Week 9

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Week 9
2012-04-08 22:04:08

acute respiratory failure
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  1. Acute Respiratory Failure
    • Hypoxemic: has low arterial blood oxygen levels
    • Ventilatory failure: perfusion is normal, but ventilation is inadequate. Chest pressure does not change enough to let air movement into and out of the lungs, as a result too little oxygen reaches the alveoli and carbon dioxide is retained. Usually a result of 3 problems:1.A physical problem of the lungs or chest wall2.A defect in the respiratory control center in the brain3.Or poor function of the respiratory muscles, esp. the diaphragm. Extrapulmonary: neuromuscular disorders (Myasthenia Gravis, Guillain-Barre syndrome), Spinal cord injury, CNS dysfunction (IICP, Stroke), Chemical depression, Obesity, External obstruction/constriction. Intrapulmonary: COPD, Pulmonary embolism, Pneumothorax, ARDSOxygenation failure: air moves in and out without difficulty but does not oxygenate the pulmonary blood sufficientlyVentilation is normal, but lung perfusion is decreased. Air movement and oxygen intake (ventilation) are normal, but lung blood flow (perfusion) is decreased. Causes: CHF with pulmonary edema, pneumonia, PE, ARDS, Hypovolemic shock, Low atmospheric oxygen (high altitude, smoke inhalation, Carbon monoxide poisoning. A combination involves hypoventilation (poor respiratory movements) of ventilatory and oxygenation failure that often occurs in patients who have abnormal lungs such as those with chronic bronchitis or emphysema or during asthma attacksDiseased bronchioles and alveoli cause oxygenation failure, and the work of breathing increases until the respiratory muscles are unable to function effectively, causing ventilatory failure
  2. Hallmark Sign of Respiratory Failure?
    Dyspnea! Assess: respiratory rate and pattern, change in lung sounds, manifestations of hypoxemia (pallor, cyanosis, increased heart rate, restlessness, confusion), pulse oximetry is okay, but order ABGs. Interventions: position of comfort, which is what usually? Conserve energy, how? Relaxation, diversion. How about drugs? MDI (albuterol for example)
  3. Acute Respiratory Distress Syndrome (ARDS)
    Often occurs after an acute lung injury as a traumatic event in people who have no previous pulmonary disease. Mortality rate is high even when intensive interventions are used. Other terms used Adult respiratory distress syndrome, shock lung, noncardiogenic pulmonary edema. The main trigger is systemic inflammatory response. No abnormal lungs sounds are present on auscultation because the edema of ARDS occurs first in the interstitial spaces, not in the airways.
  4. Causes of Lung Injury in ARDS
    the alveolar-capillary membrane is injured, which is normally only permeable to small molecules. Lung tissue normally remains relatively dry, but in patients with ARDS lung fluid increases and contains high levels of proteins. Surfactant (which maintains elasticity of lung tissue and prevents alveolar collapse) activity is decreased in ARDS. The alveoli become unstable, and tend to collapse unless they are filled with fluid, either way they cannot exchange gases. Transfusion related acute lung injury (TRALI) associated with the activation of the inflammatory response due to a recent transfusion of plasma containing products (PRBCs, platelets, FFP) are associated with ARDS in critically ill patients. When a patient is being transfused they are being exposed to plasma that contains foreign proteins and antibodies. This exposure activates WBCs and causes agglutination (clumping) of the foreign proteins and WBCs, which then travel to the lung. The clumped material injures the pulmonary capillaries causing capillary leak and additional inflammation. Common causes of acute lung injury: Shock, trauma, serious nervous system injury, pancreatitis, fat and amniotic fluid emboli, pulmonary infections, sepsis, inhalation of noxious gases, pulmonary aspiration, drug ingestion, hemolytic disorders, multiple blood transfusions, cardiopulmonary bypass, near drowning (esp. in fresh water). In many cases of ARDS, especially after trauma clot production is increased, and fibrinolysis (clot breakdown) is reduced. As a result small emboli remain in the lung.
