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Fluid and Electrolyte Basics

  • Fluids and electrolytes play a vital role in homeostasis within the body by regulating various bodily functions including cardiac, neuro, oxygen delivery and acid-base balance and much more.
  • Electrolytes are the engine behind cellular function and maintain voltages across cellular membranes.  Without proper electrolyte balance the body is unable to carry out the most basic functions.
  • Understanding the basics of these complex concepts is vital to your success in caring for complex patients.

Inside the NRSNG Academy, we have an entire Lab Values course that covers fluid and electrolytes, acid-base balance, and must know lab values.  View the NRSNG Academy.

View the NRSNG Academy

Movement of Fluid


Concentration is a number that shows the amount of solutes dissolved in a fluid.  The word solute is used to describe any substance that is dissolved in a fluid.

Concentration gradient: Molecules in a solution are in a constant state of motion.  In a liquid, they will naturally move from areas of higher concentration to areas of lower concentration.  A concentration gradient is simply variations in concentrations in a fluid.  In the following picture the container on the left has an area to the upper left that has higher concentration than the rest of the container.


Osmolarity: The number of particles in a solution by volume (mOsm/L).  It is calculated using osmolality.

Osmolality: The number of particles in a solution by mass (mOsm/kg).  This can be measured using an osmometer.  Osmolality is used- more so than osmolarity- in a clinical setting.  The osmolality of IV fluids, plasma, urine are used to help paint a picture of volume status in a patient.  Osmolality creates osmotic pressure and thus affects movement of water from different compartments in the body.


Pressure is a force applied to a surface.  Different forces affect movement of water through different areas of the body.

Osmotic Pressure: Pressure needed to stop fluid movement across a membrane created by concentration gradients.  When molecules can’t move across a membrane, fluid will move to equilibrate the concentrations.

Oncotic pressure: A type of osmotic pressure.  It is specifically talking about the pressure needed to stop movement of fluid in response to protein concentrations.  Albumin in the blood creates oncotic pressure that helps keep blood within the vessels of the circulatory system.

Hydrostatic pressure: Pressure created by the pull of gravity.  Hydrostatic pressure can also be created by blood against the surface of our vessels.  Blood pressure created by the heart pumping is hydrostatic pressure.


Osmosis: Osmosis is the movement of fluid across a membrane due to a concentration gradient.

Filtration: Filtration occurs when water moves across a membrane due to hydrostatic pressure.  An example would be pouring a solution through a colander.  The force of gravity aids in the movement of the fluid.


When we talk about tonicity we are comparing two different solutions.  Tonicity is a term to describe the effect of the particles in concentration on osmolality.  If a particle is small and can pass through the membrane it will have little effect on osmolality, because the concentration can even out by movement of the particle instead of the fluid.  All body fluids have equal tonicity, because fluids will move between compartments to balance things out.  In medicine we are typically comparing the tonicity of different IV fluids to the blood.  If we add an IV fluid and change the blood concentration that can effect water movement between plasma and the inside of red blood cells.

Hypertonic: A hypertonic solution has a higher concentration than blood.  There are more solutes dissolved in the solution.

Isotonic: An isotonic solution has the same concentration as blood.

Hypotonic: A hypotonic solution has a lower concentration of fluid than the blood.

Movement of Electrolytes

Some particles in the body can move through membranes easily, while others may need to be transported or assisted with a little pressure.  In this section we will discuss different types of movement that occur across body membranes.


Different areas of the body are separated by different types of membranes:

Cell membranes: The cell membrane separates cells from the outside environment, intracellular fluid from interstitial or intravascular fluid.

Capillary membranes: The walls of the blood vessels.  They separate intravascular fluid from interstitial fluid.

Epithelial membranes: Mucosa of the stomach, intestines, and renal tubules.

The cell membrane contains two layers of phospholipids which have a hydrophilic head (tendency to mix with water) and hydrophobic tail (repelled from water).  The hydrophilic tails point toward each other with the hydrophobic heads line each side of the membrane.  Embedded in the membranes are different proteins.  Because of the nature of the membrane some particles can move freely while others must be transported.

Diffusion:  Diffusion occurs when solutes in a solution move from an area of higher concentration to an area of lower concentration.  There must be a concentration gradient for diffusion to occur.  Diffusion in the body is affected by several different factors: temperature, concentration, size of molecule, and surface area of membrane.  Diffusion may also occur due to an electrical gradient.  If positively charged ions move into the cell they will be followed by negatively charged ions.

Simple diffusion:  Simple diffusion occurs when substances are lipid soluble (oxygen, carbon dioxide) or when they are small enough to travel through protein pores or channels (urea, water).  Simple diffusion requires a concentration or electrical gradient.

Facilitated diffusion:  Large molecules or molecules that aren’t lipid soluble require facilitated diffusion.  Concentration gradients need to be present in facilitated diffusion.  Because of its size glucose requires a carrier protein, which allows it to become lipid soluble to move through the cell membrane.  Carrier proteins can become saturated if there is a very large difference in concentration between the inside of the cell and the outside.

Active transport:  Active transport is required to move molecules against a concentration or chemical gradient.  Energy is required for active transport to take place.  The sodium-potassium pump is an example of active transport.  Carrier proteins can become saturated with excess substrate (molecule upon which an enzyme acts).

To put everything together, the body has many different compartments.  Fluids found in each compartment are regulated by membranes, concentrations, and hydrostatic pressure.

Water can move freely from vessels into cells or interstitial spaces.  The pressures described above help maintain fluids within the different compartments.  The next section describes each of the different areas where fluid is kept and how the different regulatory mechanisms help maintain homeostasis.


