💧 Fluids, Electrolytes & Acid–Base

Fluid volume deficit is a state, not a single lab number. Supporting values: serum osmolality above 295 mOsm/kg and urine specific gravity above 1.030 indicate dehydration; normal osmolality is 275 to 295 mOsm/kg and normal specific gravity is 1.005 to 1.030. In isotonic deficit (true hypovolemia) sodium stays within 135 to 145 mEq/L because water and solute are lost together.

Vomiting, diarrhea, nasogastric suction, and fistula or wound drainage. Excessive diuresis from diuretics or from uncontrolled hyperglycemia (osmotic diuresis). Hemorrhage and third spacing into the peritoneum, bowel, or burned tissue. Fever, diaphoresis, hyperventilation, and prolonged inadequate oral intake, which is common in older adults whose thirst sensation is blunted and in patients who are NPO without replacement.

Neuro: restlessness and confusion progressing to lethargy; in older adults new confusion is often the first sign. Cardiovascular: tachycardia, weak thready pulse, flat neck veins, postural hypotension, narrowed pulse pressure, delayed capillary refill. Integumentary: dry mucous membranes, poor skin turgor (check over the sternum or forehead in older adults), absent tearing, sunken eyes. Renal: urine output below 30 mL/hr, concentrated dark urine, intense thirst. Other: acute weight loss, weakness, low-grade temperature elevation.

Hemoconcentration raises hematocrit, hemoglobin, serum protein, and BUN. BUN rises out of proportion to creatinine, giving a BUN-to-creatinine ratio above 20 to 1. Serum osmolality and urine specific gravity are elevated. Sodium is high in dehydration (water loss) and normal in isotonic hypovolemia (whole-fluid loss). ECG may show sinus tachycardia; potassium and other electrolytes shift depending on the source of loss, with GI losses typically lowering potassium.

Restore volume first: establish IV access and give isotonic fluid, normal saline or lactated Ringer's, for hypovolemia; use hypotonic fluid such as 0.45 percent saline only for pure water deficit and only slowly. Monitor vital signs, level of consciousness, and hourly urine output; urine output above 30 mL/hr is the practical marker that perfusion is returning. Weigh daily at the same time on the same scale and record strict intake and output. Institute fall precautions and change positions slowly because of orthostatic hypotension. Provide frequent oral care, offer oral fluids the patient will actually drink, and treat the underlying cause, such as stopping the diuretic or controlling the vomiting. Monitor electrolytes and renal function throughout replacement, and watch for signs of overcorrection, especially crackles, dyspnea, and jugular venous distention in older adults and in patients with heart or kidney disease.

Rule: hypovolemic shock is the danger. Rehydrate with isotonic fluid and treat a sustained urine output below 30 mL/hr, a falling blood pressure with rising heart rate, or a change in level of consciousness as an emergency, not as something to recheck next shift.

Fluid volume excess is also a clinical state. In dilutional (hypotonic) overload, serum sodium falls below 135 mEq/L and serum osmolality falls below 275 mOsm/kg; urine specific gravity falls below 1.005. In isotonic overload, sodium and osmolality remain normal while total body volume rises. A gain of 1 kg of body weight equals about 1 L of retained fluid.

Heart failure, cirrhosis, nephrotic syndrome, and acute or chronic kidney injury, all of which impair excretion. Excessive or too-rapid IV fluid administration, especially isotonic saline in patients with cardiac or renal disease. Excessive sodium intake from diet, medications, or hypertonic saline. Corticosteroid therapy, hyperaldosteronism, and the syndrome of inappropriate antidiuretic hormone. Low serum albumin allows fluid to leak from the vessels into the interstitium, producing edema alongside intravascular depletion.

Respiratory: dyspnea, orthopnea, tachypnea, moist crackles, productive cough with frothy pink-tinged sputum in pulmonary edema; this is the system that kills. Cardiovascular: bounding pulse, tachycardia, elevated blood pressure, jugular venous distention, S3 gallop, elevated central venous pressure. Integumentary: dependent pitting edema, taut shiny skin, periorbital edema. Neuro: headache, confusion, and seizures when the excess is dilutional and sodium is low. Other: rapid weight gain, ascites, increased abdominal girth, polyuria if kidney function is intact.

Hemodilution lowers hematocrit, hemoglobin, BUN, and serum protein. Sodium and osmolality are low in dilutional overload and normal in isotonic overload. Urine specific gravity is decreased. Chest x-ray shows pulmonary congestion. ECG changes are nonspecific but atrial fibrillation and other dysrhythmias are common as the atria stretch; watch for changes reflecting an accompanying low potassium once diuretics are started.

Position the patient upright in semi-Fowler's or high Fowler's to ease work of breathing, and assess respiratory status and lung sounds first. Administer oxygen as prescribed and give diuretics as ordered, most often a loop diuretic. Restrict fluid and sodium as prescribed and space allowed fluids across the day. Weigh daily before breakfast in the same clothing and keep strict intake and output; a gain of more than 1 kg in 24 hours or 2 kg in a week should be reported. Monitor potassium closely once loop or thiazide diuretics begin, because both waste potassium. Elevate edematous extremities, inspect and protect edematous skin, which breaks down easily, and reposition frequently. Teach the patient to weigh daily at home, read sodium labels, and report weight gain, increasing shortness of breath, or new orthopnea.

Rule: pulmonary edema is the emergency. New crackles, dyspnea, or frothy pink sputum means sit the patient up, give oxygen, stop or slow the IV, and notify the provider immediately.

Normal serum potassium is 3.5 to 5.0 mEq/L. Hypokalemia is a level below 3.5 mEq/L; below 2.5 mEq/L is life-threatening.

Potassium-wasting diuretics (loop and thiazide) are the most common cause. GI losses through vomiting, diarrhea, nasogastric suction, laxative abuse, and ileostomy drainage. Corticosteroids and hyperaldosteronism, which trade sodium retention for potassium loss. Alkalosis and insulin administration, both of which shift potassium into the cells without changing total body stores. Inadequate intake in prolonged NPO status, alcohol use disorder, anorexia, and total parenteral nutrition without adequate potassium. Excessive diaphoresis and hyperglycemia-driven diuresis.

