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Wei Shi Liang
Intensive Care Unit
About me
Graduated from Shanxi Medical University with a degree in Clinical Medicine in 2006, and has been working in the field of Critical Care Medicine ever since.
Proficient in diseases
Treatment of severe infections, ARDS, severe trauma, MODS, and other diseases.
Voices
The earliest clinical symptoms of respiratory failure
The clinical symptoms of respiratory failure mainly manifest as hypoxemia and carbon dioxide retention. Looking at their clinical manifestations, mild hypoxia may not show any clinical symptoms. As the severity of the disease increases, there can be signs of increased respiratory drive, such as rapid breathing or difficulty breathing, along with symptoms of sympathetic nervous system activation, such as anxiety and sweating. Hypoxemia can cause dilation of peripheral arteries and constriction of veins, leading to an increased heart rate, or even severe arrhythmias. Furthermore, considering the clinical manifestations of carbon dioxide retention, they are directly related to the levels of carbon dioxide in the body, mainly depending on the rate of occurrence. Clinically, this primarily affects myocardial contractility, the contractile ability of respiratory muscles, and increases in intracranial blood flow. In mild to moderate cases, it can stimulate the respiratory center causing increased and shallow breathing, but in severe cases, it may suppress the respiratory center.
Common causes of hyperkalemia
Hyperkalemia is caused by increased intake or decreased excretion, or by the transfer of potassium ions from inside the cells to the outside. Increased intake generally does not cause hyperkalemia in individuals with normal kidney function, unless potassium is supplemented intravenously in excessive amounts or too quickly. Moreover, decreased excretion is a major cause of hyperkalemia, typically seen in renal failure, deficiency of adrenocortical hormones, and primary renal tubular disorders in potassium secretion. Additionally, a large transfer of potassium ions from inside the cells to the outside can occur in conditions such as massive cell breakdown, acidosis, tissue hypoxia, periodic paralysis, and insulin deficiency.
Common symptoms of hypokalemia and hyperkalemia
The common symptoms of hyperkalemia and hypokalemia, mainly seen in severe cases of high or low potassium, manifest as neurological and muscular symptoms as well as circulatory system symptoms, which are fairly similar in both conditions. If the blood potassium is particularly low, less than 2.0 mmol per liter, it can lead to reduced or absent reflexes. In severe cases, this may progress to paralysis of the respiratory muscles, causing respiratory pump failure. For hyperkalemia, particularly severe cases may also present with swallowing difficulties and respiratory distress. These central nervous system issues can lead to confusion and fainting. Another similar issue is the impact on the circulatory system; severe hypokalemia can cause ventricular tachycardia and even ventricular fibrillation, leading to death. In hyperkalemia, the impact on the cardiovascular system primarily causes malignant tachycardia and can also result in ventricular fibrillation. The main cause of sudden death in hyperkalemia is ventricular fibrillation and cardiac arrest, demonstrating that severe hyperkalemia and hypokalemia similarly cause significant arrhythmic conditions in the heart.
Pulmonary embolism is caused by what?
The most common cause of pulmonary embolism is a thrombus, with approximately 70%-95% of cases occurring when a deep vein thrombosis dislodges and enters the pulmonary arteries and their branches via the bloodstream, leading to pulmonary embolism. Conditions such as prolonged bed rest or immobilization of the lower limbs can lead to the occurrence of deep vein thrombosis. Therefore, the primary site of origin is mainly the deep veins of the lower limbs. Additionally, other types of emboli can also cause pulmonary embolism, such as fat emboli, air emboli, amniotic fluid emboli, parasitic emboli, and bacterial emboli, as well as detachment of cardiac tumors; all these can lead to pulmonary embolism.
Why does heart failure cause edema?
