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255 Cards in this Set

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The four main characteristics of body fluids

1. Fluid Volume

2. Concentration (osmolality)

3. Composition (electrolyte concentration)

4. Degree of acidity (pH)

What percentage of an adult man's body weight is water?


In older men how much of their body weight is water?


Obese people have more or less water than lean people? Why?

They have less water because fat contains less water than muscle

What does fluid in the context of this chapter mean?

water that contains dissolved or suspended substances such as glucose, mineral salts, and proteins

Extracellular Fluid (ECF)

Fluid outside of the cells

Intracellular Fluid (ICF)

Fluid Inside of the cells

What percentage of adult total body fluid is ICF?

In adults approximately two thirds of total body water

What percentage of adult body fluid is ECF

In adults approximately one third of total body water

What are the two major divisions of ECF?

intravascular fluid and interstitial fluid

What is a minor division of ECF?

transcellular fluids

Intravascular fluid is?

The liquid part of the blood (i.e. the plasma)

Interstitial fluid is?

located between the cells and outside the blood vessels

What is Transcellular fluid

cerebrospinal, pleural, peritoneal, and synovial fluids which are secreted by epithelial cells


Fluid in the body compartments contains mineral salts known technically as Electrolytes


Electrolyte is a compound that separates into charged particles called ions.


Positively charged Ions


Negatively charged ions

Which are the cations in body fluids

Sodium(Na+), Potassium(K+), Calcium(Ca2+) and Magnesium(Mg2+)

What are the anions in body fluid?

Chloride (Cl-) and bicarbonate (HCO3-)

What do cations and anions combine to make?


What are Millimoles per liter?

Millimoles per liter represent the number of milligrams of an electrolyte divided by its molecular weight that are contained in the liter of fluid being measured (usually blood plasma or serum)

What are Milliequivalents per liter?

Milliequivalent's per liter are the millimoles per liter multiplied by the electrolyte charge.

Why do we use Milliequivalents?

Because a milliequivalent of one electrolyte can combine with a milliequivalent of another electrolyte


the measure of the number of particles per kilogram of water


Fluid with the same tonicity as blood


a fluid more concentrated than normal blood


a solution less concentrated than normal blood

What are four processes for the movement of water in the body

Active transport, diffusion, osmosis, and filtration

Active transport

How cells maintain their high intracellular electrolyte concentration. Active transport requires ATP energy to move electrolytes against the concentration gradient

What is the concentration gradient?

Electrolytes move from areas of lower concentration to areas of higher concentration

What is one example (mentioned in the book) of active transport?

sodium-potassium pump, which moves Na+ out of a cells and K+ into it, keeping ICF lower in Na+ and higher in K+ than ECF


passive movement of electrolytes or other parties down a concentration gradient

What does diffusion of electrolytes across cell membranes require?

They require proteins that serve as ion channels

What body function does the opening of ion channels play an important role in?

muscle and nerve function


a process by which water moves through a membrane that separates fluids with different particle concentrations.

Osmotic pressure

an inward-pulling force caused by particles in the fluid


the process by which fluid moves in and out of the capillaries. It is the net effect of four forces, two that tend to move fluid out of the capillaries and small venues and two that tend to move fluid back into them

Hydrostatic Pressure

is the force of the fluid pressing outward against a surface.


Albumin and other proteins contained in the blood. They are much larger than electrolytes, glucose, and other molecules that dissolve easily. Thus they are too large to leave capillaries in the fluid that is filtered and remain in the blood.

Colloid Osmotic Pressure/Oncotic Pressure

an inward-pulling force caused by blood proteins that held move fluid from the interstitial area back into the capillaries. Interstitial fluid colloid pressure normally is a very small opposing force

At what end of a normal capillary is hydrostatic pressure the strongest?

At the arterial end and fluid moves from the capillary into the interstitial area, bringing nutrients to cells.

At what end of a normal capillary is hydrostatic pressure weaker?

At the venous end and the colloid osmotic pressure of the blood is stronger. Thus fluid moves into the capillary at the venous end, removing waste products from cellular metabolism


accumulation of excess fluid in the interstitial space

Fluid homeostasis is the dynamic interplay of three processes

fluid intake and absorption, fluid distribution, and fluid output.

How does one maintain fluid balance?

Fluid intake must equal fluid output

Which normal fluid output is a hypotonic salt solution?

Urine and Sweat

How do you balance normal fluid output

have an equivalent fluid intake of hypotonic sodium-containing fluid (or water plus foods with some salt).

What is the average fluid intake from food metabolism and fluid intake?


What are the two stimulations for the conscious desire for water, thirst?

1. when plasma osmality increases

2. when the blood volume decreases (baroreceptors-mediated thirst and angiotensin II and III-mediated thirst)

Where is the thirst control mechanism located?

within the hypothalamus in the brain. Osmoreceptors continually monitor plasma osmality; when it increases they cause thirst by stimulating neurons in the hypothalamus

fluid distribution

the movement of fluid among its various compartments.

How does fluid distribution between the extracellular and intracellular compartments occur?

Through osmosis

How does fluid distribution between the vascular and interstitial parts of the ECF occur?


Through what organs does fluid output normally occur?

Skin, lungs, GI tract, and kidneys

Examples of abnormal fluid output?

vomiting, wound drainage or hemorrhage

Which organ is the major regulator of fluid output?

