazolamide may be helpful in certain cases. Check out the CardioNerds Journal Club on the ADVOR trial!
• Amiloride and high doses of spironolactone can be used to target the collecting ducts.
• Finally, hypertonic saline has been used to address persistent diuretic resistance in certain cases, though should be done with an experienced clinician.

6. Decisions regarding cessation versus continuation of renin-angiotensin-aldosterone system (RAAS) inhibitors in the setting of CRS should be made on a case-by-case basis.

• RAAS inhibitors may not specifically cause harm, but they may make it difficult to discern whether a change in creatinine related to their use versus worsening renal function.
• On the other hand, there is an increased likelihood that RAAS inhibitors are not resumed when they are held in CRS, which is associated with worse outcomes. Therefore, it is imperative that there is a plan made to resume these medications if they are held.

References

• Jentzer, Bihorac, Brusca et al. “Contemporary Management of Severee Acute Kidney Injury and Refractory Cardiorenal Syndrome: JACC Council Perspectives.” J Am Coll Cardiol. 2020 Sep, 76 (9) 1084-1101. https://www.jacc.org/doi/abs/10.1016/j.jacc.2020.06.070
• Rangaswami J., Bhalla V., Blair J.E.A., et al. “Cardiorenal syndrome: classification, pathophysiology, diagnosis, and treatment strategies: a scientific statement from the American Heart Association”. Circulation 2019;139:e840-e878: https://www.ahajournals.org/doi/full/10.1161/CIR.0000000000000664
• Jentzer J.C., Chawla L.S. “A clinical approach to the acute cardiorenal syndrome”. Crit Care Clin 2015; 31:685-703. https://www.criticalcare.theclinics.com/article/S0749-0704(15)00048-2/abstract