Everything gets weak and slow because potassium is required for muscle and nerve excitability. Cardiac: weak irregular pulse, dysrhythmias, orthostatic hypotension, and increased sensitivity to digoxin toxicity. Neuromuscular: generalized muscle weakness starting in the legs, leg cramps, hyporeflexia, paresthesias, and in severe cases respiratory muscle weakness with shallow ineffective breathing. GI: decreased motility, anorexia, nausea, abdominal distention, hypoactive or absent bowel sounds, paralytic ileus. Neuro: lethargy, confusion. Renal: dilute urine and increased thirst.

Serum potassium below 3.5 mEq/L. ECG shows flattened or inverted T waves, ST depression, a prominent U wave, and a prolonged PR interval; premature ventricular contractions and ventricular dysrhythmias follow as the level drops. Magnesium is often low at the same time and must be checked, because potassium cannot be corrected while magnesium remains low. Arterial pH is often alkalotic. Digoxin level should be reviewed in any patient on digoxin.

Place the patient on continuous cardiac monitoring if the level is significantly low or symptoms are present. Give oral potassium with food or a full glass of water to prevent GI irritation. IV potassium must always be diluted and given by infusion pump, never by IV push and never as a bolus; a common maximum peripheral rate is 10 mEq/hr, and rates above that require central access and continuous monitoring per facility policy. Assess that urine output is adequate, above 30 mL/hr, before giving potassium, because potassium is excreted by the kidneys. Inspect the IV site frequently, since potassium is highly irritating and causes phlebitis and tissue damage on infiltration. Monitor for digoxin toxicity, hold potassium-wasting diuretics as prescribed, and teach potassium-rich foods such as bananas, oranges, potatoes, tomatoes, spinach, avocado, and dried fruit. Correct low magnesium concurrently.

Rule: potassium is never given IV push. Concentrated IV potassium given as a bolus causes cardiac arrest. Always dilute, always use a pump, always confirm urine output first.

Normal serum potassium is 3.5 to 5.0 mEq/L. Hyperkalemia is a level above 5.0 mEq/L; above 6.5 mEq/L is a medical emergency with imminent risk of lethal dysrhythmia.

Kidney failure is the leading cause, because the kidney is the main route of potassium excretion. Potassium-sparing diuretics such as spironolactone, ACE inhibitors, angiotensin receptor blockers, and NSAIDs. Excessive potassium intake including salt substitutes, potassium supplements, and rapid IV replacement. Cellular release of potassium in acidosis, crush injury, burns, rhabdomyolysis, tumor lysis syndrome, and transfusion of aged blood. Adrenal insufficiency (Addison disease) from low aldosterone. Pseudohyperkalemia from a hemolyzed specimen or prolonged tourniquet time, which must be ruled out before treating an unexpected result.

Early irritability gives way to weakness and paralysis. Cardiac: bradycardia, hypotension, irregular rhythm, and dysrhythmias progressing to ventricular fibrillation and asystole. Neuromuscular: early muscle twitching, cramps, and paresthesias, particularly around the mouth and in the hands and feet, followed by ascending flaccid weakness and loss of deep tendon reflexes. GI: hyperactive bowel sounds, nausea, cramping, diarrhea. Renal: oliguria if kidney failure is the cause.

Serum potassium above 5.0 mEq/L. ECG changes are the most important finding and appear in a predictable order: tall peaked narrow T waves first, then a widening QRS and prolonged PR interval, then flattened or absent P waves, then a sine-wave pattern preceding ventricular fibrillation or asystole. Check whether the sample was hemolyzed. Associated findings include metabolic acidosis, elevated BUN and creatinine in renal failure, and elevated creatine kinase in rhabdomyolysis.

Get an ECG and put the patient on continuous cardiac monitoring immediately; the ECG, not the number alone, drives urgency. Stop all potassium sources, including IV fluids containing potassium, supplements, and salt substitutes. For cardiac toxicity, IV calcium gluconate is given first to stabilize the myocardium; it does not lower potassium but protects the heart. Shift potassium into cells with IV regular insulin plus dextrose, and with a beta-2 agonist such as nebulized albuterol; sodium bicarbonate is used if acidosis is present. Then remove potassium from the body with a potassium-binding agent such as sodium polystyrene sulfonate or a newer binder, with loop diuretics if renal function permits, or with dialysis, which is the definitive treatment in renal failure. Teach avoidance of salt substitutes, which are potassium chloride, and of high-potassium foods.

Rule: hyperkalemia stops the heart. A potassium above 6.5 mEq/L or any peaked T waves with a widening QRS is a cardiac arrest in progress. Calcium gluconate protects the myocardium first; insulin with dextrose shifts potassium in; dialysis or a binder actually removes it.

Normal serum sodium is 135 to 145 mEq/L. Hyponatremia is a level below 135 mEq/L; below 120 mEq/L carries a high risk of seizures, cerebral edema, and coma.

Dilutional causes (too much water): syndrome of inappropriate antidiuretic hormone, heart failure, cirrhosis, nephrotic syndrome, excessive hypotonic IV fluid, psychogenic polydipsia, and water intoxication after strenuous endurance exercise. Sodium-losing causes: vomiting, diarrhea, nasogastric suction, excessive diaphoresis, wound and burn losses, thiazide diuretics, and adrenal insufficiency. Also seen with prolonged low-sodium diets combined with diuretic therapy and with irrigating body cavities using plain water.

The brain swells, so neurologic signs dominate and severity tracks with how fast the sodium fell. Neuro: headache, confusion, irritability, lethargy, personality change, seizures, and coma. Neuromuscular: generalized weakness, muscle cramps, and diminished deep tendon reflexes. GI: anorexia, nausea, vomiting, abdominal cramping, hyperactive bowel sounds. Volume-dependent findings: in hypovolemic hyponatremia expect tachycardia, hypotension, and dry mucous membranes; in hypervolemic hyponatremia expect weight gain, edema, and jugular venous distention.

