Acute Respiratory Failure

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Acute Respiratory Failure

Acute respiratory failure Clinical problems LEARNING OBJECTIVES After studying this module on Respiratory failure, you should be able to: 1. Identify patients suffering from acute respiratory failure (ARF) 2. Understand strategies for providing ventilatory support 3. Become familiar with the associated supportive measures 4. Recognise and know how to manage the complications of ventilatory support FACULTY DISCLOSURES The authors of this module have not reported any disclosures. DURATION 7 hours Copyright©2009. European Society of Intensive Care Medicine. All rights reserved. ISBN 978-92-95051-62-1 - Legal deposit D/2005/10.772/9 INTRODUCTION

Acute respiratory failure (ARF) is a common and important indication Acute respiratory failure is for admission into critical care units and is associated with a substantial always caused by an mortality. For the purpose of this module, ARF is defined as any acute underlying condition that will lung condition (with the exception of obstructive lung disease) that need urgent treatment requires active ventilatory therapy. Most ARF discussed in this The reader should also be aware that there are a variety of clinical module is due to lung failure conditions that can precipitate ARF, such as acute cardiogenic pulmonary oedema, fluid overload, massive pulmonary embolism and coma. ARF is not a disease in itself but a reaction to an underlying condition, e.g. trauma, sepsis or pneumonia. Because definitions differ, the incidence and mortality rates for ARF vary across studies. In addition, the underlying condition strongly influences prognosis.  The reported incidence of ARF, including acute lung injury (ALI) and acute respiratory distress syndrome (ARDS) varies between around 78–149 per 100 000 people >15 years of age per year.  Ninety-day mortality is close to 40% for ARF and 31–60% for ALI / ARDS. Whether mortality rates have decreased over time is still a matter of debate.  The majority of patients have ARF of pulmonary origin with pneumonia as the predominant diagnosis. 1/ HOW TO IDENTIFY/CATEGORISE/MONITOR THE PATIENT SUFFERING FROM ARF This Task will provide you with definitions, outline aetiology, risk factors, clinical manifestations and symptoms. The Task concludes with a section on how to monitor the course of acute respiratory failure. Definitions For the purpose of this module, we will focus on ALI and ARDS. The ALI/ARDS is a pulmonary definition of ARDS is under discussion but the definition proposed by a inflammatory process Joint North American–European consensus committee (NAECC) in 1994 is still accepted. ARDS is defined as an inflammatory process in the lungs with:  An acute onset of respiratory failure  New bilateral pulmonary infiltrates on frontal chest radiograph or computed tomography (CT)  Absence of left ventricular failure (clinically diagnosed or a pulmonary artery occlusion pressure <18 mmHg)  Hypoxaemia with a ratio between the partial pressure of oxygen in the arterial blood and the fraction of inspired oxygen (PaO2/FiO2) ≤27 kPa (201 mmHg) independent of the level of positive end-expiratory pressure (PEEP) ALI is defined by the same criteria except that the PaO2/FiO2 ratio is between 27 kPa (201 mmHg) and 40 kPa (300 mmHg). However, there are problems with this definition: Heart failure can exist  The definitions of left ventricular cardiac failure are concomitantly with a vague, and the interpretation of a chest radiograph may be pulmonary inflammatory difficult. process similar to ALI/ARDS  Lung recruitment manoeuvres and PEEP influence both the degree of hypoxaemia and the appearance of the chest radiograph.  The PaO2/FiO2 ratio is dependent on the FiO2 used. It has been suggested, therefore, that the definition should be modified, for example by defining 'acute' and by specifying the PEEP level and the FiO2 at which PaO2 should be obtained (see references below). Another commonly used, but more complicated definition was suggested by Murray; the Lung Injury Severity Score (LISS). In this score, the PaO2/FiO2 ratio, the chest radiograph, compliance of the respiratory system and the level of PEEP are scored on a scale 0-4. If compliance is not measured this variable can be omitted and if the patient is not receiving mechanical respiratory support PEEP can also be excluded. The sum of the scores is then divided by the number of components. A total score greater than 2.5 defines ARDS.

