Module 6: Fluid, Electrolyte, and Acid-Base Imbalances Flashcards
What are electrolytes?
Substances whose molecules dissociate into ions
when placed in water
Cations: positively charged
Anions: negatively charged
Concentration of electrolytes is expressed in
milliequivalents (mEq)/L
Composition
ICF (intracellular fluid)
Prevalent cation is K+
Prevalent anion is PO43−
ECF (extracellular fluid)
Prevalent cation is Na+
Prevalent anion is Cl−
Mechanisms Controlling Fluid/Electrolyte Movement
Diffusion
Movement of molecules across a permeable
membrane from high to low concentration
Facilitated diffusion
Uses carrier to help move molecules
Active transport
Process in which molecules move against
concentration gradient
External energy is needed for this proces
Osmosis
Movement of water “down” concentration gradient
* From a region of low solute concentration to one of high solute concentration
* Across a semipermeable membrane
Requires no outside energy sources
Osmotic pressure
-Amount of pull required to stop osmotic flow of water
Osmolarity measures the total mOsm/L of solution
Osmolality measures the number of mOsm/kg of
water
Measurement of Osmolality
Calculate the plasma osmolality
Plasma Osmolality = (2 × Na) + (BUN / 2.8) +
(glucose /18)
Normal plasma osmolality is between 280 and 295
mOsm/kg
Greater than 295 mOsm/kg= water deficit
Less than 275 mOsm/kg= water excess
Osmotic Movement of Fluids
The osmolality of the fluid surrounding cells affects
them
Isotonic—same as cell interior
Hypotonic—solutes less concentrated than in cells/
hypoosmolar
Hypertonic—solutes more concentrated than in cells/
hyperosmolar
Mechanisms Controlling Fluid and
Electrolyte Movement: Hydrostatic Pressure
-pressure exerted by the blood against the walls of blood vessels or heart chambers. It is a key factor in the movement of fluids and solutes across capillary walls, influencing the exchange between the bloodstream and the interstitial fluid surrounding cells.
Force of Fluid in a Compartment
-Hydrostatic pressure can be thought of as the force that the fluid exerts in a confined space. In blood vessels, this force is exerted by the blood itself, pushing against the vessel walls. This pressure is responsible for driving blood through the circulatory system and facilitating the exchange of nutrients, gases, and waste products between the blood and tissues.
Blood Pressure Generated by Heart’s Contraction
-The heart’s contraction generates the primary hydrostatic pressure within the circulatory system. Each time the heart beats, it pumps blood into the arteries, creating a surge of pressure known as systolic pressure. This is the maximum pressure in the arteries and occurs when the heart’s ventricles contract. The diastolic pressure, the minimum pressure, occurs between heartbeats when the heart is at rest and refilling with blood.
-The hydrostatic pressure decreases as blood moves away from the heart through the arterial system and into the capillaries due to friction and resistance within the vessels. By the time blood reaches the venous system, the pressure has significantly dropped, which is why venous blood is returned to the heart largely through the action of muscle contractions and valves in the veins, rather than hydrostatic pressure.
Role in Capillary Exchange
-The balance between hydrostatic pressure and osmotic pressure (the pressure exerted by proteins, notably albumin, in the blood plasma) determines the movement of water and solutes across capillary walls.
-At the arterial end of a capillary, hydrostatic pressure is higher than osmotic pressure, pushing fluid out of the capillaries into the interstitial space. At the venous end, hydrostatic pressure decreases, and osmotic pressure predominates, drawing fluid back into the capillaries.
Oncotic Pressure
Oncotic pressure, also known as colloid osmotic pressure, is a form of osmotic pressure exerted by proteins, notably albumin, in a blood vessel’s plasma. This pressure helps to maintain the balance of fluid between the blood vessels and the surrounding body tissues.
