NURS 533 Wk 2 Ch 8 Fluids_Electrolytes_Acid Base_Edited_Student_VO

Chapter 8: Disorders of Fluid, Electrolyte, and Acid-Base Balance

Introduction to Fluid, Electrolyte, and Acid-Base Balance

• Body Composition:

  • Brain: 75% water.

  • Blood: 83% water.

  • Muscles: 75% water.

  • Bones: 22% water.

• Functions of Water in the Body:

  • Regulates body temperature.

  • Carries nutrients and oxygen to cells.

  • Moistens oxygen for breathing.

  • Helps convert food into energy.

  • Removes waste.

  • Cushions joints and vital organs.

  • Helps the body absorb nutrients.

• Electrolytes:

  • Essential for transmission of nerve impulses and muscle contraction.

  • Maintaining electrolyte homeostasis is crucial.

• Acid-Base Balance:

  • The body maintains a narrow pH range.

  • Small pH changes can alter biological processes.

  • Too many H^+ ions make the body more acidic.

• pH Scale:

  • A measure of hydrogen ion concentration in a solution.

  • Low pH: Acidic (high H^+).

  • High pH: Alkalotic (low H^+).

• Normal pH by Body Fluid:

  • Urine: 5.0 to 6.0.

  • Gastric juices: 1.0 to 3.0.

  • Arterial blood: 7.38 to 7.42.

  • Venous blood: 7.32 to 7.37.

  • CSF: 7.32.

  • Pancreatic fluid: 7.8 to 8.0.

• Regulatory Systems:

  • Buffer system: First to respond to neutralize H^+.

  • Respiratory system: Controls CO2. Increased CO2 leads to increased H2CO3 (carbonic acid).

  • Renal system: Controls bicarbonate (HCO_3) to neutralize acid.

  • Most diseases can cause imbalances; imbalances can exacerbate the disease itself.

Body Fluids

• Composition: Fluids, ions, and nonelectrolytes.

• Fluid Occupancy: Makes up almost 60% of an adult's weight.

• Major Cations: Sodium (Na^+), potassium (K^+), calcium (Ca^{2+}), magnesium (Mg^{2+}), and hydrogen ions (H^+).

• Major Anions: Chloride (Cl^−), bicarbonate (HCO3^−), sulfate (SO4^{2-}), and proteinate ions.

Functions of Body Fluids

• Transport gases, nutrients, and wastes.

• Generate electrical activity for body functions.

• Transform food into energy.

• Maintain overall body function.

Distribution of Body Fluids

• Total Body Water (TBW):

• Intracellular Fluid (ICF): Fluid inside the cells.

• Extracellular Fluid (ECF): Fluid outside the cells.

  • Interstitial fluid: Fluid between cells.

  • Intravascular fluid: Fluid within blood vessels.

• Cerebrospinal fluid (CSF).

• Other fluids: Lymphatic, synovial, intestinal, biliary, hepatic, pancreatic, pleural, peritoneal, pericardial, intraocular fluids, sweat, and urine.

Intracellular vs. Extracellular Compartments

• Intracellular Compartment (ICF):

  • Almost no calcium.

  • Small amounts of sodium, chloride, bicarbonate, and phosphate.

  • Moderate amounts of magnesium.

  • Large amounts of potassium.

  • Larger compartment (approximately two-thirds of body water).

  • High concentration of K^+.

• Extracellular Compartment (ECF):

  • Remaining one-third of body water.

  • Contains fluids outside the cells (interstitial spaces and blood vessels).

  • High concentration of Na^+.

Age and Body Water Distribution

• Newborn: 75% of body weight is water.

• Childhood: 60% to 65% of body weight is water.

• Adults: 50% to 60% of body weight is water.

• Older Adults: Percentage declines with age.

• Men generally have a greater percentage of body water compared to women.

• Obesity decreases TBW because adipose tissue contains about 10% water.

Diffusion and Osmosis

• Concentration Gradient: Difference in concentration over a distance.

• Diffusion: Movement of particles along a concentration gradient from high to low concentration.

• Osmosis: Movement of water across a semipermeable membrane from an area with fewer particles and greater water concentration to an area with more particles and lesser water concentration.

