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Rutgers University

Dr. Garry Johnson

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respiratory failure nursing care critical care medicine

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This document provides information on nursing care for adult and geriatric clients with acute and critical respiratory failure. It covers topics such as pathophysiological mechanisms, clinical manifestations, and treatment strategies including ventilation.

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Nursing Care of the Adult and Geriatric Client with Acute and Critical Respiratory Failure N014 Dr. Garry Johnson, DHSc, RN Student Learning Outcomes Compare pathophysiological mechanisms of hypoxemia and hypercapnia Differentiate between early and late respiratory failure Describe nursing care of p...

Nursing Care of the Adult and Geriatric Client with Acute and Critical Respiratory Failure N014 Dr. Garry Johnson, DHSc, RN Student Learning Outcomes Compare pathophysiological mechanisms of hypoxemia and hypercapnia Differentiate between early and late respiratory failure Describe nursing care of patients in respiratory failure Understand clinical manifestations and nursing care of patients with ARDS Identify complications from ARDS Discuss indications for and nursing care of patients with mechanical ventilation Respiratory System Fig. 68-1. Normal gas exchange unit in the lung. f Copyright © 2011, 2007 by Mosby, Inc., an af iliate of Elsevier Inc. Lung Volumes Tidal Volume (Vt) 0.5L Volume of air inhaled and exhaled with each breath (small proportion of total lung air capacity) Residual Volume (RV) 1.5L Amount of air remaining in lungs after forced expiration Lung Volumes Total Lung Capacity (TLC) 6.0L Maximum volume of air that lungs can contain Functional Residual Capacity (FRC) 2.5L Volume of air remaining in the lungs at the end of normal exhalation Vital Capacity (VC) 4.5L Maximum volume of air that can be exhaled after maximum inspiration Advanced Respiratory De initions Elastic Recoil Compliance Is a measure of elasticity of the lungs & thorax f f Tendency of lungs to recoil after being stretched or expanded Elasticity due to elastin ibers in alveolar walls, and surrounding the bronchioles and capillaries DEFINITIONS Ventilation: Inhaling and exhaling: Moving air in and out of the lungs. Respiration : Two types: External-Gas Exchange at Alveoli in lungs Internal-Gas Exchange at Capillaries all over the body Perfusion: Oxygen delivery to the body NORMAL VALUES PaO2: Partial Pressure of O2 in Oxygenated Blood 75-100 mm Hg PCO2: Partial Pressure of O2 in Mixed Venous Blood 35-45 mm Hg Acute Respiratory Failure Fig. 68-2. Classification of respiratory failure. f Copyright © 2011, 2007 by Mosby, Inc., an af iliate of Elsevier Inc. Tissue Oxygen Extraction Mixed Venous Blood monitoring (PvO2) Amount of O2 the cells consumed Normal 38-42 mm Hg If PvO2 is less than 38 mm Hg, then the cells are stressed and are extracting more than normal O2. Suggests an inadequate O2 supply to meet O2 demand. Causes of Hypoxemic Respiratory Failure Mismatch between ventilation (V) and perfusion (Q) = V/Q mismatch Shunt Diffusion limitation Hypoventilation V/Q V=ventilation Amount of fresh gas that reaches alveoli each minute (4-5L/min) Q=perfusion Volume of blood perfusing the lungs each minute (4-5L/min) Normal V/Q ratio = 1/1=1 1 ml of air for each 1 ml of blood low f V/Q Mismatch Problems with Ventilation VQ V/Q >1 Caused by problems with perfusion Pulmonary embolus Hemorrhage Question Mr. Smith has a low V/Q ratio. This means that there is ?: a. Decreased ventilation in relation to perfusion b. Increased ventilation with decreased perfusion c. Decreased ventilation with decreased perfusion d. Increased ventilation in relation to perfusion Shunt Unoxygenated blood is passed back into the circulation without being oxygenated. 