Serum sodium below 135 mEq/L and serum osmolality typically below 275 mOsm/kg. Urine sodium and urine osmolality help distinguish causes: in SIADH the urine is inappropriately concentrated with high urine sodium while serum is dilute. Hematocrit and BUN are low in dilutional states and high in sodium-losing states with volume depletion. There is no characteristic ECG pattern; the ECG matters here mainly because accompanying potassium shifts are common.

Determine whether the problem is too little sodium or too much water, because that determines treatment. For dilutional hyponatremia, restrict fluid as prescribed and monitor daily weight and intake and output. For sodium deficit with volume loss, give isotonic normal saline as prescribed. Hypertonic saline, 3 percent, is reserved for severe symptomatic hyponatremia with seizures and must be given on a pump with frequent neurologic checks and serial sodium levels. Correct sodium slowly, generally no more than about 8 to 12 mEq/L in 24 hours, because rapid correction causes osmotic demyelination with permanent neurologic damage. Institute seizure precautions and perform frequent neurologic assessment. Monitor patients on diuretics, and teach those with SIADH about fluid restriction and daily weights.

Rule: hyponatremia is a brain problem, and correcting it too fast is as dangerous as the low sodium itself. Seizure precautions and slow, monitored correction; a sudden improvement in the number with a worsening neuro exam is a red flag.

Normal serum sodium is 135 to 145 mEq/L. Hypernatremia is a level above 145 mEq/L; above 160 mEq/L carries serious risk of neurologic injury.

Water loss exceeding sodium loss: fever, hyperventilation, heatstroke, profuse diaphoresis, watery diarrhea, diabetes insipidus, and osmotic diuresis from hyperglycemia. Inadequate water intake, which is the classic mechanism in patients who cannot access or ask for water: infants, the sedated or intubated, those with dementia, and older adults with a blunted thirst response. Sodium gain: hypertonic tube feedings without adequate free water, hypertonic IV saline, excessive sodium bicarbonate administration, near-drowning in salt water, and hyperaldosteronism or Cushing syndrome.

Water is pulled out of brain cells, so the brain shrinks and neurologic signs dominate. Neuro: restlessness and agitation early, progressing to lethargy, stupor, seizures, and coma; intense thirst is often the first complaint in an alert patient. Neuromuscular: muscle twitching, tremor, and hyperreflexia, later becoming weakness. Integumentary: dry flushed skin, dry sticky mucous membranes, decreased or absent tearing and salivation. Cardiovascular and renal: findings depend on volume status; with water loss expect tachycardia, hypotension, oliguria, and elevated temperature, while with sodium gain expect edema and elevated blood pressure.

Serum sodium above 145 mEq/L and serum osmolality above 295 mOsm/kg. Urine specific gravity and urine osmolality are high with pure water loss but inappropriately dilute in diabetes insipidus. Hematocrit and BUN rise with hemoconcentration. No specific ECG pattern is associated with sodium itself.

Identify and stop the source: free water with tube feedings, control of hyperglycemia, treatment of diabetes insipidus with desmopressin, or removal of the hypertonic fluid. Replace water gradually with hypotonic IV fluid such as 0.45 percent saline or 5 percent dextrose in water as prescribed, or with oral water if the patient can take it safely. Restrict sodium in the diet and review all medications and IV solutions for hidden sodium. Lower the sodium slowly, generally no faster than about 8 to 12 mEq/L per 24 hours, to avoid cerebral edema from water rushing back into brain cells. Monitor neurologic status, serum sodium, daily weight, and intake and output closely, and maintain seizure precautions. Offer fluids on a schedule to patients who cannot request them, and provide meticulous oral and skin care.

Rule: correct hypernatremia slowly. Rapid infusion of hypotonic fluid drives water into brain cells and causes cerebral edema and seizures. Seizure precautions stay in place during correction, not just before it.

Normal total serum calcium is 8.6 to 10.2 mg/dL (about 4.3 to 5.1 mEq/L); normal ionized calcium is about 4.5 to 5.6 mg/dL. Hypocalcemia is a total calcium below 8.6 mg/dL. Because roughly half of serum calcium is bound to albumin, a low albumin lowers total calcium without lowering ionized calcium, so check the ionized level in patients with low albumin.

Removal of or injury to the parathyroid glands during thyroidectomy or neck surgery, and hypoparathyroidism generally. Vitamin D deficiency and malabsorption states including Crohn disease, celiac disease, and after bariatric surgery. Chronic kidney disease, in which phosphate rises and calcium falls reciprocally. Acute pancreatitis, in which calcium is sequestered in the abdomen. Massive transfusion of citrated blood, which binds calcium. Alkalosis, which increases calcium binding to albumin and drops the ionized fraction even when total calcium is unchanged. Low magnesium, chronic alcohol use, and medications including loop diuretics, phosphate binders that overshoot, and some anticonvulsants.

Everything becomes irritable and twitchy, because calcium stabilizes nerve membranes. Neuromuscular: numbness and tingling around the mouth and in the fingers and toes, muscle cramps, tetany, hyperactive deep tendon reflexes, positive Trousseau sign (carpal spasm when the blood pressure cuff is inflated above systolic for up to 3 minutes) and positive Chvostek sign (facial twitching when the facial nerve is tapped anterior to the ear). Respiratory: laryngospasm and bronchospasm with stridor, which is the lethal manifestation. Cardiac: hypotension, decreased myocardial contractility, and dysrhythmias. GI: hyperactive bowel sounds, cramping, diarrhea. Chronic: seizures, brittle nails, dry skin, and osteoporosis with fractures.

Total calcium below 8.6 mg/dL with a low ionized calcium confirming true deficiency. Serum phosphate is usually elevated when the cause is renal failure or hypoparathyroidism. Magnesium and albumin must be checked. Parathyroid hormone is low in hypoparathyroidism and high when the parathyroids are responding appropriately. ECG shows a prolonged QT interval, which can deteriorate into torsades de pointes, and a prolonged ST segment.

