Water and electrolyte balance

water functions in body

solvent, transport, temperature regulation, maintain cell shape

electrolyte functions in body

maintain osmotic balance, generate electrical potentials, enzyme cofactors, acid‑base balance

daily water intake average

2300 ml (2100 ingested + 200 metabolism)

daily water output average

2300 ml (skin 350, lungs 350, sweat 100, feces 100, urine 1400)

positive water balance

intake > output

negative water balance

intake < output

major determinant of plasma fluid

plasma proteins + hydrostatic pressure

major determinant of interstitial fluid

hydrostatic and colloid osmotic forces

major determinant of intracellular fluid

ion gradients (Na+, K+, Cl‑, etc.)

plasma osmolarity formula

2.1 × plasma [Na+]

normal plasma osmolarity

280–295 mOsm/L

conditions altering plasma osmolarity

lipidaemias, hyperproteinemia, ketoacidosis, diabetes insipidus, chronic alcohol intoxication, chronic diarrhea

forces controlling fluid distribution

osmosis, colloid osmotic pressure, hydrostatic pressure

effect of isotonic saline

↑ECF volume only, no osmosis

effect of hypertonic saline

water moves out of cells, ↑ECF volume, ↓ICF volume, ↑osmolarity both compartments

effect of hypotonic saline

water moves into cells, ↑ICF > ↑ECF, ↓osmolarity both compartments

kidney role in water balance

excrete dilute urine or concentrate urine, regulate ECF Na+ and osmolarity

primary hormones regulating water/electrolytes

ADH, aldosterone, renin‑angiotensin, ANP

ADH function

stimulates water conservation, reduces free water clearance

aldosterone function

Na+ reabsorption, K+ excretion

renin‑angiotensin function

angiotensin II stimulates aldosterone release

ANP function

blocks aldosterone, ↑Na+ excretion, ↓thirst

stimuli for ADH secretion

decreased arterial pressure, decreased blood volume, nausea, vomiting, nicotine, morphine

drugs inhibiting ADH release

alcohol

urine osmolarity with max ADH

concentrated, net water gain

urine osmolarity with no ADH

dilute, net water loss

clinical case diabetes insipidus

lack of ADH → polyuria, dilute urine, hypernatremia, ↑serum osmolarity

normal plasma sodium concentration

135–145 mEq/L

average osmolarity of ECF

~300 mOsm/L (282 corrected for interionic attraction)

segmental sodium handling

major reabsorption in nephron, fractional reabsorption/excretion regulated

stimuli for aldosterone secretion

low renal blood flow, low GFR, renal sympathetic stimulation, ↑K+

ANP effect

blocks aldosterone, ↑Na+ excretion, lowers BP

hyponatremia mechanism

excess Na+ loss or excess water gain → water shifts into cells → swelling

hyponatremia symptoms

nausea, cramps, confusion, dizziness, coma, death

causes of excess sodium loss

adrenal insufficiency, diuretic use

causes of excess water gain

SIADH, ADH‑secreting tumor (bronchogenic carcinoma)

hypernatremia mechanism

water loss or sodium gain → water shifts to ECF → cell shrinkage

hypernatremia causes

dehydration, DI, IV sodium, ↑aldosterone, kidney failure, excess sodium intake

dehydration effects

↓ECF, ↑osmotic pressure, water drawn from ICF, shrunken cells, disturbed metabolism

major intracellular cation

K+

major extracellular cation

Na+

importance of potassium

maintains resting membrane potential

potassium source

diet

potassium loss

urine

factors increasing K+ excretion

↑ECF [K+], aldosterone secretion, ↑pH

renal handling of K+

90% reabsorbed in PCT, secreted in DCT under aldosterone

aldosterone effect on K+

↑K+ excretion, ↑Na+ reabsorption, ↑K+ into cells

insulin effect on K+

pushes K+ into cells with glucose uptake

epinephrine effect on K+

β‑receptor mediated K+ uptake into cells

acid‑base status effect on K+

reciprocal K+/H+ shifts between ICF and ECF

hypokalemia definition

plasma [K+] <3.5 mEq/L

hyperkalemia definition

plasma [K+] >5.5 mEq/L

hypokalemia causes

GI loss (diarrhea, vomiting), renal loss (diuretics, hyperaldosteronism), redistribution (insulin, epinephrine, alkalemia)

hypokalemia symptoms

muscle weakness, cramps, tetany, polyuria, polydipsia, orthostatic hypotension, ileus, ECG: flat T, U waves

hyperkalemia causes

acute renal failure, low aldosterone, ↑intake, acidosis, medications

hyperkalemia consequences

arrhythmia, acidaemia (H+ out of cells, K+ in)

insulin therapy in hyperkalemia

insulin + glucose drives K+ into cells

K+/H+ relationship

K+ out ↔ H+ in, K+ in ↔ H+ out to maintain neutrality

acid definition

donates H+ or accepts electrons

sources of acid

aerobic metabolism (CO2), anaerobic metabolism (lactic acid), ketoacids, sulphuric acid, phosphoric acid

base definition

neutralises acid

sources of base

dietary, metabolism of glutamate/aspartate → HCO3‑, citrate metabolism

buffer definition

resists pH change

main blood buffers

HCO3‑, hemoglobin, proteins

main tissue buffers

muscle proteins, bicarbonate, bone bicarbonate stores

normal arterial pH

7.35–7.45

acidemia definition

pH <7.35

acidosis definition

process leading to acidemia

alkalemia definition

pH >7.45

alkalosis definition

process leading to alkalemia

first line of pH buffering

blood buffers (HCO3‑, Hb, proteins)

respiratory role in pH

excrete or conserve CO2

renal role in pH

excrete H+, conserve/generate HCO3‑

equation for pH regulation

Henderson‑Hasselbalch equation

stimuli for thirst

angiotensin II, ADH, osmolarity changes

ANP effect on thirst

reduces thirst, blocks ADH and aldosterone

free water clearance definition

water excreted beyond solute clearance requirement

urine isotonic to plasma

no net gain/loss of solute or water

urine maximally concentrated

net water gain, more solute excreted than water

urine minimally concentrated

net water loss, more water lost than solute

polyuria in DI

loss of water due to absent ADH

serum osmolarity in DI

high (>295 mOsm/L)

urine osmolarity in DI

very low (<50 mOsm/L)

vasopressin therapy in DI

normalises serum and urine osmolarity

aldosterone secretion stimulus

angiotensin II from renin‑angiotensin system

renin function

cleaves angiotensinogen → angiotensin I

ACE function

converts angiotensin I → angiotensin II

angiotensin II function

stimulates aldosterone secretion

ANP secretion stimulus

high blood pressure, atrial stretch

consequence of hypernatremia

cell shrinkage, disturbed metabolism

consequence of hyponatremia

cell swelling, neurological symptoms

potent stimuli for ADH

nausea, vomiting

drug stimulating ADH release

nicotine, morphine

drug inhibiting ADH release

alcohol

fractional sodium reabsorption

percent of filtered Na+ reabsorbed in nephron segment

fractional sodium excretion

percent of filtered Na+ excreted in urine

aldosterone effect on principal cells

↑Na+ reabsorption, ↑K+ secretion

hyperkalemia ECG changes

peaked T waves, arrhythmia risk

hypokalemia ECG changes

flat T waves, U waves

relationship of acidosis and K+

acidosis → K+ out of cells → hyperkalemia