NOTE Neither LISS nor the initial degree of arterial hypoxaemia (if PaO2 is not severely low) are related to outcome. In the next five patients who are admitted to your ICU with ARF check whether they fulfil the ARDS definition by LISS, the NEACC criteria or both. Please check the level of PEEP. For more information about the different definitions of ALI/ARDS see the following references. Aetiology and risk factors ALI/ARDS is an acute inflammatory condition in the lungs and not a disease in itself, and is therefore always due to an underlying disease process. The pulmonary inflammation may be caused by:

 A direct (primary or pulmonary) injury to the lungs or  An indirect (secondary or extra-pulmonary) injury ALI/ARDS due to a direct injury comprises 50-60% of all cases, with pneumonia as the most important single cause (40-50% of all cases). Other common direct causes are aspiration of gastric contents, pulmonary contusion, inhalation of toxic gases and near drowning. Indirect ALI/ARDS is caused by systemic inflammation with generalised activation of mediators, inflammatory cells and endothelium due to infection (sepsis, peritonitis), tissue ischaemia or tissue damage (trauma, cardio-pulmonary bypass, pancreatitis, major surgery and some intoxications and overdoses). Experimental and recent clinical studies have shown that ALI/ARDS might also be due to, or be accentuated by mechanical ventilation using high tidal volumes and low levels of PEEP. The independent risk factors for ARF are old age, infection, neurological disease, alcohol abuse and multiple transfusions.

Because ALI/ARDS is always caused by an underlying disease process, treatment of precipitating factors, together with the patient's comorbidities and genetic predisposition are major determinants for the progression of the lung condition and its outcome.

THINK Why are old age, neurological disease, infection, multiple transfusions and genetic diversity important risk factors for the development of ARF? See the references below for further information. Clinical manifestations and symptoms Clinical manifestations and symptoms may be divided into:

 Pulmonary, caused by ALI/ARDS and  Extra-pulmonary, caused by the underlying disease Ascertain the diagnosis: laboratory tests and imaging According to the definitions, the diagnosis of ALI/ARDS is first established by:

 The medical history: acute onset of respiratory failure in combination with an underlying condition which has the potential to initiate pulmonary inflammation.  A recent frontal chest radiograph or thorax CT showing bilateral infiltrates.  A clinical examination (and medical history), echocardiography or pulmonary artery catheterisation (PCWP <18 mmHg) to exclude significant left ventricular failure.  An arterial blood sample together with measurement of FiO2, showing a PaO2/FiO2 ratio ≤27 kPa for the diagnosis of ARDS and <40 kPa for the diagnosis of ALI. Early in ALI/ARDS, the blood gas analysis might, in addition to hypoxaemia, show a degree of hypocapnia due to an increased ventilatory drive induced by increased stiffness of the lungs. In addition, the patient is usually apprehensive. Respiratory acidosis develops rather late in the process and signals imminent respiratory decompensation. Metabolic acidosis may be seen, but usually this is a consequence of the underlying process (sepsis or tissue hypoperfusion) rather than ALI/ARDS.

The results of other laboratory tests are usually non-specific and Clinical examination and dependent on the underlying disease. It is common to find evidence of obtaining a medical history inflammation and coagulopathy. are extremely important in the management of ALI/ARDS In ventilated patients, lung mechanics show a low respiratory system compliance and functional residual capacity is reduced.

How can you determine whether a low compliance (high elastance) is due to a pulmonary condition or to a stiff chest wall, e.g. caused by intra-abdominal distension?

See the PACT module on Respiratory monitoring for more information The chest radiograph typically shows bilateral interstitial infiltrates that later become diffuse and fluffy. In addition bilateral basal atelectasis is common. Therapeutic intervention, i.e. recruitment manoeuvres and application of PEEP, might modify the findings and sometimes even normalise the appearance of the chest radiograph.

