chapter 8: fluid, electrolyte, and acid-base imbalances

intracellular fluid compartment (ECF)

fluids inside the cells

extracellular fluid compartment (ECF)

consist of:

• intravascular fluid (IVF): blood

• interstitial fluid (ISF): fluid surrounding cells

• transcellular fluids: cerebrospinal fluid (CSF), various secretions

distribution of water within the body

• newborn infant: 75-80%

• adult male: 55-60%

• adult female: 50-55%

• % w/ more water = higher chance for dehydration

distribution of major electrolytes within extra- & intracellular fluids

• 2/3 ICF (60-67%) - K & PO (phosphate)

• 1/3 ECF (33-40%) - Na & Cl-

  • interstitial fluid: 80%

  • blood plasma: 20%

fluid circulates throughout body via:

filtration and osmosis

filtration:

pushes fluid out of blood vessel

osmosis:

pulls water back toward blood vessel

water moves between vascular and interstitial compartments, with two pressures:

hydrostatic pressure and osmostic pressure

hydrostatic pressure

promotes filtration

osmotic pressure

promotes osmosis (reabsorption)

sodium is primary cation in:

ECF

sodium regulates:

osmotic forces, and diffuses between vascular and interstitial fluids

sodium transports into and out of:

cells by sodium-potassium pump, while actively secreting into mucus and other secretions

sodium exists in form of:

sodium chloride + sodium bicarbonate

aldosterone

increases sodium reabsorption from urine back into blood, and increases potassium excretion in urine

atrial natriuretic peptide (ANP)

increases excretion of sodium into urine, and increases water excretion due to osmosis

• blood pressure decreases due to loss of blood volume!!

sodium imbalance hyponatremia

plasma sodium concentration below 135 mEq/L

• common causes: losses from excessive sweating, vomiting, use of diuretic drugs + low-salt diet, excessive water intake

  • hormonal imbalances: insufficient aldosterone - decreases Na+ reabsorption, excessive ADH secretion: increases water reabsorption

• manifestations: result of decreased osmotic pressure in ECF compartment

  • water out of blood: ISF becomes hypotonic, fluid shifts into cell, and cerebral edema results in confusion, headache, seizures

low sodium levels cause fluid imbalance between compartments, causing:

hypotonic alteration, which is when ECF is less concentrated (hypotonic)

sodium imbalance hypernatremia

plasma sodium above 145 mEq/L

• common causes: insufficient ADH, water diarrhea, ingestion of large amounts of sodium without enough water

• manifestations: dry, rough mucous membranes, weakness, increased thirst

hypertonic alteration

ECF more concentrated, hypertonic

edema

excessive amount of fluid in the interstitial compartment, which causes swelling or enlargment of tissue + may impair tissue perfussion

causes of edema:

• increased capillary hydrostatic pressure (due to high BP or incr. BV)

• loss of plasma proteins, particularly albumin (decreased plasma osmo. pressure)

• obstruction of lymphatic circulation (excess fluid not returned to general circulation)

• increased capillary permeability (result from inflammatory response or infection)

manifestations of edema

1. pitting edema: presence of excess interstitial fluid: transudate; fluid moves aside when pressure is applied by finger - causing a pit

2. non-pitting edema: presence of excess fluid rich in protein (exudate: infllamatory fluid)

3. swelling, pain, impaired circulation: ischemia leading to tissue breakdown

fluid deficit - dehydration results from:

insufficient body fluid

• inadequate intake or excessive loss

  • ex: vomiting, diarrhea, excessive sweating

• diabetic ketoacidosis: loss of fluid, electrolytes, and glucose in urine

• use of concentrated formula in infants

third spacing of fluid in dehydration:

fluid shifts out of blood into body cavity + can no longer reenter vascular compartment

• common sites: ascites (accumulation of fluid in peritoneal cavity) + pleural effusion (amount of fluid in pleural cavity)

• result of: high osmotic pressure of ISF, as in burns

  • increased capillary permeability, as in some gram-negative infections

• manifestations: dry mucous membranes in mouth, decreased skin turgor, low BP, increased hematocrit, decreased mental function

diabetes insipidus

deficiency of ADH or decreased response to it = patients unable to concentrate urine during periods of water restriction + excrete large volumes of urine

• central or neurogenic diabetes insipidus & nephrogenic diabetes insipidus

central or neurogenic diabetes insipidus

occurs because of a defect in synthesis or release of ADH

nephrogenic diabetes insipidus

occurs because kidneys do not response to ADH

SIADH (syndrome of inappropaite ADH) is:

failure of negative feedback system that regulates release + inhibition of ADH = results in excess ADH

• causes: nervous system disorders (head trauma, meningitis), excess ADH (increased reabsorption of water), causing urine to be concentrated + decreased Na+ and dilutes blood

potassium is a major cation in:

intracellular (ICF)

for potassium, serum levels are:

low, between 3.5-5.0 mEq/L

insulin promotes movement of:

potassium into cells

potassium level influenced by:

acid-base balance, with excess potassium ions in interstitial fluid potentially leading to hyperkalemia (life threatening)

potassium imbalance hypokalemia

plasma potassium concentration below 3.5 mEq/L

• causes: excessive loss due to diarrhea, diurses associated w/ some diuretic drugs, excessive aldosterone, and decreased dietary intake (EDs)

