Chapter 26: Acid/Base Balance Flashcards
Fluid Compartments:
o 2/3 intracellular o 1/3 extracellular o Males about 60 percent fld. o Females about 50 percent. o Elderly about 45 percent fld. o Infants about 75 percent fld. o Obese 40-50 percent fld. o Very lean have more body water: 60 – 70 percent fluid
Water is a Universal Solvent:
o Solutes:
o Electrolytes:
• Ions or molecules that have an electric charge.
• Carry an electric current.
• Na+, K+, H+, HCO3-.
o Non-electrolytes:
• Do not have a charge, e.g., glucose, urea.
o ALL solutes contribute to:
o Osmolarity: Concentration of molecules/ions per VOLUME of solution (mOsm/Liter).
o Osmolality: Concentration of molecules/ions per WEIGHT of solution (mOsm/Kg).
o We document concentrations of electrolytes in milliequivalents per liter (mEq/L) = # of electrical charges in one liter of body fluid.
ICF vs. ECF:
o Intracellular fluid = ICF = 2/3 of body fld.
o Potassium cation (K+).
o Phosphate anion (HPO4–, H2PO4-, PO4—).
o Magnesium cation (Mg++).
o Sulfate anion (SO4–).
o Proteins carrying negative charge.
o Extracellular fluid = ECF = 1/3 body fld.
o Sodium cation (Na+).
o Chloride anion (Cl-).
o Calcium cation (Ca++).
o Bicarbonate anion (HC03-).
Exchange Between Fluid Compartments:
o Water flows easily between compartments.
o Concentration of solutes in each compartment determines DIRECTION of water flow (water follows the particles).
o Lytes play primary role in distribution of water and total fluid content of body!!!
Regulation of Water Gain:
o Fluid INTAKE is regulated primarily by hypothalamic THIRST CENTER.
o Thirst center is stimulated if:
o Dry mouth.
o Increased Angiotensin II.
o Increased blood osmolarity picked up by central osmoreceptors in hypothalamus.
o Normally, thirst leads to increase fluid intake.
Regulation of Water Loss:
o Determined primarily by the KIDNEY o Changes in urine volume usually linked to sodium reabsorption… save Na+, pee less. o Under regulation of many hormones: o ADH (independent of Na+ reabsorption). o Aldosterone. o Angiotensin II. o ANP (and other natriuretic peptides). o Kidneys can’t COMPLETELY prevent water loss, minimum of 500 mL excreted/day to flush out urine solutes.
Disorders of Water Balance:
o 2 types of Fluid Deficiency: Fluid loss greater than fluid gain.
o 1. Volume depletion (hypovolemia).
o 2. Dehydration.
o 2 types of Fluid Overload: Fluid gain greater than fluid loss.
o 1. Volume excess.
o 2. Hypotonic hydration.
o Fluid Sequestration.
Fluid Deficiency:
Volume Depletion
o Volume Depletion = Hypovolemia.
o Proportionate amounts of water AND lytes are lost without replacement.
o Total fluid in body goes down, but fluid osmolality remains fairly normal.
o Hypovolemia occurs with:
o Hemorrhage.
o Surgical losses.
o Severe GI loss: Chronic vomiting/diarrhea/ laxative abuse/GI suction.
o Severe burns.
o Hyposecretion of ALDOSTERONE.
o Some diuretics.
Fluid Deficiency:
Dehydration
o Body loses more water than lytes.
o Total fluid in body goes down, but fluid osmolality goes up.
o Causes of dehydration:
o Decreased ingestion of fluid (and food).
o Increased losses of water greater than lytes.
o Excessive sweating.
o Heavy respirations (dry cold air).
o Excessive urination (polyuria).
Dehydration Via Excessive Urination:
o Osmotic diuresis: o Diabetes mellitus. o Ketonuria. o Some diuretics (e.g., mannitol). o Not enough ADH: o Alcohol intake. o Diabetes Insipidus. o Body cells shrink with dehydration.
Key Symptoms of Fluid Deficiency:
o Thirst. o Dry mucous membranes. o Elevated temperature. o Weight loss. o Tachycardia. o Low blood pressure (hypotension). o Weak pulses. o Circulatory shock. o Neurological sx if dehydration of neurons.