Assess the airway first and keep emergency airway equipment, including a tracheostomy tray, at the bedside for any patient after thyroid or parathyroid surgery. Place the patient on seizure precautions and cardiac monitoring, and check the QT interval. Administer oral calcium with vitamin D for chronic deficiency, taken with meals for better absorption, and IV calcium gluconate slowly through a patent line for acute symptomatic hypocalcemia, with the patient on a monitor because rapid infusion causes bradycardia and hypotension. Never give IV calcium in a line with phosphate or bicarbonate, which precipitate. Correct low magnesium first if present, because calcium will not normalize until magnesium does. Reduce environmental stimuli, and teach a diet rich in dairy, canned salmon and sardines with bones, fortified foods, and dark leafy greens.

Rule: laryngospasm is the emergency. Any tingling around the mouth, voice change, or stridor after thyroid or parathyroid surgery means airway obstruction may be minutes away. Keep calcium gluconate and airway equipment at the bedside.

Normal total serum calcium is 8.6 to 10.2 mg/dL. Hypercalcemia is a level above 10.2 mg/dL; above roughly 13 mg/dL is a hypercalcemic crisis with risk of cardiac arrest and coma.

Hyperparathyroidism and malignancy account for the large majority of cases. Bone metastases, multiple myeloma, and tumors that secrete parathyroid hormone-related protein release calcium from bone. Prolonged immobilization, which mobilizes calcium out of bone. Excessive intake of calcium supplements, vitamin D, or calcium-containing antacids. Thiazide diuretics, which reduce calcium excretion. Lithium, sarcoidosis, adrenal insufficiency, and Paget disease.

Everything slows down and dries out. Neuro: lethargy, fatigue, confusion, personality change, stupor, and coma. Neuromuscular: profound muscle weakness, diminished or absent deep tendon reflexes, bone pain and pathologic fractures. Cardiac: bradycardia initially, hypertension, and dysrhythmias including heart block, with increased sensitivity to digoxin toxicity. GI: anorexia, nausea, vomiting, constipation, hypoactive bowel sounds, and abdominal pain from possible pancreatitis or peptic ulcer. Renal: polyuria and polydipsia progressing to dehydration, and flank pain from renal calculi.

Total calcium above 10.2 mg/dL with elevated ionized calcium. Parathyroid hormone is elevated in hyperparathyroidism and suppressed in malignancy-related hypercalcemia. Serum phosphate is typically low in hyperparathyroidism. BUN and creatinine may rise from dehydration and stones. ECG shows a shortened QT interval and shortened ST segment, with prolonged PR interval, bradycardia, and heart block at higher levels.

Give IV isotonic normal saline as prescribed; volume expansion is the first-line treatment because it dilutes calcium and promotes renal excretion, and loop diuretics may be added once the patient is rehydrated. Never use thiazide diuretics, which retain calcium. Administer calcitonin for rapid short-term lowering and bisphosphonates such as IV zoledronic acid or pamidronate for durable lowering in malignancy. Discontinue calcium supplements, vitamin D, and calcium-containing antacids, and restrict dietary calcium. Encourage fluid intake of 3 to 4 L per day if not contraindicated, and encourage weight-bearing mobility to keep calcium in bone. Strain urine for stones and monitor for renal calculi. Institute fall and fracture precautions because bones are fragile and the patient is weak and confused, monitor cardiac rhythm, and watch for digoxin toxicity.

Rule: hydrate with normal saline first. Hypercalcemia causes profound dehydration, and rehydration is both the treatment and the safety measure; thiazide diuretics are contraindicated because they make the calcium go higher.

Normal serum magnesium is 1.6 to 2.6 mg/dL (about 1.3 to 2.1 mEq/L). Hypomagnesemia is a level below 1.6 mg/dL. Reference ranges vary slightly between laboratories, so always interpret against the reporting lab's stated interval.

Chronic alcohol use disorder is the classic cause, through poor intake and renal wasting. Malnutrition, starvation, prolonged NPO status, and total parenteral nutrition without adequate magnesium. Malabsorption from Crohn disease, celiac disease, and after bowel resection or bariatric surgery. GI losses through prolonged diarrhea, nasogastric suction, and fistulas. Medications: loop and thiazide diuretics, aminoglycosides, amphotericin B, cisplatin, and long-term proton pump inhibitors. Uncontrolled diabetes with osmotic diuresis, and refeeding syndrome.

Magnesium behaves like calcium's partner, so a low level makes the patient hyperexcitable, and it looks a great deal like hypocalcemia. Neuromuscular: tremors, muscle twitching, cramps, tetany, hyperactive deep tendon reflexes, and positive Trousseau and Chvostek signs. Neuro: irritability, confusion, insomnia, and seizures. Cardiac: tachycardia, hypertension, and dysrhythmias, most importantly torsades de pointes; increased risk of digoxin toxicity. GI: dysphagia, anorexia, nausea, and decreased motility.

Serum magnesium below 1.6 mg/dL. Potassium and calcium are frequently low at the same time and are refractory to replacement until the magnesium is corrected, which is the single most useful fact about this electrolyte. ECG shows a prolonged PR and QT interval, widened QRS, ST depression, and flat or inverted T waves, with a strong tendency toward torsades de pointes and ventricular dysrhythmias.

Place the patient on cardiac monitoring and seizure precautions. Give oral magnesium for mild deficiency, warning the patient that diarrhea is the common side effect and that diarrhea itself worsens the deficiency. Give IV magnesium sulfate diluted and by infusion pump for severe or symptomatic deficiency, monitoring blood pressure, respiratory rate, and deep tendon reflexes during infusion, because too-rapid administration causes hypotension and cardiac arrest. Keep calcium gluconate available as the antidote for magnesium overshoot. Check and replace potassium and calcium alongside magnesium. Assess swallowing before oral intake if dysphagia is present. Hold magnesium-wasting medications as prescribed and teach magnesium-rich foods: green leafy vegetables, nuts and seeds, whole grains, legumes, and dark chocolate. Address alcohol use where relevant.

Rule: you cannot fix potassium or calcium until you fix magnesium. A patient with a stubbornly low potassium that will not come up despite replacement has a low magnesium until proven otherwise, and is at real risk of torsades de pointes.

