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Home | CCC | Respiratory Acidosis

Respiratory Acidosis

by Dr Chris Nickson, last update April 23, 2019

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

References and Links

  • Acid-Base: ABG analysis – Anion Gap – SID – NAGMA
  • Metabolic acidosis: Overview – Evaluation – DDx
  • Metabolic alkalosis: Overview – Evaluation – DDx
  • Respiratory acidosis: Overview – DDx
  • Respiratory alkalosis: Overview – DDx

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About Dr Chris Nickson

An oslerphile emergency physician and intensivist suffering from a bad case of knowledge dipsosis. Key areas of interest include: the ED-ICU interface, toxicology, simulation and the free open-access meducation (FOAM) revolution. @Twitter | INTENSIVE| SMACC

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