Imbalances in Fluid Compartments

Edema

Too much fluid in the interstitial space, or too much volume in the space that surrounds cells

Third Spacing

Too much fluid in Transcellular space, or too much in a non-functional space

Hypovolemia

Too little fluid in the Intravascular space, or too little volume in the blood vessels

Hypervolemia

Too much fluid in the Intravascular space, or too much volume in the blood vessels

What is the etiology of Edema

• Increased capillary hydrostatic pressure

  • More fluid pushed out of capillaries

• Decreased plasma oncotic pressure

  • Reduced reabsorption of fluid back into capillaries

• Increased capillary permeability

  • Disruption in membrane integrity results in fluid leaking into interstitial space

• Lymphatic obstructions

  • Prevention of drainage of interstitial fluid; accumulation

Localized Edema

• Associated with localized conditions (Eg. Deep-vein thrombosis; clot in leg - unilateral leg swelling)

• Inflammation or injury in a specific location - warmth and redness; swelling

Anasarca

• Generalized Edema

• Systemic conditions; whole body swellling

  • Eg.) Heart failure, nephrotic syndrome

Non-pitting Edema

• Protein-rich fluid, interstitial fibrosis

Pitting Edema

• When pressure is applied to swollen area, an indentation remains for some time

• Increased hydrostatic pressure

Describe the circulatory effects of Edema, and how the RAAS is triggered

• Increase of interstitial fluid = decreased blood volume

• Renin released from kidneys to convert angiotensinogen into angiotensin I

• ACE released from lungs converts Angiotensin I into Angiotensin II

• Angiotensin II causes a few things to occur:

  • Angiotensin II causes vasoconstriction, increasing BP, increasing capillary hydrostatic pressure, causing more fluid to leak into interstitial space

  • Angiotensin II stimulates adrenal gland to release aldosterone

    • Aldosterone acts on kidneys to increase reabsorption of water & Na+ to restore blood volume, but exacerbates Edema by adding more fluid to move into interstitial space

      • Also promotes excretion of K+

Why does RAAS worsen Edema and fluid retention?

• Angiotensin II causes vasoconstriction to occur, increasing capillary hydrostatic pressure to push fluid into interstitial spaces

• Angiotensin II also causes the adrenal gland to release aldosterone, that acts on kidneys to retain water and Na+ levels in attempts to regain blood volume, further exacerbating edema since more fluid flows from Intravascular blood volume into the interstitial space

What is the clinical significance of Edema? What are the effects or outcomes?

• Impaired mobility - fall risk

• Skin integrity

  • Skin breakdown, pressure ulcers

  • Infection risk

• Organ function

  • Fluid accumulation around organs

What abnormalities can cause Third Spacing?

• Severe infections & sepsis

• Trauma & burns

• Surgery

• Liver disease

• Kidney disease

• Heart failure

• Pancreatitis

• Malnutrition

Describe the pathogenesis of Third Spacing; How does it occur?

• Increased capillary hydrostatic pressure

  • Inflammatory mediators cause capillaries to become more permeable

• Decreased plasma oncotic pressure

  • Decrease the osmotic pull of fluid back into the capillaries

• Increased capillary permeability

  • Elevated pressures in the venous system push more fluid out of the capillaries

Ascites

Fluid accumulation in the peritoneal cavity

• Liver disease, big bellies

Pleural Effusion

Fluid accumulation in pleural cavity

• impairs respiratory function; compresses lung; less space to inflate

Pericardia Effusion

• Fluid accumulation in the pericardial cavity

  • Heart not able to pump because it is constricted by surrounding fluid

What is the clinical significance of Third Spacing? What are the effects/outcomes?