Tonicity

• Definition: The effect of a solution's osmotic pressure on cell size due to water movement across the cell membrane.

• Classification of Solutions:

  • Isotonic: No change in cell size (neither shrink nor swell).

  • Hypotonic: Cells swell.

  • Hypertonic: Cells shrink.

Water Requirements

• Requirement: 100 mL of water for every 100 calories metabolized.

• Increased metabolism requires more water.

• Examples:

  • Fever: Increased body temperature increases metabolism, thus increasing the need for water.

  • Exercise: Increases metabolism, leading to increased water needs.

Mechanisms Protecting Extracellular Fluid Volume

• Alterations in Hemodynamic Variables:

  • Vasoconstriction and increased heart rate.

• Alterations in Sodium and Water Balance:

  • Isotonic contraction or expansion of ECF volume.

  • Hypotonic dilution or hypertonic concentration of extracellular sodium due to changes in extracellular water.

Alterations in Water Movement: Edema

• Edema: Accumulation of fluid in the interstitial spaces.

• Causes:

  • Increased capillary hydrostatic pressure (venous obstruction).

  • Decreased plasma oncotic pressure (losses or diminished albumin production).

  • Increased capillary permeability (inflammation and immune response).

  • Lymphatic obstruction (lymphedema).

• Edema Formation:

  • Increased capillary filtration pressure.

  • Decreased capillary colloidal osmotic pressure.

  • Increased capillary permeability.

  • Obstruction to lymph flow.

• Types of Edema:

  • Localized edema.

  • General edema.

  • Dependent edema.

Assessing Edema

• Daily weight.

• Visual assessment.

• Measurement of the affected part.

• Application of finger pressure to assess for pitting edema.

Clinical Manifestations and Treatment of Edema

• Clinical Manifestations:

  • Localized vs. generalized edema.

  • Dependent and pitting edema.

  • Third-space fluid accumulation.

  • Swelling and puffiness.

  • Tight-fitting clothes and shoes.

  • Weight gain.

• Treatment:

  • Elevate edematous limbs.

  • Use compression stockings or devices.

  • Avoid prolonged standing.

  • Restrict salt intake.

  • Take diuretic agents.

Physiologic Mechanisms Regulating Body Water

• Thirst:

  • Primary regulator of water intake.

• ADH (Antidiuretic Hormone):

  • Regulator of water output.

• Both mechanisms respond to changes in extracellular osmolality and volume.

Assessment of Body Fluid Loss

• History of conditions predisposing to sodium and water losses.

• Weight loss.

• Observations of altered physiologic function indicative of decreased fluid volume.

• Assessment of heart rate, blood pressure, venous volume/filling, and capillary refill rate.

Overview of Electrolytes

• Electrolytes exist in both ECF and ICF in different concentrations.

• Some electrolytes are more concentrated in the ICF compared to the ECF.

• Electrolytes move across compartments and must be balanced for optimal health.

Intracellular vs. Extracellular Electrolytes

• Intracellular:

  • Cation: Potassium (K^+).

  • Anions: Phosphate and organic ions.

• Extracellular:

  • Cation: Sodium (Na^+).

  • Anions: Chloride (Cl^−) and bicarbonate (HCO_3^−).

Regulators of Sodium

• Kidney: Main regulator of sodium.

  • Monitors arterial pressure; retains sodium when arterial pressure is decreased and eliminates it when arterial pressure is increased.

  • Rate is coordinated by the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS).

  • Atrial natriuretic peptide (ANP) may also regulate sodium excretion by the kidney.

• Control of Sodium: 135-145 mEq/L

Factors Regulating Sodium (Na+)

• Amount of Body Water:

  • Most important factor is the amount of water present.

  • Water is regulated by ADH (Antidiuretic Hormone).

  • ADH \, \propto \, water \, \propto \, sodium \, concentration

• Aldosterone:

  • Another regulator of sodium.

  • Renal reabsorption of sodium (works in the kidney to reabsorb sodium back into circulation).

  • Aldosterone stimulates reabsorption of sodium, sustaining blood volume and pressure, and stimulates excretion of potassium.

Water and Sodium Balance

• Baroreceptors regulate effective volume by modulating sympathetic nervous system outflow and ADH secretion.

