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RESPIRATORY FAILURE and ARDS BY NANCY JENKINS Respiration Exchange of O2 and CO2 gas exchange Respiratory Failure the inability of the cardiac and pulmonary systems to maintain an adequate exchange of oxygen and CO2 in the lungs Classification of Respiratory Failure Inhaling Exhaling Affects PaO2 Affects PCO2 Fig. 68-2 Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. Hypoxemic Respiratory Failuremost common type (Affects the pO2) Physiologic mechanisms: V/Q Mismatch Shunt Diffusion Limitation Hypoxemia-VentilationPerfusion Mismatch(V/Q) Normal V/Q =1 (1ml air/ 1ml of blood) Ventilation=lungs (breathing in and out) Perfusion or Q=perfusion- heart (delivery of blood to a capillary bed to tissues) Q greater than V , V greater than Q Ex-Pulmonary Embolus- (VQ scan) Range of V/Q Relationships Fig. 68-4 Pulmonary Embolus- V greater than Q Hypoxemia Shunt Anatomic • blood passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect Intrapulmonary • blood flows through pulmonary capillaries without participating in gas exchange ex: alveoli filled with fluid * Patients with shunts are more hypoxemic than those with VQ mismatch and they may require mechanical ventilators Hypoxemia Diffusion Limitation Gas exchange is compromised by a process that thickens or destroys the membrane 1. 2. Pulmonary fibrosis 2. ARDS * A classic sign of diffusion limitation is hypoxemia during exercise but not at rest- Why?? Hypercapnic Respiratory Failure Ventilatory Failure- affects CO2 1. Abnormalities of the airways and alveoli- air flow obstruction and air trapping- Asthma, COPD, and cystic fibrosis 2. Abnormalities of the CNS- suppresses drive to breathe drug OD, narcotics, head injury, spinal cord injury 3. Abnormalities of the chest wall- (dec tidal volume) • Flail chest, morbid obesity, kyphoscoliosis 4. Neuromuscular Conditions- respiratory muscles are weakened:- Guillain-Barre, muscular dystrophy,myasthenia gravis and multiple sclerosis Keeps air in, can’t exhale the CO2- inc. CO2 acidemia, pH < 7.35 In which of the following patients would you expect to see hypercapneic respiratory failure? Review of patients with potential respiratory failure. 1. 2. 3. 4. A patient with an anxiety attack A patient on a PCA of dilaudid A patient with COPD A patient with a RR of 30 Hypoxemia causes dec. O2 to tissues (can cause death of cells) Tissue O2 delivery is determined by: • Amount of O2 in hemoglobin- Keep at 9 • Cardiac output-4-8L/min • *Respiratory failure places patient at more risk if cardiac problems or anemia O2 delivery devices and amounts of O2 delivered- FYI 1. Room air- 21% 2. NC- 24-40% at 1-6 L 3. Face mask- 24-60% at 6-10L 4.Venturi mask- 24-60% at 4-15L 5. Partial rebreather mask- 60-90% at 8-10L 6. Non-rebreather mask-90-100% at 10-15L 7. Bag mask- up to100% 8. ET tube- up to 100% Signs and Symptoms of Respiratory Failure hypoxemia pO2<50-60 May be hypercapnia pCO2>50 • only one cause- hypoventilation *In patients with COPD watch for acute drop in pO2 and O2 sats along with inc. C02 and KNOW BASELINE!!! Hypoxemia- Signs & Symptoms Compensatory Mechanisms- early • Tachycardia- more O2 to tissues • Hypertension- fight or flight (cause?) • Tachypnea –take in more O2 Restlessness and apprehension Dyspnea Cyanosis Confusion and impaired judgment **Later dysrhythmias and metabolic acidosis, dec. B/P and Dec. CO.(MODS) Hypercapnia- signs and symptoms Dyspnea to respiratory depressionif too high CO2 narcosis Headache-vasodilation- Increases ICP Papilledema Tachycardia and inc. B/P Drowsiness and coma Respiratory acidosis • **Administering O2 may eliminate drive to breathe especially with COPD patients - WHY?? Specific Clinical ManifestationsAssessment- Respiratory Respirations- depth and rate O2 sat -oximeter, CO2- capnometer Patient position- tripod position, Pursed lip breathing Orthopnea, PND Inspiratory to expiratory ratio (normal 1:2) Retractions and use of accessory muscles Breath sounds- crackles, rhonchi, wheezes Exhaled C02 (ETC02) normal 35-45- called capnography- lots of uses now Used when trying to wean patient from a ventilator TSB- trial of spontaneous breathing Diagnosis Physical Assessment Pulse oximetry (90% is PaO2 of 