Acute kidney injury (AKI) is a common complication after cardiac surgery, with an incidence of 5-30%. Patients who develop AKI often have a combination of failure of other vital organs, increased complications, and increased morbidity and mortality. According to the Guidelines for Improving Prognosis in Global Kidney Disease Organization (KDIGO), acute kidney injury is defined as an increase in blood creatinine of at least 26.5 μmol/L within 48 hours; an increase in blood creatinine levels of at least 1.5 times the basal value over a 7-day period; or a patient’s urine output of less than 0.5 ml/h per kg body weight within 6 hours. Unlike general ICU patients with combined AKI, post-operative cardiac AKI (CS-AKI) has certain special features: the timing of renal injury is well defined; the patient tolerates volume overload very poorly due to surgical trauma affecting cardiac pump function, which is often accompanied by hemodynamic instability especially when combined with severe low cardiac output syndrome. Continuous renal replacement therapy (CRRT) can rapidly and smoothly filter out excess water from the body, effectively reducing cardiac preload and neuroendocrine system activation, thus interrupting the vicious cycle of “heart failure – relatively high volume load, low urine – heart failure”. This can be used as a treatment for heart failure. Therefore, CRRT has become an important treatment for postoperative cardiac AKI. The primary pathogenesis of postoperative acute kidney injury in cardiac surgery is the low cardiac output syndrome. The main pathogenic factors are: 1) hemodynamic factors. Cardiac output decreases significantly in heart failure, and the stagnation of renal blood flow due to insufficient renal artery supply and increased central venous pressure predisposes to AKI; 2) medical factors, mainly related to the use of contrast agents, diuretics and cardiopulmonary bypass surgery. Cardiac surgery exposes the kidney to hypothermia and pulseless hypoperfusion for a long period of time, thus triggering AKI. 3. Neurohumoral factors, excessive activation of the RAAS and SNS systems during acute cardiac events can cause intrarenal vasoconstriction, reduced renal blood flow and decreased glomerular filtration rate, resulting in renal hypoxia and inflammation, causing structural and functional damage to the kidney and ultimately irreversible renal damage. In addition to the above pathophysiological changes, the kidneys are also subjected to a wide range of pathological changes. In addition to the above pathophysiological changes, cellular dysfunction caused by oxidative stress processes, accelerated apoptosis and cell death are important causes of organ damage. Timing of CRRT – Focus on assessment of volume load Most previous studies have shown that “early” CRRT interventions do not improve the prognosis of patients with low cardiac output combined with AKI after cardiac surgery if blood urea nitrogen or creatinine indexes are used to determine the timing of CRRT initiation. AKI patients. In addition, several clinical studies have looked at the prognosis of AKI patients with varying degrees of urine output reduction at the start of CRRT, and most have found that early initiation of CRRT with reduced urine output and volume overload instead of elevated creatinine or urea nitrogen may help improve the prognosis of such patients, but the definition of early urine output reduction is inconsistent. Ostermann et al. concluded that early initiation of CRRT for AKI should be performed to avoid a relative volume load of ≥10%. 2012 Bagshaw et al. prospectively looked at 234 patients undergoing CRRT for AKI in 6 Canadian ICUs and found that CRRT initiation with a relative volume load of A relative volume loading percentage >5% may be associated with increased in-hospital mortality after correction. Recently, Prof. Teng J. of Zhongshan Hospital in Shanghai treated patients undergoing CRRT for postoperative cardiac AKI with goal-directed fluids and found that a relative volume loading percentage ≥3.6% as the threshold value had the best sensitivity and specificity for predicting 30-d mortality with a sensitivity of 65% and a specificity of 77%. Therefore, the significance of the degree of volume overload in determining the timing of CRRT initiation is gaining attention. The advantage of CRRT may be hemodynamic stability, especially in patients with severe volume overload and hemodynamic instability, and its ability to maintain volume, avoid under- or over-volume, and remove sodium and nitrogenous waste products, thus avoiding passive renal stasis and a nephrotoxic environment. and the development of a nephrotoxic environment, thus ensuring optimal renal function during a period of systemic vulnerability. New therapeutic concept: shallow hypothermic CRRT – treatment of severe hypocapnia after cardiac surgery Shallow hypothermia (34°C) has played an important role in neuroprotection and its cardioprotection has now been extensively studied. Several studies have