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![Hypoxemic Respiratory Failure
• Recognized by an acute fall in P02 or
oxyhemoglobin saturation (for example, a P02
to less than or equal to 60 mm Hg or PO2
/fraction of inspired oxygen [FiO2] less than or
equal to 200
• Conditions causing acute hypoxemic
respiratory failure include alveolar collapse
and flooding with fluid, pus, or blood.](https://image.slidesharecdn.com/3noninvasiveventilation-140519135323-phpapp02/85/3-noninvasive-ventilation-3-320.jpg)
![Acute Lung Injury & Acute Respiratory
Distress Syndrome
• Definitions
– ALI: PO2 /fraction of inspired oxygen [FiO2]in liter
is less than 300
– ARDS: PO2 /fraction of inspired oxygen [FiO2]in
liter is less than 300 ( more severe ALI)
ALI /ARDS is a noncardiogenic form of pulmonary
edema characterized by acute and persistent lung
inflammation and increased vascular permeability
( Damaged and leaky pipes)](https://image.slidesharecdn.com/3noninvasiveventilation-140519135323-phpapp02/85/3-noninvasive-ventilation-5-320.jpg)
Uploaded byKhidir Altayep
3 noninvasive ventilation
Respiratory failure can occur due to hypoxemic failure, hypercapnic (ventilatory) failure, or impaired airways. Noninvasive ventilation (NIV) delivers breaths through a tight-fitting mask and can treat various causes of respiratory failure without needing intubation. The first 30 minutes of NIV require close monitoring as clinicians work to improve gas exchange and comfort while watching for signs that intubation is needed instead. NIV is effective for acute exacerbations of COPD and cardiogenic pulmonary edema when criteria are met.
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Similar to 3 noninvasive ventilation
3 noninvasive ventilation
- 1.
- 2. Respiratory Failure • Patientswith respiratory insufficiency can be due to three conditions: • (1) hypoxemic respiratory failure • (2) ventilatory, or hypercapnic, respiratory failure • (3) impaired upper airway. However, often more than one of these factors contributes to respiratory failure. Calculation of the alveol ararterial difference (A-a gradient) can be useful.
- 3. Hypoxemic Respiratory Failure •Recognized by an acute fall in P02 or oxyhemoglobin saturation (for example, a P02 to less than or equal to 60 mm Hg or PO2 /fraction of inspired oxygen [FiO2] less than or equal to 200 • Conditions causing acute hypoxemic respiratory failure include alveolar collapse and flooding with fluid, pus, or blood.
- 4. Hypoxemic Respiratory Failure •Pathophysiology: • Continued perfusion of these unventilated lung unit can lead to profound, refractory hypoxemia • Hypoxemia does not correct with increased alveolar ventilation or supplemental oxygen. • PEEP: PEEP opens up, or "recruits," flooded or collapsed alveoli. •
- 5. Acute Lung Injury& Acute Respiratory Distress Syndrome • Definitions – ALI: PO2 /fraction of inspired oxygen [FiO2]in liter is less than 300 – ARDS: PO2 /fraction of inspired oxygen [FiO2]in liter is less than 300 ( more severe ALI) ALI /ARDS is a noncardiogenic form of pulmonary edema characterized by acute and persistent lung inflammation and increased vascular permeability ( Damaged and leaky pipes)
- 6. Acute Lung Injury& Acute Respiratory Distress Syndrome • Pulmonary artery catheters for the management of medical ICU patients offers no survival benefit. • Ruling out cardiogenic edema relies on clinical, laboratory, and echocardiographic evaluation • More than 60 disorders can precipitate ALl and ARDS • Sepsis and Pneumonia is the most common cause of ALI ?ARDS
- 7. Heart Failure • Leftventricular dysfunction can result in acute onset of bilateral pulmonary infiltrates that are radiographically indistinguishable from ALI • The hypoxemia associated with cardiogenic edema may rapidly improve with aggressive diuresis combined with temporizing measures such as noninvasive positive pressure ventilation (NPPV).
