Estimated Reading Time: 5 minutes

It’s 4am and you are working in the Emergency Department when an 80 year old if brought into the Resus Room with shortness of breath. She is tachypnoeic and tachycardic with low saturations despite high flow oxygen. She says to you “I think I’m dying”.

Learning Objectives

  • Consider the physiology of shortness of breath and how this may guide our management.
  • Think about the five top main causes of life threatening shortness of breath.

With all of the life threatening presentations the patient is struggling to get enough oxygen into their cells. Thie is why we focus on the ABC – Airway/Breathing/Circulation – of resuscitation. All three of these are vital to get oxygen into our lungs, our bloodstream and ultimately our cells.

In the patient with shortness of breath we are going to, unsurprisingly, be focussing on B. There are two predominant mechanisms that the lungs must be able to perform

Mechanical – the lungs cannot expand

In order to ‘suck’ oxygen into the alveoli, the lungs have to expand to create a negative pressure and draw gas in. To do this the chest wall has to be able to move easily and freely and in turn the lungs will expand.

Diffusion – gas cannot get into (and out of) the blood

Anything that gets in the way of the gases diffusing across the alveoli membrane, for example infection or fluid.


There may be things happening outside the lungs that mean the respiratory rate changes, such as metabolic acidosis (where the lungs are helping get rid of increaseed CO2)


As we mention often, oxygen is the key to resuscitation. Without adequate oxygen in cells they die. When enough cells die, organs die. And when organs die patients die. One of our first actions in the patient who is struggling to breath (which is usually due to a lack of oxygen) is to give them more.

The ‘non-rebreather’ oxygen mask

The so called ‘non rebreath’ mask (I prefer ‘mask with reservoir’) is our go to in the acutely unwell patient. I’m sure you have seen these, but have you ever considered how they work?

Let’s think about normal respiratory physiology.

  1. Respiratory rate – 12-20 breaths per minute
  2. Inspiratory:expiratory ratio = 1:3 (we breath in for 1 second and out for 3 seconds every breath)
  3. Tidal volume (the amount of gas we breath in at rest) = 500mls

From this we can work out the inspiratory flow rate – how fast we suck gas in to our lungs. Over one second for breath in 500mls of air, which is a rate of 30 litres per minute.

You will have seen that he maximum flow rate we can get from wall oxygen is ‘only’ 15 litres per minute, so with a standard mask (with no reservoir) the maximum the gas from the wall will only supply 50% of the patient’s breath. The other half will come from entrained room air (that is 21% oxygen). Therefore, the maximum oxygen concentration we could achieve would be about 60%.

It’s important to remember that our patients will not be breathing at his nice slow rate, and as the number of breathes per minute increases, so must the inspiratory flow rate, to get the same amount of air in, or the depth of breathing (the tidal volume) must increase, or both.

The reservoir bag is usually about 1 litre in capacity and this fills during expiration: the two sets of unidirectional valves make sure that gas can only flow into the bag and then out of the mask. In order for this to fill up at rest there must be enough flow (and time) to fill the bag.

As the mask is not completely sealed there will still be some entraining of room air, so we will never achieve an inspired concentration of 100%. The only way to do this would be a closed system (ie intubation).

But what about CO2 retainers?

Hypoxia kills quickly. Hypercarbia takes its time.

In the resuscitation room where we are watching the patient very closely we can afford to give them high flow oxygen as if there is a change we will spot it. However, you should never leave a patient on high flow oxygen for longs periods of time without close monitoring.

It is also worth noting that ‘loss of hypoxic drive’ is almost certainly not the cause of a rising CO2 in the patient on oxygen.

Acute left ventricular failure

This is a problem with ‘diffusion’ – the left ventricle isn’t working sufficiently, so the blood ‘backs up’ into the left atrium, pulmonary veins and lungs. The rise in pressure causes an increase in interstitial pressure and mean gas cannot diffuse across the alveolar membrane.


This is another situation where diffusion is affected due to the infective exudate that is sitting in the alveoli.

Asthma and COPD

These are very different diseases, but we often link them together because their treatment is similar. This is an issue with getting oxygen in (and carbon dioxide out) of the alveoli due to bronchoconstriction.

Pulmonary Embolism

Here the blood isn’t getting to the alveoli to receive the oxygen.


As the lung has lost volume, secondary to extra air between the parietal and visceral pleura, the lung is unable to expand.