The body is made of trillions of cells.  Water is found around cells, inside cells, within vessels, and around organs.  Each fluid in the body has unique characteristics that allow for the specific functions within each space.  The body has many regulatory mechanisms to maintain homeostasis of the fluids.

The different fluids in the body are unique in their electrolyte content.  The following chart lists the electrolyte content of different fluids in the body and compares them to the IV fluid that most resembles plasma: lactated ringers.

intracellular vs extracellular



Extracellular fluid:  Fluid outside of the cell.  ECF includes fluids within the blood vessels (intravascular fluid) and fluid within the interstitial spaces.  ECF totals about 15 Liters.

Intravascular Fluid: This includes all the blood within the circulatory system: veins and arteries.  IVF, also known as blood contains red blood cells and Plasma.  The plasma makes up 3 liters out of 5 liters of IVF.

Interstitial Fluid: Interstitials fluid is found in many compartments throughout the body.  Some examples include lymph, synovial fluid, cerebrospinal fluid, digestive secretions, and pericardial fluid.  11-12 liters of fluid.

Intracellular fluid:  The fluid components within the cell are the cytoplasm and neoplasm.  Intracellular fluids make up 60% of total body water.  25 liters.


Basic Anatomy

There are two kidneys in the body.  They lie on the right and left side of the abdomen below the liver and stomach respectively.  They sit toward the back of the abdomen.  An adrenal gland sits directly above each bean shaped kidney.  A renal artery enters the kidney and the renal vein and ureter exit the kidney.  The functional unit of the kidney is the nephron.  The nephron helps filter out excess water and solutes from the blood.  Filtered blood then leaves via the renal vein, and waste via the ureter.


The kidneys play many vital roles in the body including removal of waste products; regulation of blood pressure and electrolytes; acid-base balance; reabsorption of amino acids, glucose, and water; hormone production: calcitriol, erythropoietin; and enzyme production: renin.

kidneys fluid balance

kidneys electrolytes raas

Antidiuretic Hormone (ADH):  Stimulated by increased concentration of electrolytes or decreased blood pressure.  The hypothalamus has osmoreceptors that monitor osmolarity of the blood.  ADH is produced in the hypothalamus and stored in the posterior pituitary gland, it is released from the posterior pituitary into the blood to act on the kidneys.  ADH stimulates constriction of blood vessels and water conservation by increasing water reabsorption in the kidneys and decreasing sweat production by sweat glands.

Renin:  Created by the kidneys in response to decreased blood flow.  Renin stimulates the conversion of angiotensinogen to Angiotensin I, which is then converted to Angiotensin II, via the enzyme angiotensin converting enzyme.

Angiotensin II:  Causes blood vessel constriction stimulates aldosterone excretion.

Aldosterone:  A hormone made in the kidneys.  It works to increase sodium and water reabsorption and increase potassium excretion in urine.

Brain Natriuretic Peptide (BNP):  A hormone made in the heart ventricles in response to increase stretching.  When stimulated, BNP works to increase sodium and water excretion by the urine.  This leads to decreased blood volume and blood pressure.

Atrial Natriuretic Peptide (ANP):  A hormone made in the right atrium of the heart in response to increase stretching.  Just like BNP, ANP works to increase sodium and water excretion by the urine.  This leads to decreased blood volume and blood pressure.

fluid balance



(135-145 mMol/L)




Sodium is the main cation in the blood.  Small amounts are also found within the cell.


Sodium concentration is important in maintaining the cell membrane potential.  In excitable cells like neurons and muscle cells, membrane potential is essential for communication and muscle contractions respectively.  Sodium also helps maintain fluid balance in the blood.  It is the main contributor to osmolality of the blood.  Sodium contributes 280 mOsm of the 300 mOsm of the blood.  Sodium can move into cells, but is pumped out against electrochemical gradient.  Na+ absorption is proportional to intake.




Movement from ECF to ICF

If serum sodium increases some sodium will shift into the cell, maintaining the balance of sodium in the blood.


Increase total body sodium

Typical daily intake is usually much higher than our needs.



Excretion is regulated by several important hormones: aldosterone, angiotensin II, and natriuretic peptides.


Changes in serum sodium often reflect changes in fluid status.   If Na in the blood increases or decreases, the body responds by increasing or decreasing water to maintain sodium concentration.  (Remember concentration is affected by both the solute: sodium, and the solvent: water)  If you decrease the amount of water you increase concentration.  If you increase sodium you increase concentration.   Because the body compensates changes in serum sodium concentration are typically caused by changes in water.  This makes sodium a good indicator of hydration.



Hyponatremia can be caused by overhydration or body losses of salt water that is replaced with water.  The kidneys can compensate be excreting sodium free water.  If the body needs to conserve water, however, this compensatory mechanism can’t be used.  Hyponatremia causes hypoosmolality since sodium plays such a big role in serum osmolality.


When looking at hyponatremia it is important to know if it is in the setting of decreased, increased, or normal ECF volume.   In hyponatremia fluid moves out of the blood and into the interstitial spaces.


The brain has a fixed volume due to the skull.  Hyponatremia can lead to increased intracranial pressure and cerebral edema.  The body adapts over time by decreasing the concentration within the cells of the central nervous system.  Neurologic symptoms are higher in acute hyponatremia versus chronic because of this adaptation.  If serum sodium levels get below 120 mMol/L neurological symptoms may be seen.  Levels below 115 mMol/L can cause seizures or coma.


**It is dangerous to replete sodium too quickly in chronic hyponatremia.   It can cause loss of cerebral fluid due to increase in serum osmolality.


Hyponatremia with increased or normal blood volume




  • Impaired water excretion:  syndrome of inappropriate antidiuretic hormone (SIADH) – increased ADH production, oliguria


  • Fluid shifts:  edema – congestive heart failure, nephrotic syndrome, cirrhosis; hypotonic IV fluids; hyperglycemia leads to a shift of fluid from intracellular to intravascular.


