Acute respiratory failure

Definitions acute respiratory failure occurs when: pulmonary system is no longer able to meet the metabolic demands of the body hypoxaemic respiratory failure: PaO2  60mmHg when breathing room air hypercapnic respiratory failure: PaCO2  50mmHg kPa Acute respiratory failure can defined as a state in which the pulmonary system is no longer able to meet the metabolic demands of the body. It can be divided into hypoxaemic respiratory failure and hypercapnic respiratory failure. Hypoxaemic respiratory failure is defined as an arterial partial pressure of oxygen of less than or equal to 8 kPa when breathing room air and hypercapnic respiratory failure is defined as an arterial partial pressure of carbon dioxide of more than or equal to 6.7 kPa

Basic respiratory physiology

CO2 O2 The major function of the lung is to get oxygen in and carbon dioxide out

Oxygen in Depends on PAO2 Diffusing capacity Ventilation Perfusion Ventilation-perfusion matching Getting oxygen into the body depends on the partial pressure of oxygen in the alveoli, the diffusing capacity of the alveolar membrane, ventilation, perfusion and the relationship between the two.

Oxygen Carbon dioxide Water vapour Nitrogen The alveolar pressure is equal to the sum of the partial pressures of the gases within the alveolus and the partial pressure of each gas is proportional to the concentration of the gas. An increase in alveolar pressure will therefore result in a proportionate increase in the partial pressure of all of those gases

Oxygen Carbon dioxide Water vapour Nitrogen The alveolar pressure is equal to the sum of the partial pressures of the gases within the alveolus and the partial pressure of each gas is proportional to the concentration of the gas. An increase in alveolar pressure will therefore result in a proportionate increase in the partial pressure of all of those gases Nitrogen

Oxygen Carbon dioxide Water vapour Nitrogen The alveolar pressure is equal to the sum of the partial pressures of the gases within the alveolus and the partial pressure of each gas is proportional to the concentration of the gas. An increase in alveolar pressure will therefore result in a proportionate increase in the partial pressure of all of those gases Nitrogen

Oxygen in Depends on PAO2 Ventilation-perfusion matching Perfusion FIO2 Alveolar pressure PACO2 Ventilation Ventilation-perfusion matching Perfusion Diffusing capacity So to summarize, changes in alveolar PO2 result predominantly from changes in inspired oxygen concentration and alveolar pressure with a lesser contribution from alveolar PCO2 and alveolar ventilation Alveolar PO2 is, however, not the only determinant of oxygenation. Diffusing capacity, perfusion of alveoli and ventilation-perfusion matching are also important. Perfusion of non-ventilated alveoli, also known as shunting, is the most common cause of hypoxic respiratory failure in ICU

Ventilation-perfusion matching Normally ventilation and perfusion are reasonably well matched

Ventilation:perfusion ratio V/Q relationships No. of lung units With most lung units having a ventilation:perfusion ratio near to 1 1 Ventilation:perfusion ratio

Carbon dioxide out Largely dependent on alveolar ventilation Anatomical dead space constant but physiological dead space depends on ventilation-perfusion matching Carbon dioxide removal is largely dependent on alveolar ventilation which, in turn, is dependent on the respiratory rate times the difference between tidal volume and dead space. The latter will vary, depending on ventilation perfusion matching

Carbon dioxide out Respiratory rate Tidal volume Ventilation-perfusion matching Thus carbon dioxide elimination is dependent on the respiratory rate, tidal volume and ventilation perfusion matching

Pathophysiology

Pathophysiology Low inspired Po2 Hypoventilation Ventilation-perfusion mismatch Shunting Dead space ventilation Diffusion abnormality Although, in theory, acute respiratory failure may result from a low inspired PO2 this is rarely a problem in Intensive Care except in locations at high altitude. The other causes of respiratory failure involve abnormalities of respiratory physiology

75% 100% PAO2=110mmHg PACO2=38mmHg Under normal circumstances the alveoli are both ventilated and perfused with the result that blood leaving the alveolus is fully saturated with oxygen

Pathophysiology Low inspired oxygen concentration Hypoventilation Shunting Dead space ventilation Diffusion abnormality In respiratory failure due to hypoventilation

PAO2=75 mm Hg PAO2=110 mm Hg PACO2=77 mm Hg PACO2=38 mm Hg Oxygen in the alveolus is not replenished and carbon dioxide is not removed. As a result the alveolar partial pressure of oxygen falls with a corresponding fall in the arterial partial pressure and hence saturation. Similarly the rise in alveolar partial pressure of carbon dioxide results in a rise in arterial PCO2. Note that the fall in alveolar PO2 is small and is easily compensated for by small increase in inspired oxygen concentration. As a result pulse oximetry, which estimates arterial saturation is a poor guide to adequacy of ventilation, particularly in patients who are receiving supplemental oxygen.

