Acid-Base Balance PQs

Flashcards about Acid-Base Balance

Buffering properties of hemoglobin

Hemoglobin buffers blood by binding H+ ions via its histidine residue, especially in RBCs.

Haldane effect

Deoxygenated Hb binds more H+ and CO2, aiding transport from tissues.

Metabolic Acidosis

Prolonged or severe diarrhea can cause this acid-base imbalance.

Respiratory compensation for metabolic acidosis

The body increases ventilation, reducing carbonic acid (H2CO3), helping to raise blood pH.

Renal compensation for metabolic acidosis

The kidneys increase H+ excretion and enhance HCO3- reabsorption, though this occurs more slowly.

Respiratory Alkalosis

Condition that occurs when pCO2 drops due to hyperventilation, causing a rise in blood pH.

Renal Compensation for Respiratory Alkalosis

Reducing H+ secretion in the distal tubule, decreasing HCO3- reabsorption in the proximal tubule, excreting excess HCO3- in urine, and retaining H+ ions.

Intercalated Cells

These cells in the distal tubule and collecting duct of the kidney are essential for maintaining acid-base balance.

Type A (α-intercalated cells)

Secrete H+ into the tubular lumen via H+-ATPase & H+/K+ antiporters and reabsorb HCO3- into the blood; active during metabolic acidosis.

Type B (β-intercalated cells)

Secrete HCO3- into the tubular fluid via pendrin (Cl-/HCO3- exchanger) and reabsorb H+; active during metabolic alkalosis.

Respiratory Acidosis

Caused by hypoventilation, leads to CO2 retention, increased pCO2, and decreased blood pH (acidemia).

Respiratory Alkalosis

Caused by hyperventilation, leads to excess CO2 loss, decreased pCO2, and increased blood pH (alkalemia).

Metabolic Alkalosis

Chronic vomiting causes loss of gastric HCl, leading to this acid-base imbalance.

Respiratory compensation for chronic vomiting

Hypoventilation, which leads to retention of CO2, increasing H2CO3, and lowering pH.

Metabolic Alkalosis

Acid-base imbalance caused by chronic or severe vomiting.

Respiratory compensation for metabolic alkalosis due to vomiting

Hypoventilation to retain CO2, forming H2CO3 to release H+ and lower pH.

Renal compensation for metabolic alkalosis due to vomiting

Excretion of HCO3- and reabsorption of H+.

Metabolic Acidosis (Diabetic Ketoacidosis - DKA)

Condition diabetes mellitus can lead to, especially if uncontrolled.

Respiratory compensation for diabetic ketoacidosis

Increased ventilation to expel CO2, reducing carbonic acid and raising pH.

Renal compensation for diabetic ketoacidosis

Kidneys excrete H+ ions and reabsorb HCO3- to buffer the acidosis.

Acid-base regulation by ventilation

Regulates acid-base balance by controlling arterial CO2 (PaCO2), which directly influences blood pH via the carbonic acid-bicarbonate buffer system.

Hyperventilation effects

Decreased PaCO2, decreased H2CO3, decreased H+, and increased pH, leading to respiratory alkalosis.

Hypoventilation effects

Increased PaCO2, increased H2CO3, increased H+, and decreased pH, leading to respiratory acidosis.

Central chemoreceptors

Respond to CO2 (via H+ in CSF).

Peripheral chemoreceptors

Respond to increased H+, increased CO2, and decreased O2.

Buffers

Help maintain pH by neutralizing excess H+ or OH-.

Carbonic acid-bicarbonate buffer

Main extracellular buffer regulated by lungs (CO2 excretion) and kidneys (HCO3- reabsorption).

Hemoglobin buffer system

Important intracellular buffer in RBCs; deoxyhemoglobin binds H+ produced from CO2 metabolism.

Protein buffer system

Active in intracellular fluids and plasma; amino acid side chains act as weak acids/bases.

Phosphate buffer system

Active in intracellular fluid and renal tubules; important in urine acidification.

Ammonia buffer system

Functions in the renal tubules; NH3 reacts with H+ to form NH4+, which is excreted.

Hydroxyapatite/calcite (Bone buffer)

Bone salts act as long-term buffers; can release or absorb H+ and carbonate/phosphate ions.

Role of CSF in acid-base balance

Plays a crucial role in central regulation of acid-base balance by acting as the medium through which central chemoreceptors detect changes in arterial CO2 and pH.

Direct proton removal

The active secretion of H+ ions by renal tubular cells, mainly in the DCT and collecting duct.

Type A intercalated cells

Use Na+/H+ ATPase or H+/K+ exchanger proton pump on their apical membrane to actively transport H+ into the tubular lumen.

Buffering secreted protons

Secreted protons are buffered in the tubular fluid by phosphate or ammonia, forming titratable acids such as H2PO4- and ammonium, which are then excreted.