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RESPIRATORY FAILURE and ARDS BY NANCY JENKINS 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 VentilationPerfusion Mismatch (V/Q) Normal V/Q =1 (1ml air/ 1ml of blood) Ventilation=lungs Perfusion or Q=perfusion Pulmonary Embolus- (VQ scan) 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 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 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- 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. 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) 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 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 150,000 adults dev. ARDS About 50% survive **Patients with gram negative septic shock and ARDS have mortality rate of 70-90% ALI versus ARDS- continuum 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* 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 ↓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 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 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 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) *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 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). 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 Benefits to Proning Before proning ABG on 100%O2 7.28/70/70 After proning ABG on 100% 7.37/56/227 Positioning Other positioning strategies • Kinetic therapy • Continuous lateral rotation therapy 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. 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 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 Mechanical Ventilator Settings to Monitor FIO2 -% of O2 TV-<5ml/kg for ARDS (normal 8-10) Rate 12-15 • Control mode • Assist control • SIMV inspiratory pressure and flow Pressure support- only in spontaneous breathes (gets the balloon started) Pt. controls all but pressure limit 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. 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. 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 Case Study Mr. 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. Case Study You 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? Case Study 3. Which two parameters on the ABG will give you a quick overview of Mr. Hill’s status? Case Study 4. What are some possible causes of Mr. Hill’s increased respiratory rate? (Give the corresponding nursing interventions as well.) Case Study Mr. 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: PaCO2 35-45 mm Hg, pH 7.35-7.45 mm Hg, PaO2 80-100 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? 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 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 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 Ventilator Bundle Components 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 support ventilation Pressure release ventilation Pressure control ventilation Inverse ratio ventilation High-frequency ventilation Permissive hypercapnia 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.