Hypoxaemia

Original Editor - Adam Vallely Farrell


Top Contributors - Adam Vallely Farrell  

Respiratory Failure

Respiratory failure is characterised by a reduction in the function of the lungs due to lung disease or a skeletal or neuromuscular disorder.[1] It occurs when gas exchange in the lungs is significantly impaired causing a drop in the levels of oxygen in the blood (hypoxaemia) occurring with or without an increase in carbon dioxide levels (hypercapnia).[2] Respiratory failure is demonstrated in arterial blood gas (ABG) tensions. Type I respiratory failure is defined as PaO2 <8.0kPa with a normal or lowered PaCO2.[3] Type II respiratory failure (ventilatory failure) is defined as PaO2 <8.0kPa and a PaCO2 >6.0kPa. Acute respiratory failure is related to respiratory distress, with increased work of breathing and deranged gas exchange.[4] It may occur with or without the presence of excessive pulmonary secretions and/or sputum retention, and is not necessarily related to a primary respiratory problem, e.g. neurological problems may be related to respiratory depression, hypoventilation, reduced level of consciousness and inability to protect the airway[4]. Cough depression and risk of aspiration are a serious concern.

Unrecognised respiratory failure may lead to;

  • respiratory muscle fatigue
  • hypoventilation
  • sputum retention
  • Decreased O2 (hypoxaemia)[4]

An acute assessment to establish the underlying cause is imperative as, if respiratory failure is left untreated, it may progress to one or all of the following;

  • cardiac arrhytmia
  • cerebral hypoxaemia
  • respiratory acidosis
  • coma
  • cardiorespiratory arrest

Thus, timely recognition and treatment of respiratory failure is of the utmost importance and a serious part of a patients care.[4]

Hypoxaemia (Type 1 Respiratory Failure)

Hypoxaemia is defined as the inability to maintain the PaO2 above 8kPa. It is an abnormally low level of oxygen in the blood.[3][5] More specifically, it is when there is an oxygen deficiency in arterial blood.[6] Hypoxia is a more general term and represents an abnormally low oxygen content in any tissue or organ, or the body as a whole. [5] Hypoxaemia can cause hypoxia (hypoxemic hypoxia), but hypoxia may also occur via other mechanisms, such as anemia.[7]

There are many causes of Hypoxaemia, it is often due to respiratory disorders, and can cause tissue hypoxia as the blood is not supplying enough oxygen to the body.[5]

Classification and Causes of Hypoxaemia

Classification Cause
Hypoxic hypoxaemia
  • Occurs where blood flows through parts of the lung which are unventilated
  • There is an inability to transfer oxygen across the pulmonary membrane (gas diffusion limitation)
  • Acute bronchoconstriction: asthma (insufficient gas flow in and out of the lung)
  • Insufficient inspired oxygen therapy (including faulty oxygen delivery equipment)
  • Primary respiratory disease: COPD, pulmonary fibrosis, CF, pneumonia, sputum retention, decreased gas transfer across thickened (fibrotic/ oedematous) membrane
  • Primary cardiac disease: heart failure, congestive cardiac failure, pulmonary oedema (causing a diffusion limitation across the respiratory membrane)
Ischaemic hypoxaemia
  • Usually due to inadequate blood flow through the lung
  • Pulmonary embolus
  • Destruction of the pulmonary vasculature (COPD, pulmonary trauma)
Anaemic hypoxaemia
  • Reduction in the oxygen carrying capacity of the blood
  • Shock (significant blood loss with a reduced Hb)
  • Primary haematological diseases, e.g. sickle cell crisis, anaemia
Toxic hypoxaemia
  • Difficulty in the utilisation of oxygen
  • It is common in patients admitted with inhalation burns/ smoke inhalation injuries
  • E.g. carbon monoxide poisoning, cyanide poisoning

[3][4][6]

Clinical Signs

A patient with acute hypoxaemia will display some or all of the following symptom, similar to that of someone in respiratory distress;

  • central cyanosis (blue lips, tongue)
  • peripheral shut-down (cool to touch, 'cold and clammy')
  • tachypnoea - increased respiratory rate (>20 beats per minute)
  • low oxygen saturation (<90%)
  • Increased use of the chest and abdominal muscles to breathe
  • confusion or agitation if profound hypoxaemia, may be non compliant with treatment [4][8]

Chronic hypoxaemia may be compensated or uncompensated. The compensation may result in the symptoms to be overlooked initially, however, a further disease or stress such as any increase in oxygen demand may finally unmask the existing hypoxemia. [9]

Aim of Physiotherapy

The overall aim of physiotherapy is to identify and treat, if appropriate, the cause of the hypoxaemia, thus aiming to increase PaO2 >8kPa while administering appropriate oxygen therapy. [4]