  • Excess fluid intake: polydispsia (excess thirst)



Sign & Symptoms


muscle weakness, headache, lethargy, apathy, convulsions, confusion, edema, weight gain, elevated BP, muscle cramps, coma, increased  mean arterial pressure (MAP), increased, increased central venous pressure (CVP), pulmonary artery pressure (PAP)




  • Treat underlying cause: SIADH
  • Water restriction:  1000 mL/day
  • Diuretics: loop diuretics, thiazide diuretics should not be used


In hyponatremia that has persisted for more than 48 hours replete sodium slowly or permanent neurologic damage may occur.   No more than 24 mmol/L increase in the first 48 hrs.


Hyponatremia with decreased blood volume




  • GI loss: diarrhea, fistula, nasogastric suction, vomiting, laxatives


  • Renal loss: diuretics, hypoaldosteronism, renal salt wasting



Sign & Symptoms


tremors, personality changes, anxiety, cold skin, irritability, dizziness, postural hypotension, clammy skin, dry mucous membrane seizure, coma, decreased mean arterial pressure (MAP), decreased central venous pressure (CVP), pulmonary artery pressure (PAP), decreased cardiac output, increased systemic vascular resistance





  • Serum osmolality: is typically decreased (except is hyperglycemia, azotemia)
  • Serum sodium: decreased
  • Urine specific gravity: decreased as kidneys excrete excess fluid
  • Urine sodium: decreased (except in SIADH and adrenal insufficiency)





  • Replace sodium, fluid and other electrolytes like potassium and bicarbonate.
  • Hypertonic IV solution: 3% NaCl, to correct symptoms, administered with a loop diuretic to prevent fluid overload.





  • Water loss: conditions that decrease urine concentration (diabetes insipidus), increased insensible loses (respiratory infection, diarrhea)


  • Increased sodium: hypertonic saline solution, Cushing’s syndrome, sodium bicarbonate (NaHCO3), near drowning in salt water, drugs: Kayexalate


  • Inadequate water intake (issues with thirst or access to water): inadequate fluid administration in coma pt, tube feedings




Signs and Symptoms


During hypernatremia there is decreased tonicity since sodium contributes to osmolality.  In response fluid moves out of the cells and into the blood.  The cells in the brain adapt by increasing intracellular osmolality.  This ensures that the cells won’t lose excess water.  In chronic hypernatremia this adaptation has occurs, and symptoms are minimal.  As with hyponatremia if serum sodium is adjusted too quickly it can damage the adapted neurons.  It could case dangerous cerebral edema.


thirst, fatigue, irritability, altered mental status, coma, fever, flushed skin, peripheral edema, postural hypotension, tachycardia and tachypnea, muscle twitching, deep tendon reflexes


  • Sodium excess: increased central venous pressure (CVP) and  pulmonary artery pressure (PAP)
  • Water loss: Decreased central venous pressure (CVP) and  pulmonary artery pressure (PAP).





Dehydration test: hold water for 16-18 hrs, administer ADH, wait 1 hour then check serum and urine osmolality.

Serum osmolality:  increased because of increased serum sodium

Serum sodium : increased

Urine specific gravity: increased as kidneys reabsorb water.

Urine osmolality: increased as kidneys reabsorb water.

Urine sodium: decreased with renal water loss





  • Treat underlying cause:  correcting electrolyte imbalance, treat diarrhea or fever.


  • Replace water, IV or oral.  D5W or hypotonic saline solution, just to replace water deficit.


  • Diuretics and oral or IV water replacement


(3.5 – 5 mEq/L)



Potassium is the main cation inside the cell.  A small amount of potassium is found in the blood and interstitial fluid.


Potassium is transported into the cell via the sodium-potassium pump.  Three sodium ions are pumped out of the cell for every two Potassium ions pumped into the cell.  The amount of Potassium outside the cell helps maintain the resting membrane potential.  Essentially the outside of the cell is more positive and the inside more negative.  The electrical charges separated by the cell membrane give the cells in the body a resting membrane potential.  In excitable cells like neurons and muscle cells this membrane potential is essential for communication and muscle contractions respectively.




Movement of Potassium from ICF to ECF


Movement between intracellular fluid (ICF) to extracellular fluid (ECF) is affected by insulin, pH, and epinephrine:


Insulin and epinephrine stimulate glucose uptake in to the cells.  They also stimulate activity of the Na-K+ pump.  The concentration gradient of sodium that is established by the pump allows for the transport of glucose in to the cell.


The pH affects potassium as well.  When pH is low, the excess H+ ion in the blood  move into the cells.  To maintain electric equilibrium potassium moves out of the cell in response.  The opposite happens during alkalosis.  It is an inverse relationship, as pH goes down potassium goes up and vise versa.


Increased total body Potassium


  • Tissue breakdown: since the cell is where most potassium is stored, when cells are broken down that potassium is released into the system.
  • Increased Intake: excess potassium rich foods, salt substitutes, transfusions of whole blood or packed red blood cells.  Sources of K+ – fruits, vegetables, beans, dairy, meat


  • decreased K+ excretion from the kidneys due to K+ sparing diuretics, renal failure, or Addison’s disease




Potassium is excreted via the kidneys-80%, gastrointestinal tract-15%, and the skin-5%.


The kidneys play a big role in potassium regulation.  If intake is high, or tissue catabolism occurs the kidneys will quickly compensate and excrete excess serum potassium via the urine.  When plasma potassium concentrations are high the adrenal cortex releases aldosterone which will increase excretion of potassium.