60) ABG CXR CBC Electrolytes-BMP EKG Sputum and blood cultures, UA V/Q scan if ?pulmonary embolus Pulmonary function tests (PFT’s) TV, FRC Treatment Goals O2 therapy Mobilization of secretions Positive pressure ventilation(PPV) O2 Therapy If secondary to V/Q mismatch- 1-3Ln/c or 24%-32% by mask If secondary to intrapulmonary shunt- positive pressure ventilation-PPV • May be via ET tube • Tight fitting mask • **Goal is PaO2 of 55-60 with SaO2 at 90% or more at lowest O2 concentration possible • **O2 at high concentrations for longer than 48 hours causes O2 toxicity Mobilization of secretions Effective coughing- quad cough, huff cough, staged cough Positioning- HOB 45 degrees or recliner chair or bed • “Good lung down” Hydration - fluid intake 2-3 L/day Humidification- aerosol treatments- mucolytic agents Chest PT- postural drainage, percussion and vibration (30mls sputum) Airway suctioning Positive Pressure Ventilation Invasively through oro or nasotracheal intubation Noninvasively( NIPPV) through mask • Used for acute and chronic resp failure • BiPAP- different levels of pressure for inspiration and expiration- (IPAP) higher for inspiration,(EPAP) lower for expiration • CPAP- for sleep apnea • **Used best in chronic resp failure in patients with chest wall and neuromuscular disease, also with HF and COPD. Should hear equal breath sounds if in correct place. Always get a CXR to check placement also What is the correct placement of the ET tube? 1. 2. 3. 4. In the right main stem bronchus In the left main stem bronchus Above the carina Just below the vocal cords Surgical Intervention-Tracheostomy Tracheotomy Surgical procedure performed when need for an artificial airway is expected to be long term If tube in greater than 4-5 days, perform a trach-research shows benefit to early trach Drug Therapy Relief of bronchospasm- bronchodilators • alupent and albuterol-(Watch for what side effect?) Reduction of airway inflammationCorticosteroids by inhalation or IV or po (SE) Reduction of pulmonary congestion-diuretics and nitroglycerine with heart failure• why HF with pulmonary problems? Treatment of pulmonary infections- IV antibiotics, vancomycin and rocephin Reduction of anxiety, pain and agitationdiprivan, ativan, versed, propofol, opioids May need sedation or neuromuscular blocking agent if on ventilator.(Norcuron, nimbex) Medical Supportive Treatment Treat underlying cause Maintain adequate cardiac output- monitor B/P and MAP. • **Need B/P of 90 systolic and MAP of 60 to maintain perfusion to the vital organs Maintain adequate Hemoglobin concentration- need 9g/dl or greater Nutrition- During acute phase- enteral or parenteral nutrition (research enteral better) In a hypermetabolic state- need more calories • If retain CO2- avoid high carb diet-WHY Acute Respiratory Failure Gerontologic Considerations Physiologic aging results in • ↓ Ventilatory capacity • Alveolar dilation • Larger air spaces • Loss of surface area • Diminished elastic recoil • Decreased respiratory muscle strength • ↓ Chest wall compliance Causing Dec pO2 and Inc. pCO2 ARDS- intro Also known as DAD (diffuse alveolar disease) a variety of acute and diffuse infiltrative lesions which cause severe refractory arterial hypoxemia and life-threatening arrhythmias Memory Jogger Assault to the pulmonary system Respiratory distress Decreased lung compliance Severe respiratory failure 150,000 adults dev. ARDS About 50% survive **Patients with gram negative septic shock and ARDS have mortality rate of 70-90% Now distinguish between: ALI versus ARDS- continuum Same Signs and Symptoms except: Acute Lung injury PaO2/ FiO2 ratio is 200-300 Example 86/.40=215 ARDS PaO2/ FiO2 ratio is less than 200 Example 80/.80=100 Direct Causes (Inflammatory process is involved in all) Pneumonia* (community acquired) Aspiration of gastric contents* Pulmonary contusion Near drowning Inhalation injury Indirect Causes (Inflammatory process is involved) Sepsis* (most common) gm Severe trauma with shock state that requires multiple blood transfusions* Drug overdose Acute pancreatitis Stages of Edema Formation in ARDS A, Normal alveolus and pulmonary capillary B, Interstitial edema occurs with increased flow of fluid into the interstitial space C, Alveolar