HFOV

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Published on November 18, 2018

Author: ishadeshmukh2

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Slide1: Principles of Mechanical Ventilation High-Frequency Oscillatory Ventilation  : 2 High-Frequency Oscillatory Ventilation   Outline: 3 Outline Review of Acute Lung Injury & Respiratory Mechanics HFOV: A General Overview Optimizing Oxygenation Optimizing Ventilation Routine Management of the Patient on HFOV Classification of high frequency ventilators: 4 Classification of high frequency ventilators Acute Lung Injury: 5 Acute Lung Injury In acute lung injury (ALI) there are 3 regions of lung tissue: Severely diseased regions with a limited ability to "safely" recruit. Uninvolved regions with normal compliance and aeration. Possibility of overdistension with increased ventilatory support. Intermediate regions with reversible alveolar collapse and edema. harshal Respiratory Mechanics: 6 Respiratory Mechanics ALI is associated with a decrease in lung compliance. Less volume is delivered for the same pressure delivery during ALI as compared to normal conditions. Lower and upper inflection points: At the lower end of the curve, the alveoli are at risk for derecruitment and collapse. At the upper end of the curve, the alveoli are at risk of alveolar overdistension. Volume Pressure NORMAL Acute Lung Injury Ventilator Associated Lung Injury: 7 Ventilator Associated Lung Injury All forms of positive pressure ventilation (PPV) can cause ventilator associated lung injury (VALI). VALI is the result of a combination of the following processes: Barotrauma Volutrauma Atelectrauma Biotrauma Barotrauma: 8 Barotrauma High airway pressures during PPV can cause lung overdistension with gross tissue injury. This injury can allow the transfer of air into the interstitial tissues at the proximal airways. Clinically, barotrauma presents as pneumothorax, pneumomediastinum, pneumopericardium, and subcutaneous emphysema . Volutrauma: 9 Volutrauma Lung overdistension can cause diffuse alveolar damage at the pulmonary capillary membrane. This may result in increased epithelial and microvascular permeability, thus, allowing fluid filtration into the alveoli (pulmonary edema). Excessive end-inspiratory alveolar volumes are the major determinant of volutrauma. Atelectrauma: 10 Atelectrauma Mechanical ventilation at low end-expiratory volumes may be inefficient to maintain the alveoli open. Repetitive alveolar collapse and reopening of the under-recruited alveoli result in atelectrauma. The quantitative and qualitative loss of surfactant may predispose to atelectrauma. Biotrauma: 11 Biotrauma In addition to the mechanical forms of injury, PPV activates an inflammatory reaction that perpetuates lung damage. Even ARDS from non-primary etiologies will result in activation of the inflammatory cascade that can potentially worsen lung function. This biological form of trauma is known as biotrauma. Capillary Leak: 12 Capillary Leak harshal Electron microscopy demonstrates the disruption of the alveolar-capillary membrane secondary to mechanical ventilation with lung distention. Note the leakage of RBCs and other material into the alveolar space. Slide13: 13 Pressure-Volume Loop Volume Pressure Inspiration “Beaking” with overdistension Expiration Atelectasis Zones of Injury Slide14: 14 Open Lung Ventilation Strategy Volume Pressure Zone of Overdistention Safe window Zone of Derecruitment and atelectasis Goal is to avoid injury zones and operate in the safe window Outline: 15 Outline Review of Acute Lung Injury & Respiratory Mechanics HFOV: A General Overview Optimizing Oxygenation Optimizing Ventilation Routine Management of the Patient on HFOV Pressure and Volume Swings: 16 Pressure and Volume Swings INJURY INJURY CMV HFOV During CMV, there are swings between the zones of injury from inspiration to expiration. During HFOV, the entire cycle operates in the “safe window” and avoids the injury zones. Pressure Transmission: 17 Pressure Transmission With CMV, the pressures exerted by the ventilator propagate through the airway with little dampening. With HFOV, there is attenuation of the pressures as air moves toward the alveolar level. Thus, with CMV the alveoli receive the full pressure from the ventilator. Whereas in HFOV, there is minimal stretching of the alveoli and, therefore, less risk of trauma. HFOV Lung Protective Strategies: 18 Lung Protective Strategies Utilizing HFOV in an open lung strategy provides a more effective means to recruit and protect acutely injured lungs. The ability to recruit and maintain FRC with higher mean airway pressure s may: improve lung compliance decrease pulmonary vascular resistance improve gas exchange With attenuation of  P, there is less trauma to the lungs and, therefore, less