Tip:  Aldosterone can also be stimulated by postsurgical stress or volume depletion.  In these cases you may also see increase potassium excretion.  Lastly increased urine production can also cause increase losses of potassium


Mg def: potassium shifts out of cell, and increased K+ excretion occurs.





  • Inadequate intake


  • Increased urine production: aldosterone simulation (volume depletion, surgery, hyperaldosteronism), diuretics, magnesium deficiency


  • Movement of Potassium into the cells: anabolism, alkalosis, treatment of DKA with insulin, refeeding syndrome, treatment of acidosis-


  • Increased GI losses: specifically from the stomach, like NGT to suction or pyloric stenosis, vomiting, diarrhea, NG suction, GI surgery


  • Diaphoresis: excess perspiration


  • Medications: antibiotics, diuretics, laxatives, insulin, Albuterol, epinephrine



Signs & Symptoms


decreased bowel sounds, vomiting, dysrhythmia, muscle weakness, muscle cramps, fatigue, ileus, nausea, constipation, paralysis, hypoventilation, weak pulse, decreased muscle tone


hypokalemia ekg

Lab Tests


Serum potassium: decreased

Urine potassium: increased is indicative of renal cause, if decreased cause is not renal.

Transtubular K+ concentration gradient (TTKG): calculated using potassium and osmolaltiy values in the serum and urine to determine cause of increased potassium levels.

ABGs: evaluate  acidosis/alkalosis as a possible contributor.

ECG: monitor for ST- segment depression, presence of accentuated U wave, flattened T wave, ventricular dysrhythmias,


Hypokalemia may cause digitalis toxicity even if serum digitalis levels are WNL.




  • Treat underlying cause


  • Increased potassium intake:


high potassium food


  • Potassium Replacement via oral or IV medication:  40-80 mMol/day IV divided doses.  If severe K+ should be replaced via IV:  no more than 10-20 mmol/per hour or 30-40mmol/l (unless severe)  IV K+ via peripheral line can cause irritation to vessels.  Pt on more than 10 mmol/hr should be on continuous cardiac monitor: peaked t wave indicates hyperkalemia.  Types:  KCl or K phosphate.  Usually KCl since vomiting and diuretics cause Cl loss as well.  KHCO3 or K citrate if metabolic acidosis is present.


NEVER administer via IV push.


  • Potassium sparing diuretics:  spironolactone, can help increase serum potassium


  • KCl salt substitutes: 1 tsp is equal to 60 mmol KCl


Correct Mg deficiency.  If potassium is not improving with significant K+ replacement Mg deficiency might be to blame.





  • Intake:  excess IV potassium administration


  • Movement of potassium out of cells 

-insulin deficiency (esp with patients that also have chronic renal insufficiency)

-acidosis (metabolic and respiratory)

-tissue breakdown due to fever, sepsis, trauma, surgery

-hypertonicity (uncontrolled DM)


  • Excretion:

-renal failure

-potassium sparing diuretics, ACE inhibitors, NSAIDs

-adrenal insufficiency

-Addison’s disease


  • Medications: potassium sparing diuretics, ACE inhibitors, beta blockers, chemotherapy medications, heparin, digoxin, NSAIDs


In DKA potassium in the blood can be elevated despite increased loss of potassium in the urine.  During the lack of insulin, acidosis, and increased catabolism potassium moves out of the cells into the blood.


Signs & Symptoms


respiratory distress, diarrhea, irritability, anxiety, muscle weakness, paresthesia, abdominal cramping, anuria, ECG changes, hyperreflexia




ABGs: identify acidosis as possible cause of hyperkalemia

Diagnostic ECG: monitor for prolonged PR interval, ST depression, thin T wave, widened QRS, and loss of P wave.

Serum Cortisol: identify Addison’s disease

Serum Potassium: elevated

Transtubular K+ concentration gradient (TTKG): calculated using potassium and osmolaltiy values in the serum and urine to determine cause of increased potassium levels.






-Kayexalate: Kayexalate is a resin that binds to potassium in the colon so that it is excreted.

-Fludrocortisone:  increases urinary excretion of potassium

-Calcium gluconate IV can help counteract the cardiac and neurologic effects of hyperkalemia.

-IV glucose and insulin: this will help shift potassium from the blood and into the cells.  The effect lasts about 6 hours

-Sodium bicarbonate:  this will help shift potassium into the cells.  The effect lasts 1-2 hours

-Beta2 agonists: this will help shift potassium into the cell.  (Albuterol)


Limit potassium intake: following a low potassium diet or choosing an enteral product with less potassium


Discontinue medications that might be contributing to hyperkalemia: NSAIDs, ACE inhibitors, potassium-sparing diuretics


Dialysis: removes potassium from the body




Calcium is stored in the bones and teeth.  Calcium Phosphorus salts help give bones their strength.  Sodium is found in the ECF but less than 1% of total body Calcium is there.  Calcium plays a very important role in muscle contraction, and has an inhibitory affect on neurons.


There are several mechanisms that help maintain the amount of calcium in the blood.  When levels of calcium are low parathyroid hormone is released from the parathyroid gland.  PTH acts to breakdown bone so that the stored calcium can replete calcium in the ECF.  PTH also activates Vitamin D which increase calcium absorption from the intestines.  Active Vitamin D also stimulates the kidneys to conserve calcium and excrete phosphorus.  When calcium levels are too high the thyroid gland releases calcitonin.  Calcitonin stops bone breakdown.  Both dietary intake and bone breakdown can lead to increase in calcium levels Calcium is lost in gastrointestinal secretions, urinary excretion, bone deposition, and sweat (in small amounts).  Typically we only absorb 20-30% of dietary calcium.