• Decreased circulating blood volume

  • Hypovolemia = hypotension

• Organ dysfunction

  • Lungs - hypoxia & respiratory distress

  • Abdomen - impaired digestion

• Infection

  • Asities - peritonitis

  • Pleural effusion - pneumonia

Isotonic Alteration

Concentration of solutes in ECF is the same as the ICF

Hypotonic Alteration

Osmolality of the ECF is lower than the Osmolality of ICF; more solutes in ICF than ECF

Hypertonic Alteration

Osmolality of the ECF is larger than the Osmolality of ICF; solute concentration is greater in ECF than solute concentration in ICF

Isotonic loss

• Hypovolemia

• H2O loss = Na+ loss

• Serum Na+ remains the same

• Eg.) Hemorrhage, inadequate intake of fluids

Hypertonic loss

• H2O loss > Na+ loss; increased serum Na+; increased Osmolality of ECF

• Body responds by moving fluid from intracellular compartment to Intravascular compartment (high Osmolality); leading to cellular dehydration

• Eg.) Heat stroke, early kidney disease

Hypotonic loss

• Excessive Na+ > H2O loss; decreased serum Na+; hyponatremia

• Body responds by moving fluid from Intravascular compartment to intracellular compartment

  • Cells swell & decrease blood volume

How does hypertonic loss cause hypernatremia

H2O loss > Na+ loss, meaning that Na+ serums within the plasma are increased appearing higher due to water loss; causes cell shrinkage as fluid moves from intracellular compartment to Intravascular

Isotonic Excess

• Hypervolemia; H2O gain ~ Na+ gain

• Fluid in Intravascular compartment; circulatory overload

• Intercellular compartment = interstitial edema

Hypertonic excess

• Excessive Na+ intake; Na+ gain > H2O gain

• Hypernatremia

  • Eg.) rapid hypertonic saline infusion

• Fluid moves from intracellular compartment to Intravascular compartment due to high Osmolality in Intravascular compartment = cellular dehydration

Hypotonic excess

• Water intoxication

• H2O gain > Na+ gain

• Decrease in serum Na+; hyponatermia

• Body responds by moving fluid from Intravascular compartment to intracellular compartment (decrease Osmolality in ECF); cells swell but there is also excess in ECM compartment

What kind of IV fluids are provided for isotonic fluid losses?

Isotonic IV fluids

What kind of IV fluids are used to treat hypertonic fluid losses?

Hypotonic IV fluids

What kind of IV fluids are used to treat hypotonic fluid losses?

Hypertonic IV fluids

Give an example of an Isotonic IV fluids

RL - Ringer’s Lactate

What patient considerations should be taken in place prior to administration of isotonic IV RL?

• Ringers lactate contain potassium, consult with the physician if the client has high K+ prior to administration

• Clients with liver impairment/dysfunction; since they may have challenges in metabolizing lactate

What are examples of Hypotonic IV fluids?

• ½ Normal saline (0.45% NaCl)

• 1/3 Normal saline (0.35% NaCl)

• D52 (5% dextrose in water)

How do hypotonic IV fluids treat hypertonic conditions?

Hypotonic IV solutions contain fluids with a lower solute concentration than intracellular fluids

• Intracellular fluids have higher Osmolality, thus resulting with fluids being pushed into cells from Intravascular space to intracellular space

What are client considerations that should be taken in regards to D5W hypotonic IV fluid administration?

• Clients with diabetes; risk of hyperglycemia; monitor BG (blood glucose)

Why should you be considerate of clients with increased ICP (intracranial pressure) when administering hypotonic IV fluids?

You should be careful of administering hypotonic IV fluids to patients with elevated intracranial pressure because we don’t want to push more fluid into the brain and cause any further harm

What can happen when too much hypotonic solution is administered?

Hypovolemia; fluid being pushed from Intravascular space into intracellular space, can end up in other places of the body

What are examples of Hypertonic IV Fluids?

• 5% Normal Saline

• D5W with ½ Normal Saline

• D5W with Ringers Lactate (RL)

How does hypertonic IV fluids treat hypotonic conditions like Hypovolemia?

Hypertonic IV fluids contain higher concentrations of Na+/solutes than intracellular fluid solute concentrations; pulls fluid out of cells into Extracellular fluid compartments (Intravascular compartment)

What is the initial treatment for hypernatremia?

