Last late autumn, while I was bedridden in the emergency department, I witnessed a race against time in the rescue of sodium lactate injection. An elderly person who was dehydrated due to severe diarrhea was pushed into the emergency room, and the blood gas analysis results on the monitor displayed a red alert of "pH 7.15" - a typical metabolic acidosis. The doctor quickly issued an order: "Intravenous infusion of 11.2% sodium lactate injection 100ml!" I stared at the clear small bottle in the nurse's hand, with the words "Sodium lactate injection" prominently labeled on the bottle. At that time, my understanding of this drug was only limited to the vague concept of "correcting acidosis", but I never expected that this seemingly ordinary injection contained the key code to maintain the acid-base balance of life. Today, let's talk about the effects and benefits of sodium lactate injection.
---1. Basic knowledge of sodium lactate injection: To understand the role and efficacy of sodium lactate injection as a "life balancing agent", it is necessary to first clarify its "identity file". The main component of sodium lactate injection is sodium lactate (C3H5NaO3), and the commonly used clinical preparation is a 11.2% hypertonic solution (i.e. 1mol/L solution). Before use, it needs to be diluted into an isotonic solution (1.87%) for intravenous infusion according to the patient's condition. It is not a direct "acid-base neutralizer", but a "biotransformation drug" that indirectly participates in acid-base balance regulation by metabolizing it into sodium bicarbonate in the body.
（1） From Chemistry to Physiology: Pharmacokinetic Characteristics of Sodium Lactate After entering the human body, sodium lactate undergoes a pharmacokinetic process of "absorption distribution metabolism excretion". Due to intravenous injection, the drug enters the bloodstream directly and can be distributed to the extracellular fluid within 15-30 minutes; Its metabolism depends on lactate dehydrogenase in the liver. Under aerobic conditions, sodium lactate is converted to pyruvate, which then generates carbon dioxide and water through the tricarboxylic acid cycle, while producing sodium bicarbonate (NaHCO3). Every 1mmol of sodium lactate can ultimately generate 1mmol of bicarbonate (HCO3 ⁻), which is the most important alkaline reserve in the blood, responsible for neutralizing excess hydrogen ions (H ⁺). It is worth noting that this metabolic process is highly dependent on liver function and tissue oxygen supply - if a patient has liver failure or severe hypoxia (such as shock, cardiac arrest), sodium lactate may not be metabolized in a timely manner, but instead accumulate, leading to an increase in blood lactate and exacerbating the risk of acidosis.
（2） Clinical positioning: The core mission of sodium lactate injection lies in the mildness of "indirect regulation" among numerous drugs that correct acid-base imbalances, such as sodium bicarbonate and trimethylolaminomethane. It is more suitable for scenarios of metabolic acidosis combined with hyperkalemia, procainamide and other drug poisoning, while sodium bicarbonate, which directly provides HCO3 ⁻, has a faster onset of action but may lead to excessive sodium load; Although trihydroxymethyl aminomethane can enter cells and form acids, it is prone to side effects such as hypotension and hypoglycemia. Therefore, the function and efficacy of sodium lactate injection are essentially "to safely and sustainably rebuild acid-base balance through biotransformation".
---2. The role and efficacy of sodium lactate injection: A deep analysis of the role and efficacy of sodium lactate injection from mechanism to scenario, ultimately to be implemented in specific clinical applications. It is like a 'biological key' that extends its support for multiple system functions by regulating the core mechanism of acid-base balance. We can analyze from the following four scenarios:. At this point, the concentration of H ⁺ in the blood increases, pH＜7.35， Patients may experience fatigue, rapid and deep breathing (Kussmaul breathing), arrhythmia, and even coma. The function and efficacy of sodium lactate injection are reflected here: through metabolism, HCO3 ⁻ is generated, which combines with H ⁺ to form H2CO3, which is broken down into CO2 and excreted through the lungs, thereby increasing blood pH.
