1

Disorders of Fluid &Electrolyte Balance

University of San FranciscoDr. M. Maag©2003 Margaret Maag

2

Class 6 Objectives

n Upon completion of this lesson, the student willbe able to

n describe the outcomes associated with hypoand hypervolemia.

n distinguish between the different etiologies ofmajor electrolyte imbalances.

n list the manifestations of electrolyte imbalances.n identify normal distribution of ICF and ECF.n state the normal serum values for Na, K, Cl,

Mg, PO4 ,Ca.

3

Starling’s Law of the Capillary

n Fluids leave (filtration) or enter (re-absorption)the capillaries depending on how the pressurein the capillary and interstitial spaces relate toone another

n Volume re-absorbed is similar to volumefiltered: “A net equilibrium”

n Regulates relative volumes of blood &interstitial fluid

4

Capillary Exchangen The 5% of blood in the systemic capillaries =

the bulk of blood that exchanges materialswith systemic tissue cells

n Substances that pass through thin capillarywalls into interstitial fluid and then into cellsare: nutrients & oxygen

n Substances that are secreted by tissue cellsand removed from them are: wastes & CO2

5

Fluids

n Distribution of total body water (TBW)n 60% of adult body weight is fluid

• Gender, body mass & age considerationsn Intracellular (ICF, within cells = 40% of body

weight)n Extracellular (ECF, plasma, interstitial & lymph

=20% of body weight)n 1 Litre water = 2.2lb or 1 kg

6

Developmental Differences

n Infants & young childrenn Four areas of immature functioning

• Increased fluid intake and output relative to size• Total body fluid is 20% more than adults

• Greater surface area relative to size: > water lossthrough skin

• Increased metabolic rate up to 2 years• Immature kidney function

• requires more fluid to excrete wastes

7

Fluid Shifts“Third Spacing”

qExcess fluid in interstitial spaces andconnective tissues between cells [edema]

ORn Excess fluid in potential spaces [effusion]

• peritoneal cavity• pericardial sac• synovial cavities of joints• alveoli or intra-pleural spaces

8

Fluid Shifts“Third Spacing”

n Etiologyn Caused by an increase in filtration and/or decrease in

reabsorption due to altered capillary forcesn Pathophysiology

n Lymph edeman Angioedema

Mechanisms causing third spacing & edeman massive inflammationn venous obstructionn increased blood volumen low serum albumin

9

Hypovolemia

n A decrease in the ECF volumen Intravascular and interstitial volume

n Isotonic volume deficit may be due tonDecreased intake of isotonic fluidsnOr excessive

• vomiting or diarrhea• hemorrhage• urine output

10

Hypovolemian Hematocrit (Hct) is sensitive to fluid shifts

n volume (%) of erythrocytes in whole bloodn 40-54 mL/dL malesn 37-47 mL/dL femalesn 11.2-16.5 mL/dL children

n BUN will be elevated d/t < volumen 11-23 mg/dL

11

Hypovolemia: manifestationsn Decreased tissue perfusionn Check capillary refill time

n Decreased blood volumen Hypotension, tachycardia, oliguria

n Tissue dehydrationn Loss of skin turgorn Possible temperature elevation

12

Hypovolemian Nursing Responsibilities:

n calculate I & O frequently• minimal urinary output = 30cc/hr• check urine specific gravity

n check O2 saturationsn draw & analyze blood gasesn auscultate lungs (side to side)n check temperature distal from heartn give isotonic solutions (oral or IV)

• Normal saline; dextrose, Ringer’s lactaten give a fluid bolus as ordered

13

Hypervolemia

n Excess of isotonic fluid in the intravascularand interstitial spacesn Isotonic fluid retention

