Chapter 4: Fluid, Electrolyte, and Acid–Base Homeostasis

What percentage of body weight is total body water in an average adult male vs. female, and why the difference?

~60% male, ~50% female. Adipose tissue holds less water than muscle, and females proportionally have more body fat than muscle compared to males.

A newborn and an older adult are both at elevated risk for fluid imbalance, but for different structural reasons. What are they?

Newborn: TBW is ~75% of body weight (vs adult ~60%), so proportionally larger fluid losses occur faster, and infants depend on others for intake. Older adult: TBW has decreased as muscle mass was replaced by adipose tissue, combined with diminished kidney function and blunted thirst mechanism.

Of total body water, what fraction is ICF vs ECF, and what fraction of body weight does each represent?

ICF = ~2/3 of TBW = 40% of body weight. ECF = ~1/3 of TBW = 20% of body weight.

Within the ECF, how is fluid split between the intravascular and interstitial spaces?

~1/4 of ECF is intravascular (blood plasma). ~3/4 of ECF is interstitial (between cells). A small remainder (~1.5%) is lymph and transcellular fluids.

Which single electrolyte dominates the ICF, and which dominates the ECF?

Potassium dominates the ICF (highest intracellular concentration). Sodium dominates the ECF (most abundant extracellular electrolyte, sets ECF volume/osmolality).

Sodium is 135-145 mEq/L in the ECF. What is normal serum potassium, and how does its intracellular concentration compare to its extracellular one?

Normal serum K+ is 3.5-5.0 mEq/L. Intracellular concentration is roughly 30 times higher than extracellular.

A solute needs a transport protein to cross the membrane but requires no ATP. What is this mechanism called, and how does it differ from active transport?

FACILITATED DIFFUSION -- passive, needs a protein but no energy, moves the solute down its gradient (glucose transport). ACTIVE TRANSPORT requires ATP and moves substances AGAINST their gradient (Na+/K+ pump). Needing a protein does not equal needing energy.

What is osmosis, and which direction does water move relative to solute concentration?

Water moving through a semipermeable membrane toward the side with MORE dissolved particles (lower water concentration), to equalize concentration on both sides.

What drives filtration, and where in the body is it the dominant exchange mechanism?

A PRESSURE DIFFERENCE across a membrane, not a concentration gradient. Dominant at the capillary level between intravascular and interstitial compartments.

At the arteriolar end of a capillary, which force wins and which direction does fluid move? What about the venous end?

Arteriolar end: hydrostatic pressure wins -> fluid moves OUT of the capillary. Venous end: osmotic pressure (from albumin) wins -> fluid moves back IN to the capillary.

Classify a solution as isotonic, hypotonic, or hypertonic, and state what happens to a cell placed in each.

Isotonic: same osmolality as ICF, no change. Hypotonic: fewer solutes than ICF, water moves IN, cell SWELLS. Hypertonic: more solutes than ICF, water moves OUT, cell SHRINKS.

Which IV fluid is isotonic when infused but becomes effectively hypotonic once metabolized, and why?

D5W -- the dextrose is metabolized, leaving free water behind, which is hypotonic.

Trace the RAAS cascade from a drop in renal perfusion to the three effects of angiotensin II.

Decreased renal perfusion -> juxtaglomerular apparatus releases renin -> converts angiotensinogen -> angiotensin I -> ACE (in the lungs) converts it to angiotensin II, which: (1) stimulates aldosterone -> Na+/water retention, (2) stimulates thirst + ADH, (3) causes direct vasoconstriction.

How do ACE inhibitors and ARBs lower blood pressure, given what angiotensin II normally does?

ACE inhibitors block the CONVERSION of angiotensin I to II; ARBs block angiotensin II from ACTING on its receptor. Either way, no vasoconstriction, and aldosterone/ADH secretion drops -- less water reabsorption, less volume, lower BP.

What triggers ADH release, and what are its two actions?

Triggered by hypotension and hyperosmolality. Actions: (1) increases water reabsorption at the cortical-collecting ducts; (2) vasoconstriction, but only at very high ADH levels.

