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Hyponatremia causative factors:

Vomiting, diarrhea, fistulas, sweating
Diuretics, low salt diets, deficiency of aldosterone
Water intoxiction - causes water to move into the cell = ECF volume excess; seen with inappropriate ADH; hyperglycemia, tap-water enema; irrigation of g-tubes with water instead of NS; compulsive water drinker; excessive use of IV Dextrose and Water



syndrome of inappropriate ADH, so increase AHD (reabsorbs water and sodium filling up urine)
Leads to inappropriate urination of sodium
Conditions associated w SIADH = oat-cell lunc tumors, head injury, endocrine and pulmonary disorders; physiologic and psychological stress; medications – chemo agents


Hyponatremia s/s

Headache, orthostatic BP, nausea, abdominal cramping, altered mental status, can have seizures that lead to coma, poor skin turgor, dry mucosa, decreased saliva production, Anorexia, muscle cramps, exhaustion; serum sodium below 115 mEq/L; signs of increased intracranial pressure – lethargy, confusion, muscle twitching, focal weakness, hemiparesis, seizures


Hyponatremia treatment

Sodium replacement – by mouth, nasogatric tube, or IV
Water restriction – total 800 ml / 24 hours


Hypernatremia patho

fluid deprivation in unconscious patients who cannot perceive, respond to, or communicate thirst; Very old, very young, cognitively impaired persons


Hypernatremia causative factors:

Fluid deprivation, hypertonic enteral feedings (Adminstration without water supplements); watery diarrhea, hyperventilation, burns, diabetes insipidus (polydispia – increase urination, holding on to salt)
Less common causes: heat stroke, near-drowning in sea water, malfunction of HD or PD systems, IVF – hypertonic saline


Hypernatremia s/s

Neurologic (primarily neurologic – consequence of cellular dehydration – concentrated ECF), diminished DTR, restlessness, weakness, disorientation, delusions, hallucinations; thirst, dry/sticky mucus membrane, red/dry tongue; body temp rises


Hypernatremia treatment

monitor how quick, want gradual change back to normal - Gradual lowering of serum sodium by infusion of hypotonic electrolyte solution – 0.3% sodium chloride) or an isotonic nonsaline solution (D%W) – as indicated when water needs to be replaced without sodium
may give diuretics for fluid overload - to treat sodium gain
may need dialysis
monitor fluid loss



o Indicates an actual deficit in total K+ stores
o GI loss most common cause; vomiting and gastric suction may lead to hyokalemia


Hypokalemia causative factors

Diuretics, vomiting, gastric suction, diarrhea, hypersecretion of insulin, dietary, debilitated, elderly, alcoholism, anorexia, bulimia


Hypokalemia s/s

Cardiac or respiratory arrest, dysrhythmia, digitalis sensitivity, flat/inverted T wave on EKG; alkalosis; fatigue, anorexia, N/V; muscle weakness, leg cramps, decreased bowel motility (muscle contractions), paresthesias
- symptoms not likely unless beow 3.0 mEq/L


Hypokalemia treatment

Dietary or IV intake – give potassium by mouth if able, if not then dilute and give by IV - Cannot give undiluted potassium, will kill pt
• Increased intake of dietary K+, or IVF therapy, 40-80mEq/day is adequate in adults
• Foods = fruit – raisins, banana, apricots, organes, vegetables, legumes, whole grains, milk, and meat, Salt substitutes contain 50-60 mEq of K+ per teaspoon



Seldom occurs with normal renal function - is often due to treatments of other conditions
Cardiac arrest more common with elevated K+
Causes of “pseudo” hyperK+ : tight tourniquet around exercising extremity while drawing a blood sample and hemodialysis of sample before analysis
eukocytosis (WBC > 200,000); thrombocytosis (platelets > 1 million); drawing blood above K+ infusion site Measurements should be verified


Hyperkalemia causative factors

Renal failure; deficient adrenal hormones; medications; diet; burns, tissue trauma, may be because of shortening of dialysis
- Major cause: decreased renal excretion of K+ - untreated renal failure; hypoaldosteronism and Addison’s disease (deficient adrenal hormones)
- Medications – KCL, heparin, angiotensin-converting enzyme inhibitors, captopril, nonsteroidal antiinflammatories, K= sparing diuretics
- High dietary intake; K+ supplements; IVF;


Hyperkalemia s/s

- Peaked T waves, widen QRS on EKG; cardiac arrest; acidosis
- Skeletal muscle weakness; numbness, paresthesia, paralysis
- Nausea, colic, diarrhea, abdominal cramping
- cardiac effects not usually significant below 7 mEq/L but almost always present when 8 mEq/L or greater
- Earliest changes – narrow T wave, ST segment depression, shortened QT interval (6 mEq/L) if levels continue to increase, PR interval prolonged – disappearance of P wave; ventricular dysrhythmias, cardiac arrest