Fluid Overload:
o Less common—healthy kidneys are very efficient at getting rid of excess fluid (BUT not as good as compensating for inadequate intake).
o 1. Volume Excess.
o Both water and lytes are retained, so the ECF remains isotonic (osmolality does not change or not much) leads to HYPERVOLEMIA.
o Causes of volume excess:
• Too much aldosterone
• Too much cortisol
• Renal failure (acute and chronic)
• Excessive IV fluids
• Medication side effects
• Heart Failure (HF)
o 2. Hypotonic Hydration:
o More water than sodium is retained, or you lose water + lytes, but replace only with plain water.
o ECF becomes hypotonic (low osmolality).
o Causes of hypotonic hydration:
• Drinking H20 to replace isotonic losses.
• SIADH (syndrome of inappropriate ADH).
• Severe CHF or renal insufficiency.
• Psychogenic polydipsia.
o Causes cells to Swell.
Symptoms of Fluid Overload:
o Weight gain.
o Decrease in hematocrit and plasma protein concentration (diluting effect).
o Distended neck veins.
o Increased blood pressure.
o Edema: Pulmonary edema, Cerebral edema.
o Congestive heart failure.
Fluid Sequestration:
o Condition where excess fluid accumulates in a particular location. o Total body water may be normal, but it may not be distributed normally. o Causes of sequestration: o Edema. o Internal hemorrhage. o Pleural effusion. o Ascites. o Vascular (Distributive) Shock.
Patients at Risk for Lyte Imbalance:
o People who depend on others for fluid or food: o Infants, elderly, comatose. o Post-operative patients. o People with large amounts of emesis/diarrhea. o Patients with severe burns and trauma. o Certain medical treatments. o IV infusions, drainages, suctions. o Meds such as diuretics, cortisol.
Causes of Hyper- (lyte) Conditions:
o Dehydration.
o Kidney failure (can’t get rid of excess ions).
o Sudden release of ions from tissues (e.g., crushing injuries, sudden infarctions).
o Hormonal imbalances.
o Acid-base imbalances.
o Excessive intake (very rare!!).
Causes of Hypo- (lyte) Conditions:
o Increased losses. o GI, renal, meds. o Inadequate absorption/reabsorption. o Increased utilization (pregnancy, wound healing, etc.). o Hormonal imbalances. o Acid-Base Imbalances. o Hypotonic hydration d/o. o Inadequate intake (possible/not common).
Sodium:
o Most abundant ion in ECF (cation)
o Functions (many!):
o Membrane potentials, APs, nerve transmission, muscle contraction.
o Cotransport of ions across membranes.
o Sodium/potassium ATP-ase pump.
o Almost half of the osmolarity of ECF.
o Normal: About 140 mEq/liter (always a range).
o Hyponatremia: Less than 135 mEq/liter.
o Hypernatremia: Greater than 145 mEq/liter.
Regulation of Sodium (Na+) Balance:
o Aldosterone.
o Angiotensin II.
o ANP (and other natriuretic peptides).
o Estrogen (mimics aldosterone) and progesterone (reduces Na+ reabsorption).
o Ep/NE (increase sodium reabsorption).
o Adult only needs 500 mg Na+/day, typical American intake = 3 – 7 grams/day (3000 -7000 mg/day), healthy kidneys excrete the excess.
Sodium Intake:
o US Guidelines: 2300 mg/day.
o American Heart Association Guidelines: 1500 mg/day.
Hyponatremia:
o Serum Na+ less than 135 mEq/liter.
o Usually secondary to excess body H20, which in a healthy person is quickly corrected by kidney excretion of excess water.
o Sx: cellular edema (excess body water moves into cells), confusion, convulsions, coma, death.
o Increased losses
o GI: vomiting, diarrhea, GI suctions
o Burns, Renal, Meds.
o Inadequate absorption/reabsorption.
o Hypotonic hydration.
o Hormonal imbalances.
o Insufficient aldosterone; excess ADH.
o Inadequate intake (possible/not common).
