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