Fluids & Electrolytes & Acid-Base Balance

Functions of Body Fluids:

1. Transport gases, nutrients, & waste

2. Helps generate electrical activity to power body functions

3. Takes part in the transformation of food → energy

4. Environmental stresses and disease affects balance

How is Body Water distributed?

Through:

1. Intracellular water

2. Extracellular/Plasma water

3. Interstitial water

Total Body Water (TBW):

60% of total human weight

1. Intracellular fluid: 2/3 of water

2. Extracellular fluid: 1/3

Extracellular fluid is divided into:

• Interstitial fluid: around cells; most of the bunch

• Intravascular: plasma & lymph fluid

• Transcellular fluid: low amount; synovial, intestinal, CSF, sweat, urine, pleural, peritoneal, intraocular fluids; joint spaces

  • Low # but important

TBW in Peds:

• 75-80% of body weight

• Susceptible to significant changes in body fluids; dehydration in newborns

Aging in TBW:

• v % of TBW

• v free fat mass & v muscle mass & renal decline

• Diminished thirst perception

Intracellular Compartment (ICF)

• Fluid contained within all of the cells in the body

• Higher concentration of K+

• Almost no Ca

• Moderate # of magnesium

• Small Na+

Extracellular Compartment (ECF):

• Contains all outside cell fluid; interstitial or tissue spaces & b.v.

• Higher concentration of Na+

• Moderate # of bicarbonate

• Small K+

Osmolarity:

• of the extracellular fluid almost entirely due to Na+

• of the intracellular fluid almost due to K+ as the primary electrolyte

measure of the total number of solute particles dissolved in a fluid

If ECF/ICF changes in concentration _______

fluid shifts from lesser → greater concentration

Kidneys’ involvement with fluid-electrolyte balance:

• Maintains & excretes body fluids

• Selectively retains substances needed & excretes unneeded ones (like electrolytes, metabolic waste & toxins)

• Regulates pH via excretion/maintaining hydrogen ions & bicarbonate

Lungs’ involvement with fluid-electrolyte balance:

• Rids 300mL of fluid/day out of body & plays role in Acid-Base Balance

• Regulates CO2 conc.

Heart’s involvement with fluid-electrolyte balance:

• pumps blood with sufficient force → perfuse the kidneys → kidneys work ^ effectively

Adrenal gland involvement with fluid-electrolyte balance:

• Secretes aldosterone: Na+ retention (water retention) & K+ excretion

Parathyroid’s involvement with fluid-electrolyte balance:

• Regulates Ca & P balance

• PTH: ^ Ca & v PO4 (phosphate)

Pituitary gland’s involvement with fluid-electrolyte balance:

• Secretes ADH (vasopressin) → ^ water reabsorption in kidneys

• posterior part

Tonicity:

Tension/effect that effective osmotic pressure of a solution w/impermeable solutes exerts on cell size due to water movement across cell membrane

• Isotonic: neither shrink/swell

• Hypotonic: Swell; high osmolarity inside

• Hypertonic: shrink; high osmolarity outside

Water movement between fluid compartments depend on:

• Osmolality: measure of the conc. of dissolved particles (solutes) in solution

• Osmotic forces: force driving water low → high conc.

• Aquaporins: protein that selectively transports water

• Starling forces: water leaving capillary site → lymph → venae cava

  • Net filtration = forces favoring filtration - forces opposing it

Hydrostatic pressure:

caused my water, more water → ^ hydrostatic psi

Colloidal osmotic/oncotic pressure:

Have more proteins → attract water

Filtration:

caused by capillary hydrostatic psi (35mm Hg) + blood colloidal psi (25mm Hg)

• Arterial end net filtration psi = +10 mmHg

No Net movement:

capillary hydrostatic psi (25mm Hg) = blood colloidal osmotic psi (25mm Hg)

• Mid Capillary net filtration psi = 0 mm Hg

Reabsorption:

