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Signs of acute hypervolemia: Acute shortness of breath, tachycardia.

Complications of acute CHF can arise in patients with poor cardiac function given too much fluid acutely. Therefore, it is important to monitor these patients closely.

Signs of chronic hypervolemia: Peripheral edema, pulmonary edema.

Diuresis may be needed in some patients to reduce volume.

Sodium: close relationship to volume status

Hyponatremia

Definition and categories. Hyponatremia is defined as a serum sodium level of 130 mEq/L or less. The first step in diagnosis and treatment is to assess the osmolar and volemic state.

Hyperosmolar: Dilutional hyponatremia from hyperglycemia, mannitol infusion, or presence of other osmotically active particles.

Normo-osmolar: Pseudohyponatremia. Hyperglycemia, hyperlipidemia, and hyperproteinemia interfere with the lab measurement of sodium.

Hypo-osmolar: True hyponatremia.

Hypovolemic: Most common. Normally, hypovolemia leads to ADH secretion and the inability to excrete free water. Intake of free water via thirst mechanisms or infusion of hypotonic solution leads to hyponatremia. Total body sodium usually is low.

Hypervolemic: Total body sodium usually is high. The pathology is often related to low cardiac output (the kidneys see less blood flow, and free water is not excreted) or hypoalbuminemic (e.g., cirrhosis) or other edematous states where salt (renin-angiotensin system) and free water (ADH) cannot be excreted by the kidneys.

Euvolemic: Could be either of the states above, or more frequently in the perioperative patient, syndrome of inappropriate antidiuretic hormone (SIADH)

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secretion. ADH secretion can be stimulated by the stress response to trauma and surgery. Free water is retained.

Symptoms. Acute hyponatremia is associated with acute cerebral edema, seizures, and coma. Chronic hyponatremia is well tolerated to Na concentrations of 110 mEq/L. Symptoms generally include confusion/decreased mental status, irritability, and decreased deep tendon reflexes.

Diagnosis and categorization. Clinical exam and lab determination of osmolar state are often enough for diagnosis, but if in doubt, especially with hypo -osmolar hyponatremia, check urine osmolarity and sodium concentration.

Hypovolemic, hypo-osmolar hyponatremia: Urine osmolarity high; Na low.

Hypervolemic, hypo-osmolar hyponatremia: Similar picture.

Euvolemic, hypo-osmolar hyponatremia: Urine osmolarity high; urine Na high.

Treatment

Hyperosmolar: Correct hyperglycemia or source of other actively osmotic particles.

Normo-osmolar: No treatment required.

Hypo-osmolar:

Hypovolemic: Treat with isotonic fluid infusion to restore fluid and sodium deficit.

If sodium deficit is severe, sodium replacement can be considered.

Hypervolemic: Treat underlying medical cause first, then usually salt and free water restriction are appropriate.

Euvolemic: First determine if the true cause is one of the above states. If SIADH is the cause, free water restriction usually is enough. Do not replace salt because this can paradoxically lower serum sodium, as the kidney excretes sodium and conserves water.

Hypernatremia

Definition and categories. Hypernatremia is defined as a serum sodium level greater than 150 mEq/L.

Hypovolemia: Hypernatremia almost always represents a volume deficit, with more free water being lost than sodium.

Hypervolemia: Iatrogenic infusion of too much sodium can lead to hypervolemic hypernatremia, but this is rare.

Symptoms can include those of volume depletion (e.g., tachycardia, hypotension) as well as other signs of dehydration (e.g., dry mucous membranes, decreased skin turgor). Lethargy, confusion, and coma result from water shifts from the intracellular compartment in the central nervous system (CNS).

Diagnosis/etiology: Diagnosis usually simple. High serum sodium with obvious fluid losses. In surgical patients, fluid losses may be due to:

Extrarenal: Insensible losses due to fever, mechanical ventilation, burns, diarrhea, or measured losses from the gastrointestinal (GI) tract.

Renal: Excessive free water excretion.

Osmotic diuresis from hyperglycemia or mannitol administration.

High output dilute urine from the polyuric phase of acute tubular necrosis (ATN).

Treatment.