• ANP (Atrial Natriuretic Peptide).

• RAAS (Renin-Angiotensin-Aldosterone System).

  • Angiotensin II.

  • Aldosterone.

• Water Gain: Oral intake and metabolism of nutrients.

• Sodium Loss: Kidneys, skin, lungs, and gastrointestinal tract.

Sodium and Chloride Balance

• Sodium:

  • Primary ECF cation.

  • Regulates osmotic forces.

  • Roles: Neuromuscular irritability, acid-base balance, cellular reactions, and transport of substances.

  • Regulated by aldosterone and natriuretic peptides.

• Chloride:

  • Primary ECF anion.

  • Provides electroneutrality.

  • Follows sodium.

Systems Regulating Sodium and Chloride Balance

• Renin-Angiotensin-Aldosterone System:

  • Aldosterone increases potassium excretion by the distal tubule of the kidney.

• Natriuretic Peptides:

  • Decrease tubular resorption and promote urinary excretion of sodium.

  • Atrial natriuretic peptide.

  • Brain natriuretic peptide.

  • Urodilatin (kidney).

Water Balance Regulation

• Regulated by thirst perception and antidiuretic hormone (ADH).

• Thirst Perception:

  • Osmolality receptors (osmoreceptors) signal the posterior pituitary to release ADH.

  • Increases water intake.

• Baroreceptors:

  • Stimulated by depleted plasma volume.

  • Causes release of ADH.

Role of ADH in Water Balance

• Released when there is an increase in plasma osmolality or a decrease in circulating blood volume.

• Also called arginine vasopressin.

• Increases water reabsorption.

Alterations in Sodium, Chloride, and Water Balance: Hypertonic Alterations

• Hypernatremia:

  • Serum sodium > 145 mEq/L.

  • Related to sodium gain or water loss.

  • Water movement from the ICF to the ECF.

  • Intracellular dehydration.

  • Manifestations: Intracellular dehydration, seizures, muscle twitching, hyperreflexia.

  • Treatment: Isotonic salt-free fluids.

Hypertonic Alterations: Water Deficit

• Water Deficit (Dehydration):

  • Both sodium and water loss.

  • Manifestations: Low blood pressure, weak pulse, postural hypotension, elevated hematocrit and serum sodium levels, headache, dry skin, and dry mucous membranes.

  • Treatment: Oral fluids or hypotonic saline solution (5% dextrose in water).

Alterations in Sodium, Chloride, and Water Balance: Hyponatremia

• Hyponatremia:

  • Decreased osmolality.

  • Hyponatremia or free water excess.

  • Hyponatremia decreases the ECF osmotic pressure, and water moves into the cell.

Water Excess and Hyponatremia

• Water Excess:

  • Compulsive water drinking, causing water intoxication, GI losses, diuretic use.

  • Cellular edema.

  • Manifestations:

    • Lab values: Sodium below 135 mEq/L.

    • Muscle cramps, weakness, headache, depression, lethargy, stupor/coma, anorexia, nausea/vomiting/diarrhea, abdominal cramps.

  • Treatment: Fluid restriction; may need hypertonic saline solutions.

Hypotonic Alterations: Hyponatremia

• Hyponatremia:

  • Serum sodium level < 135 mEq/L.

  • Sodium deficits cause plasma hypoosmolality and cellular swelling.

  • Hypovolemic, euvolemic, hypervolemic.

  • Manifestations: Lethargy, headache, confusion, apprehension, seizures, and coma.

  • Treatment: Depends on underlying disorder; restrict water intake.

Hypernatremia Characteristics

• Hypernatremia:

  • Serum sodium level > 145 mEq/L.

  • Characterized by hypertonicity of ECF and almost always causes cellular dehydration.

  • Deficit of water in relation to the body’s sodium stores.

  • Clinical manifestations: Thirst, polydipsia, oliguria or anuria, high urine specificity, dry skin and mucous membranes, decreased tissue turgor, headache, agitation/restless, tachycardia, weak thready pulse.

  • Cells shrink.

Potassium Distribution and Regulation

• Intracellular concentration: 140 to 150 mEq/L.

• Extracellular concentration: 3.5 to 5.0 mEq/L.

• Body stores of potassium are related to body size and muscle mass.

