Pathophysiology - Fluids & Electrolytes Chapter Summary

Front 1

Fluid balance in the human body. Distribution in % and Kg, tissue it is stored in, how it varies by age, why is it important?

Back 1

In a 70 kg man, 42 kg is water (60%), and 28 kg is solids. Women have 50% water due to more fat and less muscle density.

Total body water depends on fat and age. Fat holds little water, muscle holds most of it.

Elderly - have more fat, less water, lower ability to regulate Na+ and K+, lower ability to concentrate urine.

Newborns - 70-80% water - have a higher turnover of water, higher metabolism, higher proportion of skin surface, kidneys are immature and can't concentrate urine.

Infants - 1st year 67% water - gained subcutaneous fat and muscle.

Water is important in maintaining BP and temperature, it is a medium for chemical reactions, and transports nutrients.

Front 2

What % of water is in the different spaces in tissues?

Back 2

Of the 60% water, 40% is ICF and 20% is ECF (15% interstitial, 5% intravascular). There is misc transcellular fluid that is not measured, but plays a role: Ex. CSF, lymph, synovial, pleural, intestinal...

Front 3

What are the forces that balance compartment water?

Back 3

Hydrostatic Pressure - pressure in the capillary that pushes the water out.

Colloid Osmotic Pressure (Oncotic) - Colloids pull water into capillaries through solutes that attract water.

Front 4

What are the normal blood values for colloids, solutes, and acids/bases in the blood?

Back 4

Na+ (135-145 mEq/L) Most abundant solute
K+ (3.5-5 mEq/L)
Ca+ (8.8-10 mg/dl)
Mg (1.2-2.0 mEq/L)
albumin (3.5-5 g/dl)
glucose (80-110 g/dl)
urea (BUN 10-20 mg/dl)
pH (7.35-7.45)
PCO2 (35-45 mmHg)
HCO3- (22-26)
PO2 (80-100 mmHg)
O2 Sat (90-100%)
Osmolarity/Osmolality (275-295)

Front 5

What are the values for the main arterial and venous pressures in capillary beds?

Back 5

Arterial - Net Pushing Pressure 35 mmHg
Net Pulling Pressure 25 mmHg
Total Pressure +10 mmHg

Venous - Net Pushing Pressure 15 mmHg
Net Pulling Pressure 25 mmHg
Total Pressure -10

Front 6

What are minimal and needed volumes of urine output for adults and infants/children?

Back 6

Adult:
Minimal - 30 ml/h
Need - 30ml/kg/24 hours

lbs to kg = lbs/2.2

Infants & Children:
Minimal - 1-2 m/h (typically use 2)
Maintenance Needs -
0-10 kg - 100 ml/kg/24 hours
11-20 kg - 1000 ml + 50 ml/kg/24h
>20 kg - 1500 ml + 20 ml/kg/24h

Slide 10 - Determining IV Rates

Front 7

What are the 6 regulators of water balance in the body?

Back 7

1. Thirst - osmoreceptors are on the hypothalamus and trigger the need to drink when the hypothalamus shrinks due to dehydration
2. ADH - posterior pituitary - increased osmolality increases the secretion of ADH, collecting tubules open pores, and water is reabsorbed - decreased osmolality lowers the ADH secreted, collecting tubules close pores, water is excreted
3. Glomerular Filtration Rate - increased hydrostatic pressure causes more water to be excreted, increased perfusion causes increased output
4. Aldosterone - acts on the kidney tubules, reabsorbs Na+ (retains water) and secretes K+
5. Renin-Angiotensin-Aldosterone - balances BP and water, low blood flow through glomerulus causes renin to be released, in circulation renin is changed to Ang I, in the lungs Ang I is changed to Ang II by ACE, Ang II increases blood flow through the glomerulus and stimulates aldosterone to be secreted, aldosterone stimulates retention of Na+ (and water through it) which raises blood volume/pressure and increased blood flow through the glomerulus
6. Atrial atriuretic Peptide (ANP) - increased plasma volume causes atrial tissue to stretch, thus causing the cardiac hormone ANP to be released; this lowers tubule Na+ resorption to increase urine output, increases GFR, and lowers plasma volume/BP/water

Front 8

What are the 4 pathologies of edema?

Back 8

1. Increased capillary permeability for inflammation
2. Decreased plasma albumin to increase fluid in interstitial spaces
3. Lymphatic blockage
4. Increased hydrostatic pressure in venous system, Ex. clot, obstruction, to increase interstitial fluid

Front 9

What are the 5 categories of the clinical manifestations of edema?