What distinguishes ANP from BNP in terms of what triggers their release?

ANP -- released in response to atrial stretch. BNP -- released in response to ventricular stretch from volume overload. Both promote natriuresis, vasodilation, and suppress the RAAS.

Rank the three acid-base defense systems by speed and by long-term effectiveness.

Speed: chemical buffers (immediate) > respiratory (minutes to hours) > renal (days). Long-term effectiveness: renal (most effective) > respiratory (fast but incomplete) > buffers (first-line only).

What ratio of bicarbonate to carbonic acid does the body maintain to hold normal pH, and which enzyme speeds the underlying reaction?

20:1 (HCO3- : H2CO3), sped by carbonic anhydrase.

Why is the carbonic acid-bicarbonate system considered the most important physiological buffer?

It can be independently regulated by both the lungs (via CO2 elimination) AND the kidneys (via bicarbonate reabsorption/generation) -- no other buffer system has two independent regulatory organs.

Which buffer system plays a minor role in blood pH but a major role in buffering the ICF and renal tubules/urine?

The phosphate buffer system (H2PO4- / HPO4(2-) pair).

By what two mechanisms do the kidneys achieve net acid excretion?

(1) Phosphate buffering -- H+ binds phosphate in urine, excreted as NaH2PO4, while the HCO3- generated returns to blood. (2) Ammonium excretion -- proximal tubule metabolizes glutamate to excrete NH4+ while generating new HCO3-.

How does fluid volume depletion (FVD) differ from dehydration, and which compartment does each primarily contract?

FVD = proportionate loss of BOTH sodium and water (isotonic) -> contracts BLOOD VOLUME. Dehydration = loss of WATER ALONE -> disrupts the Na+:water ratio -> hypernatremia/hypertonicity -> contracts the ICF.

In heart failure, what is the mechanism that leads to fluid volume excess?

Decreased cardiac output -> decreased renal perfusion -> RAAS activation -> sodium and water retention. (Liver failure reaches the same endpoint via systemic/splanchnic vasodilation instead.)

Name the four mechanisms of edema formation and give one example condition for each.

Increased capillary hydrostatic pressure (heart failure); decreased capillary osmotic pressure (liver disease/malnutrition -- low albumin); increased capillary permeability (burns, inflammation); lymphatic obstruction (lymph node removal, tumors).

A patient develops sudden unilateral lower-extremity edema. What must be assessed immediately, and why does bilateral edema point elsewhere?

Deep vein thrombosis -- acute unilateral edema is the classic DVT red flag. Bilateral edema is more typical of chronic systemic causes (venous disease, heart failure, medications).

Why are loop diuretics preferred over thiazide or potassium-sparing diuretics for treating edema, and what electrolyte problem do they create that spironolactone offsets?

Loop diuretics act at the loop of Henle, where the largest fraction of filtered sodium is normally reabsorbed, giving the greatest diuresis, and remain effective in renal impairment. They cause hypokalemia; spironolactone (potassium-sparing) is added to retain K+ while adding to the diuresis.

Hyponatremia and hypernatremia are both fundamentally problems with which substance, not sodium itself?

WATER. Hyponatremia = water gain relative to sodium. Hypernatremia = water loss relative to sodium.

What is the maximum safe correction rate for severe hyponatremia in 24 hours, and what complication does overcorrection risk?

No more than 8 mEq/L in 24 hours (goal 4-6). Overcorrection risks OSMOTIC DEMYELINATION SYNDROME -- rapid sodium rise pulls water out of brain cells too fast, causing potentially irreversible nerve damage.

Describe the ECG changes for hypokalemia vs hyperkalemia.

Hypokalemia: prolonged QT, ST depression, flattened T wave, U wave appears/elevates. Hyperkalemia: tall, peaked T waves, shortened QT -> as it worsens, widened QRS, prolonged PR, P wave disappears -> V-fib.

Describe the pattern of muscle weakness in both severe hypokalemia and hyperkalemia.

