Overview of acid/base Flashcards
Normal physiological pH
7.35-7.45
Acidemia pH
< 7.35
Alkalemia pH
> 7.45
Carbonic acid/bicarbonate buffer system
H+ + HCO3- <–> H2CO3 <–> CO2 + H2O
Think of the right side of the equation as occurring in the lungs and the left in the kidneys
The lungs compensate metabolic disorders while the kidneys compensate respiratory disorders
Henderson-Hasselbach equation
pH= pka + log (base/acid)
carbonic anhydrase pka= 6.1
Most of the carbonic acid in plasma is in the form of carbon dioxide gas; therefore, the concentration of carbonic acid can be estimated as the partial pressure of CO2 (pCO2) multiplied by 0,03
pH= 6.1 + log (HCO3-/ 0.03 x pCO2)
Normal blood gas values
PaCO2= 35-45 mmHg (40)
HCO2= 22-26 mEq/L (24)
PaO2= 95-100 mmHg
SaO2= > or equal to 95%
Adverse consequences
Acidemia
Alkalemia
Acidemia
Cardiovascular:
- decrease cardiac output
- Impairment of cardiac contractibility
- Increase pulmonary vascular resistance and arrhythmia’s
Metabolic:
- Insulin resistance
- Inhibition of glycolysis
- Hyperkalemia
CNS: coma or altered mental status
Others: decreased respiratory muscle strength, hyperventilation, dyspnea
Alkalemia
Cardiovascular:
- Decrease coronary blood flow
- Arteriolar constriction
- Decrease anginal threshold
- Arrhythmias
Metabolic:
- Decrease K+, Ca, and Mg
- Stimulation of glycolysis
CNS: decrease cerebral blood flow, seizures
Others: hypoventilation
Acid generation
Diet: 1 mEq/kg/day of acid consumed per day; comes from oxidation of protein and fats
Aerobic metabolism of glucose produces 15-20K mmol of CO2 each day
Anaerobic metabolism produces lactic and pyruvic acid
Three standard mechanisms of acid regulation
- Buffering
- Renal regulation
- Ventilatory regulation
Buffering
First line of defense
Buffer: ability of a weak acid and its anion to resist change in pH with addition of a strong acid or base
Bicarbonate
principle buffer
rapid onset with intermediate capacity
HCO3- buffer present in largest concentration extracellularly over any other buffers
Ability of the kidneys and lungs to excrete and retain HCO3- and CO2, respectively
Phosphates
Intermediate onset and capacity
Extracellular inorganic phosphates limited activity
Intracellular organic phosphates
Calcium phosphates in bone relatively inaccessible
Proteins
Albumin/hemoglobin: rapid onset, limited capacity
More effective from intracellular than extracellular
Renal regulation
Kidney serves 2 purposes:
1. Reabsorb filtered HCO3-
2. Excrete H+ ions released from nonvolatile acids
Bicarbonate reabsorption
85-90% reabsorbed by proximal tubule
- Filtered HCO3- combines with a secreted H+ to form H2CO3
- Through the action of carbonic anhydrase disassociated occurs to form H2O and CO2
- H2O and CO2 are reabsorbed into the tubular cell
- H2CO3 dissociates into HCO3-, which is reabsorbed into the capillary, and H+, is secreted into the urine in exchange for Na+
Net effect
filtered HCO3- is reabsorbed without any net loss of H+
Anything limiting H+ secretion into the proximal tubule lumen results in urinary bicarbonate losses
Ex: carbonic anhydrase inhibitors
Bicarbonate genration/H+ excretion
Delayed onset but large capacity
Reclamation of all filtered HCO3- is not sufficient to maintain a normal blood pH
H+ excretion take place primarily in the distal tubule
Ammonium excretion
- Secreted H+ combines with NH3 to form NH4+, NH4+ cannot cross membranes and is excreted
- HCO3- is formed during the process and is also reabsorbed in the capillaries
- New HCO3- is formed (40 mEq/day)
Titratable acidity
- Filtered HPO4- combines with H+ and is excreted as H2PO4-
- The intracellular HCO3- formed from the dissociation of H2CO3- is reabsorbed as “new” HCO3-
- Accounts for 30 mEq/day of “new” HCO3-
Distal tubular hydrogen ion excretion
Comprises 50% of net acid secretion
CO2 combines with water in the presence of carbonic anhydrase to form H2CO3, which breaksdown to H+ and HCO3-
The H+ is transported back into the tubular lumen by ATPase
Ventilatory regulation
Rapid onset and LARGE capacity
Chemoreceptors detect an increase in the PaCO2 and increase the rate and depth of ventilation
Peripheral chemoreceptors in carotid arteries and aorta: activated by arterial acidosis, hypercapnia, and hypoxia
Central chemoreceptors in medulla: activated by CSF acidosis