The kidneys

The six factors that affect the thirst mechanism

1. Increased plasma osmolality

2. Decreased plasma volume

3. Angiotensin II

4. Angiotensin III

5. Dry pharyngeal mucous membranes

6. Psychological factors

What three hormones or hormone systems affect fluid volume adjustments?

1. Antidiuretic Hormone

2. Renin-Angiotensin-Aldosterone System

3. Atrial Natriuretic Peptide


regulates the osmolality of the body fluids by influencing how much water is excreted in urine. It is synthesized by neurons in the hypothalamus that release it from the posterior pituitary gland.

What is the main trigger of ADH release

Increased blood osmolarity

What are the triggers for ADH Release

Increased blood osmolarity, decreased blood volume, pain, stressors, and some medications

What is an important fluid homeostasis function of Angiotensin II?

Stimulation of aldosterone release from the adrenal cortex

What does aldosterone do?

1. circulates to the kidneys where it causes reabsorption of sodium and water in isotonc proportion in the distal renal tubules. Removing sodium and water from the renal tubules and returning it to the blood increases the volume of the ECF

2. Also contributes to electrolyte and acid-base balance by increasing urinary excretion potassium and hydrogen ions.

The Renin-Angiotensin Aldosterone System (RAAS)

regulates ECF volume by influencing how much sodium and water are excreted in urine. It also contributes to regulation of blood pressure.

True or False, Angiotensin II also causes vasoconstriction in some vascular beds?


Atrial Natriuretic Peptide (ANP)

ANP also regulates ECV by influencing how much sodium and water are excreted in urine

Where is ANP released

ANP is released by cells in the atria of the heart when they are stretched

What hormone does ANP inhibit?

ADH by increasing the loss of sodium and water in the urine.

What are the two major types of fluid imbalances

Volume imbalances and osmolality imbalances

ECV deficit

Sodium and Water Intake Less Than Output, Causing Isotonic Loss:

* Severely decreased oral intake of water and salt

* Increased GI output: vomiting, diarrhea, laxative overuse, drainage from fistulas or tubules

* Increased renal output: use of diuretics, adrenal insufficiency (deficit of cortisol and aldosterone)

* Loss of blood or plasma: hemorrhage, burns

* Massive sweating without water and salt intake

Which fluids are affected by and ECF deficit?

Vascular and interstitial fluids


means decreased vascular volume and often is used when discussing ECV deficit

ECV excess

occurs when there is too much isotonic fluid in the extracellular compartment

Osmolality imbalances

hypernatremia and hyponatremia


also called water deficit is a hypertonic condition

What are the two general causes of hypernatremia

1. loss of relatively more water than salt

* Diabetes insipidus (ADH deficiency)

* Osmotic diuresis

* Large insensible perspiration and respiratory

water output without increased water intake

2. gain of relatively more salt than water

* Administration of tube feedings, hypertonic

parenteral fluids, or salt tablets

* Lack of access to water, deliberate water de

privation, inability to respond to thirst (e.g.

immobility, aphasia)

* Dysfunction of osmoreceptor-driven thirst


Signs and symptoms of Hypernatremia

Physical Examination: Decreased level of consciousness (confusion, lethargy, coma) perhaps thirst, seizures if develops rapidly or is very severe

Laboratory findings: Serum Na+ level above 145 mEq/L (145 mmol/L), serum osmolality above 300 mOsm/kg (300 mmol/kg)

Clinical Dehydration

The combined disorder of Hypernatremia and ECV deficit


Gain of Relatively More Water Than Salt:

* Excessive ADH (SIADH)

* Psychogenic polydipsia or forced excessive water intake

* Excessive IV administration of D5W

* Use of hypotonic irrigating solutions

* Tap-water enemas

Loss of Relatively More Salt Than Water:

* Replacement of large body fluid output (e.g. diarrhea, vomiting) with water but no salt

Causes of Hyponatremia

1. Gain of relatively more water than salt:

* Excessive ADH (SIADH)

* Psychogenic polydipsia or forced excessive water intake

* Excessive IV administration of D5W

* Use of hypotonic irrigating solutions

* Tap-water enemas

2. Loss of relatively more salt than water:

*Replacement of large body fluid output with water but no salt

Signs and Symptoms of Hyponatremia

Physical examination: Decreased level of consciousness (confusion, lethargy, coma), seizures if develops rapidly or is very severe

Laboratory findings: Serum Na+ level below 135 mEq/L (135 mmol/L), serum osmolality below 280 mOsm/kg (280 mmol/kg)

Signs and Symptoms of Extracellular Fluid Volume Deficit (Fluids have decreased Volume but Normal Osmolality)

Physical Examination: Sudden weight loss (overnight), postural hypotension, tachycardia, thready pulse, dry mucous membranes, poor skin turgor, slow vein filling, flat neck veins when supine, dark yellow urine.

