Fluid and Electrolyte Imbalances

Fluids, Electrolytes, & Acid/Base Imbalances

• Total body water and fluid distribution varies according to age and fat content.
• Total body water in an adult male is 60%, or 42 liters, in a 70kg adult male.
• Total body water in newborn infants is 70%.
• There are three functional body compartments.
• Body fluids are divided across two categories: intracellular fluid (ICF) and extracellular fluid (ECF).

Distribution and Composition of Bodily Fluids

• Intracellular fluid (ICF) is inside the cells.
• 63-70% of total body water is ICF.
• ICF contains water, proteins and electrolytes.
• Extracellular fluid (ECF) is outside the cells.
• 30-37% of total body water is ECF.
• The intravascular component of ECF is whole blood.
• The interstitial component of ECF surrounds cells in tissues.
• The transcellular component of ECF is fluid in defined spaces

Review: Movement of Water

• Osmosis is the movement of water from less concentrated to more concentrated areas.
• Water moves to equalize concentrations.

Review: Movement of Molecules

• Movement of molecules from an area of high concentration to an area of low concentration until it is equal on both sides.

Review: Movement of Molecules - Active Transport

• Active transport requires ATP to move large molecules that can't diffuse.

Movement of Body Fluids: Capillary and Interstitial Fluid Exchange

• Colloid osmotic pressure, also called oncotic pressure, relates to concentration of proteins.
• Hydrostatic pressure is the pressure of fluids or their properties when in equilibrium.

Alterations in Water Movement: Edema

• Edema is the accumulation of fluid in the interstitial spaces.
• Edema causes include:
  • Increased capillary hydrostatic pressure due to venous obstruction and sodium retention
  • Decreased plasma oncotic pressure due to losses or diminished albumin production.
  • Increased capillary permeability due to inflammation and immune response.
  • Lymph obstruction (lymphedema)

Spacing

• First spacing occurs when there is normal distribution of fluid.
• Second spacing occurs when there is abnormal accumulation of fluid in the interstitial space.
• Third spacing occurs when there is abnormal accumulation of fluid in trans-compartmental spaces, such as the serous cavity, pericardial sac, or peritoneal cavity.

Alterations in Water Movement: Edema Continued - Assessment, Treatment

• Edema can be assessed using daily weights and visual assessment which includes localized vs generalized, and assessing for pitting edema.
• Clinical manifestations of edema include localized generalized edema, dependent edema, pitting edema, "third space”, swelling and puffiness, tighter-fitting clothes and shoes, and weight gain.
• Edema can be treated by elevating edematous limbs, using compression stockings or devices and avoiding prolonged standing.
• Serum albumin, restricting salt intake and taking diuretic agents are all used to treat edema.

Overview of Electrolytes

• Electrolytes dissociate into ions in water; there are positively charged cations and negatively charged anions.
• Electrolytes are in both ECF and ICF compartments but are in different concentrations.
• Some electrolytes are more concentrated in the ICF compartment, as compared with the ECF compartment.
• All electrolytes move across compartments but must be in balance for optimal health.

Overview of Electrolytes compartments

• Intracellular electrolytes include Potassium (K+)
• Extracellular electrolytes include Sodium (Na+), Chloride (Cl-) Bicarbonate (HCO3-)
• Intracellular electrolytes include Phosphate and Organic lons.

Normal Electrolyte Values

• Normal Sodium is 135-145 mEq/L.
• Normal Chloride is 95-105 mEq/L
• Normal Potassium is 3.5 -5.0 mEq/L
• Normal Bicarbonate is 22-26 mEq/L (arterial)
• Normal Total Calcium 8.5-10.5 mg/dl
• Normal lonized Calcium 4.5-5.6 mg/dl
• Normal Magnesium 1.3-2.1 mEq/L
• Normal Phosphorus 2.5-4.5 mg/dl
• Normal Serum osmolality 280-300 mOsm/kg

Sodium

• Sodium is the primary ECF cation.
• Sodium regulates osmotic forces.
• Neuromuscular irritability, acid-base balance, cellular reactions, and transport of substances are roles of sodium. _ Sodium is regulated by aldosterone and natriuretic peptides.

