fluid,electrolyte and acid&base balance 2

Electrolyte balance

usually refers only to salt balance even though electrolytes also include acids and bases, and some proteins

• Salts control fluid movements, and provide minerals (ions) for excitability, secretory activity, and permeability of cell membranes

– Including: sodium (Na+) potassium (K+) calcium (Ca2+) and phosphate 2

(HPO4 2-)

• Salts enter body by ingestion (some liberated during metabolism)

– Lost via perspiration, feces, urine, vomit

Hypernatremia

— Na+ excess

• Causes: Dehydration; uncommon in healthy individuals; may occur in infants, older adults, or any individual unable to indicate thirst; or may result from excessive intravenous NaCl administration

• Symptoms: Thirst. CNS dehydration leads to confusion and lethargy progressing to coma; increased neuromuscular irritability evidenced by twitching and convulsions.

Hyponatremia

— Na+ deficit

• Possible Cause: Solute loss, water retention, or both (e.g., excessive Na loss through vomiting, diarrhea, burned skin, gastric suction, or excessive use of diuretics); deficiency of aldosterone renal disease; excess A D H release; excess H 2 O ingestion

• Symptoms: Neurologic dysfunction due to brain swelling:mental confusion; giddiness; coma if development occurs slowly; muscular twitching, irritability, and convulsions if the condition develops rapidly.

• In hyponatremia accompanied by water loss, the main signs are decreased blood volume and blood pressure

hyperkalemia

— K+ excess

• Possible Cause: Renal failure; deficit of aldosterone; rapid intravenous infusion of KCl; burns or severe tissue injuries that cause K super plus to leave cells

• Symptoms: Nausea, vomiting, diarrhea; bradycardia; cardiac arrhythmias and arrest; skeletal muscle weakness; flaccid paralysis.

Hypokalemia

— K+ deficit

• Possible Cause: Gastrointestinal tract disturbances (vomiting, diarrhea), gastric suction; Cushing’s syndrome (high cortisol); inadequate dietary intake (starvation); hyperaldosteronism; diuretic therapy

• Symptoms: Cardiac arrhythmias, flattened T wave on ECG; muscular weakness; metabolic alkalosis; mental confusion; nausea; vomiting.

Hyperphosphatemia

— HPO4 2- excess

• Possible Cause: Decreased urinary loss due to renal failure; hypoparathyroidism; major tissue trauma; increased intestinal absorption

• Symptoms: Clinical symptoms arise because of reciprocal changes in Ca 2+ levels rather than directly from changes in plasma phosphate concentrations

Hypophastemia

— HPO4 2- deficit

• Possible Cause: Decreased intestinal absorption; increased urinary output; hyperparathyroidism

• Symptoms: Clinical symptoms arise because of reciprocal changes in Ca 2+ levels rather than directly from changes in plasma phosphate concentrations.

Hyperchloremia

— Cl- excess

• Possible Causes: Dehydration; increased retention or intake; metabolic acidosis; hyperparathyroidism

• Symptoms: No direct clinical symptoms; symptoms generally associated with the underlying cause, which is often related to pH abnormalities.

Hypochloremia

— Cl- deficit

• Possible Causes: Metabolic alkalosis (e.g., due to vomiting or excessive ingestion of alkaline substances); aldosterone deficiency

• Symptoms: No direct clinical symptoms; symptoms generally associated with the underlying cause, which is often related to pH abnormalities.

Hypercalcemia

— Ca2+ excess

• Possible Causes: Hyperparathyroidism; excessive vitamin D; prolonged immobilization; renal disease (decreased excretion); malignancy

• Symptoms: Decreased neuromuscular excitability leading to cardiac arrhythmias and arrest, skeletal muscle weakness, confusion, stupor, and coma; kidney stones; nausea and vomiting.

Hypocalcemia

— Ca2+ deficit

• Possible Causes: Burns (calcium trapped in damaged tissues); hypoparathyroidism; vitamin D deficiency; renal tubular disease; renal failure; hyperphosphatemia; diarrhea; alkalosis

• Symptoms: Increased neuromuscular excitability leading to tingling fingers, tremors, skeletal muscle cramps, tetany, convulsions; depressed excitability of the heart; osteomalacia; fractures.

Hypermagnesemia

— Mg2+ excess

• Causes Rare; occurs in renal failure when M g 2+ is not excreted normally; excessive ingestion of M g 2+ - containing antacids

• Symptoms: Lethargy; impaired CNS functioning, coma, respiratory depression; cardiac arrest.

