What is Hypokalemia?
Hypokalemia is a condition in which the concentration of potassium in the plasma is below 3.5 mmol / L.
Hypokalemia causes severe complications (for example, life-threatening ventricular arrhythmias). Clinical signs of hypokalemia are hyporeflexia and intestinal obstruction. Violations of potassium levels are quickly signaled by ECG changes in lead II. With hyperkalemia, pointed T waves are observed, and with hypokalemia, flattened T waves and U waves are observed.
Causes of Hypokalemia
Hypokalemia develops due to:
- reduce potassium intake from food,
- moving it into cells or
- enhanced elimination.
A decrease in potassium intake is rarely the only cause of hypokalemia, since due to reabsorption in the distal nephron, urinary potassium excretion can decrease to 15 mmol / day; the amount of potassium that enters the body with food in most cases exceeds this value. The exceptions are citizens with a low standard of living and people who follow special diets.
However, insufficient potassium intake can exacerbate hypokalemia due to potassium loss through the gastrointestinal tract or kidneys.
One of the rare causes of hypokalemia is eating clay (geophagy), since it binds potassium and iron ions. Geophagy was previously widespread among blacks in the southern United States.
The movement of potassium into cells reduces the concentration of potassium in the plasma temporarily, without affecting its total content in the body. Regardless of the reason for the movement of potassium into cells, the change in its concentration is normal in this case is relatively small – not more than 1 mmol / l. However, like insufficient intake of potassium from food, the movement of potassium into cells can exacerbate hypokalemia due to potassium loss.
Hypokalemia is caused by metabolic alkalosis (due to redistribution of potassium and losses through the kidneys and gastrointestinal tract), hyperglycemia (due to osmotic diuresis), the introduction of large doses of insulin in diabetic ketoacidosis (as a result of stimulation of the counter transport Na + / H + and mediated Na +, K ± ATPase activation), increased the level of catecholamines, the appointment of beta2-adrenostimulants (due to the movement of potassium into cells and increased secretion of insulin), the growth of new cells (for example, with the appointment of vitamin B12 in Addison-Birmer disease or GM- CSF for neutropenia), transfusion of thawed and washed red blood cells (since frozen red blood cells lose up to half of potassium during storage).
Hypokalemia is also observed with familial hypopotassemia periodic paralysis – a rare disease that manifests itself with bouts of muscle weakness or paralysis.
Sweating leads to hypokalemia both directly and as a result of hypovolemia-induced increase in aldosterone and potassium excretion.
Normally, with a stool volume of 100-200 ml, the loss of potassium with it is 5-10 mmol / day.
Hypokalemia due to potassium loss through the gastrointestinal tract occurs with a villous polyp, VIP, diarrhea (often secretory) and abuse of laxatives. Loss of stomach contents during vomiting and aspiration through a nasogastric tube alone are not causes of hypokalemia (the concentration of potassium in the gastric juice is 5-10 mmol / L, and for the deficiency of 300-400 mmol, which is usually observed in such patients, it would be required losses in the amount of 30-80 l). In such cases, hypovolemia and metabolic alkalosis lead to hypokalemia. Hypovolemia stimulates the secretion of aldosterone, and metabolic alkalosis leads to bicarbonaturia and an increase in the negative charge of the fluid in the collecting tubes (the filtered bicarbonate cannot be completely reabsorbed in the proximal tubules). Both of these mechanisms increase urinary excretion of potassium.
Symptoms of Hypokalemia
Symptoms of hypokalemia are diverse and depend on its severity. They usually appear when the concentration of potassium in the plasma becomes less than 3 mmol / L. Patients complain of fatigue, weakness in the legs, myalgia. In severe cases, paresis and paralysis, respiratory failure, dynamic intestinal obstruction are observed. All these symptoms occur due to hyperpolarization of muscle cells. Due to a violation of the metabolism of muscle tissue and a decrease in working hyperemia, rhabdomyolysis is possible. With hypokalemia due to a slowdown in ventricular repolarization, ECG changes occur. With moderate hypokalemia, flattening or inversion of the T wave, an increase in the amplitude of the U wave, depression of the ST segment and prolongation of the QT interval (QU) are observed, in severe cases – prolongation of the PQ interval, expansion of the QRS complex (rarely). However, there is no clear link between ECG changes and the severity of hypokalemia. Ventricular arrhythmias are possible, especially in patients with myocardial ischemia and left ventricular hypertrophy.
Hypokalemia contributes to glycoside intoxication.
Epidemiological studies have shown a link between insufficient potassium intake and arterial hypertension in American blacks. It is also shown that taking potassium preparations reduces blood pressure in hypertension. The cause of the increase in blood pressure in hypokalemia is unknown. Perhaps this is due to increased reabsorption of sodium and chlorine in the distal nephron.
Hypokalemia is often combined with violations of the thyroid gland. Firstly, many disorders lead simultaneously to hypokalemia and to violations of the thyroid gland. Secondly, with hypokalemia, intracellular acidosis develops, bicarbonate reabsorption in the proximal convoluted tubules of the nephron, secretion of hydrogen ions in the distal tubules and ammoniogenesis increase. All this leads to metabolic alkalosis.
