Respiratory failure ØARDS ØAsthma ØCHOPN (COPD) ØAspiration ØPneumothorax ARF ØARF is not a specific disease but a reaction to an underlying condition, e.g. trauma, sepsis or pneumonia. ØDue to different definitions, the incidence and mortality rates for ARF vary across studies. ØIn addition, the underlying condition strongly influences prognosis. 2 Respiratory failure ØAcute respiratory failure (ARF) is a common and important indication for critical care with a substantial mortality. ØIt is defined as all acute lung conditions with the exception of chornic obstructive lung disease that require active therapy. Pump failure or lung failure ? ØThe respiratory system can be modelled as a gas exchanger (the lungs) ventilated by a pump. The dysfunction of each of the two parts, pump or lungs, may cause respiratory failure defined as inability to maintain adequate blood gases while breathing ambient air. 4 Pump failure ØPump failure primarily results in alveolar hypoventilation, hypercapnia and respiratory acidosis. 5 Pump failure ØInsufficient alveolar ventilation may result from a number of causes intrinsically affecting one or more of the elements of the complex chain that starts from: Øthe respiratory centres (pump controller) Øcentral and peripheral nervous ways Øchest wall, the latter including both the respiratory muscles and all the passive parts that couple the muscles with the lungs. 6 Pump failure ØInsufficient alveolar ventilation may even take place in the absence of any intrinsic problem of the pump, when a high ventilation load overcomes the natural capacity of the pump. ØExcessive load can be caused by airway obstruction, respiratory system stiffening or high ventilation requirement, and finally results in intrinsic pump dysfunction due to respiratory muscle fatigue. 7 Lung failure ØLung failure results from any damage of the natural gas exchanger: alveoli, airways and vessels. ØLung failure involves impaired oxygenation and impaired CO2 elimination depending on a variable combination of: * True intrapulmonary shunt * Increased alveolar dead space ØLung damage also involves increased ventilation requirement and mechanical dysfunctions resulting in high impedance to ventilation. 8 Cause Øintoxikation, cerbral insult Øsy Guillain Barré, trauma, poliomyelitis Ømyastenia, neuritis, tetanus, botulism ØPNO, haemothorax Øupper airway obstruction Øasthma, COPD, bronchiolitis, fibrosis, ARDS, aspiration Øcardiology 9 specific causes theat lead the respiratory ins. are ARDS - Acute Respiratory Distress Syndrome 10 common cause ARDS is defined as an inflammatory process in the lungs with: ØAn acute onset of respiratory failure meaning onset over 1 week or less ØNew onset bilateral opacites on frontal chest radiograph ØAbsence of left ventricular failure (clinically diagnosed ) ØHypoxaemia express with a ratio between the partial pressure of oxygen in the arterial blood and the fraction of inspired oxygen (PaO2/FiO2) 11 ARDS is categorized as mild, moderate, or severe: Ømild (PaO2/FIO2 ≤ 300 mm Hg) Ømoderate (PaO2/FIO2 ≤ 200 mm Hg) Øsevere (PaO2/FIO2 ≤ 100 mm Hg) 12 Aetiology and risk factor 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 is caused by: * A direct (primary or pulmonary) injury to the lungs (pneumonia) * An indirect (secondary or extra-pulmonary) injury (sepsis, pancreatitis, trauma, major surgery,…) 13 Pulmonary manifestations and symptoms ØCyanosis due to hypoxaemia ØTachypnoea ØDyspnoea due to a higher work of breathing in order to compensate for an impaired gas exchange ØHigh-pitched crackles heard in all lung fields 14 Extra-pulmonary manifestations and symptoms ØThe underlying process might dominate the clinical picture in the early phase of ARDS. lIn trauma, local signs, pain and circulatory shock are prominent lin sepsis, fever and laboratory and clinical signs of impaired perfusion are important manifestations. 15 16 ARDS - CT Lung protective ventilatory strategy ØThe goal for ventilatory therapy in ARF is to provide an adequate gas exchange (usually PaO2 >8 kPa, oxygen saturation of haemoglobin in arterial blood (SaO2) >90% and pH 7.2-7.4) ØThere are no ventilatory modes that have been conclusively proven to be superior in ARF when limiting end-inspiratory plateau pressures and tidal volumes ØVentilation with Vt 6 ml/kg ideal body weight ØThe end-inspiratory plateau airway pressures should be kept low (<30-35 cm H2O). ØLow tidal volume and low pressure ventilation might reduce CO2 elimination and this ventilatory approach has therefore been termed ‘permissive hypercapnia’. 