Hypernatremia:
o Serum Na+ greater than 145 mEq/liter. o RARELY caused by high dietary Na+. o More commonly caused by: o Inadequate fluid intake. o Excessive fluid loss (dehydration). o Osmotic diuresis. o Inappropriate amt. hypertonic saline IV. o Not enough ADH (diabetes insipidus).
Chloride (Cl-):
o Most abundant anion in ECF.
o Functions:
o Major contributor of osmolarity of ECF.
o Required to make stomach acid (HCl).
o CO2 gas transport in blood (Cl- shift).
o Regulation of acid-base balance.
o Normal: about 100 mEq/liter.
o Hypochloremia: less than 95 mEq/liter.
o Hyperchloremia: greater than 105 mEq/liter.
Potassium (K+):
o Most abundant cation in the ICF.
o Disorders of K+ can be life threatening.
o Functions:
o Membrane potentials, APs, nerve transmission, muscle contraction, Na+/K+ ATP-ase pump.
o Helps maintain normal ICF volume.
o Essential cofactor for protein and glycogen synthesis.
o Necessary for normal insulin secretion.
o Helps regulate pH (often exchanged for H+).
o Normal: about 3.5 – 5 mEq/liter.
o Hypokalemia: less than 3.5 mEq/liter.
o Hyperkalemia: greater than 5.0 mEq/liter.
Regulation of Potassium:
o Diet intake varies from 40–150 mEq/day.
o Kidneys excrete excessive amounts, fine-tuning in DCT and collecting duct.
o Aldosterone causes Na+ reabsorption but increased K+ loss (hyperkalemia stimulates adrenal cortex directly to increase aldosterone release!).
Potassium and pH Changes:
o Acidosis causes H+ to move into cells, so K+ moves out of cells; alkalosis causes the opposite shift (K+ moves into cells).
o Insulin promotes the movement of both glucose and K+ into cells (when treating DKA, really need to watch for hypokalemia).
Hypokalemia:
oPotassium is less than 3.5 mEq/liter.
o Causes:
o Inadequate intake:
o Rarely a dietary deficiency!!!!!!!!!!!
o Anorexia nervosa, bulimia, alcoholism.
o Increased losses
o Chronic emesis/diarrhea/laxatives/suction.
o Loop diuretics (e.g., Laxis).
o True licorice (glycyrrhiza).
o Hypersecretion of aldosterone (Conn’s dz).
o Hypersecretion of cortisol (Cushing’s dz).
o Transcellular shifts (K+ pushed into cells):
o Alkalosis (H+ comes out of cells/K+ goes into ICF).
o Correction of DKA with insulin.
o Catecholamines and beta adrenergic agonists.
o Correction of pernicious anemia by IV Vitamin B-12.
o Sx: K+ moves out of cell to correct ECF deficit leads to hyperpolarization leads to decreased neuromuscular excitability leads to muscle weakness, severe heart arrhythmias, depressed reflexes
Hyperkalemia:
o Serum potassium greater than 5.0 mEq/liter.
o Causes:Causes:
o Renal failure.
o Not enough aldosterone.
o Acidosis (H+ goes into cells; K+ comes out).
o Meds making you save K+ (e.g.,spironolactone, digitalis overdose which inhibits Na+/K+ pump).
o IV bolus of K+.
o Excessive intake (rare except for salt substitutes = KCl).
o Crushing traumas, hemolytic anemias, transfusion of old blood, major burns, being stung by box jellyfish!
o Sx: depends on timing!
Symptoms of Hyperkalemia:
o Remember that there are many K+ leak channels in cells…K+ continually passes out of cells by diffusion, then dragged back in by Na+/K+ ATP-ase .
o Fast increase in K+ (e.g., crush injury):
o Gradient for diffusion is lost leads to more K+ stays inside cell leads to cell closer to threshold leads to muscles/nerves hyperexcitable leads to cardiac arrest.
o Slow increase in K+ (e.g., decreased aldosterone, grad. RF):
o Not intuitive, slow depolarization of a cell inactivates.
o V-gated Na+ channels leads to no Aps leads to nerve and muscles becomes less excitable leads to muscle weakness.
o Severe hyperkalemia: muscle paralysis and cardiac arrest (heart block).
