12Shunt2 Types1. Anatomic- passes through an anatomic channel of the heart and does not pass through the lungs ex: ventricular septal defect2. 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
13Diffusion Limitations Gas exchange is compromised by a process that thickens or destroys the membrane1. Pulmonary fibrosis2. ARDS* A classic sign of diffusion limitation is hypoxemia during exercise but not at rest
15Alveolar Hypoventilation Mainly due to hypercapnic respiratory failure but can cause hypoxemiaIncreased pCO2 with decreased PO2Restrictive lung diseaseCNS diseasesNeuromuscular diseases
16Hypercapnic Respiratory Failure Ventilatory Failure- affects CO2 1. Abnormalities of the airways and alveoli- air flow obstruction and air trappingAsthma, COPD, and cystic fibrosis2. Abnormalities of the CNS- suppresses drive to breathedrug OD, narcotics, head injury, spinal cord injury
17Hypercapnic Respiratory Failure 3. Abnormalities of the chest wallFlail chest, morbid obesity, kyphoscoliosis4. Neuromuscular Conditions- respiratory muscles are weakened:Guillain-Barre, muscular dystrophy, myasthenia gravis and multiple sclerosis
18Tissue Oxygen needs Tissue O2 delivery is determined by: Amount of O2 in hemoglobinCardiac output*Respiratory failure places patient at more risk if cardiac problems or anemia
19Signs and Symptoms of Respiratory Failure- ABG’s hypoxemia pO2<50-60May be hypercapnia pCO2>50only one cause- hypoventilation*In patients with COPD watch for acute drop in pO2 and O2 sats along with inc. C02 and KNOW BASELINE!!!
20Hypoxemia Compensatory Mechanisms- early Restlessness and apprehension Tachycardia- more O2 to tissuesHypertension- fight or flightTachypnea –take in more O2Restlessness and apprehensionDyspneaCyanosisConfusion and impaired judgment**Later dysrhythmias and metabolic acidosis, dec. B/P and Dec. CO.
21HypercapniaDyspnea to respiratory depression- if too high CO2 narcosisHeadache-vasodilation- Increases ICPPapilledemaTachycardia and inc. B/PDrowsiness and comaRespiratory acidosis**Administering O2 may eliminate drive to breathe especially with COPD patients- WHY??
22Specific Clinical Manifestations Respirations- depth and ratePatient position- tripod positionPursed lip breathingOrthopneaInspiratory to expiratory ratio (normal 1:2)Retractions and use of accessory musclesBreath sounds
23Diagnosis Physical Assessment Pulse oximetry (90% is PaO2 of 60) ABG CXRCBCElectrolytesEKGSputum and blood cultures, UAV/Q scan if ?pulmonary embolusPulmonary function tests (PFT’s)
24Exhaled C02 (ETC02) normal 35-45 Used when trying to wean patient from a ventilator
25Treatment Goals O2 therapy Mobilization of secretions Positive pressure ventilation(PPV)
26O2 Therapy If secondary to V/Q mismatch- 1-3Ln/c or 24%-32% by mask If secondary to intrapulmonary shunt- positive pressure ventilation-PPVMay be via ET tubeTight fitting mask**Goal is PaO2 of with SaO2 at 90% or more at lowest O2 concentration possible**O2 at high concentrations for longer than 48 hours causes O2 toxicity
27Mobilization of secretions Effective coughing- quad cough, huff cough, staged coughPositioning- HOB 45 degrees or recliner chair or bed“Good lung down”Hydration - fluid intake 2-3 L/dayHumidification- aerosol treatments- mucolytic agentsChest PT- postural drainage, percussion and vibrationAirway suctioning
28Positive Pressure Ventilation Invasively through oro or nasotracheal intubationNoninvasively( NIPPV) through maskUsed for acute and chronic resp failureBiPAP- different levels of pressure for inspiration and expiration- (IPAP) higher for inspiration,(EPAP) lower for expirationCPAP- for sleep apnea**Used best in chronic resp failure in patients with chest wall and neuromuscular disease, also with HF and COPD.