Sodium Concentration and Water Regulation

• Sodium concentration regulation is impacted by natriuretic peptides and the renin-angiotensin-aldosterone system.
• Natriuretic peptides include Atrial natriuretic peptide and Brain natriuretic peptide.
• Atrial and brain natriuretic peptides promote sodium and water excretion
• Aldosterone of the renin-angiotensin-aldosterone system promotes water and sodium reabsorption and promotion excretion of potassium.

Water Balance

• Thirst perception and antidiuretic hormone (ADH) regulate water balance.
• ADH is released from posterior pituitary and is also called vasopressin.
• ADH is released when there is an increase in plasma osmolality or decrease in circulating blood volume, and increases water reabsorption.
• Thirst perception relates to Osmolality receptors (osmoreceptors) which are stimulated through hyperosmolality, dry mouth, plasma-volume depletion and increase water intake.

Water and Sodium Imbalances - Classifications

• Volume imbalances may be hypervolemia or hypovolemia, if these occur in equal alterations of sodium and water concentration then they are called isotonic imbalances.
• Osmolar imbalances are Unequal Alterations in the concentration between water and sodium or other solutes in ECF.
• Osmolality is the Measure of the number of milliosmoles per kilogram of water or the concentration of molecules per weight of water.
• Normal Plasma Osmolality is 280-300 mOsm/kg
• Normal role of Sodium in Osmolality is 135-145 mEq/L
• Hyponatremia is a Sodium level below 135 mEq/L.
• Hypernatremia is a Sodium level greater than 145 mEq/L.
• Isotonic solutions have solute concentrations (osmolality) equal to that of normal cells (ICF).
• Hypertonic solutions have solute concentrations (osmolality) greater than normal cells (ICF).
• Hypotonic solutions have solute concentrations (Osmolality) less than normal cells (ICF).

Classifications of IV Solutions

• IV solutions may be isotonic, hypotonic, or hypertonic, depending on what type of fluid change the provider wants to give the patient.
• QUICK GUIDE TO I.V.
  • Solutions used for I.V. therapy may be isotonic, hypotonic, or hypertonic. The type you give depends on whether you want to change or main- tain body fluid status.
• Isotonic solution
• (280-300 mOsm/liter)* An isotonic solution has an osmolarity about equal to that of serum. Because it stays in the intravascular space, it expands the intravascular compartment.
• Hypotonic solution
• (less than 280 mOsm/liter)* A hypotonic solution has an osmolarity lower than that of serum. It shifts fluid out of the intravascular compartment, hydrating cells and the intersti- tial compartments
• Hypertonic solution (greater than 300 mOsm/liter) A hypertonic solution has an osmolarity higher than that of serum. It draws fluid into the intravascular compartment from the cells and the intersti- tial compartments.

Classifications of IV Solutions, tonicity and values

• 5% dextrose in water: Iso, 250 mOsm, D5W, 5% D/W
• 10% dextrose in water: Hyper 500 mOsm,D₁W, 10% D/W
• 0.9% sodium chloride, normal saline solution: Iso, 310 mOsm, 0.9% NaCl, NSS, PSS
• 0.45% sodium chloride, 1½ normal saline solution: Hypo, 154 mOsm 0.45% NaCl, 1/2 NSS, 1/2 PSS
• 5% dextrose in 0.9% sodium chloride: Hyper, 560 mOsm DNSS, 5% D/NSS, 5% D/0.9% NaCl, D, PSS
• Dextrose 5%/0.2% sodium chloride: Iso, 326 mOsm, D5/0.2% NaCl
• 5% dextrose in 0.45% sodium chloride, 5%: Hyper, 410 mOsm, D512 NSS, 5% D/1/2
• 3% sodium chloride: Hyper, 1026 mOsm, 3% NaCl
• Lactated Ringer's solution: Iso, 274 mOsm, LRS