Normal serum magnesium is 1.6 to 2.6 mg/dL (about 1.3 to 2.1 mEq/L). Hypermagnesemia is a level above 2.6 mg/dL. Deep tendon reflexes are typically lost as the level climbs, and respiratory depression and cardiac arrest follow at higher levels.

Kidney failure is by far the most common cause, because magnesium is excreted renally. Excessive intake of magnesium-containing antacids, laxatives, and enemas, particularly in patients with reduced renal function. IV magnesium sulfate therapy for preeclampsia and eclampsia, which is the classic obstetric scenario. Adrenal insufficiency, diabetic ketoacidosis at presentation, and extensive tissue injury or tumor lysis.

Magnesium is a natural sedative and vasodilator, so everything is depressed. Neuromuscular: the earliest and most important sign is diminished or absent deep tendon reflexes, followed by generalized weakness and flaccid paralysis. Neuro: drowsiness, lethargy, and coma. Respiratory: shallow respirations progressing to respiratory depression and arrest. Cardiac: bradycardia, hypotension, and dysrhythmias progressing to complete heart block and cardiac arrest. Other: facial flushing and a sensation of warmth, nausea and vomiting.

Serum magnesium above 2.6 mg/dL. Elevated BUN and creatinine in renal failure. Calcium may be low. ECG shows a prolonged PR interval, widened QRS, and prolonged QT interval, progressing to varying degrees of heart block, bradycardia, and asystole at high levels.

Stop all magnesium sources first: IV magnesium, magnesium-containing antacids and laxatives, and enemas. Assess deep tendon reflexes, respiratory rate, level of consciousness, blood pressure, and urine output on a set schedule; in a patient receiving magnesium sulfate infusion these assessments are the monitoring plan, and hourly urine output must stay above 30 mL/hr. Have IV calcium gluconate ready as the antidote and give it as prescribed for cardiac or respiratory compromise. Support ventilation and be prepared for intubation if respirations are depressed. Give IV fluids and loop diuretics as prescribed to increase excretion if renal function allows; dialysis is the definitive treatment in renal failure. Teach patients with chronic kidney disease to avoid over-the-counter magnesium-containing antacids and laxatives.

Rule: check deep tendon reflexes. Loss of the patellar reflex is the warning sign that comes before respiratory depression and cardiac arrest during magnesium sulfate therapy. Absent reflexes, a respiratory rate below 12, or urine output under 30 mL/hr means stop the infusion and get calcium gluconate.

Normal serum phosphate is 2.5 to 4.5 mg/dL. Hypophosphatemia is a level below 2.5 mg/dL; below about 1.0 mg/dL is severe and causes respiratory muscle failure, hemolysis, and rhabdomyolysis. Phosphate and calcium move in opposite directions, so a low phosphate is often paired with a high calcium.

Refeeding syndrome, which is the most important cause to anticipate: reintroducing carbohydrate to a malnourished patient drives phosphate into cells and can drop the level catastrophically within days. Malnutrition, starvation, chronic alcohol use disorder, and anorexia nervosa. Malabsorption and prolonged diarrhea. Overuse of phosphate-binding antacids containing aluminum, magnesium, or calcium. Hyperparathyroidism, which wastes phosphate. Respiratory alkalosis and treatment of diabetic ketoacidosis with insulin, both of which shift phosphate into cells. Extensive burns during the recovery phase.

Phosphate is required to make ATP, so a deficiency shows up as failure of energy-dependent tissue. Neuromuscular: profound muscle weakness including respiratory and cardiac muscle, muscle pain, rhabdomyolysis, and difficulty weaning from a ventilator. Neuro: irritability, confusion, paresthesias, seizures, and coma. Cardiac: decreased contractility, cardiomyopathy, and dysrhythmias. Hematologic: hemolytic anemia, impaired platelet function with bleeding, and impaired white cell function with increased infection risk. Skeletal: bone pain, osteomalacia, and fractures in chronic deficiency.

Serum phosphate below 2.5 mg/dL. Serum calcium is often elevated because of the reciprocal relationship. Magnesium is frequently low as well, particularly in alcohol use disorder and refeeding. Creatine kinase rises with rhabdomyolysis. ECG changes are nonspecific but the patient may show dysrhythmias from poor contractility.

Anticipate and prevent the problem in high-risk patients: check baseline phosphate, potassium, and magnesium before starting nutrition in a malnourished patient, advance feeding slowly, and monitor levels daily during the first several days. Give oral phosphate supplements with vitamin D as prescribed, warning about diarrhea. Give IV phosphate slowly by infusion pump for severe deficiency, monitoring for hypocalcemia and tetany, because phosphate replacement drives calcium down. Monitor respiratory status and muscle strength closely, since respiratory failure is the danger, and assess the patient's ability to wean from mechanical ventilation. Discontinue phosphate-binding antacids. Institute fall precautions, handle the patient gently to reduce fracture risk, and teach a diet including dairy, meat, fish, poultry, nuts, whole grains, and legumes.

Rule: refeeding syndrome is the scenario to recognize. In a severely malnourished patient, starting nutrition can crash the phosphate and cause respiratory and cardiac failure. Start feeding low and slow, and check phosphate, potassium, and magnesium daily.

Normal serum phosphate is 2.5 to 4.5 mg/dL. Hyperphosphatemia is a level above 4.5 mg/dL. Because phosphate and calcium are reciprocal, a high phosphate almost always accompanies a low calcium, and the symptoms the patient shows are usually the symptoms of hypocalcemia.

Kidney failure is the dominant cause, since the kidney is the main route of phosphate excretion; hyperphosphatemia is nearly universal in advanced chronic kidney disease. Excessive intake of phosphate-containing laxatives, enemas, or supplements. Massive cell breakdown releasing intracellular phosphate: tumor lysis syndrome, rhabdomyolysis, crush injury, and severe hemolysis. Hypoparathyroidism, which reduces phosphate excretion. Excessive vitamin D intake, which raises absorption. Diabetic ketoacidosis at initial presentation, before insulin shifts phosphate into cells.