Taking diarrhea as an example: A patient with persistent diarrhea for 48 hours due to acute gastroenteritis lost about 3000ml of intestinal fluid (containing a large amount of HCO3 ⁻) per day. Blood gas analysis showed a pH of 7.28 and BE (residual alkali) -8mmol/L. At this time, intravenous infusion of 1.87% sodium lactate injection (isotonic solution) can gradually replenish HCO3 ⁻ reserves. After 2-4 hours, blood gas should be rechecked, and the pH can often rise to above 7.35. It should be noted that the speed of acid correction should not be too fast - if a large amount of sodium lactate is inputted in a short period of time, it may lead to hypokalemia (H ⁺ is removed from the cell and K ⁺ enters the cell) or hypocalcemia (free calcium decreases after the blood pH increases), so dynamic monitoring of electrolytes is necessary.
（2） Hyperkalemia, also known as the "cell protective shield," is an acute and critical condition that can lead to ventricular fibrillation and cardiac arrest. The mechanism of its occurrence is often related to renal failure, massive hemolysis, or acidosis (H ⁺ enters cells and K ⁺ is removed). The role and efficacy of sodium lactate injection have dual value in this scenario: on the one hand, correcting acidosis can promote the transfer of K ⁺ into cells (for every 0.1 increase in pH, blood potassium decreases by about 0.6 mmol/L); On the other hand, Na ⁺ in sodium lactate can increase extracellular fluid osmotic pressure, enhance myocardial cell excitability, and counteract the inhibitory effect of high potassium on the heart.
In clinical practice, for patients with blood potassium levels of 6.5mmol/L and abnormal ECG (high peak of T-wave and widened QRS), in addition to calcium supplements (stabilizing myocardium) and insulin+glucose (promoting K ⁺ influx into cells), sodium lactate injection is often used as a "third line weapon". There was once a patient with chronic renal failure who developed hyperkalemia due to self discontinuation of dialysis. Blood potassium was 7.2 mmol/L, and after intravenous injection of 11.2% sodium lactate injection 100ml (diluted) for 30 minutes, blood potassium decreased to 6.1 mmol/L and ECG T wave height significantly decreased. This is a typical case of sodium lactate injection acting through "acid correction+intracellular and extracellular ion balance".
（3） In major surgeries such as extracorporeal circulation and liver transplantation, patients often experience metabolic acidosis due to factors such as inadequate tissue perfusion and hypothermia, as well as organ support agents for special surgeries and critical illnesses; Patients with severe trauma and septic shock may experience "dual factor acidosis" due to increased anaerobic metabolism (lactate accumulation) and decreased liver perfusion (lactate clearance disorder). At this point, the role and efficacy of sodium lactate injection is not only to correct acidity, but also to buy time for organ function recovery.
For example, in extracorporeal circulation surgery, due to blood dilution and low temperature (28-32 ℃), lactate metabolism slows down, and patients often experience mild acidosis (pH 7.30-7.35) after surgery. At this time, low-dose (50-100ml isotonic solution) injection of sodium lactate can avoid hypernatremia caused by excessive use of sodium bicarbonate (which may worsen brain edema), and the CO2 produced by its metabolism can stimulate the respiratory center, promoting postoperative spontaneous breathing recovery in patients. In the treatment of septic shock, although there has been controversy over "early active acid correction", the latest research shows that when pH<7.20, appropriate use of sodium lactate injection can improve myocardial contractility (acidosis inhibits myocardium), enhance vascular responsiveness to vasopressors, and create conditions for fluid resuscitation and anti infective treatment.
（4） Some drug overdoses (such as procainamide, quinidine, and other Class Ia antiarrhythmic drugs) can lead to wide QRS wave tachycardia, which is related to the membrane stabilizing effect of the drug (inhibition of Na ⁺ influx). The effect and efficacy of sodium lactate injection are reflected here: high concentrations of Na ⁺ can competitively inhibit the binding of drugs to myocardial Na ⁺ channels, while correcting drug-induced acidosis (which often inhibits cell metabolism), thereby shortening the QRS complex duration and restoring normal heart rhythm.

