Week 5: Acute Respiratory Alterations

Non-invasive positive pressure ventilation (NPPV) -Advantages over invasive ventilation?

**Helps the patient breathe/ventilate Non-invasive positive pressure ventilation: Advantages over invasive ventilation = mask only, allows flexibility, less risk of infection Noninvasive ventilation (NIV) refers to the administration of ventilatory support without using an invasive artificial airway (endotracheal tube or tracheostomy tube). The use of noninvasive ventilation has markedly increased over the past two decades, and noninvasive ventilation has now become an integral tool in the management of both acute and chronic respiratory failure, Noninvasive ventilation has been used as a replacement for invasive ventilation, and its flexibility also allows it to be a valuable complement in patient management. Its use in acute respiratory failure is well accepted and widespread. Book: Non-invasive positive pressure ventilation (NPPV): is the delivery of mechanical ventilation (breathing for the pt?) without an ETT or tracheostomy tube** Provides ventilation via: 1) face mask that covers the nose, mouth or both 2) a nasal mask or pillow 3) full face mask Vocal cord injuries are reduced with these along with sedations. NPPV may prevent the need for intimation in many patients NPPV is indicated for acute exacerbations of COPD, cardiogenic pulmonary edema, early hypoxemic respiratory failure in immunocompromised patients , obstructive sleep apnea, asthma, pneumonia, Post op rep. Failure, obesity, and others. Contraindications include apnea and cardiovascular instability (hypotension, uncontrolled dysrhythmias, myocardial ischemia.)

Acute respiratory distress syndrome (ARDS) -Defining characteristic? -Diagnostic criteria for ARDS (3)**** -Diagnostic criteria? -Acute lung injury scoring? -Mild, moderate, severe ARDS? -Pulmonary capillary wedge tells us what?

ARDS: Defining characteristic = Noncardiogenic pulmonary edema (can get it from blood transfusions) Diagnostic criteria: 1) PaO2/FiO2 ratio of less than 200 2) Bilateral infiltrates (white on X-ray) 3) Pulmonary capillary wedge pressure* < 18 mm Hg Acute lung injury scoring also used for dx - Lung Injury Score (LIS) is a commonly utilized measure of lung injury severity. Draft definition proposed 3 mutually exclusive categories of ARDS based on degree of hypoxemia: -mild (200 mm Hg < PaO2/FIO2 ≤ 300 mm Hg) -moderate (100 mm Hg < PaO2/FIO2 ≤ 200 mm Hg) -Severe (PaO2/FIO2 ≤ 100 mm Hg) And 4 ancillary variables for severe ARDS: 1. radiographic severity 2.respiratory system compliance (≤40 mL/cm H2O) 3.positive end-expiratory pressure (≥10 cm H2O), and 4.corrected expired volume per minute (≥10 L/min). Pulmonary capillary wedge or occlusion pressure < 18 mm Hg] indicates non-cardiogenic pulmonary edema -Tells us whether the heart is involved. If > 18 = the heart is involved (HF) -Indication of left ventricle function (norm = 8-12 mmHg; >18 suggests heart failure)

Acute respiratory failure resulting from PE (book)

