Sodium imbalances are less likely to cause acute cardiac changes or arrest. As a result, there are no specific therapies indicated in a cardiac arrest situation. Sodium contributes the most of any electrolyte to total serum osmolality, and changes in this electrolyte will affect osmolality. This will, therefore, lead to changes in the interstitial and intravascular fluid levels to maintain osmolality levels. Acute sodium decreases can then lead to cerebral edema as fluid exits the intravascular space into the interstitial spaces in the brain. Rapid correction can also lead to significant adverse effects, so it is vital to monitor neurologic effects during treatment or both hyper- and hyponatremic states. Typically, treatment should be done slowly for 48 hours to minimize adverse events.

Regulation of sodium is via the renin-angiotensin-aldosterone pathways and antidiuretic (or arginine vasopressin). Sodium levels dictate the amount of extracellular fluid (ECF), and sodium levels reflect the status of total body water.  Sodium is primarily located outside of the cells with little amount intracellularly. Sodium overload usually causes increases in fluid overload, leading to edema. It can cause congestive heart failure, liver cirrhosis, and nephrotic syndrome. Low levels of sodium lead to ECG losses and dehydration, including orthostatic hypotension, tachycardia. Generally, sodium imbalances can indicate fluid related issues; high sodium levels indicate depletion of free water while low sodium levels indicate an overload of free water. Imbalances in vascular volume often relate to sodium imbalance. 

The normal sodium level in serum is between 135-145 mEq/L. 

Hypernatremia

Hypernatremia may arise for an increase in sodium or reduction in water with clinical symptoms, including weakness, change in mental status, neurologic deficits, seizures, and comas. The symptom severity depends on the change in sodium level as well as how quickly it develops. 

Etiologies of Hypernatremia

These range from increased aldosterone, glucocorticoid or administration of saline and sodium bicarbonate. Excess sweat, renal or GI losses can cause hypernatremia as well. The main three mechanisms include:

• Poor water ingestion leading to normovolemic hypernatremia
• Lost salt and water (more water than sodium) causing hypovolemic hypernatremia
• Gained sodium and water (more sodium than water) causing hypervolemic hypernatremia

Hypovolemic hypernatremia is the most common mechanism. These patients actually have a decrease in total sodium (due to sodium losses that are not as much as water losses). They will require replenished sodium once the serum levels are normalized.

Diagnosing Hypernatremia

Hypernatremia causes water shifts from the interstitium to the intravascular space, water also shifts out of the cells. This leads to dehydration in the cells. The range of clinical signs of hypernatremia are primarily neurologic and include fatigue, irritability, lost appetite, and nausea or emesis. Patients may present with altered mental state, confusion to coma, seizures, muscle weakness or twitching, ataxia, and focal neurologic deficits, including abnormal reflexes and paresis. In hypovolemic hypernatremia, patients will complain of thirst, fatigue and may display signs of orthostatic hypotension such as lightheadedness. 

Treating Hypernatremia

Treatment includes eliminating any free water loss and replacing water deficits. In patients without clinical symptoms, this can be done via oral administration or nasogastric tube. The hypovolemic patient should be managed with normal saline or 5% dextrose added to half the normal saline to minimize the rapid shift in serum sodium. Patient serum sodium should be monitored during treatment. 

Since many patients will have associated water changes, the typical treatment is to manage the water deficit or excess and not remove sodium. The majority will be hypovolemic with water losses, and the deficit in water must be corrected, ensuring there are no rapid changes in serum sodium levels as this can lead to dangerous intracerebral changes or other physiologic effects. 

The free water deficit is calculated to determine how much fluid must be replenished. It is key to stop any fluid losses. Typically, water deficit is replaced via normal saline. The equation is:

Free water deficit = [(serum Na – 140)/140]  x total body water

Typically, the total body water is equivalent to ½ lean body mass in males and 40% lean body mass in women. Therefore multiply weight in kg by 0.5 (for men) or 0.4 (for women). 

The replacement route is dependent on the patient’s symptoms. 

• In the asymptomatic patients, give replacement orally or via nasogastric tube. 
• If the patient is symptomatic but without significant hypovolemia, use IV half of normal saline. 
• If the patient is both symptomatic and hypovolemic, use a combination of normal saline for hypovolemia and half normal saline for free water deficits. 

Patients who are nearing arrest will have significant water losses, hypovolemia, and signs of shock. Fluid should be replaced quickly with normal saline. 

• IV 500 mL normal saline bolus. Repeat 20-30 minutes as needed while monitoring clinical status
• Another option is administering 10-20 ml/kg normal saline for 20 minutes while monitoring the clinical response. 
• Following stability, replace free water deficits.

