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RESPIRATORY FAILURE and ARDS BY NANCY JENKINS Exchange of O2 and CO2 gas exchange For normal functioning Respiratory Failure the inability of the cardiac and pulmonary systems to maintain an adequate exchange of oxygen and CO2 in the lungs Acute Respiratory Failure Hypoxemia- inadequate O2 transfer • PaO2 of 60mmHg or less when pt. Receiving 60% or greater O2 Hypercapnia- insufficient CO2 removal Increases PaCO2 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 Failure(Affects the pO2) V/Q Mismatch Shunt Diffusion Limitation Alveolar Hypoventilation- inc. CO2 and dec. PO2 Range of V/Q Relationships Fig. 68-4 VentilationPerfusion Mismatch (V/Q) Normal V/Q =1 (1ml air/ 1ml of blood) Ventilation=lungs Perfusion or Q=perfusion Pulmonary Embolus- (VQ scan) Pulmonary Embolus Shunt 2 Types • 1. Anatomic- passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect • 2. Intrapulmonary shunt- 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 Diffusion Limitations Gas exchange is compromised by a process that thickens or destroys the membrane • 1. Pulmonary fibrosis • 2. ARDS * A classic sign of diffusion limitation is hypoxemia during exercise but not at rest Diffusion Limitation Fig. 68-5 Alveolar Hypoventilation Mainly due to hypercapnic respiratory failure but can cause hypoxemia Increased pCO2 with decreased PO2 Restrictive lung disease CNS diseases Neuromuscular diseases Hypercapnic Respiratory Failure Ventilatory Failure- affects CO2 1. Abnormalities of the airways and alveoliair 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 Hypercapnic Respiratory Failure 3. Abnormalities of the chest wall • Flail chest, morbid obesity, kyphoscoliosis 4. Neuromuscular Conditions- respiratory muscles are weakened: Guillain-Barre, muscular dystrophy, myasthenia gravis and multiple sclerosis Tissue Oxygen needs Tissue O2 delivery is determined by: • Amount of O2 in hemoglobin • Cardiac output • *Respiratory failure places patient at more risk if cardiac problems or anemia Signs and Symptoms of Respiratory Failure- ABG’s 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 Compensatory Mechanisms- early • Tachycardia- more O2 to tissues • Hypertension- fight or flight • 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. Early signs of hypoxemia are: 1. 2. 3. 4. Tachycardia Tachypnea Confusion Cyanosis Hypercapnia 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 Manifestations Respirations- depth and rate Patient position- tripod position Pursed lip breathing Orthopnea Inspiratory to expiratory ratio (normal 1:2) Retractions and use of accessory muscles Breath sounds Diagnosis Physical Assessment Pulse oximetry (90% is PaO2 of 60) ABG CXR CBC Electrolytes EKG Sputum and blood cultures, UA V/Q scan if ?pulmonary embolus Pulmonary function tests (PFT’s) Exhaled C02 (ETC02) normal 35-45 Used when trying to wean patient from a ventilator TSB- trial of spontaneous 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 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. NPPV NPPV Should hear equal breath sounds if in correct place. Always get a CXR to check placement also Endotracheal Tube Fig. 66-17 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 Drug Therapy Relief of bronchospasm- bronchodilators • alupent and albuterol-(Watch for what side effect?) Reduction of airway inflammationCorticosteroids by inhalation or IV or po 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) assess with peripheral nerve stim. Medical Supportive Treatment Treat underlying cause Maintain adequate cardiac outputmonitor B/P and MAP. Maintain adequate Hemoglobin concentration- need 9g/dl or greater • **Need B/P of 90 systolic and MAP of 60 to maintain perfusion to the vital organs Nutrition During acute phase- enteral or parenteral nutrition In a hypermetabolic state- need more calories • If retain CO2- avoid high carb diet 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 • **Dec. PO2 and inc. CO2 ARDS Also known as DAD (diffuse alveolar disease) or ALI (acute lung injury) a variety of acute and diffuse infiltrative lesions which cause severe refractory arterial hypoxemia and life-threatening arrhythmias Introduction to ARDS ARDS 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% Direct Causes (Inflammatory process is involved in all) Pneumonia* 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 alveolar-capillary membrane Increased capillary hydrostatic pressure Decreased colloidal osmotic pressure Interstitial edema Alveolar edema or pulmonary edema Loss of surfactant What does surfactant do? 