18 Positive end-expiratory pressure ØMay prevent collapse of open and perfused lung regions and thus maintain arterial oxygenation ØTherefore, PEEP should ideally be set at a high level (about 10-15 cm H2O) immediately after a lung recruitment manoeuvre 19 ‘Open up the lung and keep it open’ ØStrategy lung recruitment manoeuvre to open up collapsed lung regions followed by an adequate PEEP to prevent the recruited lung regions from recollapsing. ØThis approach is usually effective in improving arterial oxygenation in early ARDS. 20 Other Therapy ØOther therapies proposed to increase oxygenation and resolution of ARDS as well as linfectious control lNutritional support lfluid management lprone position 21 COPD and Asthma ØChronic obstructive pulmonary disease (COPD) is a worldwide and rapidly growing health problem: it was the sixth leading cause of death worldwide in 1990 and is expected to become the third leading cause by 2020. ØTransient worsening of the chronically altered lung function (so-called exacerbation of COPD) may lead to life-threatening respiratory insufficiency requiring ventilatory support. ØMortality from asthma is also not negligible: it is estimated at 1-8 per 100 000 annually. 22 Asthma ØAlthough inflammation is important in both COPD and asthma, the inflammatory response is quite different in the two diseases. ØInflammation has greater clinical significance in asthma and therefore is more responsive to corticosteroids. ØThe importance of bronchospasm and the related bronchial sensitivity are much greater in asthma as well. In contrast to COPD, most of the bronchial obstruction in asthma is reversible. 23 Clinical findings (asthma): ØImmediately life-threatening clinical features are: l Silent chest, weak respiratory efforts and cyanosis l Confusion or coma l Bradycardia and hypotension l Peak expiratory flow rate (PEFR) unmeasurable Ø Clinical signs of severe asthma are: lInability to complete sentences in one breath lRespiratory rate (RR) >30/min lTachycardia >120/min lPEFR <50% of predicted normal or of best normal if known (<200 l/min if not known) lArterial paradox (the fall in systolic pressure on inspiration) >20 mmHg 24 lobal Initiative for Chronic bstructive ung isease G O L D 25 GOLD Ømain method to describe the severity of chronic obstructive pulmonary disease (COPD). Øthe GOLD staging system classifies people with COPD based on their degree of airflow limitation (obstruction). The airflow limitation is measured during pulmonary function tests (PFTs). 26 Mechanisms Underlying Airflow Limitation in COPD Small Airways Disease •Airway inflammation •Airway fibrosis, luminal plugs •Increased airway resistance Parenchymal Destruction •Loss of alveolar attachments •Decrease of elastic recoil AIRFLOW LIMITATION 27 Risk Factors for COPD •Lung growth and development •Gender •Age •Respiratory infections •Socioeconomic status •Asthma/Bronchial hyperreactivity •Chronic Bronchitis Genes Tobacco smoke Exposure to particles §Occupational dusts, organic and inorganic §Indoor air pollution from heating and cooking with biomass in poorly ventilated dwellings §Outdoor air pollution 28 SYMPTOMS chronic cough shortness of breath EXPOSURE TO RISK FACTORS tobacco occupation indoor/outdoor pollution SPIROMETRY: Required to establish diagnosis Diagnosis of COPD sputum 29 Assessment of Airflow Limitation: Spirometry ØWhen blowing out forcefully, people with normal lungs can exhale most of the air in their lungs in one second. Pulmonary function tests measure this and other values, and are used to diagnose COPD and its severity: lThe volume in a one-second forced exhalation is called the forced expiratory volume in one second (FEV1), measured in liters, In people with normal lung function, FEV1 is at least 70% of FVC. lThe total exhaled breath is called the forced vital capacity (FVC), also measured in liters. 30 Diagnosis and Assessment: ØA clinical diagnosis of COPD should be considered in any patient who has dyspnea, chronic cough or sputum production, and a history of exposure to risk factors for the disease. ØSpirometry is required to make the diagnosis; the presence of a post-bronchodilator FEV1/FVC < 0.70 confirms the presence of persistent airflow limitation and thus of COPD. 31 Classification of Severity of Airflow Limitation in COPD In patients with FEV1/FVC < 0.70: GOLD 1: Mild FEV1 > 80% predicted GOLD 2: Moderate 50% < FEV1 < 80% predicted GOLD 3: Severe 30% < FEV1 < 50% predicted GOLD 4: Very Severe FEV1 < 30% predicted Based on Post-Bronchodilator FEV1 32 Comorbidities COPD patients are at increased risk for: ØCardiovascular diseases ØOsteoporosis ØRespiratory infections ØAnxiety and Depression ØDiabetes ØLung cancer These comorbid conditions may influence mortality and hospitalizations and should be looked for routinely, and treated appropriately. 33 Differential Diagnosis: COPD and Asthma COPD Ø Onset in mid-life Ø Symptoms slowly progressive Ø Long smoking history ASTHMA ØOnset early in life (often childhood) ØSymptoms vary from day to day ØSymptoms worse at night/early morning ØAllergy, rhinitis, and/or eczema also present ØFamily history of asthma 34 Additional Investigations ØChest X-ray: Seldom diagnostic but valuable to exclude alternative diagnoses and establish presence of significant comorbidities. ØOximetry and Arterial Blood Gases: Pulse oximetry can be used to evaluate a patient’s oxygen saturation and need for supplemental oxygen therapy. 