Acute Hypoxia: An Overview

Review Article

Austin J Emergency & Crit Care Med. 2020; 6(1): 1069.

Acute Hypoxia: An Overview

Weledji EP¹*, Ngomba MN² and Njie KT³

¹Department of Surgery, Faculty of Health Sciences, University of Buea, Cameroon

²Intensive Care Unit, Regional Hospital limbe, S.W. Region, Cameroon

³Infectious Disease & Community Health, Director, Regional Hospital Limbe, S.W. Region, Cameroon

*Corresponding author: Weledji EP, Pemset House, Lumpsum Qrts, Limbe, S.W. Region, Cameroon

Received: February 15, 2020; Accepted: April 13, 2020; Published: April 20, 2020


Hypoxia kills and kills quickly. In the healthy individual total oxygen delivery far exceeds total oxygen consumption. An acute hypoxic patient would therefore be critically ill and need oxygen. The assessment of the suitability of a patient to withstand surgery and anaesthesia is closely related to their ability to increase oxygen delivery to vital tissues. Optimizing these factors would maximize the patient’s reserves. Oxygen is only one aspect of treatment and the underlying cause of the respiratory failure must be treated. This article reviewed acute hypoxia, respiratory failure and the indications for oxygen therapy.

Keywords: Hypoxia; Acute; Respiratory failure; Monitoring; Oxygen therapy


Respiratory failure occurs when pulmonary gas exchange is sufficiently impaired to cause hypoxaemia with or without hypercarbia. In practical terms, respiratory failure is present when the partial pressure of arterial oxygen (PaO2) is <8KPa (60mmHg) i.e. an arterial saturation of oxygen (Sa02) of <90% or the partial pressure of arterial carbon dioxide (PaCO2) is >7kPa (55mmHg). The normal PaO2 is 75-100mmHg (10-13.3KPa). It is the oxygen content of the arterial blood that matters and this is determined by the percentage saturation of haemoglobin (Hb) with oxygen. The measure of the oxygen saturation of Hb-oxyhaemoglobin gives an estimate +/-2% of the percentage of oxygen carrying sites which are occupied in Hb. The maximum number of sites which could be occupied is obviously 100%. Thus the normal oxygen saturation for arterial blood (SaO2) is 95- 100% (Figure 1). In health SaO2 is normally near maximal i.e. around 97%. Oxygen supplementation should ideally be given when oxygen saturation is <95%. Pulmonary distribution of blood flow is improved by hypoxia as a result of hypoxic pulmonary vasoconstriction to favour ventilation-perfusion matching. The persistence of chronic alveolar hypoxia and hypercapnoea leads to constriction of the pulmonary arterioles and subsequent pulmonary arterial hypertension [1,2]. It is also important to appreciate that the lungs normally never empty completely. At the end of each breath an ‘average’ man with a total lung capacity (TLC) of 6 litres will still have around 2.5 litres of gas in the lungs (functional residual capacity, FRC) and even if he expires as much as he can the expiratory reserve volume, (ERV) he will only reduce this to 1.2 litres (residual volume, RV) (Figure 2) [3]. In addition, the signs of hypoxia are generally non-specific and often difficult to assess. The primary aim of the management of respiratory failure is to improve the PaO2 by continuous controlled oxygen therapy. This nearly always leads to a rise in the PaCO2. A small increase in PaCO2 can be tolerated but not if the pH falls dramatically or below 7.25. Under such circumstances, increased ventilation must be achieved either by the use of a respiratory stimulant or artificial ventilation [4]. However, oxygen is only one aspect of treatment and the underlying cause of the respiratory failure must be treated.