Isotonic Fluid Volume Excess and clinical manifestations

• Symmetric Increase in extracellular sodium levels and fluid levels
• Clinical manifestations:
  • Weight gain
  • Distended neck veins
  • Blood pressure: Increased
  • Pulses: Bounding and Full
  • Increased capillary hydrostatic pressure
  • Edema
  • Pulmonary: crackles, shortness of breath
  • Peripheral edema

Isotonic Fluid Volume Excess diagnosis, treatment

• Diagnosis
  • Decreased hematocrit
  • Decreased blood urea nitrogen (BUN) levels
  • High cardiac output
• Treatment
  • Restrict fluid intake
  • Monitor I/Os
  • Correct underlying etiology

Isotonic Fluid Volume Deficit

• Symmetric depletion of water and electrolytes
• Clinical manifestations
  • Thirst
  • Decreased urine output
  • Weight loss
  • Increased hematocrit
  • Tachycardia
  • Decreased skin turgor
  • Flattened neck veins
  • Decreased blood pressure
• Potentially hypovolemic shock

Isotonic Fluid Volume Deficit - Diagnosis, Treatment

• Diagnosis
  • Increased hematocrit
  • Increased BUN: creatinine ratio
  • Increased urine osmolality
  • Increased specific gravity
• Treatment
  • Correct underlying etiology
  • Increased oral fluid
  • IV rehydration

Age Considerations for Fluid Volume Deficits

• Potential causes of dehydration in infants: Diarrhea and vomiting
• Potential causes of dehydration in older adults:
  • Smaller fluid reserves
  • Reduced ability to conserve water
  • Less acute sense of thirst

Normal Electrolyte Values

• Normal Sodium is 135-145 mEq/L.
• Normal Chloride is 95-105 mEq/L
• Normal Potassium is 3.5 -5.0 mEq/L
• Normal Bicarbonate is 22-26 mEq/L (arterial)
• Normal Total Calcium 8.5-10.5 mg/dl
• Normal lonized Calcium 4.5-5.6 mg/dl
• Normal Magnesium 1.3-2.1 mEq/L
• Normal Phosphorus 2.5-4.5 mg/dl
• Normal Serum osmolality 280-300 mOsm/kg

Sodium

• Sodium is the primary ECF cation.
• Sodium regulates osmotic forces.
• Neuromuscular irritability, acid-base balance, cellular reactions, and transport of substances are roles of sodium. _ Sodium is regulated by aldosterone and natriuretic peptides.

Hypernatremia

• Sodium concentration greater than 145 mEq/L
• Causes
  • Increased output or decreased intake of water
  • Other etiologies
• Clinical manifestations
  • Hyperosmolality
  • Increases thirst
  • Dry membranes, decreased skin turgor, salivation decreased
  • Vital Signs
  • *CNS symptoms: headaches, restlessness, agitation
  • Serious: seizures, coma

Hypernatremia - Diagnosis and Treatment

• Diagnosis
  • Increased serum sodium and increased serum osmolality
  • Increased urine specific gravity Treatment
  • Assess and correct underlying etiology
  • Decrease serum sodium
    • Hypotonic fluids
    • Gradual correction if parenteral

Hyponatremia

• Sodium concentration below 135 mEq/L with low serum Na levels
• Causes
  • prolonged vomiting and diarrhea from losing electrolytes
  • hypovolemic and hypervolemic states
  • Diuretics- loss of electrolytes
  • Other diseases and conditions
  • Diabetic Ketoacidosis- uncontrolled high amounts of glucose pulls water from inside of cells to outside
• Clinical manifestations
  • **Neurological effects: anxiety, lethargy, headaches
  • Severe = coma/seisurez hypotonic environment from water moving into cells cellular edema
  • GI: nausea/vomiting, abdominal cramps
  • MSK: muscle cramps, fatigue