• manifestations: interfere with neuromuscular function - muscles less responsive to stimuli = may progress to paralysis

potassium imbalance hyperkalemia

plasma potassium concentration above 5 mEq/L

• causes: renal failure, “potassium-sparing” diuretics, leakage of intracellular potassium into extracellular fluids, and displacement of potassium

• manifestations: cardiac dysrhythmias are common since hkalemia may progress to cardiac arrest

  • severe hyperkalemia = prolonged depolarization + impair repolarization, which decreased excitability cause cardiac arrest

  • severe hyperkalemia on EKG: wide QRS, longer PR, and tall narrow T wave

role of calcium in body:

important extracellular cation that is stored in bone and maintains stability of nerve membranes + is required for muscle concentrations and blood clotting

balance of calcium is controlled by:

parathyroid hormone (PTH) and calcitonin

vitamin D promotes:

calcium absorption from intestine, which is activated in kidneys into calcitriol

ECF calcium exists in 3 forms:

• protein bound: 40% of ECF calcium bound to albumin

• complexed: 10% is chelated with citrate, phosphate, and sulfate

• ionized (free): 50% of ECF calcium present in ionized form

calcium imbalance hypocalcemia

plasma calcium concentration below 4.3 mEq/L

• causes: hypoparathyroidism (PTH + vitamin D stimulate Ca reabsorp. in nephron)

  • deficient serum albumin (40% of ECF calcium bound to albumin)

  • renal failure: abnorm. loss of calcium from kidney

• manifestations: increase in excitability of nerve membranes + tetany (spontaneous stimulation of skeletal muscle

calcium imbalance hypercalcemia

plasma calcium concentration above 5.3 mEq/L

• causes: uncontrolled release of calcium from bones caused by neoplasms

  • hyperparathyroidism: excess PTH released more Ca from bones into blood

  • excessive calcium + vitamin D intake

• manifestations: decreased neural excitability (lethargy, stupor) + depressed neuromuscular activity (muscle weakness + loss of muscle tone)

magnesium

intracellular ion with lower range of plasma concentration 1.8-3.0 mg/dl

hypomagnesemia

occurs with alcoholism

• neuromuscular manifestations: increased reflexes, convulsion

• cardiovascular manifestations: hypertension, cardiac dysrhythmias

hypermagnesemia

occurs with renal failure

• depressed neuromuscular function: decreased reflexes + muscle weakness

acid-base balance mainly concerned with two ions:

hydrogen (H+) and bicarbonate (HCO3-)

alterations of ____ and ____ concentrantions in body fluids are:

H+ and HCO3-, common in disease process

buffers in blood respond to:

pH changes immediately

respiratory system alters:

carbonic acid levels to change pH

kidneys modify excretion rate of acids and:

absorption of bicarbonate ions to regulate pH

• kidneys slowly mechanism to initiate control, but most significant + long term

acidosis

blood pH below 7.5

respiratory acidosis

blood pH drops due to excessive retention of CO2 leading to excess H2CO3; breathing depressed CO2 elevates

respiratory acidosis may be result of + compensation:

• acute respiratory problems: pneumonia, airway obstructions, chest injuries or drugs that depress respiratory control center

• chronic respiratory disorders: common with chronic obstructive pulmonary disease

• manifestations: shortness of breath, confusion, and headaches

• compensation: kidneys conserve bicarbonate + eliminate H+

• breathing depressed, CO2 elevates, pH = <7.35

metabolic acidosis

arterial blood levels of H+ increases, HCO3- falls

metabolic acidosis is result of + compensation:

increased non-carbonic acids or excessive loss of bicarbonate ions to buffer hydrogen

• diarrhea: loss of bicarbonate from intestines

• chronic kidney disease: decreased excretion of acids

• diabetic ketoacidosis: increased formation of ketones (acidic)

• compensation: hyperventilation, and renal (kidneys conserve bicarbonate and eliminate H+)

• hydrogen increased, bicarbonate decreased = pH exceeds 7.45

manifestations of metabolic acidosis

headache, decreased BP, hyperkalemia, changes in LOC (confusion, drowsiness), muscle twitching, nausea, vomitting, etc

alkalosis

blood pH above 7.45

respiratory alkalosis

blood pH rises due to excessive loss of CO2 as in hyperventilation

respiratory alkalosis is result of + compensation:

hyperventilation

• caused by: anxiety, high fever, head injuries, brainstem tumor

• manifestations: dizziness, lightheadedness, and tingling in the hands and feet.

• compensation: kidneys conserve H+

• hyperventilation decreases CO2, pH exceeds 7.45

metabolic alkalosis

arterial blood levels of H+ falls, HCO3- rises

metabolic alkalosis is result of:

increase in serum bicarbonate ion:

• caused by loss of hydrochloric acid from stomach, excessive ingestion of antacids

• compensation: respiratory (breathing is depressed to retain CO2) + renal (kidneys conserve H+ and eliminate bicarbonate)

manifestations of metabolic alkalosis

restlessness followed by lethargy, dysrhythmias (tachycardia), compensatory (hypoventilation), confusion (LOC down, dizzy), nausea, vomitting, diarrhea

acidosis and alkalosis