There are few symptoms from the phosphate itself; what you see is hypocalcemia. Neuromuscular: numbness and tingling around the mouth and in the fingertips, muscle cramps, tetany, hyperactive reflexes, and positive Trousseau and Chvostek signs. Respiratory: laryngospasm in severe accompanying hypocalcemia. Cardiac: hypotension, prolonged QT interval, and dysrhythmias. Chronic: calcium-phosphate crystals deposit in soft tissue, causing itching, red-brown eye deposits, joint pain, and vascular calcification, and bone is weakened as calcium is pulled out of the skeleton.

Serum phosphate above 4.5 mg/dL with serum calcium usually below 8.6 mg/dL. Elevated BUN and creatinine when renal failure is the cause. Parathyroid hormone is elevated in secondary hyperparathyroidism of chronic kidney disease and low in hypoparathyroidism. Uric acid and potassium rise with tumor lysis syndrome. ECG reflects the low calcium with a prolonged QT interval.

Treat the underlying cause and remove phosphate sources: stop phosphate-containing laxatives, enemas, and supplements, and restrict dietary phosphate, which means limiting dairy, organ meats, nuts, whole grains, cola beverages, and processed foods with phosphate additives. Give phosphate-binding agents such as sevelamer, lanthanum, or calcium acetate exactly with meals or immediately after, since a binder taken between meals does nothing. Monitor calcium and manage hypocalcemia, including seizure precautions and airway assessment if the calcium is very low. Give IV fluids and loop diuretics as prescribed if renal function permits; dialysis is the definitive treatment in renal failure. For tumor lysis syndrome, expect aggressive hydration and close monitoring of potassium, uric acid, and renal function. Teach dialysis patients that binder adherence with every meal is what keeps their bones and blood vessels intact.

Rule: phosphate binders must be taken with food. Their entire mechanism is trapping dietary phosphate in the gut, and the nurse's other job is watching for the hypocalcemia that rides along with every high phosphate.

Normal values: pH 7.35 to 7.45, PaCO2 35 to 45 mm Hg, HCO3 22 to 26 mEq/L. Respiratory acidosis is pH below 7.35 with PaCO2 above 45 mm Hg. HCO3 is normal in the acute phase and rises above 26 mEq/L as the kidneys compensate over hours to days.

Anything that impairs ventilation and traps carbon dioxide. Airway and lung disease: COPD exacerbation, severe asthma, pneumonia, pulmonary edema, pneumothorax, atelectasis, and airway obstruction. Central respiratory depression: opioid or sedative overdose, anesthesia, head injury, and increased intracranial pressure. Neuromuscular failure: Guillain-Barre syndrome, myasthenic crisis, spinal cord injury above C4, amyotrophic lateral sclerosis, and residual neuromuscular blockade. Mechanical problems: chest trauma with flail chest, kyphoscoliosis, severe obesity with hypoventilation, abdominal distention, and inadequate ventilator settings.

Carbon dioxide is a cerebral vasodilator and a central nervous system depressant, so the brain shows it first. Neuro: headache, especially on waking, restlessness, drowsiness, confusion, and progression to stupor and carbon dioxide narcosis with coma. Respiratory: dyspnea, hypoventilation with shallow respirations, and in acute obstruction the patient may become quiet and tired, which is worse rather than better. Cardiovascular: tachycardia, dysrhythmias, warm flushed skin, and bounding pulses from vasodilation; hypotension in severe cases. Other: muscle twitching, tremor, and asterixis; hyperkalemia signs may appear as hydrogen ions move into cells and push potassium out.

Acute uncompensated: pH low, PaCO2 high, HCO3 normal. Partially compensated: pH still below 7.35 but HCO3 has risen above 26 mEq/L, showing the kidney has started retaining bicarbonate. Fully compensated: pH has returned into the 7.35 to 7.45 range but both PaCO2 and HCO3 remain abnormal and elevated; in full compensation the pH sits on the acidic half of normal, between 7.35 and 7.40, which is how you know acidosis was the original problem. PaO2 is often low as well. Serum potassium tends to be elevated in acute acidosis.

Assess and secure the airway, then improve ventilation, because the fix for retained carbon dioxide is always to move more air. Position the patient upright, encourage coughing and deep breathing, use incentive spirometry, and suction as needed. Administer oxygen as prescribed, using caution and low-flow delivery in chronic carbon dioxide retainers per orders. Support ventilation with bilevel positive airway pressure or mechanical ventilation when needed, and for a ventilated patient anticipate an increase in rate or tidal volume to blow off carbon dioxide. Give bronchodilators, corticosteroids, and antibiotics as prescribed, and reverse opioid-induced depression with naloxone if that is the cause. Maintain hydration to thin secretions, monitor pulse oximetry, end-tidal carbon dioxide, and serial ABGs, and monitor potassium and cardiac rhythm.

Rule: respiratory acidosis is fixed by ventilating, not by giving bicarbonate. A rising PaCO2 with a falling level of consciousness means the patient is tiring and is heading for respiratory arrest; prepare for ventilatory support rather than waiting for the next gas.

Normal values: pH 7.35 to 7.45, PaCO2 35 to 45 mm Hg, HCO3 22 to 26 mEq/L. Respiratory alkalosis is pH above 7.45 with PaCO2 below 35 mm Hg. HCO3 is normal acutely and falls below 22 mEq/L as the kidneys compensate by excreting bicarbonate.

Any cause of hyperventilation. Anxiety and panic attacks, and pain. Hypoxemia driving increased respiratory drive, as in pulmonary embolism, early pneumonia, asthma, high altitude, and anemia. Fever and sepsis, particularly early gram-negative sepsis. Central stimulation from head injury, stroke, brain tumor, salicylate (aspirin) overdose, and progesterone in pregnancy. Excessive mechanical ventilation with a rate or tidal volume set too high, which is an iatrogenic cause the nurse can detect and report.