- 8.
- 9. Hypercarbic Respiratory Failure •Ventilatory respiratory failure refers to inadequate alveolar ventilation or increased CO2 Production • P CO2 = (VCO2 , x k)/VA (where k is constant = 0.863) • Fever and increased mechanical work of breathing are important clinical causes of elevated CO2 • Decreased respiratory drive, weakness of respiratory muscles, and elevated dead-space ventilation contribute-to reduced Ventilation
- 11. Respiratory Failure: RestrictiveLung Disease • Extrapulmonary These disorders include chest wall diseases such as kyphoscoliosis, morbid obesity, large pleural effusions, and elevated intra-abdominal pressure from ascites, bowel edema etc. • Pulmonary • Ventilatory failure due to fibrotic lung disease typically is accompanied by severe hypoxemia and carries a poor prognosis
- 12.
- 13. Definition.. • Noninvasive ventilationis the delivery of ventilatory support without the need for an invasive artificial airway • In patients with new-onset respiratory fail- ure, NPPV often entails the use of a ventilator that delivers breaths through a tight-fitting mask placed over the patient's nose and/or mouth.
- 14. How does NIVwork? • Reduction in inspiratory muscle work and avoidance of respiratory muscle fatigue • Tidal volume is increased • CPAP counterbalances the inspiratory threshold work related to intrinsic PEEP. • NIV improves respiratory system compliance by reversing microatelectasis of the lung.
- 15. Advantages of NIV •Noninvasiveness – Application (compared with endotracheal intubation) – Easy to implement b. – Easy to remove Allows intermittent application – Improves patient comfort – Reduces the need for sedation – Oral patency (preserves speech, swallowing, and cough, reduces the need for nasoenteric tubes)
- 16. • Avoid theresistive work imposed by the endotracheal tube • Avoids the complications of endotracheal intubation – Early (local trauma, aspiration) – Late (injury to the the hypopharynx, larynx, and trachea, nosocomial infections)
- 17. Disadvantages of NIV •1.System – Slower correction of gas exchange abnormalities – Increased initial time commitment – Gastric distension (occurs in <2% patients) • 2.Mask – Air leakage – Transient hypoxemia from accidental removal – Eye irritation – Facial skin necrosis –most common complication. 3. Lack of airway access and protection – Suctioning of secretions – aspiration
- 18. Location of NIV •NIV can be administered in the emergency department, intermediate care unit, or general respiratory ward • It all depend on the experience of your team
- 19. Who can administerNIV? • By physicians, nurses, or respiratory care therapists, • Depends on staff experience and availability of resources for monitoring, and managing complications • For the first few hours, one-to-one monitoring by a skilled and experienced nurse, respiratory therapist, or physician is mandatory. • Immediate access to staff skilled in invasive airway management.
- 20. Interface Nasal masks • lessdead space • less claustrophobia • allow for expectoration vomiting and oral intake • vocalize facial mask dyspnoeic patients are usually mouth breathers More dead space
- 21. Humidification during NIV Nohumidification: drying of nasal mucosa; increased airway resistance; decreased compliance. HME lessens the efficacy of NIV Only pass-over humidifiers should be used Intensive Care Med. 2002;28
- 22. Aerosol bronchodilator deliveryduring NIV • Optimum nebulizer position: between the leak port and patient connection • Optimum ventilator settings: high inspiratory pressure and low expiratory pressure. • Optimum RR 20/mt. Rather than 10/mt. • 25% of salbutamol dose may be delivered Crit Care Med. 2002 Nov;30
- 23. Uses of NIV 1.COPD. Acute exacerbation/domiciliary. 2. Cardiogenic pulmonary edema. 3. Bronchial asthma 4. Post extubation RF 5. Hasten weaning.