There was a patient who accidentally took an overdose of procainamide. Upon admission, the ECG showed a QRS duration of 0.16 seconds (normal<0.12 seconds) and a blood pressure of 85/50mmHg. The doctor injected 150ml of 11.2% sodium lactate injection (diluted) intravenously while replenishing fluids and boosting blood pressure. One hour later, the QRS duration was shortened to 0.12 seconds and blood pressure rose to 105/65mmHg. In this case, sodium lactate injection not only corrected acidosis, but also directly counteracted the drug's cardiac toxicity through the "sodium ion effect".
---Thirdly, the boundary of reasonable use: precautions and contraindications for sodium lactate injection. After understanding the role and efficacy of sodium lactate injection, it is necessary to clarify the balance between "effectiveness" and "safety". The following four situations require special caution to avoid "going too far":
1. Patients with liver dysfunction: The metabolism of sodium lactate depends on liver lactate dehydrogenase. If the patient has cirrhosis or liver failure (Child Pugh C grade), sodium lactate may not be converted to HCO3 ⁻ in a timely manner, but may instead lead to an increase in blood lactate (>2mmol/L), exacerbating acidosis. At this time, sodium bicarbonate should be given priority.
2. Hypoxia or shock state: During shock, tissue perfusion is insufficient, cells are in an anaerobic metabolic state, and lactate production has increased; If sodium lactate is used simultaneously, it may cause overload of the "lactate pool" (blood lactate>4mmol/L) and induce lactic acidosis (pH<7.25). These patients need to first improve oxygen supply (such as fluid replacement, pressure boosting, mechanical ventilation), and then evaluate whether to use sodium lactate.

3. Hypernatremia or heart failure: Sodium lactate contains Na ⁺ (11.2% solution contains 167 mmol of Na ⁺ per 100 ml), and excessive use may lead to blood sodium levels greater than 145 mmol/L or exacerbate the volume load of heart failure patients. At this point, the dosage should be strictly calculated (usually according to the formula: required amount of sodium lactate=(normal BE - measured BE) x body weight x 0.3), and blood sodium and central venous pressure should be monitored.
4. Newborns and elderly: Newborns have immature liver development and weak lactate metabolism ability; Elderly people often suffer from liver and kidney dysfunction and need to reduce their dosage (usually 1/2-2/3 of the adult dose) and shorten the medication interval (such as evaluating blood gas every 6-8 hours).
---4. Summary: Sodium lactate injection is not only a medication but also a "balancing art" of life. Returning to the rescue scene at the beginning, the elderly person's blood gas analysis showed that the pH had risen to 7.32 and the heart rate had decreased from 125 beats per minute to 98 beats per minute one hour after injecting sodium lactate injection, and their consciousness gradually became clear. At that moment, I deeply realized that the role and efficacy of sodium lactate injection are far more than just "correcting a numerical value", but rather building a bridge for the recovery of various organ functions by regulating the basic state of acid-base balance in life.
It is like a 'gentle mediator' - unlike the direct violence of sodium bicarbonate, it achieves a more lasting balance through biotransformation; It is also a 'precise assistant' - playing an irreplaceable role in special scenarios such as hyperkalemia and drug poisoning through the dual mechanism of 'ion effect+metabolic regulation'. Of course, its "effectiveness" is always based on "reasonable use": it needs to be comprehensively judged based on the patient's liver and kidney function, oxygen supply status, and electrolyte level, to avoid the misconception of "correcting acid for the sake of correcting acid".

Perhaps you may ask, 'With more advanced blood gas analyzers and new acid correcting drugs, will sodium lactate injection be replaced?' My answer is no. In scenarios such as metabolic acidosis combined with high potassium and drug poisoning, it is still recommended as the first-line choice by guidelines; In organ support for major surgeries and critical illnesses, its "biotransformation" regulatory mode is more in line with physiological laws. This precisely confirms the charm of medicine - the more basic the drug, the more it requires a deep understanding of its mechanism of action in order to achieve the goal of "precision medicine" in clinical practice.
Finally, I want to say to you: the next time you see the label of "Sodium Lactate Injection" in the hospital, why not have more reverence - this small bottle contains not only chemicals, but also the "wisdom of life" summarized by countless medical predecessors through practice. Its function and efficacy will ultimately continue to safeguard the life balance of more patients through rational use.