• Olguric state r/t renal failuren Secondary Hyperaldosteronism

• Inappropriate renal reabsorption of water andsodium,and increased renal secretion of potassium

n Iatrogenic hypervolemia

14

Hypervolemia

n Pathon An excess in blood volume results in

elevated CHP and third spacingn Clinical manifestations

• Edema• Hypertension• Bounding pulse• Increased urinary output

15

Major Electrolytes

n Electrolytesn Na+, K+, Ca++, Mg+ = cationsn HCO-3, Cl-, PO-4 = anions

n ICF = K+n ECF = Na+

n osmosisn osmolarityn capillary dynamics

16

Hyponatremia(Na+ < 135 mEq/L)

n Low sodium determined by blood chemistryn The most common electrolyte imbalance:

• 2.5% of hospitalized patientsn Sodium supports neuron transmission

n Mechanism and examplesn Free water gainn Deficient sodium intaken Renal sodium loss in excess of watern Water in excess of sodium gain

17

Hyponatremia(Na+ < 135 mEq/L)

n Manifestationsn Water excess fi rapid weight gainn Na+ loss fi neurological symptoms

• irritability, seizures, < LOCn Muscle crampsn Anorexia/ Nausea/Vomiting (subtle signs)

n Treat water excessn Fluid restriction (I&O)

n Treat sodium loss• Oral or IV sodium

18

Hypernatremia(Na+ >145 mEq/L)

Etiologyn Water loss or sodium gains

n Elderly / or comatose patientsn Na+ intake > water intaken Diabetes insipidus (excessive fluid loss) fi < production of

ADHn Damage to hypothalamic thirst center?

• Tumor or CVA?n Manifestations

n Thirst, dry tonguen Restlessness; < LOC; Coma; Intracranial bleedsn Weight changes

19

Hypernatremia(Na+ >145 mEq/L)

Treatment (Rx)

n Dilute Na+ and promote secretionn Fluids (5% D/W) and diureticsn Always check LOC

n loose alertness & orientation• sepsis, head injury, intracranial bleed

n Sodium pulls fluid to cause blood vessels toburst

20

Potassium (K+)3.5-5.0 mEq/L

n Primarily an intracellular ion; small amount inplasma is essential for normal neuromuscular ancardiac function

n Maintained by the cellular sodium-potassium pumpn K+ changes fi altered excitability of musclesn Eliminated by kidneys

n renal problems causes hyperkalemian Insulin: causes K+ to move from ECF fi ICFn Acidosis, trauma to cells, and exercise

• cause K+ to move from ICF fi ECF:

21

HyperkalemiaK+ > 5.5 mEq/L

n Major Causesn Increased potassium intake

• excess or rapid delivery of K+• penicillin containing K+• Massive blood transfusion with irradiated packed red cells

Buntain and Pabari (1999)

n Shift of K+ from the ICF to ECF• Acidosis, uncontrolled DM• increased cell lysis (e.g. cytotoxic drugs)

n Decreased renal excretion• Digitalis toxicity, renal failure, overuse of potassium sparing

diuretics (spiroaldactone)

22

HyperkalemiaK+ > 5.5 mEq/L

n Mainfestations:n weak skeletal muscles/ paralysis > 8 mEq/Ln paresthesiasn irritabilityn abdominal cramping with diarrhean irregular pulse fi EKG changes fi cardiac standstilln EKG changes

• peaked T-waves and a shortened QT interval occur• Depressed ST segment and widened QRS interval

23

HyperkalemiaK+ > 5.5 mEq/L

Managementn Eliminate K+

n Diuretics (Lasix)n Dialysisn Kayexalaten Increased fluids

n IV insulinn Cardiac monitor

24

HypokalemiaK+ < 3.5 mEq

n Major causesn < intake of potassium or > cellular uptake of

potassium• Insulin: promotes K+ uptake by muscle & liver cells• When insulin is given: K+ goes into ICF fi < serum K+

leveln Uncontrolled diabetes mellitus:

• > Glucose: osmotic diuretic fi > potassium viaurinary excretion

• Diabetic Ketoacidosis: › H+ ions in ECF fiexchange across cell membranes fi K+ is firstelevated and then K+ stores are excreted via urine