Hyponatremia - Diagnosis and Treatment

• Diagnosis
  • Decreased serum sodium, chloride levels
  • Increased hematocrit (if vol deficient also present)
• Treatment
  • Treat underlying etiology
  • Mild: oral sodium replacement-
  • Moderate: Isotonic IV fluids 0.9 normal saline sodium chloride
  • Severe: hypertonic fluids- 3% NaCl
    • Rapid administration can lead to central pontine myelinolysis:breakdown of myelin in the pons center of the brain
  • Brain cells can adapt in hypotonic fluid environments

Chloride

• Chloride is the primary ECF anion.
• Normal level is 95-105 mEq/L
• Provides electroneutrality.
• Follows sodium.
• Component of hydrochloric acid in the stomach
• Essential for carbon dioxide transport in red blood cells

Hyperchloremia

• Abnormally high plasma concentration of chloride ions
• Causes:
  • Metabolic acidosis
  • Water loss, dehydration
  • Head injury that causes endocrine abnormalities
  • Hypernatremia, severe diarrhea, respiratory alkalosis
• Clinical manifestations
  • Resemble hypernatremia
  • Symptoms related to dehydration

Hyperchloremia - diagnosis and treatment

• Diagnosis
  • Increased serum chloride
  • Metabolic acidosis or respiratory alkalosis
• Treatment
  • IV hypotonic fluids, lactated Ringer's, and sodium bicarbonate (acid-base imbalances)
  • Diuretic therapy (concurrent hypernatremia)
  • Restriction of sodium and chloride in diet

Hypochloremia

• Abnormally low plasma concentration of chloride ions
• Causes
  • Vomiting, diarrhea, nasogastric suctioning
  • Alkalosis
  • Burns
  • Diuretics
  • Hormones

Hypochloremia - clinical manifestations, diagnosis and treatment

• Clinical manifestations
  • Resemble hyponatremia
  • Cerebral edema
  • Headache, weakness, nausea, tetany
• Diagnosis
  • Decreased serum chloride
  • Metabolic alkalosis
• Treatment
  • Isotonic saline or hypertonic saline
  • Replacement with oral sodium chloride

Potassium

• Potassium is the major intracellular cation.
• Normal concentration is 3.5-5.0 mEq/L
• Regulates ICF osmolality-
• Essential for the transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction
• The sodium-potassium (Na + /K +) pump maintains concentration

Potassium - Key Facators

• Factors influencing the movement of potassium
  • Acid/Base Balance
    • Acidosis- Facilitates movement of k+ out of cell in exchange for h+(hyperkolemia)
    • Alkalosis- Facilitates movement of k+ into cell in exchange for h+ (hypokolemia)
  • Exercise -causes movement of K outside of cell
  • Epinephrine- Facilitates movement of k+ into cell with ATPase pump
  • Aldosterone- Promotes k+ excretion in distal tubule of kidneys
  • Insulin- Used for hypokalemia, lowers potassium levels in the blood- Facilitates movement of K+ into liver and muscle cells

Hyperkalemia

• Abnormally high plasma concentration of potassium ions [ >5 mEq/L]
• Causes
  • Over supplementation of K
  • Decreased renal excretion or renal failure (associated with metabolic acidosis) ARBS have side effects of Hyperkalemia- Pril, Losartan, Spironolactone
  • Shifts from k+ to ECF
    • Acidosis- body will try to compensate and move excess H ions out of ECF and into the cell, K is then moved outside of the cell
    • Insulin deficiency- won't be able to move K into muscle cells
    • Cell hypoxia
  • Endocrine abnormalities- low aldosterone level productions
  • Aldosterone= retains Na and H20 and moves out K

Hyperkalemia - Clinical manifestations

• Clinical manifestations
  • Cardiac: ECG changes [PEAKED T Waves], dysrhythmias Increased neuromuscular excitability-Severe hyperkalemia = cardiac arrest and Tall T waves
  • Neuromuscular- Initial increased neuromuscular irritability, More Severe (Prolonged) : muscle weakness, loss of muscle tone, paralysis
  • Gl: nausea, vomiting, diarrhea , cramps

