- Respiratory acidosis = a primary acid-base disorder in which arterial pCO2 rises to an abnormally high level.
- arterial pCO2 is normally maintained at a level of about 40 mmHg by a balance between production of CO2 by the body and its removal by alveolar ventilation.
PaCO2 is proportional to VCO2/VA VCO2 = CO2 production by the body VA = alveolar ventilation
- an increase in arterial pCO2 can occur by one of three possible mechanisms:
- presence of excess CO2 in the inspired gas
- decreased alveolar ventilation
- increased production of CO2 by the body
Inadequate Alveolar Ventilation
- central respiratory depression
- drug depression of respiratory centre (eg by opiates, sedatives, anaesthetics)
- neuromuscular disorders
- lung or chest wall defects
- airway obstruction
- inadequate mechanical ventilation
Over-production of CO2 -> hypercatabolic disorders
- Malignant hyperthermia
- Thyroid storm
- Early sepsis
- Liver failure
Increased Intake of Carbon Dioxide
- Rebreathing of CO2-containing expired gas
- Addition of CO2 to inspired gas
- Insufflation of CO2 into body cavity (eg for laparoscopic surgery)
- CO2 is lipid soluble -> depressing effects on intracellular metabolism
- increased minute ventilation via both central and peripheral chemoreceptors
- increased sympathetic tone
- peripheral vasodilation by direct effect on vessels
- acutely the acidosis will cause a right shift of the oxygen dissociation curve
- if the acidosis persists, a decrease in red cell 2,3 DPG occurs which shifts the curve back to the left
- cerebral vasodilation increasing cerebral blood flow and intracranial pressure
- central depression at very high levels of pCO2
- potent stimulation of ventilation
- this can result in dyspnoea, disorientation, acute confusion, headache, mental obtundation or even focal neurologic signs
Acute – buffering only
- mostly takes place intracellularly
- buffers: Hb, protein, phosphate
- H2CO3 not involved as it can’t buffer itself
Chronic – renal bicarbonate retention
- kidneys respond by retaining bicarbonate
- takes 3 or 4 days to reach its maximum
- increased arterial pCO2 -> increases intracellular pCO2 in proximal tubular cells -> increased H+ secretion from the PCT cells into the tubular lumen:
- increased HCO3 production which enters the circulation (plasma HCO3 increases)
- increased Na+ reabsorption in exchange for H+ and less in exchange for Cl- (plasma [Cl-] falls)
- increased ‘NH3’ production to ‘buffer’ the H+ in the tubular lumen (urinary excretion of NH4Cl increases)
Restoration of Ventilation
- the pCO2 rapidly returns to normal with restoration of adequate alveolar ventilation
- treatment usually needs to be directed to correction of the primary cause if this is possible.
- in severe cases, intubation and mechanical ventilation will be necessary to restore alveolar ventilation -> patient can deteriorate post intubation from decrease in sympathetic tone with falling CO2
‘Post Hypercapnic Alkalosis’
- the correction of the elevated bicarbonate (renal compensation) associated with chronic respiratory acidosis may not be rapid.
- return of plasma bicarbonate to normal requires renal excretion of the excess bicarbonate -> the kidney has a large capacity to excrete bicarbonate but in certain abnormal conditions this capacity is impaired and the bicarbonate level remains elevated.
- the persistence of elevated bicarbonate despite resolution of the chronic respiratory acidosis is referred to by some as ‘post-hypercapnic alkalosis’.
- the best available quantitative index of the magnitude of a respiratory acidosis is the difference between the ‘actual’ pCO2 and the ‘expected’ pCO2
- actual pCO2 = the measured value obtained from arterial blood gas analysis.
- expected pCO2 = the value of pCO2 that we calculate would be present taking into account the presence of any metabolic acid-base disorder
Expected pCO2 = 1.5 (Actual [HCO3]) + 8 mmHg (this is known as Winter’s formula)
- monitoring with capnography -> the end-tidal pCO2 is typically lower than the arterial pCO2 and the difference between these values is an index of the magnitude of the alveolar dead space -> so if the end-tidal pCO2 is elevated then the arterial pCO2 is usually even more elevated.
- inadequate ventilation will also necessarily affect arterial oxygenation -> give oxygen