Controlled water replacement is the usual hypernatremia treatment.

Hyponatremia

In these cases, there is too much water in relationship to sodium.

Etiologies of Hyponatremia

Typically, this condition is due to decreased water excretion or excess salt wasting by the kidneys. Several situations can lead to this condition, including thiazide diuresis, edematous states, syndrome of inappropriate antidiuresis hormone (SIADH), hypothyroidism, renal failure, or adrenal insufficiency. SIADH is the most common cause of significant or emergent hyponatremia.

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In most cases, there will be associated hypoosmolality. One significant exception is with uncontrolled diabetes in which the hyperglycemic state cause increased osmolality, overcoming the low sodium state. 

Syndrome: Inappropriate Antidiuresis Hormone (SIADH)

SIADH is secondary to an abnormal increase in vasopressin (or arginine vasopressin, antidiuresis hormone). Its release is from the posterior pituitary or from an alternate source such as a neoplasm. Vasopressin leads to increased retention of free water by the kidneys as sodium is excreted. Patients will then have normovolemic hyponatremia associated with high urine osmolality (usually over 100 mOsm/kg). SIADH leads to overly concentrated urine with an osmolality that is greater than serum.

Syndrome of Inappropriate Antidiuretic Hormone secretion occurs when the body makes too much antidiuretic hormone.

SIADH can progress to significant neurologic complications and death and should always be considered in any patient with symptomatic hyponatremia. 

Diagnosing Hyponatremia

The condition is often asymptomatic unless severe or acute. This is typical with sodium levels under 120 mEq/L. With a sudden sodium change, patients may develop irritability, headache, seizure, nausea/vomiting, and death. 

Treating hyponatremia

To treat hyponatremia, sodium must be replaced, and free water must be excreted. In cases of SIADH, fluid restriction between 55-66% of requirements is begun. Sodium changes should be corrected slowly, with an increase of 0.5mEq/L each hour or 12mEq/L over 24 hours. Rapid changes can be life-threatening and can lead to coma or central pontine myelinolysis (rapid extracellular fluid shift in the brain), which can be fatal. 

In asymptomatic patients, the sodium that can be administered each hour is determined by multiplying total body water (weight in kg multiplied by 0.6 in men or 0.5 in women) by 0.5mEg/L. 

For symptomatic patients, use 3% hypertonic saline to increase sodium levels by as much as 1 mEq/L each hour until symptoms resolve. The maximum should be a change of 4mEq/L in 4 hours. This may be increased in patients with seizure activity up to 2-4 mEq/L each hour. Following the resolution of symptoms, the correction should return to 0.5 mEq/L. 

In symptomatic patients, the sodium replacement is with 3% hypertonic saline and is determined by the equation

• Sodium dosing=  4mEq/L x [0.6men or 0.5women] x weight in kg

Once calculated, determine the 3% hypertonic saline volume (by dividing by 513 mEg/L), then provide the amount over the recommended time. Typically, this will be the total (4mEq/L) over four hours. Once the patient is asymptomatic, return to the slower rate of 0.5mEq/L. Be sure to monitor sodium levels regularly. Never use 3% saline to completely correct sodium levels. This is only used to allow the resolution of significant hyponatremia symptoms. Once symptoms have resolved, return to the use of normal saline. 

 It is also important to monitor the volume as well:

• Determine if hypo-, hyper-, or normovolemic. Hypovolemia signs include tachycardia, hypotension, and signs of poor perfusion. Hypervolemia signs include peripheral edema, CHF, distended jugular veins, 3rd heart sound, and rales. 
• Treatment is based on volume and symptoms. 
  • If low volume, replace it with normal saline. 
  • If excess volume, restrict water while beginning diuresis. Alternatively, 3% saline may be used. 
  • If normovolemic, decrease fluid intake to ½ – 1/3 and manage etiology. 
  • If asymptomatic slowly correct sodium level at most 0.5mEq/L each hour with a maximum of 12 mEq/L over 24 hours. 
• Rapid changes in sodium level lead to coma or central pontine myelinolysis (rapid extracellular fluid shift in the brain), which can be fatal.

Patients who are nearing arrest will have significant symptoms, including seizures, coma, or signs of a severe increase in intracranial pressures. Patients will rapidly deteriorate.  In cases of neurologic symptoms, immediately manage with 3% hypertonic saline to increase sodium levels by 1mEq/L until symptoms resolve. Then, increase levels by 0.5 mEq/L each hour.