2 types: anatomic and intrapulmonary Anatomic: when blood passes through an anatomic channel in the heart (ventricular septal defect or patent ductus arteriosus) and bypasses the lungs Shunt Intrapulmonary: When blood lows through pulmonary capillaries without participating in gas exchange. ARDS Pulmonary Edema Pneumonia f When the alveoli ill with luid: f f Shunt If increasing the FiO2 does not change the PaO2, then you may have a shunt. Resistant to O2 therapy Treating shunt with more FiO2 is useless Acute Respiratory Failure Fig. 68-4. Range of ventilation to perfusion (V/Q) relationships. A, Absolute shunt, no ventilation due to fluid filling the alveoli. B, V/Q mismatch, ventilation partially compromised by secretions in the airway. C, Normal lung unit. D, V/Q mismatch, perfusion partially compromised by emboli obstructing blood flow. E, Dead space, no perfusion due to obstruction of the pulmonary capillary. f Copyright © 2011, 2007 by Mosby, Inc., an af iliate of Elsevier Inc. Diffusion Limitation When gas exchange across the alveolar capillary membrane is impaired from: Obstruction or destruction of capillary membrane (severe emphysema, recurrent pulmonary emboli) Thickening of membrane, slowing gas transport (pulmonary ibrosis, interstitial lung disease, ARDS) f Diffusion Limitation More likely to cause hypoxemia during exercise than at rest. Increased RBC transit time through pulmonary capillaries decreases time for gas transport Acute Respiratory Failure Fig. 68-5. Diffusion limitation. Exchange of CO 2 and O2 cannot occur because of the thickened alveolar-capillary membrane. f Copyright © 2011, 2007 by Mosby, Inc., an af iliate of Elsevier Inc. Hypoventilation Generalized decrease in ventilation that leads to increased PaCO2 with a consequent decrease in PaO2. Causes are many Lung disease CNS disease Chest wall dysfunction Neuromuscular disease Hypoventilation Increasing hypercapnia leads to hypoxemia. Gases compete for space in alveoli PaCO2 PaO2 Can be acute or chronic Hypercapnic Respiratory Failure Limitation of ventilatory supply Abnormalities of the airways/ alveoli Abnormalities of the CNS Abnormalities of the chest wall Neuromuscular conditions (see table 67-1, 67-2) Airways and Alveoli (air low obstruction and air trapping) Asthma COPD Cystic ibrosis f f Central Nervous System (nonresponsive medulla) Narcotic and other drug abuse Brainstem infarction and/or head injury Chest Wall (limitation of chest expansion) Flail chest Kyphoscoliosis Massive Obesity (Pickwickian Syndrome) Neuromuscular Conditions Cervical Cord injury Phrenic nerve injury Amytrophic lateral sclerosis (ALS) Guillain-Barre Muscular Dystrophy Multiple Sclerosis Poliomyelitis Hypoxemia vs. Hypoxia Hypoxemia-low amount of O2 in blood Hypoxia-PaO2 has fallen suf iciently to cause signs and symptoms of inadequate oxygenation (poor tissue perfusion). Hypoxemia can lead to hypoxia if not corrected. Hypoxia can lead to anaerobic metabolism which leads to __________ acidosis. f Signs of Hypoxemia Restlessness, agitation, confusion Tachycardia, HTN Dypsnea, tachypnea Prolonged expiration Intercostal retraction Accessory respiratory use Signs of Hypoxemia Fatigue Arrhythmias (late), Hypotension (late) Cyanosis (late) Signs of Hypoxia Blood shunts to major organs (trunk) Slowed peripheral capillary re ill Cold extremities with thready pulses Skin pale and mottled Urinary Output Coma (late) from brain perfusion to Organ shut down leading to failure f Respiratory Failure Respiratory failure is de ined as: PaCO2 > 45 mm Hg pH < 7.35 PaO2 < 60 mm Hg on O2 >60% f Oxygen Therapy NC High Flow (Heated Humidi ied High Flow Nasal Oxygen- HFNO) Positive pressure ventilation CPAP, BiPAP Mechanical ventilation 100% NRB Avoid causing O2 toxicity High O2 concentrations eliminate nitrogen in alveoli causing instability & atelectasis Results in ibrotic changes in alveoli f f Venti Mask O2 Narcosis in Hypercapnea Hypercapnea (CO2 retainer) at risk Respiratory drive stimulated by hypoxia If PaO2 suddenly increases, will no longer be hypoxemic and may have respiratory arrest. Suggest no more than 3L per NC or no greater than Venti mask 24-28% FiO2 unless necessary. Collaborative Management Effective coughing and positioning Hydration and humidi ication Chest physical therapy Airway suctioning f Collaborative Management: Acute Respiratory Failure Medication Therapy Goals Relief of bronchospasm Reduction of airway in lammation Reduction of pulmonary congestion Treatment of pulmonary infections Reduction of severe anxiety, pain, and agitation Copyright © 2011, 2007 by Mosby, Inc., an af iliate of Elsevier Inc. f f Medication Therapy Relief of Bronchospasm Short acting bronchodilators via inhaler or hand held