Hyperkalemia treatment

- Restrict K+ intake – oral and IV, eliminate salt substitutes
- Retention enema; Kayexalate – orally or retention enema (do not use if paralytic ileus or intestinal perforation can occur)
- EKG to detect changes; repeat serum K+ level from vein


Hypocalcemia causative factors

Hypoparathyroidism, also associate with surgery on thyroid and parathyroid glands and radical neck dissections, Inflammation of pancreas; renal failure; insufficient Vitamin D; Magnesium deficiency; thyroid carcinoma; low albumin, alkalosis, alcohol abuse


Hypocalcemia s/s

Tetany, tingling fingers, mouth, feet; spasms in extremities or face; seizures; mental changes, delirium; prolonged QT interval on EKG, Ventricular tachycardia
- tetany – the entire symptom complex induced by increase neural excitabilty – sx due to spontaneous discharges of both sensory and motor fibers in peripheral nerves
- Trousseau’s sign – inflate bp cuff, carpal spasms (abduction thumb, flexed wrist, fingers together)
- Chvosterk’s sign - tap side of cheek and notice twitching
- seizures may occur – increased irritability of CNS; mental changes – depression, impaired memory, confusion, delirium, hallucination


Hypocalcemia assessment

Serum calcium, albumin Level, arterial pH; PTH level; Magnesium & phosphorus levels


Hypocalcemia treatment

Calcium salts via IVF therapy; Vitamin D therapy; aluminum hydroxide antacids; dietary replacement
- acute symptoms are life-threatening and require prompt treatment with IV calcium
- Parenteral calcium salts – calcium gluconate, calcium chloride, calcium gluceptate
- Too rapid IV admin can cause cardiac arrest – dangerous in patients receiving digitalis-derived meds
- IV calcium should be diluted in D5W –given slow IV bolus or slow IV infusion (0.9% NS should NOT be used with calcium because it increases renal calcium loss)
- Solutions with phosphates or bicarb should NOT be used -> percipitates when calcium is added
- Calcium can cause postural hypotension – keep in bed for IV replacement and monitor BP
- Vit D therapy – increase calcium absorption from GI tract
- Aluminum-hydroxide antacids
- Dietary intake to at least 1000 – 1500 mg/day in adult
- Foods high in calcium = milk products, green leafy vegetable, canned salmon, sardines, fresh oysters


hypercalcemia crisis

17** severe thirst and polyuria; muscle weakness, intractable nausea, abdominal cramps, obstipation or diarrhea, peptic ulcer symptoms, bone pain; lethargy, confusion, and coma – very dangerous condition – may lead to cardiac arrest.
• mortality rate as high as 50% if not treated promptly.


hypercalcemia causative factors

Malignancy, bone cancer, hyperparathyroidsim ; excessive PTH (secretion = increased release of calcium from bones and increased intestinal and renal absorption); immobilization (Bone mineral is lost during immobilization – may cause increase in total calcium); thiazide diuretics (may cause slight elevation – they potentiate the action of PTH on kidneys = reduced urinary calcium excretion); vitamin A & D intoxication, lithium


hypercalcemia s/s

Muscle weakness, depressed DTR, uncoordination; lethargy, confusion, coma, short QT on EKG; renal stones
- hyper ca+ reduces neuromuscular excitability – suppresses activity at myoneural junction
- Muscle weakness, incoordination, anorexia, constipation
- Cardiac standstill may occur when serum calcium is 18mg/dl
- Dig toxicity is aggravated by hypercalcemia
- Anorexia, N/V, constipation; dehydration; abdominal / bone pain; abdominal distention and paralytic ileus; excessive urination; severe thirst; peptic ulcer sx – increased secretion of acid and pepsin by stomach
- Confusion, impaired memory, slurred speech, lethargy, acute psychotic behavior, or coma may occur


hypercalcemia treatment

Treat underlying cause; IVF therapy; mobilize patient; restrict dietary intake



o Approximately 1/3 of Mg is bound to protein the rest is free cations
o Should be evaluated with albumin levels – low albumin levels will decrease total Mg
o Route for loss: GI tract – NG suction, diarrhea, fistulas
o Mg concentration is higher in lower GI tract so diarrhea and fistuala will cause greater deficit
o The distal small bowel is where most Mg is absorbed so any disruption (intestinal resection, inflammatory bowel disease) can lead to hypoMg