32Surgical Intervention-Tracheostomy If tube in greater than 4-5 days, perform a trachTracheotomySurgical procedure performed when need for an artificial airway is expected to be long term
33Drug Therapy Relief of bronchospasm- bronchodilators alupent and albuterol-(Watch for what side effect?)Reduction of airway inflammation-Corticosteroids by inhalation or IV or poReduction of pulmonary congestion-diuretics and nitroglycerine with heart failure-why HF with pulmonary problems?Treatment of pulmonary infections- IV antibiotics, vancomycin and rocephinReduction of anxiety, pain and agitation- diprivan, ativan, versed, propofol, opioidsMay need sedation or neuromuscular blocking agent if on ventilator.(Norcuron, nimbex) assess with peripheral nerve stim.
34Medical Supportive Treatment Treat underlying causeMaintain adequate cardiac output- monitor 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
35Nutrition During acute phase- enteral or parenteral nutrition In a hypermetabolic state- need more caloriesIf retain CO2- avoid high carb diet
36Acute Respiratory Failure Gerontologic Considerations Physiologic aging results in↓ Ventilatory capacityAlveolar dilationLarger air spacesLoss of surface areaDiminished elastic recoilDecreased respiratory muscle strength↓ Chest wall compliance**Dec. PO2 and inc. CO2
37ARDS 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-threateningarrhythmias
38Memory Jogger Assault to the pulmonary system Respiratory distress Decreased lung complianceSevere respiratory failure
46Pathophysiology of ARDS Damage to alveolar-capillary membraneIncreased capillary hydrostatic pressureDecreased colloidal osmotic pressureInterstitial edemaAlveolar edema or pulmonary edemaLoss of surfactant
49Pathophysiologic Stages in ARDS Injury or Exudative- 1-7 daysInterstitial and alveolar edema and atelectasisRefractory hypoxemia and stiff lungsReparative or Proliferative-1-2 weeks afterDense fibrous tissue, increased PVR and pulmonary hypertension occursFibrotic-2-3 week afterDiffuse scarring and fibrosis, decreased surface area, decreased compliance and pulmonary hypertension
50The essential disturbances of ARDS **interstitial and alveolar edema and atelectasis
51**Progressive arterial hypoxemia in spite of inc. O2 is hallmark of ARDS
52Clinical Manifestations: Early Dyspnea-(almost always present), tachypnea, cough, restlessnessChest auscultation may be normal or reveal fine, scattered cracklesABGs**Mild hypoxemia and respiratory alkalosis caused by hyperventilation
53Clinical Manifestations: Early Chest x-ray may be normal or show minimal scattered interstitial infiltratesEdema may not show until 30% increase in lung fluid content
54Clinical Manifestations: Late Symptoms worsen with progression of fluid accumulation and decreased lung compliancePulmonary function tests reveal decreased compliance and lung volumeEvident discomfort and increased WOB
55Clinical Manifestations: Late Suprasternal retractionsTachycardia, diaphoresis, changes in sensorium with decreased mentation, cyanosis, and pallorHypoxemia and a PaO2/FIO2 ratio <200 despite increased FIO2 ( ex: 80/.8=100)
56Clinical Manifestations As ARDS progresses, profound respiratory distress requires endotracheal intubation and positive pressure ventilationChest x-ray termed whiteout or white lung because of consolidation and widespread infiltrates throughout lungs
66Diagnostic 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
67ABG Review and Practice RealNurseEd (Education for Real Nurses by a Real Nurse)
71*Goal of Treatment for ARDS Maintain adequate ventilation and respirations.Prevent injuryManage anxiety
72TreatmentMechanical Ventilation-goal PO2>60 and 02 sat 90% with FIO2 < 50PEEP- can cause dec. CO, B/P and barotraumaPositioning- prone, continuous lateral rotation therapy and kinetic therapyHemodynamic Monitoring- fluid replacement or diureticsEnteral 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
73Cont. Crystalloids versus colloids Mild fluid restriction and diuretics
74pt. can not expire completely. Causes alveoli to remain inflated PEEPpt. can not expire completely. Causes alveoli to remain inflated(Complications can include decreased cardiac output, pneumothorax, and increased intracranial pressure).YouTube - Peep
80ProningProning typically reserved for refractory hypoxemia not responding to other therapiesPlan for immediate repositioning for cardiopulmonary resuscitation
81Proning-Principles Positioning strategies Mediastinal and heart contents place more pressure on lungs when in supine position than when in pronePredisposes to atelectasisTurn from supine to prone positionMay be sufficient to reduce inspired O2 or PEEPFluid pools in dependent regions of lung