Sites at which disease may cause hypoventilation

Pathophysiology Low inspired oxygen concentration Hypoventilation Shunting Dead space ventilation Diffusion abnormality Shunting is the most common cause for hypoxaemic respiratory failure in ICU patients.

Shunt It is a form of ventilation-perfusion mismatch in which alveoli which are not ventilated (eg due to collapse or pus or oedema fluid) are still perfused. Because the alveoli are not ventilated blood perfusing these alveoli remains poorly oxygenated, with the result that blood leaving the lungs is not fully saturated.

Furthermore oxygen therapy has relatively little effect on hypoxia due to shunting. Increasing the inspired oxygen concentration cannot further increase the saturation of blood leaving normally ventilated alveoli as it is already 100% saturated and the higher oxygen concentration does not reach non-ventilated alveoli 75% 75% 100% 75% 87.5%

However, in time, hypoxic vasoconstriction will result in a reduction in perfusion to non-ventilated alveoli and a relative increase in perfusion to ventilated alveoli, thus reducing the magnitude of the shunt and increasing the arterial saturation 75% 75% 100% 75% 90%

Shunting Intra-pulmonary Intra-cardiac Pneumonia Pulmonary oedema Atelectasis Collapse Pulmonary haemorrhage or contusion Intra-cardiac Any cause of right to left shunt eg Fallot’s, Eisenmenger, Pulmonary hypertension with patent foramen ovale Causes of intrapulmonary shunting include pneumonia, pulmonary oedema, atelectasis, collapse and pulmonary haemorrhage or contusion Shunting can also occur at an intra-cardiac level but this is an unusual cause of hypoxaemia in the ICU. Any cause of pulm hyptension eg ARDS with patent foramen ovale can lead to right to left shunting.

Pathophysiology Low inspired oxygen concentration Hypoventilation Shunting Dead space ventilation Diffusion abnormality The other extreme of VQ mismatch is dead space ventilation

Dead space This occurs when alveoli are ventilated but not perfused

Ventilation:perfusion ratio V/Q relationships No. of lung units Diseased Clearly shunting and dead space ventilation are the extremes of ventilation:perfusion mismatch and less extreme forms of mismatch exist. Indeed acute respiratory failure is characterised by increase in the spread of ventilation perfusion ratios as opposed the normal situation where ratios are closely clustered around 1 Normal 1 Ventilation:perfusion ratio

Pathophysiology Low inspired oxygen concentration Hypoventilation Shunting Dead space ventilation Diffusion abnormality Diffusion abnormalities can result from a failure of diffusion across the alveolar membrane or a reduction in the number of alveoli resulting in a reduction in the alveolar surface area. Causes include ARDS and fibrotic lung disease. Although diffusion abnormalities are very common their contribution to respiratory failure is usually small.

Respiratory monitoring

Clinical Respiratory compensation Sympathetic stimulation Tissue hypoxia Haemoglobin desaturation Clinical signs of respiratory failure can be divided into signs of respiratory compensation

Clinical Respiratory compensation Sympathetic stimulation Tachypnoea Accessory muscles Recesssion Nasal flaring Sympathetic stimulation Tissue hypoxia Haemoglobin desaturation Such as tachypnoea, use of accessory muscles, recession and nasal flaring

Clinical Respiratory compensation Sympathetic stimulation HR BP (early) sweating Tissue hypoxia Haemoglobin desaturation Signs of sympathetic stimulation such as tachycardia, hypertension and sweating

Clinical Respiratory compensation Sympathetic stimulation Tissue hypoxia Altered mental state HR and BP (late) Haemoglobin desaturation Signs of tissue hypoxia such as altered mental status and at a very late stage bradycardia and hypotension

Clinical Respiratory compensation Sympathetic stimulation Tissue hypoxia Haemoglobin desaturation cyanosis And haemoglobin desaturation which is manifested as central cyanosis

Pulse oximetry Hb saturation (%) PaO2 (mmHg) 90 60 Pulse oximetry is one of the most useful monitors. Oxygen therapy should be titrated to ensure a saturation of at least 90% in most circumstances. Above this level a large rise in PaO2 is required to increase saturation marginally, while below this level a small fall in PaO2 produces a large fall in saturation 60 PaO2 (mmHg)