• Normally derived from dietary sources.

• Plasma potassium is regulated through two mechanisms:

  • Renal mechanisms that conserve or eliminate potassium.

  • A transcellular shift between the ICF and ECF compartments.

Potassium Overview

• ECF concentration: 3.5–5.0 mEq/L.

• Major intracellular cation.

• Aldosterone, insulin, and epinephrine facilitate K^+ into the cells.

• Insulin deficiency, aldosterone deficiency, acidosis, and strenuous exercise facilitate K^+ out of the cells.

• The sodium-potassium (Na^+/K^+) pump maintains concentration.

Potassium Functions

• Essential for the transmission and conduction of nerve impulses, normal cardiac rhythms, and skeletal and smooth muscle contraction.

• Regulates ICF osmolality and deposits glycogen in liver and skeletal muscle cells.

• Kidneys, aldosterone and insulin secretion, and changes in pH regulate K^+ balance.

• K^+ adaptation allows the body to accommodate slowly to increased levels of K^+ intake.

Diagnosis and Treatment of Potassium Disorders

• Diagnosis is based on complete history, physical examination to detect muscle weakness and signs of volume depletion, plasma potassium levels, and ECG findings.

• Treatment:

  • Calcium antagonizes the potassium-induced decrease in membrane excitability.

  • Sodium bicarbonate will cause K^+ to move into ICF.

  • Insulin will decrease ECF K^+ concentration.

  • Curtailing intake or absorption, increasing renal excretion, and increasing cellular uptake.

Abnormal Potassium Levels

• Hypokalemia: Decrease in plasma potassium levels below 3.5 mEq/L.

  • Inadequate intake.

  • Excessive gastrointestinal, renal, and skin losses.

  • Redistribution between the ICF and ECF compartments.

• Hyperkalemia: Increase in plasma levels of potassium in excess of 5.0 mEq/L.

  • Decreased renal elimination.

  • Excessively rapid administration.

  • Movement of potassium from the ICF to ECF compartment.

Hypokalemia Details

• Potassium level < 3.5 mEq/L.

• Causes:

  • Reduced potassium intake.

  • Increased potassium entry into cell.

  • Increased potassium loss.

• Treatment: Replace potassium orally and/or intravenously.

• Manifestations:

  • Membrane hyperpolarization causes decreased neuromuscular excitability.

  • Confusion.

  • Skeletal muscle weakness.

  • Muscle cramps.

  • Smooth muscle atony.

  • Cardiac dysrhythmias.

  • Postural hypotension.

  • U wave on electrocardiogram (ECG).

Hyperkalemia Details

• Potassium level > 5.0 mEq/L.

• Rare due to efficient renal excretion.

• Causes:

  • Increased intake.

  • Shift of K^+ from ICF to ECF.

  • Decreased renal excretion.

  • Hypoxia, acidosis, insulin deficiency, cell trauma, digitalis overdose.

Effects and Treatment of Hyperkalemia

• Mild Attacks:

  • Tingling of lips and fingers, restlessness, intestinal cramping, and diarrhea, T waves on the ECG.

• Severe Attacks:

  • Muscle weakness, loss of muscle tone, paralysis.

• Treatment:

  • Calcium gluconate, insulin and/or glucose, buffered solutions, dialysis.

  • Dysrhythmias – the most serious effects, wideness of QRS; prolonged PR interval.

  • The progressively worsening of hyperkalaemia leads to suppression of impulse generation by the SA node and reduced conduction by the AV node and His-Purkinje system, resulting in bradycardia with junctional & ventricular escape rhythms and conduction blocks and ultimately cardiac arrest.

Calcium, Phosphate, and Magnesium Regulation

• Vitamin D, calcitonin, and parathyroid hormone regulate calcium, phosphate, and magnesium levels.

• Vitamin D sustains normal plasma levels of calcium and phosphate via increased intestinal absorption.

• Calcitonin acts on the kidney and bone to remove calcium from the extracellular circulation.

Mechanisms Regulating Calcium, Phosphate, and Magnesium Balance

• Ingested in the diet.

• Absorbed from the intestine.

• Filtered in the glomerulus of the kidney.

• Reabsorbed in the renal tubules.