If severe: thirst, restlessness, confusion, hypotension; oliguria (urine output below 30mL/h); cold, clammy skink; hypovolemic shock

Laboratory Findings: Increased hematocrit increased BUN above 25mg/dL (8.9 mmol/L) (hemoconcentration); urine specific gravity usually above 1.030, unless renal cause


the production of abnormally small amounts of urine


Low Serum Potassium (K+) Concentration:

Decreased K+ Intake: Excessive use of K+ free IV solution

Shift of K+ into Cells: Alkalosis; treatment of diabetic ketoacidosis with insulin

Increased K+ Output: Acute or chronic diarrhea; vomiting; other GI losses (e.g. nasogastric or fistula drainage); use of potassium-wasting diuretics; aldosterone excess; polyuria; glucocorticoid therapy

Signs and Symptoms of Hypokalemia

Physical Examination: Bilateral muscle weakness that begins in quadriceps and may ascend to respiratory muscles, abdominal distention decreased bowel sounds, constipation, dysrhythmias

Laboratory findings: Serum K+ level below 3.5 mEq/L (3.5 mmol/L); ECG abnormalities: Uwaves, flattened or inverted T waves; ST segment depression


High Serum Potassium (K+) Concentration

Increased K+ Intake: Iatrogenic administration of late amounts of IV K+; rapid infusion of stored blood; excess ingestion of K+ salt substitutes

Shift of K+ out of cells: Massive cellular damage (ex. crushing trauma, cytotoxic chemotherapy); Insufficient insulin (e.g., diabetic ketoacidosis); some types of acidosis

Decreased K+ Output: Acute or chronic oliguria (e.g. severe ECV deficit, end-stage renal disease); use of potassium-sparing diuretics; adrenal insufficiency (deficit of cortisol and aldosterone)


Low Serum Calcium (Ca2+) Concentration

Decreased CA2+ Intake and Absorption:

Calcium-Deficient diet; vitamin D deficiency (includes end-stage renal disease); chronic diarrhea; laxative misuse; steatorrhea

Shift of Ca2+ into Bone or Inactive Form:

Hypoparathyroidism; rapid administration of citrated blood; hypoabunimemia; alkalosis; pancreatitis; hyperphosphatemia (includes end-stage renal disease)

Increased CA2+ Output: Chronic diarrhea; steatorrhea


High Serum Calcium (Ca2+) Concentration

Increase Ca2+ Intake and Absorption:

Milk-alkali syndrome

Shift of Ca2+ out of Bone: Prolonged immobilization; hyperparathyroidism; bone tumors; nonosseous cancers that secrete bone-resorbing factors

Decreased Ca2+ Output: Use of thiazide diuretics

Hypercalcemia signs and symptoms

Physical Examination: Anorexia, nausea and vomiting, constipation, fatigue, diminished reflexes, lethargy, decreased level of consciousness, confusion, personality change, cardiac arrest if severe

Laboratory findings: Total serum Ca2+ level above 10.5 mg/dL (2.6 mmol/L) or serum ionized Ca2+ level above 5.3 mg/dL (1.3 mmol/L;

Hypomagnesemia- Low Serum Magnesium (Mg2+) Concentration

Decreased Mg2+ Intake and Absorption: Malnutrition; chronic alcoholism; chronic diarrhea: laxative misuse; steatorrhea

Shift of Mg2+ Into Inactive Form: Rapid administration of citrated blood

Increased Mg2+ Output: Chronic diarrhea; steatorrhea; other GI losses (e.g. vomiting, nasogastric or fistula drainage); use of thiazide or loop diuretics; aldosterone excess

Hypermagnesemia- High Serum Magnesium (Mg2+) Concentration

Increased Mg2+ Intake and Absorption: Excessive use of Mg2+ containing laxatives and antacids; parenteral overload of magnesium

Decreased Mg2+ Output: Oliguric end-stage renal disease; adrenal insufficiency

Signs and Symptoms of Hypomagnesemia

Physical Examination: Positive Chvostek's sign, hyperactive deep tendon reflexes, muscle cramps and twitching, grimacing, dysphagia, tetany, seizures, insomnia, tachycardia, hypertension, dysrhythmias

Laboratory Findings: Serum Mg2+ level below 1.5 mEq/L (0.75 mmol/L); ECG abnormalities; prolonged QT interval

Signs and symptoms of hypermagnesemia- High serum Magnesium (Mg2+) Concentration

Physical Examination: Lethargy, hypoactive deep tendon reflexes, bradycardia, hypotension

Acute elevation in Mg2+ levels: flushing sensation of warmth

Severe acute hypermagnesemia: Decreased rate and depth of respirations, dysrhythmias, cardiac arrest

Laboratory Findings: Serum Mg 2+ level above 2.5 mEq/L (1.25 mmol/L); ECG abnormalities: prolonged PR interval

Sings and Symptoms of Hyperkalemia

Physical Examination: Bilateral muscle weakness in quadriceps, transient abdominal cramps, diarrhea, dysrhythmias, cardiac arrest if severe.

Laboratory Findings: Serum K+ level above 5 mEq/L (3.5 mmol/L; ECG abnormalities: peaked T waves; widened QRS complex; PR prolongation; terminal sine-waves pattern.

Acid-base homeostasis is the dynamic interplay of what three processes?

Acid production, acid buffering, and acid excretion

Arterial Blood Gases (ABGs)

Laboratory tests of sample arterial blood used to monitor a patient's acid-base balance.

Cellular metabolism constantly creates what two types of acids

Carbonic acid and metabolic acid

Carbonic Acid

Cells produce Carbon Dioxide (CO2) which acts like an acid in the body y concerting to carbonic acid (H2CO3)

Metabolic Acids

Are any acids that are not carbonic acid


are pairs of chemical that work together to maintain normal pH. Buffers normally keep the blood from becoming too acid when acids that are produced by cells circulate to the lungs and kidneys for excretion.