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 **interstitial and alveolar edema and atelectasis **Progressive arterial hypoxemia in spite of inc. O2 is hallmark of ARDS 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 Clinical Manifestations: Early 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 Pulmonary function tests reveal decreased compliance and lung volume Evident discomfort and increased WOB Clinical Manifestations: Late 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 Chest X-Ray of ARDS Fig. 68-10 Clinical Manifestations If prompt therapy not initiated, severe hypoxemia, hypercapnia, and metabolic acidosis may ensue Nursing Diagnoses 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 • SaO2 > 90% • Patent airway • Clear lungs or auscultation Dyspnea and Tachypnea The Auscultation Assistant - Breath Sounds Cyanosis Nursing Assessment Lung sounds ABG’s CXR Capillary refill Neuro assessment Vital signs O2 sats Hemodynamic monitoring values Diagnostic Tests ABG-review 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 ABG Review and Practice ABG review RealNurseEd (Education for Real Nurses by a Real Nurse) ARDS X-Rays X-RAY on 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 Hemodynamic Monitoring- fluid replacement or diuretics 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 Cont. Crystalloids versus colloids Mild fluid restriction and diuretics PEEP pt. can not expire completely. Causes alveoli to remain inflated (Complications can include decreased cardiac output, pneumothorax, and increased intracranial pressure). 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-Principles Positioning strategies • Mediastinal and heart contents place more pressure on lungs when in supine position than when in prone – Predisposes to atelectasis • Turn from supine to prone position – May be sufficient to reduce inspired O2 or PEEP • Fluid pools in dependent regions of lung Prone Device •Prone positioning With position change to prone, previously nondependent air-filled alveoli become dependent, perfusion becomes greater to air-filled alveoli opposed to previously fluid-filled dependent alveoli, thereby improving ventilation-perfusion matching. No benefit in mortality Rotoprone bed Benefits to Proning Before proning ABG on 100%O2 7.28/70/70 After proning ABG on 100% 7.37/56/227 Other Positioning: Continuous Lateral Rotation Fig. 68-12 Medications Inhaled Nitric Oxide Surfactant therapy NSAIDS and corticosteroids Nitric Oxide Dilates pulmonary blood vessels and helps reduce shunting Assessment Data and Priority Respiratory rate of 10 Absent breath sounds on the left O2 sat 82% High pressure alarm on vent going off Bilateral wheezing Respiratory rate of 30 ABG respiratory acidosis ARDS Prioritization and Critical Thinking Questions #28 When assessing a 22 Y/o client admitted 3 days ago with pulmonary contusions after an MVA, the nurse finds shallow respirations at a rate of 38. The client states he feels dizzy and scared. O2 sat is 80% on 6 Ln/c. which action is most appropriate? A.Inc. flow rate of O2 to 10 L/min and reassess in 10 min. B.Assist client to use IS and splint chest using a pillow as he coughs. C.Adminster ordered MSO4 to client to dec. anxiety and reduce hyperventilation. D.Place client on non-rebreather mask at 95-100% FiO2 and call the Dr. #25.The nursing assistant is taking VS for an intubated client after being suctioned by RT. Which VS should be immediately reported to the RN? A. HR 98 B.RR 24 C.B/P 168/90 D.Temp 101.4 #15. After change of shift report, you are assigned to care of the following clients. Which should be assessed first? 68 y/o on ventilator who needs a sterile sputum specimen sent to the lab. 59y/o with COPD and has a pulse ox on previous shift of 90%. 72y/o with pneumonia who needs to be started on IV antibiotics. 51y/o with asthma c/o shortness of breath after using his bronchodilator inhaler. Ventilators song Ventilate me Ventilator VentWorld What is a Ventilator? a machine that moves air in and out of the lungs Mechanical Ventilation Indications • • • • Apnea or impending inability to breathe Acute respiratory failure Severe hypoxia Respiratory muscle fatigue Mechanical Vent Objective support circulation and maintain pt. respirations until can breathe on own Goal of Mechanical Ventilation adequate controlled ventilation relief of hypoxia without hypercapnia relief of work of breathing access to airways Criteria to put on vent Apnea or impending inability to breathe Acute respiratory failure • pH<7.25 • pCO2>50 Severe hypoxia - pO2<50 Respiratory muscle fatigue Mechanical Ventilation Types of mechanical ventilation • Negative pressure ventilation – Uses chambers that encase chest or body and surround it with intermittent subatmospheric or negative pressure – Noninvasive ventilation that does not require an artificial airway – Not used extensively for acutely