Heart failure is not the end of the heart function, but a difficult pit-saw battle between heart and disease. Drug treatment is the most critical “strategic weapon” in this campaign, like a group of trained “heartguards”, who work together from different angles to alleviate symptoms, slow progress, improve the quality of life of patients and re-establish a dynamic heart defence for patients with heart failure.
I. Urine: Reduced heart “water load”
The heart of a heart-deficit patient, like an exhausting and poorly drained “pump”, cannot effectively pump the blood out, resulting in body fluids remaining in the body, thus increasing the heart burden and creating a vicious circle. The urea is the “right hand” to break the cycle. It helps to remove excess water and salinity from the body by facilitating the generation and excretion of the kidneys, thereby rapidly reducing the front load of the heart and the symptoms of oedema and respiratory difficulties.
The commonly used urinants are gilloxins (e.g. fur serries), gills (e.g. HCl) and potassium urea (e.g. propyls). The lysergic urea is powerful and rapid and can be used in large quantities in a short period of time for acute heart failure or heavy oedema. Peritone is often used for mild heart failure or in combination with other urea. Potassium urea is used to reduce the loss of potassium ion, often in combination with gill or gill urea to maintain the balance of potassium ion in the body and to avoid complications such as cardiac disorders caused by low potassium haemaemia. However, due to the caution in the use of urinants, excessive doses may lead to adverse effects such as dehydration, low blood pressure, electrolytic disorders, it is essential that the patient adjust the dose to his/her own condition under the strict guidance of a doctor and regularly monitor indicators such as body weight, blood pressure, electrolyte, etc.
II. ACEI and vascular stressor II Receptor (ARB): Stifling vascular pressure
ACEI-type drugs are one of the cornerstones of heart failure treatment. They can inhibit the activity of vascular stressors to convert enzymes and reduce the generation of vascular stressors II, thus helping to expand the blood vessels, reduce blood pressure and reduce post-heart loads. At the same time, such drugs have a unique function of inhibiting myocardial reorganism, preventing structural and functional changes in the heart caused by chronic stress loads and slowing down the process of heart failure. Inapuli and Catopli, for example, are clinically common ACEI drugs.
However, some patients may not be able to withstand ACEI-type drugs because of adverse reactions such as cough, at which point ARB-type drugs can be used as an alternative option. ARB-type drugs can also achieve expansion of the blood vessels, improvement of the heart function and inhibition of myocardial reorganisation by disrupting the combination of vascular stressor II and receptor, with relatively few side effects. ARB drugs such as chlorsartam and thaltan also play an important role in the treatment of heart failure. In the use of these two types of drugs, patients need to pay close attention to changes in blood pressure, kidney function and potassium blood levels, especially at the initial stage of use and at the dose adjustment stage, in order to detect and address in a timely manner possible adverse effects, such as low blood pressure, high potassium haemorrhage, deterioration of kidney function, etc.
iii. Beta receptor retardant: stable heart rhythm
The application of β-receptor retardants in the field of heart failure treatment is a major breakthrough in modern medicine. Such drugs can interrupt the β-receptor in the heart, slow down the heart rate and reduce myocardial condensation, which appears to be “deficit” in the heart, and have a deeper meaning. By slowing down the heart rate, the heart can have more time to fill and rest, thus increasing the blood efficiency of each heartbeat; reducing myocardial condensation can reduce the oxygen consumption of myocardial muscles and avoid excessive heart fatigue. More crucial is the ability of beta receptor retardants to inhibit over-activation of the sensory nerves in the long term, to reverse myocardial reorganisation and to improve the long-term prognosis of the heart.
Metolore, Bislore and others are clinically common beta-receptor retardants. In the course of their use, however, the adjustment of their doses needs to be made with particular caution, since such drugs may temporarily exacerbate the symptoms of heart failure at the time of initial application, so it is usually necessary to gradually increase the dose, starting at a small dose, and to find the best acceptable dose for each patient on the basis of close observation of the patient ‘ s symptoms, heart rate, blood pressure and heart function changes. Patients cannot reduce their own doses or stop drugs while they are on medication, which could lead to a backsliding and serious cardiovascular events.
IV. Selbasterone receptors: enhanced heart protection
As an important member of the renal, vascular and formal sterilisation system (RAAS), formaldehydedone acts as an “aides” in the development of heart failure. It also promotes cardiac fibrosis and cardiac reorganisation, in addition to its role of sodium sodium sodium sodium. A formaldegenone receptor is capable of disrupting these adverse effects, further reducing the burden on the heart and reducing the mortality rate of heart failure patients.
Pyrethrin is the most representative receptor of lydone, and in recent years new lydone receptor of lydone has been gradually applied to clinically. Such drugs can be used in conjunction with ACEI, beta receptor retardants, etc., in synergy and provide more comprehensive and robust protection of the heart. It should be noted, however, that lysinone receptor receptors may lead to high potassium haematosis, and therefore the levels of potassium blood must be closely monitored during the use of the drug, especially in cases where the kidney function is incomplete and the use of potassium urea or ACEI/ARB-type drugs is accompanied by increased monitoring of potassium blood and timely adjustment of treatment programmes to ensure safe use.
V. Positive cardiac help
At the stage of acutely severe or terminal heart failure, the heart function is extremely weak, and conventional drugs are no longer able to sustain normal heart pumping. At this point, positive muscle drugs can be used as “emergency pioneers” to provide additional dynamic support to the heart.
Oceanic yellow drugs (e.g., geo-goxin) are traditional positive muscle drugs that enhance myocardial constriction and increase heart output, while also having the effect of slowing down heart rates and inhibiting heart transfer systems to improve the symptoms of heart failure. However, the treatment window for yellow-like drugs in the ocean is narrower and susceptible to poisoning, and indicators such as blood concentration, heart rate, heart rate, etc. need to be closely monitored during drug use to avoid adverse effects of yellow poisoning in the ocean, such as heart disorder, nausea, vomiting, visual abnormalities, etc.
In addition to yellow-like drugs in the ocean, in recent years new types of positive muscles have been introduced, such as phosphate diesterase inhibitors (e.g., miricon), calcium-sensitizers (e.g., Left West Mondam). While these drugs, which function through different mechanisms of action, have some advantage in improving heart function in the short term, the safety and effectiveness of long-term applications still need further study. Positive muscle drugs are usually used and monitored by doctors within the hospital, depending on the patient ‘ s specific condition, to ensure that they can work best at critical times while minimizing the occurrence of adverse reactions.
The treatment of heart failure is a complex and sophisticated system that requires doctors to develop individualized treatments based on the patient ‘ s specific condition, age, sex, and syndrome. Patients, on the other hand, are required to have full confidence in the doctor, to take the medication on time and in accordance with medical instructions, to follow closely the changes in their symptoms, to visit the hospital on a regular basis and to provide timely feedback on the problems that arise in the course of their use. Only by working together can the “guards” of these drugs be given the greatest power on the battleground for treatment of heart failure, protecting the patient’s heart’s health, and helping the patient to gain more life and hope in the fight against disease and to return to a vibrant and better life.