Hypovolemic: Need to replace volume. Calculate free water deficit first:

Water deficit = 0.6 × body weight in kilograms × (pNA/140 - 1)

Then, calculate one half the deficit to replace in the first 8 hours and the remainder in the next 16 hours. If the hypovolemic state is severe (i.e., shock), initial therapy can be isotonic fluids for resuscitation. If the deficit is less severe, or once perfusion adequate, it is permissible to switch to 0.5% NS or dextrose 5% in water (D5W).

Hypervolemia: If the patient's total body water is increased, first decrease the amount of sodium administered. If sodium intake (e.g., antibiotics, TPN, drips in normal saline) cannot be decreased, free water can be infused to lower the serum sodium level, but this does not decrease the total body sodium or water content. Diuretics can be used as well.

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Potassium

Hypokalemia

Definition. In general, K + <3.5 mEq/L is considered hypokalemia. Severe hypokalemia is defined as a serum potassium level of 3 mEq/L or less. In some patients (cardiac), it is desirable to have a K + >4.0.

Symptoms of hypokalemia include ileus and weakness. Weakness can become profound enough to cause respiratory failure. Profound depletion results in cardiac dysrhythmias.

Electrocardiogram (ECG) changes can become manifest below a K + of 3.0 mEq/L and include, in increasing order of severity, T -wave flattening or inversion, depressed ST segments, development of U waves, prolonged QT interval, and finally ventricular tachycardia.

Diagnosis/etiology: Diagnosis simple and based on blood chemistry. More important is to understand the cause. Rarely found in healthy humans with a normal diet and normal kidneys. Causes can be one of four categories.

Renal: Diuretics, vomiting (renal excretion of K + to preserve Na +), renal tubular acidosis.

Extrarenal: Diarrhea, burns.

Intracellular shift: Insulin, alkalotic state.

Medical disease: Hyperaldosteronism, Cushing syndrome

Treatment. If symptoms are severe, administer as much potassium IV as needed to reduce symptoms. If symptoms are mild or nonexistent, can infuse 20 mEq/hour maximum in the unmonitored patient and 40 mEq/hour in the monitored patient. A general rule of thumb is that every 10 mEq of K + should raise serum concentration by 0.1 mEq/L. Administration for more chronic conditions can be via enteral supplements. Remember, serum K + concentration is not an indication of total body stores of potassium. If the serum K + is repleted but total body stores are low (as most K + is intracellular), serum K + will drop again quickly as K + shifts into cells.

Hyperkalemia

Definition. Hyperkalemia is usually defined as a serum potassium level of 6 mEq/L or greater.

Symptoms of hyperkalemia are rare but include diarrhea, cramping, nervousness, weakness,

and flaccid paralysis. More often, cardiac dysrryhthmias are manifest before other symptoms become severe. ECG changes include peaked T waves , widened QRS, and can eventually degenerate into ventricular fibrillation.

Diagnosis/etiology. There are numerous causes, among the more common are the following:

Renal failure: With inappropriate consumption/administration of K +

Extracellular shift:

Rhabdomyolysis

Massive tissue necrosis

Metabolic acidosis

Hyperglycemia

Medical disease:

Addison's disease

Treatment. Can be divided into two phases. Acutely, the goal is to stabilize the cardiac membrane and to lower serum potassium. Once the patient is stabilized, maneuvers to remove K + permanently from the system should be instituted.

Acutely symptomatic patient:

IV calcium stabilizes cardiac myocyte membranes and can prevent dysrhythmias. One gram of Ca ++ gluconate IV is a standard dose.

Glucose/insulin administration can be used to shift K intracellularly acutely and quickly. One ampule of D50 with 10 units of regular insulin is often enough.

Bicarbonate administration will also shift K + intracellularly.

To remove K+ and to lower body stores permanently:

Ion-exchange resin: used either by mouth (PO) or rectally. Binds K + in the colon, facilitating excretion.

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Lasix: Only use if kidneys are able to excrete, and keep a close eye on other electrolytes and fluid balance.

Dialysis.

Chloride

Hypochloremia

Definition. Hypochloremia is defined as a chloride level less than 90 mEq/L.

Symptoms. Usually associated with dehydration or hypokalemia due to vomiting or other GI loss.

Diagnosis/etiology. Hydrochloric acid (HCl) from the stomach is lost from vomiting, leading to low chloride and a buildup of bicarbonate. This causes a metabolic alkalosis. It is often associated with paradoxic aciduria. Normally, the kidneys would excrete bicarbonate to reduce pH; however, as the dehydration becomes more severe, the kidneys drive to retain sodium

predominates. The kidney excretes both K + and H+ to conserve sodium.