  • Increased calcium loss: diuretics


  • Decreased intake: decreased absorption (diarrhea, gastric surgery), reduced intake, vitamin D deficiency,


  • Altered regulation

– hypoparathyroidism.

– hyperphosphatemia (rhabdomyolysis, renal failure, tumor lysis syndrome) elevated phosphorus can lead to low calcium.  Calcium and phosphorus have a reciprocal relationship, as one goes up the other goes down.


-Thyroidectomy (calcium moves from blood back into bone)


  • Acute pancreatitis, chronic alcoholism, bone cancer, alkalosis


Since some Calcium in the blood is bound to protein (albumin), when albumin is low total calcium may be low.  This is not a problem and doesn’t need treatment as long as ionized Calcium is within normal limits.



Signs and Symptoms


arrhythmias, numbness,  tingling fingers, hyperactive reflexes, muscle cramps, tetany, convulsions, tetany, stridor and spasms, lethargy, anxiety, depression, psychosis, decreased heart contractility and heart failure, positive chvostek’s sign and trousseau’s sign


ECG changes: prolonged QT, elongation of ST segment–> ventricle tachycardia.




Ionized serum Ca: decreased – most useful measure to detect calcium deficiency

Magnesium: low Mg may cause low Ca

Parathyroid hormone: Decreased levels indicate hypoparathyroidism which is related to low calcium

Phosphorus: elevated Phos may cause low Ca

Total serum Ca: total Calcium in the blood may be declined due to decreased protein that calcium is bound to.  Look at albumin levels and pH when assessing for deficiency




Treat the underlying cause:


  • Replete calcium: This can be done orally or via IV.   With symptoms present usually IV calcium gluconate is best option.
  • Replete magnesium:  If Mg is the cause of deficiency, replace.
  • Vitamin D: Vitamin D increases absorption of Calcium if repleting calcium orally.
  • Phosphate binder: This can help reduce elevated phosphorus levels in patients with renal failure.
  • Increased intake:  replete via oral intake: 1000-1500 mg/ day

Oral supplements: calcium carbonate


high calcium foods





  • Increased intake:  Excess IV calcium


  • Decreased excretion: renal failure, thiazide diuretics


  • Bone breakdown: prolonged immobility, fractures, malignant diseases, Paget’s disease, hyperparathyroidism, hyperthyroidism,  hypophosphatemia


  • Increase absorption: Vitamin D or Vitamin A overdose


  • Medications: diuretics, ace inhibitors


Signs & Symptoms


weakness, lethargy, nausea, vomiting, anorexia, polyuria ( from nephrogenic diabetes insipidus), bone pain, fractures, itching, flank pain ( renal calculi), confusion, depression, stupor, coma, personality changes, paresthesia, ECG findings: shortening of ST segment and QT interval, prolonged PR interval.  more severe: ventricular dysrhythmia.  Risk for digitalis toxicity


Lab Tests


Imaging: assess bone density, identify kidney stones  

Ionized Calcium: elevated

Parathyroid hormone:  increased in hyperparathyroidism

Serum Calcium: elevated, assess serum albumin level: for every 1g/dL drop in albumin there is a drop in calcium of 0.8- 1 mg/dL decrease in serum calcium




Treat underlying cause: partial parathyroidectomy for hyperparathyroidism, chemotherapy for malignant disease, or discontinue ca supplements, vitamin A, vitamin D, thiazide diuretics in renal patients


IV NS solution: Administer rapidly to increased Ca excretion via urine.  Administer diuretics at the same time to prevent volume overload and to increase calcium excretion.


Low calcium diet:  limit calcium intake.



  • Bisphosphates: Pamidronate or etidronate:  These medications inhibit bone resorption.  This medication is most often used for malignant disease
  • Plicamycin:  cytotoxic antibiotics that decreases bone resorption.  Used with neoplastic disorders.
  • Calcitonin: Reduces bone resorption and increase bone deposition of Ca and phos.  increase urinary ca and phosphorus excretion.
  • Gallium nitrate:  inhibit bone resorption – used in malignant disease.
  • Cortisone: Steroids compete with Vitamin D for absorption in the small intestines.  This decreases calcium absorption as well.


Hemodialysis: with low calcium dialysate in renal failure patients


(2.5-4.5 mg/dL        0.81 – 1.45 mMol/L)



Phosphorus is the main anion in inside the cell.  The majority of Phosphorus is stored with Calcium in bones and teeth – 85%.  The inside of the cell contains 14% of phosphorus, and the blood has about 1%.  Most phosphorus in the body is in the form of phosphate.



  • Essential for nerve and muscle function
  • Involved in acid/base balance
  • Formation of red blood cells
  • Component of ATP (important form of stored energy in the body)
  • Carbohydrate, protein, fat metabolism
  • A part of structure of bones and teeth




Decrease phosphorus: insulin, glucose, carbohydrate (phosphorus shifts into the cell due to increased needs for of phosphorus during metabolism), alkalosis, specifically respiratory alkalosis due to intracellular shift of phosphorus


Increase phosphorus: respiratory acidosis can cause shift of phosphorus out of cell, increased intake, intestinal absorption increased, bone reabsorption, impaired renal excretion.


PTH causes increased GI absorption, increased movement of phosphorus out of bone.  PTH also increases renal excretion.


Close relationship between calcium and phosphorus





  • Inadequate intake: TPN with inadequate phosphorus


  • Intracellular fluid shifts: insulin, carbohydrate load, respiratory alkalosis, androgen therapy, refeeding syndrome, malnutrition


  • Tissue repair: phosphorus is needed to help with energy supply during tissue repair


  • Increased Excretion: decreased magnesium, decreased potassium, hyperparathyroidism, thiazide diuretics, ATN, Fanconi’s syndrome


  • Decreased absorption or intestinal loss:  phosphorus binding antacids (aluminum, calcium, magnesium), vomiting, nasogastric suction, diarrhea, malabsorption, vitamin D deficiency


  • Combination: Alcohol, alcohol withdrawal, DKA treatment, severe burns.