35 Beta2-agonists Short-acting beta2-agonists Long-acting beta2-agonists Anticholinergics Short-acting anticholinergics Long-acting anticholinergics Combination short-acting beta2-agonists + anticholinergic in one inhaler Methylxanthines Inhaled corticosteroids Combination long-acting beta2-agonists + corticosteroids in one inhaler Systemic corticosteroids §An inhaled corticosteroid combined with a long-acting beta2-agonist is more effective than the individual components in improving lung function and health status and reducing exacerbations in moderate to very severe COPD. §Combination therapy is associated with an increased risk of pneumonia. §Addition of a long-acting beta2-agonist/inhaled glucorticosteroid combination to an anticholinergic appears to provide additional benefits. Therapeutic Options: Combination Therapy 37 ØChronic treatment with systemic corticosteroids should be avoided because of an unfavorable benefit-to-risk ratio. Therapeutic Options: Systemic Corticosteroids 38 Therapeutic Options: Theophylline ØTheophylline is less effective and less well tolerated than inhaled long-acting bronchodilators and is not recommended if those drugs are available and affordable. ØThere is evidence for a modest bronchodilator effect and some symptomatic benefit compared with placebo in stable COPD. Addition of theophylline to salmeterol produces a greater increase in FEV1 and breathlessness than salmeterol alone. ØLow dose theophylline reduces exacerbations but does not improve post-bronchodilator lung function. 39 ØInfluenza vaccines can reduce serious illness. Pneumococcal polysaccharide vaccine is recommended for COPD patients 65 years and older and for COPD patients younger than age 65 with an FEV1 < 40% predicted. ØThe use of antibiotics, for treating infectious exacerbations of COPD and other bacterial infections. Therapeutic Options: Other Pharmacologic Treatments 40 ØMucolytic: Patients with viscous sputum may benefit from mucolytics; overall benefits are very small. ØAntitussives: Not recommended. Therapeutic Options: Other Pharmacologic Treatments 41 ØOxygen Therapy: The long-term administration of oxygen (> 15 hours per day) to patients with chronic respiratory failure has been shown to increase survival in patients with severe, resting hypoxemia. ØVentilatory Support: Combination of noninvasive ventilation (NIV) with long-term oxygen therapy may be of some use in a selected subset of patients, particularly in those with pronounced daytime hypercapnia. Therapeutic Options: Other Treatments 42 Palliative Care, End-of-life Care, Hospice Care: ØCommunication with advanced COPD patients about end-of-life care and advance care planning gives patients and their families the opportunity to make informed decisions. Therapeutic Options: Other Treatments 43 Exacerbation of COPD Øis an event in the natural course of the disease characterised by a change in the patient’s baseline dyspnoea, cough and/or sputum beyond day-to-day variability, sufficient to warrant a change in management 44 ØThe most common causes of COPD exacerbations are viral upper respiratory tract infections and infection of the tracheobronchial tree. ØThe goal of treatment is to minimize the impact of the current exacerbation and to prevent the development of subsequent exacerbations. Manage Exacerbations: 45 ØShort-acting inhaled beta2-agonists with or without short-acting anticholinergics are usually the preferred bronchodilators for treatment of an exacerbation. ØSystemic corticosteroids and antibiotics can shorten recovery time, improve lung function (FEV1) and arterial hypoxemia (PaO2), and reduce the risk of early relapse, treatment failure, and length of hospital stay. ØCOPD exacerbations can often be prevented. Manage Exacerbations: 46 Antibiotics should be given to patients with three cardinal symptoms : 1.increased dyspnea 2.increased sputum volume 3.increased sputum purulence. ØWho require mechanical ventilation. Manage Exacerbations:Treatment Options 47 Noninvasive ventilation (NIV) for patients hospitalized for acute exacerbations of COPD: ØImproves respiratory acidosis, decreases respiratory rate, severity of dyspnea, complications and length of hospital stay. ØDecreases mortality and needs for intubation. Manage Exacerbations: Treatment Options 48 Oxygen ØIf the patient is hypoxaemic, oxygen must be applied in acute asthma and also in COPD exacerbation. ØIt is, however, important to know that in COPD, pCO2 might rise, requiring iterative blood gases to avoid CO2 narcosis, and titration of FiO2 so that SaO2 reaches but does not exceed 90%. ØIf reaching this target induces a significant worsening of the respiratory acidosis, there is a clear indication for ventilatory support! 