Week 3: Acid-Base Balance

normal blood pH

7.35-7.45

acids

release hydrogen ions when dissolved in water or body fluids

bases

bind with hydrogen ions in solutions ans lower the amount of free hydrogen ions in solution

buffers

can react either as an acid or a base; first line of defense against changes in free hydrogen ion levels

normal pCO2

35-45 mmHg

normal pO2

75-100 mmHg

normal HCO3-

23-30 mEq/L

normal O2 Sat

>95%

pH < 7.35

acidic

pH > 7.45

alkaline

CO2 > 45 mmHg

respiratory acidosis

CO2 < 35 mmHg

respiratory alkalosis

HCO3 < 23 mEq/L

metabolic acidosis

HCO3 > 30 mEq/L

metabolic alkalosis

homeostasis

balance; depends on hydrogen ion production being consistent; CO2 loss from the body through breathing keeping pace with all forms of hydrogen ion production

carbonic anhydrase equation

carbon dioxide + water = carbonic acid = bicarbonate + hydrogen ion

CO2 + H2O ←→ H2CO3 ←→ HCO3- + H+

relationship between free hydrogen and CO2

increase in one causes an increase in the other; increased CO2 in blood → more bicarbonate and free floating hydrogen → risk of acidosis

second line of defense for acid base imbalance

respiratory system; hyperventilation, hypoventilation

respiratory acid-base control cycle

decreased rate/depth of respiration (hypoventilation) → increased pCO2 and H+ → stimulation of central chemoreceptors → increased rate/depth of respiration (hyperventilation) → decreased pCO2 and H+ → inhibition of central chemoreceptors → hypoventilation

third line of defense for acid-base imbalance

kidneys; stronger but slower than respiratory; takes 24-48 hrs

metabolic acid-base control

when pH is low, bicarb is reabsorbed by the kidneys back into circulation to buffer the free hydrogen ions, kidneys can also make more bicarb if necessary, which is then reabsorbed into circulation

when pH is high (alkaline), bicarb stays in the urine ans is excreted

formation of acids in urine

anions like phosphate in the urine pull hydrogen ions into the urine and form an acid which is excreted into the urine

formation of ammonium

ammonia (from protein breakdown) is converted to ammonium in the urine by trapping hydrogen ions allowing them to be excreted

controls CO2 levels

lungs

controlls HCO3 levels

kidneys

fatal pH

<6.9 or >7.8

acid base balance and pH

the result if how well the kidneys are functioning to retain or eliminate bicarb ions and how well the lungs are functioning to eliminate CO2

acidosis

pH <7.35

diabetic ketoacidosis and seizures increase acid production; respiratory and kidney impairment decrease acid elimination; deficit of bases (over elimination or underproduction of bicarbonate ions)

greatest risk: pts with breathing problems, older adults with chronic health problems

hydrogen ions in metabolic acidosis

overproduction: exess breakdown of fatty acids due to DKA or starvation, excessive intake of acids in alcohol and aspirin

under elimination: severe lung impairment (retention of CO2) and kidney failure (retention of hydrogen ions)

bicarbonate ions in metabolic acidosis

under production: kidney failure, impaired liver or pancreatic function

over elimination: diarrhea

causes of metabolic acidosis

diabetic ketoacidosis (DKA), severe diarrhea, renal failure, starvation, shock

metabolic acidosis symptoms

hyperkalemia, kussmaul respiration (deep, rapid; compensatory hyperventilation)

headache, decreased BP, confusion, drowsiness, muscle twitching, warm/flushed skin, nausea, vomiting, diarrhea

combined metabolic and respiratory acidosis

metabolic and respiratory acidosis occurring at the same time; pt with DKA and COPD

respiratory acidosis

retention of CO2: respiratory depression, inadequate chest expansion, airway obstruction, reduced alveolar capillary diffusion

causes of respiratory acidosis

pneumonia, COPD, atelectasis, acute pulmonary edema, cardiac arrest, over sedation, chest trauma

respiratory acidosis symptoms

hyperkalemia (always check K+ on pt with acidosis)

hypoventilation (hypoxia), reapid/shallow respirations, drowsiness, dizziness, disorientation, decreased BP with vasodialation, muscle weakness, hyperreflexia, headache, dysrrhythmias

acidosis assessment

physical: incerased HR, hyperkalemia, hypotension, lethargy, confusion in elders, reduced muscle tone and DTR, muscle weakness, kussmaul respirations (deep/rapid), pale to cyanotic skin (respiratory) or reddish warm and dry (metabolic)

cognitive changes may be first sign

metabolic acidosis labs

pH <7.35

bicarbonate < 21 mEq/L

PaO2 normal

PaCO2 normal or slightly decreased

serum potassium high

respiratory acidosis labs

pH <7.35

PaO2 low

PaCO2 high

serum bicarbonate variable (usually normal in acute cases, elevated in chronic cases due to kidney compensation)

acidosis planning and implementation

improving gas exhange: drug therapy (bronchodialators, anti inflammatory, mucolytics), O2 therapy, pulmonary hygiene (sit up, deep breathing, positioning), ventilatory support

control the cause: insulin to treat DKA, rehydration and antidiarrheals to treat prolonged diarrhea

alkalosis

pH >7.45

excess bases, especially bicarbonate; decrease in free hydrogen ion level of the blood

metabolic alkalosis

increase of bases or decease of acids

base excess: caused by excessive intake of bicarbonates, carbonates, acetates, citrates

acid deficit: caued by disease processes or medical treatments

causes of metabolic alkalosis

severe vomiting, excessive GI suctioning, diuretic therapy; excessive use of bicarbonate containing antacids

metabolic alkalosis symptoms

hypokalemia

restlessness followed by lethargy, confusion, decreased LOC, dizziness, irritable, dystrhythmias, tachycardia, nausea, vomiting, diarrhea, compensatory hypoventilation, tremors, muscle cramps, tingling of fingers and toes

respiratory alkalosis

excessive loss of CO2 through hyperventilation

hallmark: ABG result with an elevated pH coupled with low CO2 level

causes of respiratory alkalosis

hyperventilation (anxiety, PE, fear), mechanical ventilation

respiratory alkalosis symptoms

hypokalemia

seizures, lethargy and confusion, deep/rapid breathing, light headedness, hyperventilation, nausea, vomiting, tachycardia, decreased or normal BP, numbness and tingling of extremities

alkalosis assessment

low calcium levels (hypocalcemia) and low potassium (hypokalemia) often occur; CNS, neuromuscular, cardiovascular, respiratory S&S

alkalosis interventions

prevent further losses of hydrogen, potassium, calcium, and chloride ions; restore fluid balance, monitor changes, provide for safety, stop treatments that may have caused alkalosis, drug therapy, fluid and electrolyte replacement