Total Body Water
Intracellular and extracellular fluid
2/3 of TBW = ICF
1/3 of TBW = ECF
Intracellular Fluid
2/3 of TBW
fluid inside the cells
Extracellular Fluid
1/3 of TBW
fluid outside the cell
Subdivided into 2 compartments;
Interstitial Fluid (between the cells) 80%
Plasma (bloodstream) 20%
T/F: Water shifts by diffusion/osmosis back and forth between the ICF and ECF based on concentration gradients between the 2 compartments?
True
T/F: If the ICF and ECF concentrations are in equilibrium then there will be no net shift of water between the 2 compartments?
True
T/F: Water only shifts between the ICF and ECF when there is a concentration gradient between the 2 compartments?
True
Intracellular/Extracellular makeup
solutions comprised of water and solutes (dissolved substances) such as Na+, Cl-, K+, glucose, etc
Isotonic range
280-300
T/F: If there is a normal amount of water and a normal amount of solute, then the concentration of the solution is normal; Isotonic
True
Hypertonic
relatively more solute/relatively less water
>300
Solution is greater than the normal
Hypotonic
relatively less solute/relatively more water
<280
Solution is less than the normal
T/F: Water will always move from more dilute to more concentrated?
True
T/F: The abnormalities are not incredibly severe, 280-300 is normal, but even the slightest change either direction causes shifts?
True
If the ICF is isotonic and the ECF is hypotonic, how will the fluid shift?
The fluid will shift from the ECF to the ICF. The ECF is slightly more dilute/less concentrated than the ICF, therefore the fluid will shift to inside the cells causing them to expand.
If the ICF is isotonic and the ECF is hypertonic, how will the fluid shift?
The fluid will shift from the ICF to the ECF. The ICF is less concentrated/more dilute than the ECF, therefore the fluid will shift out of the cells and into the ECF, causing the cells to shrink.
T/F: The ECF concentration changes more easily than the ICF concentration?
True
Hydrostatic Pressure
pressure trying to push water out
In the plasma: water is trying to be pushed out by hydrostatic pressure
Has a direct correlation to Blood Volume
Increased BV, Increased HP
Decreased BV, Decreased HP
Oncotic Pressure
pressure trying to hold or keep water in
In the plasma: water is trying to stay in by oncotic pressure
Oncotic Pressure Plasma Protein: Albumin (made in the liver)
Albumin establishes oncotic pressure
Edema
accumulation of fluid in the interstitial space
is a distribution problem
can occur in almost every organ and can be focal (localized), regional, or diffuse (widespread)
4 Factors Contributing to Edema Formation
Increased Plasma Hydrostatic Pressure
resulting from increased BV
ex: Pulmonary Edema, CHF (not enough cardiac output = fluid retention)
Decreased Plasma Oncotic Pressure
resulting from reduced plasma albumin levels
ex: liver failure
Increased Capillary Permeability
resulting from trauma and/or inflammation
"increased leakiness"
Lymphatic Obstruction
resulting from internal blockage or external compression or lymphatic drainage
reduced lymphatic circulation
Any of the above-contributing factors can occur alone or in combination
Normal Sodium Values/Affects
135-145 mEq/L
Most abundant ECF electrolyte; sodium abnormalities affect ECF osmolarity and BV/BP
Na+ homeostasis is regulated by the GI tract, kidneys, and endocrine system (aldosterone)
Hypernatremia
blood Na+ >145 mEq/L
most commonly occurs in hospitalized patients and the elderly; and is almost always caused by water deficit, reduced water intake, or increased water loss
as a result of hypernatremia, ECF will be hypertonic, causing water to shift out of the cells (ICF to ECF) and causing shrinkage (cellular dehydration)
If severe (blood Na+ > 165), more significant effects are on the CNS
Treat by correcting the water deficit
Hyponatremia
blood Na+ <135 mEq/L
results from either sodium loss or the addition of water
common causes include diuretic use, diarrhea (caused by sodium loss with decreased BV), and heart failure (caused by water retention with an increased BV)
as a result of hyponatremia, ECF will be hypotonic causing water to shift into the cells (ECF to ICF) causing cells to expand/swell
