Blog from the Guest Lecture Series at East Carolina University – Brody School of Medicine

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Lecturer: Hassan Alhosaini, MD
Blogger: Tejas Desai, MD

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The Cardio-Renal Syndrome

Dr. Alhosaini started with a case of a young man with advanced heart failure, NYHA class 4. Dyspneic at rest and right-sided pressures are elevated in the upright position. Also evidence of high pulmonary filling pressures. The patient is admitted for IV diuretics and his BUN/Cr start rising.

Should we continue with the diuretics or begin to administer IV fluids?

The 2010 American Heart Association update estimates $30 billion for complications from heart failure. The rate of hospital discharge for heart failure is actually increasing, unlike the rate for hospital discharge after myocardial ischemia.

The agenda for this lecture was:
– define the cardiorenal syndrome
– epidemiology and treatment of cardiorenal syndrome
– classification of cardiorenal syndrome (there are 5)
– pathophysiology of the cardiorenal syndrome
– therapeutic considerations

In 2007, the National Heart, Lung, and Blood Institute looked into the cardiorenal syndrome. Their working definition of cardiorenal syndrome was: therapy to treat heart failure leads to worsening renal function. Dr. Alhosaini feels that the definition must be expanded in order to reflect the pathophysiologic changes, especially because treatments are developed based on the definition of the disease.

He recommends the following definition: each dysfunctional organ initiates and perpetuates disease in the other organ through biochemical, neurohormonal, immunologic , and vascular pathways.

Conventional wisdom in cardiorenal syndrome is that the renal dysfunction is due to the prerenal state. The prerenal state occurs as a result of poor cardiac output or excessive diuresis.

In the last 10-15 years, the prevalence of cardiorenal syndrome in hospitalized decompensated heart failure is 30%; 21% have a creatinine > 2 mg/dl; 9% have a creatinine > 3 mg/dl (ADHERE Registry). In a study looking at 750 heart failure outpatients, prevalence rates for cardiorenal syndrome were: NYHA IV 40%, NYHA III 30%. Renal dysfunction effects outcomes in heart failure patients. Patients who had poor quality of life had a higher rate of cardiorenal syndrome. Creatinine level is powerful predictor of poor events in these patients.

A recent JACC paper categorized cardiorenal syndrome into 5 categories, based on chronicity and whether the primary problem is cardiac or renal. Dr. Alhosaini focused on type 1 (acute) and type 2 (chronic) cardiorenal syndrome (CRS). In both these categories, the primary organ dysfunction is cardiac. Type 2 patients are usually seen as outpatients; becoming more resistant to diuretics with worsening creatinine.

Dr. Alhosaini then turned his attention to novel pathogenetic mechanisms for CRS. For example, he discussed intra-abdominal pressure (IAP) as a mechanism by which the CRS can be perpetuated. Elevated IAP’s lead to worsening renal function. Elevated central venous pressure is also another novel mechanism. In the Damman study, patients with normal eGFR had normal levels of CVP, but rising CVP’s cause a worsening of eGFR (this is counter-intuitive, since the conventional wisdom is that lower CVP’s (lower preloads) should lead to worsening eGFR because of a generalized pre-renal/hypovolemic state)). A group at the Cleveland Clinic looked at cardiac index vs. CVP to determine which would be a better predictor of developing worsening renal failure. Surprisingly, CVP was a better marker. With these new findings, one can say that renal function is related to the pressure gradient between the afferent and efferent arteriolar systems (the renal perfusion pressure).

Dr. Alhosaini then detailed a number of examples in the Lynne Stevenson model of heart failure profiles. For example, patients with the “wet-warm” profile have a relatively normal cardiac output but an elevated right atrial pressure. This leads to a greater CVP, which makes the renal perfusion pressure drop. In the “wet-cold” profile, both an elevated right atrial pressure and lower cardiac output lead to a significant decrease in renal perfusion pressure. Thus, therapies directed to re-establish the renal perfusion pressure (the pressure gradient) should help alleviate CRS.

Therapeutic Considerations
Is it right to give both lasix and fluids to a patient with CRS? Contrary to belief, this is a legitimate strategy provided that the fluids given are 3% saline or albumin. A group in Italy is using 3% saline to mobilize fluid into the vasculature and then administering diuretics to eliminate that fluid. This is primarily being used in heart failure patients who are defined as diuretic-resistant.

Dr. Alhosaini recommends using a continuous infusion of diuretics rather than intermittent boluses, but the studies are equivocal, primarily because of small sample sizes.

Adenosine antagonism (the PROTECT Study): this idea came from the observation that coffee causes a diuresis because of its antagonistic affects. Dr. Alhosaini did not go into the mechanism except to say that coffee inhibits afferent arteriolar tone. Unfortunately, the results of the PROTECT study were not as impressive as one would have hoped.

Nesiritide (a natriuretic peptide) has not shown to be effective in acute CRS patients.

Continuous Ultrafiltration: data is not back yet and it is not clear if this strategy would be the most effective. Studies are underway.

Vasopressin antagonists: these vaptans are not yet approved for heart failure and CRS patients.

Dr. Alhosaini is of the opinion that most CRS patients require volume removal rather than volume resuscitation. It appears that most cardiologists feel CRS patients are volume overloaded based on a European review.

Dr. Alhosaini has provided his slides for review (if needed).




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