  • Medications: phosphate binders, antacids, diuretics, laxative abuse


Signs & Symptoms


Acute : coma, decreased grip strength, lack of coordination, seizures, chest pain secondary to poor oxygenation, muscle pain, increased risk of infection, confusion, numbness tingling of fingers and circumoral region, difficulty weaning from the vent, decreased  strength: difficulty speaking, respiratory muscle weakness (the weakenss in th respiratory muscles can lead to hypoxemia  and hyperventilation which may lead to respiratory alkalosis which aggravates the hypophosphatemia), bleeding due to platelet dysfunction, rhabdomyolysis and hemolysis in severe cases.


Chronic: joint pain, weakness, pseudo fractures,  lethargy, memory loss, cyanosis, joint stiffness, osteomalacia



Lab Tests


Serum Phosphorus: decreased  (moderate: 1-2.5 mg/dL, severe: < 1mg/dL)

PTH: identify hyperparathyroidism

Serum Magnesium: may be decreased due to increased excretion during hypophosphatemia

Alkaline Phosphatase: increased during building of bones (osteoblast activity)

Imaging: identify changes in bone density, shape: osteomalacia, rickets





  • Treat underlying cause: avoid phosphate binders ( aluminum, magensium, calcium antacids)


Increase Phosphorus intake:  consume high Phos foods (meat organ  meats especially, fish, poultry, milk, dairy, whole grains, seeds, nuts, eggs, dried beans/peas),  take and oral supplement: NeutraPhos, IV phosphorus if severe: NaPhos or KPhos.






  • Decreased excretion: hypoparathyroidism, acute or chronic renal failure, volume depletion.


  • Increased intake:  vitamin D excess with increased GI absorption, fertilizer poisoning, excess administration of phosphorus supplements,  excess use of Phosphorus containing laxatives or enemas


  • Extracellular shifts: respiratory acidosis and metabolic acidosis, diabetic ketoacidosis, infection


  • Movement of phosphorus out of cells:  Neoplastic disease (leukemia, lymphoma),  increased tissue catabolism (trauma, crush injury), tumor lysis syndrome, chemotherapy, rhabdomyolysis (breakdown of striated muscle)



Signs & Symptoms


tetany, muscle weakness, nausea, vomiting, anorexia, tachycardia, hyperreflexia


Most symptoms associated with hyperphosphatemia are actually associated with the accompanying hypocalcemia that often occurs.  Other symptoms may occur in metastatic disease due to soft tissue calcification: corneal haziness, conjunctivitis, oliguria, irregular HR, and papular eruptions.





Blood urea nitrogen (BUN): assess renal status

Creatinine: assess renal status

Imaging: assess bone density: osteodystrophy

Parathyroid hormone: decreased – identify hyperparathyroidism

Serum calcium: help identify primary cause

Serum phosphorus: increased




Treat underlying cause: correct volume depletion, treat secondary hyperparathyroidism in chronic renal failure:  in chronic renal failure excess PTH can lead to elevated phosphorus and bone disease.  Vitamin D can help reduce PTH levels.


Limit Phosphorus intake:  avoid high phosphorus foods.


Phosphate binders: (Renvela) Phosphate binders bind to Phosphorus in the GI tract to decrease absorption.


Antacids to bind phosphorus (Aluminum, Calcium, or Magnesium antacids): These medications will bind to phosphorus and decrease absorption.  In renal failure Calcium is preferred to Magnesium or Aluminum.


Dialysis: Dialysis may be necessary in severe acute hyperphosphatemia, with symptomatic hypocalcemia.


(1.5-2.5 mEq/L)


The majority of magnesium is stored in the bone, 50-60%.  Only 1% of magnesium is in the blood, and the remainder is inside the cell.


Magnesium activates enzymes that breakdown carbohydrate and protein, triggers the Na/K pump, and plays a role is neuron communication and heart function.  Most of Magnesium in the blood is ionized, but there is a portion bound to protein.





Absorption of magnesium is controlled by vitamin D.  Excretion is regulated by the kidneys.  Excretion is affected  by 3 things: excretion of sodium and calcium, blood volume, and parathyroid hormone.


↑ PTH → ↓ Mg Excretion

↓ Sodium and Calcium excretion  → ↓ Mg Excretion

↓ blood volume → ↓ Mg Excretion





  • Decreased intake: decreased GI absorption- malabsorption


  • Shift of magnesium into cell


  • Increased magnesium excretion: diuretics


  • Excess GI loss (vomiting, diarrhea, nasogastric suction, fistula)


  • alcoholism, cirrhosis, hyperthyroidism, hypothyroidism, pancreatitis, preeclampsia, hemodialysis, hypercalcemia, hypothermia, burns, sepsis, wound debridement


Signs & Symptoms


paresthesia, insomnia, loss of appetite, mood changes, confusion, fatigue, weakness, hallucinations




ECG: may see changes related to magnesium, potassium or calcium deficiencies.

