Pissing Away the Chloride

Using Chloride Levels in Heart Failure Management

I started using serum chloride (Cl^-1 ) in 1979 after  I took care of a young adult, with a terrible cardiomyopathy from hemosiderosis caused by repetitive transfusion for a hemoglobinopathy associated anemia.  She had had 13 admissions for fluid overload, and I noticed that every time she came in, her Cl^-1 was over 110 mg/dl and every time she went home it was less than 95.   When I asked her about taking her medicines, she told me that she did not take them because she did not want to have her disease.  Since that encounter, I have looked at serum Cl^-1 to judge if the patient is compliant with his/her diuretic.     

Sodium and chloride (NaCl) are absorbed together in the renal tubule. (Figure)  But if a person becomes volume depleted for any reason, the renal tubules become sodium (Na⁺¹) avid.  Na⁺¹ escaping absorption as NaCl can be reabsorbed alone in the distal convoluted tubule in exchange for potassium (K⁺¹) or hydrogen ions (H⁺¹).  The H⁺¹ is catalyzed from H₂CO³ by carbonic anhydrase in the renal tubular cells.  The remaining bicarbonate (HCO₃) is  absorbed, and the Cl^-1 is lost in the urine.  The loss of Cl^-1, K⁺¹, and H⁺¹  produces the classic hypochloremic, hypokalemic metabolic alkalosis also called “volume contraction alkalosis.”   Diuretics block the absorption of NaCl making the kidney act as if the patient were volume depleted even though there is still lots of edema. 

This phenomenon makes the serum Cl^-1 concentration an important electrolyte for cardiologists to follow.  Diuretics such as furosemide block NaCl absorption, so that patients taking their diuretic should have a low Cl^-1.  A chronic heart failure patient presenting to the emergency department in heart failure with a high normal Cl^-1 is probably not taking their diuretic if their kidney function is reasonable.  Cl^-1 is also useful in assessing if the diuretic is working and how much more the patient needs to be diuresed. 

I consider Cl^-1 to be one of the most important electrolytes when managing hospitalized heart failure patients.  I use Cl^-1 as a measure of compliance and as an indicator as to whether or not the patient is getting close to where he/she is fully diuresed.  It is not the only parameter I use to judge volume status, but an extremely important one.  Not everyone agrees with using Cl^-1 in this fashion.  When I was on the American Board of Internal Medicine’s Board Exam Committee for Cardiovascular Diseases, I wrote a question using Cl^-1.  None of the other 11 exam writers had even heard of the concept.  The question was not included in the exam.  I simply ask you to think about using Cl ^-1, try using it and see if it helps manage patients with heart failure.