Respiratory failure occurs when there is an impairment in the gas exchange between blood and the lungs leading to a failure to meet metabolic demands for oxygen. It can be divided into two types that are characterised by hypoxaemia ± hypercapnia. We will discuss this further, but first let’s recap the physiology of respiratory drive:
🏃♀️ Physiology
Chemoreceptors are integral to the respiratory system and regulation of our breathing. We have 2 groups of chemoreceptors to consider:
- Peripheral chemoreceptors - located in the carotid body and aortic body. They are sensitive to partial pressure of oxygen (pO2). Low levels of oxygen are detected here, sending afferent impulses via the glossopharyngeal nerve and vagus nerve → medulla oblongota and pons. These respond with 3 mechanism to restore the pO2:
- Increased respiratory rate and tidal volume - to allow more oxygen to enter the lungs and subsequently the blood.
- Blood flow - more blood is directed to our kidneys and brain as they are most sensitive to hypoxia.
- Increased cardiac output - to maintain blood flow to the lungs to receive more oxygen and thus supply to the tissues.
- Central chemoreceptors - located in the medulla of the brainstem. They are sensitive to partial pressure of carbon dioxide (pCO2). Changes that are detected here cause impulses to be sent to the respiratory centres in the brainstem to either increase or decrease ventilation to restore the normal pCO2. The mechanism by which they detect these changes relates to cerebral spinal fluid (CSF):
The pH of CSF is based on the ratio of pCO2:[HCO3-]. The HCO3- in the CSF is relatively constant but CO2 is able to move in and out of the BBB freely. It then reacts with H2O to produce carbonic acid (H2CO3) to lower the pH. Therefore if there is too much CO2, we produce excess carbonic acid and we get acidaemia.
- A decrease in pCO2 increases the pH of the CSF → respiratory centres stimulated to decrease ventilation.
- An increase in pCO2 decreases the pH of the CSF → respiratory centres stimulated to increase ventilation.
However, if there is a prolonged change to pCO2 levels, the choroid plexus allows HCO3- ions to enter the CSF which alters the pH but also alters the baseline and as a result we are able to retain more CO2. This is especially true in diseases such as COPD.
Pathophysiology
Ventilation-perfusion ratio (V/Q ratio) refers to the volume of air inhaled and exhaled from the lungs in a minute (tidal volume x respiratory rate) in comparison with the total volume of blood reaching the pulmonary capillaries in the same amount of time.
The average ventilation rate in a man is 6L/min.
The ratio differs at the apex of the lungs compared to the base:
- Apex - 3.3 (more ventilation and less perfusion).
- Base - 0.63 (less ventilation and more perfusion).
These differences occur due to the effect of gravity increasing the amount of perfusion we get relative to the amount of ventilation. The overall average V/Q ratio is close to 0.8 actually.
V/Q mismatches can occur due to either reduced ventilation or reduced perfusion which results in a failure for the oxygen demand to meet the body’s metabolic demands. This leads to acid-base imbalances
A reduction in ventilation affects oxygen levels primarily as CO2 is able to diffuse despite the impairment. This leads to hypoxia but not hypercapnia as the CO2 is still able to diffuse out despite the impairment. However, it may progress to a point where CO2 saturation cannot diffuse out at a sufficient rate which leads to hypercapnia eventually.
🔢 Classification and causes
There are 2 types of respiratory failure that can occur:
- Type 1 respiratory failure (hypoxaemic respiratory failure) - low levels of oxygen in the blood without high levels of carbon dioxide. It is characterised by a PaO2 <8kPa (however, in chronic lung disease it can be as a low as 6.7kPa and this is defined as a decrease 10% below the baseline). It is caused by either poor ventilation or poor perfusion.
- Type 2 respiratory failure (hypercapnic respiratory failure) - low levels of oxygen in the blood coupled with high levels of carbon dioxide (PaCO2 >6kPa).
Type 1 respiratory failure
The volume of air passing in and out of the lungs is smaller than the volume of blood that perfumes the lungs. However, it in pulmonary embolism it may cause a mismatch with less perfusion than ventilation.