82Prone Device No benefit in mortality 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
83Benefits to Proning Before proning ABG on 100%O2 7.28/70/70 After proning ABG on 100% 7.37/56/227
84Positioning Other positioning strategies Kinetic therapy Continuous lateral rotation therapy
86Oxygen Therapy Oxygen High flow systems used to maximize O2 delivery SaO2 continuously monitored, Usually have arterial line for frequent ABG’sGive lowest concentration that results in PaO2 60 mm Hg or greater
87Respiratory TherapyRisk for O2 toxicity increases when FIO2 exceeds 60% for more than 48 hoursPatients will commonly need intubation with mechanical ventilation because PaO2 cannot be maintained at acceptable levels
88Mechanical ventilation PEEPHigher levels of PEEP are often needed to maintain PaO2 at 60 mm Hg or greater**High levels of PEEP can compromise venous return↓ Preload, CO, and BP
89Medical Supportive Therapy Maintenance of cardiac output and tissue perfusionContinuous hemodynamic monitoringContinuous BP measurement via arterial catheter
90Medical Supportive Therapy Pulmonary artery catheter to monitor pulmonary artery pressure, pulmonary artery wedge pressures, and COAdministration of crystalloid fluids or colloid fluids, or lower PEEP if CO falls
91Medical Supportive Therapy Use of inotropic drugs may be necessaryHemoglobin usually kept at levels greater than 9 or 10 with SaO2 ≥90%Packed RBCsMaintenance of fluid balance
92Medical Supportive Therapy May be volume depleted and prone to hypotension and decreased CO from mechanical ventilation and PEEPMonitor PAWP, daily weights, and I and O’s to assess fluid status
93Medications Inhaled Nitric Oxide Surfactant therapy NSAIDS and corticosteroids
94Nitric OxideDilates pulmonary blood vessels and helps reduce shunting
96Assessment Data and Priority Respiratory rate of 10Absent breath sounds on the leftO2 sat 82%High pressure alarm on vent going offBilateral wheezingRespiratory rate of 30ABG respiratory acidosis
97ARDS 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 % FiO2 and call the Dr.
98#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 98B.RR 24C.B/P 168/90D.Temp 101.4
99#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.
101a machine that moves air in and out of the lungs VentilatorVentWorld - What is a Ventilator?a machine that moves air in and out of the lungs
102Mechanical Ventilation IndicationsApnea or impending inability to breatheAcute respiratory failureSevere hypoxiaRespiratory muscle fatigue
103Mechanical Vent Objective support circulation and maintain pt. respirations until can breathe on own
104Goal of Mechanical Ventilation adequate controlled ventilationrelief of hypoxia without hypercapniarelief of work of breathingaccess to airways
105Criteria to put on vent Apnea or impending inability to breathe Acute respiratory failurepH<7.25pCO2>50Severe hypoxia - pO2<50Respiratory muscle fatigue
106Mechanical Ventilation Types of mechanical ventilationNegative pressure ventilationUses chambers that encase chest or body and surround it with intermittent subatmospheric or negative pressureNoninvasive ventilation that does not require an artificial airwayNot used extensively for acutely ill patientsMostly used for neuromuscular diseases, CNS and injuries of the spinal cord
107Mechanical Ventilation Types of mechanical ventilation (cont’d)Positive pressure ventilation (PPV)Used primarily in acutely ill patientsPushes air into lungs under positive pressure during inspirationExpiration occurs passively
110Settings to Monitor FIO2 -% of O2 TV-<5ml/kg for ARDS (normal 8-10) Rate 12-15Control (CMV) Continuous Mandatory Ventilationassist controlSIMVinspiratory pressure and flowPressure support- only in spontaneous breathes (gets the balloon started) Pt. controls all but pressure limit
112Ventilator 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.
113Mechanical Ventilation Modes of volume ventilationBased on how much work of breathing (WOB) patient should or can performDetermined by patient’s ventilatory status, respiratory drive, and ABGs
114Control Mode or CMV TV and RR are fixed. 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 effortSpontaneously breathing patients must be sedated and/or pharmacologically paralyzed so they don’t breathe out of synchrony with the ventilator.*Ventilator does all the work
115Assist ContolA/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.Patient Assists or triggers the vent –can breathe faster but not slowerVent has back-up rateMay need to be sedated to limit the number of spontaneous breaths since hyperventilation can occur.This mode is used for patients who can initiate a breath but who have weakened respiratory muscles.