Fluid re-enters capillary due to capillary hydrostatic psi (18 mmHg) < blood colloidal osmotic psi (25 mm Hg)

• Venous end net filtration psi = -7 mm Hg

Net Filtration:

• Forces favoring filtration:

  • Capillary hydrostatic psi (BP)

  • Interstitial oncotic psi (water pulling)

• Forces favoring reabsorption

  • Plasma (capillary) oncotic psi (water-pulling)

  • Interstitial hydrostatic psi

Edema:

Accumulation of fluid within interstitial spaces

• Causes:

  1. ^ in capillary hydrostatic psi

  2. v in plasma(capillary) oncotic psi

  3. ^ in capillary permeability

  4. Lymph obstruction

• Localized vs generalized:

• Pitting Edema

• Assessing via daily weight, visual assessment, measuring affected part, finger pressor for pitting edema

What are the causes of decreased capillary oncotic psi that would lead to Edema?

Either

1. Loss of plasma protein to interstitial space from increased capillary permeability

2. Lower synthesis of plasma proteins from cirrhosis or malnutrition

3. Increased loss of plasma proteins from nephrotic syndrome

4. Increased plasma Na- and water retention from dilution of plasma proteins

What are the causes of increased capillary permeability that would lead to Edema?

Burns or inflammation

causes loss of plasma proteins to interstitial space

What are the causes of increased tissue oncotic pressure that would lead to edema?

1. Loss of plasma proteins to interstitial space

2. Lymph obstruction → v transport of capillary filtered protein

What are the causes of increased capillary hydrostatic psi that would lead to edema?

Venous obstruction, salt & water retention, and heart failure

Causes fluid movement to tissues

Lymph obstruction and its effects on edema:

1. Fluid movement to tissues

2. lower transport of capillary filtered proteins

Antidiuretic Hormone (ADH):

^ water reabsorption → plasma

• ^ plasma osmolarity → detected by receptors → either fluid intake (will lead to v osmolarity straight up) or hypothalamus detects it → PP pars nervosa → ADH → aquaporins ^ → renal water retention → v plasma osmolality

• v plasma volume → detected by receptors → hypothalamus detects it → PP pars nervosa → ADH → aquaporins ^ → renal water retention → ^ plasma volume

Atrial Natriuretic Peptide (ANP):

^ plasma volume → atrial stretching detected by endocrine cells → ANH release → (glomerulus starts to ^ Glomerular Filtration Rate → excrete more water) or (proximal tubule lowers Na+ reabsorption → excrete ^ Na)

• High amounts suggest heart failure

Renin Angiotensin Aldosterone System (RAAS):

either v extracellular fluid/arterial BP → kidneys sense low # of fluid → Juxtaglomerular cells secrete Renin → turn angiotensinogen to angiotensin 1 → converting enzymes in lungs turn 1 to Angiotensin 2 → (goes to adrenal cortex → induce aldosterone → ^ Na+ reabsorption of kidney thus water too → ^ Vascular volume & arterial BP) or/and (goes to arterioles → vasoconstriction of systematic arterioles → ^ arterial BP)

Osmolarity Alterations:

All occur in interstitial compartment; normal osmolarity is from 275-295 mm Hg

Can either be:

• Isotonic

• Hypertonic

• Hypotonic

Isotonic Alterations:

• TBW change w/proportional electrolyte & water change (no conc. change)

• Isotonic fluid loss/excess

Hypertonic alterations:

• Na gain & water loss → intracellular dehydration & hypernatremia

• ICF → ECF

Hypotonic alterations:

• v osmolality → cells expand & hyponatremia

• water moves into cells via osmosis

Fluid Volume Deficit:

in the Interstitial compartment

1. Isotonic Dehydration

2. Hypertonic Dehydration

3. Hypotonic Dehydration:

Isotonic Dehydration:

• Inadequate intake of fluids & solutes

• Excessive losses of isotonic body fluids

Hypertonic Dehydration

• Excessive perspiration, hyperventilation, ketoacidosis, prolonged fevers, diarrhea, diabetes insipidus all lead to ^ fluid loss