Colloid Osmotic Pressure
Oncotic pressure is termed “colloid” osmotic pressure because it is generated by the presence of large protein molecules (colloids) in the plasma, which are too large to easily cross the capillary walls. These proteins effectively draw water towards themselves.
Osmotic Pressure Caused by Plasma Proteins
The primary plasma protein contributing to oncotic pressure is albumin, although globulins and fibrinogen also play roles. Albumin’s role is critical because it constitutes about 60% of the total plasma proteins and has a significant influence on the blood’s osmotic pressure.
Oncotic pressure is essential for the reabsorption of water from the interstitial fluid back into the capillaries. At the venous end of capillaries, where the hydrostatic pressure has dropped, the oncotic pressure predominates, facilitating the movement of water from the tissue spaces back into the bloodstream, thus preventing excessive fluid loss from the capillaries and edema (swelling due to fluid accumulation in tissues).
Fluid Movement in Capillaries
The amount and direction of fluid movement across capillary walls are determined by the interplay of four primary forces, collectively known as Starling forces. These forces include capillary hydrostatic pressure, plasma oncotic pressure, interstitial hydrostatic pressure, and interstitial oncotic pressure. Together, they govern the exchange of water and solutes between the capillaries and the interstitial space surrounding the cells.
Capillary Hydrostatic Pressure (CHP)
Definition: The pressure exerted by the blood within the capillary walls. It tends to push fluid out of the capillaries into the interstitial space.
Role in Fluid Movement: CHP is a major force driving fluid out of the capillaries at the arteriolar end, facilitating the delivery of nutrients and oxygen to the tissues.
Plasma Oncotic Pressure (POP)
Definition: The osmotic pressure exerted by plasma proteins, primarily albumin, which cannot easily cross the capillary wall. It pulls water from the interstitial space back into the capillaries.
Role in Fluid Movement: POP promotes the reabsorption of water into the capillaries at the venous end, helping to maintain blood volume and pressure.
Interstitial Hydrostatic Pressure (IHP)
Definition: The pressure exerted by the fluid in the interstitial space outside the capillaries. It tends to push fluid from the interstitial space back into the capillaries.
Role in Fluid Movement: Generally lower than CHP, IHP can vary in different tissues but usually opposes the outward movement of fluid from capillaries, aiding in reabsorption.
Interstitial Oncotic Pressure (IOP)
Definition: The osmotic pressure exerted by proteins in the interstitial fluid. Since plasma proteins can occasionally leak into the interstitial space, they can exert a small osmotic pressure that draws fluid out of the capillaries into the interstitial space.
Role in Fluid Movement: IOP is typically much lower than POP but works in conjunction with CHP to promote the filtration of fluid from capillaries into the interstitial space.
The net movement of fluid across the capillary wall is determined by the balance of these forces, described by the Starling equation. When the sum of forces pushing fluid out of the capillaries (CHP and IOP) exceeds the sum of forces pulling fluid into the capillaries (POP and IHP), filtration occurs, moving fluid into the interstitial space. Conversely, when the reabsorptive forces (POP and IHP) exceed the filtrative forces (CHP and IOP), fluid moves back into the capillaries from the interstitial space.
This dynamic balance ensures adequate tissue hydration and nutrient delivery while preventing excessive accumulation of fluid in tissues (edema) or within the vascular system. Disruptions in any of these forces can lead to pathological conditions affecting fluid distribution and balance in the body.