Hypomagnesemia causative factors

- Alcohol withdrawal - Withdrawal from alcohol is most common cause in US (should be measured q 2-3 days)
- Malnutrition, malabsorption - Administration of nourishment – TPN or tube feedings
- Other causes: aminoglycosides, cyclosporine, diuretics, digitalis, amphotericin, and citrated blood – especially in pt with renal or hepatic disease
- Diabetic ketoacidosis – secondary to increased renal excretion duiring osmotic diuresis – Mg shifts into the cells with insulin therapy
- Contributing causes: sepsis, burns, and hypothermia


Hypomagnesemia s/s

Hyperexcitability with muscle weakness, tremors; tetany, seizures; mood alterations; cardiac dysrhythmias
- sx usually not seen until level <1 mEq/L
- neuromuscular – hyperexcitability w/ muscle weakness, tremors, athetoid movements (slow, involuntary twisting and writhing)
- Tetany, generalized tonic-clonic or focal seizures, laryngeal stridor,
- ECK – prolonged QRS, depress ST segment, and predisposed to cardiac dysrhythmias – PVC, supraventricular tachycardia, V-fib
- Increased susceptibility to digitalis toxicity
- May also see marked alterations in mood – apathy, depression, apprehension, or extreme agitation
- Ataxia, dizziness, insomnia, confusion, delirium, auditory/visual hallucinations, psychoses


Hypomagnesemia treatment

Dietary; IVF therapy; monitor urine output



May be falsely elevated when blood hemolyze or is drawn from extremity with excessively tight tourniquet


Hypermagnesemia causative factors

Renal failure; untreated diabetic ketoacidosis; excessive administration of Magnesium; excessive use of antacids and laxatives
- Most common cause: renal failure
- May occur in patient with untreated diabetic ketoacidosis when catabolism causes the release of cellular Mg that cannot be excreted because of profound fluid volume depletion and oliguria.
- Excessive administration to treat eclampsia or to lower serum Mg levels
- Adrenocortical insufficiency; Addison’s disease, hypothermia; excessive use of antacids (maalox, Riopan) and laxatives (MOM)


Hypermagnesemia s/s

Low BP, N/V, soft-tissue calcification; facial flushing; sensation of warmth;
- High levels = lethargy; dysarthria; drowsiness; DTR lost; muscle weakness/paralysis may occur; cardiac & respiratory arrest if untreated
- depressed CNS and peripheral neuromuscular junction
- Tendency to low BP due to peripheral vasodilation;
- N/V, soft-tissue calcification; facial flushing, sensation of warmth;
- High levels = lethargy, difficulty speaking, drowsiness; deep tendon reflex may be lost; muscle weakness and paralysis may develop
- Resp center is depress when serum Mg exceed 10 mEq/L – coma, atrioventricular heart block and cardiac arrest may occur if left untreated


Hypermagnesemia treatment

EKG monitor; ventilate if necessary; hemodialysis; IVF therapy
- Avoid administration of Mg with renal failure;
- Carefully monitor those receiving Mg salts – D/C use if hyperMg
- Emergencies – Resp. depression or defective cardiac conduction – may require venilatory support and IV calcium
- Hemodialysis with Mg-free dialysate can reduce Mg to safe level within hours
- Loop diuretics and 0.45%NS enhance Mg excretion if adequate renal function
- IV calcium gluconate antagonizes the neuromuscular effects of Mg



(phosphorus and calcium have an inverse relationship)
Although it often indicates phosphorus deficiency – it may occur under a variety of circumstances - May be hypo – even if normal body stores are normal –
Phosphorus deficiency is an abnormally low content of phosphorus in lean tissues and may exist in the absence of hypophosphatemia


Hypophosphatemia causative factors

Malnutrition; alcohol withdrawal; elderly; debilitated; diabetic ketoacidosis; burns; certain antacids;Vitamin D deficiency
- Often seen during administration of calories to patient with severe protein-calorie malnutrition
- Likely to occur with overzealous intake or administration of simple carbohydrates
- Examples: anorexia, alcoholism, elderly, debilitated, those unable to eat
- As many as 50% alcoholics will have hypoPh
- May be seen in malnourished pt receiving TPN
- Prolonged hyperventilation, alcohol withdrawal, poor dietary intake, diabetic ketoacidosis, major thermal burns
- Resp. alkalosis
- Excess-phosphorus binding by antacids containing Mg, calcium or albumin may decrese phosphorus available from the diet to amount below that required to maintain serum balance
- Vitamin D regulates intestinal absorption – deficiency of Vit D may cause decreased calcium and phosphorus levels = osteomalacia (softened, brittle bones)


Hypophosphatemia s/s

Irritability, weakness, numbness, confusion, seizures, coma; hypoxia, bruising or bleeding
- irritability, fatigue, apprehension, weakness, numbness, paresthesias, confusion, seizures, coma
- Hypoxia -> increased resp rate & alkalosis
- hypoPh predisposes a person to infection
- Muscle weakness, muscle pain; weakness of respiratory muscles may impair ventilation
- HypoPh may predispose to insulin resistance and hyperglycemia
- Chronic loss of phosphorus can cause bruising and bleeding from platelet dysfunction