NOTE A chest radiograph obtained during expiration, compared with one taken during inspiration will show more pronounced changes. Computed tomography (CT) examinations are useful for evaluation of the lung pathology. CT can more accurately define infiltrates, pleural effusions and small pneumothoraces especially those lying anteriorly or posteriorly. In extrapulmonary ARDS, bilateral symmetrical dorsal and caudal densities, indicating lung collapse and alveolar oedema, are common when the patient is supine. Bilateral pleural effusions are also typical findings. In pulmonary ARDS the more dense lung regions tend to be asymmetrical and localised to the areas most affected by the primary process. However, these differences in apprearance between pulmonary and extra-pulmonary ARDS are not always conclusive. Furthermore the findings change with time as the process evolves.

THINK Consider the benefits of obtaining a CT versus the costs and risk of moving the patient from the ICU. How to monitor the course of ARF

See also the PACT modules on Mechanical ventilation , Respiratory monitoring and Haemodynamic monitoring

ALI/ARDS is frequently part of the multiple organ dysfunction Monitoring is useless without syndrome. Therefore, it is important to monitor and detect early signs correct interpretation of the of additional organ involvement, e.g. renal dysfunction, and to rapidly data and appropriate decision institute measures to prevent further deterioration. Maintaining making adequate tissue perfusion is of paramount importance, especially when arterial oxygenation is compromised. NOTE Before initiating monitoring, particularly with invasive devices, always consider whether such monitoring has the potential to usefully influence patient management. In all types of ARF, continuous monitoring should include:

 Depth of sedation  Respiratory frequency  FiO2  Peripheral oxygen saturation by pulse oximetry In addition:

 If the patient is mechanically ventilated, all relevant Do not forget to examine the ventilatory variables are automatically and continuously patient frequently! obtained. It is important to check that alarm limits for tidal volumes and pressures are set correctly.  Ventilatory variables (mode, PEEP, auto-PEEP, peak and plateau pressures, tidal volume, inspiratory:expiratory (I:E) ratio, ventilator rate) should be noted at prescribed regular intervals.  Arterial blood gases should be sampled at regular intervals and when deterioration in the patient's condition is clinically evident.  A chest X-ray should be performed at least twice weekly if the course is benign and more often in those with severe lung injury.  Continuous measurement of systemic blood pressure.  Fluid balance and urine output should be updated hourly. Additional monitoring (airway pressure-lung volume relationships, lung volume measurements, mixed venous or central venous oxygen saturation, cardiac output measurement, echocardiography, pulmonary artery catheterisation, or arterial transpulmonary indicator dilution catheter) should be instituted according to the severity of respiratory failure and the level of support required, as well as the degree of additional organ dysfunction and support. Nutritional therapy should be monitored biochemically. The clinical utility of a promising new monitoring method, electrical impedance tomography, is not clear. In the next five patients with ARF in your ICU observe the monitoring techniques employed. Do you agree with these monitoring protocols? Give arguments (pros and cons). Discuss the issues with your supervisor or a colleague.

2/ STRATEGIES FOR VENTILATORY SUPPORT (LUNG PROTECTIVE VENTILATION)

See also the PACT module on Mechanical ventilation The goal for ventilatory therapy in ARF is to achieve adequate gas exchange (usually PaO2 >8 kPa, oxygen saturation of haemoglobin in arterial blood (SaO2) >90% and pH 7.2- 7.4) without causing additional iatrogenic damage to the lungs and other organs, i.e. a lung protective ventilatory strategy. In this context it is important to recognise that a ventilator can only replace the work performed by the respiratory muscles and not the gas exchange function of the lungs. However, by using lung recruitment manoeuvres, positive end- expiratory pressure and by changing the inspired oxygen concentration, gas exchange can be improved and supported. In the reference below you will find more information about ventilatory support of patients with ARDS.

When to initiate ventilatory support? As a general rule, The mean inspired oxygen  All patients with ALI/ARDS should immediately receive concentration via a standard oxygen via a mask. face mask is only 40-50% at

 If hypoxaemia persists and the clinical condition does not flow rates of 10-15 l O2 /min improve rapidly more active measures are urgently required.  If the patient has concomitant conditions that compromise cardiopulmonary function, more active measures should be considered early. The patient's clinical condition is more important than the values obtained by blood gas analysis in deciding when to start ventilator support.