Oxygen delivery Remember that the aim of therapy is to restore oxygen delivery to tissues and that saturation not PO2 is a major determinant of oxygen delivery. Oxygen delivery is the product of the cardiac output, the oxygen content of blood and a correction factor. The oxygen content of blood is mainly dependent on the oxygen saturation and the haemoglobin saturation, with the a very small contribution from dissolved oxygen. As a result it is the saturation which is important in determining oxygen delivery rather than the PaO2

Sources of error Poor peripheral perfusion Poorly adherent/positioned probe False nails or nail varnish Lipaemia Bright ambient light Excessive motion Carboxyhaemoglobin or methaemoglobin There are a number of sources of error in pulse oximetry of which the two most common are poor peripheral perfusion and a poorly adherent or positioned probe.

123 80 40 Both of these errors can be detected with fair reliability by comparing the pulse rate detected by the pulse oximeter with the heart rate determined from the ECG. If there is a significant discrepancy the oxygen saturation estimated by pulse oximetry is probably inaccurate. It is also important to be aware that the saturation may remain normal in the face of significantly impaired ventilation, particularly if the patient is receiving oxygen therapy 87% HR=95

Summary worry if remember RR > 30/min (or < 8/min) unable to speak 1/2 sentence without pausing agitated, confused or comatose cyanosed or SpO2 < 90% deteriorating despite therapy remember normal SpO2 does not mean severe ventilatory problems are not present In practical terms worry if the respiratory rate is more than 30 or less than 8, if the patient is unable to speak 1/2 a sentence without pausing, is agitated, confused or comatosed, is cyanosed or has a saturation of less than 90 or is deteriorating despite therapy And remember that a normal saturation does not mean that severe ventilatory problems are not present

Treatment

Treat the cause Treatment Supportive treatment Oxygen therapy CPAP Mechanical ventilation As always, it is vital to treat the cause as supportive therapy is futile if the underlying problem is not corrected. Supportive treatment consists of oxygen therapy, CPAP and mechanical ventilation. Click on a button to select a topic or click on the return button to return to the main menu

Oxygen therapy Progressive hypercarbia due to loss of hypoxic drive is RARE Hypoxia KILLS The appropriate response to progressive hypercarbia is assisted ventilation NOT removal of oxygen

Oxygen therapy Fixed performance devices Variable performance devices Oxygen delivery devices can be divided into fixed performance devices and variable performance devices

Variable performance device 30 37% O2 Flow 6 l/min O2 In a variable performance device the oxygen concentration the patient receives will depend on the pattern of ventilation. In this example, where the subject is receiving oxygen at 6l/min, the inspired oxygen concentration is 100% while the inspiratory flow rate is <6 l/min as the inspiratory requirement can be met entirely by the fresh gas flow through the mask 6 Time

Variable performance device 24 l/min air 30 37% O2 Flow 6 l/min O2 Howver, when the inspiratory flow rate rises above 6 l/min the fresh gas flow is inadequate to meet inspiratory requirements and air is entrained through and around the mask, with air entrainment reaching a maximum at the peak inspiratory flow rate. At this point the subject is breathing in at a rate of approximately 30 l/min of which 6 l/min will be the oxygen flowing through the mask and the remaining 24 l/min will be entrained air. The net result is that the inspired oxygen concentration in the trachea has fallen to 37%. The average inspired oxygen concentration will depend on the peak inspiratory flow rate and the pattern of inspiration. In general the harder the patient breaths the lower the inspired concentration and vice versa 6 Time

Fixed performance device 60% O2 30 l/min 60% O2 With fixed performance devices not only is the concentration of oxygen in the device constant but the entire inspiratory requirement can be met from gas flowing through the device. A common example of this sort of device is the venturi mask. With these masks air is entrained in a fixed proportion to oxygen ensuring a constant concentration of oxygen in the mask. The oxygen flow rate is then adjusted so that the total gas flow (ie oxygen plus air) is at least 30 l/min, thus ensuring that the gas flow through the device is sufficient to meet even the peak inspiratory flow. 15 l/min air 100% O2 15 l/min

Other devices Bag valve resuscitator Other oxygen delivery devices include bag valve resuscitators which supply 100% oxygen if applied tightly to the face. It is important to realise that patients can breath spontaneously through a bag valve resuscitator.