Calcium:
o Higher amts in ECF, but important in ICF in small, regulated (sequestered) amounts.
o Functions:
o Muscular contraction/muscle tone.
o Neurotransmitter release (exocytosis).
o Required for the secretion of many hormones.
o Important for plasma membrane stability.
o “Second messenger” for many hormones/NT.
o Essential in blood clotting.
o Structural component of bones and teeth.
o Normal: 4.5-5.2 mEq/L (9 - 11 mg/dL).
o Hypocalcemia: less than 4.5 mEq/liter.
o Hypercalcemia: greater than 5.2 mEq/liter.
o Note: About 50% of calcium in blood is bound to plasma proteins.
Regulation of Calcium:
o Primarily regulated by hormones:
o PTH:
• Targets bone/activates osteoclasts/ ↑ bone resorption
• Targets kidneys to reduce calcium excretion
• Targets kidneys to activate Vit D calcitriol
o Calcitriol (very potent hormone!!!):
• Targets small intestine: increases calcium absorption
• Targets kidneys to reduce calcium excretion
• Targets bone to increase bone resorption
o Calcitonin:
• Probably not significant in adults.
Hypocalcemia:
o Serum calcium less than 4.5 mEq/L (less than 9 mg/dl).
o Causes:
o Hypoparathyroidism (insufficient PTH).
o Vitamin D deficiency (insufficient uv light).
o Renal disease ( less than calcitriol formation).
o Blood transfusions (citrate binds Ca++).
o Hypomagnesemia.
o Alkalosis increases the binding of calcium to plasma proteins leads to decreases free ion availability leads to get sx of hypocalcemia even though total blood calcium may be normal.
Symptoms of Hypocalcemia:
o TETANY of hypocalcemia (makes membrane unstable by increasing sodium permeability) leads to skeletal and smooth muscles and nerves hyperexcitable.
o Tingling in fingers/toes/mouth (paresthesias).
o Skeletal muscle cramps and intestinal cramps.
o Carpo-pedal spasms (Trousseau’s sign).
o Exaggerated reflexes.
o Convulsions.
o Tetany (laryngeal spasms = death).
o Decreases myocardial contractility (prolonged QT interval; remember plateau requires calcium influx from ECF).
o Cardiac arrhythmias (pacemaker cells require calcium influx).
Hypercalcemia:
o Serum calcium greater than 5.2 mEq/liter.
o Causes:
o Hyperparathyroidism.
o Excess calcitriol (hypervitaminosis D).
o Multiple Myeloma ( increases osteoclastic bone resorption/destruction).
o Bone metastases with increases bone resorption.
o Acidosis decreases the binding of calcium to plasma proteins leads to increases free ion availability leads to get sx of hypercalcemia even though total blood calcium may be normal.
Symptoms of Hypercalcemia:
o Reduces sodium permeability of plasma membranes leads to decreases neuromuscular excitability.
o Muscle weakness and decreased tone.
o Depressed reflexes.
o Constipation.
o Lethargy and fatigue.
o Depression/mental confusion/coma.
o Cardiac arrhythmias and heart block.
o Kidney stones ( increases calcification of soft tissues).
o Increased PUD (hypercalcemia increases gastrin secretion).
Phosphate Anions:
o Important anions in ICF
o Exists in 3 forms: HPO4–, H2PO4-, PO4—.
o Normal: 1.6—2.9 mEq/L (sometimes up to 4.0 mEq/L).
o Elevated in renal failure.
o Functions:
o ATP production/use (also GTP, cAMP, creatine phosphate, etc.).
o Synthesis (e.g., protein synthesis).
o Synthesis of nucleotides (DNA and RNA).
o Biochemical rxns using phosphorylation or dephosphorylation for activation/deactivation.
o Structural part of membranes (phospholipids), bones and teeth.
o Important in acid-base balance (buffering)—esp. urine.
