Hypokalemia cardiac respiratory arrest, why hypokalemia induces arrhythmias

Cardiac arrest due to hyperkalemia is common, and hypokalemia is generally not likely unless someone else has been sick for several days! The slight blow caused me to be a doctor for more than ten years, and I have not seen or heard of it!

Hypokalemia is prone to arrhythmias due to increased myocardial excitability, prolongation of abnormal periods, and increased automaticity of ectopic pacemakers. Conduction slowness and unidirectional block due to decreased conductivity, combined with a shortening of the effective refractory period, can also cause arrhythmias including ventricular fibrillation.

Yes, it's not **, it's a trigger. Details: Which is the first to stop the heartbeat or breathing? This is important.

Friend hypokalemia can weaken muscle contractions, and the lower the blood potassium, the more likely it is to occur.

Hypokalemia in chronic respiratory failure is associated with hypercapnia, decreased appetite, and inadequate potassium intake due to decreased eating, and increased potassium excretion due to sweating and vomiting in respiratory failure. In respiratory acidosis, intracellular potassium moves extracellularly, and the use of diuretics results in insufficient total potassium.

The use of glucocorticoids can promote the increase of renal tubular exchange, cause water and sodium retention, and promote potassium excretion, so hypokalemia is predisposed. Insulin and alkalosis promote the transfer of serum potassium to the details, manifesting as hypokalemia.

It can be seen that hypokalemia is related to many factors in addition to hypercapnia, and type I respiratory failure is mainly hyperkalemia, but hypokalemia can also be seen in clinical work.

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Potassium is an important substance for maintaining heart function, and hypokalemia can easily induce arrhythmia.

When the cells are back or the blood is potassium ions.

When the concentration decreases, the difference between the potassium concentration inside and outside the cell membrane increases, and the potassium permeability of the membrane decreases. In hypokalemia, myocardial excitability increases, automaticity increases, and conductivity decreases.

When the difference between potassium concentration inside and outside cardiomyocytes increases, the potassium permeability of the membrane decreases, and the potassium outflow decreases, which reduces the resting potential of cardiomyocytes. As the membrane potential decreases close to the threshold potential, cardiomyocyte excitability increases. At the same time, the effect of relative sodium ion influx is weakened, which accelerates the automatic depolarization speed of cardiomyocytes during diastole, shortens the time for diastolic potential to reach threshold potential after repolarization, and increases the automaticity of cardiomyocytes.

In addition, due to the decrease in resting potential, the influx and depolarization speed and amplitude of sodium ions are reduced, and the conduction of excitation is slowed down.

It can be seen that hypokalemia is due to the change of sodium ion and potassium ion channel permeability on myocardial cells, which increases myocardial excitability, automaticity, and conduction, and is easy to form excitatory reentment, and induces arrhythmia.

The early symptoms of hypokalemia are limb muscle weakness, general weakness, abdominal distension, nausea, constipation, lack of energy and other symptoms, while the arrhythmias caused by mild hypokalemia are mostly sinus tachycardia, premature atrial contractions or ventricular premature contractions.

When hypokalemia is low, myocardial excitability is usually enhanced, and palpitations and arrhythmias may occur. In severe cases, atrioventricular block, ventricular tachycardia, and ventricular fibrillation may occur, and finally the heart may stop beating in contraction. In addition, it can also cause myocardial tone loss, heart enlargement, peripheral blood vessel dilation, blood pressure drop, etc.

The main manifestations are total inhibition, that is, the excitability, conduction, automaticity, and contractility are all decreased.

Excitability should be increased because the negative resting membrane potential decreases in mild hyperkalemia, but when hyperkalemia worsens, the fast sodium channel is inactivated and excitability decreases.

As the absolute value of the resting membrane potential decreases, the depolarization rate also decreases, so the conductivity decreases, and when the fast sodium channel is inactivated, the depolarization is completed by the influx of calcium ions, and the conductivity also decreases.

In hyperkalemia, the concentration of potassium ions outside the cell increases, the permeability of the cell membrane to potassium ions increases, the potassium efflux of stage 4 increases, and the automatic depolarization is affected, so the automaticity is reduced.

The high concentration of potassium ions in the extracellular fluid reduces the influx of calcium ions, affects the excitation-contraction coupling of cells, and decreases contractility.

In summary, the heart is prone to a series of fatal arrhythmias, such as cardiac arrest, in hyperkalemia.

As mentioned earlier, high potassium can induce arrhythmias, and low potassium can also induce arrhythmias. When extracellular potassium or serum potassium concentrations decrease, the difference between potassium concentrations inside and outside the membrane increases, while the potassium permeability of the membrane decreases. (1) Increase excitability

When the concentration of extracellular potassium or potassium in the blood decreases, the difference between the concentration of potassium inside and outside the membrane increases, and theoretically the potassium efflux increases, which increases the resting potential, but in fact, when the potassium in the blood decreases, the membrane potential decreases instead of increasing. This is because the permeability of the membrane to potassium decreases at low potassium levels, so the membrane potential decreases despite the increase in potassium concentration between the inside and outside of the membrane. Excitability is increased as the membrane potential decreases close to the threshold potential.

2) Increased automaticity: The permeability of the myocardial cell membrane to potassium is reduced, the outflow of potassium ions is slowed down, and the effect of relative sodium influx is weakened, resulting in the acceleration of automatic diastolic depolarization, and the time from diastolic potential after repolarization to threshold potential is shortened, so the automaticity is increased. (3) Reduced conductivity:

As the resting potential decreases, the influx and depolarization of sodium ions decrease in speed and amplitude, thus slowing the conduction of excitation. It can be seen that due to the increase of excitability and the increase of automaticity and the decrease of conductivity in hypokalemia, it is easy to form excitatory reentry and induce arrhythmia.