The clinical manifestations of hyperkalemia are primarily cardiovascular and neuromuscular. The severity of the symptoms depends on the degree and rate of elevation of blood potassium, the presence of other plasma electrolyte and water metabolism disorders in combination.
1.Cardiovascular symptoms: High potassium depresses the myocardium and decreases myocardial tone, so there is bradycardia and cardiac enlargement, heart sounds are weakened, and arrhythmia is easily occurred, but heart failure does not occur. The electrocardiogram has characteristic changes and correlates with the degree of elevated blood potassium. When blood potassium is greater than 5.5mmol/L, ECG shows shortening of Q-T interval, symmetry of T-wave high tip, narrowing of base and tenting; when blood potassium is 7-8mmol/L, P-wave amplitude decreases, P-R interval prolongs to the point of P-wave disappearance, which may be sinus node block or sinus arrest, and "sinus-ventricular" conduction (sinus-ventricular) may also be seen. This may be sinus block or sinus arrest, and there may also be "sinus-ventricular" conduction (the sinus node does not pass through the normal conduction system in the atrium and passes through the special fiber bundles in the atrium into the ventricle); when the blood potassium rises to 9-10 mmol/L, the intraventricular conduction is more slow, the QRS wave is widened, the R-wave amplitude is reduced, the S-wave is deepened, and it connects with the T-wave and fuses with the T-wave straight line; when the blood potassium rises to 11 mmol/L, the QRS wave, the ST-segment, and the T-wave are fused into a biphasic zigzag waveform. At 12mmol/L, a part of myocardium was first excited and recovered, and the other part was not depolarized yet, which was very easy to cause folding movement and ventricular ectopic rhythm, manifested as ventricular tachycardia, ventricular flutter and ventricular fibrillation, and finally cardiac arrest in diastole.
2. Neuromuscular symptoms: early on, there are often numbness in the limbs and perioral sensation, extreme fatigue, muscle pain, pale limbs, wet and cold. When the blood potassium concentration reaches 7mmol/L, the limbs become numb and limp, first for the trunk, then for the limbs, and finally affect the respiratory muscles, and asphyxia occurs. The central nervous system may manifest as agitation or confusion.
3. Other symptoms can cause nausea, vomiting and abdominal pain due to the increased release of acetylcholine caused by hyperkalemia. Due to the toxic effect of hyperkalemia on muscles, it can cause quadriplegia and respiratory arrest. All hyperkalemia is associated with varying degrees of azotemia and metabolic acidosis, the latter of which can exacerbate hyperkalemia.
Diagnosis
The diagnosis of hyperkalemia begins with the exclusion of pseudohyperkalemia due to hemolysis, for example, and laboratory errors. Electrocardiography clarifies the occurrence of serious cardiotoxicity, and an electrocardiogram that shows hyperkalemia is a sign of danger that warrants aggressive therapeutic measures. Drugs (including potassium salts) and renal insufficiency are the most common causes of hyperkalemia. Patients with normal renal function but with severe prerenal azotemia may have hyperkalemia. Defects in aldosterone and insulin secretion or action may also lead to hyperkalemia. Hyperkalemia is present in 40% of patients initially diagnosed with adrenocortical insufficiency. Persistent hyperkalemia with acidosis may be hyperkalemic renal tubular acidosis, which is common in moderate renal insufficiency, especially in patients with diabetes mellitus, interstitial nephritis, or obstruction. In addition, tissue necrosis, rhabdomyolysis, and depolarizing states of the membranes (e.g., succinylcholine use and hyperkalemic periodic paralysis) are not difficult to diagnose from the clinical presentation. Some rare genetic defects resulting in inherited disorders can also lead to hyperkalemia.