49 Ventilatory support ØThe indications for ventilatory support (two out of three should be present) include: ØAt least moderate dyspnoea, with use of accessory muscles and paradoxical abdominal motion ØHypercapnic acidosis (pH <7.35) 50 Ventilation ØThe most commonly used ventilatory mode is pressure support with PEEP, or BIPAP in case of insufficient respiratory drive. ØThere are no clearly defined criteria for the initiation of invasive mechanical ventilation in COPD or asthma. ØIn COPD, the current approach is to intubate the patient if non-invasive ventilation fails, i.e. if blood gases and clinical status do not improve within one hour of initiation of non-invasive mechanical ventilation. ØIn asthma, the primary goal of intubation and mechanical ventilation is to maintain oxygenation and prevent respiratory arrest. Once a decision to intubate has been made, the goal is to gain rapid and complete control of the patient’s cardiorespiratory status. 51 Ventilation ØIf it is not possible to reach normoventilation within the safe parameters as mentioned above, it is recommended to use so-called permissive hypercapnia to avoid mechanical lung damage. Hypercapnic acidosis is usually well tolerated 52 Trauma 53 54 ram make a trauma 55 56 57 58 Mechanical ventilation ØToday, major technological advancements allow use of mechanical ventilators as sophisticated assistants of the respiratory pump. ØPositive pressure ventilation can also be very effective in lung failure. ØThe safe management of mechanical ventilation requires precise information about the individual disorders of respiratory mechanics 59 main mode Mechanical ventilation ØThe mechanical ventilator is an artificial organ, external to the body, which was conceived originally to replace, and later to assist, the inspiratory muscles. ØIts primary action is promotion of alveolar ventilation and CO2 elimination, but it is normally used also for the difficult task of correcting impaired oxygenation. 60 task- úkol O2 CO2 The function of the ventilator is to help get oxygen into the patient and carbon dioxide out 61 The function of the ventilator is to help get oxygen into the patient and carbon dioxide out Invasive vs non-invasive techniques ØIn intensive care, positive pressure ventilators are used most commonly, i.e. machines that promote alveolar ventilation by applying positive pressures at the airway opening of the patient. ØIn intensive care, two kinds of interface are used: lEndotracheal tube (or tracheostomy): The classic, invasive approach lMask: The non-invasive approach 62 Intubation ØThe invasive approach has a number of disadvantages associated with endotracheal intubation, such as: ØDeprese of cough effectiveness ØIncrease of airway resistance ØRisk of different types of damage of the bypassed airway ØLoss of the ability to speak ØLoss of the protective functions of the upper airway (gas heating, gas humidification, and protection from infections) 63 NIV ØSafe and effective management of mask ventilation has precise requirements: ØAt least some residual ability of spontaneous breathing (the need for full mechanical support is an absolute contraindication for a non-invasive approach) ØNo estimated need of high levels of positive pressure ØHaemodynamic stability ØGood cooperation from the patient ØThe ability of the patient to protect his own airway ØNo acute facial trauma, skull base fracture, or recent digestive surgery 64 65 diagram Spontaneous breathing 66 axis CPAP (Continuous Positive Airwav Pressure) ØSpontaneous breathing with CPAP. All breaths are fully spontaneous, and the inspiratory pressure is ideally equal to the set PEEP level. Technically, when applied with a mechanical ventilator, spontaneous breathing with CPAP is identical to PSV with a pressure support of zero. 67 PS (Pressure Support) Pressure Support Ventilation (PSV). This is based on spontaneous breaths assisted by a pre-set pressure. 68 SIMV (Synchronized Intermittent Mandatory Ventilation) This mode alternates assist-control volumetric inflations (delivered according to a user-set mandatory frequency) and breaths that can be either assisted-spontaneous (when pressure support is set above zero) 69 ACV (Assist Control) 70 PCV/VCV(Pressure/Volum Controlled Ventilation) ØVolume-Controlled Ventilation (VCV). In this mode the tidal volume (Vt) is preset. Breaths are either controlled or assist-controlled, depending on the lack or presence of patient’s inspiratory activity ØPressure-Controlled Ventilation (PCV). In this mode inspiration is promoted by a pre-set pressure. Breaths are either controlled or assist-controlled, depending on the lack or presence of patient’s inspiratory activity 71 PCV/VCV(Pressure/Volum Controlled Ventilation) 72 Cycling to exhalation: Machine vs patient ØWhen controlled by the machine, cycling is normally time-based. Time cycling means that the ventilator switches to exhalation as soon as the set inspiratory time (Ti) is elapsed. ØPatient-controlled cycling is used in assisted-spontaneous and fully spontaneous breaths. The expiratory trigger is based on the measurement of the inspiratory flow. When the inspiratory flow falls below a threshold value, the ventilator considers that the inspiratory effort should be close to the end, and hence cycles to exhalation. 