  5. ARDS: Diagnostic Assessment
    ABGs with lower PaO2 (partial pressure of arterial oxygen)Pulmonary artery catheter (Swan-Ganz) placement and hemodynamic monitoring is a diagnostic tool. In the patient with ARDS the pulmonary capillary wedge pressure (PCWP) is usually low to normal (in cardiac induced pulmonary edema the wedge pressure is elevated. FYI: The PCWP is measured by inserting a balloon-tipped, multi-lumen catheter (Swan-Ganz catheter) into a peripheral vein, then advancing the catheter into the right atrium, right ventricle, pulmonary artery, and then into a branch of the pulmonary artery. Just behind the tip of the catheter is a small balloon that can be inflated with air (~1 cc). The catheter has one opening (port) at the tip (distal to the balloon) and a second port several centimeters proximal to the balloon. These ports are connected to pressure transducers. When properly positioned in a branch of the pulmonary artery, the distal port measures pulmonary artery pressure (~ 25/10 mmHg) and the proximal port measures right atrial pressure (~ 0-3 mmHg). The balloon is then inflated, which occludes the branch of the pulmonary artery. When this occurs, the pressure in the distal port rapidly falls, and after several seconds, reaches a stable lower value that is very similar to left atrial pressure (LAP, normally about 8-10 mmHg). The balloon is then deflated. The same catheter can be used to measure cardiac output by the thermodilution technique
  6. ARDS: Interventions
    May need sedation and paralysis for adequate ventilation and to reduce tissue oxygen needs. Patient positioning is important in promoting gas exchange although the exact position is controversial. Some patients do well in the prone postion, esp. if started early in the course of the disease. It is very awkward to turn the patient. Continuously turning the patient to 40 degrees from side to side or using a 90 degree lateral position also appears to improve perfusion. Drugs: corticosteroids may be used because they decrease WBC movement and stabilize capillary membranes. Antibiotics are used to treat infections. Recent research shows that conservative fluid therapy is most beneficial, it shortens the duration of mechanical ventalation, shortens ICU length of stay. Conservative fluid therapy involves smaller fluid amounts and the use of diuretics to maintain fluid balance. Nutrition therapy: at risk for malnutrition which further reduces the resp. muscle function and the immune response. Nutrition is started ASAP. Phase 1: early changes of dyspnea, and tachynea. Early interventions focus on supporting the patient and supplying oxygenPhase 2: Patchy infiltrates form from increasing pulmonary edema. Interventions include mechanical ventilation and prevention of complications.Phase 3: occurs over days 2 through 10, and the patient has progressive hypoxemia that responds poorly to high levels of oxygen. Interventions focus on maintaining adequate oxygen transport, preventing complications and supporting the failing lung until it has had time to heal. Phase 4: Pulmonary fibrosis with progression occurs after 10 days. This phase is irreversible and is often called late or chronic ARDS. Patients who develop this stage and survive it will have some permanent lung damage. Interventions focus on preventing sepsis pneumonia and MODS, as well as weaning the patient from the ventilator. The patient in this phase will be ventilator dependent for weeks to months. Some patients may not be weanable.
  7. Endotracheal Tube
    Patients who require mechanical ventilation first need an artificial airway. Most common is an ET tube, for short term. A tracheostomy is used if a patient will need an artificial airway for longer than 10 to 14 days to reduce tracheal and vocal cord damage. The goals of intubation are to maintain a patent airway, provide a means to remove secretions, and provide ventilation and oxygen.
  8. Verifying Tube Placement
    Possibly in the right main brochus- if breath sounds and chest movement are absent on the left. May be in the stomach if the abdomen is distended.