Other devices Reservoir face mask Reservoir face masks can deliver up to 70% oxygen depending on the oxygen flow rate but need to be adjusted so that they are tightly applied to the face. Otherwise it is easier to entrain air from around the mask than to inspire oxygen from the reservoir bag

CPAP reduces shunt by recruiting partially collapsed alveoli For patients with respiratory failure which is predominantly due to shunting CPAP may improve oxygenation dramatically by re-opening and keeping open collapsed alveoli

Lung compliance and FRC reduces work of breathing Volume This recruitment of alveoli increases the functional residual capacity, shifting patient to more compliant part of lung volume-pressure curve and thus reducing the work of breathing. CPAP is particularly useful for patients with acute cardiogenic pulmonary oedema as it also reduces preload, afterload and decreases myocardial oxygen consumption. Pressure

Mechanical ventilation Decision to ventilate Complex Multifactorial No simple rules The decision whether or not to ventilate a patient is a complex decision which takes into account many factors and as a result there are no simple rules for when to ventilate a patient.

Ventilate? Severity of respiratory failure Major factors to be considered include severity of respiratory failure

Ventilate? Severity of respiratory failure Cardiopulmonary reserve Cardiopulmonary reserve, patients with low reserve should be ventilated earlier

Ventilate? Severity of respiratory failure Cardiopulmonary reserve Adequacy of compensation Ventilatory requirement Adequacy of compensation. When considering this factor the likelihood of adequate compensation continuing should also be considered. Patients with a high ventilatory requirement are more likely to become exhausted and decompensate.

Ventilate? Severity of respiratory failure Cardiopulmonary reserve Adequacy of compensation Ventilatory requirement Expected speed of response Underlying disease Treatment already given Expected speed of response to treatment. This will depend not only on the underlying disease but also on the treatment that has already been given. Thus a patient with an acute asthmatic attack who has continued to deteriorate despite nebulized salbutamol and oral steroids is unlikely to respond rapidly.

Ventilate? Severity of respiratory failure Cardiopulmonary reserve Adequacy of compensation Ventilatory requirement Expected speed of response Underlying disease Treatment already given Risks of mechanical ventilation Risks of mechanical ventilation. These vary with the underlying disease. For example the risks of mechanical ventilation in acute asthma are greater than the risks of ventilation in acute pulmonary oedema.

Ventilate? Severity of respiratory failure Cardiopulmonary reserve Adequacy of compensation Ventilatory requirement Expected speed of response Underlying disease Treatment already given Risks of mechanical ventilation Non-respiratory indication for intubation Non-respiratory indications for intubation. For example the patient may require intubation and mechanical ventilation for surgery,

Whenever considering mechanical ventilation, consider whether the patient can be ventilated non-invasively as this is generally associated with a lower risk of complications

Ventilate? 43 year old male Community acquired pneumonia Day 1 of antibiotics PaO2 60 mmHg, PaCO2 30 mmHg, pH 7.15 on 15 l/min O2 via reservoir facemask Respiratory rate 35/min Agitated These principles are best illustrated by clinical examples. The first is a 43 year old male with community acquired pneumonia who was started on appropriate antibiotics the previous day. On 15 l/min of oxygen via a reservoir facemask his arterial blood gases show a Po2 of 8 kPa, Pco2 of 4 kpa and a pH of 7.15, his respiratory rate is 35/min and he is agitated. Should he be ventilated?

Yes 43 year old male Community acquired pneumonia Day 1 of antibiotics PaO2 60 mmHg, PaCO2 30 mmHg, pH 7.15 on 15 l/min O2 via reservoir facemask Respiratory rate 35/min Agitated The patient is hypoxaemic

Yes 43 year old male Community acquired pneumonia Day 1 of antibiotics PaO2 60 mmHg, PaCO2 30 mmHg, pH 7.15 on 15 l/min O2 via reservoir facemask Respiratory rate 35/min Agitated Despite near maximal oxygen therapy by facemask

Yes 43 year old male Community acquired pneumonia Day 1 of antibiotics PaO2 60 mmHg), PaCO2 30 mmHg, pH 7.15 on 15 l/min O2 via reservoir facemask Respiratory rate 35/min Agitated His tachypnoea also indicates that his respiratory failure is severe

Yes 43 year old male Community acquired pneumonia Day 1 of antibiotics PaO2 8 kPa (60 mmHg), PaCO2 4 kPa (30 mmHg), pH 7.15 on 15 l/min O2 via reservoir facemask Respiratory rate 35/min Agitated And his agitation and metabolic acidosis indicate tissue hypoxia

Yes 43 year old male Community acquired pneumonia Day 1 of antibiotics PaO2 8 kPa (60 mmHg), PaCO2 4 kPa (30 mmHg), pH 7.15 on 15 l/min O2 via reservoir facemask Respiratory rate 35/min Agitated Furthermore he is only on the first day of antibiotic therapy for community acquired pneumonia and he is therefore unlikely to respond rapidly to treatment of his underlying condition. The risk benefit ratio therefore favours ventilation.

