3. Fluids, Electrolytes and Acid-Base Balance

What does total body water (TBW) mean?

The total quantity of water in the body, distributed between intracellular and extracellular fluid compartments.

What proportion of body weight is TBW in non-elderly adult men and women according to the lecture?

About 60% in men and 50% in women.

How does the proportion of total body water change with age?

It generally decreases in older adults; the lecture lists approximately 50% for elderly men and 45% for elderly women.

What are the major fluid compartments and their approximate fractions of body weight?

Intracellular fluid about 40%; interstitial fluid about 15%; plasma about 5% (illustrated for a typical adult male).

What are the approximate fluid volumes in a 70-kg adult male from the lecture figure?

TBW 42 L: intracellular 28 L, interstitial 10.5 L and plasma 3.5 L.

What is the main extracellular cation and the main intracellular cation?

Sodium (Na+) is the main extracellular cation; potassium (K+) is the main intracellular cation.

How are mmol/L, mEq/L and mOsm/L different?

mmol/L describes amount of particles; mEq/L describes electrical charge equivalents; mOsm/L describes osmotically active particles.

What is the average daily water intake in the lecture?

Approximately 2,000 mL/day, roughly 75% from drinks and 25% from food.

What are the approximate daily water losses described in the lecture?

Urine 800–1,200 mL, stool about 250 mL, insensible loss about 600 mL; additional sweating or gastrointestinal losses vary.

How are insensible water losses distributed between skin and lungs?

Approximately 75% through the skin and 25% through the lungs.

Which conditions increase insensible water loss?

Fever, hypermetabolism and hyperventilation.

Which receptors help regulate water and circulating volume?

Osmoreceptors and baroreceptors.

What is the most common fluid disorder in surgical patients according to the lecture?

Extracellular fluid volume deficit (hypovolemia).

What are common causes of hypovolemia in surgical patients?

Gastrointestinal loss, third spacing, prolonged surgery, trauma, burns, peritonitis and bowel obstruction.

What are common causes of hypervolemia?

Excess administered fluids, renal insufficiency, congestive heart failure and cirrhosis.

What are typical signs of extracellular volume depletion?

Weight loss, decreased skin turgor, tachycardia, orthostatic hypotension, collapsed neck veins and oliguria.

What are typical signs of fluid overload?

Weight gain, peripheral edema, raised venous pressure, pulmonary edema and sometimes bowel edema or ileus.

Which commonly used parenteral solutions are listed?

0.9% sodium chloride, lactated Ringer's, 0.45% saline with dextrose, 5% dextrose in water and balanced electrolyte solutions.

How much sodium and chloride does 0.9% saline contain in the lecture table?

Approximately 154 mEq/L each of sodium and chloride.

What is the approximate electrolyte composition of lactated Ringer's solution in the lecture table?

Na+ 130, Cl− 109, K+ 4, calcium 3 and metabolizable buffer approximately 28 mEq/L.

What categories of alternative resuscitation fluids are presented?

Hypertonic saline and colloids such as albumin, dextran, hetastarch and gelatin-containing solutions.

What preoperative maintenance fluid regimen is given as an example in the lecture?

5% dextrose in 0.45% saline at 100 mL/h, with potassium only when renal function is normal.

What fluid type is recommended by the lecture for an obvious intravascular volume deficit?

An isotonic crystalloid solution.

What initial fluid challenge does the lecture describe for adults with cardiovascular signs of volume deficit?

An isotonic fluid bolus of 1–2 L followed by reassessment and continued tailored replacement.

What adult urine output target indicates adequate perfusion during resuscitation?

About 0.5–1 mL/kg/hour according to the lecture.

Which parameters guide fluid resuscitation effectiveness?

Vital signs, urine output, and in complicated cases improvement in base deficit and lactate.

What is an important principle of intraoperative fluid therapy?

Correct pre-existing deficits and replace ongoing losses while monitoring hemodynamic stability.

What postoperative fluid approach does the lecture describe?

Initially use isotonic fluid to treat hypovolemia and losses; later switch to maintenance therapy if oral intake is inadequate and replace measured drains or gastrointestinal losses.

When may potassium be added to postoperative IV fluid?