Severe hyponatremia (blood Na+ <120) is potentially life-threatening because it can lead to brain swelling. Hyponatremia should be corrected slowly (<8mEq/L over 24 hours) to prevent Osmotic demyelinization syndrome (CNS complication)
Normal Postassium Values/ Affects
Blood K+ 3.5-5.0 mEq/L
K+ is the most abundant ICF electrolyte
the vast majority of K+ is in the cells
Abnormalities affect the NM excitability, most notably affecting the heart
K+ homeostasis is regulated by the GI tract, kidneys, and endocrine system (aldosterone and insulin) -Aldosterone: lower BP with release of K+; holds onto Na+, releases K+
lowers K+ by shifting into cells
Hyperkalemia
blood K+ >5.0mEq/L
most dangerous electrolyte abnormality due to the development of potentially lethal cardiac dysrhythmias
Severe hyperkalemia (blood K+ > 6.5) slows conduction velocity in the heart; can cause asystole or causes VFib (ventricular fibrillation)
Common causes are drugs that increase K+ retention (K+ sparing drugs; ACE inhibitors and ARBs), renal impairment, adrenal insufficiency (both decrease K+ excretion), metabolic acidosis, cancer treatments, etc
Resting potential goes up as a result of hyperkalemia
Treat moderate to severe hyperkalemia with IV insulin (insulin shifts K+ back into cells), glucose (to compensate for the insulin), and Calcium gluconate to protect the heart
Hypokalemia
Blood K+ <3.5mEq/L
most commonly caused by increased K+ loss in the urine (diuretic use & hyperaldosteronism; increased aldosterone, increased K+ excretion) or from the GI tract. Can also be caused by reduced dietary K+ intake or the increased shift of K+ into cells
The primary manifestations result from decreased NM excitability
Resting potential goes down as a result of hypokalemia
Treat the underlying cause
Normal Calcium Values/ Affects
Blood Ca+ 8.5-10.5 mg/dL
Calcium is abundantly stored in the bones and teeth
Calcium abnormalities affect NM excitability
Calcium homeostasis is regulated by the GI tract, kidneys, skeletal system, and endocrine system (PTH [increases blood Ca+] & Vitamin D)
Hypercalcemia
blood Ca+ >10.5 mg/dL
most commonly caused by hyperparathyroidism and cancer
hypercalcemia causes a decrease in NM excitability (by moving threshold potential further away from resting membrane potential) possibly resulting in constipation and hypercalciuria (increased urine Ca+) with kidney stones
If hypercalcemia is severe (blood Ca+ >~13.0 mg/dL), skeletal muscle weakness, confusion, and coma can occur
Treat underlying cause. Treatment can also include the administration of a loop diuretic (LASIX) to enhance urinary Ca+ excretion
Hypocalcemia
Blood Ca+ <8.5 mg/dL
commonly caused by hypoparathyroidism, Vitamin D deficiency (you need Vit. D so the body can absorb Ca+), and renal failure
Hypocalcemia causes an increase in NM excitability (by moving threshold potential closer to resting membrane potential)
Mild hypocalcemia may be asymptomatic or cause muscle cramps
Severe hypocalcemia (blood Ca+ <~7.0 mg/dL) can cause tetany (continuous skeletal muscle contraction), hyperreflexia (increased reflexes), paresthesia (tingling) of the tongue, lips, fingers, feet, or seizures
Treat mild hypocalcemia with oral Ca+ supplements; treat hypocalcemic tetany with IV Ca+ gluconate
Acid-Base Balance normal values/affects
3 Ways the Body Acts to Maintain Acid-Base Balance
Buffer systems work to resist pH changes
Kidneys: regulate acid/base excretion as needed
Lungs: regulate CO2 (volatile acid) excretion as needed
Buffer systems and kidneys collectively are responsible for the metabolic regulation of acid-base balance (Bicarbonate ion; HCO3- levels reflect the function of the metabolic component of acid-base regulation) HCO3- is a base/alkaline
Lungs are responsible for the respiratory regulation of acid-base balance. CO2 levels reflect the function of the respiratory component of acid-base regulation. CO2 is an acid/acidic
Acid-Base Disturbance
Respiratory Acidosis/Alkalosis
Respiratory Acidosis: high CO2 Respiratory Alkalosis: low CO2
Metabolic Acidosis/Alkalosis
Metabolic Acidosis: low HCO3- Metabolic Alkalosis: high HCO3-
Combination Acidosis/Alkalosis
Combination Acidosis: high CO2, low HCO3- Combination Alkalosis: low CO2, high HCO3-
There's both a respiratory and metabolic cause for the acidosis/alkalosis
What test is used to determine the Acid-Base balance of a patient?