  9. Mechanical Ventilation
    Traditionally divided into negative-pressure ventilation, where air is essentially sucked into the lungs, or positive pressure ventilation, where air (or another gas mix) is pushed into the trachea.Negative-pressure ventilators: the “iron lung”. In the iron lung by means of a pump, the air is withdrawn mechanically to produce a vacuum inside the tank, thus creating negative pressure. This negative pressure leads to expansion of the chest, which causes a decrease in intrapulmonary pressure, and increases flow of ambient air into the lungs. As the vacuum is released, the pressure inside the tank equalizes to that of the ambient pressure, and the elastic coil of the chest and lungs leads to passive exhalation.Positive-pressure ventilators: most ventilators in use today are this type. Positive pressure ventilators are classified by the mechanism that ends inspiration and starts expiration. Inspiration is terminate in 3 ways: Pressure-cycled ventilators: push air into the lungs until a preset airway pressure is reached. Tidal volumes and inspiration time vary. Used for short periods. Bi-level positive airway pressure (Bi-PAP) ventilators are a modern form of pressure-cycled ventilator in which the ventilator provides a preset inspiratory pressure and an expiratory pressure similar to positive end-expiratory pressure (PEEP). Time-cycled ventilators: push air into the lungs until a preset time has elapsed. Tidal volume and pressure vary, depending on the needs of the patient and the type of ventilator. Volume-cycled ventilators: push air into the lungs until a preset volume is delivered. A constant tidal volume is delivered regardless of the pressure needed to deliver the tidal volume. A set pressure limit, however, prevents excessive pressure from being exerted on the lungs. The advantage is that a constant tidal volume is delivered regardless of the changing compliance of the lungs and chest wall or the airway resistance. Microprocessor vents: computer managed positive pressure ventilators. Allows ongoing monitoring of ventilatory functions, alarms, andpatient conditions. More responsive to patients who have severe lung disease
  10. Modes of Ventilation
    Assist-control ventilation (AC): used most often, The ventilator takes over the work of breathing of the patient. The tidal volume and ventilatory rate are preset. If the patient does not trigger spontaneous breaths a minimal ventilatory pattern is established by the vent. It is programmed to respond to the patient’s inspiratory effort if he/she does begin a breath. In this case the vent delivers the preset tidal volume while allowing the pt. to control the rate. Disadvantage: If the patients spontaneous breathing increases the vent continues to deliver the preset tidal volume, the patient can hyperventilate and respirtory alkalosis can occur. Investigate the cause of hyperventilation (pain, anxiety) and correct them. Synchronized intermittent mandatory ventilation (SIMV): similar to AC ventilation in that tidal volume and ventilatory rate are preset. If the patient does not breathe, a minimal ventilatory pattern is established by the ventilator. Unlike the AC mode, SIMV allows spontaneous breathing at the patient's own rate and tidal volume between the ventilator breaths. It can be used as a main ventilatory mode or as a weaning mode. When used for weaning, the number of mechanical breaths (SIMV breaths) is gradually decreased (e.g., from 12 to 2) and the patient gradually resumes spontaneous breathing.Bi-level positive airway pressure (BiPAP): provides noninvasive pressure support ventilation by nasal mask or facemask. Although BiPAP is most often used for patients with sleep apnea, it also may be used for patients with respiratory muscle fatigue to avoid more invasive ventilation methods.Other modes of ventilation: such as pressure support and continuous flow (flow-by), are part of most microprocessor ventilators. Both types decrease the work of breathing and are often used for weaning patients from mechanical ventilation. Other modes are maximum mandatory ventilation (MMV), inverse inspiration-expiration (I/E) ratio, permissive hypercarbia, airway pressure–release ventilation, proportional assist ventilation, high-frequency ventilation, and high-frequency oscillation. Many of these modes use special ventilators, tubing, or airways.