 If the patient is fully awake, haemodynamically stable Oxygen consumption and

and is not fatigued there is no immediate need for CO2production increase by 6- ventilatory support even if blood gases indicate hypoxaemia. 10% per °C. This increased On the other hand, because almost all patients with demand can exacerbate ALI/ARDS require some form of ventilatory support, respiratory distress mechanical ventilation should always be considered early in the disease process.  If the patient is exhausted, has a respiratory rate above 30-35/min, blood gases indicate significant hypoxaemia (PaO2 <7-8 kPa) on oxygen via mask, an increasing carbon dioxide pressure in the arterial blood (PaCO2) or pH is below 7.3 (showing that the patient cannot maintain a normal pH by spontaneous breathing) mechanical ventilation should be instituted expeditiously.  If the patient is haemodynamically unstable but can maintain PaO2 above 8 kPa on oxygen via mask, haemodynamic support is indicated under careful ventilatory monitoring before invasive ventilatory support (intubation) is initiated.

Why does a low PaO2 not necessarily indicate tissue hypoxia? How can you improve tissue oxygenation without increasing PaO2?

See PACT module on Respiratory monitoring for further information Sedation and initiation of positive pressure ventilation may cause severe cardiovascular collapse in hypovolaemic patients.

In the last five patients with ARF in your department what were the PaO2, PaCO2, arterial pH and respiratory rate before initiating ventilator therapy.

Should we start a trial with non-invasive ventilation (NIV)?

Non-invasive support with continuous positive airway pressure (CPAP) may be considered in otherwise stable patients with hypoxaemia in the absence of CO2 retention. Non-invasive positive pressure ventilation is otherwise the preferred method in patients with ARF. NIV can only be considered if the staff members are experienced with the method and if the patient is:

 Fully conscious  Cooperative  Haemodynamically stable  Tolerant of short periods without ventilatory support  Able to take adequate tidal volumes  Not fatigued The trial of NIV should be terminated if the patient does not markedly Never delay initiating invasive improve clinically within an hour. ventilation by applying NIV to NIV should always be considered in patients who are a patient who is exhausted. immunosuppressed because of the importance of preventing nosocomial infections in such patients (tracheal intubation is associated with nosocomial pneumonia and sinusitis). This approach has been associated with improved outcomes. ANECDOTE A patient infected with human immunodeficiency virus (HIV) with bilateral pulmonary interstitial infiltrates on the chest radiograph was transferred to the ICU at 2.00 a.m. He was at that time fully awake, his respiratory rate was 40/min and his PaO2 was 7 kPa on face mask O2 at 15 l /min. Pneumocystis jiroveci pneumonia was suspected and trimethoprim-sulfmethoxazole was started. Because the patient was cooperative NIV was started with pressure support ventilation (see PACT module on Mechanical ventilation) of 15 cm H2O above 5 cm H2O PEEP and FiO2 of 1.0. The patient improved initially. After two hours the patient became more tired with increasing PaCO2 and decreasing pH. However, since it was early morning (5.00 a.m.) the nurse decided to wait a further hour before informing the intensivist on call. When the intensivist arrived just after 6.00 a.m. he found the patient severely lethargic and exhausted with an arterial oxygen saturation of 77% on pulse oximetry. An emergency oral tracheal intubation was performed but unfortunately the patient developed cardiac arrest, which could not be reversed. This case illustrates the need for continuous close attention by experienced staff and that invasive ventilation should be instituted promptly if NIV is not successful.

What are the advantages and disadvantages of NIV in patients with hypoxaemic respiratory failure?

See PACT module on Mechanical ventilation Be aware that the administration of 100% oxygen for a prolonged period can exacerbate atelectasis.