found that shallow hypothermia not only reduces mortality but also significantly improves hemodynamic parameters such as stroke volume and blood pressure in animal models of post-infarction cardiogenic shock. The application of high doses of vasoactive drugs and increased volume load to manage acute heart failure in patients with severe postoperative cardiac surgery complications only increases the load on the failing heart and leads to irreversible failure. The concept of resting the failing heart to restore its function is now well established. Based on the concept that a partially compensated heart can still recover with adequate rest, Zhang Haitao, director of the ICU of Cardiac Surgery at Fu Wai Cardiovascular Hospital in Beijing, and Du Yu, MD, PhD, were the first to combine CRRT with shallow hypothermia (34°C) (CRRT/MHT) to treat “acute severe heart failure”. acute severe heart failure”, by reducing the body’s demand, reducing the work done by the heart, resting the heart and providing the patient with the possibility of recovery. Shallow hypothermic CRRT treatment has led to a significant decrease in the dosage of catecholamines, which has played an important role in the decrease of mortality in patients. Despite the well-known toxic effects of catecholamines on the heart, intravenous application of vasoconstrictor and positive inotropic drugs to maintain circulation is very common in patients with severe acute heart failure after cardiac surgery. Because adrenergic agonists can cause myocardial damage and receptor “desensitization” can occur with continued use, they should be kept at low doses for short periods or intermittently during clinical procedures. This “fast and furious” treatment is really a “last resort” method, which should be “used quickly and withdrawn quickly”. High doses of adrenergic drugs, while “fast and furious” lead to increased cardiac work, also cause corresponding myocardial damage: direct cytotoxic effects; hypertrophy, necrosis, fibrotic remodeling of myocardial cells; decreased myocardial Ca2+-ATP function, decreased contractility; IL6/IL10 inflammatory response, myocardial tonus; extracellular matrix changes. extracellular matrix changes. As cardiac function deteriorates, adrenergic reserve decreases in heart failure, myocardial β-adrenergic receptor density is downregulated, and the effects of adrenergic drugs will be significantly reduced. In recent studies, the reduction in catecholamine drug dosage may be related to the positive inotropic effect of hypothermia with increased peripheral resistance. The advantages of shallow hypothermic CRRT for severe postoperative cardiac hypocapnia syndrome are: 1. CRRT controls the body in shallow hypothermia (central blood temperature 34°C), and for every 1°C decrease in body temperature, the basal metabolic rate decreases by 8-10% (central blood temperature 37.5°C → 34°C, which can reduce the body metabolism by 30-40%); together with simultaneous adequate sedation, complete ventilator-controlled breathing, and parenteral nutrition, relying on CRRT to maintain the stability of the internal environment, the body’s metabolism needs to be reduced to the lowest imaginable, which means that the work done by the heart may be reduced to a minimum, at this time can still meet the needs of the body to survive, to achieve this dynamic balance, to win time for cardiac rehabilitation. 2, through CRRT to quickly filter out water, reduce the heart preload, while reducing vasoactive drugs, so that the heart work and oxygen consumption are reduced, the heart to “unload”, to achieve the effect of allowing the heart to fully rest. 3, CRRT ensures the stability of the internal environment in the case of reduced renal urine output due to reduced cardiac work. 4, CRRT clears inflammatory mediators and myocardial inhibitory factors to reduce the impact on the heart; at the same time, shallow hypothermia also inhibits the inflammatory response of ischemia-reperfusion tissue and the activity of pro-inflammatory factors to reduce the damage to the heart and promote the recovery of the heart. 5, shallow hypothermia improves the peripheral vascular tone, reduces the dosage of vasoactive drugs, and reduces the adverse effects of vasoactive drugs on cardiac remodeling. Shallow hypothermia increases the tolerance of the body to ischemia and hypoxia in the low perfusion state. 6, CRRT quickly and accurately carry out blood cooling, effectively avoiding chills and skin pressure injury of body surface cooling. For the implementation of “shallow hypothermia, cardiac decompression therapy” provides a very practical “one-two punch” effect. Therefore, shallow hypothermia CRRT can be used for the treatment of patients with severe cardiovascular surgery, which can reduce the preload of the heart, reduce the work of the heart, make the myocardium fully rest, and at the same time reduce the metabolic rate of the body, and finally improve the cardiac function, opening up a new method for the treatment of severe heart failure.