Edema
Edema is caused by
Shifts of plasma to interstitial fluid
Elevation of venous hydrostatic pressure
Decrease in plasma oncotic pressure
Elevation of interstitial oncotic pressur
Fluid Spacing
First spacing— Normal distribution in ICF and
ECF
Second spacing— Abnormal accumulation of
interstitial fluid (edema)
Third spacing— Fluid is trapped where it is
difficult or impossible for it to move back into
cells or blood vessels
Regulation of Water Balance: Hypothalamic-pituitary regulation
Osmoreceptors in hypothalamus sense fluid deficit or
increase
Deficit stimulates thirst and antidiuretic hormone
(ADH) release
Decreased plasma osmolality (water excess)
suppresses ADH release
Regulation of Water Balance: Renal Regulation
Main organ for regulating fluid and electrolyte balance
Adjusting urine volume
* Selective reabsorption of water and electrolytes
* Renal tubules are sites of action of ADH and
aldosterone
Regulation of Water Balance: Adrenal cortical regulation
Releases hormones to regulate water and electrolytes
Glucocorticoids
* Cortisol
Mineralocorticoids
* Aldosterone
Regulation of Water Balance: Cardiac regulation
Natriuretic peptides are antagonists to the RAAS
Hormones made by cardiomyocytes in response to
increased atrial pressure
They suppress secretion of aldosterone, renin, and
ADH to decrease blood volume and pressure
Regulation of Water Balance: GI regulation
Oral intake accounts for most water
Small amounts of water are eliminated by GI tract in
feces
Diarrhea and vomiting can lead to significant fluid and
electrolyte loss
Considerations for Geriatric Population
Structural changes in kidneys decrease ability to
conserve water
Hormonal changes include a decrease in renin
and aldosterone and increase in ADH and ANP
Subcutaneous tissue loss leads to increased
moisture lost
Fluid Volume Imbalances
Fluid volume deficit (FVD) or hypovolemia
Abnormal loss of body fluids, inadequate fluid intake,
or plasma to interstitial fluid shift
Dehydration
Loss of pure water without corresponding loss of
sodium
Correct the underlying cause and replace water and
electrolytes
* Orally
* Blood products
* Isotonic IV solutions
Fluid volume excess (hypervolemia)
Excess fluid intake, abnormal fluid retention, or
interstitial-to-plasma fluid shift
Clinical manifestations related to excess volume
* Weight gain is the most common
Remove fluid without changing electrolyte
composition or osmolality of ECF
Diuretics
Fluid restriction
Possible restriction of sodium intake
Removal of fluid to treat ascites or pleural effusion
Sodium
Imbalances typically associated with parallel
changes in osmolality
Plays a major role in
ECF volume and concentration
Generating and transmitting nerve impulses
Muscle contractility
Regulating acid-base balance
Hypernatremia
-High serum sodium may occur with inadequate
water intake, excess water loss or sodium gain
Causes hyperosmolality leading to cellular
dehydration
Primary protection is thirst
Clinical manifestations
Thirst
Changes in mental status, ranging from drowsiness,
restlessness, confusion and lethargy to seizures and
coma
Symptoms of fluid volume deficit
Hypernatremia Management
Treat underlying cause
Primary water deficit—replace fluid orally or IV with
isotonic or hypotonic fluids
Excess sodium—dilute with sodium-free IV fluids and
promote sodium excretion with diuretic
Hyponatremia
Results from loss of sodium-containing fluids and/or
from water excess
Clinical manifestations
Mild—headache, irritability, difficulty concentrating.