Treatment of Hypoxaemia

The primary treatment for hypoxaemia is controlled oxygen therapy, alongside the identification and treatment of the underlying cause. Patients who are unable to maintain a SaO2 >90% with a face mask may require additional respiratory support. This might include either continuous positive airway pressure (CPAP) or intubation and mechanical ventilation. Patients presenting with a unilateral lung disease can be positioned in side-lying, with the unaffected lung down, to try to improve V/Q matching.[4]

Controlled Oxygen Therapy

Controlled oxygen therapy is prescribed for hypoxaemic patients to increase alveolar oxygen tension and decrease their work of breathing.[10] It is important to remember that oxygen is a drug and should always be prescribed with the required percentage and/or flow rate. It is usually delivered at 24-60% and can be given by an oxygen mask. Lower requirements of 2-4L/min are commonly supplied via nasal cannulae; however, often a mask may be preferable if hypoxic and/or the patient is a mouth breather.[4] If a patient is requiring over 60% oxygen with persistently low oxygen saturation (<90%) a non-rebreather mask should be used to administer constant flow of high concentration oxygen. CPAP is also useful with profound hypoxaemia once a pneumothorax has been excluded.[11]

Humidification

Oxygen therapy is known to dry out the airways. Humidifying oxygen is often used in an attempt to help prevent the drying of the upper respiratory tract. The BTS oxygen guidelines (2008) state that humidification is not required for the delivery of low flow oxygen (4L/minute and under) or short term use of high flow oxygen for short periods.[12] In patients who are requiring high flow oxygen or oxygen for longer periods consider cold or heated humidification. Heated humidification is believed to be better for tenacious secretions or severe bronchospasm. [4]

Treat the cause, e.g. bronchospasm, sputum retention, volume loss

Whilst the delivery of oxygen therapy is the primary treatment for hypoxaemia it is essential to treat the cause. If it is a primary respiratory problem, treat this. If the primary problem is cardiac or renal in origin, discuss this with the medical team to help resolve the presenting issue.[4]

Increased work of breathing

Patients will commonly present with an increased work of breathing. Positioning is essential to reduce breathlessness and improve ventilation perfusion matching[4]. Airway clearance techniques can also be useful if needed. IPPB may be considered (with a high flow rate) to rest the respiratory muscles and improve efficacy of other treatments.

Common Issues in Hypoxaemia

Bronchopneumonia

Bronchopneumonia is a form of pneumonia, sometimes referred to as lobar pneumonia, that also causes inflammation in the bronchi. [13] A patient presenting with bronchopneumonia will present with troubled breathing due to airway constriction. Due to inflammation, their lungs are not adequately ventilated. Symptoms can range from mild to severe. Physiotherapy treatment can include;

  • Ensure medication is optimised (oxygen, analgesia, bronchodilators, antibiotics, etc.)
  • Positioning to decrease work of breathing
  • Airway clearance techniques
  • Humidification[4]

Acute lobar pneumonia

Lobar pneumonia is an acute exudative inflammation of an entire pulmonary lobe, produced in 95% of cases by Streptococcus pneumoniae (pneumococci). If not treated lobar pneumonia progresses in 4 stages; namely consolidation, red hepatization, grey hepatization and resolution.[14] Treatment is dependent on the severity of symptoms and may include some of the following techniques;

  • During the unproductive phase advice on positioning may reduce WOB
  • CPAP is useful for hypoxaemia
  • Sputum clearance s only indicated if the patient becomes productive

Pulmonary embolus

Pulmonary embolism (PE) is a blockage of an artery in the lungs by a substance that has moved from elsewhere in the body through the bloodstream (embolism).[15] Symptoms of a PE may include shortness of breath, chest pain particularly upon breathing in, and coughing up blood. Physiotherapy is not indicated. CPAP may help with severe hypoxaemia.

Pulmonary fibrosis

Pulmonary fibrosis describes a collection of diseases which lead to interstitial lung damage and ultimately fibrosis and loss of the elasticity of the lungs. It is a chronic condition characterised by shortness of breath.[16] The lung tissue becomes thickened, stiff and scarred over a period of time. The development of scar tissue is called fibrosis. As the lung tissue becomes scarred and thicker, the lungs start to lose their ability to transfer oxygen into the bloodstream. Treatment of pulmonary fibrosis may involve;

  • Present with profound hypoxaemia. Humidified CPAP is effective
  • Ensure sufficient oxygen is available when CPAP removed

Pulmonary oedema

Pulmonary oedema occurs when fluid accumulates in the alveoli of the lungs causing an increased work of breathing. This fluid accumulation interferes with gas exchange and can cause respiratory failure.[17] Treating a patient with pulmonary oedema may include;

  • CPAP is effective in the treatment of pulmonary oedema
  • If hypotensive, check that BP does not drop with increased intrathoracic pressure.
  • NIV (pressure support with EPAP) may be useful in the patient tiring on CPAP[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.