risk of VALI. HFOV improves outcome by  shear forces associated with the cyclic opening of collapsed alveoli. HFOV - General Principles: 19 HFOV - General Principles A CPAP system with piston displacement of gas Active exhalation Tidal volume less than anatomic dead space (1 to 3 ml/kg) Rates of 180 – 900 breaths per minute Lower peak inspiratory pressures for a given mean airway pressure as compared to CMV Decoupling of oxygenation & ventilation Indications for HFOV: 20 Indications for HFOV Inadequate oxygenation that cannot safely be treated without potentially toxic ventilator settings and, thus, increased risk of VALI. Objectively defined by: Peak inspiratory pressure (PIP) > 30-35 cm H 2 O F i O 2 > 0.60 or the inability to wean Mean airway pressure (P aw ) > 15 cm H 2 O Peak end expiratory pressure (PEEP) > 10 cm H 2 O Oxygenation index > 13-15 (P aw  F i O 2 ) P a O 2  100 OI = Relative Indications for HFOV (Regardless of ventilator settings or gas exchange): 21 Relative Indications for HFOV (Regardless of ventilator settings or gas exchange) Alveolar hemorrhage Sickle cell disease in acute chest syndrome Large airleak with inability to keep lungs open Inadequate alveolar ventilation with respiratory acidosis Patient Selection: 22 Patient Selection The clinical goals and guidelines presented are for the “typical” patient with ALI/ARDS. The goals may differ for: Other disease states – reactive airway disease, acute chest syndrome, flail chest, congenital diaphragmatic hernia, sepsis, pulmonary hypertension. Certain patient groups – congenital cardiac disease, closed head injury. Clinical Goals: 23 Clinical Goals Reasonable oxygenation to limit oxygen toxicity S a O 2 86 to 92% P a O 2 55 to 90 mm Hg Permissive hypercapnea Provide “just enough” ventilatory support to maintain normal cellular function. Monitor cardiac function, perfusion, lactate, pH Allow P a CO 2 to rise but keep arterial pH 7.25 to 7.30. This strategy helps to minimize VALI. ‘Normal’ pH, P a CO 2 , & P a O 2 are indictors of OVERventilation!! Outline: 24 Outline Review of Acute Lung Injury & Respiratory Mechanics HFOV: A General Overview Optimizing Oxygenation Optimizing Ventilation Routine Management of the Patient on HFOV Variables in Oxygenation: 25 Variables in Oxygenation The two primarily variables that control oxygenation are: F i O 2 Mean airway pressure (P aw ) Slide26: 26 23 35 33 7.5 P aw is displayed here Mean Airway Pressure (P aw ) is controlled here Mean Airway Pressure (Paw): 27 Mean Airway Pressure (P aw ) Use to optimize lung volume and, thus, alveolar surface area for gas exchange. Utilize P aw to: recruit atelectatic alveoli prevent alveoli from collapsing (derecruitment) Although the lung must be recruited, guard against overdistension. Alveolar atelectasis or overdistension can result in  pulmonary vascular resistance (PVR). Effect of Lung Volume on PVR: 28 Effect of Lung Volume on PVR Lung Volume PVR Total PVR Large Vessels Small Vessels Atelectasis Overexpansion FRC PVR is the lowest at FRC Overexpansion of small vessels  PVR Atelectasis of large vessels  PVR Oxygenation – Clinical Tips: 29 Oxygenation – Clinical Tips Initiate HFOV with F i O 2 1.0 P aw 5-8 cm H 2 O greater than P aw on CMV Increase P aw by 1 - 4 cm H 2 O to achieve optimal lung volume. Optimal lung volume is determined by: increase in S a O 2 allowing the F i O 2 to be weaned diaphragm is at T9 on chest radiograph Maintain the P aw and wean the F i O 2 until ≤ 0.60. Oxygenation – Clinical Tips: 30 Oxygenation – Clinical Tips Follow CXR’s to assess lung expansion. If the diaphragm is between 8 and 8 ½ , continue to wean the oxygen. If the diaphragm is between 9 and 9 ½ , wean the P aw by 1 cm H 2 O. You should be able to wean the F i O 2 to < 0.60 within the first 12 hours of HFOV. If unable to wean F i O 2 , consider: a recruitment maneuver (sustained inflation) increasing the P aw Oxygenation – Clinical Tips: 31 Oxygenation – Clinical Tips Lung perfusion must be matched to ventilation for adequate oxygenation (V/Q matching). Ensure adequate intravascular volume & cardiac output. The higher intrathoracic pressure may adversely affect cardiac preload. Consider volume loading (  5 mL/kg) or initiating inotropes. Closely monitor hemodynamic status. Utilize pulse oximetry and transcutaneous monitors to wean F i O 2 between blood gas analyses. Gas exchange & ventilator adjustments during high frequency ventilation: 32 Gas exchange & ventilator adjustments during high frequency ventilation Outline: 33 Outline Review of Acute Lung Injury & Respiratory Mechanics HFOV: A General Overview Optimizing Oxygenation Optimizing Ventilation Routine Management of the Patient on HFOV Ventilation: 34 Ventilation The two primarily variables that control ventilation are: Tidal volume (  P