A) Restriction of fluids

B) Administration of a diuretic

C) Hypertonic fluid administration

D) Hypotonic salt-free fluid (D5W)

D) Hypotonic salt-free fluid (D5W)

• Hypernatremia is elevated levels of sodium in the blood, Osmolality of intravenous fluid compartment is greater than the Osmolality of intracellular fluid compartments, drawing fluid out of cells causing cellular dehydration, Administration of hypotonic IV solution (D5W) will push fluid back into the cells as the hypotonic solution contains a solute concentration lower than the solute concentration of intracellular fluid. This causes fluid to move from intravenous compartment to intracellular compartments, hydrating the cells

What is the etiology of Hypovolemia? Why does it occur?

Hypovolemia - too little fluid in Intravascular space; low blood volume

• Fluid loss (hemorrhage, dehydration, third spacing)

• Increased fluid output (polyurea, adrenal insufficiency)

• Inadequate fluid intake (nutritional deficits)

What is MAP? What is the normal range?

• Mean Arterial Pressure, 70-100 mmHg

What is the equation of MAP

MAP = CO x TPR

• CO = SV x HR

MAP = SV x HR x TPR

How does Hypovolemia affect tissue perfusion?

Hypovolemia, the decrease in Intravascular volume causes a decrease in venous return

• A decrease in venous return decreases stroke volume

• Decreased stroke volume causes decreased cardio output; overall decreasing MAP

What are the compensatory mechanisms of Hypovolemia?

• Sympathetic Nervous System Activation

• Renin-Angiotensin-Aldosterone System (RAAS)

• Antidiuretic Hormone (ADH) Release

How does Hypovolemia trigger ADH release?

• Baroreceptors detect changes in blood volume due to Hypovolemia

• Osmoreceptors detect changes in Intravascular Osmolality

• Both signal the hypothalamus and the hypothalamus responds by signalling the posterior pituitary to release ADH

• ADH increases water resorption in the kidneys, decreases urine output, and causes vasoconstriction

How does vasoconstriction caused by ADH release compensate for Hypovolemia?

Vasoconstriction increases peripheral vascular resistance, increasing blood pressure

What are micro-level structural alteration of Hypovolemia; visible under microscope

• Decreased capillary perfusion

  • Hypoxia & cellular injury

• Shift to anaerobic metabolism

  • Inadequate O2 deliver = lactic acidosis

What are macro-level structural alterations of Hypovolemia; visible to the eye

• Decreased perfusion of vital organs

  • Ischemia & organ damage

• Cardiovascular compensation

  • Increase HR; tachycardia to maintain cardiac output

  • Severe Hypovolemia (plasma fluid loss) = Hypovolemia shock = impaired organ function and decrease in blood pressure

A client has Hypovolemia. How would their hematocrit levels appear?

A client with Hypovolemia would have high hematocrit levels, since Intravascular fluids are lost, and RBC concentration appears higher compared to total volume of blood

Renal causes of Hypervolemia

• Acute kidney injury, chronic kidney disease

• Nephrotic syndrome

Cardiac causes of Hypervolemia

Congestive heart failure

Liver causes of Hypervolemia

Cirrhosis

Endocrine causes of Hypervolemia

• Hyperaldosteronism

• Syndrome of inappropriate antidiuretic hormone (SIADH)

Iatrogenic (medical interventions) causes of Hypervolemia

• excessive intravenous fluid administration

• Blood transfusions or albumin transfusions

What factors lead to the cause of Hypervolemia

• Sodium retention

  • Increased sodium intake, decreased sodium excretion

• Water retention

  • Conditions like SIADH

• Capillary dynamics

  • Decreased capillary permeability

  • Increased Oncotic pressure

What are structural alterations of Hypervolemia?

• Edema - fluid accumulation in interstitial spaces

• Ascites - fluid accumulation in peritoneal cavity

• Pleural Effusion - fluid accumulation in the pleural space

• Cardiac Enlargement - cardiac hypertrophy and heart failure