Acid-Base Imbalances

acids

molecules that release hydrogen ions in solution

bases

molecules that accept hydrogen ions in solution

normal arterial blood range

7.35-7.45

henderson-hasselbalch equation

explains how pH is determined by the ratio of bicarbonate to carbonic acid

alkalosis

if bicarbonate goes up, pH rises

acidosis

if CO2 rises, pH falls

three major mechanisms to regulate blood pH

• chemical buffers

• respiratory system

• renal system

arterial blood gas (ABG)

indicates acid-base status in the arterial blood (extracellular fluid)

what do you do before taking ABG?

allen’s test

chemical buffers

first line of defense against pH changes; acts immediately to resist pH change

biocarbonate buffers

primarily extracellular fluid, most clinically important

phosphate buffers

intracellular fluid and renal regulation

hemoglobin buffers

inside erythrocytes

protein buffers

intracellular and blood

bicarbonate buffer system with acidosis

H+ binds to HCO3- → forms H2CO3 → converted to CO2+H2O → CO2 exhaled by lungs

bicarbonate buffer system with alkalosis

H2CO3 dissociates → releases H+ → lowers pH

respiratory contribution with acid base imbalance

CO2 combines with water to form carbonic acid; lungs eliminate CO2 and water from body; reduces carbonic acid

chemoreceptors

in carotids and aortic arch sense increase in PaCO2 or pH changes and adjust breathing rate and depth

chemoreceptor action with respiratory alkalosis

increased ventilation → CO2 exhaled → pH rises

chemoreceptor action with respiratory alkalosis

decreased ventilation → CO2 retained → pH falls

compensation

respiratory system adjusts breathing to help restore pH balance during metabolic acid base

metabolic alkolosis compensation

increased ventilation, decreased CO2 and increased pH

metabolic alkalosis compensation

decreased ventilation, increased CO2 and decreased pH

renal contribution

provide the most powerful long-term regulation of acid base balance; excrete all metabolic acids except carbonic acid

powerful functions of renal contribution

excretes acids generated by normal metabolism; adjusts increased H+ excretion when blood is acidic and reabsorbs HCO3- or decreases H+ excretion when blood is alkaline and excrete HCO3-

renal contribution; increased H+ excretion (acidosis)

• increased production of ammonia in renal tubular cells

• H+ + NH3 → NH4 which is trapped in urine and excreted

• helps remove excess acid and restore pH

renal contribution; decreased H+ excretion (alkalosis)

• decreased production of ammonia

• less H+ secreted; some H+ absorbed into blood

• kidneys excrete bicarbonate to help lower pH

renal contribution; HCO3- in plasma

• reflects the metabolic/kidney side of acid-base regulation

• acts as the major extracellular base/buffer

• normal plasma HCO3- is approximately 22-26 mEq/L

• changes in HCO3- help identify metabolic acidosis or metabolic alkalosis

renal contribution; decreased HCO3-

• indicates excess metabolic acids in blood

• HCO3- is consumed buffering these acids

• plasma HCO3- concentration falls below normal

renal contribution; increased HCO3-

• indicates a deficit of metabolic acids

• plasma HCO3- rises above normal

compensatory response for acidosis

increase excretion of hydrogen ions and metabolci acids; reabsorbs more HCO3-

compensatory response for alkalosis

decrese H+ excretion; excrete more HCO3-

respiratory acidosis

any condition that causes an excess of carbonic acid in the blood; CO2 retention from hypoventilation; caused by impaired CO2 elimination by the lungs

respiratory acidosis effects

impaired ventilation or gas exchange; depressed respiratory drive; impaired neuromuscular function

clinical manifestations of respiratory acidosis

neurological (early: HA, confusion, blurred vision; progressive: tremors, lethargy, disorientation, somnolence, coma); cardiac (tachycardia, dysrhythmias; severe: vasodilation → hypotension)

ABG of respiratory acidosis

low pH, high PaCO2, HCO3- normal

compensatory response for respiratory acidosis

kidneys cannot excrete carbonic acid to they increase the renal excretion of H+ and reabsorb HCO3; increase in HCO3- ion moves the pH towards normal

compensated respiratory acidosis

high PaCO2, high HCO3-, low/normal pH

respiratory alkalosis

any condition that causes a carbonic acid deficit; usually the only cause is hyperventilation

respiratory alkalosis causes

• hypoxemia-related

• psychogenic: anxiety, psychological distress, prolonged sobbing

• neurologic/drug related: alcohol withdrawal, salicylate overdose, meningitis, head injury, sepsis