Which is the major buffer in the ECF

bicarbonate (HCO3-) which buffers metabolic acids

What are the body's two acid-excretion systems

lungs and kidneys

The lungs excrete carbonic or metabolic acid?

Carbonic acid. The kidneys excrete metabolic acid

What are the two types of acidosis?

respiratory and metabolic acidosis

What are the two types of alkalosis

respiratory and metabolic acidosis

Respiratory acidosis

Excess Carbonic Acid Caused by Alveolar Hypoventilation. Causes

1. Impaired Gas Exchange

2. Impaired Neuromuscular Function:

3. Dysfunctional Brainstem Respiratory Control

Signs and Symptoms of Respiratory Acidosis

Physical Examination:

Headache, light-headedness, decreased level of consciousness (confusion, lethargy, coma) dysrhythmias

Laboratory Findings: Arterial blood gas alterations: pH below 7.35, PaCO2 above 45 mm Hg (6kPa), HCO3- level normal if uncompensated or above 26 mEq/L (26 mmol/L) if compensated

Respiratory Alkalosis

Deficient Carbonic Acid Caused by Alveolar Hyperventilation

Hypoxemia from any cause (e.g. initial part of asthma episode, pneumonia)

Acute Pain

Anxiety, psychological distress, sobbing

Inappropriate mechanical ventilator settings

Stimulation of brainstem respiratory control (e.g. meningitis, gram negative sepsis, head injury, aspirin overdose

Metabolic Acidosis

Excessive Metabolic Acids

1. Increase of Metabolic Acids (High Anion Gap):

Ketoacidosis (diabetes, starvation, alcoholism)

Hyper metabolic state (severe hyperthyroidism, burns, severe infection)

Oliguric renal disease (acute kidney injury, end-stage renal disease)

Circulatory shock

Ingestion of acid or acid precursors (e.g., methanol, ethylene glycol, boric acid, aspirin overdose)

2. Loss of Bicarbonate (Normal Anion Gap)


Pancreatic Fistula

Renal tubular acidosis

Metabolic Alkalosis

Deficient Metabolic Acids

1. Increase of Bicarbonate:

Excessive administration of sodium bicarbonate

Massive blood transfusion (liver converts citrate to HCO3-)

Mild or moderate ECV deficit (contracting alkalosis)

2. Loss of Metabolic Acid:

Excessive vomiting or gastric suctioning


Excess aldosterone

Signs and Symptoms of Metabolic Acidosis

Physical Examination: Decreased level of consciousness (lethargy, confusion, coma), abdominal pain, dysrhythmias, increased rate and depth of respirations (compensatory hyperventilation)

Laboratory Findings: Arterial blood gas alterations: pH below 7.35, PaCO2 normal if uncompensated or below 35 mm Hg (4.7 kPa) if compensated, HCO3- level below 22 mEq/L (22 mmol/L)

Signs and Symptoms of Metabolic Alkalosis

Physical Examination: Light-headedness, numbness and tingling of fingers, toes, and circumoral region; muscle cramps; possible excitement and confusion followed by decreased level of consciousness, dysrhythmias (may be caused by concurrent hypokalemia)

Laboratory Findings: Arterial blood gas alterations: pH above 7.45, PaCO2 normal if uncompensated or above 45 mm Hg (6.0 kPa) if compensated, HCO3- above 26 mEq/L (26 mmol/L)

What is the normal pH range for adult arterial blood?

7.35 to 7.45


an abnormal sensation, typically tingling or pricking (associated with respiratory alkalosis)

anion gap

a laboratory calculation that reflects the unmeasured anions in plasma. It is calculated by subtracting the sum of plasma concentration of the anions (Cl- and HCO3-) from the plasma concentration of the cations (Na+).

Total Na+ - (Cl- + HCO3-)

Nursing History Consists of?

1. Age

2. Environment

3. Dietary Intake

4. Lifestyle

5. Medications

Impact of Age on Fluid, Electrolyte, and acid Base Imbalance?

1. Infants have a total water weight of 70-80% of total body weight

2. Children 2-12 have fevers when sick

3. Adolescents have increased metabolism and water production

4. Old people- have more difficulty recovering from imbalances because of age, medication, and illnesses

Impact of the Environment on Fluid, Electrolyte, and acid Base Imbalance?

1. Hot Environment increases sweating which is a hypotonic sodium-containing solution. Sweating can lead to Clinical Dehydration

Impact of Dietary Intake on Fluid, Electrolyte and acid base imbalance

1. Assess intake of fluids, salt, and foods rich in potassium, calcium, and magnesium.

2. Starvation diets, high in fat and no carbohydrate content lead to metabolic acidosis.

3. Assess a patients ability to chew and swallow.

Impact of Lifestyle on Fluid Electrolyte and acid base imbalance

Chronic alcohol abuse commonly causes hypomagnesemia in part because it increases renal magnesium excretion.

Impact of Medication on Fluid Electrolyte and acid base imbalance

1. Obtain a complete list of medications

2. ask about the use of baking soda as an antacid which can cause ECV excess because of its high sodium content that holds water in the EC compartments.