Hyperkalemia - Mild and Severe

• Mild Hyperkalemia
  • Tingling of lips and fingers,restlessness, intestinal cramping and diarrhea and Peaked T waves on the ECG
• Severe Hyperkalemia
  • Muscle weakness, loss of muscle tone, flaccid paralysis and cardiac arrest

Hyperkalemia - Diagnosis and Treatment

• Diagnosis include Increased serum potassium levels. Peaked T waves in EKG
• Treatment
  • Sodium polystyrene sulfonate- cal oxalate. Exchanges Na or Ca, PO or enema: Do not mix with juice due to high K in oj.
  • Hemodialysis if there is renal failure.
  • Change diuretic medication
  • IV calcium gluconate- antagonizes the increased muscular excitability, stabilizes cardiac potential (short fix)
  • IV Insulin helps increase K entry into the cell and Dextrose 50%-

Hypokalemia

• Abnormally low plasma concentration of potassium ions [ <3.5 mEq/L]
• Causes
  • Decreased potassium intake
  • Shifts of k+ into cell
    • Alkalosis- H ions are low and compensate by moving outside of cells and K follows
    • Insulin used in DKA to treat hyperkalemia
  • Increased k+ losses
    • Hyperaldosteronism- excessive aldosterone secretion and retaining too much NA &H2o and losing K
    • Diuretics, Thiazides, Loop,
    • GI Loss

Hypokalemia - Clinical manifestations

• Clinical manifestations
  • Cardiac: ECG Changes [flat T waves], dysrhythmias as well as Severe: hypotension, cardiac arrest
    • Hypokalemia increases Digoxin Toxicity
    • Membrane potential is more (-) and moved away from the threshold
  • Neuromuscular: muscle weakness, cramps as well as Severe: paralysis
  • Gl: anorexia, nausea, vomiting, constipation and Severe: paralytic ileus-

Hypokalemia - Diagnosis and Treatment

• Diagnosis
  • Decreased serum potassium
  • Electrocardiogram abnormalities Flat T waves
• Treatment
  • Oral potassium supplements
  • IV potassium supplements (slow maintenance to avoid hyperkalemia )
  • Increase foods rich in K: Bananas, oranges, broccoli, spinach,Thiazides- K will be excreted

Calcium

• Total serum calcium concentration= 8.5-10.5 mg/dl (bound)
• lonized calcium = 4.5 -5.6 mg/dl (Free)
• Majority found in bone and teeth
• Essential for:
  • Coagulation-
    • 40% is bound to the protein albumin (not biologically active- low albumin= higher ionized free Ca)
    • 10% bound to phosphate or citrate
    • 50% is free in ECF (Active Free lonized)
  • Muscular contraction- excitability
  • Cellular electrophysiology and membrane potential
• Acts as a second messenger in hormonal and neurotransmitter pathways

Calcium hormones

• Regulated by three hormones:
  • Parathyroid hormone (PTH)= Increases Ca+
    • 1. Increase Gl absorption of ca+
    • 2. Increases plasma calcium levels via kidney reabsorption and phosphate excretion
    • 3. Increase ca+ bone resorption (breakdown)
  • Vitamin D
    • Is a fat-soluble steroid; Synthesised by the skin then sent to calcitriol in the kidneys
    • increases calcium absorption from the gastrointestinal (GI) tract
  • Calcitonin= decreases ca+ released by thyroid
    • 1. Decreases renal tubular reabsorption
    • 2. Decreases ca+ resorption from bones
    • Opposite of PTH

Hypocalcemia

• Abnormally low plasma concentration of calcium ion
• Causes
  • Hypoparathyroidism
  • Renal Failure, Hyperphosphatemia-
  • Vitamin D deficiency- decreased intestinal absorption of Ca
  • Less Ca blocking NA channels allows more Na into neurons
• Clinical manifestations
  • CNS and increased neuromuscular excitability
    • tetany, seizures, hyperreflexive DTRs, muscle spasms, wheezing strider
  • Hyperactive bowel sounds, facial spacms
  • Chvostek sign- in the cheek
  • Trousseau sign- in the arm
  • ECG abnormalities
  • Respiratory, laryngeal spasms