or amplitude) Controlled by the force with which the oscillatory piston moves. (represented as stroke volume or P) Frequency ( ) Referenced in Hertz (1 Hz = 60 breaths/second) Range: 3 - 15 Hz Variables in Ventilation: 35 Variables in Ventilation In CMV, ventilation is defined as: f x V t In HFOV, ventilation is defined as: f x V t 1.5-2.5 Therefore, changes in V t delivery have a larger effect on ventilation than changes in frequency. Amplitude (P): 36 Amplitude (  P) The power control regulates the force and distance with which the piston moves from baseline. The degree of deflection of the piston (amplitude) determines the tidal volume. This deflection is clinically demonstrated as the “wiggle” seen in the patient. The wiggle factor can be utilized in assessing the patient. “Wiggle Factor”: 37 “Wiggle Factor” Reassess after positional changes If chest oscillation is diminished or absent consider: decreased pulmonary compliance ETT disconnect ETT obstruction severe bronchospasm If the chest oscillation is unilateral, consider: ETT displacement (right mainstem) pneumothorax Amplitude Selection: 38 Amplitude Selection Start amplitude in the 30’s and adjust until the “wiggle” extends to the lower level of patient’s groin. Adjust in increments of 3 to 5 cm H 2 O Subjectively follow the wiggle Objectively follow transcutaneous CO 2 and P a CO 2 Remember, the goal is not to achieve ‘normal’ P a CO 2 and pH, but to minimize VALI. Slide39: 39 23 35 33 7.5 The power dial controls the degree of piston deflection This is displayed as the amplitude or P Resonance Frequency: 40 Resonance Frequency There is a resonance frequency of the lungs in which optimal ventilation (CO 2 removal) occurs. Resonance frequency varies based on: lung size the degree of lung injury Resonance Frequency: 41 Resonance Frequency The resonance frequency depends on: the amount of functional lung the type and extent of the disease state the size of the patient Therefore, the resonance frequency can vary between patients and in the same patient over the time. Initial Frequency Settings: 42 Initial Frequency Settings Guidelines for setting the initial frequency. Adjustments in frequency are made in steps of ½ to 1 Hz. Patient Weight Hertz Preterm Neonates 10 to 15 Term Neonates 8 to 10 Children 6 to 8 Adults 5 to 6 Frequency (): 43 Frequency ( ) To evaluate the effects of changes in frequency with regards to CO 2 elimination, let us look at 2 different frequencies. 4 Hz 8 Hz Frequency (): 44 Time X 4 Hz 8 Hz Frequency ( ) Lets consider a time interval of X Frequency (): 45 Time X 4 Hz 8 Hz The lower the frequency setting, the larger the volume displacement. Frequency ( ) Frequency (): 46 Time X 4 Hz 8 Hz The higher the frequency setting, the smaller the volume displacement. Frequency ( ) Frequency (): 47 Time X Therefore, lower frequencies have a larger volume displacement and improved CO 2 elimination. Frequency ( ) Slide48: 48 23 35 33 7.5 The frequency is controlled and read here Improving Ventilation: 49 Improving Ventilation To improve ventilation first increase the amplitude. If this does not improve CO 2 elimination, consider decreasing the frequency. Although controversial, some centers consider decreasing the frequency by 1 Hz once the amplitude is  3 times the P aw . Inspiratory Time: 50 Inspiratory Time The initial inspiratory time setting is 33%. If carbon dioxide elimination is inadequate, despite deflating the ETT cuff (or if the patient has an uncuffed tube), consider increasing the i-time (max 50%). Increasing the i-time allows for a larger tidal volume delivery. Slide51: 51 23 35 33 7.5 The inspiratory time is controlled and read here Improved Ventilation: 52 Improved Ventilation If there is appropriate chest wiggle and the P a CO 2 is too low, consider increasing the frequency. Once you have improved ventilation or are in the weaning phase, do not forget to: decrease i-time to 33%. reinflate the ETT cuff (if deflated). raise/adjust the frequency as the resonance frequency of the lungs changes. wean the amplitude. Outline: 53 Outline Review of Acute Lung Injury & Respiratory Mechanics HFOV: A General Overview Optimizing Oxygenation Optimizing Ventilation Routine Management of the Patient on HFOV Sedation/Neuromuscular Blockade: 54 Sedation/Neuromuscular Blockade Transitioning a patient from CMV to HFOV typically indicates that the patient’s respiratory distress has worsened. To facilitate ‘capturing’ the patient, additional sedation may be required. Neuromuscular blockade may be required. As the patient improves, discontinue the paralysis and wean the sedation as tolerated. Auscultation: 55 Auscultation Listen to the lung fields to primarily assess the presence and symmetry of piston sounds. Asymmetry may indicate improper ETT placement, pneumothorax, heterogeneous