116Synchronous Intermittent Mandatory Ventilation-SIMV SIMV delivers the preset volume or pressure and rate while allowing the patient to breathe spontaneously in between ventilator breaths.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.SIMV is used as a primary mode of ventilation, as well as a weaning mode.During weaning, the preset rate is gradually reduced, allowing the patient to slowly regain breathing on their own.The disadvantage of this mode is that it may increase the work of breathing and respiratory muscle fatigue
119Pressure Support Ventilation PSV is preset pressure that augments the patient’s spontaneous inspiratory effort and decreases the work of breathing.The patient completely controls the respiratory rate and tidal volume.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.
121High Frequency Ventilation HFV delivers a small amount of gas at a rapid rate (as much as breaths per minute.)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.Sedation and pharmacological paralysis are required.
122Inverse Ratio Ventilation The normal inspiratory:expiratory ratio is 1:2 but this is reversed during IRV to 2:1 or greater (the maximum is 4:1).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.The shorter expiratory time prevents the alveoli from collapsing again.Sedation and pharmacological paralysis are required since it’s very uncomfortable for the patient.For patients with ARDS continuing refractory hypoxemia despite high levels of PEEP
123Case StudyMr. Hill has been on the ventilator for 24 hours. You volunteered to care for him today, since you know him from the intubation yesterday. The settings ordered by the pulmonologist after intubation were as follows: A/C, rate 14, VT 700, FIO2 60%. Since 0700, Mr. Hill has been assisting the ventilator with a respiratory rate of 24 (It’s now 1100).1. 1. Describe the ventilator settings.
124AnswerThe ventilator delivers 14 breaths per minute, each with a tidal volume of 700 ml. The A/C mode delivers the breaths in response to Mr. Hill’s own respiratory effort, but will initiate the breath if he doesn’t within the set amount of time. (He’s currently breathing above the vent setting.) The oxygen concentration is 60%.
125Case StudyYou notice that Mr. Hill’s pulse oximetry has been consistently documented as 100% since intubation. You also notice that his respiratory rate is quite high and that he’s fidgety, doesn’t follow commands, and doesn’t maintain eye contact when you talk to him. He hasn’t had any sedation since he was intubated.2. 2. Which lab test should you check to find out what his true ventilatory status is?
126AnswerArterial blood gas (ABG) - which he should have had done with his morning labs. If not, check with the pulmonologist about getting one.
127Case Study3. Which two parameters on the ABG will give you a quick overview of Mr. Hill’s status?
128AnswerPaCO2 (which affects the pH) and PaO2. With his high respiratory rate, Mr. Hill is at risk for hypocapnia from “blowing off CO2.” If the PaO2 is adequate, the FIO2 could be decreased, since his oxygen saturation has been consistently 100%.
129Case Study4. What are some possible causes of Mr. Hill’s increased respiratory rate? (Give the corresponding nursing interventions as well.)
130Answer 1. Secretions - suction through the ETT, as well as his mouth. 2. Anxiety or pain - Mr. Hill hasn’t received any sedation since he was intubated. At this point, he should at least have a prn order for sedation, if not a continuous IV infusion.3. The vent settings may not be appropriate – check the ABG’s and notify the pulmonologist
131Case StudyMr. Hill didn’t have an ABG done this morning, so you get an order from the pulmonologist to get one now (1130). When it comes back, the PaCO2 is 28, the pH is 7.48, and the PaO2 is 120 (normals: PaCO mm Hg, pH mm Hg, PaO mm Hg).5. Based on the ABG, the pulmonologist changes the vent settings to SIMV, rate 10, PS 10, FIO2 40%. The VT remains 700. How will these new settings help Mr. Hill?
132AnswerSIMV will deliver 10 breaths with the full tidal volume each minute, but in synchrony with Mr. Hill’s spontaneous breaths. This mode is not triggered to deliver a breath each time Mr. Hill inhales, and the tidal volume of his spontaneous breaths is under his control. Pressure support decreases the work of breathing that results from breathing through the ventilator circuits and tubing. The PaO2 was higher than desired, indicating that the FIO2 could be decreased. We need to be careful to prevent oxygen toxicity.The pulmonologist also orders midazolam (Versed) 1-2 mg every hour prn for sedation.