Hypocalcemia - Diagnosis and Treatment

• Diagnosis
  • Decreased total and ionized calcium levels
• Treatment
  • IV calcium salts (given for rapid corrections)
  • Vitamin D supplementation (kidneys need to work for Vit D to be processed) and Dietary management- more dairy

Hypercalcemia

• Abnormally high plasma concentration of calcium ions
• Causes
  • Malignancy
  • Hyperparathyroidism- too much release of PTH
  • Immobilization- lack of breakdown of Ca
  • Thiazide diuretics- holds onto Ca and kicks out other electrolytes- also causes hypokalemia and hypernatremia
  • Excessive ingestion of calcium and/or vitamin D
• Clinical manifestations
  • Decrease in CNS and neuromuscular excitability in cardiac and sm, by blocking sodium
    • Muscle weakness, weak reflexes, fatigue, lethargy
  • GI: constipation
• Others: "Stones, bones, groans, and psychiatric moans"

Hypercalcemia

• Diagnosis
  • Elevated serum calcium
  • Elevated parathyroid hormone level
  • Elevated vitamin D level
  • If all normal, consider pathology immobilization
• Treatment
  • Intramuscular calcitonin to decrease Ca serum levels, and promote excretion of Ca in urine.
  • IV fluids to dilute serum calcium and enhancing renal excretion
  • Oral phosphate- binds to Ca in the gut
  • Bisphosphonates: decreases bone resorption

Phosphorus

• Normal concentration: 2.5-4.5 mg/dL
• 85% found in the bones and 14% found ICF and 1% found in ECf
• Inorganic=phosphate Organic- nucleic acids/phospholipids
• Buffer in acid-base regulation
• Component in bone and ATP formation
• Involved in glucose, fat, and protein metabolism
• Maintains control of calcium and phosphate concentrations and vitamin D regulation

Phosphorus function

• Necessary for high-energy bonds located in creatine phosphate and adenosine triphosphate (ATP) and acts as an anion buffer and needed for muscle contraction energy
• Calcium and phosphate concentrations are rigidly controlled and work in opposite ways- As Ca levels go up Phosphate goes down - Ca++ x HPO4= = K (K is a constant) - If the concentration of one increases, the concentration of the other decreases
• Regulation of Phosphorous
  • PTH: stimulates release of phosphorous from the bone, increases renal excretion of phosphorous, enhances Gl absorption of phosphorous (reduces re-absorbtion from kidneys and urine)
  • Vit D : increases serum phosphorous

Hyperphosphatemia

• Abnormally high plasma concentration of phosphate ions
• Causes
  • Acute or Chronic renal failure common in CKD patients
  • Administration of excess phosphate containing antacids, laxatives, enemas
• Clinical manifestations
  • Correlate with those of hypocalcemia
• Diagnosis: elevated serum phosphate
• Treatment:
  • Restriction of dietary phosphorous
  • Phosphate binders- given with food and binds to phosphorus in gut so the body will not re-absorb

Hypophosphatemia

• Abnormally low plasma concentration of phosphate ions
• Causes include malnutrition and alcohol withdrawal, and decreased intestinal absorption.
• Increased renal excretion of phosphate is associated with hyperparathyroidism, where too much PTH drops phosphate levels
• Clinical manifestations Correlate with those of hypercalcemia
• Diagnosis- decreased serum phosphate
• Treat with oral phosphorous and high-phosphorus diet

Magnesium

• Magnesium major Intracellular cation
• Normal concentration: 1.3-2.1 mg/dL
• Cofactor in hundreds of enzymatic reactions
• Plays role in ATP generation, DNA replication, and mRNA production and translation, membrane stabilization, nerve conduction, ion transport
• Prevents potassium from exiting cardiac cells, smooth musclue relaxant and contributes to neuromuscular integrity