gross lung disease, or mucus plugging. Pause the piston to perform a cardiac exam and assess heart sounds. With the piston paused you have placed the patient in a CPAP mode and will have maintained P aw . Chest Radiographs: 56 Chest Radiographs Typically obtain a chest radiograph 1 hour after initiating HFOV and then Q12-24 hours. Assess ETT placement Rib expansion (goal is  9 ribs) Pneumothorax / airleak syndrome Change in lung disease Suctioning: 57 Suctioning Indications: Routine suctioning to ensure the ETT remains patent Frequency of suctioning varies by institution. Our policy is every 12 to 24 hours and prn. Decreased/absent wiggle Possibly from mucus plugs/secretions Decrease in S p O 2 or transcutaneous O 2 level Increase in transcutaneous CO 2 level Suctioning de-recruits lung volume May be minimized but not fully eliminated with closed suction system. May require a sustained inflation recruitment maneuver following suctioning . Sustained Inflation (SI): 58 Sustained Inflation (SI) A sustained inflation is a lung recruitment maneuver. There are several ways in which to perform a SI maneuver. In our institution, the piston is paused (thus leaving the patient in CPAP) and the P aw is increased by 8-10 cm H 2 O for 30-60 seconds. Once the SI maneuver is completed, the piston is restarted. Potential complications: Pneumothorax CV compromise / altered hemodynamics When To Utilize A SI Maneuver: 59 When To Utilize A SI Maneuver When initiating HFOV to recruit lung After a disconnect or loss of FRC/P aw After suctioning (even with a closed suction system) Inability to wean F i O 2 When considering increasing P aw A recruitment maneuver may recruit lung allowing you to maintain the baseline P aw and, thus, not increase support. Weaning : 60 Weaning Once goals and adequate ventilation nad oxygenation are achieved. FiO2 < 30% gradually decreased MAP to 6-8 cm H2O Big babies extubate directly from HFV Small babies switch over to CMV or CPAP Potential Complications of HFOV: 61 Potential Complications of HFOV The higher intrathoracic pressures with HFOV may decrease RV preload and require volume administration ± inotropic support. Pneumothorax Migration/displacement of ETT Bronchospasm Acute airway obstruction from mucus plugging, secretions, hemorrhage or clot. Summary: 62 Summary Open the lungs and keep them open HFOV improves outcome by  shear forces associated with the cyclic opening of collapsed alveoli. Minimize P (i.e., shear injury) to the lungs by minimizing the swings from inspiration to expiration. Ventilate in the “safe window”. Oxygenation and ventilation are dissociated. Adjust P aw independently of P Looking towards the future: 63 Looking towards the future A great deal remains unknown about HFOV: the exact mechanism of gas exchange the most effective strategy to manipulate ventilator settings the safest approach to manipulate ventilator settings a reliable method to measure tidal volume the appropriate use of sedation and neuromuscular blockade to optimize patient-ventilator interactions Additional research in these and other issues related to HFOV are necessary to maximize the benefit and minimize the potential risks associated with HFOV. Looking towards the future: 64 Looking towards the future A great deal remains unknown about ARDS in the pediatric patient. Although there has been a substantial quantity of research performed in using various treatment options in adults (prone positioning, steroids, iNO, tidal volume, etc.), many of these therapies have not been evaluated in pediatric patients with ARDS. Additional research in the pathophysiology of pediatric ARDS and various treatment options is necessary. Remember : 65 Remember Newborn is a demanding individual whichever method of ventilation is used, clinical observations, bedside vigilance, timely action, human touch and tender care can not be replaced by any technology.. Harshal References: 66 References Priebe GP, Arnold JH: High-frequency oscillatory ventilation in pediatric patients. Respir Care Clin N Am 2001; 7(4):633-645 Arnold JH, Anas NG, Luckett P, Cheifetz IM, Reyes G, Newth CJ, Kocis KC, Heidemann SM, Hanson JH, Brogan TV , et al. : High-frequency oscillatory ventilation in pediatric respiratory failure: a multicenter experience. Crit Care Med 2000; 28(12):3913-3919 Arnold JH: High-frequency ventilation in the pediatric intensive care unit. Pediatr Crit Care Med 2000; 1(2):93-99 Slutsky, AS: Lung Injury Caused by Mechanical Ventilation. Chest 1999; 116(1):9S-14S dos Santos CC, Slutsky AS: Overview of high-frequency ventilation modes, clinical rationale, and gas transport mechanisms. Respir Care Clin N Am 2001; 7(4):549-575 Duke PICU Handbook (revised 2003) Duke Ventilator Management Protocol (2004)

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