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What is respiratory failure? What are the different types?

Respiratory failure may be acute, chronic or acute on chronic (e.g. a patient with an exacerbation of COPD and pre-existing hypoxia). Abnormal levels of arterial oxygen (<8kPa) or carbon dioxide (>6kPa) are used to define the presence of respiratory failure, which is divided into 2 types:

1) Type I (hypoxic) failure: failure of oxygenation
2) Type 2 (hypercapnic) failure: failure of ventilation to remove CO2

Generally, hypercapnic failure is the result of a disorder with respiratory muscles ("pump failure"), whereas hypoxaemic failure is usually due to pulmonary pathology. However, type II failure often supersedes type I failure as the patient becomes exhausted.


What is the A-a gradient?

Alveolar O2 and CO2 are interdependent and high alveolar partial pressures of carbon dioxide results in a lower partial pressure of oxygen. The alveolar - arterial gradient, is calculated from the alveolar gas equation and is a measure of ventilation and perfusion mismatch (reflecting the severity of lung disease).

A-a gradient = FiO2 - PaO2 - 1.25(PCO2)


What is a normal A-a gradient?

2-4kPa is the normal range. It increases with age and FiO2 >0.28 (FiO2 = fraction of oxygen in inspired air).


What diseases increase the A-a gradient?

Hypoxaemia is low arterial partial pressure of oxygen (this is slightly different to hypoxia, which is a low TISSUE partial pressure of oxygen).

It is caused by decreased PAO2, diffusion defect, V/Q mismatch, and right to left shunts.

The A-a gradient can be used to compare the causes of hypoxaemia. As already mentioned, it is normally between 2 - 4 kPa, since O2 normally equilibrates between alveolar gas and arterial blood PAO2 is approximately equal to PaO2.

The A-a gradient is increased (i.e. >4kPa) if O2 does not equilibrate between alveolar gas and arterial blood and PAO2 is GREATER than PaO2.


What are the causes of hypoxaemia (and therefore type 1 respiratory failure)?

Hypoxaemia can be caused by:
1) Shunt (e.g. Eisenmenger's): the lung is perfused but not ventilated (the opposite of dead space). A right to left shunt leads to hypoxaemia

2)Ventilation/ perfusion mismatch (e.g. PE, pulmonary oedema, COPD/ obstruction, pneumonia): THIS IS THE MOST COMMON CAUSE OF HYPOXAEMIA. Even in diseases like pulmonary fibrosis where one might expect diffusion block. Poorly ventilated alveoli contribute to hypoxaemia which cannot be compensated for alone by increasing ventilation.

3) Diffusion block (e.g. Fibrosis): a thickened interstitium between alveolus and capillary (uncommon). Only important during exercise when erythrocytes have insufficient time to equilibrate for gas exchange.

4) Low FiO2 (e.g. altitude)

5) Hypoventilation (e.g. drug overdose - opiates): ventilation is inversely proportional to PaCO2. The interdependence of PaO2 and PaCO2 thus leads to hypoxaemia in hypoventilation


Of the causes of hypoxaemia and therefore type I failure, which are associated with an increased A-a gradient?

The A-a gradient increases only when oxygen cannot equilibrate across the alveolar capillary membrane, therefore in hypoxaemia caused by hypoventilation and low FiO2 the A-a gradient is normal. All other causes of hypoxaemia are associated with increased A-a gradients.


Which cause of hypoxaemia cannot be corrected for by increasing FIO2 (i.e. with supplementary oxygen)?

A right to left shunt leads to hypoxaemia that does NOT respond to 100% oxygen.


What are the signs of type I respiratory failure?

- central cyanosis
- decreased PaO2; normal PaCO2
- agitated
- confused
- coma
- tachypnoeic
- dyspnoeic
- tachycardic


What is hypoxia?

Is decreased oxygen delivery to tissues. It is caused by decreased blood flow, hypoxaemia, decreased Hb concentrations, CO poisoning and cyanide poisoning.


What determines oxygen delivery to tissues?

This is described by the following equation:

O2 delivery = Cardiac output x O2 content

O2 content of blood depends on Hb concentration, O2 binding capacity of Hb and PO2 (which determines % saturation of Hb by O2).

Anything that affects cardiac output and O2 content can lead to hypoxia (not just hypoxaemia).


Name some causes of hypoxia?

1) Decreased cardiac output - causes hypoxia by decreased blood flow
2) Hypoxaemia - decreased PaO2 causes decr. % saturation of Hb
3) Anaemia - decreased [Hb] causes decr. oxygen content of blood
4) CO poisoning - decr. O2 content
5) Cyanide poisoning - decr. O2 utilization by tissues


How does the body respond to tissue hypoxia?