After ensuring adequate urine output and normal renal function.

What are the main ERAS principles for perioperative fluid management?

Allow clear liquids until about 2 hours preoperatively when appropriate; encourage early enteral intake; avoid excessive sodium/IV fluids and stop IV fluids promptly when possible.

Why is excessive perioperative fluid administration undesirable?

Fluid overload is associated with tissue edema, prolonged ileus and other postoperative complications.

How does the lecture define hyponatremia and when can severe symptoms occur?

The lecture uses Na+ below 130 mmol/L; severe symptoms often develop around Na+ below 120 mmol/L.

What are the two main mechanisms of hyponatremia?

Relative water excess (dilution) and sodium depletion.

How is chronic hyponatremia generally managed in the lecture?

Free-water restriction and sometimes salt supplementation, with slow, monitored sodium correction.

Why must chronic hyponatremia be corrected slowly?

Overly rapid correction can cause osmotic demyelination syndrome.

What correction limit does the lecture specify for chronic hyponatremia?

Up to 0.5 mmol/L/hour and about 4–6 mmol/L per 24 hours (lecture-specific target).

What treatment is described for acute symptomatic hyponatremia?

Carefully monitored hypertonic saline in an intensive-care setting.

How does the lecture define hypernatremia and when do prominent symptoms often appear?

Above approximately 145–150 mmol/L; symptoms are often prominent above 160 mmol/L.

How does hypernatremia commonly arise?

Relative water deficit compared with sodium, due to inadequate water intake or excessive free-water loss.

What options are described for replacing free water in hypernatremia?

Enteral free water when feasible or intravenous 5% dextrose, after stabilization of any intravascular volume deficit.

What correction rates for hypernatremia are described in the lecture?

Acute: up to 2 mmol/L/hour, no more than about 12 mmol/L/24 hours; chronic: approximately 0.5 mmol/L/hour.

How does the lecture define hyperkalemia and severe hyperkalemia?

Potassium above 5 mmol/L; severe values above 6.5 mmol/L require emergency assessment/treatment.

Why can a small rise in extracellular potassium be dangerous?

Only about 2% of total body potassium is extracellular, but it strongly affects cardiac and neuromuscular excitability.

What ECG changes are associated with hyperkalemia?

Peaked T waves, PR prolongation, reduced or absent P waves, QRS widening and potentially ventricular fibrillation.

What are the initial treatments for severe hyperkalemia in the lecture?

IV calcium gluconate for cardiac membrane stabilization; insulin with glucose and inhaled beta-agonist to shift potassium into cells; dialysis or renal excretion measures to remove potassium.

When may dialysis be needed in hyperkalemia?

If severe hyperkalemia persists despite initial treatment, especially with impaired renal function.

How is hypokalemia defined in the lecture?

Potassium below 3.5 mmol/L; severe hypokalemia below 2.5 mmol/L.

What ECG changes suggest hypokalemia?

Flattened T waves, ST changes, prominent U waves and arrhythmias.

How is hypokalemia treated according to severity?

Oral potassium for mild, asymptomatic chronic cases; carefully monitored IV potassium for severe or symptomatic cases.

Why should magnesium be checked when hypokalemia does not correct?

Hypomagnesemia can cause persistent renal potassium loss and refractory hypokalemia.

What is the function of calcium in the body?

Bone structure, neuromuscular activity and many cellular processes; the ionized, unbound fraction is physiologically active.

What ECG change is associated with hypercalcemia?

Shortened QT interval.

What are important causes of hypercalcemia in surgical patients?

Hyperparathyroidism, malignancy/bone metastases, PTH-related peptide production, hyperthyroidism and thiazides.

What is the treatment principle for severe hypercalcemia in the lecture?

Volume repletion as appropriate, calcitonin or bisphosphonates in selected severe cases, and sometimes dialysis.

What ECG change is associated with hypocalcemia?

Prolonged QT interval.

What causes of hypocalcemia are listed?

Hypoparathyroidism, pancreatitis, renal dysfunction, crush injury and severe soft-tissue infection.

How is symptomatic hypocalcemia treated in the lecture?

Parenteral calcium gluconate.

What is the main physiological role of phosphorus/phosphate?

