intravascular fluid 5%

interstitial fluid 15%

Increased plasma crystalloid osmolality

Decreased effective blood volume

An increase in angiotensin II

Intravenous injection of mannitol, hyperglycemia, and increased plasma osmotic concentration

Water moves out of the cell, increasing circulation capacity

Hyperlipidemia and hyperalbuminemia increase plasma solid solutes

The water content and sodium concentration per unit volume decrease proportionally.

low effective osmotic pressure state

High capacity Water retention > Sodium retention

Isovolumetric excessive water intake, abnormal renal drainage

Low capacity: more electrolytes lost and less replenished

Water enters brain cells quickly

Signs and symptoms are significant

Intracellular solutes slowly move out, and water inflow into the cell decreases.

Symptoms and signs are mild

Hypotonic fluid was discontinued and TURP was discontinued.

Sodium deficiency (mmol) = [125-serum sodium (mmol/L)] × body weight (kg) × 0.

Half/8h, other half/1-3d

Severe hyponatremia with severe neurological symptoms is treated with 3% sodium chloride solution to increase serum sodium by 0.6-1mmol/L/h, with a target increase of 4-6mmol/L.

It is not advisable to correct hyponatremia too quickly

osmotic demyelination

central nervous system damage

Severe diarrhea, vomiting, diabetes insipidus

Also known as hypertonic dehydration, the most common

Less water intake, more drainage, and increased invisible water loss

Often iatrogenic

Infusion of too much sodium bicarbonate or hypertonic sodium chloride or formaldehyde

Apathy, lethargy, tremor, agitation, increased muscle tone, stupor, lethargy, coma and death

Brain shrinkage, meningeal blood vessel tears, and intracranial hemorrhage

Give diuretics and hypotonic fluids

Restore normal osmotic concentration and volume of extracellular fluid

Eliminate excess sodium from the body

Acute: Rapidly reduce plasma osmolality and restore brain volume

Chronic speed control

Sodium reduction rate 0.7mmol/L/h

The amplitude does not exceed 10% of the serum sodium concentration

Long-term fasting, gastrointestinal attraction

Hyperaldosteronism, diuretics

Excessive infusion of sodium bicarbonate can cause severe alkalosis and hypokalemia

Insulin therapy and hypokalemic periodic paralysis

β2 receptor excitation activates K-Na-ATP

Muscle weakness, slow or absent tendon reflexes, paralysis, and in severe cases, respiratory muscles are involved

Abdominal bloating, constipation, and paralytic ileus

Easily agitated, irritable, lethargic, and mentally disturbed

intracellular acidosis

ECF alkalosis, paradoxical aciduria

Premature ventricular and atrial contractions Ventricular and atrial tachycardia Second- or third-degree atrioventricular block In severe cases, ventricular fibrillation or cardiac arrest occurs during systole

Potassium supplementation in urine

Fast first and then slow

Alkalosis can be corrected after potassium correction, and potassium can be replenished before acid correction.

Closely monitor electrocardiogram and monitor serum potassium at the same time

Refractory hypokalemia is often accompanied by hypomagnesemia, which should be corrected by supplementing magnesium at the same time.

ischemia reperfusion

metabolic acidosis

insulin deficiency

Increased protein catabolism

Escape of intracellular potassium ions in patients with severe crush injuries and burns

increased excitability

Hyperkalemia reduces neuromuscular excitability

Have nausea and vomiting

stomach ache

When >5.5mmol/L, the QT interval is shortened and the T wave is high and sharp.

When >6.5mmol/L, the PR interval is prolonged, the QRS complex is widened, the P wave decreases or disappears, and nodal or ventricular arrhythmias occur.

When >9mmol/L, the QRS deforms and becomes sinusoidal, ventricular asystole or ventricular fibrillation.

Remove the cause and limit potassium intake

Promote intracellular transfer

Promote potassium excretion

Antagonizes the cardiotoxic effects of potassium: 10% calcium gluconate