Hypermagnesemia

• Abnormally high plasma concentration of magnesium ions = > 2.1 mg/dL
• Causes
  • Renal failure
  • Excessive use of magnesium-containing medications like Antacids and laxatives
• Clinical manifestations
  • Decreased neuromuscular excitability
    • Lethargy, hyporeflexia, confusion, muscle weakness
  • Cardiac Hypotension Cardiac arrest in severe hypermagnesemia
• Diagnosis: increased serum magnesium
• Treatment: cease all magnesium-containing medications

Hypomagnesemia

• Abnormally low plasma concentration of magnesium ions < 1.3 mg/dL
• Causes
  • Decrease dietary intake/absorption in Gl tract
  • Other etiologies : diarrhea, malabsorption syndrome, prolonged NG suction, chronic alcoholism Clinical manifestations:
  • Increased neuromuscular excitability
    • • Chvostek and Trousseau; tetany, paresthesia
  • CV: Tachycardia, HTN
• Diagnosis: decreased serum magnesium
• Treatment
  • Dietary management
  • Magnesium supplements

Acid and Base Balance

• pH-What is it?
  • Negative logarithm of the H+ concentration. Each number represents a factor of 10.
  • If the solution moves from a pH of 7 to a pH of 6, then the H+ ions have increased tenfold.
  • If H+ is high in number, pH is low (acidic).
  • If H+ is low in number, pH is high (alkaline).

Acid - Base Balance values

• Acids are formed as end products of protein, carbohydrate, and fat metabolism
• the body's normal pH is (7.35-7.45) and H+ must be neutralized by the retention of bicarbonate or excreted.
• Bones, lungs, and kidneys are major organs involved in the regulation of acid-base balance and the normal PH
• pH below 6.8 = death and pH above 7.8 = death

Bicarbonate and Hydrogen Ions and Acid Base Balance

• Acid-base balance is mainly concerned with two ions
  • Hydrogen (H+) and Bicarbonate (HCO3-) with Alterations of hydrogen and bicarbonate concentrations in body fluids are common in disease processes.

Acid- base Balance values

• Volatile Acids in the Body include carbonic acid (H2CO3) and can be eliminated as carbon dioxide (CO2) gas via the lungs
• Nonvolatile Acids in the body include sulfuric, phosphoric, and other metabolic acids can be eliminated by the renal tubules with the regulation of HCO3-

Sources of H+ ions - Regulating Factors

Sources of H+ ions when Carbon source (CO2) diffuses into the bloodstream

• Regulated by the Lung: CO2 + H2O H2CO3
• Regulated by the Kidney HCOS+ H+

Compensation vs Correction

• Compensation includes Chemical buffers, renal or respiratory function to return pH within normal range while the Underlying disease process is still present
• Correction is when Condition responsible for imbalance is controlled or no longer present and therefore the pH shifts within normal range

Renal regulation of Acid - Base Balance

• Kidney is essential for maintenance of acid-base balance plus they Regulate bicarbonate and nonvolatile acids.

• Three mechanisms:

  • Conservation and Reabsorption of bicarbonate as well as Secretion of H⁺ into urine

• Synthesis of new bicarbonate

  • Others: Buffering of H+ with Ammonia and Phosphate

• Renal compensation is less effective in presence of kidney disease.

Buffering Systems

• A main Buffering system utilizes protein. Proteins have negative charges and, as a result, they can serve as buffers for H+; mainly intracellular buffer with hemoglobin.
• Secondary options include Respiratory and renal buffering
  • Respiratory: Acidemia causes increased ventilation; alkalosis slows respirations
  • Renal: Secretion of H+ in urine and reabsorption of HCO3; synthesis of new bicarb plus Buffering of H+ with ammonia and phosphate creating monobasic or dibasic phosphate and ammonium
• Cell Cellular ion exchange
• Exchanges of K+ for H+ in acidosis and alkalosis

Acid - Base Imbalances

• Normal arterial blood pH range is 7.35 to 7.45, and Obtained by arterial blood gas (ABG) sampling
• Acidosis is when the pH is less than 7.35 and there is a Systemic increase in H+ concentration
• Alkalosis is when the pH is greater than 7.45 and there is a Systemic decrease in H+ concentration or excess of base