• Eliminated in the urine.

Hormonal Regulation of Calcium and Phosphate

• Regulated by three hormones:

  1. Parathyroid hormone (PTH): Increases plasma calcium levels via kidney reabsorption.

  2. Vitamin D: Increases calcium absorption from the gastrointestinal (GI) tract.

  3. Calcitonin: Decreases plasma calcium levels.

Calcium Overview

• Ionized form: 5.5–5.6 mg/dL.

• Most calcium is located in the bone as hydroxyapatite (99% in bone; 1% in plasma and body cells).

• Necessary for:

  • Structure of bones and teeth.

  • Blood clotting.

  • Hormone secretion.

  • Cell receptor function.

  • Muscle contractions.

Physiological Forms of Calcium

• ECF calcium exists in three forms:

  1. Protein-bound: 40% of ECF calcium is bound to albumin.

  2. Complexed: 10% is chelated with citrate, phosphate, and sulfate.

  3. Ionized: 50% of ECF calcium is present in the ionized form.

Calcium Gain and Loss

• Gains:

  • Dietary dairy foods.

  • PTH and vitamin D stimulate calcium reabsorption in the nephron.

• Losses:

  • When dietary intake (and calcium absorption) is less than intestinal secretion.

Hypocalcemia Details

• Calcium levels < 9.0 mg/dL.

• Causes:

  • Inadequate intake or absorption.

  • Decreases in PTH and vitamin D.

  • Blood transfusions.

• Treatment: Calcium gluconate, calcium replacement, decrease phosphate intake.

• Manifestations:

  • Increased neuromuscular excitability (partial depolarization).

  • Muscle spasms.

  • Chvostek and Trousseau signs.

  • Convulsions.

  • Tetany.

Hypocalcemia Actions

• Decreases depolarization threshold which results in increased neuromuscular excitability

Causes and Symptoms of Hypocalcemia

• Causes:

  • Impaired ability to mobilize calcium from bone stores.

  • Abnormal losses of calcium from the kidney.

  • Increased protein binding or chelation such that greater proportions of calcium are in the nonionized form.

  • Soft tissue sequestration.

• Symptoms:

  • Increased neuromuscular excitability.

  • Cardiovascular effect.

  • Nerve cells less sensitive to stimuli.

Hypercalcemia Details

• Calcium levels > 10.5 mg/dL.

• Causes:

  • Hyperparathyroidism.

  • Bone metastasis.

  • Excess vitamin D.

  • Immobilization.

  • Acidosis.

  • Sarcoidosis.

• Manifestations:

  • Decreased neuromuscular excitability, weakness, kidney stones, constipation, heart block.

• Treatment: Oral phosphate, IV normal saline, bisphosphonates, calcitonin, denosumab.

Causes and Symptoms of Hypercalcemia

• Increased intestinal absorption (excessive vitamin D and calcium, milk-alkali syndrome).

• Increased bone resorption (↑ parathyroid hormone, malignant neoplasms, prolonged immobilization).

• Decreased elimination (thiazide, lithium therapy).

• Symptoms: Changes in neural excitability, alterations in smooth and cardiac muscle function, exposure of the kidneys to high concentrations of calcium.

Role of Phosphate in the Body

• Plays a major role in bone formation.

• Essential to certain metabolic processes, the formation of ATP, and the enzymes needed for metabolism of glucose, fat, and protein.

• A necessary component of several vital parts of the cell.

• Incorporated into the nucleic acids of DNA and RNA and the phospholipids of the cell membrane.

• Serves as an acid–base buffer in the extracellular fluid and in the renal excretion of hydrogen ions.

• Necessary for delivery of oxygen by the red blood cells.

• Needed for normal function of other blood cells.

Phosphate levels

• Serum levels: 2.5–4.5 mg/dL (adults).

• Similar to calcium, most phosphate (85%) is also located in the bone.

• Necessary for high-energy bonds.

• Calcium and phosphate concentrations are rigidly controlled.

• Ca^{++} \times HPO_4^{=} = K (K is a constant).

• If the concentration of one increases, the concentration of the other decreases.

Causes of Hypophosphatemia and Hyperphosphatemia

• Hypophosphatemia:

  • Depletion of phosphate because of insufficient intestinal absorption.