It is usually a small portion of lung tissue that is affected Leading to a compensation with other lung tissue excreting carbon dioxide normally.
Some common causes include:
- Pneumonia
- Pulmonary oedema
- Pulmonary embolism
- Pneumothorax
- Pulmonary fibrosis
However, it is important to note that the causes of type 1 and type 2 respiratory failure are not exclusive to the groups alone.
Type 2 respiratory failure
It is due to alveolar hypoventilation which causes impaired CO2 excretion. It is usually due to a mismatch across a larger region/entire lung as opposed to a small region of lung tissue.
Some common causes include:
- COPD - increased resistance of airways.
- Kyphosis/scoliosis
- CNS depression - opioids or sedatives
- Severe asthma
- Myasthenia gravis - impaired pumping performance.
- Guillan-Barre syndrome - also causes respiratory muscle weakness.
- Obesity
- ARDS
- Upper airway obstruction
It is more dangerous as an increased PaCO2 leads to respiratory acidosis which can be potentially fatal.
😷 Presentation
- Dyspnoea
- Tachypnoea
- Accessory muscle use
- Cyanosis
Hypercapnia can lead to some specific features such as: headache, confusion, behavioural changes, asterixis, papilloedema (due to cerebral vascular dilation and increased ICP).
🔍 Investigations
- Pulse oximetry - generally speaking when SpO2 is <92% at sea level, there will be clinical signs of acute respiratory failure. An
- ABG - we will discuss a lot more on respiratory acidosis/alkalosis and metabolic acidosis/alkalosis on the page on ABGs.
- Type 1 respiratory failure - hypoxaemia (PaO2 <8kPa) with normocapnia (PaCO2 <6.0kPa).
- Type 2 respiratory failure - hypoxaemia (PaO2 <8kPa) with hypercapnia (PaCO2 >6.0kPa).
- Other aspects to note are the pH, HCO3-, for signs of acidosis/alkalosis. However, this will be discussed in a separate section.
- Spirometry
- ECG - cardiac arrhythmias may occur secondary to acidosis and hypoxaemia.
🧰 Management
The most appropriate management is to treat underlying cause.
- Supplemental oxygen - can be provided via a nasal cannula, Venturi mask or non-rebreathe mask.
- In patients who need further respiratory support we can step it up to non-invasive ventilation (NIV).
- If this is not sufficient endotracheal intubation or tracheostomy may be done.
This is the alternative option to intubating a patient and ventilating the lungs artifically. NIV involves a full face mask or nasal mask that blows air into the lungs to ventilate them without the need to intubate them.
There are 2 main options:
- Bilevel positive airway pressure (BiPAP)
- Continuous positive airway pressure (CPAP)
BiPAP
BiPAP involves cyclical high and low pressures that correspond with inspiration and expiration from the patient.
The criteria for BiPAP is respiratory acidosis (pH <7.35 and PaCO2 >6.0kPa) despite medical treatment.
We should ensure that there is no pneumothorax prior to giving NIV. A chest X-ray should be done to confirm this if it does not cause a delay. It is also important to discuss what the progression from NIV would be if it fails (escalating to intubation and ICU or to move to palliative care).
As we said it is cyclical, so there are 2 types of pressures with BiPAP:
- Inspiratory PAP - the pressure provided during inspiration forcing air into the lungs. For an average male the starting point is 16-20cm H2O.
- Expiratory PAP - the pressure provided during expiration to ensure that the airways don’t collapse and also facilitating remove of all in patients with obstructive lung diseases. For an average male the starting point is 4-6cm H2O.
We should increase by 2-5cm increments until the acidosis resolves.
CPAP
Provides air by continuously blowing into the lungs to keep them expanded to allow air to travel in and out easily, especially in patients who are at risk of airway collapse.
Indications for CPAP include:
- Obstructive sleep apnoea
- Congestive heart failure
- Acute pulmonary oedema