Serum Albumin: if albumin is decreased it may cause decreased magnesium level

Serum Calcium: decreased – due to decreased action of PTH caused by

Serum Ionized Mg: decreased – tends to reflect intracellular magnesium

Serum Magnesium: decreased (can be normal despite low intracellular magnesium)

Serum Potassium: decreased – hypokalemia may be resistant to replacement if the cause is a problem with the sodium-potassium pump – magnesium may need to be repleted first


Urine Mg: identify renal cause




  • oral Mag-Ox in mild or chronic hypomagnesemia
  • IV or IM mgSo4 in sever hypomagnesaemia
  • add to TPN if pt receiving IV nutrition

increased dietary intake:

high magnesium foods




  • Increased intake:  antacids laxatives that contain magnesium, enemas, laxatives, excess admin of IV MgSo4, excess magnesium  in TPN


  • Decreased excretion:  renal failure, adrenocortical insufficiency (Addison’s disease, hypothermia)


  • Untreated DKA, cortical insufficiency, hemodialysis using magnesium rich dialysate


Signs & Symptoms


sensation of heat, decreased deep tissue reflexes, soft tissue calcification, hypotension, weakness, nausea, vomiting, decreased arterial pressure, bradycardia, lost knee jerk reflex (patellar reflex), diaphoresis, coma, flushing, altered mental function, drowsiness, paralysis, paralysis of respiratory muscles may occur when Mg > 10 mEq/L



ECG: AV block, prolonged QT interval


Serum Magnesium: increased




Treat underlying cause:  if magnesium is high due to medication, d/c the medication (antacids or laxatives that have magnesium: Maalox, Mylanta, Mag Citrate, Milk of Magnesia, Mag-Sulfate)


Diuretics and 0.45% normal saline: will help increase magnesium excretion, as long as patient has adequate renal function.


IV Ca gluconate: counteract neuromuscular effects of Mg if Hypermagnesemia is severe.


Dialysis with a low magnesium dialysate (pt with severe renal impairment)




Hypervolemia is an increase in extracellular fluid (intravascular and interstitial fluid).  In hypervolemia the body compensates with the release of natriuretic peptides- which increase excretion of sodium and water by the kidneys- and inhibition of aldosterone.




  • Retention of water and sodium: cirrhosis, nephrotic syndrome, heart failure, excess glucocorticoids


  • Excess fluid administration: excess IV fluids, excess fluid in total parenteral nutrition


  • Decreased renal function: acute or chronic renal failure with decreased urine output.


  • Fluid shift from interstitial space to intravascular fluid:  treatment after a burn, hypertonic saline administration, administration of a colloid solution like albumin


Signs & Symptoms


moist skin, edema, ascites, crackles, weight gain, increased blood pressure (decreased BP as heart rate falls), orthopnea, shortness of breath, bounding pulses, wheezes, rhonchi, rales, distended neck veins, tachypnea, tachycardia, gallop rhythm, increased CVP, increased pulmonary artery pressure (PAP), increased pulmonary artery wedge pressure (PAWP), increased mean arterial pressure (MAP) unless pt with heart failure.




ABGs: identify hypoxemia (decreased PaO2), and respiratory alkalosis (increased pH and decreased PaCO2)

Chest x-ray: assess for vascular congestion to identify pulmonary congestion.

BNP: increased

BUN: increased in renal failure

Hematocrit: decreased due to dilution

Serum Sodium: decreased in the presence of water retention

Urinary Sodium: possibly elevated if the kidneys are excreting excess sodium.

Urine specific gravity: decreased when kidneys are removing excess fluid



Water and sodium restriction: oral, enteral, parenteral


Limit high sodium foods 

Diuretics: IV or oral diuretics, loop diuretics (Furosemide) in severe hypervolemia, or renal failure


Renal replacement therapy (dialysis):  in renal failure or very severe volume overload




input and output, weight (monitor weights daily, a 2 kg wt gain equals 2 L fluid gain), specific gravity, edema



Hypovolemia is a decrease in intravascular fluid/blood volume.  With hypovolemia the body will attempt to compensate by increasing stimulation of the central nervous system:  increase heart rate, vascular resistance, thirst, ADH, and aldosterone.



  • Skin: exercise, fever, burns, or cystic fibrosis.


  • Decreased fluid intake:  coma patient, dementia, limited access to water


  • Renal: loss of fluid excreted via the kidney can be caused by diabetes mellitus, diabetes insipidus, diuretics, renal disease, and adrenal insufficiency


  • Blood loss:  loss of blood could occur with hemorrhage or surgery


  • Gastrointestinal: GI loss of fluid due to nausea, vomiting, diarrhea, fistula, nasogastric suction


  • Fluid shift (from intravascular space into interstitial): peritonitis, small bowel obstruction, pulmonary edema, burns



Signs & Symptoms


sunken eyeballs, increased temp, fatigue, syncope, weight loss, vomiting, increased HR, weakness, constipation, anorexia, thirst, dry tongue, nausea, confusion, oliguria, dizziness, decreased BP, decreased central venous pressure (CVP), decreased pulmonary artery pressure (PAP), decreased cardiac output, decreased mean arterial pressure (MAP), increased systemic vascular resistance


children: decreased tear production, depressed anterior fontanelle, and poor skin turgor.


hypovolemic shock: pale, diaphoretic, rapid thready pulse, oliguria, confusion, decreased blood pressure (BP)



ABGs: metabolic acidosis secondary to DKA or lower GI loses, and metabolic alkalosis secondary to diuretics, or upper GI losses

BUN: increased, as a result of increased production or decreased excretion (due sodium and water reabsorption)

BUN/creatinine ratio: in hypovolemia BUN will rise more than creatinine.  An equal  rise in BUN and creatinine is an indicator of renal problems

Hematocrit:  increased, due to increased concentration

Serum CO2: increased in metabolic alkalosis, decreased in metabolic acidosis

Serum electrolytes:

– Potassium: low in GI or renal loss; high in adrenal insufficiency

– Sodium: low due to thirst and increased water intake, high with sweat loss

Serum osmolality: depends on type of fluid lost and amount of compensation

Urine Na: decreased as long as kidney function is normal.