edema occurs when the fluid crosses the blood-gas barrier Fig. 68-8 Copyright © 2007, 2004, 2000, Mosby, Inc., an affiliate of Elsevier Inc. All Rights Reserved. ↓CO Metabolic acidosis ↑CO Interstitial & alveolar edema Severe & refractory hypoxemia *Causes (see notes) DIFFUSE lung injury (SIRS or MODS) Damage to alveolar capillary membrane Pulmonary capillary leak SHUNTING Stiff lungs Inactivation of surfactant Alveolar atalectasis Hyperventilation Hypocapnea Respiratory Alkalosis Hypoventilation Hypercapnea Respiratory Acidosis Pathophysiology of ARDS Damage to alveolarcapillary membrane Increased capillary hydrostatic pressure Decreased colloidal osmotic pressure Interstitial edema Alveolar edema or pulmonary edema Loss of surfactant What does surfactant do? stiff lungs Pathophysiologic Stages in ARDS Injury or Exudative- 1-7 days • Interstitial and alveolar edema and atelectasis • Refractory hypoxemia and stiff lungs Reparative or Proliferative-1-2 weeks after • Dense fibrous tissue, increased PVR and pulmonary hypertension occurs Fibrotic-2-3 week after • Diffuse scarring and fibrosis, decreased surface area, decreased compliance and pulmonary hypertension The essential disturbances of ARDS are **interstitial and alveolar edema and atelectasis causing **Progressive arterial hypoxemia in spite of inc. O2 which is hallmark of ARDS (refractory hypoxemia) Clinical Manifestations: Early Dyspnea-(almost always present), tachypnea, cough, restlessness Chest auscultation may be normal or reveal fine, scattered crackles ABGs • **Mild hypoxemia and respiratory alkalosis caused by hyperventilation Chest x-ray may be normal or show minimal scattered interstitial infiltrates • Edema may not show until 30% increase in lung fluid content Clinical Manifestations: Late Symptoms worsen with progression of fluid accumulation and decreased lung compliance • PFTs show decreased compliance and lung volumes • Evident discomfort and increased WOB – Suprasternal retractions • Tachycardia, Diaphoresis • Changes in sensorium with decreased mentation, cyanosis, and pallor Hypoxemia and a PaO2/FIO2 ratio <200 despite increased FIO2 ( ex: 80/.8=100) Clinical Manifestations As ARDS progresses, profound respiratory distress requires endotracheal intubation and positive pressure ventilation Chest x-ray termed whiteout or white lung because of consolidation and widespread infiltrates throughout lungs Clinical Manifestations If prompt therapy not initiated, severe hypoxemia, hypercapnia, and metabolic acidosis may ensue Nursing Diagnoses Potential Safety Issues?? Nursing Care Ineffective airway clearance Ineffective breathing pattern Risk for fluid volume imbalance Anxiety Impaired gas exchange Imbalanced nutrition: Less than body requirements Planning Following recovery • PaO2 within normal limits or at baseline ( may not be possible) • SaO2 > 90% • Patent airway • Clear lungs or auscultation Nursing Assessment Lung sounds-The Auscultation Assistant - Breath Sounds ABG’s CXR Capillary refill Neuro assessment Vital signs O2 sats Hemodynamic monitoring values Diagnostic Tests- Most important ABG reviewRealNurseEd (Education for Real Nurses by a Real Nurse) CXR Pulmonary Function Tests- dec. compliance and dec vital capacity- (max exhaled after max inhale) Hemodynamic Monitoring- (Pulmonary artery pressures) to rule out pulmonary edema. **If ARDS, PAW normal Severe ARDS ARDS Autopsy *Goal of Treatment for ARDS Maintain adequate ventilation and respirations. Prevent injury Manage anxiety Treatment Mechanical Ventilation-goal PO2>60 and 02 sat 90% with FIO2 < 50 PEEP- can cause dec. CO, B/P and barotrauma Positioning- prone, continuous lateral rotation therapy and kinetic therapy ECMO Hemodynamic Monitoring- fluid replacement or diuretics. Monitor cardiac outputs and daily weights Hemodynamics- (distiguish between pulmonary edema from heart versus from ARDS) wedge PAWP increases with Heart Failure ,PAWP does not increase with ARDS. Enteral or Parenteral Feeding- high calorie, high fat. Research shows that formulas enriched with omega -3 fatty acids may improve the outcomes of those with ARDS Crystalloids versus colloids Mild fluid restriction and diuretics- watch for pulmonary edema, strict I and O