Hypoxia induces EPO synthesis. This is a growth factor that is synthesized in the kidneys in response to hypoxia. Decreased oxygen delivery to the kidney causes increased production of hypoxia-inducible factor 1 alpha. This directs the synthesis of mRNA for EPO which ultimately promotes development of mature RBCs.


What causes hypercapnia?

This is a PaCO2 of <6kPA. Hypercapnia is associated with type 2 respiratory failure alongside low PaO2. It is caused by pump failure or ventilatory failure, causes include:

1) defective central control of breathing - e.g. drug overdose, most causes of coma
2) neuromuscular disease - ALS, spinal cord lesions, MG, GBS, polio
3) chest wall disease - kyphoscoliosis, large effusions
4)primary lung disease - COPD


What is key in the management of respiratory failure?

It is important to establish whether the onset of respiratory failure is acute, chronic or acute on chronic. The key to managing respiratory failure is treating the underlying disease process. There are various strategies for treating hypoxia and hypercapnia that occur in respiratory failure.


What variable performance oxygen devices can be used in the treatment of hypoxaemia associated with respiratory failure?

Oxygen can be delivered by variable or fixed performance devices:

Variable performance devices: air is entrained during breathing whilst oxygen is delivered from a reservoir. The latter may be the nasopharynx, mask or reservoir bag. The FiO2 delivered to the lungs therefore depends on the oxygen flow rate, the patients inspiratory flow, respiratory rate, and the amount of air entrained.

- e.g. nasal cannulae: flow rates up to 4L/min, nasopharynx is the reservoir
- e.g. face mask: flow rates exceed 5L/min to stop rebreathing of CO2
- e.g. non re breath masks: these have a reservoir bag. A one way valve stops exhaled air entering the oxygen reservoir. High flow rates 10-15L/min provide FiO2 >60%


What fixed performance devices are used in the management of hypoxaemia associated with respiratory failure?

These are independent of the patients pattern of breathing and use the Venturi device to entrain air into the mask, exceeding inspiratory flow and thus deliver a fixed oxygen concentration. These are typically colour coded.


What is CPAP?

CPAP, or continuous positive airways pressure, uses a tight fitting mask and a flow generator to deliver a positive pressure throughout the respiratory cycle (5-15cmH2O). This increases functional residual capacity, thereby recruiting more alveoli and improving oxygenation. CPAP is applied in the same way as NIV but it is NOT a form of ventilation.

Intubation and mechanical ventilation may be required if hypoxia does not respond to treating the underlying disease, oxygen therapy or CPAP.


When is CPAP used?

CPAP recruits collapsed lung units and keeps them open during expiration by applying a continuous positive pressure. Consequently, V/Q relationships improve and oxygenation increases.

CPAP is used in cardiogenic pulmonary oedema, pneumonia, and in obstructive sleep apnoea where it helps prevent upper airway collapse.


What level of oxygenation should be achieved in respiratory failure?

Generally, one should aim for oxygen saturations exceeding 90% as this puts the patient on the flat part of the oxygen dissociation curve. Further increases in PaO2 will only have small effects on oxygen delivery (as almost all the oxygen in blood is bound to haemaglobin)

BTS guidelines recommend saturations of 94-98% in acutely ill patients, or 88-92% for those at risk of hypercapnia.


What patients should not be given 100% oxygen?

Patients at risk of hypercapnic respiratory failure, most commonly seen in COPD. Patients who have tolerated high levels of CO2 may become dependent on hypoxaemia providing a drive to breath. Oxygen delivery may remove this drive and stop them breathing (even if they are well oxygenated!).


How should hypercapnia seen in respiratory failure be managed?

Any sedative drugs should be reversed or avoided (e.g. opiates, BDZ). If hypercapnia and respiratory acidosis persist despite treating the underlying condition, artificial ventilation should be considered. Non invasive ventilation is now widely available and can be delivered via nasal, face, full face or helmet interfaces. It is not a substitute for invasive ventilation, which should be given if this method fails.


What are the normal values of arterial blood gases?

pH 7.35-7.45
PaCO2 4.5-6kPa
PaO2 10-13kPa
HCO3 22-26mmol/L
BE -2 to +2


When is BIPAP used?

BIPAP (Bilevel Positive Airway Pressure) is a form of non-invasive ventilation that has been shown to be very effective in acute type two respiratory failure. It works by stenting alveoli open to increase the surface area available for ventilation and gas exchange. A BIPAP machine alternates between the IPAP (Inspiratory Positive Airway pressure) applied when a patient breathes in and the EPAP (Expiratory Positive Airway Pressure) which is applied between patient triggered breaths. A minimum respiratory rate can be set on the machine and the pressures up-titrated as tolerated. Regular arterial blood gas analysis in needed to asses the patients response to NIV.

CPAP (Continuous Positive Airway Pressure) is another form of non-invasive ventilation but is not as effective as BIPAP in COPD. It is used in type one respiratory failure and is particularly useful in pulmonary oedema.

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