Back 9

1. Localized edema - limited to injured part
2. Generalized edema - throughout all body tissues, hard to recognize
3. Dependent edema - gravity dependent parts like the feet/legs when upright and buttocks when lying down
4. Pitting edema - leaves an indentation when pressed on
5. Other clinical manifestations - weight gain, swelling, puffy appearance, shoes fitting tight

Front 10

What problems does edema create and what is the treatment?

Back 10

Problems - 1. Creates increased distance for nutrients, oxygen, and water to travel between capillaries and tissues 2. Wounds heal more slowly

Treatments - 1. Elevate body part to increase venous and lymphatic return 2. Compression on the limbs 3. Lower salt intake 4. Use diuretic medications

Front 11

FLUID BALANCE ALTERATION:
Isotonic Alterations:

Back 11

Isotonic Loss - electrolytes and water are lost proportionally, no shift of water, no cellular shrinking; caused by hemorrhage, renal retention of Na+ and water; manifested as serum sodium normal, weight loss, decreased urine output, hypovolemia (lower BP, increased HR-90); treat by giving water and soute (Gatoraid, normal saline IV, etc)

Isotonic Excess - Electrolytes and water gained are proportional, no shift of water and no cellular swelling; caused by too much IV fluid, drugs such as cortisone; manifested as normal serum Na+, weight gain, hypervolemia (increased BP, distended jugular veins; in the elderly it causes heart failure AEB pulmonary edema; treat by restricting free water and decrease IV rate

Front 12

FLUID BALANCE ALTERATIONS
Hypertonic and Hypotonic

Back 12

Hypertonic - solute gain of Na+ and glucose causes and increase in osmolality; water loss; solute gain is caused by excess Na+ (by IV or diet), concentrated infant formula, and hyperglycemia (diabetes); water deficit caused by comatose or paralyzed individuals are not able to drink fluids, infants depend on someone to feed them, water loss with fever or rapid RR, inability of kidney to concentrate urine, clinical manifestations of 'normal' BP, postural hypotension, hypernaturemia (Na+ >147), increased HCT, decreased urine output, intracellular dehydration, dry mucous membranes (mouth), dry skin, confusion (esp. in elderly) due to shrinkage of the brain, poor skin turgor; treatment of giving free water by mouth or hypotonic IV until Na+ is normal

Hypotoic - Na+ loss and water excess; Na+ loss caused by GI losses (vomiting, diarrhea, GI suctioning), water gain caused by excess water intake, hypotonic IV fluids (D5W), increased ADH (SIADH), and heart failure; clinical manifestations of hyponatremia (Na+ <135), low HCT, confusion/HA/lethargy RT brain swelling, generalized and/or dependent edema manifested by weight gain; treatment of restricting free water and decrease IV rate, give glucose immediately

Front 13

FLUID BALANCE ALTERATIONS
Hypotonic Alteration of Water Gain (SIADH)

Back 13

Syndrome of Inappropriate Antidiuretic Hormone - ADH decreases water secretion by the kidney; water is absorbed and decreases Na+; secretion of ADH occurs with fear, pain, surgery, infection, narcotic analgesic medications, and anesthesia; clinical manifestations of decreased BP, decreased urine output, weight gain, and hyponatremia; treat by restricting free water

Front 14

What are the 2 types of fluid shifts when regulatory mechanisms can't compensate?

Back 14

1. 3rd Spacing - fluid is trapped and is not available, creating excess fluid in interstitial spaces; caused by major trauma, heart and kidney failure; pathology of increased capillary hydrostatic pressure or decreased oncotic pressure which can be caused by inflammation, increased BV, venous obstruction, and low secretion of albumin; clinical manifestations of pitting edema in dependent parts, pulmonary edema (fluid shifted into alveoli), generalized edema, weight gain (overnight) of 2.2 lbs; treat the cause by waiting or giving increased protein

2. Interstitial to plasma shift - decreased hydrostatic pressure as with severe blood loss, which is hypovolemia decreased hydrostatic pressure causing fluid to move from interstitial spaces to the plasma; increased oncotic pressure as with increased glucose or a large solute load

Front 15

ELECTROLYTES
Source, regulation, 5 things infuenced by direct hormonal regulation

Back 15

Intake is from dietary sources
Regulation depends on water intake and hormonal regulation
Direct Hormonal Regulation:
1. Aldosterone - it increases resorption of water and Na+, influences secretion of K+
2. ANP - Atrial Natropathic Hormone - suppresses aldosterone effects on the kidney and decreases resorption of Na+
3. PTH - Parathyroid Hormone - regulates serum Ca+ and pulls it out of the bones
4. Vitamin D - stimulates Ca+ and Phosphate (P) absorption from the gut
5. Calcitonin - Drives Ca+ back into the bone

Front 16

ELECTROLYTES
Sodium and it's functions

Back 16

Na+ is the most abundant electrolyte in the ECF (135-145 mEq/L); it regulates osmolarity and volume of fluid, is used in action potentials, has cellular functions

Hyponaturemia (<135) manifests like a hypotonic solution in fluid balance alterations (slide 36)

Hypernaturemia (>147) creates the same manifestations as a hypertonic solution (slide 32)

Front 17

ELECTROLYTES
Potassium

Back 17

K+ is most abundant in the ICF, only source is dietary or IV intake, important in CHO metabolism, exchanges for H+ in acid base imbalances, necessary for an action potential. If a system is acidotic, Na+ and K+ can change places and serum levels rise.