Magnesium (Mg++):
o Normal: 1.5 – 2.5 mEq/Liter.
o Important intracellular cation—involved in over 300 biochemical reactions, including fxn of Na+/K+ ATP-ase pump, protein synthesis & use of ATP by contracting muscles.
o Regulated by kidneys, PTH, calcitriol.
o Hypomagnesemia sx = hypocalcemia sx.
o From diuretics, alcoholism, malnutrition.
o Hypermagnesemia sx = hypercalcemia sx.
o From renal failure.
Bicarbonate Ion (HCO3-):
o Important ECF anion.
o Normal: 22 – 26 mEq/liter.
o Functions:
o Regulation of pH of ECF
• Metabolic acidosis: HCO3- less than 22 mEq/L.
• Metabolic alkalosis: HCO3- greater than 26 mEq/L.
o Transport of CO2 in the blood.
o Regulated primarily by kidneys and acid/base balance mechanisms.
Normal pH:
o Normal blood pH
o 7.35 to 7.45.
o ARTERIAL blood is About 7.4.
o VENOUS blood is About 7.35.
o 8’s are FATAL (less than 6.8 or greater than 8.0).
o Why do we care??
o [ H+ ] affects activity of proteins.
o [ H+ ] affects other electrolytes.
o [ H+ ] affects activity of medications.
o [ H+ ] affects activity of neurons and muscle.
Neuromuscular Disorders Due to Abnormal pH:
o Acidosis (pH less than 7.35) o CNS depression o Sluggish reflexes o Confusion o Coma o Death o Alkalosis (pH greater than 7.45) o Hyperexcitability of neuromuscular systems. o Muscle spasms. o Muscle tetany. o Convulsions. o Paralysis of respiratory muscles leading to death.
pH:
o Measure of H +.
o The greater the concentration of H +, the LOWER the pH.
o Fewer H + in solution means a HIGHER pH.
o Only free H + ions matter.
Acids:
o Acid = any chemical that releases H + into a solution.
o H + is hydrogen without its electron (really it is just a proton).
o When you place an acid in water, the H + “dissociates” (dissolves).
o It is only the FREE (unbound) H + ion that affects pH.
o Strong Acids:
o Strong acids dissociate (ionize) almost completely in a watery solution.
o HCl Becomes H + + Cl ‾ .
o Almost 100% of the HCl ionizes.
o Weak Acids:
o Weak acids dissociate only SLIGHTLY in a watery solution.
o Carbonic acid is a WEAK acid and only gives up SOME of its H+ in solution.
o H2CO3 becomes HCO3 + H or vice versa.
Bases:
o Base = chemical that ACCEPTS H+ .
o Proton “acceptor”.
o When a base “accepts” H+, it takes H+ out of solution… thus the pH will go up (lower concentration of free H+ ).
o Many bases dissociate into hydroxide ions OHˉ.
o OHˉ then binds to H+ to form water.
o OHˉ plus H+ leads to H₂ O (takes H+ out of solution).
Strong vs. Weak Bases:
o Strong bases dissociate (ionize) easily in water, quickly tying up any free H+ ions: NaOH becomes Na⁺ + OHˉ .
o Weak bases bind only a small portion of available H+ in solution (less of an effect on pH): HCO₃‾ + H+ becomes H₂CO₃ or NH₃ + H+ becomes NH₄+ .
Buffers:
o Buffers = chemicals (or organ systems) that prevent rapid changes in pH.
o Chemical buffers: molecules/ions that bind H+ when pH is going down or release H+ when pH is going up.
o Physiological buffer: organ system that stabilizes pH by controlling how the body gets rid of acids, bases, or CO2.
Chemical Buffers:
o Chemical Buffers act immediately!
o The quantity of acid or base that can be “buffered” depends on 2 factors:
o The concentration of the buffers (quantity…you can run out of buffers).
o The pH of the environment (each chemical buffering system has its own optimal pH for functioning).
o Chemical buffering systems = first line of defense (act immediately).
o 1. Protein Buffer System:
• carboxyl (COOH) group.
• amino (NH₂) group.
o 2. Phosphate Buffer System:
• H₂PO4 ˉ ⇄ HPO₄ ² - + H+.
o 3. Bicarbonate Buffer System
• H₂CO₃ ⇄ HCO₃‾ + H+.