3. Laxatives - multiple loose stools remove fluid and electrolytes from the body

Medical History impact on Fluid and Electrolyte and acid base imbalance

1. Recent Surgery

2. Gastrointestinal Output

3. Acute Illness or Trauma

A. Respiratory Disorders

B. Burns

C. Trauma

4. Chronic Illness

A. Cancer

B. Heart Failure

C. Oliguric Renal Disease

Impact of Surgery

Recent surgery (24-48hrs)- increased secretion of aldosterone, glucocorticoids and ADH cause increased ECV, decreased osmolality, and increased potassium excretion.

Impact of GI output

Diarrhea, vomiting cause ECV deficit, hypernatremia, clinical dehydration and hypokalemia. Chronic Diarrhea can cause hypocalcemia and hypomagnesemia due to decrease in electrolyte absorption.

Removal of gastric acid can cause metabolic alkalosis.

Removal of the bicarbonate rich intestinal or pancreatic fluids can cause metabolic acidosis.

Impact of Respiratory Disorders

Many acute respiratory disorders predispose patients to respiratory acidosis.

Impact of Burns

Place a patient at a hight risk for ECV deficit. Patients with burns have cellular damage that releases potassium into the blood and they become hyperkalemic. In addition these patient often develop metabolic acidosis because of great increased cellular metabolism which produces more metabolic acids than their kidneys are able to excrete.

Impact of Trauma

Hemorrhage causes ECV deficit from blood loss

crush injuries destroy cellular structure, causing hyperkalemia by massive release of intracellular K+ into the blood.

Head injury typically alters ADH secretion. It may cause diabetes insipid (deficit of ADH) in which patients excrete large volumes of very dilute urine and develop hypernatremia. In contrast it can also cause the syndrome of inappropriate antidiuretic hormone (SIADH) in which excess secretion of ADH causes hyponatremia by retaining too much water and concentrating the urine

Impact of Cancer

Depends on the type of cancer and treatment

Many PT's w/cancer develop hypercalcemia when their cancer cells secrete chemicals that circulate to bones and causes calcium to enter the blood.

Other imbalances can occur because tumors can cause metabolic and endocrine abnormalities.

In addition, PT's with cancer are at risk for fluid and electrolyte imbalances as a result of side effects of chemotherapy, biological response modifiers, or radiation.

Impact of Heart Failure

PT's with chronic HF have diminished cardiac output which reduces kidney perfusion and activates RAAS. Aldosterone on the kidneys causes ECV excess and hypokalemia

Most diuretics used to treat HF increase the risk of hypokalemia while reducing the ECV excess. Sodium restriction is important with HF because it causes further water retention.

In severe HF both fluid and sodium is restricted to decrease the heart workload by reducing fluid volume.

Oliguric Renal Disease

Oliguria occurs when the kidneys have a reduced capacity to make urine resulting in ECV excess, hyperkalemia, hypermagnesemia, hyperphosphatemia, metabolic acidosis.

Assessment: Loss of 2.2 lbs (1kg) or more in 24 hours for adults


ECV deficit

Assessment: Gain of 2.2 lbs (1kg) or more in 24 hours for adults


ECV excess

Assessment: Hypotension or orthostatic hypotension.


ECV deficit

Assessment: Lightheaded ness or sitting upright or standing


ECV deficit

Pulse rate and character:

Rapid, thready

ECV deficit

Pulse rate and character:



ECV excess


Fullness of Neck Veins:

Flat or collapsing with inhalation when supine


ECV deficit


Fullness of Neck Veins:

Full or distended when upright or semi-upright


ECV Excess


Other assessments of vascular volume:

Capillary refill: sluggish

ECV deficit


Other assessment of vascular volume

Lung auscultation, dependent lobe: Crackles or bronchi with progressive dyspnea

ECV excess


Other assessment of Vascular volume:

Urine Output: Small volume of Dark yellow urine

ECV deficit

Clinical Markers of Interstitial Volume

Presence of Edema: Present in dependent areas (ankles or sacrum) and possibly fingers or around eyes

ECV excess

Clinical Markers of Interstitial Volume

Mucous Membranes: Dry between cheek and gum, decreased or absent tearing

ECV deficit

Clinical Markers of Interstitial Volume

Skin Turgor: Pinched skin fails to return to normal position within 3 seconds

ECV deficit

Clinical Markers of Interstitial Volume

Presence of thirst

Hypernatremia, severe ECV deficit

Clinical Markers of Interstitial Volume

Behavior and level of consciousness:

Restlessness and mild confusion

Severe ECV deficit

Clinical Markers of Interstitial Volume

Behavior and level of consciousness:

Decreased level of consciousness (lethargy, confusion, coma)

Hyponatremia, hypernatremia, hypercalcemia, acid-base imbalances

Cardiac and Respiratory Signs of Electrolyte or Acid-Base Imbalances

Pulse rhythm and ECG: Irregular pulse and ECG changes

K+, Ca2+, Mg2+, and/or acid-base imbalances

Cardiac and Respiratory Signs of Electrolyte or Acid-Base Imbalances

Rate and Depth of respirations:

Increased rate and depth

Metabolic acidosis (compensatory mechanism); Respiratory alkalosis (cause)

Cardiac and Respiratory Signs of Electrolyte or Acid-Base Imbalances

Rate and Depth of respirations:

Decreased Rate and Depth

Metabolic alkalosis (compensator mechanism); respiratory acidosis (cause)

Neuromuscular Markers of Electrolyte or Acid-Base Imbalances

Muscle strength bilaterally, especially quadriceps muscles:

Muscle Weakness

Hypokalemia, hyperkalemia

Neuromuscular Markers of Electrolyte or Acid-Base Imbalances

Reflexes and sensations:

Decreased deep tendon reflexes

Hypercalcemia, hypermagnesemia

Neuromuscular Markers of Electrolyte or Acid-Base Imbalances

Reflexes and sensations:

Hyperactive Reflexes, muscle twitching and cramps, tetany

Hypocalcemia, hypomagnesemia

Neuromuscular Markers of Electrolyte or Acid-Base Imbalances

Reflexes and sensations:

Numbness, tingling in fingertips, around mouth

Hypocalcemia, hypomagnesemia, respiratory alkalosis

Neuromuscular Markers of Electrolyte or Acid-Base Imbalances

Reflexes and sensations:

Muscle cramps, tetany

Hypocalcemia, hypomagnesemia, respiratory alkalosis

Neuromuscular Markers of Electrolyte or Acid-Base Imbalances

Reflexes and sensations:



Gastrointestinal Signals of Electrolyte Imbalances

Inspection and auscultation:

Abdominal distention

Hypokalemia; third-spacing of fluid

Gastrointestinal Signals of Electrolyte Imbalances

Inspection and auscultation:

Decreased bowel sounds


Gastrointestinal Signals of Electrolyte Imbalances

Motility: Constipation

Hypokalemia, hypercalcemia

Normal Value of Osmolality

280-300 mosm/kg Water (H2O) (280-300 mmol/kg H2O)

Normal Value of Sodium (Na+)

136-145 mEq/L (136-145 mmol/L)

Normal Value of Potassium (K+)

3.5-5.0 mEq/L (3.5-5 mmol/L)

Normal Value of Chloride (Cl-)

98-106 mEq/L (98-106 mmol/L)

Normal Value of Total CO2 (CO2 total content)

22-30 mEq/L (22-30 mmol/L)

Normal Values

Bicarbonate (HCO3-)

Arterial 22-26 mEq/L (22-26 mmol/L)

Venous 24-30 mEq/L (24-30 mmol/L)

Normal Values

Total Calcium

8.4 - 10.5 mg/dL (2.1-2.6) mmol/L

Normal Value of Ionized Calcium

4.5-5.3 mg/dL

Normal Values of Magnesium (Mg2+)

1.5 - 2.5 mEq/L

Normal Values of Phosphate

2.7-4.5 mg/dL

Normal Anion Gap

5-11 mEq/L

Normal pH


Normal PaCO2

35-45 mm Hg (4.7-6 kPa)

Normal PaO2

80-100 mmHg

Normal O2 saturation

95% - 100%

Normal Base Excess

-2 + 2 mm Eq/L (mmol/L)

Each Kg (2.2 lbs) of weight loss is equal to how much fluid loss?

1L or 1,000 mL

Can you delegate parts of I&O measurement to NAP with competent skills?


Which is Kussmaul Respirations associated with?

Metabolic Acidosis, Respiratory Acidosis, Metabolic Alkalosis or Respiratory Alkalosis?

Metabolic Acidosis

Lungs excrete?


Kidneys Excrete?

HCO3 Bi Carbonate

In many instances NAP's record oral intake but not?

intake through feeding or IV tubes

In many instances NAP's record urine, diarrhea, and vomitus output but not?

Drainage through tubes

Normal HCO3- values

22-26 mEq/L

Possible Nursing Diagnoses for patients with fluid, electrolyte, and acid-base alterations include the following:

* Decreased Cardiac Output

* Acute Confusion

* Risk for Electrolyte Imbalance

* Deficient Fluid Volume

* Excess Fluid Volume

* Impaired Gas Exchange

* Risk for Injury

* Deficient Knowledge regarding Disease Management

Can you delegate administration of IV fluid and hemodynamic assessment to NAP?


Can you delegate daily weights, I&O, and direct physical care of a stable patient to NAP?


Who helps identify medications or combinations of medications likely to cause electrolyte or acid-base disturbances and offered information regarding patient education about side effects to anticipate for prescribed drugs?

A Pharmacist

What do you need to restrict for a patient in end-stage renal disease?

intake of fluid, sodium, potassium, magnesium, and phosphate

When is oral replacement of fluids contraindicated?

1. When a patient has a mechanical obstruction of the GI tract

2. Is at hight risk of aspiration

3. or has impaired swallowing

How do you record the volume of an ice chip for I&O purposes?

You record one half the volume. For example, if a patient ingested 240 mL of ice chips, you record 120 mL of intake

When replacing fluids by mouth in a patient with ECV deficient, you should choose fluids that contain what?

Sodium (e.g., Pedialyte and Gasrolyte)

When is a feeding tube appropriate for a patient?

When the patient's GI tract is health but he or she cannot ingest fluids.

What are the options for administering fluids when oral intake is not an option?

Gastronomy, Jejunostomy instillations or infusions through small-bore nasogastric feeding tubes

A patient who has severe ECV excess is sometimes restricted to have both ________ and _______.

sodium and water

Patients can swallow pills with as little as _____ of water.

