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Complications of invasive mechanical ventilation Related to tube insertion Aspiration of gastric contents Trauma of teeth, pharynx, oesophagus, larynx, trachea Sinusitis (nasotracheal intubation) Need for sedation Related to mechanical ventilation Arrhythmias and hypotension Barotrauma Related to tracheostomy Haemorrhage Trauma of trachea and oesophagus False lumen intubation Stomal infections and mediastinitis Tracheomalacia, tracheal stenoses and granulation tissue formation Tracheo-oesophageal or tracheoarterial fistulas Caused by loss of airway defence mechanisms Airway colonisation with Gram-negative bacteria Pneumonia Occurring after removal of the endotracheal tube Hoarseness, sore throat, cough and sputum Haemoptysis Vocal cord dysfunction and laryngeal swelling
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NPPV is defined as any form of ventilatory support applied without ETI, and is considered to include:.1 CPAP, with or without inspiratory pressure support;.2 volume- and pressure-cycled systems;.3proportional assist ventilation (PAV);.4 helium–oxygen (heliox) gas mixtures.
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Effectiveness and appropriate location for noninvasive positive pressure ventilation in acute respiratory failure (ARF) from different causes Cause of ARF Level of evidence# Location AECOPD A Ward, RIICU, ICU Depending on severity Weaning (AECOPD) A ICU, RIICU CPO A ICU, RIICU Immunocompromised patient A ICU, RIICU Post-operative respiratory failure B ICU Pre-intubation oxygenation B ICU Endoscopy B Depending on severity Asthma exacerbations C ICU, RIICU ALI/ARDS C ICU Extubation failure C ICU Do-not-intubate status C Ward, RIICU Pneumonia C ICU, RIICU
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Compared with standard medical therapy alone,NPPV improved survival, reduced the need for ETI and the rate of complications, and shortened the hospital and intensivecare unit (ICU) length of stay. Based on these observations, NPPV has been proposed as the first-line ventilatory strategy in this condition with different timing and location according to the level of ARF severity (fig. 2) [23, 24].
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NPPV v. standard therapy We recommend the use of NPPV in addition to usual care in patients who have a severe exacerbation of COPD(PH< 7.35 and relative hypercarbia ) (1A)
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We suggest that heliox not be routineiy used (NA) NPPV v.conventional mechanical ventilation We make no recommendation about the use of NPPV versus intubation and mechanical ventilation in patient whit severe exerbation of COPD because of insufficient evidence (NA)
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severity PH>7.35 PH7.35-7.25 PH<7.20 and/or: Neurological status Fatigue ETI indication MOF PH<7.25,alertness Locatio n Ward RIICU ICU T-Trial# SuccessFailure ExtubationEarly extubation DischargeNPPV Intervention Drug + oxygen NPPV ETI
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In contrast to AECOPD, the use of NPPV in severe exacerbations of asthma leading to ARF is supported by less evidenc. Thoracic Society Standards of Care Committee Statements: ‘‘NPPV should not be used routinely in acute asthma, but a trial might be considered in patients not promptly responding to standard treatments’’[34].e.
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NPPV or CPAP : We make no recommendation (NA)
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defined by a Pa,O2/oxygen inspiratory fraction (FI,O2) ratio f300 mmHg. Therefore, the following subsets of patients will be considered: acute cardiogenic pulmonary oedema; pneumonia; acute lung injury/acute respiratory distress syndrome; and post-operative respiratory failure.
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The use of NPPV in acute CPO is supported by RCTs [37–47] and meta-analyses [48–52]. Both mask CPAP and NPPV (inspiratory combined with positive end- expiratory pressure (PEEP); so-called bi-level ventilation) reduce ETI rate and, with a lower level of evidence, mortality rate, compared with standard medical therapy and oxygen. CPAP resulted in easier and less expensive application, and a meta-analysis suggests a greater efficacy in reducing mortality for this modality [51]. However, some studies [38, 39] suggest that NPPV may be preferable for patients with persisting dyspnoea or hypercapnia after initiation of CPAP, whereas early concerns about possible greater risks of myocardial infarction with NPPV [38] were not confirmed [53]. The main physiological benefit of CPAP in these patients is related to decreased left ventricular pre-load and afterload owing to increased intrathoracic pressure, resulting in improved cardiac performance; an increase in functional residual capacity reopens collapsed alveoli and improves oxygenation. This also reduces work of breathing [54].