Urine osmolality: increased, increased concentration

Urine specific gravity: increased, more concentrated urine as the body tries to conserve fluid




Treatment is based on the type of fluid that is lost.  In severe depletion, rapid increase in intravascular fluid is priority.


Treatment with IV Fluids




  • Isotonic Normal Saline: increases intravascular fluid, without increasing intracellular fluid
  • Saline/Electrolyte solutions: provides fluid and electrolytes (K+, Ca+, Lactate, acetate)
  • hypotonic fluid is used for maintenance fluids
  • isotonic fluid will replace fluid loss (most fluids lost are isotonic)
  • Dextrose solutions: provides free water which is distributed to intracellular fluid and extracellular fluid, replete total body water deficit.





  • Blood products: increase intravascular fluid only
  • Plasma: Increase intravascular fluid


Patient History


Medical History:


Look for medical history that might be associated with fluid or electrolyte disturbances


Medical conditions: Crohn’s disease, diabetes mellitus, etc

Medications: diuretics


Psychological/ Religious/ Cultural History:


Behavioral, emotional, cultural, socioeconomic, or religious disorders that might be associated with fluid or electrolyte disturbances: bulimia, religious fasting, financial constraints that limit purchase of medications etc.

Clinical Assessment




Central venous pressure (CVP):  Amount of blood returning to right atria.  If elevated may indicate fluid overload, pulmonary edema, right sided heart failure.  The CVP is measured with a catheter in the right atrium.


Pulmonary artery pressure (PAP): The amount of blood pressure in the pulmonary artery.  The PAP is measured via a catheter placed in the pulmonary artery.  Increased PAP may indicate increases in fluid volume.


Systemic vascular resistance (SVR): Resistance in peripheral circulation that must be overcome to pump blood to the body.


Cardiac output (CO):  The amount of blood pumped out of the heart each minute.  heart rate x stroke volume = cardiac output


Mean arterial pressure (MAP):  Average pressure in the arteries during one cardiac cycle.  It can be calculated using diastolic and systolic blood pressure.  MAP = [(2 x diastolic BP)+systolic BP]/ 3


Heart Rate: A measurement of the number of heart beats in one minute.


Stroke Volume: A measure of blood moved during a contraction of the left ventricle.


Blood Pressure (BP):  The pressure exerted on the blood vessels by circulating blood.  When blood pressure is decreased it can indicate decrease in fluid volume or possible dysrhythmia from electrolyte abnormalities.  Increased blood pressure may indicate increased fluid volume.  BP=SVR x CO




Taking daily weights is an important indicator of fluid status.  Weights should be taken at the same time each day using the same scale if possible.  Rapid short term weight changes are a sign of fluid status.   A weight change of 1 kg is equivalent to a loss or gain of 1 liter of fluid.   Total body water gains could be in any of the body compartments.




Fluid status can be monitored by measuring daily intake and output of fluid.


Intake:  PO fluids (all drinks and foods that are liquid at room temperature), IV Fluids (exact amounts given should be recorded), irrigation (any irrigation that is not pulled back out should be documented), tube feedings (all administered tube feeds and any water flushes).


Output: urine output, profuse sweating, nasogastric tube suction, draining fistula, rapid breathing  liquid stool, wound drainage, vomiting



Vital Signs


Body Temp


Elevated temperature leads to increase fluid and electrolyte losses.  Fluid volume can also affect temperature: hypovolemia can lead to decreased temperature and vice versa.


Respiratory Rate


Increased respiratory rate leads to increase fluid losses via breathing.  Respiratory rate will be elevated in metabolic acidosis.  With fluid overload in the lungs crackles or rhonchi may be present.


Heart Rate


Heart rate will increase with decreased fluid volume.  In volume overload a bounding pulse is seen.  In volume deficit a weak or thready pulse is seen.


Heart rate may be altered with disorders of potassium or magnesium.


Blood Pressure


When blood pressure is decreased it can indicate decrease in fluid volume or possible dysrhythmia from electrolyte abnormalities.  Increased blood pressure may indicate increased fluid volume.

Physical Assessment


Integument System


Edema: increases in interstitial volume leads to edema which can be localized or generalized.  Bony surfaces like the sacrum or tibia should be used to assess for pitting edema.  Edema is rated based on severity 1+ to 4+, with 4+ being most severe.

Skin Moisture: check for flushed and dry skin

Skin Turgor: may indicated changes in interstitial volume, assess by pinching the skin over the forearm, sternum to assess if skin quickly returns to original position.

Tongue: furrowing (rut or groove in the tongue) indicates decrease in fluid volume

Moisture between cheek and tongue: if moisture is decreased it indicates volume deficit


Cardiovascular System


Heart Sounds: The third heart sound (S3) may indicate fluid overload


Veins: the veins in the hands – when the hand is raised hand veins collapse within 3-5 seconds.  In fluid volume overload this time may be delayed.


Dysrhythmias: may be related to electrolyte abnormalities: calcium, magnesium, potassium


Neurologic System 


Assess reflexes: may be altered with magnesium and calcium abnormalities

Changes in mental status: confusion may be present in hypovolemia, or acid/base imbalances

Trousseau’s and Chvostek’s sign: will be positive with decreased calcium or magnesium

Muscular function: weakness, paralysis can be seen with potassium and calcium deficits


Gastrointestinal System 


Anorexia, nausea, vomiting, nasogastric suction are all modes of fluid loss.  Increased thirst can be a sign of fluid deficit.


Treatment for disorders of fluid balance depends on the cause.  It is important to understand the different characteristics of IV fluids available.  They are useful in different situations.

Colloid Solutions

Colloids consist of blood and blood components: blood, packed red blood cells, fresh frozen plasma, plasma, albumin