Mechanical Ventilation Patients will commonly need intubation with mechanical ventilation because PaO2 cannot be maintained at acceptable level High flow systems used to maximize O2 delivery SaO2 continuously monitored Give lowest concentration that results in PaO2 60 mm Hg or greater Risk for O2 toxicity increases when FIO2 exceeds 60% for more than 48 hours PEEPPositive End Expiratory Pressure pt. can not expire completely. Causes alveoli to remain inflated- so can dec the FIO2 (Complications can include decreased cardiac output, pneumothorax, and inc. ICP. FRC- air in after normal exhalation PEEP- Positive end-expiratory pressure Vent settings to improve <oxygenation> PEEP and FiO2 are adjusted in tandem • PEEP • Increases FRC • Prevents progressive atelectasis and intrapulmonary shunting • Prevents repetitive opening/closing (injury) • Recruits collapsed alveoli and improves V/Q matching • Resolves intrapulmonary shunting • Improves compliance • Enables maintenance of adequate PaO2 at a safe FiO2 level • Disadvantages • Increases intrathoracic pressure (may require pulmonary a. catheter) • May lead to ARDS • Rupture: PTX, pulmonary edema Oxygen delivery (DO2), not PaO2, should be used to assess optimal PEEP. Proning Proning typically reserved for refractory hypoxemia not responding to other therapies • Plan for immediate repositioning for cardiopulmonary resuscitation Proning- Rotoprone • Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone • Fluid pools in dependent regions of lung • Predisposes to atelectasis – With prone position • nondependent air-filled alveoli become dependent • perfusion becomes greater to air-filled alveoli • thereby improving ventilation-perfusion matching. Benefits to ProningNone to mortality Before proning ABG on 100%O2 7.28/70/70 After proning ABG on 100% 7.37/56/227 Other positioning strategies Kinetic therapy Continuous lateral rotation therapy Ecmo story ECMO- Blood drains by gravity from the patient through a tube (catheter) placed in a large neck vein. This blood passes through a plastic pouch, or bladder, and then in pumped through the membrane oxygenator that serves as an artificial lung, putting oxygen into the blood and removing carbon dioxide. The blood then passes through a heat exchanger that maintains the blood at normal body temperature. Finally, the blood reenters the body through a large catheter placed in an artery in the neck. ECMO Extracorporeal membrane oxygenation • Alternative form of pulmonary support for patient with severe respiratory failure • Modification of cardiopulmonary bypass • Involves partially removing blood through use of large-bore catheters, infusing oxygen, removing CO2, and returning blood back to patient Medications Inhaled Nitric Oxide Surfactant therapy NSAIDS and corticosteroids Nitric Oxide Dilates pulmonary blood vessels and helps reduce shunting Ventilator song Ventilate me a machine that moves air in and out of the lungs Mechanical Ventilation Indications • Apnea or impending inability to breathe • Acute respiratory failure – pH<7.25 – pCO2>50 • Severe hypoxia – pO2<50 • Respiratory muscle fatigue – RR<12 Mechanical Ventilation Purpose • Support circulation and • Maintain pt. respirations until can breathe on own Goal • Adequate controlled ventilation • Relief of hypoxia without hypercapnia • Relief of work of breathing Types of Mechanical Ventilation Negative PressureVentilation – Chambers encase chest or – – – – – body Surround with intermittent subatmospheric or negative pressure Noninvasive ventilation Does not require an artificial airway Not used extensively for acutely ill patients Used for neuromuscular diseases, CNS and injuries of the spinal cord Types of Mechanical Ventilation Positive pressure ventilation (PPV) Used primarily in acutely ill patients Pushes air into lungs under positive pressure during inspiration Expiration occurs passively Mechanical Ventilator Settings to Monitor FIO2 -% of O2 TV-<5ml/kg for ARDS (normal 8-10) Rate 12-15 Mode-WOB • • • • Control mode Assist control SIMV Pressure support- only in spontaneous breathes (gets the balloon started) Pt. controls all but pressure limit inspiratory pressure and flow SETTING FUNCTION USUAL PARAMETERS Respiratory Rate (RR) Number