- 24. COPD EXACERBATION: NIV •Success rates of 80-85% • Increases pH, reduces PaCO2, reduces the severity of breathlessness in first 4 h of treatment • Decreases the length of hospital stay • Mortality, intubation rate—is reduced GOLD 2003
- 25. CRITERIA FOR NIVIN ACUTE EXACERBATION OF COPD GOLD 2005
- 28. Cardiogenic Pulmonary edema…. •Sufficiently high level evidence to favor the use of CPAP • There is insufficient evidence to recommend the use of BiPAP, probably the exception being patients with hypercapnic CPE.
- 29. Methodology • Initial ventilatorsettings: CPAP (EPAP) 2 cm H2O & PSV (IPAP) 5 cm H20. • Mask is held gently on patient’s face. • Increase the pressures until adequate Vt (7ml/kg), RR<25/mt, and patient comfortable. • Titrate FiO2 to achieve SpO2>90%. • Keep peak pressure <25-30 cm • Head of the bed elevated
- 30. Monitoring Response Physiological a) Continuousoximetry b) Exhaled tidal volume c) ABG should be obtained with 1 hour and, as necessary, at 2 to 6 hour intervals. Objective a) Respiratory rate b) blood pressure c) pulse rate Subjective a) dyspnea b) comfort c) mental alertness
- 31. Monitoring….. Mask Fit, Comfort, Airleak, Secretions, Skin necrosis Respiratory muscle unloading Accessory muscle activity, paradoxical abdominal motion Abdomen Gastric distension
- 32. The Bottom Line •First 30 min. of NPPV is labor intensive. • Bedside presence of a respiratory therapist or nurse • familiar with this mode is essential. • Providing reassurance and adequate explanation • Be ready to intubate and start on invasive ventilation.
- 33. First 30 min.of NPPV is labor intensive. Bedside presence of a respiratory therapist or nurse familiar with this mode is essential. Providing reassurance and adequate explanation Be ready to intubate and start on invasive ventilation.
- 34. Criteria to discontinueNIV • Inability to tolerate the mask because of discomfort or pain • Inability to improve gas exchange or dyspnea • Need for endotracheal intubation to manage secretions or protect airway • Hemodynamic instability • ECG – ischemia/arrhythmia • Failure to improve mental status in those with CO2 narcosis.
Editor's Notes
- #4 Hypoxemic Respiratory Failure Acute hypoxemic respiratory failure is recognized by an acute fall in P02 or oxyhemoglobin saturation (for example, a P02to less than or equal to 60 mrn Hg or POy'fraction of inspired oxygen [Pio.] less than or equal to 200 [Po.fess than 200 on 100% oxygen or less than 100 on 50% oxygen]). In pure hypoxemic respiratory failure, the Pco, is typically normal or reduced. Conditions causing acute hypoxemic respiratory fail- ure include alveolar collapse and flooding with fluid, pus, or blood. Continued perfusi9n of these unventilated lung units
- #5 Continued perfusion of these unventilated lung unitcan lead to profound, refractory hypoxemia that does not adequately correct with increased alveolar ventilation or supplemental oxygen. Rather, hypoxemia is reversed by application of positive end-expiratory pressure (PEEP) to the lung, which opens up, or "recruits," flooded or collapsed alveoli.