  11. Ventilator Controls and Settings
    Tidal volume (Vt): the volume of air the patient receives with each breath. It can be measured either on inspiration or expiration. Rate—breaths/min: the number of breaths delivered each minuteFraction of inspired oxygen (FiO2): The oxygen level delivered to the patient. Determined by the ABG value and the patient’s condition. Vents can provide 21% to 100% oxygen. Oxygen is warmed and humidified. Peak airway (inspiratory) pressure: (PIP) indicates the pressure needed by the ventilator to deliver a set tidal volume at a given lung compliance. The PIP value appears on the display on the front or top of the ventilator. It is the highest pressure reached during inspiration. Monitoring trends in PIP reflect changes in resistance of the lungs and resistance in the ventilator. An increased PIP reading means increased airway resi stance in the patient or in the ventilator tubing (bronchospasm or pinched tubing), increased amount of secretions, pulmonary edema, or decreased pulmonary compliance (the lungs or chest wall is “stiffer” or harder to inflate). An upper pressure limit is set on the ventilator to prevent barotrauma. When the limit is reached, the high-pressure alarm sounds and the remaining volume is not given. Continuous positive airway pressure (CPAP): applies positive airway pressure throughout the entire respiratory cycle for spontaneously breathing patients. Sedating drugs are given cautiously or not at all when the patient is receiving CPAP so that respiratory effort is not suppressed. CPAP keeps the alveoli open during inspiration and prevents alveolar collapse during expiration. This process increases functional residual capacity (FRC), improves gas exchange, and improves oxygenation.Positive end-expiratory pressure (PEEP): is positive pressure exerted during the expiratory phase of ventilation. PEEP improves oxygenation by enhancing gas exchange and preventing atelectasis. It is used to treat persistent hypoxemia that does not improve with an acceptable oxygen delivery level. PEEP is often added when the partial pressure of arterial oxygen (PaO2) remains low with an Fio2 of 50% to 70% or greater.Flow and other settings: Flow is how fast each breath is delivered and is usually set at 40 L/min. If a patient is agitated or restless, has a widely fluctuating pressure reading on inspiration, or has other signs of air hunger, the flow may be set too low. Increasing the flow should be tried before using chemical restraints.
  12. Nursing Management
    Monitor the patient’s response: assess VS, listen to breath sounds every 30 to 60 minutes, Monitor resp. parameteres (capnography, pulse oximeter) check ABG values. Vital signs change during hypercarbia and hypoxemia. Assess breathing pattern in relation to the breathing cycle, are they tolerating or fighting the vent. Breath sounds, need for suctioning? Assess around the ET tube or trach tube at least every four hours. Pace activities, Look for slight changes in vital signs or ABGs, fatigue or distress. Skilled and sensitive nursing care promotes psychological well being. Communication methods, magic slates, writing paper, computers, and trach tubes that promote talking. Call light in reach, try to anticipate needs, encourage family visits. Managing the ventilator system: Settings are prescribed by the physician (often in conjunction with the RT). Perform and document ventilator checks. Respond rapidly to alarms, compare prescribed settings to the actual settings, check level of water and temperature of humidifier. Drain water in the vent tubing into the collection receptacles. Never silence the alarms. 2 major alarms ar high pressure and low exhaled volume. (page 695 table 34-4). Prevent complications:Capnography is the monitoring of the concentration or partial pressure of carbon dioxide (CO2) in the respiratory gases.hypercapnia: the physical condition of having the presence of an abnormally high level of carbon dioxide in the circulating blood
  13. Mechanical Ventilation: Complications
    Hypotension: caused by positive pressure that increases chest pressure and inhibits blood return to the heart. Decreased venous return decreases cardiac output reflected as hypotension. Most often seen in patients with dehydration or need high PIP. Fluid Retention: D/T decreased cardiac output, the kidneys receive less blood flow which stimulates the body to retain fluid (renin angiotensin aldosterone system).Valsalva Maneuver: teach the patient to avoid valsalva maneuver.
  14. Mechanical Ventilation: Complications (Cont’d)
    GI problems: result from the stress of mechanical ventilation (stress ulcers are common). The ulcers complicate the nutritional status and increase the risk of infection. Antacids, antiulcer (carafate), histimine blockers (rantidine:Zantac), proton pump inhibitors (esomeprazole: Nexium) are often ordered in vent patients. Changes in chest and abdominal cavity pressure can lead to a paralytic ileus. Nutritional problems: malnutrition weakens muscles including the diaphragm making it difficult to wean these patients. Infections—ventilator-associated pneumonia: perform oral care at least every 2 hours, implement pulmonary hygiene, including chest physiotherapy, postural drainage and turning and positioning (page 660 chart 33-5, not included in the reading)Muscle deconditioningVentilator dependence: the longer a patient is on a vent the more dependent they become.