Protein Buffering System:
o Proteins are in high concentration in both the ICF and ECF.
o Proteins provide about ¾ of the chemical buffering capacity of body!
o Proteins can buffer both acids and bases because of the unique chemical make up of their amino acid chains:
o COOH group can donate H+.
o NH2 group can accept H+.
Phosphate Buffering System:
o Phosphate ion can exist in 3 different forms: H₂PO4 ˉ HPO4 2- PO4 3-
o When there is too much H+ (pH is low), then HPO4 2- can act as a weak base and accept H+, taking H+ out of solution to normalize pH:
o HPO₄ ² - + H+ becomes H₂PO4 ˉ .
o When there is too little H+ (pH is high), then H₂PO4 ˉ can donate one of its H+ to increase the H+ in solution (thus decreases pH).
o H₂PO4 ˉ becomes HPO₄ ² - + H+.
Bicarbonate Buffering System:
o If there is excess H+ (pH is low), bicarbonate ion acts as a weak base and takes the H+ out of solution.
o HCO₃‾ + H+ becomes H₂CO₃ .
o If there is a shortage of H+ (pH is high), then carbonic acid acts as a weak acid and donates H+ to the solution.
o H₂CO₃ becomes HCO₃‾ + H+.
2 Physiologic Buffering Systems:
o Respiratory System (CO2)
o Urinary System (HCO3-)
If pH Homeostasis is Disturbed:
o 1st line of defense: o Chemical buffering systems. o Act immediately. o 2nd line of defense: o Respiratory system. o Acts within seconds to a few minutes. o 3rd line of defense: o Urinary system. o Takes hours to days.
Respiratory Control of pH:
o Regulates pH by controlling how fast or slow CO₂ is exhaled through lungs
o CO₂ + H₂O leads to H₂CO₃ leads to HCO₃‾ + H+ and vice versa.
o Normal pCO₂: 35 – 45 mm Hg
o Decreased ventilation: Decreases the CO2 leaving body and increases the pCO2 in the blood.
o Increased ventilation: Increases the CO₂ leaving body and decreases the pCO2 in the blood.
o Acts rapidly (within minutes).
Respiratory “Reminders”:
o Eupnea: o 12 – 15 breaths/minute. o Resting tidal volume ~ 500 ml/breath. o Normal pCO₂: 35 – 45 mm Hg (Arterial blood). o Hypercapnia vs. Hypocapnia. o Regulation of Rate/Depth of breathing. o Central chemoreceptors. o Peripheral chemoreceptors. o Carotid bodies. o Aortic bodies.
Effectiveness of Respiratory Control of pH:
o Halving ventilation can lower pH from 7.4 to 7.2.
o Quartering ventilation can lower pH from 7.4 to 7.0.
o Doubling ventilation can raise pH from 7.4 to 7.63.
o Very powerful system!!!
Respiratory Acidosis:
o Rate of alveolar ventilation can’t get rid of the amount of CO2 produced.
o pCO2: Increases to greater than 45 mm Hg (hypercapnia).
o pH: Decreases to less than 7.35 (acidemia or acidosis).
o Causes:
o COPD:
• Severe emphysema or chronic bronchitis.
o Pulmonary edema:
• Pneumonia or left-sided heart failure.
o Airway obstruction:
• Asthma or cystic fibrosis.
o Depression or injury to brainstem respiratory centers:
• Narcotic or barbiturate overdose.
• Stroke, tumors, trauma to brainstem.
Respiratory Alkalosis:
o Rate of alveolar ventilation is greater than the rate of CO2 production. o pCO2: Decreases to less than 35 mm Hg (hypocapnia). o pH: Increases to greater than 7.45 (alkalemia or alkalosis). o Causes: o Anything causing hyperventilation • Pain • Anxiety • Panic attacks • Brainstem injury • Improper ventilator setting (Most common). • Significant hypoxemia (very low pO2 ). • Very high altitudes. o Symptoms: o Neuromuscular hyperexcitability • Skeletal muscle spasms • Carpopedal spasm • Laryngospasm o Decreased cerebral blood flow • pCO₂ dropping from 40 to 25 mm Hg can decrease cerebral blood flow by 60 percent. • Light headedness leads to LOC.