of breaths delivered by the Usually 4-20 breaths per minute ventilator per minute Tidal Volume (VT) Volume of gas delivered during each Usually 5-15 cc/kg ventilator breath Fractional Inspired Oxygen (FIO2) Inspiratory:Expiratory (I:E) Ratio Pressure Limit Amount of oxygen delivered by ventilator 21% to 100%; usually set to keep PaO2 > 60 to patient mmHg or SaO2 > 90% Length of inspiration compared to length of Usually 1:2 or 1:1.5 unless inverse ratio expiration ventilation is required Maximum amount of pressure the ventilator 10-20 cm H2O above peak inspiratory can use to deliver breath pressure; maximum is 35 cm H2O Ventilator Modes Mode • How the machine will ventilate the patient in relation to the patient’s own respiratory efforts • There is a mode for nearly every patient situation • Can be used in conjunction with each other Two types • Volume • Pressure Modes of Volume Ventilation Based on how much work of breathing (WOB) patient should or can perform Determined by patient’s ventilatory status, respiratory drive, and ABGs Types • CMV- Control Mode • AC- Assist Control- Most used mode • SIMV- Synchronous Intermittent Mandatory Ventilation Control Mode or CMV 1. TV and RR are fixed. 2. Used for patients who are unable to initiate a breath (anesthetized or paralyzed). CMV delivers the preset volume or pressure at pre-set rate regardless of the patient’s own inspiratory effort 3. Spontaneously breathing patients must be sedated and/or pharmacologically paralyzed so they don’t breathe out of synchrony with the ventilator. 3. *Ventilator does all the work Assist Contol 1. A/C delivers the preset volume or pressure in response to the patient’s own inspiratory effort, but will initiate the breath if the patient does not do so within the set amount of time. 2. Patient Assists or triggers the vent –can breathe faster but not slower 3. Vent has back-up rate 4. May need to be sedated to limit the number of spontaneous breaths since hyperventilation can occur. 5. This mode is used for patients who can initiate a breath but who have weakened respiratory Synchronous Intermittent Mandatory Ventilation-SIMV 1. SIMV delivers the preset volume or pressure and rate while allowing the patient to breathe spontaneously in between ventilator breaths. 2. Each ventilator breath is delivered in synchrony with the patient’s breaths, yet the patient is allowed to completely control the spontaneous breaths at own TV. 3. SIMV is used as a primary mode of ventilation, as well as a weaning mode. 4. During weaning, the preset rate is gradually reduced, allowing the patient to slowly regain breathing on their own. 5. The disadvantage of this mode is that it may increase the work of breathing and respiratory muscle fatigue Pressure Support Ventilationonly with spontaneous breaths 1.Preset pressure that augments patients own inspiratory effort- (gets balloon started) 2.Decreases WOB 3.Patient completely controls rate and volume 4.Used for stable patients often with SIMV to overcome resistance of breathing through ventilator tubing High Frequency Ventilation Small amounts of gas delivered at a rapid rate • As much as 60-100 breaths /minute Used when conventional mechanical ventilation would compromise hemodynamic stability For short term procedures For patients at high risk for pneumothorax Sedation and pharmacological paralysis required Pressure Control Inverse Ratio Ventilation 1. The normal inspiratory:expiratory ratio is 1:2 but this is reversed during IRV to 2:1 or greater (the maximum is 4:1). 2. This mode is used for patients who are still hypoxic even with the use of PEEP. The longer inspiratory time increases the amount of air in the lungs at the end of expiration (the functional residual capacity) and improves oxygenation by re-expanding collapsed alveoli- acts like PEEP. 3. The shorter expiratory time prevents the alveoli from collapsing again. 4. Sedation and pharmacological paralysis are required since it’s very uncomfortable for the patient. 