ABG (Arterial Blood Gas)
What is the ABG made up of?
pH, CO2, HCO3-
Normal Values for the ABG
pH: 7.35-7.45 (indicates acid-base balance) CO2: 35-45 mmHg (respiratory component) HCO3-: 22-28 mEq/L (metabolic component)
Respiratory Alkalosis
occurs when CO2 is removed (exhaled) faster than it is produced; results in low CO2 (hypocapnia) and a corresponding increase in pH (>7.45) because acid is being removed faster than it is replaced
can be caused by anything that results in hyperventilation (increased ventilation rate), hypoxemia, panic attacks, severe anxiety, etc
Respiratory Acidosis
occurs when CO2 is removed (exhaled) slower than it is being produced; results in high CO2 (hypercapnia) and a corresponding decrease in pH (<7.35) because acid is released more slowly than it is accumulating
can be caused by anything that results in hypoventilation (decreased ventilation rate), asthma, COPD, pneumonia, ARDS, etc
Metabolic Alkalosis
occurs when HCO3- accumulates due to a loss of acid, reduced HCO3- excretion, or the addition of HCO3-, this results in a high HCO3- and a corresponding increase in pH (>7.45) because base (HCO3-) is accumulating
commonly caused by volume depletion (low blood volume) secondary to vomiting (loss of acid) or diuretic use (reduced HCO3- excretion)
Metabolic Acidosis
occurs when HCO3- is reduced due to the accumulation of organic acid (lactic acid, keto acids, others) or increased HCO3- excretion (loss); resulting in low HCO3- and a corresponding decrease in pH (<7.35) because base (HCO3-) is reduced
Can be classified as either normal anion gap (AG) or elevated anion gap (AG)
Normal Anion Gap (AG)
caused by loss of HCO3-; most common cause s prolonged diarrhea
-normal range= 3-12 mEq/L
Elevated Anion Gap (AG)
caused by the accumulation of organic acid
most common causes are lactic acids (from hypoxia [low tissue oxygenation]), DKA (diabetic ketoacidosis; complication of Type 1 DM), or uremia associated with CKD (chronic kidney disease)
Formula for Elevated AG: AG= Na+ - (Cl- + HCO3-)
Metabolic Acidosis formula to determine if respiratory compensation is appropriate
CO2= (1.5 * HCO3-) +8 +/- 2
+/-2 gives us the range
Combinations
in a combination acidosis/ alkalosis, there is BOTH a respiratory and metabolic cause for the acidosis or alkalosis
Compensation
in acid-base regulation, compensation refers to physiologic changes that occur to try to maintain acid-base balance
EX: metabolic acidosis; the pH is low because there is a primary metabolic cause. The respiratory component (reflected by CO2) may then compensate for the metabolic cause of the acidosis in an attempt to keep the pH as close to normal as possible
T/F: Compensation can occur for any acid-base disorder?
True