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Hyperchloremia is an electrolyte disturbance in which there is an elevated level of chloride ions in the blood. [1] The normal serum range for chloride is 96 to 106 mEq/L, [2] therefore chloride levels at or above 110 mEq/L usually indicate kidney dysfunction as it is a regulator of chloride concentration. [3]
Chloride is part of gastric acid (HCl), which plays a role in absorption of electrolytes, activating enzymes, and killing bacteria. The levels of chloride in the blood can help determine if there are underlying metabolic disorders. [20] Generally, chloride has an inverse relationship with bicarbonate, an electrolyte that indicates acid-base ...
The normal blood reference range of chloride for adults in most labs is 96 to 106 milliequivalents (mEq) per liter. The normal range may vary slightly from lab to lab. Normal ranges are usually shown next to results in the lab report. A diagnostic test may use a chloridometer to determine the serum chloride level.
Hyperparathyroidism – can cause hyperchloremia and increase renal bicarbonate loss, which may result in a normal anion gap metabolic acidosis. Patients with hyperparathyroidism may have a lower than normal pH, slightly decreased PaCO2 due to respiratory compensation, a decreased bicarbonate level, and a normal anion gap.
Chloride shift (also known as the Hamburger phenomenon or lineas phenomenon, named after Hartog Jakob Hamburger) is a process which occurs in a cardiovascular system and refers to the exchange of bicarbonate (HCO 3 −) and chloride (Cl −) across the membrane of red blood cells (RBCs).
Still, the blood values are approximately equal between the arterial and venous sides for most substances, with the exception of acid–base, blood gases and drugs (used in therapeutic drug monitoring (TDM) assays). [6] Arterial levels for drugs are generally higher than venous levels because of extraction while passing through tissues. [6]
This is to maintain the plasma's electrical balance, as the chloride anions have been extracted. The bicarbonate content causes the venous blood to leave the stomach more alkaline than the arterial blood delivered to it. The alkaline tide is neutralised by the secretion of H + into the blood during HCO 3 − secretion in the pancreas. [2]
Gastric vomiting leads to the loss of acid (protons) [clarification needed] and chloride directly. Combined with the resulting alkaline tide, this leads to hypochloremic metabolic alkalosis (low chloride levels together with high HCO − 3 and CO 2 and increased blood pH) and often hypokalemia (potassium depletion).