Alkalosis makes nerves hyperexcitable, and the low carbon dioxide constricts cerebral vessels. Neuro: lightheadedness, dizziness, inability to concentrate, anxiety, and syncope. Neuromuscular: numbness and tingling around the mouth and in the fingers and toes, muscle cramps, twitching, hyperactive reflexes, carpal-pedal spasm, tetany, and seizures in severe cases. Respiratory: rapid deep breathing, air hunger, and chest tightness. Cardiovascular: tachycardia and dysrhythmias, particularly if potassium is low. Alkalosis also increases calcium binding to albumin, which drops ionized calcium and explains the tetany.

Acute uncompensated: pH high, PaCO2 low, HCO3 normal. Partially compensated: pH still above 7.45 with HCO3 fallen below 22 mEq/L. Fully compensated: pH back within 7.35 to 7.45 but sitting on the alkaline half, between 7.40 and 7.45, with both PaCO2 and HCO3 low. Serum potassium and phosphate often fall as they shift into cells, and ionized calcium falls. Check a salicylate level when the cause is not obvious.

Treat the cause rather than the number: relieve pain, treat fever and infection, correct hypoxemia with oxygen, and address anxiety. Stay with the anxious patient and coach slow controlled breathing; breathing into a paper bag is no longer recommended as routine practice because it risks hypoxia and masks serious causes such as pulmonary embolism. Never assume hyperventilation is anxiety until hypoxemia, pulmonary embolism, and sepsis have been considered. For the mechanically ventilated patient, anticipate reducing the respiratory rate or tidal volume as prescribed. Administer sedation or anxiolytics as prescribed, monitor ABGs and pulse oximetry, and monitor potassium, calcium, and cardiac rhythm. Institute safety measures for dizziness and possible syncope.

Rule: hyperventilation is a symptom, not a diagnosis. In a postoperative or immobilized patient, a sudden low PaCO2 with a high pH and shortness of breath is a pulmonary embolism until proven otherwise.

Normal values: pH 7.35 to 7.45, PaCO2 35 to 45 mm Hg, HCO3 22 to 26 mEq/L. Metabolic acidosis is pH below 7.35 with HCO3 below 22 mEq/L. PaCO2 is normal initially and falls below 35 mm Hg as the lungs compensate by hyperventilating.

Two mechanisms: gaining acid or losing base. Acid gain with a high anion gap: diabetic ketoacidosis, starvation ketosis, alcoholic ketoacidosis, lactic acidosis from shock, sepsis, or cardiac arrest, kidney failure with retained acids, and ingestions including salicylates, methanol, and ethylene glycol. Base loss with a normal anion gap: severe diarrhea, which loses bicarbonate-rich intestinal fluid, and is the classic exam cause; also intestinal or pancreatic fistulas, ileostomy output, ureteral diversions, renal tubular acidosis, carbonic anhydrase inhibitors such as acetazolamide, and excessive normal saline administration.

Neuro: headache, confusion, drowsiness, and progression to stupor and coma, which is often the presenting picture in diabetic ketoacidosis. Respiratory: Kussmaul respirations, deep and rapid breathing, which is the body compensating by blowing off carbon dioxide, plus a fruity acetone breath odor in ketoacidosis. Cardiovascular: hypotension, decreased cardiac contractility, warm flushed skin from vasodilation, and dysrhythmias, particularly from the accompanying hyperkalemia. GI: nausea, vomiting, abdominal pain, and anorexia. Neuromuscular: weakness and diminished reflexes.

Uncompensated: pH low, HCO3 low, PaCO2 normal. Partially compensated: pH still below 7.35 with PaCO2 fallen below 35 mm Hg as the lungs work. Fully compensated: pH back into 7.35 to 7.40, on the acidic half of normal, with both HCO3 and PaCO2 low. Calculate the anion gap (sodium minus the sum of chloride and bicarbonate; normal is roughly 8 to 12 mEq/L) to separate acid-gain from bicarbonate-loss causes. Serum potassium is typically elevated as hydrogen moves into cells and potassium moves out, even though total body potassium in diabetic ketoacidosis is depleted. Expect elevated glucose and ketones in DKA and elevated lactate in shock.

Treat the underlying cause, which is what actually fixes the pH: insulin and fluids for diabetic ketoacidosis, restoring perfusion in shock, stopping the diarrhea, or dialysis in renal failure. Maintain the airway and monitor respiratory status; Kussmaul breathing is protective, so do not sedate it away. Establish IV access and give fluids as prescribed. Monitor potassium relentlessly, because it looks high at presentation in DKA but falls sharply once insulin and fluids begin, and hypokalemia then becomes the threat; potassium replacement is usually started early in DKA treatment. Keep the patient on cardiac monitoring and perform frequent neurologic assessment with seizure and fall precautions. Sodium bicarbonate is reserved for severe acidosis, generally pH below about 7.1, and is given cautiously because it can worsen intracellular acidosis and cause hypokalemia. Monitor serial ABGs, glucose, and electrolytes.

Rule: watch the potassium during treatment. In diabetic ketoacidosis the potassium reads high but the patient is actually potassium-depleted, and insulin drives it into cells fast. The most dangerous moment is not admission, it is a few hours into treatment when the potassium plummets.

Normal values: pH 7.35 to 7.45, PaCO2 35 to 45 mm Hg, HCO3 22 to 26 mEq/L. Metabolic alkalosis is pH above 7.45 with HCO3 above 26 mEq/L. PaCO2 is normal initially and rises above 45 mm Hg as the lungs compensate by hypoventilating, though this compensation is limited because the patient still has to breathe.

Two mechanisms: losing acid or gaining base. Acid loss: prolonged vomiting and continuous nasogastric suction, which strip hydrochloric acid from the stomach and are the classic causes. Base gain: excessive sodium bicarbonate administration, overuse of bicarbonate-containing antacids, and massive transfusion of citrated blood, since citrate is metabolized to bicarbonate. Also loop and thiazide diuretics, hyperaldosteronism and Cushing syndrome, and severe hypokalemia, which drives hydrogen into cells. Milk-alkali syndrome from large intakes of calcium plus absorbable alkali.

