- 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
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
Chris is an Intensivist and ECMO specialist at the Alfred ICU in Melbourne. He is also the Innovation Lead for the Australian Centre for Health Innovation at Alfred Health, a Clinical Adjunct Associate Professor at Monash University, and the Chair of the Australian and New Zealand Intensive Care Society (ANZICS) Education Committee. He is a co-founder of the Australia and New Zealand Clinician Educator Network (ANZCEN) and is the Lead for the ANZCEN Clinician Educator Incubator programme. He is on the Board of Directors for the Intensive Care Foundation and is a First Part Examiner for the College of Intensive Care Medicine. He is an internationally recognised Clinician Educator with a passion for helping clinicians learn and for improving the clinical performance of individuals and collectives.
After finishing his medical degree at the University of Auckland, he continued post-graduate training in New Zealand as well as Australia’s Northern Territory, Perth and Melbourne. He has completed fellowship training in both intensive care medicine and emergency medicine, as well as post-graduate training in biochemistry, clinical toxicology, clinical epidemiology, and health professional education.
He is actively involved in in using translational simulation to improve patient care and the design of processes and systems at Alfred Health. He coordinates the Alfred ICU’s education and simulation programmes and runs the unit’s education website, INTENSIVE. He created the ‘Critically Ill Airway’ course and teaches on numerous courses around the world. He is one of the founders of the FOAM movement (Free Open-Access Medical education) and is co-creator of LITFL.com, the RAGE podcast, the Resuscitology course, and the SMACC conference.
His one great achievement is being the father of two amazing children.
On Twitter, he is @precordialthump.