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NPPV or CPAP v.standard therapy We recommend the use of either NPPV or CPAP in patients who have CPE and respiratory failure in the absent of shock or ACS (1A )
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NPPV seems disappointing in ARF owing to pneumonia [55,56], showing failure rates of up to 66% in patients with severe community-acquired pneumonia (CAP) [57]. An RCT of patients with severe CAP showed that NPPV reduced ETI rates, ICU length of stay and 2-month mortality rate, but only in the subgroup with underlying COPD [58]. Another RCT of patients with hypoxaemic ARF [59] showed that NPPV reduced the need for ETI among patients with pneumonia, but a more recent RCT [60], in which NPPV was used as an alternative to ETI in patients with various types of ARF, found that in the subgroup with pneumonia the technique was very unsuccessful. These data do not support the routine use of NPPV in patients with severe pneumonia. However, a cautious trial of NPPV may be considered in patients with pneumonia and underlying COPD under careful monitoring and in the appropriate setting.
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NPPV or CPAP v.standard therapy We make no recommendation in patient with no history of COPD ( NA )
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Studies of NPPV for the treatment of ALI/ARDS have reported failure rates ranging 50–80%, but no RCTs have focused on ALI/ARDS exclusively.Independent risk factors for NPPV failure in this group of patients include severe hypoxaemia, shock and metabolic acidosis [64]. Need for ETI was more likely in olderpatients, with a higher Simplified Acute Physiology Score (SAPS) II and severe hypoxaemia, or when a higher level of PEEP and pressure support was needed [67]. NPPV cannot be recommended as routine therapy for ALI/ARDS.
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NPPV v.standard therapy We no recommend ( NA ) CPAP v.standard therapy We recommend not be used (1C )
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NPPV or CPAP in all patients : We make no recommendation (NA)
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A small, single-centre study [74] showed that NPPV also has a role in ARF after solid organ transplantation (liver, lung, renal). RCTs in transplant recipients with haematological diseases and hypoxaemic ARF have shown decreased ETI and ICU mortality rates and shorter ICU lengths of stay in patients treated with NPPV as compared with conventional therapy [75]. An RCT in patients with ARF and immunosuppression from various causes reported lower mortality and ETI rates in the subgroupof patients treated with NPPV compared with standard treatment. The reduction in mortality was mainly related to the reduction in ETI rate and in the risk of VAP [76]. Similar findings have been reported by a nonrandomised study in patients with AIDS [77]. The reduced mortality rate is likely to be related to reduced infectious complications associated with NPPV compared with ETI, including VAP, other nosocomial infections and septic shock [78]. These findings support NPPV as the preferred initial ventilatory modality for these patients to avoid ETI and its associated risks.
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NPPV v.standard therapy : We suggest (2B) CPAP v.standard therapy : We make no recommendation (NA)
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The use of NPPV during fibreoptic bronchoscopy is supported by previous evidence and should be considered for use, especially when risks of ETI are high, such as in immunocompromised patients.
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NPPV has been proposed as a means of facilitating weaningfrom invasive mechanical ventilation in patients with AECOPD and acute on chronic respiratory failure failing a single [79, 80] or repeated T-piece trial [81]. In extubated patients who were switched to NPPV and weaned according to a standard protocol using pressure support ventilation, RCTs showed increased weaning rates, decreased duration of mechanical ventilation and ICU stay, and reduced rates of VAP compared with CMV. A meta-analysis of studies comparing ‘‘usual’’ weaning strategies to early extubation with immediate application ofNPPV, confirmed that switch toNPPV resulted in a favourable outcome, including lower mortality rate, lower rate of VAP and shorter total time of mechanical ventilation [82]. The physiopathological basis underlying these results is that NPPV is as capable as invasive ventilation for unloading respiratory muscles and improving gas exchanges; however, this can only partially explain the success of this technique in weaning [83]. Based on these findings, patients intubated for hypercapnic ARF due to AECOPD who fail spontaneous breathing trials should be considered for a trial of extubation to NPPV.