  • 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

Fatigue

  • Hypoxaemic patients may start to fatigue. This is seen by a rising PaCO2 - type II respiratory failure failure. An important clinical sign requiring immediate attention

Chronic chest patients

  • Patients who have longstanding chest diseases may have a regular chest clearing routine they adhere to e.g. Bronchiectatic, CF patient
  • It is important to discuss this and mould your treatment plan so that it fits within their existing regimen and their current physiotherapy problems[4]

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[4]

Distended abdomen, e.g. pancreatitis, ascites

  • Positioning in alternate side-lying or well supported high side-lying is useful
  • Standing where possible[4]

References

  1. Respiratory Failure. (2017, October 5). Physiopedia, . Retrieved 12:19, March 27, 2018 from https://www.physio-pedia.com/index.php?title=Respiratory_Failure&oldid=179534.
  2. Tulaimat A, Patel A, Wisniewski M, Gueret R. The validity and reliability of the clinical assessment of increased work of breathing in acutely ill patients. August 2016. Journal of crit care 34:111-5
  3. 3.0 3.1 3.2 Pollak, Charles P.; Thorpy, Michael J.; Yager, Jan (2010). The encyclopedia of sleep and sleep disorders (3rd ed.). New York, NY. p. 104.
  4. 4.00 4.01 4.02 4.03 4.04 4.05 4.06 4.07 4.08 4.09 4.10 4.11 4.12 4.13 4.14 4.15 4.16 Harden B, Cross J, Broad MA. Respiratory physiotherapy: An on-call survival guide. Elsevier Health Sciences; 2009.
  5. 5.0 5.1 5.2 Martin, Lawrence (1999). All you really need to know to interpret arterial blood gases (2nd ed.). Philadelphia: Lippincott Williams & Wilkins.
  6. 6.0 6.1 Eckman, Margaret (2010). Professional guide to pathophysiology (3rd ed.). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins. p. 208. 
  7. Robert J. Mason, V. Courtney Broaddus, Thomas R. Martin, Talmadge E. King, Dean E. Schraufnagel, John F. Murray and Jay A. Nadel (eds.) (2010) Murray & Nadel's Textbook of Respiratory Medicine, 5th ed. Philadelphia: Saunders Elsevier
  8. Colledge NR, Walker BR, Ralston SH, eds. (2010). Davidson's principles and practice of medicine (21st ed.). Edinburgh: Churchill Livingstone/Elsevier.
  9. Adde, FV; Alvarez, AE; Barbisan, BN; Guimarães, BR (Jan–Feb 2013). "Recommendations for long-term home oxygen therapy in children and adolescents". Jornal de pediatria. 89 (1): 6–17. 
  10. Hardinge M, Annandale J, Bourne S, Cooper B, Evans A, Freeman D, Green A, Hippolyte S, Knowles V, MacNee W, McDonnell L. British Thoracic Society guidelines for home oxygen use in adults: accredited by NICE. Thorax. 2015 Jun 1;70(Suppl 1):i1-43.
  11. Machado ML, Vollmer WM, Togeiro SM, Bilderback AL, Oliveira MC, Leitão FS, Queiroga F, Lorenzi-Filho G, Krishnan JA. CPAP and survival in moderate-to-severe obstructive sleep apnoea syndrome and hypoxaemic COPD. European Respiratory Journal. 2010 Jan 1;35(1):132-7.
  12. O’driscoll BR, Howard LS, Davison AG. BTS guideline for emergency oxygen use in adult patients. Thorax. 2008 Oct 1;63(Suppl 6):vi1-68.
  13. Blaisdell FW. Pathophysiology of the respiratory distress syndrome. Arch Surg. 1974 Jan 1;108(1):44-9.
  14. Pneumonia. (2018, January 9). Physiopedia, . Retrieved 11:29, March 31, 2018 from https://www.physio-pedia.com/index.php?title=Pneumonia&oldid=182184.
  15. Dalen JE, Alpert JS. Natural history of pulmonary embolism. Progress in cardiovascular diseases. 1975 Jan 1;17(4):259-70.
  16. Gribbin J, Hubbard RB, Le Jeune I, Smith CJ, West J, Tata LJ. Incidence and mortality of idiopathic pulmonary fibrosis and sarcoidosis in the UK. Thorax. 2006 Nov 1;61(11):980-5.
  17. Masip J, Betbesé AJ, Páez J, Vecilla F, Cañizares R, Padró J, Paz MA, de Otero J, Ballús J. Non-invasive pressure support ventilation versus conventional oxygen therapy in acute cardiogenic pulmonary oedema: a randomised trial. The Lancet. 2000 Dec 23;356(9248):2126-32.