Acute Respiratory Failure Resulting from Pulmonary Embolism (PE): An embolus is a clot of a plug of material that travels from one blood vessel to another, smaller blood vessel (the clot lodges in the smaller blood vessel and obstructs flow.) (PE = embolus lodged in the pulmonary vasculature.) -The embolus could be a clot broken off from a DVT, a fat globule from a long bone fracture or a catheter tip fragment or amniotic fluid in pregnancy. Most PE's originate from a DVT of the lower extremity. PE and DVT are two components of the disease process VTE (Venous thromboembolism) A massive PE manifests as systolic hypotension < 90 mm Hg (30-80 mortality rate) A non-massive PE manifests with a BP of at least 90 mm Hg and results in a 5% mortality rate Virchow's triad: favor development of a VTE 1) Venous stasis 2) Hypercoagulability of blood 3) Damage to the vessel walls DVT is the underlying cause for 90% of PE's* Pathophysiology: pulmonary circulation has an enormous capacity to compensate for a PE which is why many patients with a PE do not initially decompensate. An embolus lodges in the pulmonary vasculature completely or partially occluding a pulmonary artery or one of its branches. Lack of perfusion to ventilation alveoli results in increased dead space, V/Q mismatch - gas exchange cannot occur Release of inflammatory mediators cause constriction of bronchi and widespread vasoconstriction causing poor pulmonary perfusion and increased dead space. This causes inadequate production of surfactant resulting in atelectasis Assessment: classic presentation includes sudden onset of pleuritic chest pain, SOB, and hypoexmia. Tachypnea, crackles, S2 sound, tachycardia and fever. Diagnosis: D-dimer Assay: a positive test indicates a thrombus formation but it is non-specific and not recommended for dx; used to safely rule out PE in young healthy people Ventilation-Perfusion scan: calculates pulmonary airflow and blood flow; may detect dead space from impaired perfusion of ventilated alveoli. Not confirmatory/diagnosis for PE Compression ultrasound: useful for detecting lower-extremity DVTs, not PE's High-resolution multidetector computed tomography angiography (MDCTA): aka a spiral CT is the preferred tool for detecting PE (standard of care) Pulmonary angiography: provides direct anatomical visualization of pulmonary vasculature and provides close to 100% certainty of PE but it is invasive and difficult to perform Treatment: Prevention is the best therapy for VTE; treatment is anticoagulation therapy with heparin. -Low molecular weight heparin (LMWH) is begun immediately after acute PE (also for VTE prevention.) -Compression stocking/devices are recommended for VTE prophylaxis -**Oral anticoagulant warfarin is started at the time of PE diagnosis and is continued for at least 3 months. Heparin-induced thrombocytopenia (HIT) is a complication of LMWH and UFH. It is caused by antibodies that activate platelets leading to thrombocytopenia. Results in thromboembolism such as DVT or PE; patients will have decreasing platelet counts, skin lesions at injection site, fever, cills. **If the location of the PE is known, positioning the patient with the "good" lung in the dependent position is warranted

Acute respiratory failure in Asthma (book)

Acute Respiratory Failure in Asthma: Asthma is a chronic inflammatory disorder of the airways. The inflammation causes the airways to become hyperresponsive when the patient inhales allergens, viruses, or other irritants Episodic airflow obstruction results because these irritants cause bronchoconstriction, airway edema, mucus plugging and airway remodeling. Asthma is largely reversible** Clinical manifestations include: expiratory wheezing, dyspnea, chest tightness, prolonged expiration, tachycardia, tachypnea, and nonproductive cough. The pt initially hyperventilates (resp. alkalosis) with PEEP readings less than 50% and may be using accessory muscles to breathe. Status asthmaticus: is a severe asthma exacerbation when the bronchoconstriction does not respond to bronchodilator therapy and ARF ensues (resp acidosis and severe hypoxemia.) **Auscultation of a "silent" chest indicates complete absence of air movement and is an impending medical emergency. Mild exacerbations of asthma are managed with inhaled short acting beta2-agonists to treat bronchoconstriction and inhaled corticosteroid from inflammation. Acute severe exacerbations of asthma require O2 therapy, repeated administration of rapid acting inhaled bronchodilators and systemic steroid administration (some may need intubation and mechanical ventilation) **Oxygenation may be improved by delivering a mixture of helium and O2 (heliox) to the lungs because helium is less dense than O2, it enhances gas flow through the constricted airways and may improved oxygenation

Acute respiratory failure in adult patients with cystic fibrosis (book)

Acute respiratory failure in adult patients with cystic fibrosis: CF is a genetic disorder (autosomal recessive disease- both parents must be carriers of a variant gene) that results from defective chloride ion transport which leads to the formation of thick mucus. The thick mucus obstructs glands of the lungs, pancreas, liver, glands and testes causing organ dysfunction. It is a multisystem disease but has its greatest effects on the lungs with respiratory failure being the primary cause of death Affects mostly white people Sweat chloride test is the gold standard (60 mmol/L or greater indicate CF is likely) If ventilator support is needed, noninvasive mechanical ventilation is the first line of therapy. ETT is next. *Lung transplant requirement includes a life expectancy of less than 24-36 months.

