Gunn: Acid/Base Physiology 2 Flashcards
What is respiratory acidosis?
This is a condition in which the concentration of PCO2 is increased due to an inability to excrete it as efficiently due to impaired ventilation.
What is respiratory alkalosis?
This is a condition in which the concentration of PCO2 is decreased due to an increased ventilation.
What causes metabolic acidosis?
Excess nonvolatile acid production due to diabetic ketoacidosis or accumulation of lactic acid in circulatory shock, for instance, failure to excrete sufficient acid in renal failure or loss of bicarbonate (in diarrhoea).
What are the causes of metabolic alkalosis?
This condition can occur through the addition of nonvolatile alkali to the body - such as through the ingestion of antacids - or through the loss of nonvolatile acids due to vomiting or nasogastric suction.
What causes respiratory acidosis?
This occurs due to inadequate alveolar gas exchange relative to carbon dioxide production.
- Inadequate ventilation - Depression of respiratory centres.
- Impaired Gas Diffusion - COPD or Pulmonary Oedema.
What causes respiratory alkalosis?
Due to a result of excess alveolar gas exchange relative to CO2 production. Hyperventilation may be due to endogenous or drug-induced stimulation of respiratory centres. It may also occur due to anxiety or fear.
What is a common example of a mixed disorder?
In heart failure, respiratory acidosis occurs due to impaired gas diffusion and reduced cardiac output leads to reduced systemic oxygen delivery resulting in anaerobic metabolism and lactic acidosis. That is respiratory acidosis in combination with metabolic acidosis.
How is respiratory rate regulated?
Arterial PCO2 and pH are sensed by chemoreceptors in the brain (ventrolateral medulla -senses CO2 and secondary pH changes in metabolism) and aortic/carotid bodies. When the PCO2 increases - or the pH decreases - it stimulates ventilatory drive and vice versa.
- Hypoxia also acts as a potent stimulus for the ventilatory drive - This PO2 is sensed by peripheral chemoreceptors (aortic and carotid bodies).
What is the kidneys role in acid/base regulation?
The kidney is involved in the reabsorption of all HCO3- filtered by the kidney and in the regeneration of all HCO3- lost in the buffering of nonvolatile acids. Also, has roles in the removal of fixed acids incorporated into non-bicarbonate buffer systems.
Where in the kidney is bicarbonate filtered?
- Bicarbonate is freely filtered by the renal glomeruli.
- 80 - 90% is reabsorbed in the proximal convoluted tubules.
- 10-15% recovered in the Loop of Henle and Distal Tubule.
How is bicarbonate filtered?
Filtered bicarbonate is exchanged for hydrogen ions in a process that involves the vector transport of sodium ions from the tubular lumen into the peritubular space.
What are the steps involved in the renal excretion of H+ and conservation of HCO3- ?
- Bicarbonate combines with secreted hydrogen ions in the renal tubule forming carbonic acid.
- Carbonic acid then dissociates to form CO2 and H2O - This reaction is catalysed by carbon anhydrase present in the brush border of the renal tubular cells.
- CO2 crosses the tubular cell border down its concentration gradient easily.
- Inside proximal tubule, CO2 recombines with H2O to form carbonic acid - Again under the influence of carbon anhydrase.
- Carbonic Acid disassociates to bicarbonate and hydrogen ions.
- Bicarbonate transported into the bloodstream with sodium down its conc and electrical gradient.
- H+ passes back into tubular space in exchange for sodium.
What are the processes involved in the renal excretion of H+ and regeneration of HCO3-?
Regeneration of the bicarbonate lost as a result of nonvolatile acid production occurs in proximal, distal tubules and collecting ducts and is associated with the active transport of hydrogen ions into the tubular lumen, where they combine with phosphate ions and ammonia.
- Glutamine is split into a-ketoglutarate and NH4+
- a-ketoglutarate forms bicarb and NH4+ is symportered with Na+ into the lumen to bind with Cl- and be excreted
- HCO3- is moved into the peritubular space from the distal nephron in exchange for Cl- .
What are the limitations of HCO3- regeneration?
- Depletion of the phosphate ion stores.
- Depletion of the ammonia stores - Ammonia is produced in the kidney from glutamine but this requires several days.
What regulates HCO3- reabsorption?
- In acidosis, secretion of H+ by the nephron is increased and there is near complete reabsorption of HCO3- .
- In alkalosis, secretion of H+ by the nephron is decreased and there is a reduction in the reabsorption of HCO3- .
What happens in response to a sustained respiratory alkalosis?
- Hyperventilation reduces PCO2 and raises pH - As bicarbonate reabsorption is directly related to PCO2 this reabsorption reduces.
- Reduced renal net acid excretion also acts to restore pH and acts reduce HCO3- .
What occurs in response to acute metabolic acidosis?
- Metabolic acidosis causes a fall in HCO3- concentrations and therefore a reduction in the pH.
- This drives an increase in the respiratory drive and alveolar ventilation.
- This leads to a fall in the PCO2.
- This leads to a return in pH towards normal.
What are the time periods for each buffer/compensatory action to reach full effect?
- Distribution and Buffering in ECF = 1-2 hours
- Cellular Buffering Processes = 8 hours
- Respiratory Compensation = 12 hours
- Renal Base Excretion = 48 hours - Faster than renal acid excretion as you only need to turn off the reabsorption of bicarbonate.
- Renal Acid Excretion = 72 hours - Limited by the stores of ammonia and phosphate.
Match the letter to the number column they relate to…
- A = II
- B = III
- C = I
- D = V
- E = IV
What acid-base disturbance do these values correspond to?
Acute Respiratory Acidosis
