Acid-Base Balance

How does Hb buffer H+?

deoxy-Hb has a greater affinity for H+ than oxy-Hb

important consequences for acid-base balance

Which is more acidic, venous or arterial blood?

venous—only slightly more, at 7.36 vs 7.4

only a small amount of H+ remains

free in blood

H+ concentration (pH) has important effects on

many metabolic processes

regulation is essential for homeostasis

normal plasma [H+]

40 nmol/L (pH 7.4)

HCO3- acts as a

buffer for H+

Henderson-Hasselbalch equation

pH= pKa + log [HCO3-]/alpha*[PCO2]

describes relationship between pH, PCO2, and HCO3-

derived from H2CO3 ←→ H+ + HCO3-

alpha= solubility of CO2 in plasma per kPa PCO2 at body temperature= 0.03

pKa= acid dissociation constant= 6.1

PCO2 normally is 40?

normal HCO3- concentration in arterial blood

24 mmol/L

what governs balance of HCO3-?

renal excretion

what governs PCO2?

lung ventilation

Davenport diagram

shows relationship between pH, HCO3-, and PCO2

BAC line shows relationship between HCO3- and pH as carbonic acid is added to whole blood—buffer line

slope is steeper than for plasma alone because Hb has its own buffering capacity

increased [HCO3-] displaces line upward, base excess line D-E

decreased [HCO3-] displaces line downward, base deficit line G-F

respiratory acidosis

caused by an increase in PCO2, which reduces [HCO3-]:PCO2 ratio; pH decreases

ventilation is too little, hypoventilation, or ventilation-perfusion inequality

respiratory alkalosis

caused by a decrease in PCO2, which increases [HCO3-]:PCO2 ratio; pH increases

ventilation is too great, hyperventilation, such as high altitude

metabolic acidosis

caused by a decrease in [HCO3-] which reduces [HCO3-]:PCO2 ratio; pH decreases

excess acid is ingested or generated, e.g. tissue hypoxia releases lactic acid

metabolic alkalosis

caused by an increase in [HCO3-] which increases [HCO3-]:PCO2 ratio; pH increases

excessive ingestion alkalis or loss gastric acid by vomiting

respiratory acidosis compensatory mechanisms

if CO2 retention persists, the kidneys respond by preserving HCO3-

increased PCO2 in renal tubular cells results in excretion of more acid urine (H+ excreted as H2PO4- or NH4-); HCO3- reabsorbed

[HCO3-]:PCO2 ratio increases toward normal level

renal compensation not usually perfect, so pH remains a little low

respiratory alkalosis compensatory mechanisms

renal compensation via increased HCO3- excretion

after prolonged stay at high altitude, renal compensation may be complete

metabolic acidosis compensatory mechanisms

increased ventilation rate to lower PCO2

stimulus is the action of H+ ions on peripheral chemoreceptors

metabolic alkalosis compensatory mechanisms

some degree of compensation may occur via reduced alveolar ventilation, but compensation is small or absent

causes of respiratory acidosis

inhibition of medullary respiratory centre, disorders of respiratory muscles, airway obstruction, disorders of gas exchange

inhibition of medullary respiratory centre examples

opiates, barbiturates, anesthetics

lesions of CNS

central sleep apnea

disorders of respiratory muscles examples

Guillaine-Barre syndrome

polio

amyotrophic lateral sclerosis (ALS)

multiple sclerosis

airway obstruction examples

aspiration, obstructive sleep apnea, laryngospasm

disorders of gas exchange examples

acute respiratory distress syndrome (ARDS)

COPD

pneumonia

pulmonary edema

causes of respiratory alkalosis

stimulation of the medullary respiratory centre, hypoxemia, mechanical ventilation

stimulation of medullary respiratory centre examples

hysterical hyperventilation, gram negative septicemia, salicylate poisoning, neurological disorders (tumour, stroke)

hypoxia examples

high altitude (hypoxemia stimulates peripheral chemoreceptors), pneumonia, pulmonary embolism