Acid-Base Imbalance Categories

-There are four categories: - Respiratory acidosis-Elevation of pCO2 as a result of ventilation depression - Respiratory alkalosis-Depression of pCO2 as a result of hyperventilation - Metabolic acidosis-Depression of HCO3- or an increase in nonocarbonic acids - Metabolic alkalosis-Elevation of HCO3-, usually as a result of an excessive loss of metabolic acids

Effects of Acidosis and Effects of Alkalosis

• Effects of acidosis which can lead to Similar things in respiratory and metabolic acidosis
• Similar effects of alkalosis in respiratory and metabolic alkalosis

Stepwise Analysis of Acid - Base Imbalances

• Type is determined by patient's history, Clinical manifestations and Lab tests, including arterial or venous blood gas data
• Utilize the ROME mnemonic which dictates the direction of change of values for each imbalance
  • If it is respiratory think "Opposite". If it is metabolic think "Equal"

Stepwise Analysis of Acid - Base Imbalances - the effect of PH

• Respiratory acid-base imbalances include when the pH and PaCO2 move in opposite directions
• Metabolic imbalances include when pH and HCO3 move in same direction

Acidosis

• Normal range of pH is 7.35-7.45
• Below 7.35 is Acidosis and Above 7.45 is Alkalosis
• in Respiratory acidosis you typically see this presentation (pH and pCO2) as well as in Metabolic acidosis.

Laboratory Tests: Arterial Blood Gases (ABGs)

Most useful test for acid-base assessment that measures arterial blood values. Including.. -pH (normal: 7.35-7.45) -PaCO2 (normal: 35-45 mmHg) -PaO2 (normal: 80-100 mmHg; 60-70 mmHg in newborns)

• HCO3 (normal: 22-26 mEq/L) Measures all forms of CO₂ in blood

Laboratory Tests: Venous Blood Gases (VBGs)

• Same measures as ABGs but in venous blood with slightly different Normal ranges:

  • pH: 7.3-7.41
  • HCO3¯: 21-22 mEq/L

• In cardiovascular collapse venous blood gas values cannot substitute for arterial blood gases

Laboratory Tests: Base Excess Test

• Detects excess of base (positive number) or deficit of base (negative number) and Measure of all bases in blood
  • Positive number which is greater than 2.0 mEq/L means there may be Metabolic alkalosis or Renal compensation for respiratory acidosis
  • Negative number, less than -2.0 mEq/L, means there may be Metabolic acidosis or Renal compensation for respiratory alkalosis

###Laboratory Tests: Anion Gap The following will describe the the amount of measured anions:

• High net gain of acid, such as with renal failure, lactic acidosis, and DKA Represent unmeasured negative ions. such as ketos The other extreme is Normal, which describes the loss of bicarbonate, and may be due to diarrhea, and renal tubular acidosis

Laboratory Test: Anion Gap

The following table helps break down Elevated vs Normal Anion Gap:

• Elevated Anion Gap with Ketoacidosis, Lactic Acidosis or Decreased rental H+ as a result of renal failure
• Normal Anion Gap with Diarrhea plus Intestinal suctioning, Ileostomy drainage, or Early renal failure

Respiratory Acidosis

• Acidosis: Pathogenesis Occurs with alveolar hypoventilation with CO2 elevated from hypercapnia and therefore the pH is below 7.35 Impaired elimination of CO₂ by lungs

• Causes of Inadequate CO2 Release: Respiratory diseases or conditions, Respiratory muscle paralysis and Disorders of the chest wall as a result of kyphoscoliosis, pickwickian syndrome, flail chest, CNS as a result of Dysfunction and depression of the respiratory center secondary to brainstem trauma, oversedation and electrolyte as a result of imbalances Metabolic conditions

Test your knowledge of fluid and electrolyte imbalances, including causes, symptoms, and appropriate nursing interventions. Questions cover hyponatremia, hyperkalemia, the role of aldosterone, and the impact of natriuretic peptides. Review electrolyte distribution between intracellular and extracellular fluids.