Fluids and Electrolytes

human body is BLANK % water

60

intracellular fluid (ICF)

fluid inside cells

extracellular fluid (ECF)

fluid outside the cells

interstitial fluid (ISF)

between the cells, tissue

intravascular fluid

inside the blood vessels

transcellular fluid (TSF)

body spaces

osmosis

movement of water across a membrane, water moves from low solute concentration to high solute concentration

osmotic pressure

determined by the volume of fluid in a compartment

hormones that can have control over body fluids

antidiuretic hormone, aldosterone, atrial natriuretic peptide

antidiuretic hormone

promotes reabsorption of water in the kidneys

aldosterone

increases reabsorption of sodium and water in the kidneys

atrial natriuretic peptide

stimulates renal vasodilation and suppresses aldosterone, increasing urinary output

nervous control of body fluids

thirst mechanism triggered by deceased blood volume and increased osmolarity

edema

excess fluid in the interstitial space

hypervolemia

fluid volume excess in intravascular space

water intoxication

excess fluid in the intracellular space

what is fluid excess caused by

excessive sodium/water intake or inadequate sodium/water elimination (heart, lung, liver, and renal failure)

manifestations of fluid excess

peripheral edema, periorbital edema, cerebral edema, jugular vein distension, hypertension, polyuria, rapid weight gain, crackles, bulging fontanelles

hypovolemia

fluid volume deficit, decreased fluid in the intravascular space

what are fluid deficits caused by

inadequate fluid intake or excessive fluid/sodium losses

fluid deficits

decrease in fluid level leads to increase in level of blood solutes, cell shrinkage, and hypotension

manifestations of fluid deficits

thirst, altered level of consciousness, hypotension, flat jugular veins, dry mucous membranes, decreased skin turgor, oliguria, weight loss, sunken fontanelles

cations

positively charged electrolytes

anions

negatively charged electrolytes

electrolyte balance plays a role in →

muscle and neural activity and acid-base and fluid balance

soidum

most significant cation, controls serum osmolarity/water balance, facilitates muscles and nerve impulses, plays role in acid-base balance

depolarization

sodium moves into cells

repolarization

sodium moves out of the cell

what is the main source of sodium and potassium?

dietary intake

how are sodium and potassium excreted?

excreted through the kidneys and GI tract

what is sodium controlled by?

• aldosterone: sodium retention in kidneys

• angiotensin: sodium retention

• sympathetic system: increases glomerular filtration rate, increases sodium excretion

hypernatremia

too much sodium, serum osmolarity increases, resulting in fluid shifts into the vascular compartments

causes of hypernatremia

excessive sodium, deficient water

manifestations of hypernatremia

increased thirst, dry and sticky mucous membranes, headache, seizures, dysphagia, lethargy, coma, BP changes, tachycardia, decreased urine output

hyponatremia

too little sodium, serum osmolarity decreases, water shifts into cells causing cellular swelling

causes of hyponatremia

deficient sodium, excessive water

manifestations of hyponatremia

upset GI, poor skin turgor, dry mucous membranes, BP changes, pulse changes, edema, headache, diminished deep tendon reflexes, muscle weakness, seizure, and coma

potassium

primary intracellular cation; plays role in electrical conduction, acid-base balance, and metabolism; inverse relationship with sodium, serum potassium cannot fluctuate much without causing serious issue especially to heart

what happens when potassium is out of normal range?

paresthesia, muscle weakness, flaccid paralysis, dysrhythmias, cardiac arrest, respiratory depression, abdominal cramping, nausea, constipation or diarrhea

hyperkalemia

too much potassium

causes of hyperkalemia

• deficient excretion: renal failure, addison’s disease, certain medications and syndromes

• excessive intake: oral potassium supplements, salt substitutes, and rapid IV administration of potassium

• increased release from cells: acidosis, blood transfusions, and burns or any other cellular injuries

hypokalemia

too little potassium

causes of hypokalemia

• excessive loss: vomiting, diarrhea, laxatives, diuretic, and corticosteroids

• deficient intake: malnutrition, extreme dieting, and alcoholism

• increased shift into the cell: alkalosis and insulin excess

calcium

found in bone and teeth; plays a role in blood clotting, hormone secretion, receptor functions, nerve transmission, and muscular contraction

what is the main source of calcium?

vitamin d aids absorption, absorbed through the GI tract (small intestine), excreted in urine and stool

what is calcium regulated by?