Hypophosphatemia treatment

IVF therapy; monitor concentration of enteral feedings; oral supplements; monitor serum phosphate


Hyperphosphatemia causative factors

Renal failure; hypoparathyroidism; diabetic ketoacidosis; diet intake
- Various conditions can lead to this imbalance – renal failure is most common
- Others: chemotherapy for neoplastic disease, hypoparathyroidism; resp acidosis or diabetic ketoacidosis, high phosphate intake, profound muscle necrosis, increase phsophorus absorption


Hyperphosphatemia s/s

Related to decreased calcium= tetany; anorexia, N/V; muscle weakness; hyperreflexia; tachycardia; soft tissue calcification
- Most result from decreased calcium level and soft tissue calcifaction
- Tetany – causing tingling sensation in fingertips and around mouth
- Anorexia, N/V, muscle weakness, hyper-reflexia; tachycardia
- Long-term consequence: soft-tissue calcification – seen with reduced glomerular filtration rates
- High levels promote precipitation of calcium phosphate in nonosseous sites, decreasing urine output, impairing vision, and producing palpitations


Hyperphosphatemia assessment

- Serum phosphate level over 4.5 (normally higher in children because of high rate of skeletal growth)
- Serum calcium useful for diagnosing primary problem and assessing effect of treatments
- X-ray to show skeletal changes


Hyperphosphatemia treatment

Treat underlying cause (renal or parathyroid) IE: renal failure – measure to decrease serum phosphate are indicated – administer phosphate-binding gels, restrict dietary intake and dialysis


Hypochloremia causative factors

Deficient intake or reabsorption; salt-restricted diets; GI tube drainage; severe vomiting or diarrhea, worry about GI suctioning
- Chloride control depends on intake of chloride and excretion and reabsorption of its ions in the kidneys
- Chloride produced in stomach as hydrochloric acid – small amount is lost in feces
- Risk factors = salt-restricted diets, GI tube drainage, severe vomiting & diarrhea


Hypochloremia s/s

Same as with sodium & potassium deficit and metabolic alkalosis; hyperexcitability of muscle; tetany; hyperactive DTR; weakness, twitching; cramps; cardiac dysrhythmia; seizures
- acid-base and el+ imbalances
- Hyponatremia, hypokalemia, and metabolic alkalosis (high pH and high bicarb)
- Hyperexcitability of muscles, tetany, hyperactive DTR, weakness, twitching, muscle cramps
- Cardiac dysrhythmia and seizures as noted with other El+ changes


Hypochloremia assessment

Serum chloride ; Sodium and K+ levels; ABG; Urine chloride


Hypochloremia treatment

IVF therapy; D/C or change diuretics; dietary intake; ammonium chloride;
- Correct the cause –
- IVF therapy with 0.9% or 0.45% NS is used
- May D/C use of diuretics or change to another kind
- Foods high in chloride = tomato juice, salty broth, canned vegetables, processed meats, and fruits
- Avoid large amounts of free / bottled water because it causes body to excrete large amounts of chloride
- Ammonium chloride – an acidifying agent may be Rx for metabolic alkalosis
- Monitor I & O, ABGs, vital signs, respiratory status


Hyperchloremia causative factors

Loss of bicarbonate ions via kidney or GI tract with corresponding increase in chloride ions


Hypochloremia s/s

Same as with hypernatremia; metabolic acidosis; tachypnea; weakness; lethargy; deep rapid resp; diminished cognitive ability; hypertension
- same as metabolic acidosis; hypervolemia; hypernatremia
- Tachypnea; weakness; lethargy; deep, rapid resp; diminished cognitive ability; hypertension
- If untreated – decrease in cardiac output; dysrhythmia; coma
- High Chloride is seen with high sodium and fluid retention


Hypochloremia assessment

Serum chloride 108 or greater; Sodium > 145; pH < 7.35, Bicarb < 22, Normal anion gap, Urine excretion increases


Hypochloremia treatment

IVF Therapy with LR; diuretics, restrict sodium and chloride; monitor vital signs, I & O
- Correct cause – restore El+, fluid, an acid-base balance
- Lactated Ringer’s may be used to convert lactate to bicarb in liver - > increase base bacarb level and correct acidosis
- Sodium bicarb may be given IV to promote renal excretion
- Diuretics may be used to eliminate chloride
- Restrict sodium, fluids, and chlorides
- Monitor vital signs, ABG, I & O
- Respiratory, neurologic and cardiac systems