Intubation /tracheostomy

The indications for intubation in ARF are:

 Inadequate gas exchange with non-invasive respiratory support (oxygen via mask, CPAP or NIV) or  When NIV is contraindicated or believed to be insufficient, e.g. o Severe hypoxaemia (PaO2 <6-7 kPa) o Severe respiratory acidosis (pH <7.2, PCO2 > 9-10 kPa) o Semi-or unconscious/ unable to maintain and protect the airway o Concomitant central nervous system compromise (head injury, brain oedema due to meningitis, intracerebral bleeding, spinal injury) o Recent surgery In patients with ARF there is a significant risk of complications during tracheal intubation:

 Pronounced hypoxaemia  Aspiration of gastric contents  Misplacement of the endotracheal tube  Haemodynamic compromise Intubation, therefore, should be performed with great caution. Because Always use capnography to the indications are hypoxaemia or respiratory fatigue, immediate confirm that the tube is successful tracheal intubation is essential. All means to rapidly secure correctly positioned in the a safe airway should therefore be available; a variety of laryngoscopes, trachea different designs and sizes of endotracheal tubes, stylets, bougies, forceps, a fibre optic bronchoscope or laryngoscope, airways and devices for cricothyroidotomy. It must be possible to suction and to administer 100% oxygen. It is important to avoid worsening of hypoxaemia during the procedure by administering 100% oxygen or maintaining NIV as long as possible before intubation. There are three different approaches for intubation:  Oral intubation  Fibre optic awake intubation  Blind nasal intubation

Oral intubation If the patient is obtunded, oral intubation is the technique of choice. Oral intubation is easier, quicker and safer to perform than nasal intubation and in addition is associated with a lower incidence of sinusitis. Before intubation, the equipment and the tube should be checked, and a decision made about the amount and type of drugs to be used to facilitate intubation. A skilled assistant should be available. These patients usually have slow gastric emptying and are at risk of regurgitation of stomach contents followed by pulmonary aspiration. Therefore a rapid sequence intubation with cricoid pressure should be performed.

THINK What do you do if you cannot intubate at the first attempt in a patient with ARF? What are your department's guidelines?

See PACT module on Airway management for more information Fibre optic intubation Fibre optic intubation is a good and safe choice in an awake patient, particularly if the upper airways are compromised. Fibre optic intubation should replace blind nasal intubation in patients with ARF. Nasal intubation may induce serious nasal bleeding in patients with thrombocytopenia or coagulation disorders.

How do you confirm correct positioning of an endotracheal tube?

Tracheostomy

Tracheostomy is

 Seldom a first-line measure except when the patient has a compromised upper airway.  Performed when it is anticipated that the patient needs lengthy ventilatory support or to facilitate the weaning process, as in severe head trauma.  Relatively contraindicated during the critical phase when the patient requires high inspired oxygen and difficult to ventilate.  Relatively contraindicated in patients with bleeding tendency or coagulation disorders. It is not clear whether tracheostomy, even when performed early can decrease morbidity or mortality compared with prolonged tracheal intubation. In clinical practice, however, tracheostomy is more comfortable for the patient, facilitates suctioning and oral hygiene as well as the weaning process. In patients with ARF, tracheostomy should be performed by a skilled and NOTE experienced member of staff. The procedure can be performed surgically or percutaneously. The approach adopted is mainly determined by local practices. Assist at five tracheostomies (percutaneous or surgical). Discuss with the operator and your supervisor / colleagues, what the arguments are for surgical, percutaneous or both procedures being used.

What are the targets of ventilatory support? The objective is to achieve adequate gas exchange without injuring the lungs and other organs. The gas exchange targets are not clearly defined. It is common practice to aim for a PaO2 and SaO2 above 8 kPa and 90%, respectively, but lower values may be acceptable as long as there are no signs of tissue hypoxia. In fact, no studies have shown that increasing PaO2 improves outcome. PCO2 in itself is seldom important, but pH should usually be maintained between 7.2 and 7.4.

See the PACT modules on Mechanical ventilation and Respiratory monitoring.

Hypocapnia constricts coronary and cerebral arteries and hampers oxygen unloading

What are the benefits or drawbacks of hypercapnia? See reference below for more information.