More severe—confusion, vomiting, seizures, coma
If the cause is water excess,
Fluid restriction may be only treatment
Loop diuretics and demeclocycline
Severe symptoms (seizures)
* Give small amount of IV hypertonic saline solution (3%
NaCl)
If the cause is abnormal fluid loss,
Fluid replacement with isotonic sodium-containing
solution
Encouraging oral intake
Withholding diuretics
Drugs that block vasopressin (ADH)
* Convaptan (Vaprisol) IV
* Tolvaptan (Samsca) ora
Potassium
Major ICF cation
-Necessary for
Resting membrane potential of nerve and muscle
cells
Regulates intracellular osmolality
Promotes cellular growth
Maintenance of cardiac rhythms
Acid-base balance
Sources
Protein-rich foods
Fruits and vegetables
Salt substitutes
Potassium medications (PO, IV)
Stored blood
Regulated by kidneys
Hyperkalemia
High serum potassium caused by
Impaired renal excretion
Shift from ICF to ECF
Massive intake of potassium
Some drugs
Most common in renal failure
Manifestations
Life-threatening arrhythmias
Fatigue, confusion
Tetany, muscle cramps
Weak or paralyzed skeletal muscles
Abdominal cramping or diarrhea
Management of Hyperkalemia
Stop oral and IV K+ intake
Increase K+ excretion (thiazide diuretics, dialysis)
patiromer (Veltessa), sodium zirconium cyclosilicate
(ZS-9, Lokelma), and/or sodium polystyrene sulfonate
(Kayexalate)
Force K+ from ECF to ICF by IV regular insulin with
dextrose and a -adrenergic agonist or sodium
bicarbonate
Stabilize cardiac cell membrane by administering
calcium chloride or calcium gluconate IV
Use continuous ECG monitoring
Hypokalemia
Low serum potassium caused by
Increased loss of K+ via the kidneys or gastrointestinal
tract
Increased shift of K+ from ECF to ICF
Decreased dietary K+ (rare)
Renal losses from loop or potassium depleting
diuresis
Low magnesium level
Clinical manifestations
Cardiac most serious
Skeletal muscle weakness and paresthesia
Weakness of respiratory muscles
Decreased GI motility
Hyperglycemia
Management of Hypokalemia
KCl supplements orally or IV
Always dilute IV KCl
NEVER give KCl via IV push or as a bolus
Should not exceed 10 mEq/hr
Use an infusion pump
Calcium
Functions
Formation of teeth and bone
Blood clotting
Transmission of nerve impulses
Myocardial contractions
Muscle contractions
Major source is dietary intake
Need vitamin D to absorb
Present in bones and plasma
Ionized or free calcium is biologically active
Changes in pH and serum albumin affect levels
Balance controlled by
Parathyroid hormone (PTH)
* Increases bone resorption, GI absorption, and renal
tubule reabsorption of calcium
Calcitonin
* Increases calcium deposition into bone, increases renal calcium excretion, and decreases GI absorption
Hypercalcemia
High levels of serum calcium
caused by
Hyperparathyroidism (two-thirds
of cases)
Cancers, especially kidney, breast, prostate, ovarian,
hematologic,, and lung cancers
Manifestations
Fatigue, lethargy, weakness, confusion
Hallucinations, seizures, coma
Dysrhythmias
Bone pain, fractures, nephrolithiasis
Polyuria, dehydration
Hypercalcemia Interventions
Low calcium diet
Stop medications related to hypercalcemia
Increased weight-bearing activity
Increased fluid intake
* 3000 to 4000 ml daily
* Cranberry or prune juice
Hydration with isotonic saline infusion
Bisphosphonates—gold standard
Calcitonin
Hypocalcemia
Low serum Ca levels caused by
Decreased production of PTH
Multiple blood transfusions
Alkalosis
Increased calcium loss
Manifestations
Positive Trousseau’s or Chvostek’s sign
Trousseau’s Sign
Description: Trousseau’s sign is elicited by inflating a blood pressure cuff on the upper arm to a pressure greater than the systolic blood pressure and maintaining it for 3 to 5 minutes. A positive Trousseau’s sign is indicated by the occurrence of carpal spasm, which involves flexion of the wrist and metacarpophalangeal joints, extension of the fingers, and adduction of the thumb and fingers (a position sometimes referred to as the “obstetrician’s hand”).
Associated Conditions: Trousseau’s sign is most commonly associated with hypocalcemia but can also be seen in patients with hypomagnesemia (low magnesium levels) and alkalosis (increased blood pH).
Chvostek’s Sign
Description: Chvostek’s sign is tested by tapping on the facial nerve just in front of the ear and watching for a twitch of the facial muscles, particularly the nose or lips. A positive Chvostek’s sign indicates facial muscle contraction in response to the tapping.
