Hypoxaemia: Difference between revisions

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== Respiratory Failure ==
== Respiratory Failure ==
[https://www.physio-pedia.com/Respiratory_Failure Respiratory failure] is demonstrated in [https://www.physio-pedia.com/Arterial_Blood_Gases arterial blood gas] (ABG) tensions. Type I respiratory failure is defined as PaO2 <8.0kPa with a normal or lowered PaCO2. 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. 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. Cough depression and risk of aspiration are a serious concern. Unrecognised respiratory failure leads to;
[https://www.physio-pedia.com/Respiratory_Failure Respiratory failure] is demonstrated in [https://www.physio-pedia.com/Arterial_Blood_Gases arterial blood gas] (ABG) tensions. Type I respiratory failure is defined as PaO2 <8.0kPa with a normal or lowered PaCO2.<ref name=":0">Pollak, Charles P.; Thorpy, Michael J.; Yager, Jan (2010). ''The encyclopedia of sleep and sleep disorders'' (3rd ed.). New York, NY. p. 104.</ref> 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.<ref name=":1">Harden B, Cross J, Broad MA. Respiratory physiotherapy: An on-call survival guide. Elsevier Health Sciences; 2009.</ref> 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. Cough depression and risk of aspiration are a serious concern. Unrecognised respiratory failure leads to;
* respiratory muscle fatigue
* respiratory muscle fatigue
* hypoventilation
* hypoventilation
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* coma
* coma
* cardiorespiratory arrest
* cardiorespiratory arrest
Thus, timely recognition and treatment of respiratory failure is of the utmost importance and a serious part of a patients care.  
Thus, timely recognition and treatment of respiratory failure is of the utmost importance and a serious part of a patients care.<ref name=":1" />


== Hypoxaemia (Type 1 Respiratory Failure)  ==
== Hypoxaemia (Type 1 Respiratory Failure)  ==
Hypoxaemia is defined as the inability to maintain the PaO2 above 8kPa
Hypoxaemia is defined as the inability to maintain the PaO2 above 8kPa. It is an abnormally low level of oxygen in the blood.<ref name=":0" /><ref name=":2">Martin, Lawrence (1999). ''All you really need to know to interpret arterial blood gases'' (2nd ed.). Philadelphia: Lippincott Williams & Wilkins.</ref> More specifically, it is when there is an oxygen deficiency in arterial blood.<ref name=":3">Eckman, Margaret (2010). ''Professional guide to pathophysiology'' (3rd ed.). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins. p. 208. </ref> 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.<ref name=":2" />


== Classification and Causes of Hypoxaemia  ==
== Classification and Causes of Hypoxaemia  ==
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|E.g. carbon monoxide poisoning, cyanide poisoning
|E.g. carbon monoxide poisoning, cyanide poisoning
|}
|}
<ref name=":0" /><ref name=":1" /><ref name=":3" />


== Clinical Signs ==
== Clinical Signs ==

Revision as of 14:16, 27 March 2018

Respiratory Failure[edit | edit source]

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.[1] 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.[2] 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. Cough depression and risk of aspiration are a serious concern. Unrecognised respiratory failure leads to;

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

Acute assessment to establish the underlying cause is imperative as, if left untreated, it may progress to any 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.[2]

Hypoxaemia (Type 1 Respiratory Failure)[edit | edit source]

Hypoxaemia is defined as the inability to maintain the PaO2 above 8kPa. It is an abnormally low level of oxygen in the blood.[1][3] More specifically, it is when there is an oxygen deficiency in arterial blood.[4] 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.[3]

Classification and Causes of Hypoxaemia[edit | edit source]

Classification Cause
Hypoxic hypoxaemia
  • Where blood flows through parts of the lung which are unventilated
  • 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 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 oxygen utilisation - common in patients admitted with inhalation burns/ smoke inhalation injury
E.g. carbon monoxide poisoning, cyanide poisoning

[1][2][4]

Clinical Signs[edit | edit source]

A patient with hypoxaemia will display some/all of the following symptoms;

  • 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%)
  • confusion or agitation if profound hypoxaemia, may be non compliant with treatment

Aim of Physiotherapy[edit | edit source]

To identify and treat, if appropriate, the cause of the hypoxaemia, thus aiming to increase PaO2 >8kPa while administering appropriate oxygen therapy

Treatment of Hypoxaemia[edit | edit source]

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

Controlled Oxygen Therapy[edit | edit source]

  • Oxygen is a drug which should be prescribed for the required percentage and/or flow rate
  • Usually 24-60% can be given by an oxygen mask
  • 2-4L/min via nasal cannulae; however, a mask may be preferable if hypoxic and/or mouth breather
  • Over 60% oxygen with persistently low sats (<90%) use a non-rebreather mask to administer constant flow of high concentration oxygen
  • CPAP is useful with profound hypoxaemia once pneumothorax excluded

Humidification[edit | edit source]

  • Consider cold or heated humidification
  • Heated is better for tenacious secretions or severe bronchospasm

Treat the cause, e.g. bronchospasm, sputum retention, volume loss[edit | edit source]

  • If primary respiratory problem, treat this
  • If primary problem is cardiac or renal, discuss this with the medical team

Increased work of breathing[edit | edit source]

  • Use airway clearance techniques if needed
  • Positioning is essential to reduce breathlessness and improve ventilation perfusion matching
  • IPPB may be useful (with a high flow rate) to rest the muscles and improve efficacy of other treatments

Common Issues in Hypoxaemia[edit | edit source]

Bronchopneumonia[edit | edit source]

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

Acute lobar pneumonia[edit | edit source]

  • 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[edit | edit source]

  • physiotherapy is not indicated. CPAP may help with severe hypoxaemia

Pulmonary fibrosis[edit | edit source]

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

Pulmonary oedema[edit | edit source]

  • 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

CO2 retention[edit | edit source]

  • 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[edit | edit source]

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

Chronic chest patients[edit | edit source]

  • 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

Renal failure[edit | edit source]

  • 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

Distended abdomen, e.g. pancreatitis, ascites[edit | edit source]

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

Oesophageal varices[edit | edit source]

  • Dilated blood vessels in the oesophagus can rupture with increased pressure
  • Care should be taken when coughing, suctioning is contraindicated
  • Prevent chest infection by positioning, teaching huff, mobilize if tolerated

References[edit | edit source]

  1. 1.0 1.1 1.2 Pollak, Charles P.; Thorpy, Michael J.; Yager, Jan (2010). The encyclopedia of sleep and sleep disorders (3rd ed.). New York, NY. p. 104.
  2. 2.0 2.1 2.2 Harden B, Cross J, Broad MA. Respiratory physiotherapy: An on-call survival guide. Elsevier Health Sciences; 2009.
  3. 3.0 3.1 Martin, Lawrence (1999). All you really need to know to interpret arterial blood gases (2nd ed.). Philadelphia: Lippincott Williams & Wilkins.
  4. 4.0 4.1 Eckman, Margaret (2010). Professional guide to pathophysiology (3rd ed.). Philadelphia: Wolters Kluwer/Lippincott Williams & Wilkins. p. 208.