Preventing complications of Mechanical Ventilation (MV) -Barotrauma -Volutrauma

Barotrauma: Examples -Pneumothorax -Tension pneumothorax Detect: -High PAP, mean airway pressure -Decreased breath sounds -Tracheal shift -Subcutaneous crepitus -Hypoxemia Treat tension pneumothorax emergently -Manually ventilate -Needle thoracostomy -Trauma can occur secondary to mechanical ventilation. -Types include barotrauma and volutrauma. -Can be life-threatening. Volutrauma: -Overdistention of alveoli -Damages the lung similar to early ARDS -Keep PIP < 40 cm H2O -Acid-Base Disturbances: -Respiratory acidosis -Respiratory alkalosis Excess volume can create damage similar to that of ARDS. Important to monitor PIP and plateau pressure. Book: Pulmonary system: Trauma aka baraotrauma means pressure trauma from injury to the lungs associated with mechanical ventilation. Alveolar injury or rupture occurs as a result of excessive pressure, excessive peak inflating volume (volutrauma) or both. Baraortrauma may occur when the alveoli are overextended (Positive pressure ventilation). Precipitating factors include diseases where the lungs have reduced compliance (ARDS), pneumonia associated with high PIP The alveoli rupture or tear so that air escapes into various parts of the thoracic cavity causing subcutaneous emphysema (air in the tissue space.), pneumothorax, and more. s/s of barotrauma include decreasing SpI2, decreased breath sounds, tracheal shift, subcutaneous crepitus, new air leak or increase in air leak in a chest drainage system and symptoms associated with hypoxemia A tension pneumothorax occurs when pressurized air enters the pleural space. It is unable to exit and continues to accumulate causing increased intrathoracic pressure, increasing amounts of lung collapse, shifting of the heart and great vessels to the opposite thorax (mediastinal shift,( tachycardia, and hypotension. Treatment is immediate insertion of a chest tube or needle thoracostomy** Lung tissue injury induced by local or regional ocerdisting volume is called volutrauma. Similar to pathological findings of ARDS (stiff lungs) and result of local stress and strain on the alveolar capillary membrane

Mrs. J Case Study (continued): Mrs. J.'s condition continues to worsen. A decision is made to try the oscillator ventilator. -Why is this decision made? -What is the related nursing care? -As Mrs. J. gets worse, what other complications can occur with ARDS?

Because Mrs. J. was unable to be oxygenated with high levels of FiO2 and PEEP, a new ventilatory strategy is needed. The oscillator may successfully recruit alveoli in cases of severe ARDS. Review text for nursing care, which includes sedation, neuromuscular blockade, prevention of complications of bed rest, etc. Psychological support for the family is also critical (and has been given throughout). Mrs. J Case Study (continued): -Despite the oscillator, Mrs. J.'s condition worsens. -The physicians discuss her grave condition with her husband. They mutually agree to make her a DNR. -The husband and her parents are encouraged to spend time with her in the room and are supported by the staff. -Mrs. J. dies about 4 hours after the DNR decision. Discussion: -What are the psychosocial implications of this case? -How can you support the family? -Responses will vary. Discuss the relative youth of the patient and providing support to a young spouse and parents who do not expect their child to die. Pastoral care services or other bereavement services may be needed. Support and debriefing may also be needed by the multiprofessional team members.

Preventing complications of Mechanical Ventilation (MV) -Weaning patients from Ventilator -Assessment for readiness to wean -Evidence-based weaning guidelines

Weaning Patients from Ventilator: Liberation -Individualized decisions -Collaborative team effort -Breathe!! *Weaning is a team effort Assessment for readiness to wean: -Underlying cause for mechanical ventilation resolved -Hemodynamic stability; adequate cardiac output -Adequate respiratory muscle strength -Adequate oxygenation without a high FiO2 and/or high PEEP -Absence of factors that impair weaning -Mental readiness -Minimal need for medicines that cause respiratory depression -Must assess readiness to wean patients from mechanical ventilation. -Resolution of underlying cause for mechanical ventilation is critical. Evidence-Based Weaning Guidelines: 1) Identify causes for ventilatory dependence 2) Assess potential for weaning success 3) Conduct spontaneous breathing trial (SBT) 4) Determine cause, if SBT is unsuccessful 5) Assess airway patency and ability of patient to protect airway 6) Implement nursing and respiratory therapy weaning protocols 7) Use sedation strategies aimed at early extubation 8) Consider tracheostomy for prolonged assisted ventilation 9) Conduct slow-paced weaning for patients with prolonged mechanical ventilation 10) Patient is not ventilator-dependent until 3 months of failed SBTs 11) Transfer patient who has failed weaning trials to long-term facility specializing in ventilator management