Associated Conditions: Like Trousseau’s sign, a positive Chvostek’s sign is commonly associated with hypocalcemia but can also occur in hypomagnesemia and other conditions that cause neuromuscular excitability.
Laryngeal stridor
Dysphagia
Numbness and tingling around the mouth or in the
extremities
Dysrhythmias
Management of Hypocalcemia
Treat cause
Calcium and Vitamin D supplements
IV calcium gluconate
Rebreathe into paper bag
Treat pain and anxiety to prevent hyperventilation-
induced respiratory alkalosis
Phosphate
Primary anion in ICF
Essential to function of muscle, red blood cells,
and nervous system
Involved in acid-base buffering system, ATP
production, cellular uptake of glucose, and
metabolism of carbohydrates, proteins, and fats
Serum levels controlled by parathyroid hormone
Maintenance requires adequate renal
functioning
Reciprocal relationship with calcium
Hyperphosphatemia
High serum PO43− caused by
Acute kidney injury or chronic kidney disease
Excess intake of phosphate or vitamin D
Hypoparathyroidism
Manifestations
Tetany, muscle cramps, paresthesias, hypotension,
dysrhythmias, seizures (hypocalcemia)
Calcified deposits in soft tissue such as joints,
arteries, skin, kidneys, and corneas (cause organ
dysfunction, notably renal failure)
Hyperphosphatemia Management
Identify and treat underlying cause
Restrict intake of foods and fluids containing
phosphorus
Oral phosphate-binding agents
Hemodialysis
Volume expansion and forced diuresis
Correct any hypocalcemia
Hypophosphatemia
Low serum PO43− caused by
Malnourishment/malabsorption
Diarrhea
Use of phosphate-binding antacids
Inadequate replacement during parenteral nutrition
Manifestations
CNS depression
Muscle weakness and pain
Respiratory and heart failure
Rickets and osteomalacia
Hypophosphatemia Management
Increasing oral intake with dairy products
Oral supplements
IV administration of sodium or potassium phosphate
* Monitor serum calcium and phosphorus levels every 6
to 12 hours
Magnesium
Cofactor in enzyme for metabolism of
carbohydrates
Required for DNA and protein synthesis
Blood glucose control
BP regulation
Needed for ATP production
Acts directly on myoneural junction
Important for normal cardiac function
50% to 60% contained in bone
30% in cells
Only 1% in ECF
Absorbed in GI tract
Excreted by kidneys
Hypermagnesemia
High serum Mg caused by
Increased intake of products containing magnesium
when renal insufficiency or failure is present
Excess IV magnesium administration
Manifestations
Hypotension, facial flushing
Lethargy
Nausea and vomiting
Impaired deep tendon reflexes
Muscle paralysis
Respiratory and cardiac arrest
Hypermagnesemia Management
Prevention first—stop magnesium-containing drugs
and limit dietary intake of magnesium-containing
foods
IV calcium gluconate if symptomatic
Fluids and diuretics to promote urinary excretion
Dialysis
Hypomagnesemia
Low serum Mg caused by
Prolonged fasting or starvation
Chronic alcoholism
Fluid loss from GI tract
Prolonged PN without supplementation
Diuretics, proton-pump inhibitors, some antibiotics
Hyperglycemic osmotic diuresis
Manifestations
Resembles hypocalcemia
* Muscle cramps, tremors
* Hyperactive deep tendon reflexes
* Chvostek’s and Trousseau’s signs
* Confusion, vertigo, seizures
Dysrhythmias
Hypomagnesemia Management
Management
Treat underlying cause
Oral supplements
Increase dietary intake
IV magnesium when severe
pH
Measure of H+ ion concentration
