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Brain & Heart Hypochloremia in refractory heart failure

to the Cleveland Clinic from July 2008 to December 2013 The results of the above studies provide the basis that
also documented Cl changes. Hypochloremia was found when dealing with HF patients, it is important to look at and
in 10.7% of the HF patients, 12.6% of those with HFrEF, monitor Cl levels as essentially as Na. However, these studies
and 9.3% of individuals with HFpEF. They reported that Cl have limitations that should be interpreted judiciously.
levels independently predicted long-term mortality during Most studies were either prospective or retrospective
hospitalization, and both were inversely associated (hazard cohort or registry-based studies. None of these studies
ratio [HR], 0.94; 95% CI: 0.92 – 0.95; P < 0.001). This study was a randomized controlled trial or interventional study.
demonstrated that even after multivariate risk adjustment, However, all the studies reported data from a significant
serum Cl was significantly associated with mortality in number of patients. Further, most studies report similar
ADHF (HR, 0.93; 95% CI: 0.90 – 0.97; P < 0.001). 15,16 outcomes, which makes these findings worth examining.
Another study of 39,298 hospitalized patients from 5. Intracellular electrolytes in HF
2009 – 2013 compared serum Cl levels at admission and
at least twice during hospitalization and its effects on Several compensatory mechanisms are activated in chronic
in-hospital death. Of the total patients, 59% had normal HF (CHF), which affect the metabolism of electrolytes.
Cl levels throughout hospitalization, 21% had hospital- Activation of the renin-angiotensin-aldosterone (RAAS)
acquired hypochloremia, 15% developed hyperchloremia, system causes Na retention and loss of K and magnesium.
and 5% had both abnormalities. Their mortality was The secondary hyperaldosteronism may lead to high
associated with hyperchloremia (odds ratio [OR]: 2.84; intracellular Na and low intracellular K through the cell
P < 0.001) and both hyper- and hypochloremia (OR: 1.72; membrane permeability effect. Magnesium deficiency may
P = 0.004). Hypochloremia alone was not significantly further increase intracellular Na and decrease intracellular
associated with in-hospital mortality (OR: 0.91; P = 0.54). K, as Mg is a mandatory ion for the Na-K pump. 21
This study showed that nearly half of hospitalized 6. Mechanisms of Cl interaction in HF
patients had serum Cl abnormalities. It was concluded
that hyperchloremia, rather than hypochloremia, 6.1. Cl and blood pressure
was associated with high mortality. The relationship Some studies suggest that high dietary Na does not increase
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between hypochloremia and hyponatremia and their blood pressure without Cl. An old study from 1929 described
effects on mortality was demonstrated in a prospective that the Cl component raised blood pressure because Na salts
and single-center observational study. At the 3-month of bicarbonate (HCO ) did not elicit the equivalent pressor
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follow-up, 45% of adult patients with acute HF (AHF) and effect as did NaCl in hypertensive subjects. Furthermore,
hypochloremia on admission developed hyponatremia at in those with hypertension, dietary K reduced blood
3 months, and only 3% without baseline hypochloremia pressure in the form of KCl compared to potassium citrate
developed hyponatremia. Hypochloremia at admission was (K C H O ). However, there is little scientific evidence that
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significantly associated with hyponatremia after 3 months the accompanying Cl anion is necessary to determine the
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(P < 0.001; OR: 27.08; 95% CI: 4.3 – 170.7). It was observed pressor effect of NaCl. NA salts of C H O , HCO , and PO
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that patients who had low Cl and normal Na at admission do not appear to affect the rise in blood pressure. 22,23 4
exhibited statistically significantly higher in-hospital
mortality (OR: 4.08; CI: 1.08 – 15.43; P = 0.039). 18 6.2. Physiology of Cl
A cohort study of 1996 individuals from December 2016 Cl is the most abundant extracellular and intracellular
to June 2019 showed that the prevalence of hypochloremia anion, accounting for 70% of total negative ions. Due
was 26.1% (521/1996) in patients with HF. It shows to its high concentration, Cl is essential for maintaining
that serum Cl levels at admission have an independent electroneutrality. Cl contributes about 100 out of 300
and inverse association with all-cause mortality in HF mOsm/L of ECF tonicity. Volume-homeostasis-regulating
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(HR: 0.967; 95% CI: 0.939 – 0.996; P = 0.026) as compared mechanisms generally activate through changes in the Na
to Na, which after multivariable adjustment was no and Cl levels. There is a negative relationship between
longer significant (P > 0.05). A study of ADHF subjects Cl and HCO , which maintains the acid-base balance
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shows that low serum Cl (hypochloremia) predicts the through reciprocal transport in and out of RBCs and renal
risk of cardiac death at discharge, irrespective of the EF. tubules. Cl clearance is a crucial pathway in the renal
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It shows that hypochloremic individuals had a significant adaptation of metabolic acidosis and chronic respiratory
risk of cardiac death as compared to those without acid-base disorders. The gut and kidneys mainly regulate
it in the HFrEF (HR: 3.38 [1.03 – 11.08], P = 0.007), circulating Cl levels in the body. Cl is absorbed across the
HEmrEF (HR: 4.37 [1.20–15. , P = 0.025), and HFpEF entire length of the intestine and secreted in the form of
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(HR: 3.13 [1.01 – 9.74], P = 0.048) groups. 20 HCl from parietal stomach cells. 23,24
Volume 2 Issue 1 (2024) 3 https://doi.org/10.36922/bh.2257