1 oz (30mL)

In acute care settings when a patient is on a fluid restriction how do you allot their total fluid intake?

Usually you a lot half the total oral fluids between 7am and 3pm (when their most active, receive two meals, and take most of their meds)

True or False. Patients on fluid restriction require less frequent mouth care?

False. Patients on fluid restriction need frequent mouth care to moisten mucous membranes, decrease the chance of mucosal drying and cracking, and maintain comfort.

What are the means of parenteral fluid and electrolyte replacement?

Parenteral nutrition (PN), IV fluid and electrolyte therapy (crystalloids), and blood and blood component (colloids) administration.

What is a peripheral IV?

When the catheter tip lies in a vein in one of the extremities

What is a central venous IV?

When the catheter tip lies in the central circulatory system (e.g. in the vena cava close to the right atrium of the heart)

What is a PN also called a total PN (TPN)?

IV administration of a complex highly concentrated solution containing nutrients and electrolytes that is formulated to meet a patient's needs.

Which IV is a high osmolality PN solution administered through?

Central IV Catheter

Which IV is a low osmolality PN solution administered through?

peripheral IV

What is the benefit of IV therapy?

It allows for direct access to the vascular system, permitting the continuous infusion of fluids over a period of time.

What does an order for IV therapy require?

It requires a health care provider's order for type, amount, and speed of administration.

What are Vascular Access Devices (VAD's)

they are catheters or infusion ports designed for repeated access to the vascular system

What's a PICC line?

It's a Peripherally inserted central catheter, they enter a peripheral arm vein and extend through the venous system to the superior vena cava where they terminate

What are central lines better for than peripheral lines?

They are more effective than peripheral catheters for administering large volumes of fluid, PN, and medications or fluids that irritate veins.

Why is it important to take proper care of a central line insertion site?

To prevent a central line-associated bloodstream infection (CLABSI)

Is the insertion of an IV a sterile or clean procedure?

Sterile because fluids infuse directly into the bloodstream

What is the necessary IV equipment?

VADs, tourniquet, clean gloves, dressings; IV fluid containers, various types of tubing, and electronic infusion devices (EID's) also called infusion pumps.

Which gauge peripheral IV catheter is commonly used?

20 and 22

What is the tubing called that the main IV fluid used in a continuous infusion flows through?

primary line

Which is the most common IV site?

the inner arm

Which sites should you not use on older adults or ambulatory patients

Do not use hand veins or foot veins in adults. (foot veins increase the risk of thrombophlebitis)

When is venipuncture contraindicated?

in a site that has signs of infection, infiltration, or thrombosis, an extremity with a vascular (dialysis) graft/fistula or on the same side as a mastectomy.

What are the signs of an infected site?

red, tender, swollen, and possibly warm to the touch. Exudate may also be present.

What is the danger in using an infected site for an IV insertion?

the danger of introducing bacteria from the skin surface into the blood stream.

What is a venipuncture?

is a technique in which a vein is punctured through the skin by a sharp rigid stylet (e.g. metal needle)

What are the general purposes of venipuncture?

collect a blood specimen, start an IV infusion, provide vascular access for later use, instill a medication, or inject a radiopaque or other tracer for special diagnostic exam.

The IV flow rate can be slowed by?

1. A blocked catheter

2. infiltration

3. vasospasm

4. knot or kink in the tubing

5. External pressure on the tubing

6. Position changes of the Patient's extremity

What does IV line maintenance involve?

1. Keeping the system sterile and intact

2. Changing the IV fluid container and tubing, and contaminated site dressings.

3. helping a patient with self-care activities so as not to disrupt the system.

4. Monitoring for complication of IV therapy.

What are catheter stabilization devices?

Protective devices designed to prevent movement or accidental displacement of a VAD. It is preferred over taping when feasible.

How soon can you change a continuous infusion tubing?

INS standards specify that continuous infusion tubings occur no more frequently than every 96 hours unless the tubing has been compromised or become contaminated.

How often should you change intermittent infusion tubing?

Every 24 hours because of the increased risk of contamination from opening the IV system

How often should you change tubing for blood and blood components?

Every 4 hours

How often should you change tubing for IV lipids?

Every 24 hours and use tubing that is free of diethylexyl-phtalate (DEHP), a toxin that leaches into lipid solutions

How often should you change a transparent dressing (most common) placed on the IV site?

Leave in place until the IV tubing is replaced

How often should you change a gauze dressing placed on an IV site?

Every 48 hours.

Infiltration or extravasation:


DESCRIPTION: IV fluid entering subcutaneous tissue around venipuncture site

EXTRAVASATION: Technical term used when a vesicant (tissue damaging) drug (e.g. chemo) enters tissue.

ASSESSMENT FINDINGS: Skin around catheter taut, blanched, cool to touch, edematous, may be painful. Flow may slow or stop.

INTERVENTION: stop infusion. Discontinue IV if no vesicant drug. If vesicant drug disconnect IV tubing and aspirate drug from catheter.


Description, Assessment Findings, and Intervention

DESCRIPTION: Inflammation of inner layer of vein

ASSESSMENT: Redness, tenderness, pain, warmth along course of vein starting at access site; possible red streak and/or palpable cord along vein.