Hypotonic Dehydration:

• Chronic illness, renal failure, chronic malnutrition

To assess body fluid losses measure:

• HR, BP, venous volume/filling, capillary refill rate

• Conditions that predispose Na + water loss, weight loss or body functions indicate v fluid volume

Fluid Volume Excess:

Interstitial compartment

• Isotonic Overhydration

• Hypertonic Overhydration:

• Hypotonic Overhydration:

Isotonic Overhydration

• Hypervolemia

  Excessive fluid in extracellular compartment

  fluid does not shift

  Causes circulatory overload & interstitial edema

Hypertonic Overhydration:

• Rare, excess Na intake

• fluid is drawn from ICF

Hypotonic Overhydration:

• Water intoxication

• Fluid moves into ICF → expansion

Proportionate changes in Na & H20 in Interstitial compartment

Loss of water & sodium → fluid loss in ECF

Gain of water & sodium → fluid excess in ECF

Disproportionate changes in Na & H20 in Interstitial compartment:

Loss of sodium or gain of water → Hyponatremia

Gain of sodium or loss of water → Hypernatremia

What are all the electrolytes?

• Na, K, Ca, P, Mg

Sodium (Na):

• Major cation(+ charged atom that lost electrons) in ECF

• 135-145 mEq/L normal serum lvl

• Determinant of plasma osmolarity; works with Cl-

• Nerve impulse transmission, muscle contraction, movement of glucose & amino acids

Hyponatremia:

• sodium lvl <135 mEq/L → plasma hypoosmolality & cellular swelling

• Imbalances of Na+ → fluid volume imbalances

• Most common electrolyte disorder; older age ^ risk

Causes of Hyponatremia:

1. Pure sodium loss

2. Low intake

3. Dilutional hyponatremia: gain lots of water → Na+ diluted

4. Diuretics, diaphoresis, GI loss

Manifestations of Hyponatremia:

1. Cellular swelling occurs

2. Early signs: muscle cramps, weak, fatigue (heavy exercise)

3. N.S. most seriously affected: lethargy, disorientation, confusion, seizures, comma

4. Loss of ECF & hypovolemia → hypotension, tachycardia, v urine output

5. Dilutional from excess water (hypervolemic hyponatremia) → weight gain, edema, ascites, jugular vein distention

Hypernatremia:

• Serum sodium> 145mEq/L

Causes of Hypernatremia:

• Decreased Na excretion

  • Cushing syndrome: too much cortisol → retains water & sodium → excrete K

  • Renal Failure: problem excreting waste

  • Hyperaldosteronism: retains sodium & water

• ^ Na intake

  • Excessive oral sodium ingestion

  • Hypertonic saline solutions

• v water intake

  • NPO: nothing per oral

  • Infants, elderly, comatose

• ^ water loss

  • severe burns/fever

  • Diabetes insipidus: too low ADH → unable to retain water → peeing lots

  • Water diarrhea

Manifestations of Hypernatremia:

• Thirst- early symptom

• v urine output

• ^ urine & serum osmolality

• Dry skin & mouth

• Seizures

• Tachycardia

Potassium:

• Major ICF cation

• Normal serum levels 3.5-5.0 mEq/L

• Concentration maintained by Na+/K+ AtPase Pump

• Transmission & conduction of nerve impulses, normal cardiac rhythm, skeletal/muscle contractions

• Derived from diet

• Regulated by renal & transcellular buffer systems

• Changes in pH affect K+ balance

  • Aldosterone, insulin & epinephrine influence lvls

  • Kidney most efficient regulators

Hyperosmolality:

• Water leaves cell → intracellular K + → K+ moves out of cell

Metabolic Acidosis/Alkalosis:

Metabolic Acidosis:

• H moves into cell for buffering; K moves out to ECF

Metabolic Alkalosis:

• H moves out of cell → K moves into cell

Epinephrine. Albuterol, & insulin: Move K → cell

Repeated muscle contractions: Moves K → out of cell

Hypokalemia:

• K levels <3.5

• K Balance described by changes in plasma potassium lvls

• Causes:

  • v K intake

  • ^ K entry to cells (hyperinsulinism), steroids, cushing syndrome

  • ^ K loss (GI, renal, skin, diuretics, diarrhea, vomiting, NG suction

s/s of Hypokalemia:

• (depend on rate & severity):

  • Membrane hyperpolarization → v in neuromuscular excitability, skeletal muscle weakness, smooth muscle atony, cardiac dysrhythmias

  • Muscle paralysis if life-threatening respiratory v (<2.5)

  • EKG changes: ^ PR interval, depression of ST segment, flat t wave, prominent U wave; lower stimulus (voltage) → not enough to reach threshold for action potential

Hyperkalemia:

• K levels >5.0

• Rare due to efficient renal excretion

• Causes:

  • ^ intake

  • shift of K+ ICF → ECF (acidosis)

  • v renal excretion (renal failure, Addison’s disease (OPP of Cushing disease))

  • Many blood transfusions

  • Cell Trauma

s/s of Hyperkalemia:

• Mild attacks: membrane cell depolarization → initial ^ neuromuscular irritability (restless, diarrhea, intestinal cramps

• Severe: EKG: peaked narrow T waves, wide QRS, cardia arrest; v resting membrane potential; weakness, loss of muscle tone, paralysis

EKG of Potassium:

Calcium & Phosphate:

• Both controlled by parathyroid hormone (PTH), vitamin D, & calcitonin

• Vitamin D : controls normal plasma lvls of Ca & PO4 via ^ intestinal absorption

• Calcitonin acts on kidney & bone → removes Ca from extracellular circulation

• Approx 99% of calc, 85% of P & 50-60% of Mg is found in bone

Calcium:

Bones, teeth, blood clotting, hormone secretion, cell receptor function, plasma membrane stability & muscle contraction (nerves)

• Normal serum conc. 8.6-10.5 mg/dl

• ECF Calcium exists in 3 forms:

  1. Protein bound: 40% bound to albumin

  2. Complexed: 10% chelated in citrate, PO4, Sulfate

  3. Ionized: 50% in ionized form

Parathyroid Hormone:

maintains calcium conc in ECF, can also decrease PO4 lvls whilst ^ Ca lvls

• If plasma Ca ^ → PTH inhibited → calcium stores in bones

• If plasma Ca v → PTH secretion ^ & Ca mobilized from bone

• Secretion, synthesis, & PTH action influenced by Mg: cofactor in cellular ATP generation

Hypoparathyroidism:

v Ca

• caused by hyposecretion of PTH

• May be congenital

• Can occur after neck surgery (removal of parathyroid tissue in a thyroidectomy)

Hypocalcemia:

• <8.5mg/dl Ca

• Causes:

  • Inhibition of Ca absorption from GI tract

    • Inadequate oral intake

    • Lactose intolerant

    • Malabsorption (Chrons)

  • ^ Ca Excretion:

    • Renal failure

    • Diarrhea

    • Steatorrhea: attached to fat instead of intestinal oxalate

  • Conditions that v ionized fraction of Ca:

    • Hyperphosphatemia

    • Removal/destruction of PT glands

Hypocalcemia:

• Chvostek’s sign: twitch of facial nerve in response to tap of nerve

• Trousseau’s sign: Spasm of forearm on blood supply obstruction (BP cuff)

• Tetany: spasm in muscles; Worst form is laryngospasm (prevents breathing)

• Muscle Twitching

• Later signs:

  • Arrhythmias: prolonged ST & QT interval

Hypercalcemia:

• >10.5 mg/dl

• Causes:

  • ^ intestinal absorption

    • Excessive oral intake of Ca & Vitamin D

  • v Ca excretion

    • Use of thiazide diuretics

  • ^ Bone resorption of Ca:

