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Periodic Paralysis—Hyperkalemic/Hypokalemic
Published in Charles Theisler, Adjuvant Medical Care, 2023
Hyperkalemic periodic paralysis is a condition that causes episodes of extreme muscle weakness or paralysis, usually beginning in infancy or early childhood. Attacks are usually brief, lasting a few minutes to an hour or two, but tend to occur frequently. Most often, these episodes involve a temporary inability to move muscles in the arms and legs. Some people with hyperkalemic periodic paralysis have elevated serum levels of potassium (hyperkalemia) during attacks. Hyperkalemia results when the weak or paralyzed muscles release potassium ions into the bloodstream. In most patients, potassium levels do not actually rise above normal. Hyperkalemic refers more to the fact that attacks may be triggered by eating potassium-rich foods or by giving the patient potassium.
The Sequence and Mechanisms of Ventricular Arrhythmia in Acute Myocardial Ischemia and Reperfusion — An Introduction
Published in Samuel Sideman, Rafael Beyar, Analysis and Simulation of the Cardiac System — Ischemia, 2020
Following an occlusion of a coronary artery, the ischemia and hypoxia are immediate, arrhythmias occur minutes later, and necrosis is the last event. Irreversible necrosis sets in after phase I-A and phase I-B of ischemic arrhythmias, but before phase II. For a clearer understanding of the mechanisms, it is important to stress that acute ischemia is associated with two phenomena: first, the lack of energy and second, the marked reduction in perfusion. The result of the first phenomenon (loss of energy) is the loss of contractile function and the leakage of the potassium ion from cells. Another obvious result is the production of acidosis. Due to the second phenomenon, namely, lack of perfusion, the above-mentioned elements and many more accumulate in the ischemic tissue. The myocardial fiber suffers then from both the lack of energy and from the accumulation of the “toxic” metabolites. Of these, the potassium ion is well known to have profound electrophysiological effects.
Tubular Function
Published in Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal, Principles of Physiology for the Anaesthetist, 2020
Peter Kam, Ian Power, Michael J. Cousins, Philip J. Siddal
Various factors alter the intracellular/extracellular distribution of potassium ions. Insulin and epinephrine stimulate the cell membrane Na+/K+-ATPase so that potassium is shifted into the cell after a meal and during exercise, respectively. During acidosis, when the plasma hydrogen ion concentration is high, potassium ions move out of the cells and hydrogen ions move in. During alkalosis, potassium moves into the cells and hydrogen ions move out.
Prediction of hyperkalemia in ESRD patients by identification of multiple leads and multiple features on ECG
Published in Renal Failure, 2023
Daojun Xu, Bin Zhou, Jiaqi Zhang, Chenyu Li, Chen Guan, Yuxuan Liu, Lin Li, Haina Li, Li Cui, Lingyu Xu, Hang Liu, Li Zhen, Yan Xu
A total of 1024 sets of serum potassium concentration and ECG data sets were included in this study. The mean potassium concentration of these 1024 datasets was 4.83 ± 1.01 mmol/L. The average values of different characteristics on each lead are shown in Table S2. Among them, 576 had serum potassium concentration less than 5.0 mmol/L, 173 had serum potassium concentration greater than or equal to 5 mmol/L and less than 5.5 mmol/L, 136 had serum potassium concentration greater than or equal to 5.5 mmol/L and less than 6.0 mmol/L, 85 had serum potassium concentration greater than or equal to 6.0 mmol/L and less than 6.5 mmol/L, and 54 had serum potassium concentration greater than or equal to 6.5 mmol/L. The concentration distribution of potassium ions is relatively concentrated between 3.5 mmol/L and 6.0 mmol/L (Figure 3). The prevalence of hyperkalemia was 43.8% when 5.0 mmol/L was used as the threshold for blood potassium concentration. When 5.5 mmol/L was used as the threshold for hyperkalemia, the prevalence was 26.9%. The prevalence of hyperkalemia with a blood potassium concentration above 6.0 mmol/L was 13.6%, and the prevalence of severe hyperkalemia with a blood potassium concentration above 6.5 mmol/L was 5.3%.
Association of vitamin A and its organic compounds with stroke – a systematic review and meta-analysis
Published in Nutritional Neuroscience, 2023
Sajjad Farashi, Siamak Shahidi, Abdolrahman Sarihi, Mohammad Zarei
After the stroke, oxygen insufficiency in some brain areas causes a reduction in oxidative phosphorylation and a drop in ATP synthesis. This disrupts the hemostasis of ionic pumps and consequently reduces intracellular potassium ions. The next link in the chain is membrane depolarization and the uncontrolled entrance of calcium ions inside the cell. Furthermore, after stroke, the glutamate level increases rapidly. This excites the N-methyl-D-aspartate-type glutamate receptors and intensifies the flow of Ca2+ into the cytosol. Increased Ca2+ level disrupts mitochondrial function and activates enzymes that destroy proteins, nucleic acids and phospholipids and consequently increased free radicals [12]. Free radicals contribute to LDL oxidation and in this way cause the development of atherosclerosis [53]. Vitamin A can prevent the membrane from lipid peroxidation and in this way protects the cell from damages [24]. Furthermore, beta-carotene that is converted to vitamin A in the human body is a free radical scavenger and deletes singlet oxygen, superoxide and hydroxyl radicals [27] and in this way prevents the risk of stroke. The association between stroke and vitamin A is also sensitive to other blood plasma substances such as homocysteine [14]. In lower homocysteine concentrations, the inverse association between retinol and stroke was reinforced [14].
Efficient simulations of stretch growth axon based on improved HH model
Published in Neurological Research, 2023
Xiao Li, Xianxin Dong, Xikai Tu, Hailong Huang
The HH model can accurately interpret the experimental results of electrophysiological activity of squid axons and quantitatively describe the changes in voltage and current on the neuron membrane. Firstly, by changing the concentration of the extracellular ions (mainly sodium and potassium ions), the current carried by the ions is deduced, and then the experimental results are fitted with the mathematical model to solve the mathematical model. By comparing the action potentials of the model with those recorded in the experiment, the correctness of the model is verified. The mechanism of the action potential under electrical stimulation was discovered by Hodgkin and Huxley [4]. When nerve cells are stimulated with adequate excitatory current, the cell membrane potential rises and the permeability of the cell membrane changes, allowing a huge amount of sodium ions to influx, raising the membrane potential even higher and producing an action potential. Potassium ions began to flow out in huge quantities when the membrane potential reached its peak value, causing the membrane potential to drop until it reverted to its resting condition. Cell depolarization above the threshold, according to Hodgkin and Bernard Katz [5], causes a brief increase in the permeability of the cell membrane to sodium ions. The permeability of sodium ions outweighed the permeability of potassium ions throughout this time. This establishes a research foundation for the development of axon action potentials in response to mechanical traction.