73 Inspiratory time lThe normal I:E ratio is between 1:2 and 1:1.5, corresponding to an inspiratory duty cycle of 33-40%. 74 It can be set as a percentage of the respiratory cycle or as a ratio of inspiration to expiration, the so called I:E ratio. Note that on most ventilators the expiratory time is not set directly but is merely the remaining time after inspiration before the next breath Trigger Øpressure-trigger: the ventilator watches the airway pressure during exhalation. When the patient contracts his inspiratory muscles, the airway opening pressure drops below the baseline. When this drop reaches a pressure threshold defined by the trigger sensitivity control, the machine responds by starting the inspiratory phase of the respiratory cycle. Øflow-trigger: the ventilator watches the airflow. When the patient contracts his inspiratory muscles, the airflow reverses from expiratory or zero to inspiratory values. When the inspiratory flow generated by the patient reaches the trigger sensitivity threshold, the machine responds. 75 The trigger sensitivity determines how easy it is for the patient to trigger the ventilator to deliver a breath. In general increased sensitivity is preferable in order to improve patient-ventilator synchrony but excessively high sensitivity may result in false or auto-triggering .Triggering may be flow-triggered or pressure triggered. Flow triggering is generally more sensitive. The smaller the flow or the smaller the negative pressure the more sensitive the trigger PEEP ØPEEP contributes to the reopening of collapsed alveoli and opposes alveolar collapse. PEEP artificially increases the functional residual capacity and, by increasing the number of alveoli that are open to ventilation, it improves the lung compliance. ØPEEP level of up to 5 cmH2O has minor adverse effects and contraindications, and can be used in most patients. In most ALI-ARDS cases, a PEEP of 10-15 cmH2O is necessary ØImproves oxygenation 76 However PEEP has the major advantage that it may decrease shunting by re-opening alveoli. Respiratory complications ØNosocomial pneumonia ØBarotrauma: ØHigh pressures (barotrauma) ØHigh volumes (volutrauma) ØShear injury ØGas trapping 77 Respiratory complications of mechanical ventilation include nosocomial pneumonia, barotrauma and gas trapping Cardiovascular effects ØPreload Øpositive intrathoracic pressure reduces venous return Øexacerbated by Øhigh inspiratory pressure Øprolonged inspiratory time ØPEEP 78 Preload is reduced. This is predominantly due to reduced venous return. Normally venous return is enhanced by the negative intrathoracic pressure during inspiration. Not only is this abolished by positive pressure ventilation but venous return is actually impeded by the positive intrathoracic pressures. This effect will by exacerbated by any factors that increase the mean intrathoracic pressure such as high inspiratory pressures, prolonged inspiratory times and the application of PEEP. Ventilators are comprised of four main groups of elements: ØAn internal source of pressurised gas including a blender for air and oxygen ØThe inspiratory valve, the expiratory valve and the ventilator circuit ØA control system, including control panel, monitoring and alarms ØA system for ventilator-patient synchronisation 79 kempraiz- skládat se Parts of the external circuit Øthe inspiratory line, expiratory line ØY-piece Øflexible tube for patient connection Øthe external circuit can be very different, depending on the location of the expiratory valve, and on the system used for gas conditioning 80 Gas conditioning ØThe inspiratory gas delivered to the patient must be adequately heated and humidified. Gas conditioning can be obtained by means of: ØHeat and Moisture Exchanger (HME) mounted at the Y-piece ØHeated humidifier mounted within the inspiratory line. 81 De-escalation and weaning ØDe-escalation is a process that should be started as soon as a generic, even minimum improvement in patient’s respiratory state is found. ØDe-escalation involves FiO2, PEEP, and mechanical support to alveolar ventilation and respiratory muscles. ØWeaning the final step of deescalation, involving the patient’s complete and durable freedom from the need for mechanical support and artificial airway. 82