137Low Pressure AlarmsCircuit leaks Airway leaks Chest tube leaks Patient disconnection High Pressure AlarmsPatient 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
141Mechanical Ventilation Complications of PPV (cont’d)Cardiovascular system (cont’d)↑ Intrathoracic pressure compresses thoracic vessels↓ Venous return to heart, ↓ left ventricular end- diastolic volume (preload), ↓ cardiac outputHypotensionMean airway pressure is further ↑ if PEEP >5 cm H2O
142Mechanical Ventilation Complications of PPV (cont’d)Pulmonary systemBarotraumaAir can escape into pleural space from alveoli or interstitium, accumulate, and become trapped pneumothorax , subcutaneous emphysemaPatients with compliant lungs are at ↑ riskChest tubes may be placed prophylactically
144Mechanical Ventilation Complications of PPV (cont’d)Ventilator-associated pneumonia (VAP)Pneumonia that occurs 48 hours or more after ET intubationClinical evidenceFever and/or elevated white blood cell countPurulent or odorous sputumCrackles or rhonchi on auscultationPulmonary infiltrates on chest x-ray
145Mechanical Ventilation Complications of PPV (cont’d)Guidelines to prevent VAPHOB elevation at least 30 to 45 degrees unless medically contraindicatedNo routine changes of ventilator circuit tubing
146Mechanical Ventilation Complications of PPV (cont’d)Guidelines to prevent VAP (cont’d)Use of an ET that allows continuous suctioning of secretions in subglottic areaDrain condensation that collects in ventilator tubing
147Mechanical Ventilation Complications of PPV (cont’d)Fluid retentionOccurs after 48 to 72 hours of PPV, especially PPV with PEEPMay be due to ↓ cardiac outputResultsDiminished renal perfusionRelease of renin-angiotensin-aldosteroneLeads to sodium and water retention
148Mechanical Ventilation Complications of PPV (cont’d)Fluid retention (cont’d)Pressure changes within thorax are associated with ↓ release of atrial natriuretic peptide, also causing sodium retentionAs part of the stress response, antidiuretic hormone and cortisol may be ↑Contributes to sodium and water retention
149Mechanical Ventilation Complications of PPV (cont’d)Gastrointestinal systemRisk for stress ulcers and GI bleeding↑ Risk of translocation of GI bacteria↓ Cardiac output may contribute to gut ischemiaPeptic ulcer prophylaxisHistamine (H2)-receptor blockers, proton pump inhibitors, tube feedings↓ Gastric acidity, ↓ risk of stress ulcer/hemorrhage
150Mechanical Ventilation Complications of PPV (cont’d)Musculoskeletal systemMaintain muscle strength and prevent problems associated with immobilityProgressive ambulation of patients receiving long-term PPV can be attained without interruption of mechanical ventilation
151Mechanical Ventilation Psychosocial needsPhysical and emotional stress due to inability to speak, eat, move, or breathe normallyPain, fear, and anxiety related to tubes/ machinesOrdinary ADLs are complicated or impossible
152Mechanical Ventilation Psychosocial needs (cont’d)Involve patients in decision makingEncourage hope and build trusting relationships with patient and familyProvide sedation and/or analgesia to facilitate optimal ventilation
153Mechanical Ventilation Psychosocial needs (cont’d)If necessary, provide paralysis to achieve more effective synchrony with ventilator and increase oxygenationParalyzed patient can hear, see, think, feelSedation and analgesia must always be administered concurrently
154Respiratory TherapyAlternative modes of mechanical ventilation if hypoxemia persistsPressure support ventilationPressure release ventilationPressure control ventilationInverse ratio ventilationHigh-frequency ventilationPermissive hypercapniaIndependent Lung Ventilation
156ResearchLiquiVent 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.
157Liquid Ventilation Partial liquid ventilation with perflubron Perflubron is an inert, biocompatible, clear, odorless liquid that has affinity for O2 and CO2 and surfactant-like qualitiesTrickled down ET tube into lungs
158Blood 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.
159Research and NewvideoYouTube - Superman breather - USA
160Prioritization 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.
161#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.