Increase H+ concentration= acidity
Decrease H+ concentration= alkalinity
Blood is slightly alkaline at pH 7.35 to 7.45
Less than 7.35 is acidosis
Greater than 7.45 is alkalosis
Acid-Base Regulation
3 mechanisms to regulate acid-base balance and
keep pH between 7.35 and 7.45
Buffer system
Respiratory system
Renal system
Buffer System
Primary regulator of acid-base balance
Act chemically to change strong acids to weak
acids or bind acids to neutralize them
Respiratory and renal systems need to be
functioning adequately
HCl + NaH2CO3 NaCl + H2CO3
Strong acid + strong base is buffered into salt
and weak acid
Major buffer system
Other Buffer Systems
Phosphate
Protein
Hemoglobin
Cellular
Shifts H+ in and out of cell in exchange for potassium
Respiratory System Regulation
CO2 + H2O –> H2CO3 –> H+ + HCO3−
Respiratory center in medulla controls breathing
Increased respirations lead to increased CO2
elimination and decreased CO2 in blood
Decreased respirations lead to CO2 retention
Renal System Regulation
Kidneys conserve bicarbonate and excretes some
acid
- 3 mechanisms for acid excretion
Secrete free hydrogen
Combine H+ with ammonia (NH3)
Excrete weak acids
Alterations in Acid-Base Balance
Imbalances occur when compensatory mechanisms
fail
-Classification of imbalances
Respiratory (CO2) or metabolic (HCO3)
Acidosis or alkalosis
Acute or chronic
Blood Gas Values
Arterial blood gas (ABG) values give objective
information about
Acid-base status
Underlying cause of imbalance
Body’s ability to regulate pH
ABG analysis also shows the partial pressure of
arterial O2 (PaO2) and O2 saturation
Interpretation of ABGs
- Look at each of the values
Start by reviewing all the values provided in the ABG report, which typically includes:
pH: Indicates the acidity or alkalinity of the blood.
PaCO2 (Partial Pressure of Carbon Dioxide): Reflects the respiratory component of acid-base balance.
HCO3- (Bicarbonate): Represents the metabolic component of acid-base balance.
PaO2 (Partial Pressure of Oxygen): Measures the oxygen level in the blood.
O2 Saturation (Oxygen Saturation): Indicates the percentage of hemoglobin saturated with oxygen.
- Look at pH first
The pH value will tell you if the blood is acidic, alkaline, or normal:
Normal pH: 7.35 - 7.45
Acidemia: pH < 7.35
Alkalemia: pH > 7.45
- Use ROME to determine respiratory or
metabolic
ROME stands for “Respiratory Opposite, Metabolic Equal”:
Respiratory: Changes in PaCO2. If pH and PaCO2 are in opposite directions (pH down, PaCO2 up = acidosis; pH up, PaCO2 down = alkalosis), it indicates a respiratory issue.
Metabolic: Changes in HCO3-. If pH and HCO3- move in the same direction (both up or both down), it indicates a metabolic issue
- Determine if patient is compensating
Compensation refers to the body’s attempt to restore normal pH:
Fully Compensated: pH has returned to normal, but PaCO2 and HCO3- are abnormal.
Partially Compensated: pH, PaCO2, and HCO3- are all abnormal, indicating the body is attempting to compensate, but has not yet normalized the pH.
Uncompensated: Only one of either PaCO2 or HCO3- is abnormal along with an abnormal pH, indicating no compensation has occurred.
- Assess the PaO2 and O2 saturation
These values provide information about the patient’s oxygenation status:
PaO2: Normal values range from 75 to 100 mmHg. Values below this range indicate hypoxemia.
O2 Saturation: Normal saturation is 95-100%. Values below 95% may indicate insufficient oxygenation.