vitamin K, parathyroid hormone, and calcitonin

hypercalcemia

too much calcium

causes of hypercalcemia

• increased intake or release: calcium antacids, calcium supplements, cancer, immobilization, vitamin D deficiency

• deficit excretion: renal failure, diuretics, and hyperparathyroidism

manifestations of hypercalcemia

dysrhythmias, personality changes, confusion, decreased memory, headache, lethargy, stupor, coma, muscle weakness, decreased deep tendon reflexes, nausea, vomiting, constipation, abdominal pain, pancreatitis, renal calculi, polyuria, and dehydration

hypocalcemia

too little calcium, increases cellular excitability

causes of hypocalcemia

• excessive losses: hypoparathyroidism, renal failure, alkalosis, pancreatitis, diarrhea

• deficient intake: decreased dietary intake, alcoholism, absorption disorders, and hypoalbuminemia

manifestations of hypocalcemia

dysrhythmias, increased bleeding, anxiety, confusion, depression, irritability, fatigue, paresthesia, increased deep tendon reflexes, tremors, muscle spasms, seizures, laryngeal spasms, increased bowel sounds, abdominal cramping, positive Trousseau’s and Chvostek’s signs

acid-base balance

measured by pH

what helps maintain acid-base balance?

body fluids, kidneys, and lungs

what forms carbonic acids?

CO2 molecules combine with water in your blood

what does carbonic acid break down into?

Carbonic acid breaks down in the kidneys into H ions and Bicarbonate ions increasing the acidity (lower pH)

what does excess CO2 equal?

Excess CO2 = Increased H ions = lower pH

what three systems work to maintain acid-base balance?

the buffers, respiratory system, renal system

buffer system

chemicals that combine with an acid or base to change pH, critical in maintaining blood pH, bind to acid or base to neutralize, immediate reaction to counteract pH variations until compensation is initiated

four major buffer mechanisms

• bicarbonate: carbonic acid system, buffers blood and interstitial fluids

• protein system: intra and extracellular acids and bases — most abundant buffers

• phosphate system: renal tubules

• hemoglobin system: weak acid, capillary system

respiratory system in pH regulation

manages pH by altering CO2 excretion, uses chemoreceptors, responds quickly but is short lived

what does speeding up respirations do to pH?

Speeding up respirations will excrete more carbon dioxide, decreasing acidity (lower pH)

what does slowing down respirations do to pH?

Slowing down respirations will excrete less carbon dioxide, increasing acidity (higher pH)

renal system in pH regulation

alters the excretion or retention of hydrogen or bicarbonate, more effective because it permanently removing hydrogen, responds slowest but lasts longest

acidosis

increased acidity, increased blood CO2 because of decreased respirations, acid build up

alkalosis

increased alkalinity, decreased blood CO2 because of increased respiration, acid loss

respiratory acidosis

results from CO2 retention, increased carbonic acid

what is respiratory acidosis caused by?

conditions that result in hypoventilation or decreased gas exchange — acute asthma exacerbations, COPD, airway obstructions, pulmonary edema, pneumonia, drug overdose, CNS depression

manifestations of respiratory acidosis

headache, blurred vision, tremors, muscle twitching, vertigo, irritability, disorientation, lethargy, coma, BP fluctuations, diaphoresis

metabolic acidosis

results from a deficiency or bicarbonate or an excess of hydrogen

causes of metabolic acidosis

• bicarbonate deficit: intestinal and renal losses

• acid excess: tissue resulting hypoxia resulting in lactic acid accumulation, ketoacidosis, drugs, toxins, and renal retention

respiratory alkalosis

results from excess exhalation of CO2, leads to carbonic acid deficits

causes of respiratory alkalosis

caused by conditions that result in hyperventilation — acute anxiety, pain, fever, hypoxia, gram-negative septicemia, aspirin overdose, excessive mechanical ventilation, and hypermetabolic states

manifestations of respiratory alkalosis

occur in combination with manifestations of underlying condition — paresthesia, dizziness, vertigo, syncope, muscle twitching, seizures, tachycardia, dysrhythmias, dry mouth, excessive diaphoresis, anxiety and coma

metabolic alkalosis

results from excess bicarbonate, deficient acid or both

causes of metabolic alkalosis

• excess bicarbonate: excessive antacid use, use of bicarbonate-containing fluids, hypochloremia

• deficient acid: GI loss, hypokalemia, renal loss, hypovolemia, hyperaldosteronism

manifestations of metabolic alkalosis

occur in combination with manifestations of underlying condition — mental confusion, hyperactive reflexes, paresthesia, seizures, respiratory depression, dysrhythmias, and coma