nebulizer Metaproterenol (Alupent) Albuterol (Ventolin) Medication Therapy Reduction of Airway In lammation Corticosteroids (inhaled not for emergencies) Methylprednisolone IV for immediate effects Reduction of Pulmonary Congestion IV diuretics to reduce pulmonary edema Antibiotics Antifungals f Treatment of Pulmonary Infections Medication Therapy Reduction of Severe Anxiety and Restlessness CAUTION: Low dose sedation since these could be symptoms of cerebral hypoxia Example: Ativan Must monitor especially for respiratory depression. Collaborative Management of Respiratory Failure Treat underlying cause Maintain adequate CO Maintain adequate hemoglobin concentration Nutritional therapy Effects of Aging on Respiratory System in elastic recoil of the lung in chest wall compliance anteroposterior (AP) diameter of the thoracic cage in the # of functional alveoli Small airways in lung bases close earlier on expiration This leads to V/Q mismatch Normal ventilation Decreased pulmonary capillary perfusion Leads to decreased PaO2 Effects of Aging on Respiratory System Less effective respiratory defense mechanisms Decline in cell-mediated immunity Decline in antibody formation Alveolar macrophages are less effective at phagocytosis Less forceful cough Fewer and less functioning cilia Effects of Aging on Respiratory System Decline in formation of IgA, which neutralizes viruses Decline in respiratory control Slower response to changes in PaO2 & PaCO2 Changes compounded if smoker or obese Acute Respiratory Distress Syndrome ARDS Hypoxemia refractory to supplemental 02 Severe dyspnea Reduced lung compliance Diffuse pulmonary in iltrates No evidence of heart failure A predisposing condition for ARDS within 48 hours of clinical manifestations f Etiology and Pathophysiology Conditions Predisposing to ARDS: Acute lung injury (ALI) Systemic in lammatory response Multiple organ dysfunction f 3 phases of ARDS 1. Injury or Exudate Phase: Interstitial and alveolar edema (noncardiogenic) Atelectasis Severe V/Q mismatch, shunting Hypoxemia unresponsive to 02 2. Reparative or proliferative Dense, ibrous tissue 3. Fibrotic f remodeling phase: phase: Clinical Manifestations Insidious onset Tachypnea, retractions, scattered crackles and rhonchi, interstitial and alveolar in iltrates: not r/t cardiac function Progresses to respiratory distress Intubation: (positive pressure ventilation), severe hypoxemia, hypercapnia, metabolic acidosis f Nursing Diagnoses Impaired gas exchange r/t Alveolar hypoventilation Intrapulmonary shunting V/Q mismatch Diffusion impairment Nursing Diagnoses Ineffective airway clearance r/t Excess secretions Decreased level of consciousness Presence of an arti icial airway Neuromuscular dysfunction pain f Nursing Diagnoses Ineffective breathing pattern r/t Neuromuscular impairment of respirations Pain Anxiety Decreased level of consciousness Respiratory muscle fatigue bronchospasm Nursing Diagnoses Risk for imbalanced luid volume r/t Sodium and water retention f Collaborative management Interventions: O2 administration, positioning strategies Mild luid restriction and diuretics as necessary Overall goal: f Pa02 of > 60mmHg, pH: 7.35-7.45 Sa02 90%, patent airway, clear lungs on auscultation Ventilators Criteria for Ventilator Use Apnea or impending inability to breathe Respiratory failure Hypoxia PaCO2 > 50 and pH < 7.25 PaO2 < 50 Respiratory muscle fatigue Types of Ventilators Negative pressure Ventilator Reduces intrathoracic pressure “Iron lung” Positive Pressure Ventilators During inspiration pushes air into the lungs under positive pressure Volume ventilation: a predetermined tidal volume is delivered on each inspiration, pressure varies with lung compliance and airway resistance Pressure ventilation: the peak inspiratory pressure is predetermined and the Vt delivered varies based on the pressure and compliance and resistance factors Ventilator Settings Tidal Volume Amount of air that moves in and out of lungs in a normal breath Normal is 10-12ml/kg (500-800ml in adult) FiO2 21%-100% Ventilator Settings Inspiratory:Expiratory Ratio (I:E) IE in the ventilated Prolongs positive pressure which can recruit more alveoli Helps with V in V/Q Inverse Ratio Ventilation Critical Thinking Questions What would you want to “recruit” the alveoli to do? Ventilator Settings Mode Assist