INTERVENTION: Stop Infusion and discontinue IV line. Start new IV line in other extremity or proximal to previous insertion site of continued IV therapy if necessary. Apply warm, moist compress or contact IV therapy team or health care provider if area needs additional treatment.

Local Infection:

Description, Assessment Findings, and Intervention

DESCRIPTION: Infection at catheter skin entry point during infusion or after removal of IV catheter

ASSESMENT: Redness heat, swelling at catheter skin entry point; possible purulent drainage

INTERVENTION: Culture any drainage (if ordered), clean skin with alcohol; remove catheter and save for culture; apply sterile dressing

Notify health care provider

Start new IV line in other extremity. Initiate appropriate wound care if needed.

Bleeding at Venipuncture site:

Description, Assessment Findings, and Intervention

DESCRIPTION: Oozing or slow, continuous seepage of blood from venipuncture site

ASSESSMENT FINDINGS: Fresh blood evident at venipuncture site, sometimes pooling under extremity

INTERVENTIONS: Assess if IV system is intact

If catheter is within vein, apply pressure dressing over site or change dressing.

Start new IV line in other extremity or proximal to previous insertion site if VAD is dislodged, IV is disconnected, or bleeding from site does not stop.

Circulatory Overload of IV solution:

Description, Assessment Findings, and Intervention

Description: IV solution infused too rapidly or in too great an amount

Assessment Findings: Depends on type of solution ECV excess with Na+ containing isotonic fluid (crackles in dependent parts of lungs, shortness of breath, dependent edema)

Hyponatremia with hypotonic fluid (confusion, seizures)

Hypernatremia with Na+ containing hypertonic fluid (confusion, seizures)

Hyperkalemia from K+ containing fluid (cardiac dysrhythmias, muscle weakness, abdominal distention

Objectives for administering blood transfusion:

1. Increasing circulating blood volume after surgery, trauma, or hemorrhage

2. Increasing the number of RBC's and maintaining hemoglobin levels in patients with severe anemia

3. Preceding selected cellular components as replacement therapy (e.g. clotting factors, platelets, albumin)

Transfusion Reaction

If incompatible blood is transfused the patient's antibodies trigger RBC destruction.

Who is considered the universal blood donor?

type O blood

Rh factor

another antigen in RBC membranes. Dos people have this antigen and are Rh positive; a person without it is Rh negative.

Someone who is Rh negative can receive what kind of blood transfusion?

only Rh negative blood components

Autologous transfusion (auto transfusion)

the collection and reinfusion of a patient's own blood.

Before initiating any blood therapy for patient safety we always verify three things:

1. that blood components delivered are the ones that were ordered.

2. that blood delivered to a patient is compatible with the blood type listed in the medical record

3. that the right patient receives the blood.

Together two RN's or one RN and an LPN (must check the label on the blood product against the medical record and the patient's ID #, blood group, and complete name.

Patients who received a large-volume transfusion of citrated blood have high risk of.....

hyperkalemia, hypocalcemia, hypomagnesemia, and metabolic alkalosis therefore they need careful monitoring.

ACE Inhibitors (e.g. captopril [Capoten]) and angiotensin II receptor blockers (e.g. Losartan [Cozaar)) :


Antidepressants, SSRI (e.g. fluoxetine [Prozac]):


Calcium carbonate antacids:

Hypercalcemia, mild metabolic alkalosis

Corticosteroids (e.g. prednisone) :

Hypokalemia, metabolic alkalosis

Diuretics, potassium-wasting (e.g. furosemide [Lasix], thiazides):

ECV deficit, hyponatremia (thiazides), hypokalemia, hypomagnesemia, mild metabolic alkalosis

Diuretics, potassium-sparring (e.g., spironolactone [Aldactone]):

Hyperkalemia, mild metabolic acidosis

Effervescent (fizzy) antacids and cold medications (high Na+ content):

ECV Excess


ECV deficit, hypokalemia, hypocalcemia, hypomagnesemia, metabolic acidosis

Magnesium Hydroxide (e.g. milk of magnesia):


Non steroidal anti-inflammatory drugs (e.g. ibuprofen [Advil]):

Mild ECV excess, hyponatremia

Penicillins, high-dose (e.g., carbenicillin)

Hypokalemia, metabolic alkalosis, hyperkalemia with penicillin G (contains K+)

Transfusion Reaction: Acute Intravascular Hemolytic

Cause: Infusion of ABO incompatible whole blood RBC's or components containing 10mL or more of RBC's Antibodies in recipient's plasma attach to antigens on transfused RBC's, causing RBC destruction.

Clinical Manifestations: Chills, fever, low back pain, flushing, tachycardia, tachypnea, hypotension, hemoglobinuria, hemoglobinemia, sudden oliguria (acute kidney injury) circulatory shock, cardiac arrest, death.

Management: stop transfusion and save blood back and administration set for follow-up. Keep IV site open with normal saline infused through new tubing. Maintain BP and treat shock as ordered, if present obtain blood samples slowly to avoid hemolysis; send for serological testing. Send urine specimen to laboratory. Give diuretics to maintain urine flow. Insert indwelling urinary catheter or measure each voiding to monitor hourly urine output. Dialysis may be required if acute kidney injury occurs.

PATIENT ALERT: Do not transfuse additional RBC containing components until transfusion service provides newly cross-matched units.