Hypoxaemia: Reversible Causes of Cardiac Arrest
Published: 29 April 2020
Published: 29 April 2020
Hypoxaemia is the reduction in the values for partial pressure of oxygen dissolved in arterial blood (PaO2) and arterial oxygen saturation (SaO2) (Bullock & Hales 2013). Pa02 is best measured by arterial blood gas (ABG) analysis, while SaO2 can be routinely assessed using a non-invasive test called pulse oximetry.
During clinical assessment, hypoxaemia should be considered if a patient has a respiratory rate greater than 24 per minute, and arterial oxygen saturations (SaO2) below 94% on room air (Rittayamai et al. 2015). Clinically, however, hypoxaemia is defined as: PaO2 < 8 kilopascals (kPa), or 60 millimetres of mercury (mmHg), on ABG (Bullock & Hales 2013).
The degree of hypoxaemia is reflected in the PaO2 value. There is no standardisation of hypoxic thresholds (Allwood et al. 2018), however they are commonly divided into three categories:
|Mild hypoxaemia||Moderate hypoxaemia||Severe hypoxaemia|
When hypoxaemia and acute dyspnoea occur together – such as in acute pulmonary oedema (APO), pneumonia, or during exacerbation of chronic obstructive pulmonary diseases (COPD) – it constitutes a medical emergency. If the hypoxaemia is not reversed by administering oxygen it can precipitate cardiac arrest (Rittayamai et al. 2015).
Prolonged or severe hypoxaemia causes tissue to become hypoxic, resulting in anaerobic metabolism and altering the patient’s acid-base balance (Deranged Physiology 2020; Pruitt 2004). This can precipitate cardiac arrest.
Oxygen therapy should be administered to treat hypoxaemia, however, exposing a patient to high concentrations of oxygen for long periods of time can result in life-threatening oxygen toxicity (Cooper & Shah 2019). Hyperoxia, the state of too much oxygen, can affect the pulmonary system, the retinas and the central nervous system (Bullock & Hale 2013; ANZCOR 2016).
It is therefore imperative to provide sufficient oxygen to manage the patient safely and prevent deterioration, whilst ensuring that excessive amounts are not delivered. Clarify correct therapeutic oxygen levels with the medical team prior to commencing.
Firstly, ensure that the patient’s airway is open and clear. Mechanical causes of airway obstruction – such as foreign bodies (food, mucous plugs etc.) – should be excluded, and addressed if able, before proceeding (Resus Council UK 2020).
Ensure that your oxygen source is connected properly. Give the maximal feasible inspired oxygen concentration via a bag valve mask (BVM) connected to a face mask or airway adjunct such as an endotracheal tube (ETT) or laryngeal mask airway (LMA).
Assess for adequate ventilation by performing a thorough respiratory assessment including observing the patient for bilateral chest rise and fall, chest auscultation and ETCO2 monitoring.
If administering with an ETT, capnography is the most reliable indicator that an endotracheal tube is placed in the trachea after intubation, followed by a thorough respiratory assessment (Krauss et al. 2020).
Note: Accredited clinicians have less than five seconds to intubate under critical circumstances, as priority is recommencing CPR immediately to maintain perfusion. Tracheal intubation should therefore only be attempted by those who are trained, competent and experienced in the skill (Australian Resuscitation Council 2020).
Early intubation is no longer advocated as the preferred method of managing an airway during cardiac arrest (Australian Resuscitation Council and New Zealand Resuscitation Council Whakahauora Aotearoa 2016), but exceptions are high-risk patients for whom laryngoscopy and intubation may become more difficult over time (includes those with airway burns, laryngeal oedema secondary to anaphylaxis, or severe facial trauma).
After return of spontaneous circulation (ROSC), as soon as arterial blood oxygen saturation can be monitored reliably using ABGS and pulse oximetry, the inspired oxygen concentration level should be titrated to maintain SaO2 between 94% and 98% (Soar et al. 2015).
Cardiac arrest is not always a sudden, unpredictable event, and some patients can demonstrate slow but progressive physiological deterioration. When this is unnoticed or mismanaged, poorer outcomes are the result.
Early, effective recognition and response to signs of hypoxaemia will prevent some cardiac arrests, deaths and unanticipated ICU admissions (Soar et al. 2015).