Hypercapnia: Difference between revisions
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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. | 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 == | == Pathology<ref name=":3">Rawat D, Sharma S. Hypercapnea. [Updated 2019 Jun 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: h[https://www.ncbi.nlm.nih.gov/books/NBK500012/ ttps://www.ncbi.nlm.nih.gov/books/NBK500012/]</ref> == | ||
{{#ev:youtube|v=QrvhApnoKDM}}<ref>MrA91000. Pathology of Hypercapnia. Available from: https://www.youtube.com/watch?v=QrvhApnoKDM [last accessed 20/8/2012]</ref> | {{#ev:youtube|v=QrvhApnoKDM}}<ref>MrA91000. Pathology of Hypercapnia. Available from: https://www.youtube.com/watch?v=QrvhApnoKDM [last accessed 20/8/2012]</ref> | ||
# | # Increased CO2 in the body can be caused by metabolic compensation or respiratory failure | ||
# A CNS (central nervous system) injury such as [[Guillain-Barre Syndrome|guillain-barré syndrome]] or [[Overview of Traumatic Brain Injury|traumatic brain injury]] can lead to a reduced respiratory drive | |||
# Reduced respiratory rate leads low tidal volume and hypoventilation | |||
# Causing poor [[Respiratory System|gas exchange]] in the alveoli | |||
# This causes a retention of CO2 and therefore hypercapnia or type 2 respiratory failure | |||
# | |||
# | |||
== Causes of Hypercapnia == | == Causes of Hypercapnia == | ||
=== Respiratory | === Respiratory failure === | ||
* Poor ventilation/ perfusion (V/Q) matching leads to reduced gas exchange of O2 and CO2. | * 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 | * Sputum retention - means there is less surface area for gases to exchange | ||
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*** This can be diagnosed by interpretation of recent [[Arterial Blood Gases|blood gas]] results, assessing pH, in relation to PaCO2 | *** This can be diagnosed by interpretation of recent [[Arterial Blood Gases|blood gas]] results, assessing pH, in relation to PaCO2 | ||
=== | === Metabolic compensation === | ||
* | * Patients in renal failure may present with an increased work of breathing. | ||
* [[Arterial Blood Gases|ABGs]] will show metabolic acidosis, generally with some form of respiratory compensation e.g. Decreased O2 | ** [[Arterial Blood Gases|ABGs]] will show metabolic acidosis, generally with some form of respiratory compensation e.g. Decreased O2 | ||
* Pulmonary oedema and pleural effusion may also be present | ** Pulmonary oedema and pleural effusion may also be present | ||
* Sepsis<ref name=":3" /> | |||
* Increased steroid use<ref name=":3" /> | |||
== Medical Treatment == | == Medical Treatment == | ||
Revision as of 10:34, 16 April 2020
Original Editor - Abbey Wright
Top Contributors - Abbey Wright, Lucinda hampton and Kim Jackson
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[edit | edit source]
In an acute setting a hypercapnic patient may present with some or all of the following symptoms[1][4]:
| 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 |
| Tachypnoae | Increased respiratory rate and shallow/apical breathing, increased accessory muscle use | RR > 20 BPM |
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[5][edit | edit source]
- Increased CO2 in the body can be caused by metabolic compensation or respiratory failure
- A CNS (central nervous system) injury such as guillain-barré syndrome or traumatic brain injury can lead to a reduced respiratory drive
- Reduced respiratory rate leads low tidal volume and hypoventilation
- Causing poor gas exchange in the alveoli
- This causes a retention of CO2 and therefore hypercapnia or type 2 respiratory failure
Causes of Hypercapnia[edit | edit source]
Respiratory failure[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
- Ventilatory pump failure
- Lung hyperinflation[4]
- 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.[7]
- 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
Metabolic compensation[edit | edit source]
- Patients in renal failure may present with an increased work of breathing.
- ABGs will show metabolic acidosis, generally with some form of respiratory compensation e.g. Decreased O2
- Pulmonary oedema and pleural effusion may also be present
- Sepsis[5]
- Increased steroid use[5]
Medical Treatment[edit | edit source]
Initial treatment of hypercapnia is oxygen therapy with the goal of increasing the inspired oxygen volume.[4] If left untreated or under-treated it is highly likely hypoxia and hypoxaemia will occur.