25

HypokalemiaK+ < 3.5 mEq

n Epinephrine: promotes uptake into cells• stress, acute illness, hypoglycemia

n Excessive GI loss: diarrhea & ng suction fimetabolic alkalosis

n Diuretics: Lasix (watch K+ levels)n Excessive renal excretion fi elevated

aldosterone fi diuresis

26

HypokalemiaK+ < 3.5 mEq

n Signs & Symptomsn Muscle weakness: hypotonian Cardiac dysrhytmias (T-wave inversion or PVCs)n Atony of smooth muscle

• intestinal distention• constipation• paralytic ileus• urinary retention

n Confusion or disorientation

27

HypokalemiaK+ < 3.5 mEqManagement

n Administer KCL slowly and accuratelyn dilute properly with other IV fluids

• 10 mEqs/1 hourn can cause pain and necrosis of veins

• use central IV line for large rapid amountsn Bring pt out of immediate danger & restore

graduallyn Consider discontinuing diuretic therapyn Consider chloride for metabolic alkalosis

28

Calcium8.8 - 10 mg/dL

n Major functions:n Transmission of nerve impulsesn Cardiac muscle contractionsn Blood clotting factorn Formation of teeth & bonen Muscle contraction

n Requires:n Vitamin Dn Parathyroid hormone (PTH)n Calcitonin from thyroid gland

29http://lpi.oregonstate.edu/infocenter/minerals/calcium/capth.html

30

HypocalcemiaCa+ < 8.5 mg/dL

n Nutritional deficiency of calcium or Vitamin Dn Parathyroid deficiency d/t surgical removaln Children & elderly d/t dietary deficiencyn Bone cancer: excess bone formation

n “Hungry Tumor” syndromen Treatment of prostrate cancer with estrogen depletes

ECF calcium levelsn Blood transfusions

n preserve blood with citrate & this binds with calcium

31

HypocalcemiaCa+ < 8.5 mg/dL

n Manifestations:n Chvostek’s signn Trousseau’s signn Dysrythmias:< threshold for depolarization in

cardiac cellsn Paresthesias: “pins & needles”n Abdominal cramping & diarrhean Tetany, Seizures (severe hypocalcemia)

32

HypercalcemiaCa+ > 10.5 mg/dL

n Malignancies or hyperparathyroidismn PTH secreting tumor (adenoma)

n Skeletal calcium secreted into bloodstreamn Metastatic breast cancer & multiple myeloma

n Prolonged immobility: loose Ca+ from bone into bloodn Osteoporosis: Ca+ is liberated into bloodstreamn Manifestations:n lethargy/ weakness/fatigue/constipationn pathogenic fractures fi calcium loss from bone

33

Phosphate (PO4 -) 3.0 - 4.5mg/dL or 1.8 - 2.6 mEq/L

n Stored with Ca+ in bones & teethn PO-4 & Ca+ are equilibrated

• > Ca+ = < PO-4• excreted by kidneys

n Hypophosphatemia: < 2.7 mg/dLn clinical manifestations

• confusion, weakness, seizures, numbness, coman Hyperphosphatemia: > 4.5 mg/dL

n common in renal failure

34

Magnesium (Mg+)1.5 - 2.5 mEq/L

n Second most abundant ICF cationn essential for neuromuscular functionn changes in serum Mg+ levels effect other

electrolytesn Hypermagnesemia: > 2.5mEq/L

n muscle weakness, bradycardia, hypotension,nausea & vomiting

n Hypomagnesemia:< 1.5mEq/Ln increased neuromuscular irritability

• Muscle spasms, tetany, seizures

35

References

n Braxmeyer, D. L. & Keyes, J. L. (1996). Thepathophysiology of potassium balance. CriticalCare Nurse, 16(5), 59-71.

n Hansen, M. (1998). Pathophysiology:Foundations of disease and clinicalintervention. Philadelphia: Saunders.

n Huether, S. E., & McCance, K. L. (2002).Pathophysiology. St. Louis: Mosby.