Hypokalemia can be the cause of nephrogenic diabetes insipidus. Due to impaired insulin secretion and the development of insulin resistance with hypokalemia, glucose tolerance is often impaired.
Diagnosis of Hypokalemia
The cause of hypokalemia in most cases can be established on the basis of anamnesis. Clarify whether the patient is taking laxatives or diuretics. It is also important to find out if it causes artificial vomiting. With severe leukocytosis (for example, in patients with acute myeloid leukemia), if blood samples are stored at room temperature, pseudo-hypokalemia is rarely observed (potassium is captured by leukocytes). To avoid this, you should store the samples in the refrigerator or quickly separate the plasma or serum from the cells. Then exclude a decrease in potassium intake with food and causes leading to the movement of potassium into cells. A source of potassium loss helps establish a urine test. If renal function is not changed, then as a result of decreased secretion and increased potassium reabsorption, its excretion during hypokalemia decreases to 15 mmol / day. This is observed with potassium loss through the skin and gastrointestinal tract, as well as some time after taking diuretics or repeated vomiting.
Renal loss of potassium increases with increasing fluid intake in the distal nephron and increasing potassium concentration in the cortical sections of the collecting tubules. In the differential diagnosis of the causes of renal loss of potassium, an assessment of the volume of extracellular fluid, ASC, and measurement of blood pressure help.
A quick and easy method for evaluating potassium secretion is to determine the trans-tubular gradient of potassium concentration. This indicator is equal to the ratio of the concentration of potassium in the lumen of the cortical sections of the collecting tubules and in the peritubular capillaries (i.e., in the plasma). His calculation is based on three conditional assumptions:
- reabsorption of dissolved substances does not occur in the brain sections of the collecting ducts;
- in these departments potassium is not secreted and not reabsorbed;
- osmolality of the fluid at the ends of the cortical sections of the collecting tubules is known.
In most cases, these assumptions are more or less complied with:
- reabsorption of sodium in the distal sections of the collecting tubules usually has little effect on the trans-tubular gradient of potassium concentration;
- secretion or reabsorption of potassium in these departments occurs only with severe hypokalemia or hyperkalemia;
- under the action of ADH, the osmolality of the liquid at the ends of the cortical sections of the collecting tubes is equal to the osmolality of the plasma, and then the concentration of potassium in them (K + cst) can be calculated by the formula:
(K + kst) = (K +) m x Opl / Ohm, where
(K +) m – the concentration of potassium in the urine,
Opl – osmolality of plasma,
Ohm – osmolality of urine.
ChGKK = (K + kst) / (K + pl) = ((K +) m x Opl / Ohm) / (K + pl), where
ChGKK – trans-tubular concentration gradient of potassium,
(K +) PL – the concentration of potassium in the plasma.
The above calculations are true if the osmolality of urine is higher than the osmolality of plasma.
There are no normal values of the trans-tubular gradient of potassium concentration, since they depend on the balance of potassium.
Hypokalemia with a trans-canalicular gradient of potassium concentration of more than 4 indicates renal loss of potassium due to increased secretion of this ion in the distal nephron. One possible cause of this condition is hyperaldosteronism.
For differential diagnosis of different forms of hyperaldosteronism, the level of renin and aldrsterone in the plasma is determined.
Bicarbonaturia, as well as the presence in the urine of other non-absorbable anions, increases the trans-tubular gradient of potassium concentration and stimulates the excretion of this ion.
Treatment aims to stop the loss of potassium and eliminate its deficiency. In case of hypokalemia due to redistribution of potassium iv, the administration of potassium preparations is not indicated, as it can lead to rebound hyperkalemia (with the exception of familial hypokalemic periodic paralysis). Potassium intake is safe.
The concentration of potassium in the plasma does not accurately reflect its total content in the body. Thus, a decrease in the concentration of potassium in the plasma to 3 mmol / L may correspond to a deficit of 200 to 400 mmol of potassium. If the concentration of potassium in the plasma is below 3 mmol / l, then its deficiency often reaches 600 mmol. When moving potassium from cells (in particular, with diabetic ketoacidosis), potassium deficiency can be underestimated. In this regard, during treatment, it is necessary to constantly monitor the concentration of potassium in the plasma.
With hypokalemia with metabolic alkalosis, potassium chloride is prescribed.
With hypokalemia with metabolic acidosis (with prolonged diarrhea or renal tubular acidosis), bicarbonate and potassium citrate are used (the latter breaks down to form bicarbonate).
Intravenous administration of potassium preparations is indicated for severe hypokalemia or the inability to take drugs internally. When introduced into the peripheral vein, the concentration of potassium in the solution should not exceed 40 mmol / l, when introduced into the central vein – 60 mmol / l. If there are no paresis and life-threatening arrhythmias, the infusion rate should not exceed 20 mmol / h. Potassium chloride is best added in 0.9% NaCl.
The introduction of potassium with glucose solutions can lead to an even greater decrease in the concentration of potassium in the plasma due to the insulin-mediated movement of potassium into the cells. Fast iv administration of potassium chloride requires careful monitoring of the patient (ECG, study of motor functions).
A proper diet will help prevent the development of the disease. It is difficult to determine whether hypoglycemia will occur after vomiting or diarrhea, after taking diuretics.