Hypercapnia

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Introduction[edit | edit source]

Hypercapnia is when there is too much carbon dioxide (CO2) in the blood. This is normally caused by hypoventilation of the body which leads to CO2 retention. Hypercapnia is defined as PaCO2 greater than 4.2kPa on an arterial blood gas (ABG).[1]

Hypercapnia can eventually cause hypoxaemia due to reduced respiratory drive.

However; hypercapnia can conversely be caused by long term hypoxaemia which causes the body to compensate leading to increased CO2 in the blood. This is known as type 2 respiratory failure.

Type 2 respiratory failure[edit | edit source]

Type 2 respiratory failure is defined as: PaCO2 greater than 4.2kPa and PaO2 less than 8kPa.[1] (these ranges can differ slightly depending on the book or article).[2]

It is caused reduced respiratory drive which commonly is due to a neurological impairment. These neurological impairments could be traumatic or insidious in nature.

Type 2 respiratory failure is also common in advanced COPD patients due to: long term hypoxaemia or lack of gas exchange occurring in the alveoli thanks to poor tissue quality. [3]

On the contrary to hypoxaemia the patient will present as drowsy and with low respiratory rate as a result of the increased CO2 in the brain. [1]

Clinical signs[1][edit | edit source]

In an acute setting a hypercapnic patient may present with some or all of the following symptoms:

Sign Clinical feature Observation
Tachycardia Increased heart rate HR > 100 bpm
Dyspnoea Deranged respiratory rate RR inconsistent
Bradypnea Low respiratory rate RR < 12 bpm
Flushed skin Redness of face or body May be hyperthermic (not always)
Hot calor Warm extremities May be hyperthermic (not always)
Altered mental state Confusion, drowsy, difficult to wake
Astrexis Arm flapping Jerking motion of the hands, inability to stay still

In chronic respiratory diseases these symptoms can develop over time, however, symptoms can become severe which can lead to coma or death if left untreated.

Pathology[edit | edit source]

[4]

Causes of hypercapnia[edit | edit source]

Respiratory cause:[edit | edit source]

  • Poor ventilation/ perfusion (V/Q) matching leads to reduced gas exchange of O2 and CO2.
  • Sputum retention - means there is less surface area for gases to exchange
  • Over oxygenating - causing CO2 retention (especially present in COPD)[5]
  • CO2 retention Uncontrolled oxygen therapy, or receiving too much oxygen, can make people who usually have higher CO2 levels retain more until it reaches dangerous levels.
    • Acute CO2 retention is not a reason to reduce FiO2 unless patients have evidence of acute-on-chronic CO2 retention secondary to chronic respiratory disease
    • This can be diagnosed by interpretation of recent blood gas results, assessing pH, in relation to PaCO2, standard bicarbonate and base excess. Only this group of patients require judicious oxygen administration )24-28%), which should be prescribed accordingly
  1. Renal failure
  • Patient in renal failure may present with an increased work of breathing
  • ABGs will show metabolic acidosis, generally with some form of respiratory ompensation e.g. Decreased CO2
  • Pulmonary oedema and pleural effusion may also be present[1]

Resources[edit | edit source]

References[edit | edit source]

  1. 1.0 1.1 1.2 1.3 Patel S, Miao JH, Majmundar SH. Physiology, Carbon Dioxide Retention. InStatPearls [Internet] 2020 Feb 12. StatPearls Publishing.
  2. Kenyon K, Kenyon J. The Physiotherapist's Pocketbook. Essential Facts at your Fingertips. 2nd ed. London: Churchill Livingstone, Elsevier. 2009.
  3. McEvoy RD, Pierce RJ, Hillman D, Esterman A, Ellis EE, Catcheside PG, O’Donoghue FJ, Barnes DJ, Grunstein RR. Nocturnal non-invasive nasal ventilation in stable hypercapnic COPD: a randomised controlled trial. Thorax. 2009 Jul 1;64(7):561-6.
  4. MrA91000. Pathology of Hypercapnia. Available from: https://www.youtube.com/watch?v=QrvhApnoKDM [last accessed 20/8/2012]
  5. West JB. Causes of and compensations for hypoxemia and hypercapnia. Comprehensive physiology. 2011 Jan;1(3):1541-53.