5. For patients with ARDS continuing refractory hypoxemia despite high levels of PEEP Alarms high pressure low pressure Low Pressure Alarms •Circuit leaks •Airway leaks •Chest tube leaks •Patient disconnection High Pressure Alarms •Patient coughing •Secretions or mucus in the airway •Patient biting tube •Airway problems •Reduced lung compliance (eg. pneumothorax) •Patient fighting the ventilator •Accumulation of water in the circuit •Kinking in the circuit NEVER TURN ALARMS OFF! Assess your patient not the alarms Complications of Postive Pressure Ventilaton • Cardiovascular system • ↑ Intrathoracic pressure compresses thoracic vessels • ↓ Venous return to heart • ↓ left ventricular end- diastolic volume (preload) • ↓ cardiac output • Hypotension • Mean airway pressure is further ↑ if PEEP >5 cm H2O Complications of PPV Pulmonary System Barotrauma • Air can escape into pleural space from alveoli or interstitium • Accumulate, and become trapped • Pneumothorax • subcutaneous emphysema Patients with compliant lungs are at ↑ risk Chest tubes may be placed prophylactically What could happen? Mechanical Ventilation Complications of PPV (cont’d) • Ventilator-associated pneumonia (VAP) – Definition-Pneumonia that occurs 48 hours or more after ET intubation – Clinical evidence- Detection • • • • Fever and/or elevated white blood cell count Purulent or odorous sputum Crackles or rhonchi on auscultation Pulmonary infiltrates on chest x-ray VAP Prevention • Guidelines to prevent VAP – HOB elevation at least 30 to 45 degrees unless medically contraindicated – No routine changes of ventilator circuit tubing – Use of an ET that allows continuous suctioning of secretions in subglottic area – oral care Drain condensation that collects in ventilator tubing http://www.youtube.co m/watch?v=ska5mS_T oA4 Mechanical Ventilation Complications of PPV (cont’d) • Fluid retention – Occurs after 48 to 72 hours of PPV, especially PPV with PEEP – May be due to ↓ cardiac output – Results • Diminished renal perfusion • Release of renin-angiotensin-aldosterone – Leads to sodium and water retention Mechanical Ventilation Complications of PPV (cont’d) • Gastrointestinal system – Risk for stress ulcers and GI bleeding – ↑ Risk of translocation of GI bacteria • ↓ Cardiac output may contribute to gut ischemia – Peptic ulcer prophylaxis • Histamine (H2)-receptor blockers, proton pump inhibitors, tube feedings – ↓ Gastric acidity, ↓ risk of stress ulcer/hemorrhage Mechanical Ventilation Complications of PPV (cont’d) • Musculoskeletal system – Maintain muscle strength and prevent problems associated with immobility – Progressive ambulation of patients receiving long-term PPV can be attained without interruption of mechanical ventilation Mechanical Ventilation Psychosocial needs • Physical and emotional stress due to inability to speak, eat, move, or breathe normally • Pain, fear, and anxiety related to tubes/ machines • Ordinary ADLs are complicated or impossible Mechanical Ventilation Psychosocial needs (cont’d) • Involve patients in decision making • Encourage hope and build trusting relationships with patient and family • Provide sedation and/or analgesia to facilitate optimal ventilation • If necessary, provide paralysis to achieve more effective synchrony with ventilator and increase oxygenation • Paralyzed patient can hear, see, think, feel – Sedation and analgesia must always be administered concurrently Evidence Based Practice Ventilator Bundle Components What is a Bundle? 1. Elevate HOB 30-45 degrees 2. Daily sedation vacations and assessment of readiness to extubate 3. Peptic ulcer disease prophylaxis 4. Venous thromboembolism prophylaxis Respiratory Therapy Alternative modes of mechanical ventilation if hypoxemia persists • • • • Pressure release ventilation Pressure control ventilation Permissive hypercapnia- from low TV Independent Lung Ventilation Research LiquiVent is an oxygen-carrying liquid drug (perflubron) used for respiratory distress syndrome. The goal of "liquid ventilation" therapy is to open up collapsed alveoli (air sacs) and facilitate the exchange of respiratory gases while protecting the lungs from the harmful effects of conventional mechanical ventilation. Liquid Ventilation Partial liquid ventilation with perflubron • Perflubron is an inert, biocompatible, clear, odorless liquid that has affinity for O2 and CO2 and surfactant-like qualities • Trickled down ET tube into lungs Research and New video YouTube - Superman breather - USA