Ventilate? 24 year old woman Presents to A&E with acute asthma SOB for 2 days Salbutamol inhaler, no steroids PFR 60 L/min, HR 105/min pH 7.25 PaCO2 51 mmHg, PaO2 315 mmHg on FiO2 0.6 RR 35/min Alert The second case is a 24 year old woman with acute asthma. She has been using a salbutamol inhaler but has not received steroids, her peak flow is 60 l/min, heart rate is 105/min, PCO2 6.8 kPa and respiratory rate 35 l/min. She is alert.

No 24 year old woman Presents to A&E with acute asthma SOB for 2 days Salbutamol inhaler, no steroids PFR 60 L/min, HR 105/min pH 7.25 PaCO2 51 mmHg, PaO2 315 mmHg on FiO2 0.6 RR 35/min Alert Although she has severe asthma as indicated by her low peak flow, tachycardia

No 24 year old woman Presents to A&E with acute asthma SOB for 2 days Salbutamol inhaler, no steroids PFR 60 L/min, HR 105/min pH 7.25, PaCO2 51 mmHg, PaO2 315 mmHg on FiO2 0.6 RR 35/min Alert Hypercarbia and tachypnoea

No 24 year old woman Presents to A&E with acute asthma SOB for 2 days Salbutamol inhaler, no steroids PFR 60 L/min, HR 105/min pH 7.25 PaCO2 51 mmHg, PaO2 315 mmHg on FiO2 0.6 RR 35/min Alert She is alert

No 24 year old woman Presents to A&E with acute asthma SOB for 2 days Salbutamol inhaler, no steroids PFR 60 L/min, HR 105/min pH 7.25 PaCO2 51 mmHg, PaO2 315 mmHg on FiO2 0.6 RR 35/min Alert And has received relatively little treatment. There is therefore a significant chance that, with appropriate treatment, she may improve significantly in the next few hours

No 24 year old woman Presents to A&E with acute asthma SOB for 2 days Salbutamol inhaler, no steroids PFR 60 L/min, HR 105/min pH 7.25 PaCO2 6.8 kPa (51 mmHg), PaO2 42 kPa (315 mmHg) on FiO2 0.6 RR 35/min Alert Furthermore her underlying problem is asthma and ventilation of patients with severe asthma is fraught with difficulty.

No 24 year old woman Presents to A&E with acute asthma SOB for 2 days Salbutamol inhaler, no steroids PFR 60 L/min, HR 105/min pH 7.25, PaCO2 51 mmHg, PaO2 315 mmHg on FiO2 0.6 RR 35/min Alert The risk:benefit ratio does not, therefore, favour ventilation in this case

Summary Shunting is the most common cause of acute respiratory failure in acutely ill patients High concentrations of oxygen are required Hypoventilation due to abolition of hypoxic drive is RARE

Summary worry if remember RR > 30/min (or < 8/min) unable to speak 1/2 sentence without pausing agitated, confused or comatose cyanosed or SpO2 < 90% deteriorating despite therapy remember normal SpO2 does not mean severe ventilatory problems are not present In practical terms worry if the respiratory rate is more than 30 or less than 8, if the patient is unable to speak 1/2 a sentence without pausing, is agitated, confused or comatosed, is cyanosed or has a saturation of less than 90 or is deteriorating despite therapy And remember that a normal saturation does not mean that severe ventilatory problems are not present

Treat the cause Treatment Supportive treatment Oxygen therapy CPAP Mechanical ventilation As always, it is vital to treat the cause as supportive therapy is futile if the underlying problem is not corrected. Supportive treatment consists of oxygen therapy, CPAP and mechanical ventilation. Click on a button to select a topic or click on the return button to return to the main menu

Ventilation Severity of respiratory failure Cardiopulmonary reserve Adequacy of compensation Ventilatory requirement Expected speed of response Underlying disease Treatment already given Risks of mechanical ventilation Non-respiratory indication for intubation The decision to intubate is complex and should take into account……