    • ^ PTH

    • Malignant neoplasm

    • Prolonged immobilization

Hypercalcemia s/s:

• Cardiovascular: ^ HR (early), Bradycardia (later)

  • Bounding/full pulse

  • EKG changes: short ST segment, wide T wave

• Respiratory: skeletal weakness → ineffective respiration

• Renal:

  • Polyuria: ^ urine output → dehydration

  • Renal Calculi (stones)

• GI

  • v motility & bowel sounds

  • Anorexia

  • Nausea, vomiting

  • Abdominal distention

  • Constipation

Phosphate:

• Energy for muscle contraction

• PTH, Vitamin D3, calcitonin act together → controls phosphate absorption/excretion

• Normal value = 2.5-4,5 mg/dl

Hypophosphatemia:

• Causes:

  • Intestinal Malabsorption

    • Vitamin D deficiency

    • Antacids containing Mg & Al

    • Long term alcohol abuse

  • Malnutrition

  • Respiratory alkalosis (intracellular shift)

  • ^ Renal excretion of PO4 associated w/ hyperparathyroidism

Hypophosphatemia s/s:

• s/s:

  • Muscle Pain & weakness

  • Mental changes: irritated, confused, numb, coma, convulsions

  • Respiratory Failure

  • Cardiomyopathies

Hyperphosphatemia:

• >4.5 mg/dl

• Due to Hypocalcemia

• Causes:

  • v renal excretion (renal failure)

  • ^ intake

  • Hypoparathyroidism

Hyperphosphatemia s/s:

• s/s:

  • v serum Ca lvls due to ^ PO4 lvls; sim to hypocalcemia results

Magnesium:

• Intracellular cation

• 1.5 - 2.5 mEq/L

• Cofactor for intracellular enzymatic enzymes

• ^ neuromuscular excitability

Hypomagnesemia:

• Causes:

  • Malnutrtion

  • Gastric Suction

  • Malabsorption syndromes

  • Alcoholism

  • Urinary losses

Hypomagnesemia s/s:

• s/s:

  • Anorexia

  • Neuromuscular irritability

  • ^ reflexes

  • Depression

  • Disorientation

Hypermagnesemia:

• Causes:

  • Renal insufficiency/failure

  • ^ intake of Mg-containing antiacids

  • Adrenal insufficiency; v renal excretion

Hypermagnesemia s/s:

• s/s:

  • Lethargy & drowsiness

  • Hypotension

  • Muscle weakness

  • v deep tendon reflexes (DTR)

  • v respirations

  • Bradycardia

  • Important in Pregnant woman: checks DTR, respirations

Acid-Base Balance:

Regulated to maintain normal pH via many mechanisms

• Normal blood/body pH is from 7.35-7.45 pH

• Measured by arterial blood gas (ABG) sampling; take from radial pulse w/needle

• Determined by H+ conc in body fluids

• 3 Systems:

3 Systems of Acid-Base Balance:

1. Chemical Buffer System (HCO3-H2CO3 [Bicarbonate acid])

2. Kidneys (HCO3 [Bicarbonate)

3. Lungs (CO2)

pH:

• -log of H+ conc

• ^ H+ = acidic

• v H+ = alkaline

• 0-14 scale

• Acid can be eliminated via:

  1. Lungs → CO2 gas

  2. Renal tubules w/regulation of HCO3-

  3. Secretion regulation of H+ into urine

Buffering systems:

• used to control pH

• Buffer: chemical that binds excessive H+/OH- w/out significant pH change

  • Most important plasma-buffer systems: carbonic-bicarbonate pair

  • 20 molecules of HCO3- to 1 H2CO3 (carbonic acid) = 7.4 pH

  • Acidosis: <7.35; ^H+ & v HCO3

  • Alkalosis: >7.45; vH+ & ^ HCO3

2 Systems can compensate when pH altered:

1. Respiratory System: ^/v ventilation → expire/retain CO2

   • CNS medulla controls & regulates RR

2. Renal System: produces acidic/alkaline urine (HCO3/H+)

   • Slow compensatory mechanism

Lungs regulation of Acid-Base Balance:

• PaCO2: partial psi of CO2 in arterial blood

  • 35-45 mmHg

  • Acute rise in PaCo2 is powerful respiration stimulant

Kidneys Roles in Acid-Base Balance

• Regulate pH of ECF

• If pH low:

  1. Elimination of H+ in urine

  2. HCO3 reabsorption

  3. HCO3 production

NORMAL VALUES of Acid-Base Balance:

• pH: 7.35-7.45

• PaCO2: 35-45 mm Hg

  • >45 acidosis ; <35 alkalosis; Respiratory altered

• HCO3: 21-28 mEq/L

  • <21 acidosis; >28 alkalosis; Metabolic altered

• PaO2: 80-100 mm Hg

• O2 sat: 95%+

Acid-base imbalances:

• Respiratory Acidosis: ^ PCO2 due to ventilation depression

• Respiratory Alkalosis: v of PCO2 due to hyperventilation

• Metabolic Acidosis: v of HCO3/ ^ in noncarbonic acids

• Metabolic alkalosis: ^ of HCO3, caused by excessive loss of metabolic acids

• Mixed acidosis: resp + metabolic acidosis

• Mixed alkalosis: rep + metabolic alkalosis

Metabolic Acidosis:

• v HCO3 → v pH

• Caused by

  1. ^ metabolic acids

     • Diabetic ketoacidosis (Dka): Usage of fat instead of glucose for energy

     • Starvation ketoacidosis

     • Anerobic metabolism

     • Ferrous sulfate overdose

     • Renal failure, uremia

  2. Inability of kidneys → excrete acid

  3. Excess loss of HCO3 via kidney/GI

     • Severe Diarrhea

     • Pancreatic secretions lost via pancreatic fistulas

     • Excessive acetazolamide (Diamox)/ammonium chloride

     • Renal failure

Metabolic Acidosis Compensation:

• Compensation:

  • Ventilating faster

  • Acidic urine

  • Therapy: lactate containing solution used in therapy → convert to HCO3 ions in live

Metabolic Acidosis s/s:

• s/s:

  • Headache

  • v BP

  • Hyperkalemia

  • Muscle Twitchin

  • Kussmaul Respirations

  • Diarrhea, Nausea

Metabolic Alkalosis:

• >7.45 ^ HCO3

• Causes:

  • ^ HCO3 loading

    • Antacids

    • Ringer’s lactate

  • Loss of acid

    • Gastric suctioning: taking H+ out of stomach

    • Vomiting

    • Thiazide/loop diuretics

  • Contraction of ECF

    • v in ECF due to vomiting/NGT suction → loss of Cl & reabsorption of Na+ & HCO3

Metabolic Alkalosis compensation:

• Compensation:

  • Breathing suppress → hold CO2

  • Kidney conserves H+ & makes HCO3 urine

  • Chloride-containing solution → HCO3 replaced by Cl

Metabolic Alkalosis s/s:

• s/s:

  • Compensatory Hypoventilation

  • Tremors, muscle cramps, finger/toes tingling

Respiratory Acidosis:

• ^ in CO2 → v pH

• Causes:

  • Hypoventilation

  • Acute disorders of Ventilation:

    • Impaired respiratory center function in medulla & pons (overdoses & tumors)

    • Lung disease

    • Chest injury

    • Weak respiratory muscles

    • Airway obstruction

  • Chronic Disorders of Ventilation:

    • COPD

    • Pulmonary Fibrosis

  • ^PaCo2 production:

    • Exercise

    • Fever

    • Sepsis

    • Burns

    • Carb rich diet

Respiratory Acidosis Compensation:

• Compensation:

  • Conserve HCO3 via kidneys

Respiratory Acidosis s/s:

• s/s:

  • Headaches

  • Hyperkalemia

  • Dysrhythmias (K+)

  • Hypoxia ← Hypoventilation