Weakness is ASCENDING: lower extremities -> trunk -> upper extremities, potentially progressing to respiratory paralysis in severe cases of either.

In a hyperkalemic cardiac emergency, why is IV calcium given first, even though it doesn't lower serum potassium?

It STABILIZES THE CARDIAC CELL MEMBRANE within 1-3 minutes, counteracting hyperkalemia's excitatory effect on the heart. Insulin/glucose, beta-2 agonists, and potassium binders lower serum K+ but work more slowly and don't address the immediate membrane instability.

What is the hallmark clinical sign of acute hypocalcemia, and name the two bedside tests used to elicit it.

TETANY. Trousseau sign (BP cuff inflated above systolic x3 min -> carpal spasm) and Chvostek sign (tap facial nerve near the ear -> facial twitch).

A patient has low total serum calcium but also low albumin. What should the nurse suspect, and what confirms it?

PSEUDOHYPOCALCEMIA -- since ~40% of calcium is normally bound to albumin, low albumin makes total calcium look falsely low. Checking IONIZED calcium (the active, unbound fraction) clarifies whether true hypocalcemia is present.

Which electrolyte deficiency must be corrected first before potassium or calcium replacement will work, and why?

MAGNESIUM -- required for normal PTH secretion/response (affecting calcium) and independently causes renal potassium wasting when deficient.

What is the earliest sign of magnesium toxicity, and what is the antidote?

Diminished/absent deep tendon reflexes (DTRs) is the earliest sign. Calcium gluconate is the antidote.

Contrast hypomagnesemia and hypermagnesemia in terms of neuromuscular and CNS effects.

Hypomagnesemia -> HYPEREXCITABILITY: tremors, increased DTRs, tetany, seizures. Hypermagnesemia -> CNS/neuromuscular DEPRESSION: decreased DTRs (earliest sign), progressing to paralysis and respiratory failure. Mirror images of each other.

State the normal ranges for pH, PCO2, HCO3-, and the anion gap.

pH 7.35-7.45. PCO2 35-45 mm Hg. HCO3- 22-26 mEq/L. Anion gap 8-16 mEq/L (12-20 if potassium included).

Walk through the stepwise method for interpreting an ABG.

(1) Check pH -- acidosis or alkalosis? (2) Check PCO2 -- does it move with the pH (respiratory primary)? (3) Check HCO3- -- does it move with the pH (metabolic primary)? (4) Match the parameter that moved WITH the pH to identify the primary disorder. (5) Check whether the OTHER parameter moved OPPOSITE the pH -- that's compensation. (6) Check PaO2/SaO2 for hypoxemia.

Distinguish a high anion gap metabolic acidosis from a normal anion gap metabolic acidosis, and give two causes of each.

High AG = excess acid production -- e.g. lactic acidosis, DKA. Normal AG = bicarbonate loss (hyperchloremic) -- e.g. severe diarrhea, renal tubular acidosis.

An ABG shows a low pH, elevated PCO2, and a bicarbonate that has risen to compensate but pH is still only 7.33. What is this, and what's the timeframe difference from an acute presentation?

Chronic (partially compensated) respiratory acidosis -- classic for COPD. Renal compensation takes DAYS to develop; an acute presentation wouldn't show this compensation yet, and pH would be more severely abnormal.

Why must supplemental oxygen be given cautiously to a patient with chronic COPD and chronic respiratory acidosis?

Chronic CO2 retention desensitizes the normal CO2-driven respiratory drive, so low PO2 becomes the primary stimulus to breathe. Giving too much oxygen can remove that hypoxic drive -> respiratory depression -> worsening PCO2.

Trace the full mechanism by which an infant's projectile vomiting from pyloric stenosis produces metabolic alkalosis, hypokalemia, and hypochloremia simultaneously.

Vomiting loses gastric HCl and KCl. Losing H+ -> metabolic ALKALOSIS. Losing Cl- -> HYPOCHLOREMIA. Losing K+ -> HYPOKALEMIA. These losses also cause volume depletion, which further drives renal bicarbonate retention, sustaining the alkalosis.