Front 18

ELECTROLYTES
Hyperkalemia & Hypokalemia

Back 18

Hypokalemia K+ serum level <3.5; caused from low K+ in food, loss with ETOH intake, alkalosis from K+ shifting into cells when H+ shifts out, loss from GI tract (vomiting, diarrhea, GI suctioning), or loss from the urinary tract (loop diuretics); pathology is it alters resting membrane potential making cells less excitable; manifests as decreased contractilility of smooth, skeletal, cardiac muscles, diaphragm weakness causing respiratory arrest, paralysis, decreased reflexes, cardiac dysrhythmias, decreased smooth muscle contractions resulting in decreased peristalsis in the ileus; treatment is to replace the K+ slowly, no IV push!

Front 19

Hyperkalemia

Back 19

K+ elevated above 5.5; caused by increased intake, transfusion of whole blood (contains free K+), acidosis, severe burns or crush injuries, renal failure, hemolysis of RBC; pathology is that it makes membrane potentials more excitable; manifests as restlessness, intestinal cramping, diarrhea, heart dysrhythmias from increased excitability; treat by giving insulin and glucose to get K+ to shift into the cells, Calcium gluconate IV helps raise threshold and decreases cardiac cell irritability, dialysis, exchange resin (Kayexalate) exchanges Na+ for K+ in the gut

Front 20

ELECTROLYTES
Calcium

Back 20

99% is in the bones and teeth, the 1% in body fluids is what is tested in the lab and it is bound to serum albumin, ionized Ca+ is not usually measured; it is essential for action potentials and muscle contraction, required for synaptic release of neurotransmitters, and necessary for clotting cascade

Front 21

ELECTROLYTES
Hypocalcemia& Hypercalcemia

Back 21

Hypocalcemia is a serum level >8.5; caused by decreased food intake, decreased Vitamin D, cancers, removal/injury of PT glands; pathology results in increased irritability of muscle cells, decreased threshold of action potentials; manifested in the neuro system as “pins and needles” feeling (parenthesis), hyperreflexia/tetany (Chvostek’s sign – tap cheek (CN V) and muscle in cheek will contract) (Trousseau’s sign – inflate a BP cuff and hand will curl up and bend to the anterior); GI effects of hypermotility with cramping and diarrhea; cardiac effects are dysrhythmias; treat by replacing Ca+ and Vitamin D orally or through IV

Front 22

Hypercalcemia

Back 22

A serum level of >10.5; causes hyperparathyroidism, resorptive bone metastasis (breast CA, prostate CA, cervix CA, and multiple myeloma); pathology is neuromuscular decrease resulting in weakness; manifestations include kidney stones (usually 1st sx), pathological fractures, neuro issues like fatigue, weakness and lethargy, GI issues such as hypomotility, N/V, and constipation; treat with fluids to dilute Ca+, diuretics, meds to inhibit bone resorption

Front 23

ELECTROLYTES
Magnesium

Back 23

50% is stored in the bones, 45% intracellular, 5% intravascular, serum levels of 1.2-2.0, regulation is interrelated with K+ and Ca+, most absorbed in the intestine

Front 24

ELECTROLYTES
Hypomagnesaemia & Hypermagnesaemia

Back 24

Hypomagnesaemia is a level of <1; caused by decreased intake, malabsorption, diuretics; pathology is it coexists with hypocalcemia and hypokalemia, increased irritability; manifests like hypoclcemia and hypokalemia; treat through the administration of Mg like antacids or IV

Front 25

Hypermagnesaemia

Back 25

a level >2.5; caused by decreased renal excretion, over use of laxatives (MOM); pathology results in decreased neuromuscular excitability; manifested through muscle weakness and deep tendon reflexes, bradycardia and decreased BP, N/V; treat resulting renal failure through dialysis