Edema caused by heart failure is mainly due to heart dysfunction, resulting in systemic circulation, venous congestion, and excessive fluid accumulation in the body's tissue spaces. The primary cause is right heart failure or total heart failure, and some special cases of pericarditis. The edema caused by this type of heart failure is often symmetrical, indenting, and sagging, and usually worsens with activity and lessens with rest. The common locations for fluid accumulation are in the sacral and perineal areas, while bedridden patients often show it in the ankle area. In severe cases, patients may experience generalized edema, and even develop ascites and pleural effusion. This condition is known as heart failure, and the type of edema it causes is called cardiogenic edema.
How to radically cure hypokalemia?
Hypokalemia must be treated with potassium supplementation while simultaneously addressing the primary condition. For mild hypokalemia, oral potassium can be given in doses of 40 to 80 mmol/day. In cases of severe hypokalemia, where blood potassium is less than 2.0 mmol/L or when life-threatening symptoms are present, intravenous potassium should be administered at a rate of 10 to 20 mmol/L per hour. Regular monitoring of blood potassium levels is necessary, especially in cases of renal dysfunction and cellular uptake impairment. For life-threatening severe hypokalemia, potassium can be administered via central venous lines with close monitoring of blood potassium levels, and the infusion rate can reach up to 40 mmol/L, which can effectively cure hypokalemia.
How is subarachnoid hemorrhage treated?
The treatment of subarachnoid hemorrhage primarily aims to prevent rebleeding, vasospasm, hydrocephalus, and other complications, reducing mortality and disability rates. During the acute phase, keep the patient's head in a raised position, lying on their side, and provide dehydration, sedation, and pain relief; absolute bed rest; monitor blood pressure; and when bleeding is significant, undertake ventricular puncture for drainage. Patients with subarachnoid hemorrhage should generally be admitted to the ICU, monitoring vital signs and changes in neurological signs, ensuring airway patency, maintaining stable respiratory and circulatory functions, resting quietly, avoiding emotional agitation, ensuring smooth bowel movements, and for patients with increased intracranial pressure, appropriately restricting fluid intake.
The role of calcium agents in hyperkalemia
Change the excitability of autonomic cells to protect the heart. Hyperkalemia mainly affects the conduction of the heart and neuromuscular system. Typical clinical manifestations include severe bradycardia, atrioventricular block, and even sinus arrest. By using calcium agents to change the excitability of autonomic cells, we can protect the heart from the damage to the conduction system caused by hyperkalemia. This allows the potassium ions to move from outside the cell to inside the cell. While protecting the myocardium, it is also necessary to use some medications to lower blood potassium. If the blood potassium is particularly high, dialysis or continuous bedside blood filtration can be used to reduce the blood potassium to a normal range.
Severe pancreatitis complications
Complications of severe pancreatitis primarily include: 1. Acute peripancreatic fluid collection and interstitial edematous pancreatitis, where fluid accumulates around the pancreas without necrosis. This can be diagnosed with enhanced CT. 2. Pancreatic pseudocysts, characterized by fluid encapsulated by a clearly defined inflammatory cyst wall around the pancreas, with no or minimal necrosis, commonly occurring around four weeks after an episode of interstitial edematous pancreatitis. 3. Accumulation of acute necrotic material, involving necrotic tissue and liquids from necrotizing pancreatitis, including the parenchyma and peripancreatic tissues, also diagnosable through enhanced CT. 4. Encapsulated necrosis, observable as a clearly defined inflammatory encapsulation of the pancreas and peripancreatic tissues, commonly occurring four weeks post an episode of necrotizing pancreatitis.
Hypokalemia is a condition.
Potassium is one of the essential electrolytes for life. Its physiological functions mainly include maintaining cellular metabolism, regulating osmotic pressure, acid-base balance, and maintaining cell stress functions. The human body intakes about 100 millimoles of potassium each day, of which 90% is excreted through the kidneys, and the remainder is excreted through the gastrointestinal tract. Potassium mainly exists inside cells, with serum potassium accounting for only 2% of the total potassium in the body. The concentration of potassium in serum is between 3.5 to 5.5 mmol/L. If the concentration of serum potassium is below 3.5 mmol/L, it is considered hypokalemia, which is often due to insufficient potassium intake or excessive potassium excretion.