By-Products of Metabolism:
o “fixed” acids o Sulfuric acid o Phosphoric acid o “organic” acids o Uric acid o Lactic acid o Ketones o Up to 60-100 mEq of H+ each day.
Renal Control of pH:
o Regulates pH by controlling renal tubular:
o Reabsorption of HCO₃‾.
o Generation of new HCO₃‾.
o Secretion of H+.
o Can neutralize MORE acid/base than either respiratory system or the chemical buffering systems combined.
o Acts slowly (hours to days).
Reabsorption of Filtered Bicarbonate Ion HCO3:
o Na+ antiporters reabsorb Na+ and secrete H+.
o PCT cells produce the H+ and release bicarbonate ion to the peritubular capillaries.
o For every H+ secreted into the tubular fluid, one filtered bicarbonate eventually returns to the blood.
Intercalated Cells of Collecting Ducts:
o Proton pumps (H+ ATPases) secrete H+ into tubular fluid.
o Can secrete against a concentration gradient so urine can be 1000 times more acidic than blood.
o Urine is buffered by HPO4 2- and ammonia, both of which combine irreversibly with H+ and are excreted.
Generation of New HCO3-:
o Tubular cells make new HCO₃‾ by breaking down the a.a. GLUTAMINE.
o This creates 2 molecules of NH₄+ and 2 molecules of HCO₃-.
o NH₄+ is secreted into filtrate.
o HCO₃‾ is reabsorbed into peritubular capillaries.
o Takes time to “rev up”.
Metabolic Acidosis:
o Too much H+ produced/ingested. o Too much H+ is retained or lost/not made. o HCO3-: Decreases to less than 25 mEq/L o pH: Decreases to less than 7.35. o Causes: o Too much acid ingested/produced: • Overdose of aspirin. • Salicylic ACID. • Excessive ETOH intake. • Increased Ketone production. • DKA (diabetic ketoacidosis). • Starvation. • Increased Lactic acid production. • Shock. • Acute MI with heart failure. o Too much HCO₃‾ is lost: • Severe and chronic diarrhea. • Colostomy or ileostomy. o Not enough HCO₃‾ is made: • Renal disease. o Not enough H+ is secreted: • Renal disease.
Other Things That Could Cause Metabolic Acidosis Besides Severe MI:
o Chronic diarrhea/colostomies. o Renal disease, especially renal failure. o Overdose of aspirin. o Excessive ETOH intake. o Increased Ketone production. o Starvation and DKA (diabetic ketoacidosis). o Increased Lactic acid production. o Acute MI/Shock.
Metabolic Alkalosis:
o Too much HCO3 Ingested or too much acid(H+) is lost. o Serum HCO3-: Increases to greater than 26 mEq/L. o pH: Increases to greater than 7.45. o Causes: o Too much HCO₃‾ is ingested: • Sodium bicarbonate products. • Antacids. o Too much acid (H+ ) is lost: • Chronic emesis (vomiting). • Gastric suctioning. • Conn’s disease (hyperaldosteronism). o Symptoms: o Neuromuscular hyperexcitability • Skeletal muscle spasms. • Carpopedal spasm. • Laryngospasm. o Respiratory System: • Decreased respirations. • Increased pCO₂. • Trying to COMPENSATE.
Compensation:
o When the respiratory system is causing the acid-base disorder, the kidneys will come to the rescue.
o When there is a metabolic problem, the respiratory system will try to help.
o Compensation can be complete (pH is within normal range) or partial (pH is still not normal).
Diagnosing pH Disorders:
o 1) Diagnose acidosis vs. alkalosis (based on blood pH)
o 2) Check the pCO₂: is respiratory the cause of the acidosis or alkalosis?
o 3) If respiratory is NOT the cause, check the HCO₃‾ level to confirm a metabolic acidosis or alkalosis.
o 4) Is the other physiologic buffering system trying to compensate?