How to adjust the ventilator settings in a patient with acute respiratory failure

The ventilator settings should be adjusted to ensure adequate gas exchange without causing:

 Overdistension  Repeated opening and closing of distal units Thus, tidal volumes and the transpulmonary pressure difference between inspiration and expiration should be kept low. Ventilatory mode There are no ventilatory modes (including high frequency oscillatory Use your clinical judgment at ventilation) that have been conclusively proven to be superior in ARF the bedside when adjusting as long as end-inspiratory plateau pressures and tidal volumes are the ventilator settings limited. However, there is some suggestion that modes which allow for spontaneous breathing (e.g. airway pressure release ventilation, APRV), improve oxygenation and haemodynamics, contribute to lung recruitment and decrease the need for sedation. On the other hand, recent studies suggest that a short initial period with heavy sedation combined with muscle relaxation might be beneficial. See the references below for further information about APRV and muscle relaxation. If possible, use modes early See PACT module on Mechanical ventilation that allow spontaneous breathing as early as possible Tidal volume and airway pressures  Ventilation with a tidal volume of 6 ml/kg ideal body weight has been shown to significantly decrease mortality (by 9%) when compared with ventilation with 12 ml/kg tidal volumes. However, the acceptable tidal volume may be more dependent on the condition of the lungs; in small and highly inflamed lungs tidal volumes should probably be lower than 6 ml/kg but in larger and less inflamed lungs tidal volumes somewhat larger than 6 ml/kg are probably safe.  The end-inspiratory plateau airway pressures should be kept low (<28–30 cm H2O). However, because the transpulmonary pressure is more important than the airway pressure, the compliance of the chest wall should be taken into consideration. In a patient with a compliant chest wall, e.g. a small child, an airway pressure of 30 cm H2O will translate into a high transpulmonary pressure and is likely to injure the lungs, while in an adult, obese patient with intraperitoneal pathology, an airway pressure of 40 cm H2O might generate a low, risk-free, transpulmonary pressure.  Low tidal volume and low pressure ventilation may be associated with a reduction in CO2 elimination. The rise in a PaCO2 should be tolerated (an approach termed permissive hypercapnia).

How can you improve CO2 removal without increasing the tidal volume?

What are the drawbacks of low tidal volume ventilation? See the PACT modules on Mechanical ventilation and on Respiratory monitoring Case 2 You get a request from the surgical ward for possible transfer of a 42-year-old woman, with previously normal cardio-pulmonary health, to the ICU. She had been operated on four days previously with a right-sided colectomy and ileo-colic anastomosis colon. The surgery and anaesthesia were uncomplicated, but afterwards she developed nausea, vomiting and abdominal pain. Now she is complaining about difficulties with breathing and her temperature has increased to 39.5 °C. The surgical resident suspects pneumonia and wants her transferred to the ICU. When you arrive at the surgical ward you examine the patient. She is pale, slightly cyanotic but has good peripheral circulation. She has a respiratory rate of 28/min and is somewhat dyspnoeic. Over both basal lungs you can hear crepitations. The abdomen is tender and tense. The wound is not infected. Blood pressure is 100/60 mmHg and pulse rate is 120/min. The patient has no urinary catheter and does not remember when she voided. She has received thromboembolic prophylaxis (low molecular weight heparin) and prophylactic antibiotics during surgery.

Which diagnosis is most probable and why? Learning issues

Aetiology of secondary ALI/ARDS

Clinical signs of secondary ALI/ARDS

Differential diagnosis of postoperative lung disorders

What other diagnoses do you consider?

What is your first measure to improve the patient's condition? Why? Refresh your knowledge about treatment of severe infections. NOTE See PACT module on Severe infection

See PACT module on Sepsis and MODS Case 2 Screen 2 You immediately discuss your findings with the surgical consultant. He is convinced that the patient can be handled in the surgical ward and that no further actions are necessary. Learning issues

Definition of ALI/ARDS

Pathogenesis of secondary ALI/ARDS

Management of secondary ALI/ARDS

Give arguments to convince him this is not the best approach for this patient? You and the surgeon decide that the patient should be transferred to the ICU for optimisation before

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