Respiratory Acidosis
Carbonic acid excess caused by
Hypoventilation
Respiratory failure
Compensation
Kidneys conserve HCO3– and secrete
H+ into urine
Respiratory Alkalosis
Carbonic acid deficit caused by
Hypoxemia from acute pulmonary disorders
Hyperventilation
Compensation
Rarely occurs when acute
Can buffer with bicarbonate shift
Renal compensation if chronic
Metabolic Acidosis
Base bicarbonate deficit caused by
Diabetic ketoacidosis
Lactic acid accumulation (shock)
Severe diarrhea
Kidney disease
Compensatory mechanisms
Increased CO2 excretion by lungs
* Kussmaul respirations (deep and rapid)
Kidneys excrete acid
-Anion gap
= Na+ – (HCO3– + Cl–)
Normal: 8–12 mmol/L
Increased with acid gain
Metabolic Alkalosis
Base bicarbonate excess caused by
Prolonged vomiting or gastric suction
Gain of HCO3–
Compensatory mechanisms
Renal excretion of HCO3–
Decreased respiratory rate to increase plasma CO2
(limited)
ABG Interpretation Guide
ABG Interpretation Guide
1. Evaluate pH:
Normal: 7.35-7.45
Acidemia: pH < 7.35 (indicates acidosis)
Alkalemia: pH > 7.45 (indicates alkalosis)
- Analyze PaCO2 & HCO3-:
PaCO2 (Respiratory Component):
Normal: 35-45 mmHg
↑ PaCO2 suggests respiratory acidosis
↓ PaCO2 suggests respiratory alkalosis
HCO3- (Metabolic Component):
Normal: 22-26 mEq/L
↑ HCO3- suggests metabolic alkalosis
↓ HCO3- suggests metabolic acidosis
- Apply ROME:
Respiratory Opposite:
pH ↓ & PaCO2 ↑ = Respiratory Acidosis
pH ↑ & PaCO2 ↓ = Respiratory Alkalosis
Metabolic Equal:
pH & HCO3- both ↓ = Metabolic Acidosis
pH & HCO3- both ↑ = Metabolic Alkalosis
- Assess Compensation:
Uncompensated: Abnormal pH with one other abnormal value (PaCO2 or HCO3-)
Partially Compensated: All three values (pH, PaCO2, HCO3-) are abnormal
Fully Compensated: Normal pH, but both PaCO2 and HCO3- are abnormal
- Examine Oxygenation:
PaO2 (Oxygen Level): Normal range is 75-100 mmHg. Values below this range suggest hypoxemia.
O2 Saturation: Normal saturation is 95-100%. Values below 95% may indicate inadequate oxygenation.
Oral Fluid and Electrolyte
Replacement
Used to correct mild fluid and electrolyte deficits
Water
Glucose
Potassium
Sodium
IV Fluid and Electrolyte
Replacement
Purposes
Maintenance
* When oral intake is not adequate
Replacement
* When losses have occurred or are ongoing
Types of fluids categorized by tonicity
IV Fluids: Hypotonic
Hypotonic
Lower osmolality when compared to plasma
* Dilutes ECF
Water moves from ECF to ICF by osmosis
Good maintenance fluids
Also used to treat hypernatremia
Monitor for changes in mentation
IV Fluids: D5W
Technically isotonic
Dextrose quickly metabolizes
Net result free water
Provides 170 cal/L
Used to replace water losses, helps prevent ketosis
IV Fluids: Isotonic
Isotonic
Similar osmolality to ECF
* Expands only ECF
No net loss or gain from ICF
Ideal to replace ECF volume deficit
IV Fluids: Normal Saline
NS, 0.9% saline, NSS
Isotonic
Slightly more NaCl than ECF
Used when both fluid and sodium lost
Only solution used with blood
IV Fluids: Lactated Ringer’s
Isotonic
Contains sodium, potassium, chloride, calcium
and lactate
Expands ECF—ideal for surgery, burns and
GI losses
Contraindicated with liver problems,
hyperkalemia, and severe hypovolemia
IV Fluids: Hypertonic
Hypertonic
Higher osmolality compared with plasma
Draws water out of cells into ECF
Require frequent monitoring of
* Blood pressure
* Lung sounds
* Serum sodium levels
IV Fluids: D5 ½ NS
Hypertonic
Common maintenance fluid
Replaces fluid loss
KCl added for maintenance or replacement
IV Fluids: D10W
Hypertonic
Provides 340 kcal/L
Provides free water but no electrolytes
Limit of dextrose concentration that may be
infused peripherally
IV Fluids: Colloids
Stay in vascular space and increase oncotic
pressure
All colloids affect blood coagulation, by
interfering with coagulation factor VII
Include:
Human plasma products (albumin, fresh frozen
plasma, blood)
Semisynthetics (dextran and starches, [Hespan]
Remembering IV Fluids
IV Solution Uses Guide:
Normal Saline (0.9% NaCl): Used for fluid resuscitation, hydration, and managing shock.