  15. Lung Problems
    Barotrauma: damage to the lungs by positive pressure. Includes pneumothorax, subcutaneous emphysema and pneumomediastinum. Patients at high risk have blebs, are on PEEP, or require high pressure to ventilate the lungs, because of stiff lungs as in ARDS. Volutrauma: damage to the lungs by excess volume delivered to one lung over the other. Picture above: This patient developed a left tension pneumothorax during treatment of a severe pneumonia. Note the marked shift of the mediastinal structures to the right, the partial collapse of the left lung, and the inversion and downward displacement of the left hemidiaphragm.The mediastinum is a non-delineated group of structures in the thorax, surrounded by loose connective tissue. It is the central compartment of the thoracic cavity. It contains the heart, the great vessels of the heart, esophagus, trachea, phrenic nerve, cardiac nerve, thoracic duct, thymus, and lymph nodes of the central chest.
  16. Weaning
    SIMV synchronous intermittent mandatory ventilation: The patient breaths between the machines preset bpm rate. The machine is initially set at 12, meaning the patient receives a minimum of 12 breaths/min, the rate will be gradually decreased to 1 or 2T-Piece: the patient is taken off the ventilator for short periods of time (initially 5 to 10 minutes) and allowed to breath spontaneously. The ventilator is replaced with a T-piece, weaning progresses as the client tolerates progressively longer periods off the ventilator. Pressure support: allows the patient’s respiratory effort to be augmented by a predetermined pressure assist from the ventilator, as the weaning ensues the amount of pressure is gradually decreased.
  17. Extubation
    Vitals every 5 minutes at first. IS every 2 hours, it is common for them to be hoarse at first and have a sore throatSit in semi-fowlers, use incentive spirometer every 2 hours, take deep breaths every ½ hourLimit speaking right after extubation. What are you monitoring for? Respiratory fatigue and airway obstruction. Look for mild dyspnea, coughing, inability to expectorate secretions. Stridor….bad! Late manifestation of a narrowing airway. Requires rapid response.
  18. Multiple Organ Dysfunction Syndrome
    Damage to organs may be primary or secondary. In primary direct damage to an organ from shock, trauma, burn injury or infection. Secondary MODS is a result of a wide spread inflammatory response that results in organ dysfunction not involved in the initial insult. From Iggy: Multiple Organ Dysfunction SyndromeThe sequence of cell damage caused by the massive release of toxic metabolites and enzymes is termed multiple organ dysfunction syndrome (MODS). Once the damage has started, the sequence becomes a vicious cycle as more dead cells break open and release harmful metabolites. The metabolites trigger small clots (microthrombi) to form. The clots block tissue oxygenation and damage more cells, thus continuing the devastating cycle. MODS occurs first in the liver, heart, brain, and kidney. The most profound change is damage to the heart muscle. One cause of this damage is the release of myocardial depressant factor (MDF) from the ischemic pancreas.
  19. Multiple Organ Dysfunction Syndrome (continued)
    Circulation to the gastrointestinal tract (splanchnic flow). The anatomy of the circulation of the gut (splanchnic circulation) is unusual in that the venous blood does not return directly to the heart, but instead it flows in the portal vein to the liver, and only after this does it reach the hepatic vein and the inferior vena cava. Pronounced Splank-nick
  20. Pathophysiology of DIC
    Characterized by exagerated microvasculature coagulation (clotting), which prompts the release of clotting factors which eventually depletes the clotting factor, which leads to bleeding.
  21. Treatment of DIC
    The product is manufactured by slowly thawing a unit of FFP at temperatures just above freezing (1-6 °C), typically in a water bath or a refrigerator. The product is then centrifuged to remove the majority of the plasma, and the precipitate is resuspended in the remaining plasma or in sterile saline.