ill patients – Mostly used for neuromuscular diseases, CNS and injuries of the spinal cord Mechanical Ventilation Types of mechanical ventilation (cont’d) • Positive pressure ventilation (PPV) – Used primarily in acutely ill patients – Pushes air into lungs under positive pressure during inspiration – Expiration occurs passively Patient Receiving PPV Fig. 66-22 Mechanical Ventilator Settings to Monitor FIO2 -% of O2 TV-<5ml/kg for ARDS (normal 8-10) Rate 12-15 • Control (CMV) Continuous Mandatory Ventilation • assist control • SIMV inspiratory pressure and flow Pressure support- only in spontaneous breathes (gets the balloon started) Pt. controls all but pressure limit SETTING FUNCTION USUAL PARAMETERS RespiratoryRate (RR) Number of breaths delivered bythe Usually4-20 breaths per minute ventilator per minute Tidal Volume (VT) Volume of gas delivered duringeach Usually5-15 cc/kg ventilator breath Fractional Inspired Oxygen(FIO2) Inspiratory:Expiratory (I:E) Ratio Pressure Limit Amount of oxygendelivered by ventilator 21%to100%; usually set tokeepPaO2 >60 topatient mmHgor SaO2 >90% Lengthof inspirationcompared tolengthof Usually1:2 or 1:1.5unless inverse ratio expiration ventilationis required Maximumamount of pressure the ventilator 10-20 cmH2Oabove peak inspiratory canuse todeliver breath pressure; maximumis 35 cmH2O Ventilator Modes- depends on WOB Mode refers to 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, plus many can be used in conjunction with each other. Mechanical Ventilation 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 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 Ventilation 1. PSV is preset pressure that augments the patient’s spontaneous inspiratory effort and decreases the work of breathing. 2. The patient completely controls the respiratory rate and tidal volume. 3. PSV is used for patients with a stable respiratory status and is often used with SIMV to overcome the resistance of breathing through ventilator circuits and tubing. Pressure support High Frequency Ventilation 1. HFV delivers a small amount of gas at a rapid rate (as much as 60-100 breaths per minute.) 2. This is used when conventional mechanical ventilation would compromise hemodynamic stability, during short-term procedures, or for patients who are at high risk for pneumothorax. 3. Sedation and pharmacological paralysis are required. 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 Mechanical Ventilation Complications of PPV (cont’d) • Cardiovascular system (cont’d) – ↑ Intrathoracic pressure compresses thoracic vessels • ↓ Venous return to heart, ↓ left ventricular enddiastolic volume (preload), ↓ cardiac output • Hypotension • Mean airway pressure is further ↑ if PEEP >5 cm H2O Mechanical Ventilation Complications of PPV (cont’d) • 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 Subcutaneous Emphysema Mechanical Ventilation Complications of PPV (cont’d) • Ventilator-associated pneumonia (VAP) – Pneumonia that occurs 48 hours or more after ET intubation – Clinical evidence • • • • Fever and/or elevated white blood cell count Purulent or odorous sputum Crackles or rhonchi on auscultation Pulmonary infiltrates on chest x-ray Mechanical Ventilation Complications of PPV (cont’d) • 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 – Drain condensation that collects in ventilator tubing 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 Respiratory Therapy Alternative modes of mechanical ventilation if hypoxemia persists • • • • • • • Pressure support ventilation Pressure release ventilation Pressure control ventilation Inverse ratio ventilation High-frequency ventilation Permissive hypercapnia Independent Lung Ventilation 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 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. Research and New video YouTube - Superman breather - USA Prioritization and Delegation Questions on Vent The nurse is assigned to provide nursing care for a client receiving mechanical ventilation. Which action should be delegated to the experienced nursing assistant? A. Assess respiratory status q 4 hours. B. Take VS and pulse ox reading q4 hours. C. Check ventilator settings to make sure they are as prescribed. D.Observe client’s need for suctioning q 2 hours. #27 The high pressure alarm on the vent goes off and when you enter the room to assess a client with ARDS, her O2 sat is 87% and she is struggling to sit up. What action should be taken next? A. Reassure client that the vent will do the work of breathing for her. B. Manually ventilate the client while assessing possible reasons for the alarm. C. Inc. the FiO2 to 100% in preparation for endotracheal suction. D. Insert an oral airway to prevent client from biting the endotracheal tube.