Treatment for hypochloremia involves replacement of the chloride and volume deficit with sodium chloride solutions and replacement of K + as needed.

Hyperchloremia

Definition. Hyperchloremia is defined as a plasma chloride level greater than 110 mEq/L.

Cause. The most common cause of hyperchloremia in surgical patients is the administration of large amounts of chloride in IV solutions. The chloride content in normal saline (154 mEq/L) is significantly higher than that in plasma (90–110 mEq/L).

Diagnosis/etiology. Excess chloride in relation to sodium decreases the strong ion difference, thereby causing more water to dissociate and more H+ ions to be present.

Treatment. Decrease the amount of chloride being infused. Look for all sources (IV antibiotics) in addition to IV fluids. If isotonic saline needs to be administered for other reasons, consider sodium bicarbonate or sodium acetate to reduce chloride load. For instance, 1/2 NS with 1.5 amps NaHCO 3 /L has 152 mEq/L Na, only 77 mEq/L chloride and 75 mEq/L bicarbonate.

Calcium

Hypocalcemia

Definition. Hypocalcemia is defined as a serum calcium level less than 8 mg/dL.

Symptoms of hypocalcemia include neuromuscular irritability, with perioral and extremity numbness that may progress to carpopedal spasm and tetany. Premature ventricular contractions can be reduced with treatment of hypocalcemia as prolongation of the QT interval is noted in these patients. Classic signs include Trousseau and Chvostek's signs.

Diagnosis/etiology. There are numerous causes of hypocalcemia. In surgical patients, the suppression of normal parathyroid function from adenomatous or hyperplastic glands that have been removed is most common, followed by accidental removal of the parathyroids during thyroid surgery. In critically ill patients, lactate, citrate from blood transfusions, and numerous medicines can cause hypocalcemia.

Treatment.

Asymptomatic outpatients can be supplemented orally. An investigation into possible medical causes (vitamin D deficiency, renal failure, excess dietary phosphate, or other causes of hyperphosohatemia, etc.) should be investigated.

Symptomatic patients need to be monitored and treated. If symptoms are mild, large doses of oral calcium are often adequate (especially in the postparathyroidectomy patient). Severely symptomatic patients should be repleted with IV calcium until symptoms resolve and an appropriate oral regimen is tolerated.

Hypercalcemia

Definition. Hypercalcemia is defined as a serum calcium level of 10.5 mg/dL or greater.

Symptoms. Fatigue, confusion, nausea, vomiting, diarrhea, dehydration, and anorexia are common. When related to hyperparathyroidism, renal calculi and ulcer disease are more common.

Diagnosis/etiology. Hypercalcemia has a multitude of causes.

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Endocrine: primary hyperparathryoidism (most common), thyrotoxicosis.

Malignancy: Most common, up to 20%–30% of cancer patients will have hypercalcemia. Osteolytic lesions, PTHrP-secreting lesions are often the cause.

Granulomatous disease: sarcoidosis, tuberculosis.

Medications: excess calcium ingestion, vitamin D toxicity, thiazide diuretics.

Other causes: renal disease, milk alkali syndrome, familial hypocalciuric hypocalcemia.

Treatment. Severe, symptomatic hypercalcemia is a medical emergency and requires immediate treatment. The first line of therapy is aggressive isotonic resuscitation, leading to diuresis and excretion of calcium. If unsuccessful, lasix can be added, assuming that the patient is fluid resuscitated. The next line of therapy is medical. Medications to stop osteoclastic activity is the mainstream. Bisphonates, calcitonin, and steroids are all used. Mithromycin is no longer available in the United States.

II Acid–base Disturbances

A Regulatory systems

The human body requires a very narrow pH range of 7.35 to 7.45 to function properly. There are three main systems in the body that maintain the pH within normal parameters. CO2 , strong ions, and weak acids.

Carbon dioxide: CO2 production can exceed 15,000 mmol/day from metabolic processes. The lungs effectively excrete this entire amount to maintain normal CO2 . If PCO 2 increases, water dissociates and HCO3 - and H+ form based on the Henderson-Hasselbach equation, thus decreasing pH. The reverse happens for lower PCO 2 concentrations. Either a loss of bicarbonate or again in protons can cause acidosis.