If low PaO2 and high PaCO2 continues some form of ventilation may be required: CPAP, non-invasive (NIPPV) or invasive depending on the severity or risk to life.[8] [4] The goal of treatment is to prevent further respiratory failure and hypoxiaemia of the tissues especially the brain.
Chronic Hypercapnia[edit | edit source]
Chronic hypercapnia is seen in COPD patients and can be managed through different ways:
- Pharmacology: Long acting bronchodilators[9], anti-inflammation therapy, systemic steroids and antibiotics in the case of acute respiratory failure[4][10].
- Pulmonary rehabilitation: exercise therapy to improve quality of life and prevent muscular deconditioning[10]
- Long term oxygen therapy
- Non-invasive ventilation: the use of NIPPV (non-invasive postive-pressure ventilation) can be of use for night-time hypercapnic patients or sleep apoena[4]
- CPAP (continous positive airway pressure): has been used as an alternative to ventilation in management of hypercapia[11]
Complications[4][edit | edit source]
- Altered mental state and confusion
- Loss of consciousness and coma[12]
- Cardiac arrhythmia
- Hypoxaemia and tissue death
- Irreversible brain damage
- Death
Resources[edit | edit source]
Measuring respiratory rate and common breathing patterns
References[edit | edit source]
- ↑ 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.
- ↑ Kenyon K, Kenyon J. The Physiotherapist's Pocketbook. Essential Facts at your Fingertips. 2nd ed. London: Churchill Livingstone, Elsevier. 2009.
- ↑ 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.
- ↑ 4.0 4.1 4.2 4.3 4.4 4.5 4.6 Budweiser S, Jörres RA, Pfeifer M. Treatment of respiratory failure in COPD. International journal of chronic obstructive pulmonary disease. 2008 Dec;3(4):605.
- ↑ 5.0 5.1 5.2 Rawat D, Sharma S. Hypercapnea. [Updated 2019 Jun 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK500012/
- ↑ MrA91000. Pathology of Hypercapnia. Available from: https://www.youtube.com/watch?v=QrvhApnoKDM [last accessed 20/8/2012]
- ↑ West JB. Causes of and compensations for hypoxemia and hypercapnia. Comprehensive physiology. 2011 Jan;1(3):1541-53.
- ↑ Antonelli M, Pennisi MA, Pelosi P, Gregoretti C, Squadrone V, Rocco M, Cecchini L, Chiumello D, Severgnini P, Proietti R, Navalesi P. Noninvasive Positive Pressure Ventilation Using a Helmet in Patients with Acute Exacerbation of Chronic Obstructive Pulmonary DiseaseA Feasibility Study. Anesthesiology: The Journal of the American Society of Anesthesiologists. 2004 Jan 1;100(1):16-24.
- ↑ Niewoehner DE, Rice K, Cote C, Paulson D, Cooper JA, Korducki L, Cassino C, Kesten S. Prevention of exacerbations of chronic obstructive pulmonary disease with tiotropium, a once-daily inhaled anticholinergic bronchodilator: a randomized trial. Annals of internal medicine. 2005 Sep 6;143(5):317-26.
- ↑ 10.0 10.1 Rabe KF, Hurd S, Anzueto A, Barnes PJ, Buist SA, Calverley P, Fukuchi Y, Jenkins C, Rodriguez-Roisin R, Van Weel C, Zielinski J. Global strategy for the diagnosis, management, and prevention of chronic obstructive pulmonary disease: GOLD executive summary. American journal of respiratory and critical care medicine. 2007 Sep 15;176(6):532-55.
- ↑ Dial S, Menzies D. Is there a role for mask continuous positive airway pressure in acute respiratory failure due to COPD? Lessons from a retrospective audit of 3 different cohorts. International journal of chronic obstructive pulmonary disease. 2006 Mar;1(1):65.
- ↑ Sakuta Y, Kuroda N, Tsuge M, Fujita Y. Hypercapnic respiratory distress and loss of consciousness: a complication of supraclavicular brachial plexus block. JA clinical reports. 2015 Dec 1;1(1):13.