What is positive end-expiratory pressure (PEEP)? Auto-PEEP? Ventilation setting - PEEP

What is Positive End-Expiratory Pressure (PEEP)?: With PEEP, positive pressure is maintained throughout expiration, but when the patient inhales spontaneously, airway pressure decreases to below zero to trigger airflow. With CPAP, a low-resistance demand valve is used to allow positive pressure to be maintained continuously. Positive-pressure ventilation increases intrathoracic pressure and thus may decrease cardiac output and blood pressure. Because mean airway pressure is greater with CPAP than PEEP, CPAP may have a more profound effect on blood pressure. In general, patients tolerate CPAP well, and CPAP is usually used rather than PEEP. The use of appropriate levels of CPAP is thought to improve the outcome in ARDS Auto-PEEP: -Spontaneous development of PEEP -Caused by gas trapping: -Insufficient expiratory time -Incomplete exhalation -Rapid RR -Airflow obstruction -Inverse I:E ventilation -Auto-PEEP can sometimes occur in conditions of gas trapping. -Respiratory therapist can assess this maneuver. Ventilator Setting - PEEP: -Positive end-expiratory pressure (PEEP) -Typical ventilatory setting = 5-20 cmH2O -Increases FRC to improve oxygenation -Can cause reduced cardiac output if high and impedes venous return -Auto - PEEP = Total PEEP - Set PEEP Protocols are often used to determine ventilator settings; respiratory therapists commonly make these adjustments. PEEP is commonly applied to reduce oxygen needs; explain physiology of PEEP. With PEEP, positive pressure is maintained throughout expiration, but when the patient inhales spontaneously, airway pressure decreases to below zero to trigger airflow. With CPAP, a low-resistance demand valve is used to allow positive pressure to be maintained continuously. Positive-pressure ventilation increases intrathoracic pressure and thus may decrease cardiac output and blood pressure. Because mean airway pressure is greater with CPAP than PEEP, CPAP may have a more profound effect on blood pressure. In general, patients tolerate CPAP well, and CPAP is usually used rather than PEEP. The use of appropriate levels of CPAP is thought to improve the outcome in ARDS

If the PaO2 is 60 mm Hg and the FiO2 is 0.6, the PaO2/FiO2 ratio is: a) 100 b) 1000 c) 360 d) 3600

A PaO2 / FiO2 60 / 0.6 = 100 This pt would be in ARDS since its less than the cut off of 200

ARDS pathophysiology -Main patho of ARDS?** -Surfactant is decreased from damage to _________? -Two pathways from an indication of lung damage that lead to ARDS? (2) -Early cases of ARDS have which metabolic disorder? Why?

ARDS Pathophysiology: -Insult—systemic inflammatory response syndrome (SIRS) -Release of inflammatory mediators -Damage to alveolar-capillary membrane -Increased capillary permeability -Pulmonary edema (noncardiogenic)**(test) (pathophysiology of ARDS)* ARDS Pathophysiology -Microatelectasis (little spots in the alveoli that are collapsing) -Decreased compliance (stiff lungs) -Decreased surfactant (damage to type II pneumocytes) -Impaired gas exchange -V/Q mismatch ​​​​Take- home message: This is a complex process related to inflammation, infection, and cell damage There are two pathways from an indication of lung damage to the most severe form of Acute Respiratory Failure - ARDS. -Alveolar epithelial damage and endothelial damage. 1) Alveolar epithelial damage - related to infection (such as pneumonia) and decreased surfactant production and/or atelectasis 2) Endothelial damage - due to aggregation of platelets (clots) and/or inflammatory mediators or cytokines, such as interleudin 1 and tumor necrosis factor Alkalotic at FIRST (early in ARDS) but then become acidotic later on** Patients hyperventilate early in the course of the disease as an attempt to increase oxygen delivery. Early cases will have respiratory alkalosis.