Henderson-Hasselbach: pH = pK × log [HCO3 - /(0.03 × PCO 2 )]

Strong ions are defined as ions that completely dissociate in water. Na +, Cl - , Ca ++ , Mg++ , K + are examples. In a pure salt solution, ion concentrations are equal, and pH is neutral. In plasma, however, there are more cations that anions. To maintain electrical neutrality, water dissociates, H + is excreted, and HCO3 - concentration increases, hence a pH of 7.4 and not 7.0.

Weak acids. This includes the buffering systems of the body. Weak acids can exist as negatively charged

molecules or accept H+ and exist uncharged. They include proteins and phosphates.

B Acidosis

The body's pH decreases when the PCO 2 increases, the concentration of HCO3 - increases, the concentration of

strong anions increases, or the concentration of weak acids increases. A pH less than 7.35 is considered pathologic, but patients can compensate from the following disorders of acid–base metabolism or have a mixed picture with a pH in the normal range.

Respiratory acidosis. Decreased ventilation relative to CO2 production leads to increased CO2 concentration.

Causes

The most common cause of respiratory acidosis is decreased alveolar ventilation.

Respiratory depression

Drugs (narcotics)

Alcohol

Excess sedation/analgesia (opioids, benzodiazepines)

Anesthetic agents

Central nervous disorders

Stroke

Trauma

Physical

Iatrogenic (too-low minute ventilation on the ventilator)

Intrisic lung disease (acute respiratory distress syndrome [ARDS], chronic obstructive pulmonary disease [COPD])

Respiratory muscle weakness (myasthenia gravis, spinal cord injury)

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Increased CO2 production. Excess administration of carbohydrate via enteral or parenteral administration can increase the respiratory quotient and increase production of CO2 . Most

patients can compensate, but if the patient is weak or mechanically ventilated he or she may not be able to do so. Also, if the overfeeding is severe, compensation may be difficult.

Treatment. The primary method of treatment for respiratory acidosis is to increase alveolar ventilation. In cases of drug overdose, this may be accomplished with appropriate reversing agents. However, most of the causes of alveolar hypoventilation require intubation with mechanical ventilation to clear CO2 and return the pH to normal values.

Metabolic acidosis results either from a loss of HCO3 - , an accumulation of strong anions, or accumulation of weak acids.

Causes

Weak acid accumulation. All will have anion gap, etiology includes loss of HCO 3 - to maintain electric neutrality.

Acid accumulation can occur because of renal failure and the inability of the kidneys to clear the acids that are by-products of metabolism.

Lactic acidosis. A common cause of metabolic acidosis is lactic acid. Lactic acid could be considered a strong anion, however, as it nearly completely dissociates in water. It usually results from inadequate tissue perfusion, leading to anaerobic metabolism.

Diabetic ketoacidosis. Acetoacetate and β-hydroxybutarate are weak acids.

Toxins. Polyethylene glycol, methanol. Methanol is metabolized to formaldehyde and then formic acid.

Strong anion accumulation. Normal anion gap.

Hyperchloremic acidosis. Excess chloride induces water to dissociate, H to accumulate and pH to drop.

Loss of bicarbonate. Normal anion gap.

Excess renal excretion of bicarbonate.

Diarrhea.

Treatment. The primary treatment for metabolic acidosis is correction of the underlying metabolic problem and proper fluid and electrolyte management. Bicarbonate administration should rarely be used unless pH is dangerously low (<7.2) and the underlying defect is in the process of being corrected. If the primary defect is excess loss of bicarbonate (diarrhea, renal tubular acidosis), bicarbonate therapy should be considered as treatment.

C Alkalosis

Respiratory alkalosis

Causes

Respiratory alkalosis in the spontaneously breathing patient is caused by an increase in alveolar ventilation and subsequent reduction in CO2 levels. This situation can be caused by

any entity that causes hyperventilation, such as anxiety, pain, shock, sepsis, toxic substances (salicylate poisoning), or CNS dysfunction. Some processes causing hypoxia or intrapulmonary shunts can lead to hypocarbia and alkalosis (think of pulmonary embolus!). In the mechanically ventilated patient, iatrogenic overventillation is frequent.

Treatment of respiratory alkalosis includes decreasing minute ventilation and allowing the CO2 levels

to return to normal. Turning down the ventilator and increasing sedation and analgesia will correct nearly all cases. Most cases are self-limited, however, as patients cannot keep excessive ventilatory