  • Transcompartmental shifts.

  • Increased renal losses.

• Hyperphosphatemia:

  • From failure of the kidneys to excrete excess phosphate.

  • Rapid redistribution of intracellular phosphate to the ECF compartment.

  • Excessive intake of phosphate.

Hypophosphatemia Details

• Serum phosphate level < 2.0 mg/dL.

• Causes: Intestinal malabsorption and renal excretion, vitamin D deficiency, antacid use, alcohol abuse, malabsorption syndromes, refeeding syndromes.

• Manifestations: Diminished release of oxygen, osteomalacia (soft bones), muscle weakness, bleeding disorders (platelet impairment), leukocyte alterations, rickets.

• Treatment: Treat underlying condition such as respiratory alkalosis and hyperparathyroidism.

Hyperphosphatemia Details

• Serum level > 4.7 mg/dL.

• Causes: Exogenous or endogenous addition of phosphate to ECF, chemotherapy, long-term use of phosphate enemas or laxatives, renal failure.

• High phosphate levels related to low calcium levels.

• Manifestations: Same as hypocalcemia with possible calcification of soft tissue.

• Treatment: Treat underlying condition, aluminum hydroxide, and dialysis.

Magnesium Overview

• Intracellular cation.

• Stored mostly in the muscle and bones.

• Interacts with calcium.

• Plasma concentration of 1.5–3.0 mg/dL.

• Cofactor in intracellular reactions, protein synthesis, nucleic acid stability, and neuromuscular excitability.

Magnesium Balance

• Essential to all reactions that require ATP.

• Regulation at the kidney level.

• Magnesium absorption in the thick ascending loop of Henle is the positive voltage gradient created in the tubular lumen by the Na^+ - K^+ - 2Cl^− cotransporter system.

• Ingested in the diet, absorbed from the intestine, and excreted by the kidneys.

Hypomagnesemia and Hypermagnesemia

• Hypomagnesemia:

  • From malabsorption.

  • Associated with hypocalcemia and hypokalemia.

  • Neuromuscular irritability, tetany, convulsions, increased reflexes.

  • Treatment: Magnesium sulfate.

• Hypermagnesemia:

  • From renal failure.

  • Skeletal muscle depression, muscle weakness, hypotension, respiratory depression, bradycardia.

  • Treatment: Avoid magnesium; dialysis.

Causes of Hypermagnesemia

• Excessive Intake:

  • Intravenous administration of magnesium for treatment of preeclampsia.

  • Excessive use of oral magnesium-containing medications.

• Decreased Excretion:

  • Kidney disease.

  • Acute renal failure.

Manifestations of Hypomagnesemia

• Laboratory Values: Serum magnesium level less than 1.8 mg/dL.

• Neuromuscular Manifestations: Personality change, athetoid or choreiform movements, nystagmus, tetany, positive Babinski, Chvostek, Trousseau signs.

• Cardiovascular Manifestations: Tachycardia, hypertension, cardiac dysrhythmias.

Acid-Base Balance

• pH Scale: 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 10-fold.

  • If H+ is high in number, pH is low (acidic).

  • If H+ is low in number, pH is high (alkaline).
    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 10-fold.
    If H^+ is high in number, pH is low (acidic).
    If H^+ is low in number, pH is high (alkaline).

Maintenance of Acid-Base Balance

• Acids are formed as end products of protein, carbohydrate, and fat metabolism.

• To maintain the body’s normal pH (7.35–7.45), the 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.

• pH below 6.8 = death; pH above 7.8 = death.

Key Ions in Acid-Base Balance

• Acid-base balance is mainly concerned with two ions:

  1. Hydrogen (H^+).

  2. Bicarbonate (HCO_3^−).

• Alterations of hydrogen and bicarbonate concentrations in body fluids are common in disease processes.

Volatile vs. Nonvolatile Acids

• Volatile Acids:

  • Carbonic acid (H2CO3) can be eliminated as carbon dioxide (CO_2) gas via the lungs.

• Nonvolatile Acids:

  • Sulfuric, phosphoric, and other metabolic acids.

  • Eliminated by the renal tubules with the regulation of HCO_3^−.