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Adjunct to early liberation from MV NPPV v.conventional MV With COPD: We suggest in centers that have expertise(2B) Without COPD: No recommendaion (NA)
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NPPV v.standard (high risk patients ) : we suggest (2B) NPPV v.standard ( low risk patient ) : we suggest not be used(2C)
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NPPV failed to reduce re-intubations and resulted in increased ICU mortality, possibly related to delays in re- intubation. These findings do not support the use of NPPV as a means of treatment of respiratory failure after extubation.
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Two other RCTs [87, 88] carried out on patients at high risk for extubation failure found that NPPV, applied immediately after extubation, prevented ARF and reduced the need for reintubation and ICU mortality, with the subset of COPD patients showing the most benefit [88]. NPPV has also been successfully used for the prevention of ARF in the first 48 h post-extubation in severely obese patients [89]. These data support the use of NPPV as a means of prevention of ARF in patients at high risk of extubation failure, in selected patient and in appropriate settings allowing for strict monitoring and prompt ETI. Routine use in all patients is discouraged [90].
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NPPV is being increasingly used as an alternative to invasive ventilation in end-stage symptomatic patients [91–95]. The use of NPPV for patients with ARF could be classified into three categories: 1) NPPV as life support with no pre- set limitations on life-sustaining treatments; 2) NPPV as life support when patients and families have decided to forego ETI; and 3) NPPV as a palliative measure when patients and families have chosen to forego all life support, receiving comfort measures only.
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For perivention of RF: No recommendation (NA) For treatment of RF : Abdominal surgery : We suggest CPAP (2C) Lung resection surgery : We suggest NPPV(2C)
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Reported contraindications for noninvasive ventilation Cardiac or respiratory arrest Severe encephalopathy Severe gastrointestinal bleeding Severe haemodynamic instability with or without unstable cardiac angina Facial surgery or trauma Upper airway obstruction Inability to protect the airway and/or high risk of aspiration Inability to clear secretions
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Clinical Sensorium Dyspnoea Respiratory rate Respiratory distress Mask comfort Compliance with ventilator setting Vital signs Physiology Arterial oxygen saturation Arterial blood pressure ECG Ventilator setting Air leaks Patient–ventilator interaction Set parameters
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Two or more of the following should be present: ◦ Use of accessory muscles ◦ Paradoxical breathing ◦ Respiratory rate≥25 breaths/min ◦ Dyspnea (moderate to severe or increased in COPD patients) ◦ PaCO2>45 mmHg with pH<7.35 ◦ PaO2/FiO2<200
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Clinical Criteria Gas Exchange Criteria Exclusion Criteria ◦ Respiratory arrest or immediate need for intubation ◦ Medically unstable Acute MI, uncontrolled arrhythmias, cardiac ischemia, upper GI bleeding, hypotensive shock ◦ Unable to protect airway Impaired swallowing or cough Excessive secretion ◦ Agitated or uncooperative ◦ Recent upper airway or esophageal surgery ◦ Unable to fit mask
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Inclusion: History of COPD Acute hypercapnic respiratory failure Clinical impression of impending intubation Exclusion: Apnea Unable to cooperate Need for airway protection (coma, seizure, vomiting) Systolic pressure < 90 mmHg Recent facial, esophageal. Or gastric surgery or trauma Unstable angina/acute MI Initial settings : Oronasal mask Pressure support ventilation Titrate inspiratory pressure to patient comfort Set expiratory pressure ≤ 5 cm H2O Titrate FiO2 for SpO2>90% Monitor: Patient comfort Level of dyspnea Respiratory rate Heart rate and blood pressure SpO2 Accessory muscle use; respiratory paradox Patient-ventilator synchrony Mask leak Arterial blood gas after 30 to 60 minutes Adjustments to improve patient compliance Coaching Mask fit Inspiratory and expiratory pressure levels FiO2 Sedation Continuous versus intermittent use Failure: Hemodynamic instability Decreased mental status Respiratory rate > 35/min Worsening respiratory acidosis Inability to maintain SpO2>90% Inability to tolerate mask Inability to manage secretions Patient preference CONSIDER INTUBATION yes no