Control (A/C) Intermittent Mandatory Ventilation (IMV) Synchronous IMV (SIMV) Pressure Support Ventilation (PS) Used as an adjunct to SIMV Used alone when weaning AC (Assist control) Takes over the work of breathing “Assist” means the ventilator is sensitive to the inspiratory efforts of the patient. When the patient begins to inhale, the ventilator triggers a breath at certain settings “Control” means a minimum number of breaths are delivered per minute if patient apneic IMV Patient spontaneously breaths, taking on most of the work of breathing Ventilator delivers a breath with a pre-set TV intermittently Spontaneous breaths happen inbetween mandatory breaths and generate intrinsic TV SIMV Ventilator synchronizes a mandatory breath to follow the patient’s exhalation (synchronized) Mandatory breath is not “stacked up” on top of a spontaneous breath More comfortable for the patient than IMV PS Adjunct weaning mode Enhances spontaneous inspiratory effort by application of positive pressure Triggered by patient’s spontaneous breathing effort Decreases the work of breathing Applies and maintains a pre-set pressure throughout the entire inspiration phase Ventilator Settings Rate Calculate the minute ventilation Amount of air that moves in and out of the lungs in 1 minute Normal rate is 8-12/minute on ventilator Dependant on mode and spontaneous respiratory efforts Ventilator Settings PEEP Positive End Expiratory Pressure Provides the alveoli with a constant pre-set amount of positive pressure at the end of expiration Keeps alveoli open and prevents atelectasis Maximizes O2 diffusion Raises intrathoracic pressure during inspiration, which decreases venous return Ventilator Settings PEEP Physiologic PEEP is 3-5cm H2O Airway pressure gauge on ventilator will not return to “0” if the patient is on PEEP Ventilator Settings PEEP 5-15 cm H2O for mild forms of lung injury 10-30 cm H2O for more severe lung injury > 30 cm H2O extremely severe lung injury like ARDS Complications from barotrauma Ventilator Settings Air delivered should always be humidi ied. f Reservoir should be “full” Air should be warmed 34-37 degrees centigrade Warmer for hypothermia Assessment of the Ventilator Dependent Patient ABCs Ventilator rate versus total RR Cuff pressure ETT measurement at the lips in cm Ventilator settings and function/ alarms Frequency of suctioning and quality of sputum ABGs CXR trends Readiness to wean Care of the Mechanically Ventilated Patient Goals of Care: Keep airway patent and ventilated Prevent ventilator associated pneumonia (VAP) Prevent barotrauma and subsequent tension pneumothorax Comfort Prevent hemodynamic instability Ventilator Associated Pneumonia (VAP) Second most common nosocomial infection in the US Is frequently referred to as the most common ICU infection Care of the Mechanically Ventilated Patient Prevent ventilator associated pneumonia (VAP) Effective oral care Critically ill colonize more lethal lora in oral cavities Staphylococcus aureus Streptococcus pneumoniae Pseudomonas aeruginosa Dental plaque serves as a reservoir for lora f f Critical Thinking exercise case study Acute respiratory distress syndrome See case study, Lewis 11th ed. Pg. 1603, with Patient pro ile of J.N. 1.What is the cause Of ARDS for this pt? 2. How does the pathophysiology of ARDS predispose him to refractory hypoxemia? 3. What manifestations does “he” have the support a diagnosis of ARDS? 4. Calculate the Pa02/FIO2 ratio. What does this value tell you about the seriousness of his condition? 5. What other complications is “he” at risk for developing from ARDS? 7.What priority interventions should be implemented to improve “his” respiratory status and hypoxemia? f References ATI- Phram modules Adams, M.& Urban, C. (2020) Pharmacology Connections to Nursing Practice (4th ed) Boston:Pearson Lewis, S.M., Heitkemper, M.M., & Dirksen, S.R. (2021). Medical Surgical Nursing: Assessment and Management of Clinical Problems, 11th ed. Mosby Munro, C.L. & Grap, M.J. (2004). Oral health and care in the intensive care unit: state of the science. American Journal of Critical Care. References Neis, B.R. & Neis, P. (2004). Gastric factors that can cause ventilator associated pneumonia. Of icial News Magazine of the Society of Critical Care Medicine. f

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