Respiratory Acidosis

DEFINITION

• Respiratory acidosis = a primary acid-base disorder in which arterial pCO2 rises to an abnormally high level.

PATHOPHYSIOLOGY

• 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:

1. presence of excess CO2 in the inspired gas
2. decreased alveolar ventilation
3. increased production of CO2 by the body

CAUSES

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
• Phaeochromocytoma
• 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)

EFFECTS

• CO2 is lipid soluble -> depressing effects on intracellular metabolism

RESP

• increased minute ventilation via both central and peripheral chemoreceptors

CVS

• 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

CNS

• 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

COMPENSATION

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:

1. increased HCO3 production which enters the circulation (plasma HCO3 increases)
2. increased Na+ reabsorption in exchange for H+ and less in exchange for Cl- (plasma [Cl-] falls)
3. 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’.

ASSESSMENT

• 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)

PREVENTION

• 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