• voluntary hyperventilation

clinical manifestations of respiratory alkalosis

• neuromuscular excitability (paresthesia, carpopedal spasm, tetany)

• CNS effects (confusion, dizziness, excitation → seizures; cerebral vasoconstriction)

ABG of respiratory alkalosis

low PaCO2, high pH, normal HCO3-

compensatory response to respiratory alkalosis

• kidneys retain H+ and excrete HCO3-

• slows renal excretion of metabolic acids (helps restore the ratio of bicarbonate to carbonic acid and moves pH back toward normal)

aldosterone and hypokalemia

increase in Na+ reabsorption; promotes K+ and H+ excretion in urine

hyperaldosteronism

excess H+ and K+ excretion

hypokalemia

H+ shifts into cells in exchange for K+ and contributes to metabolic acidosis

compensated respiratory alkalosis

low PaCO2, low HCO3-, pH high but closer to normal

metabolic acidosis

excess of metabolic acids or loss of bicarbonate

main causes of metabolic acidosis

increase acid production (lactic acidosis, ketoacidosis); decreased bicarbonate (diarrhea, renal tubular loss); combination of increased acid and decreased base

starvation ketoacidosis

decrease caloric/glucose intake leads to increase fat breakdown that causes ketone body accumulation → acidosis

causes of metabolic acidosis

• ketoacidosis (diabetes, alcoholism)

• lactic acidosis (shock, impaired hypoxia, severe hyperthyroidism, burns)

• renal failure (impaired acid excretion)

• toxins/precursors (salicylates, methanol, ethylene glycol)

loss of bicarbonate common causes

• renal tubular acidosis

• diarrhea

clinical manifestations of loss of bicarbonate

• headache, abdominal pain

• CNS depression: confusion, lethargy, coma

• severe cases: tachycardia, ventricular dysrhythmias, decreased cardiac contractility

ABG of metabolic acidosis

low HCO3-, low pH, normal PaCO2

compensation for metabolic acidosis

hyperventilation; decreased pH stimulates peripheral chemoreceptors → respiratory center increases rate and depth of breathing → lungs blow off more CO2 leading to decreased carbonic acid → pH rises towards normal

compensated ABG of metabolic acidosis

low HCO3-, low PaCO2, pH low/normal

kussmaul respirations

deep, rapid breathing is the body’s attempt to compensate for metabolic acidosis

anion gap

determines whether metabolic acidosis is caused by added acids or by bicarbonate loss

anion gap: gap > than normal =

unmeasured acids (lactate, ketones, toxins, renal failure)

if anion gap in normal but person is still acidic…

body lost HCO3- and replaced it with chloride

normal anion gap

4-12 mEq/L

causes of high anion gap metabolic acidosis

Glycols, Oxoproline, Lactate, Dlactate, Methanol, Aspirin, Renal failure, Ketoacidosis

metabolic alkalosis

primary increase in serum HCO3- due to gain or base or loss of acid

causes of metabolic alkalosis

• gain of base (increase HCO3-) → excess intake of bicarbonate, massive blood transfusion with citrate, contraction alkalosis

• loss of acid (decrease H+) → vomiting or NG suction/hyperaldosteronism or Cushing’s

decrease in acid mechanisms

• GI loss of H+: vomiting, gastric suction

• renal loss of H+: hyperaldosteronism, diuretics

• cellular shifts: hypokalemia

• volume contraction: extracellular fluid loss

• most common cause = vomiting or gastric suction

clinical manifestations of metabolic alkalosis

• cardiovascular (postural hypotension)

• electrolyte effects (hypokalemia → bilat. muscle weakness, K+ shifts into cells; ionized hypocalcemia → tingling, tetany, seizures)

• neurological (irritability, agitation → confusion, lethargy, coma; fatal if pH > 7.8)

ABG for metabolic alkalosis

high CO3-, normal PaCO2, high pH

compensatory response for metabolic alkalosis

• hypoventilation

• usually incomplete (cannot hypoventilate forever)

compensated metabolic acidosis ABG

high HCO3, high PaCO2, slightly high pH