Front 26

ACIDS & BASES
Normal pH, acids, bases

Back 26

Normal pH is 7.35-7.45; acidity is determined by H+ in excess, acids can be volatile: carbonic acid changes to a gas CO2 and water, can be non-volatile: sulfuric acid and fatty acids don’t change to a gas; body sources of acid include glucose catabolism (carbonic acid), protein catabolism (sulfuric acid), fat catabolism (fatty acids), ischemia; basic pH is dependent on bicarbonate (HCO3-); body sources of bases are catabolism of carbonic acid (H2CO3 = HCO3 + H+), GI intake of bicarb, pancreas secretion of bicarb, kidney resorption of bicarb

Front 27

ACIDS & BASES
pH regulation & buffer system

Back 27

Carbonic acid = bicarb buffer; CO2 + H2O (happens in the lungs in minutes) = H2CO3 (carbonic acid) = H+ +HCO3- (bicarb) (happens in the kidneys in hours to days); protein buffer = HGB; renal buffers = secretes H+ and reabsorbs HCO3; cellular buffer = K+ moves out of cell as H+ moves in during acidosis;

Front 28

ACIDS & BASES
Compensation

Back 28

Temp adjustment of increase or decrease in acid or base; kidneys compensate for the respiratory problems by retaining H+ or excreting H+; respiratory system (medulla) compensates for metabolic problems by allowing respiration to retain H2CO3 or increasing respiration to excrete H2CO3

Front 29

ACID BASE IMBALANCES
Metabolic Acidosis

Back 29

Acidosis, pH <7.35; pathology is ECF gain of metabolic acids (not carbonic acid!) or loss of bicarb; ANION GAP – measures ions not usually measured/difference between (Na+ + K+) – (HCO3 + Cl) = 10-12 mEq; elevation means increase in nonvolatile acid; caused by lactic acid from the muscles, renal failure, diabetic ketoacidosis (DKA) (can’t process sugar), starvation and increased FA metabolism, and severe diarrhea; breakdown of FA’s = keytones = ONCODOSIS; clinical manifestations of HA’s, letharegy = coma = death, keep respirations (Kussmaul) (increase in resp to blow off CO2, anorexia, N/V, diarrhea, hyperkalemai (H+ into cells and K+ out = increased K+; diagnosis is made by ABG’s of pH <7.35, PCO2 35-45, HCO3 22, increased K+ >5.5, anion gap >12; treat the cause (ex. Diabetic ketoacidosis – give insulin); respireatory comp through increased RR to blow off CO2 (thus carbonic acid)

Front 30

ACID BASE IMBALANCES
Metabolic Alkalosis

Back 30

pH >7.45; pathology is usually caused by loss of acids (GI suctioning, vomiting), excess HCO3 intake from antacids, diuretics, hypoparathyroidism; manifests in decreased RR; diagnosed by ABG’s of pH >7.45, CO2 >40 if compensating, 47-50 if not compensating, HCO3 >26, K+ <3.5 mEq; treat the cause with normal saline IV and K+; respiratory compensation for Alkalosis is decreased ventilation to increase CO2 and carbonic acid

Front 31

ACID BASE IMBALANCES
Respiratory Acidosis

Back 31

pH <7.35, pathology results from decreased alveolar ventilation resulting in CO2 retention, increased H2CO3 = H+ +HCO3 (bicarb); caused by CNS respiratory depression (narcotics) (#1 reason!), resp muscle paralysis, scoliosis, Pickwickian syndrome (obesity pushes on the diaphragm, pt can’t take a deep breath due to weight from top), pneumonia, pulmonary edema, COPD (#2 reason) from emphysema and asthma; manifestations related to severity and length of time, restlessness, apprehension, lethargy, muscle tremors, convulsions, coma; diagnosed by pH <7.35, PCO2 >45, HCO3 >22 or >26 for compensation by kidneys after 24 h; treat by increasing ventilation, metabolic compensation through kidneys, acute respiratory acidosis,(airway obstruction pH <7.35, PCO2 >45, HCO3 >22 for under 24h; chronic resp acidosis COPD pH <7.35 or normal, PCO2 >45, HCO3 >26 for over 24h

Front 32

ACID BASE IMBALANCES
Respiratory Alkalosis

Back 32

pH >7.45; pathology of decreased O2 intake, hyperventilation; caused by hypoxemia (increased RR from blowing off CO2), pulmonary disease (COPD, pneumonia) (retaining CO2), high altitude, fever, anemia, hysteria (increased RR); manifests in deep rapid RR (primary symptom), dizziness, confusion, tingling of extremities, confusion, coma, carpopedal spasms toward ventral surface; diagnosed through pH >7.45, PCO2 <35, HCO3 normal or <22 with chronic alkalosis; treat underlying causes, correct hypoxemia, for hysteria give pt a paper bag; metabolic compensation of H+ coming out of cells into ECF, kidney saves H+ and excretes HCO3 (bicarb)