Sources of H+ Ions

• CO_2 diffuses into the bloodstream where the following reaction occurs:

• Regulated by the Lung; Regulated by the Kidney

• CO2 + H2O \leftrarrows H2CO3 \leftrarrows HCO_3^− + H^+

• Carbonic acid

pH Control Mechanisms

• Tissue

  • CO_2

• Plasma
  E \rightleftharpoons CO2 dissolved CO2+H2Oh \rightleftharpoons H2 CO3 \rightleftharpoons H^* + HCO3
  CO2+Protein-NH2 \rightleftharpoons Protein-NHCOO^* + H^*

• Erythrocyte
  H2O + CO2 \rightleftharpoons H2 CO3 \rightleftharpoons H^* + HCO3 H^* + Hb + CO2 \rightleftharpoons HHbCO_2

Buffering Systems

• Buffer: Chemical that can bind excessive H^+ or OH^− without a significant change in pH.

• Located in the ICF and ECF.

• Consist of a buffering pair: weak acid and its conjugate base.

• Most important plasma buffering systems: carbonic acid-bicarbonate system and hemoglobin.

• Associate and dissociate very quickly (instantaneous).

Carbonic Acid-Bicarbonate Buffering

• Operates in the lung and the kidney.

• The greater the partial pressure of carbon dioxide (pCO_2), the more carbonic acid is formed.

• At a pH of 7.4, the ratio of bicarbonate to carbonic acid is 20:1.

• Bicarbonate and carbonic acid can increase or decrease, but the ratio must be maintained.

• Lungs can decrease carbonic acid; kidneys can reabsorb or regenerate bicarbonate

Carbonic Acid-Bicarbonate Buffering (Cont.)

• If bicarbonate decreases, then the pH decreases and can cause acidosis.

• pH can be returned to normal if carbonic acid also decreases.

• This type of pH adjustment is called compensation.

• The respiratory system compensates by increasing or decreasing ventilation.

• The renal system compensates by producing acidic or alkaline urine.

Other Buffering Systems

• Protein Buffering:

  • Proteins have negative charges; as a result, they can serve as buffers for H^+; mainly intracellular buffer with hemoglobin.

• Respiratory and Renal Buffering:

  • Respiratory: Acidemia causes increased ventilation; alkalosis slows respirations.

  • Renal: Secretion of H^+ in urine and reabsorption of HCO_3^−; dibasic phosphate and ammonia.

• Cellular Ion Exchange:

  • Exchanges of K^+ for H^+ in acidosis and alkalosis.

Overview of Acid-Base Imbalances

• Normal arterial blood pH: 7.35–7.45.

• Obtained by arterial blood gas (ABG) sampling.

• Acidosis:

  • pH is less than 7.35.

  • Systemic increase in H^+ concentration.

• Alkalosis:

  • pH is greater than 7.45.

  • Systemic decrease in H^+ concentration or excess of base.

Four Categories of Acid-Base Imbalances

1. Respiratory acidosis: Elevation of pCO_2 as a result of ventilation depression.

2. Respiratory alkalosis: Depression of pCO_2 as a result of hyperventilation.

3. Metabolic acidosis: Depression of HCO_3^− or an increase in noncarbonic acids.

4. Metabolic alkalosis: Elevation of HCO_3^−, usually as a result of an excessive loss of metabolic acids.

Causes of Metabolic Acidosis

• Lactic acidosis

• Renal failure

• Diabetic ketoacidosis

• Diarrhea

• Starvation

Metabolic Acidosis Explained

• Noncarbonic acids increase or bicarbonate (base) is lost from ECF or cannot be regenerated by the kidney.

• pH drops below 7.35; HCO_3^− drops: less than 24 mEq/L.

• Compensation: Hyperventilation and renal excretion of excess acid.

Manifestations and Treatment of Metabolic Acidosis

• Manifestations: Headache, lethargy, Kussmaul respirations.

• Treatment:

  • Buffering solution administration.

  • Treat the underlying cause(s).

  • Base administration.

  • Correct sodium and water deficits.

Anion Gap in Metabolic Acidosis

• Used cautiously to distinguish different types of metabolic acidosis.

• By rule, anions (−) should equal cations (+).

• Not all normal anions are routinely measured.

• Represents