Hypomagnesemia

— Mg2+ deficit

• Causes: Alcohol use disorder; chronic diarrhea, severe malnutrition; diuretic therapy

• Symptoms: Tremors, increased neuromuscular excitability, tetany, convulsions.

Central role of sodium

• Sodium most abundant cation, sodium salts most abundant solutes, in ECF

– NaHCO3 and NaCl contribute 280 of total 300 mOsm ECF solute concentration

• Only cation exerting significant osmotic pressure

– Controls ECF volume and water distribution because water follows salt

– Change in blood Na+ levels affect blood volume and pressure, but also ICF and IF volumes

• Na+ that leaks into cells is pumped out against its electrochemical gradient

• Na+ moves between ECF and body secretions (e.g., digestive secretions)

• Renal acid-base control mechanisms are coupled to Na+ transport

Concentration of Na+

▪ Stable because of water shifts between compartments

▪ Determines ECF osmolality, and influences excitability of neurons and muscles

▪ Controlled long term by thirst and ADH

Content of Na+

▪ Total Na+ content determines ECF volume and therefore blood pressure

▪ Regulated by hormones:

– Renin-angiotensin-aldosterone system increases Na+ content

– Atrial natriuretic peptide (ANP) decreases Na+ content

regulation of sodium balance

• Na+ -water balance coupled to blood pressure and volume control mechanisms (no known receptors that directly monitor Na+ levels in body fluids)

• Changes in BP or volume trigger neural and hormonal controls to regulate Na+ content

Aldosterone

plays biggest role in regulation of Na+

▪ Regardless of aldosterone presence

– 65% of filtered Na+ is reabsorbed in the PCT and another 25% in the nephron loops; only 10%∼ remains entering DCT and CD

Aldosterone concentrations are high

most of the remaining filtered Na+ is actively reabsorbed in the DCT and CD

– Water follows, so ECF volume increases

Aldosterone concentration are low

most of the remaining filtered Na+ is excreted

– Water follows (into urine), so ECF volume decreases

Atrial natriuretic peptide

– High BP stretches atrial (heart) cells, causing them to secrete______

– ________ decreases blood pressure and blood volume via:

▪ Inhibits ADH, renin (so angiotensin II),and aldosterone production

– Increases excretion of Na+ (natriuresis) and water (diuresis)

– Promotes vasodilation directly, and by decreasing production of angiotensin I

Female sex hormones

▪ Estrogens (like aldosterone chemically) increase Na+ (salt) reabsorption in renal tubules (like aldosterone), which can lead to:

– Salt and water retention during menstrual cycles and pregnancy

▪ Progesterone causes mild diuresis (probably blocks aldosterone receptors)

Glucocorticoids

▪ At high levels, ________ increase salt reabsorption in renal tubules (like aldosterone); water follows, which can lead to edema

Cardiovascular baroreceptors

– Baroreceptors alert brain to reduce S N S stimulation of the kidneys if blood volume and B P rise (opposite if they fall); decreased sympathetic output causes:

▪ Afferent arterioles dilate →G F R increases →Na+ (salt) and water output increase → blood volume and pressure decline back to normal

Potassium balance

• Potassium (K )+ is most abundant ICF cation; required for essential metabolic activities, including functioning of the “excitable” cells (neurons and muscle cells)

– ICF-ECF K+ concentrations directly affect resting membrane potential (RMP)

– Abnormal [K ]+ (hyper- or hypokalemia) in heart can interfere with electrical conduction, leading to sudden death

• K+ is also part of body’s buffer system: H+ shifts into and out of cells in exchange for K+ to maintain cation balance

– So ECF K+ levels rise with acidosis and fall with alkalosis

– pH driven shifts in K+ can affect ECF [K ]+ and therefore activity of excitable cells

regulatory site of potassium

the DCT and collecting duct

– K+ balance is controlled in DCT and collecting ducts by regulating amount secreted into filtrate (after reabsorbing 90%∼ in the PCT and nephron loop)

▪ High ECF K+ content favors principal cell secretion of K+

▪ Low ECF K+ causes principal cells to minimize secretion of K+

– Also, type A intercalated cells can reabsorb some K+ left in filtrate

– Kidneys have limited ability to retain K+ (regulation revolves around excretion), so K+ loss (in urine) that exceeds K+ intake leads to hypokalemia

influence of plasma potassium concentration

– Most important factor affecting K + secretion is its concentration in E C F

– High K + diet leads to increased K +content of E C F, which increases K + entry into principal cells, and their subsequent secretion

▪ Low K + diet or accelerated K + loss reduces its secretion and promotes its limited reabsorption