Alkalosis makes nerves and muscles irritable and drops ionized calcium. Neuromuscular: numbness and tingling of the fingers, toes, and around the mouth, muscle cramps and twitching, hyperactive deep tendon reflexes, carpal-pedal spasm, tetany, and positive Trousseau and Chvostek signs. Neuro: dizziness, irritability, agitation, confusion, and seizures. Respiratory: slow shallow compensatory breathing, sometimes with periods of apnea. Cardiovascular: tachycardia and dysrhythmias, worsened by the hypokalemia that usually accompanies it. GI: nausea, vomiting, and anorexia, which may be both cause and effect.

Uncompensated: pH high, HCO3 high, PaCO2 normal. Partially compensated: pH still above 7.45 with PaCO2 risen above 45 mm Hg. Fully compensated: pH back into 7.40 to 7.45, on the alkaline half of normal, with both HCO3 and PaCO2 elevated. Serum potassium is usually low as potassium shifts into cells in exchange for hydrogen, and serum chloride is often low, particularly with vomiting or nasogastric suction. Ionized calcium falls, explaining the tetany. ECG may show the flattened T waves and U waves of hypokalemia.

Treat the cause: control vomiting with antiemetics, minimize and correctly manage nasogastric suction, and stop bicarbonate or antacid overuse. Irrigate nasogastric tubes with normal saline rather than plain water, because water irrigation washes out more electrolytes. Replace fluid and electrolytes with isotonic normal saline as prescribed, which supplies the chloride the kidney needs to excrete bicarbonate; replace potassium as prescribed, since alkalosis rarely resolves while potassium remains low. Monitor potassium, chloride, calcium, and serial ABGs, keep the patient on cardiac monitoring, and institute seizure and safety precautions. Monitor respiratory status, since compensatory hypoventilation can cause hypoxemia, and administer oxygen as prescribed. Teach patients not to self-treat indigestion with large amounts of bicarbonate-containing antacids.

Rule: metabolic alkalosis and hypokalemia travel together. Vomiting or nasogastric suction predicts a high pH, a high bicarbonate, and a low potassium and chloride; correct the potassium and give chloride-containing fluid or the alkalosis will not resolve.

Normal arterial values: pH 7.35 to 7.45 (midpoint 7.40), PaCO2 35 to 45 mm Hg, HCO3 22 to 26 mEq/L, PaO2 80 to 100 mm Hg, SaO2 95 to 100 percent, and base excess minus 2 to plus 2 mEq/L. Remember which value belongs to which system: PaCO2 is the respiratory value and is an acid; HCO3 is the metabolic value and is a base. Below pH 7.35 is acidosis, above 7.45 is alkalosis.

ABGs are drawn to evaluate oxygenation, ventilation, and acid-base status: in respiratory failure, during mechanical ventilation and after ventilator changes, in shock and sepsis, in diabetic ketoacidosis, in kidney failure, in overdose, and after cardiac arrest. Sampling is from an artery, usually the radial, and the Allen test is performed first to confirm collateral ulnar circulation. The sample is placed on ice and transported immediately, air bubbles are expelled because they falsely raise PaO2, and firm pressure is held over the site for at least 5 minutes, or longer if the patient is anticoagulated.

Use this five-step method on any ABG. Step 1: look at the pH. Below 7.35 is acidosis, above 7.45 is alkalosis, and within range means either normal or fully compensated. Step 2: look at the PaCO2. Above 45 is acidic, below 35 is alkaline. Step 3: look at the HCO3. Below 22 is acidic, above 26 is alkaline. Step 4: decide which value matches the pH. If the PaCO2 moved in the same acid-base direction as the pH, the problem is respiratory; if the HCO3 matches the pH, the problem is metabolic. A quick way to hold this: pH and PaCO2 moving in opposite directions (one up, one down) points respiratory, while pH and HCO3 moving in the same direction points metabolic. Step 5: decide the degree of compensation, then always finish by reading the PaO2 and SaO2 separately to judge oxygenation, because a patient can have a perfect pH and still be hypoxemic.

Compensation has three states. Uncompensated: the pH is abnormal and only one of PaCO2 or HCO3 has moved; the other is still normal. Partially compensated: the pH is still abnormal, and both PaCO2 and HCO3 are abnormal, meaning the opposing system has started to correct but has not finished. Fully compensated: the pH has returned inside 7.35 to 7.45, but both PaCO2 and HCO3 remain abnormal. To name a fully compensated gas, use which side of 7.40 the pH sits on, because the body never overcorrects: a pH of 7.35 to 7.39 with both values abnormal is a compensated acidosis, and a pH of 7.41 to 7.45 with both values abnormal is a compensated alkalosis. Then look at whether the PaCO2 or the HCO3 is the one causing rather than correcting that direction to say whether it is respiratory or metabolic. Worked examples: pH 7.28, PaCO2 58, HCO3 24 is uncompensated respiratory acidosis. pH 7.30, PaCO2 58, HCO3 32 is partially compensated respiratory acidosis. pH 7.37, PaCO2 60, HCO3 34 is fully compensated respiratory acidosis. pH 7.22, PaCO2 30, HCO3 14 is partially compensated metabolic acidosis. pH 7.50, PaCO2 30, HCO3 23 is uncompensated respiratory alkalosis. pH 7.52, PaCO2 48, HCO3 34 is partially compensated metabolic alkalosis.

Perform the Allen test before radial puncture and document the result. After the draw, hold direct pressure for at least 5 minutes and longer for anticoagulated patients, then assess the site and distal circulation, color, temperature, and pulse. Send the iced sample immediately, and note on the requisition the patient's oxygen delivery and flow rate and body temperature, since all of these change interpretation. Recheck ABGs about 20 to 30 minutes after a ventilator setting change or a significant intervention, or as ordered. Correlate the gas with the patient in front of you: the trend and the clinical picture matter more than a single value. Report a pH below 7.35 or above 7.45 with new symptoms, a PaO2 below 60 mm Hg, or an SaO2 below 90 percent promptly.

Rule: match the abnormal value to the pH to name the problem, then judge compensation, then read the oxygen last and separately. And no matter what the gas says, assess the patient: a normal pH with a rising PaCO2 and a sleepy patient is a failing patient, not a stable one.