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12 hr rest on NPPV if tolerated Nursing/respiratory care considerations : Monitor for signs of gastric distension Administer aerosolized bronchodilators Assess for drying of eyes and facial skin breakdown Titrated as tolerated : Pressure support target of 10 cm H2O; wean as tolerated FiO2 target of 0.40; wean provided SpO2≥90% Trials off NPPV as tolerated Monitor for signs of fatigue; resume NPPV if: Respiratory rate > 25/min Worsening dyspnea Increased use of accessory muscles Patient request Free from NPPV For 24 hr Without fatigue Discontinue NPPV yes
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Ventilator Capabilities ◦ Mandatory rate ~ to 30 breaths/min ◦ Patient trigger capabilities yes ◦ FiO2 0.21-0.5 ◦ Inspsiratory pressure to 30 cm H2O ◦ PEEP to 15 cm H2O ◦ 2-Hours battery back-up optional ◦ Pressure relief yes ◦ Antiasphyxia capabilities yes ◦ Airway attachments mask/mouthpiece ◦ Rebreathing potential minimal ◦ Inspiratory flow 60 L/min at 20 cm H2O ◦ ASTM circuit yes ◦ Humidification optional ◦ Leak tolerance yes Type 1 : Application of NPPV in a condition in which cessation of ventilatory support could lead to imminent death
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Monitors/alarms ◦ Pressure monitor optional ◦ Volume monitor optional ◦ High pressure alarm optional ◦ Disconnection alarm yes ◦ Power loss yes ◦ Battery loss yes (if battery present) Type 1 : Application of NPPV in a condition in which cessation of ventilatory support could lead to imminent death
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Inspiratory pressure Initial 8-10 cm H2O Eventual 12-20 cmH2O Expiratory pressure Initial 4- 5 cm H2O Eventual 4- 8 cm H2O Higher pressure for auto-PEEP improving oxygenation eliminating obstructive apnea eliminating rebreathing
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Back-up rate 12- 20 /min Oxygenation Bilevel ventilators O2 flow 2-15 L/min via mask or circuit Critical care ventilator Titrate FiO2 or flow for O2 sat>90-92% Humidification Heated pass-over humidifier recommended for >24 h applications
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Mask-related Frequency (%) Discomfort 30-50 Facial skin erythema 20-34 Claustrophobia 5-10 Nasal bridge ulceration 5-10 Acneiform rash 5-10
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Air-pressure- or flow-related Frequency Problem (%) Nasal congestion 20-50 Sinus/ear pain 10-30 Nasal/oral dryness 10-20 Eye irritation 10-20 Gastric insufflation 5-10
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Frequency (%) Air leaks 80-100 Major complications Aspiration pneumonia < 2 Hypotention < 2 Pneumothorax < 2
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Discomfort ◦ Check fit ◦ Adjust strap ◦ Apply water based jelly to mask contact points ◦ Try new mask type Facial skin erythema ◦ Loosen strap tension ◦ Apply artificial skin
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Claustrophobia ◦ Small mask ◦ Sedation Nasal bridge ulceration ◦ Loosen strap tension ◦ Apply artificial skin ◦ New mask Acneiform rash ◦ Topical steroids or antibiotics
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Nasal congestion ◦ Nasal steroids ◦ Decongesestants/antihistamine Sinus/oral dryness ◦ Nasal saline ◦ Add humidifier ◦ Reduce air leak Sinus/ear pain ◦ Reduce pressure if intolerable
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Eye irritation ◦ Check mask fit ◦ Readjust straps Gastric insufflation ◦ Reassure ◦ Simethacone ◦ Reduce pressure if intolerable
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Encourage mouth closure Try chin straps Oro-nasal mask if using nasal mask Apply water-based jelly to mask contact points Reduce pressure slightly
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