Major intracellular anion important for ATP production, energy metabolism and bone structure.

Which patients are at risk of hypophosphatemia?

Malnourished or alcoholic patients, refeeding syndrome, excessive antacid use and patients after liver resection.

What are symptoms of severe hypophosphatemia?

Muscle and diaphragmatic weakness, respiratory failure, reduced cardiac output, diplopia, confusion, delirium and coma.

How is severe hypophosphatemia treated?

Carefully monitored IV sodium or potassium phosphate according to the patient's electrolyte status.

What can cause hyperphosphatemia, and what complication can it cause?

Severe renal disease or tissue injury; calcium-phosphate precipitation can produce hypocalcemia.

How is hyperphosphatemia managed in the lecture?

Treat the cause, use phosphate binders, enhance excretion when appropriate, and consider dialysis in renal failure.

What are the normal and abnormal magnesium cutoffs given in the lecture?

Hypomagnesemia below 0.65 mmol/L; hypermagnesemia above 1.05 mmol/L.

What causes and manifestations of hypomagnesemia are emphasized?

Malnutrition, alcoholism, prolonged diarrhea, diuretics or aminoglycosides; can cause tetany, weakness, seizures and refractory hypokalemia/hypocalcemia.

How is clinically significant hypomagnesemia treated?

Magnesium replacement, including IV magnesium sulfate when severe or symptomatic.

What are clinical findings of hypermagnesemia?

Weakness, lethargy, reduced deep-tendon reflexes and potentially cardiac arrhythmias.

How can severe hypermagnesemia be managed?

IV calcium gluconate for cardiac or neuromuscular toxicity, plus enhanced excretion or dialysis if necessary.

What is the normal arterial blood pH range?

7.35–7.45.

What are the main physiological blood buffer systems?

Bicarbonate–carbonic acid, hemoglobin, plasma proteins and phosphate.

How does respiratory compensation respond to metabolic acidosis or alkalosis?

Metabolic acidosis stimulates ventilation to lower PaCO2; metabolic alkalosis suppresses ventilation to retain CO2.

How do the kidneys compensate for respiratory acid-base abnormalities?

By changing hydrogen ion excretion and bicarbonate reabsorption/production.

What ABG findings define metabolic acidosis?

Reduced pH and low bicarbonate (HCO3− below about 24 mEq/L), with compensatory decrease in PaCO2.

What ABG findings define metabolic alkalosis?

Elevated pH and increased bicarbonate (HCO3− above about 24 mEq/L), with compensatory increase in PaCO2.

What ABG findings define respiratory acidosis?

Low pH with elevated PaCO2 (above about 40 mmHg in the lecture diagram), followed by renal bicarbonate retention.

What ABG findings define respiratory alkalosis?

High pH with decreased PaCO2 (below about 40 mmHg in the lecture diagram), followed by renal bicarbonate excretion.

How is the plasma anion gap calculated?

AG = Na+ − (Cl− + HCO3−).

What anion gap reference value is given in the lecture?

Less than approximately 12 mmol/L.

What are the broad mechanisms of metabolic acidosis?

Increased acid production or intake, reduced acid excretion, or loss of bicarbonate.

What is the central treatment of lactic metabolic acidosis due to shock?

Restore tissue perfusion and treat the underlying shock rather than treating a laboratory pH value alone.

When does the lecture consider bicarbonate therapy for metabolic acidosis?

Selected cases with severe acidemia (about pH 7.0–7.2 or below), normal-anion-gap acidosis or renal failure, under close supervision.

What are the main treatment principles for metabolic alkalosis?

Correct volume/chloride depletion with isotonic saline if appropriate, replace potassium and treat the cause; consider acetazolamide in selected euvolemic patients.

How is acute respiratory acidosis treated?

Treat the cause of hypoventilation and provide ventilatory support, including mechanical ventilation when severe.

How is respiratory alkalosis treated?

Treat the underlying cause of hyperventilation (e.g., pain or anxiety when relevant); well-compensated chronic cases may need no direct correction.

Why must chronic respiratory acid-base disorders not be corrected abruptly?

Rapid correction can create a significant secondary metabolic acid-base disturbance.