Ch 20 - Fluids, Electrolytes, Acid-Base

Intracellular fluid

2/3rds or 66%

Extracellular fluid

1/3rd or 33% of all bodily fluids. Consists of 80% interstitial fluid, 20% plasma.

Water gain

Ingestion and metabolic synthesis

Water loss

Urine, feces, perspiration, lung exhalation

Thirst response

Increased osmolarity, low BP → stimulates thirst center in hypothalamus to drink more water

Antidiuretic hormone (vasopressin)

Increased osmolarity, low blood volume, low BP → Posterior pituitary releases hormone → Inserts aquaporin-2s into principal cells of distal tubule and collecting duct → increased water reabsorption → Corrected osmolarity, blood volume, BP

Receptors for thirst response and ADH release

Hypothalamic osmoreceptors, Atrial blood volume receptors, Baroreceptors in aortic arch, carotid artery, juxtaglomerular cells of kidney

Renin-angiotensin-aldosterone pathway

Low BP → Renin from kidney → Conversion of angiotensinogen (from liver) to angiotensin 1 → ACE in lungs converts to angiotensin 2 → vasoconstriction, aldosterone from adrenal cortex → increased Na+/H2O reabsorption → Increased blood volume and BP

Aldosterone

Released from adrenal cortex to increase Na+ reabsorption in late distal tubule, which promotes water reabsorption. Stimulated by low BP or Na+. Final component of RAA pathway

Atrial natriuretic peptide

Atrial volume receptors detect increased volume, stretch → Released to increase Na+ excretion in urine to promote water loss → Lower blood volume, BP

Electrolytes

Ions dissolved in bodily fluids that control osmosis between fluids, maintain acid base balance, carry electrical current, and serve as enzyme cofactors

Higher concentration outside cell

Na+, Ca2+, Cl-, HCO3-

Higher concentration inside cell

K+, Mg2+, HPO4 (2-), protein anions

Na+

Most abundant extracellular cation. Role in APs. Increased by ANP, ADH (indirectly via H2O). Lowered by ANP.

Cl-

Most abundant extracellular anion. Mostly moves across membranes via leak channels. Balances anion levels in different compartments

K+

Most abundant intracellular cation. Establishes resting membrane potential, controls repolarizing phase.

HCO3-

Mechanism of CO2 homeostasis, increases blood pH.

Ca2+

Major NT signaling molecule that is PTH regulated, largely stored in bone.

HPO4(2-)

Buffer, especially in kidneys - controls H+/urine pH.

Mg2+

Cofactor for many enzymes

Carbonic acid-bicarb buffer system

High pH: H2CO3 dissociates into H+ and HCO3-

Low pH: H+ and HCO3- combine to form H2CO3

Largely intracellular - RBCs, alveoli, kidneys

protein buffer system

High pH: C-term releases H+

Low pH: N-term bonds H+, forming NH3+

Hgb is most important in RBCs

Hemoglobin

High pH: H2CO3 → H+ + HCO3-

Low pH: Binds H and releases O. Hb-O2 + H+ → Hb-H + O2

phosphate buffer system

High pH: Donates H to OH- to form water — OH- + H2PO4- → H2O + HPO4 (2-)

Low pH: Binds H+ to form dihydrogen phosphate. H+ + HPO4 (2-) → H2PO4-

Intracellular, controls urine pH.

High CO2 - Low pH

RR increases

Low CO2 - High pH

RR decreases

respiratory acidosis

High CO2 (consequently high H+ via carbonic acid rxn) - low pH. Caused by hypoventilation - drug OD, emphysema.

Compensation: increased HCO3- reabsorption and H+ excretion

metabolic acidosis

Low HCO3- (consequently low CO2) and low pH due to loss of base - severe diarrhea, acid accumulation, renal dysfunction, DKA.

Compensation: hyperventilation

respiratory alkalosis

Low CO2 level, high pH caused by hyperventilation.

Compensation: decreasing HCO3- reabsorption and H+ excretion.

metabolic alkalosis

High HCO3- due to acid loss - excessive vomiting, endocrine disorder, excessive antacids.

Compensation: hypoventilation.

Female body mass

45% solids, 55% fluids

Male body mass

40% solids, 60% fluids