Hypertonic Saline: Used to treat cerebral edema and hyponatremia.
D5W (5% Dextrose in Water): Used for hypoglycemia, fluid loss, and dehydration.
Isotonic Solutions: Used for fluid replacement and electrolyte balance.
Lactated Ringer’s: Used for burns, fluid loss from third spacing.
D5 1/2 Normal Saline (D5 0.45% NaCl): Used for hypotonic hydration and SIADH (Syndrome of Inappropriate Antidiuretic Hormone) treatment.
D10W (10% Dextrose in Water): Used for nutritional supplementation and high-calorie fluid replacement.
Colloids: Used for volume expansion, managing shock, and compensating for blood loss.
CVADs
Catheters placed in large blood vessels
Subclavian vein, jugular vein
3 main types
Centrally inserted catheters
Peripherally inserted central catheters (PICCs)
Implanted ports
Permit frequent, continuous, rapid, or
intermittent administration of fluids and
medications
Allow us to more safely administer drugs that are
potential vesicants
Used to administer blood/blood products and PN
Useful for patients with limited peripheral
vascular access or need for long-term vascular
access
Hemodynamic monitoring
Venous blood samples
Injection of radiopaque contrast media
CVADs Advantages/Disadvantages
Advantages
Immediate access
Reduced venipunctures
Decreased risk of extravasation
Disadvantages
Increased risk of systemic infection
Invasive procedure
Centrally Inserted Catheter (CVC)
Inserted into a vein in the chest or abdominal
wall with tip resting in distal end of superior vena
cava
Nontunneled or tunneled
Dacron cuff anchors catheter and decreases
incidence of infection
Single-, double-, or triple-lumen
Examples of long-term (tunneled) catheters
Hickman
Broviac
Groshong
PICC
Central venous catheter inserted into a vein in
arm
Single- or multi-lumen, nontunneled
For patients who need vascular access for 1
week to 6 months
Cannot use arm for BP or blood draw
PICC Advantages/Disadvantages
Advantages
Lower infection rate
Fewer insertion-related complications
Decreased cost
Complications
Deep vein thrombosis
Phlebitis
Implanted Infusion Port
Central venous catheter connected to an
implanted, single or double subcutaneous
injection port
Port is titanium or plastic with self-sealing
silicone septum
Port is accessed using a special non-coring
needle with a deflected tip
Drugs are placed in the reservoir of the port through
skin by a direct injection or through injection into
an established IV line
Advantages
Good for long-term therapy
Low risk of infection
Cosmetic discretion
Midline Catheters
Peripheral catheters
3 to 8 in long
Single- or double-lumen
Use and care similar to PICC
May stay in place up to 4 weeks
Complications
Catheter occlusion
Clamped or kinked catheter
Tip against wall of vessel
Thrombosis
Precipitate buildup in lumen
Embolism
Catheter breaking
Dislodgement of thrombus
Entry of air into circulation
Infection
Contamination during insertion or use
Migration of organisms along catheter
Immunosuppressed patient
Pneumothorax
Perforation of visceral pleura
Catheter migration
Improper suturing
Trauma, forceful flushing
Spontaneous