- #6 Acute Lung Injury and the Acute Respiratory Distress Syndrome Acute lung injury (ALl) is a noncardiogenic form of pul- monary edema characterized by acute and persistent lung inflammation and increased vascular permeability. Diffuse inflammatory injury of the alveolar epithelial cells and cap- illary endothelial cells results in leakage of fluid, protein, and inflammatory cells into the interstitium and alveoli. The pathologic correlate is diffuse alveolar damage, but the diagnosis typically is made clinically rather than histologi- cally (Table 39). ALl causes hypoxemic respiratory failure, defined by a Po2/Fio2 less than or equal to 300. The subset of patients with ALl who have severe hypoxemia (Po2/Fio2 less than or equal to 200) is considered to have the acute respiratory dis- tress syndrome (ARDS). In addition to a decreased Po2/Fio2ratio, the diagnosis of either ALlor ARDS requires the pres- ence of bilateral pulmonary infiltrates on a chest radiograph and the absence of evidence to suggest increased left atrial pressure (for example, left ventricular dysfunction). There is substantial evidence that the routine use of pul- monary artery catheters for the management of medical I CD patients (including those with ARDS) offers no survival ben- efit. Therefore, the exclusion of cardiogenic edema increas- ingly relies on clinical, laboratory, and echocardiographic eval- uation to exclude left ventricular dysfunction rather than measurement of the pulmonary capillary wedge pressure. More than 60 disorders can precipitate ALl and ARDS by either direct insult to the lung or by marked systemic inflam- mation elsewhere in the body that releases mediators that can cause pulmonary capillary leak (and also affect multiple
- #7 Acute Lung Injury and the Acute Respiratory Distress Syndrome Acute lung injury (ALl) is a noncardiogenic form of pul- monary edema characterized by acute and persistent lung inflammation and increased vascular permeability. Diffuse inflammatory injury of the alveolar epithelial cells and cap- illary endothelial cells results in leakage of fluid, protein, and inflammatory cells into the interstitium and alveoli. The pathologic correlate is diffuse alveolar damage, but the diagnosis typically is made clinically rather than histologi- cally (Table 39). ALl causes hypoxemic respiratory failure, defined by a Po2/Fio2 less than or equal to 300. The subset of patients with ALl who have severe hypoxemia (Po2/Fio2 less than or equal to 200) is considered to have the acute respiratory dis- tress syndrome (ARDS). In addition to a decreased Po2/Fio2ratio, the diagnosis of either ALlor ARDS requires the pres- ence of bilateral pulmonary infiltrates on a chest radiograph and the absence of evidence to suggest increased left atrial pressure (for example, left ventricular dysfunction). There is substantial evidence that the routine use of pul- monary artery catheters for the management of medical I CD patients (including those with ARDS) offers no survival ben- efit. Therefore, the exclusion of cardiogenic edema increas- ingly relies on clinical, laboratory, and echocardiographic eval- uation to exclude left ventricular dysfunction rather than measurement of the pulmonary capillary wedge pressure. More than 60 disorders can precipitate ALl and ARDS by either direct insult to the lung or by marked systemic inflam- mation elsewhere in the body that releases mediators that can cause pulmonary capillary leak (and also affect multiple
- #8 Heart Failure Left ventricular dysfunction can result in acute onset ofbilat- eral pulmonary infiltrates that are radiographicallyindistin- guishable from ALL Differentiating cardiogenic from non- cardiogenic edema has important clinical implications because the hypoxemia associated with cardiogenic edema may rapidly improve with aggressive diuresis combined with temporizing measures such as noninvasive positive pressure ventilation (NPPV).
- #12 Restrictive Lung Disease Extrapulmonary The mechanical work of breathing is markedly increased in some disorders, thereby precipitating ventilatory failure even in the" absence of intrinsic lung disease or weakness. Such patients have a restrictive pattern on pulmonary function tests. These disorders include chest wall diseases such as kyphosco- liosis, morbid obesity, large pleural effusions, and elevated intra-abdominal pressure from ascites, bowel edJina, or intraoperative gas insufflation. Kyphoscoliosis cannot be sur- gically corrected in adults, but affected patients are suitable candidates for NPPV, particularly at night when accessory muscle compensation is not as effective. Patients with extra- pulmonary causes of restriction who develop infection or other acute illnesses 'may experience sudden declines in ven- tilatoryfunction resulting in the need for intensive care. Pulmonary Ventilatory failure due to fibrotic lung disease typically is accompanied by severe hypoxemia and carries a poor prog- nosis. Exacerbation of idiopathic pulmonary fibrosis, which is characterized by diffuse alveolar damage superimposed on fibrosis, is increasingly recognized as a cause of death in patients with even mild baseline decrements in pulmonary function tests (see also Diffuse Parenchymal Lung Disease).