Respiratory failure in Acute Respiratory Distress Syndrome (ARDS): (book) -Criteria -Etiology -Pathology -Assessment -Inteventions

ARDS in the most severe form of ARF** Criteria for ARDS: 1) acute onset within 1 week after clinical insult, 2) bilateral pulmonary opacities not explained by other conditions, 3) altered PaO2/FiO2 ratio. The severity of ARDS is determined by the PaO2/FiO2 ratio when the patient is treated with positive end-expiratory pressure (PEEP) or continuous positive airway pressure (CPAP) of 5 cm H2O ir higher Mild ARDS = 200 - 300 mm Hg Moderate ARDS = 100 - 200 mm Hg Severe ARDS = less than 100 mm Hg Etiology: risk factors such as pneumonia, spesis, aspiration and trauma have a higher association frequency of ARDS (the presence of two or more factors increases the risk.) Direct causes: aspiration of gastric contents, fat embolism, inhalation of toxic gasses, multisystem trauma (chest/lung injury,) near drowning, pneumonia Indirect causes: burns, cardiopulmonary bypass, drug overdose, fractures (pelvis, long bones,) multiple transfusions*, multisystem trauma (without chest/lung injury,( pancreatitis, sepsis *After recovery, people are weak, have mobility issues, nausea, swallowing difficulties, fatigue, problems with memory, anxiety, depression and more. Pathology of ARDS: ARDS is characterized by acute and diffuse injury to the lungs leading to respiratory failure. Occurs in 3 phases: Acute phase: characterized by uncontrolled inflammation. Inflammatory mediators damage the pulmonary/capillary endothelium activation massive aggregation of platelets and formation of intravascular thrombi** Fluid, protein, and blood cells leak from the capillary beds into the alveoli causing pulmonary edema. Pulmonary hypertension occurs secondary vasoconstriction caused by the inflammatory mediators (both lead to V/Q mismatching.) Production of surfactant is stopped, and the damaged cells become susceptible to bacterial infection/pneumonia. The lungs become less compliant (resulting in decreased ventilation.) A right to left shunt of pulmonary blood develops. WOB increases. Proliferative phase: overlaps with the fibrotic phase and occurs between 1-3 weeks after onset. During this phase, pulmonary edema resolves, and fibrin matrix forms resulting in progressive hypoxemia Fibrotic phase: is the final phase and occurs 2-3 weeks after the initial insult. Fibrosis obliterates the alveoli, bronchioles, and interstitium. The lungs become fibrotic with decreased functional residual capacity and severe right to left shunting The inflammation and edema become worse with narrowing of the airways, resistance to airflow and atelectasis increase. Inflammatory mediators cause widespread edema and multiple organ failure/dysfunction syndrome (MODS.) Cause of death may not be related to ARF but more likely MODS related to ARDS* Assessment: clinical findings include dyspnea, tachypnea and hypoxemia that does not respond to O2 therapy (refractory hypoxemia.) Hypoxemia triggers hyperventilation (resp. alkalosis.) Initial signs are fine crackles, restlessness, disorientation and change of LOC. -Chest CT shows interstitial and alveolar infiltrates over the first 24-48 hours after onset. -As pulmonary edema develops and the lungs become non-compliant, hypoventilation and resp acidosis occur. Interventions: adequate oxygenation is the primary goal in the treatment of ARDS. NPPV or ETT intubation and mechanical ventilation may be needed. Patients with ARDS usually require intubation and mechanical ventilation to meet oxygenation needs* -To prevent O2 toxicity and increased mortality, the goal is to maintain the PaO2 with levels of FiO2 at 0.50 -Ventilatory support for patients with ARDS typically included PEEP (positive-end expiratory pressure) - PEEP is a mode of therapy used in conjunction with mechanical ventilation. At the end of mechanical or spontaneous exhalation, PEEP maintains the patient's airway pressure above the atmospheric level by exerting pressure that opposes passive emptying of the lung. Pharmacological treatment: this is no pharmacological agents that are considered standard therapy for ARDS Sedation and comfort: patients with ARDS are routinely sedated to promote comfort, rest, and sleep; alleviate anxiety, prevent self-extubation or harm, and ensure adequate ventilation. **Prone positioning: (face down) Pt's with severe ARDS may benefit from prone positioning; placing them prone for more than 12 hours has been shown to decrease mortality when used with lower Vt ventilation -Turning the pt prone alters the V/Q ratio by maintaining posterior perfusion while allowing optional ventilation in the larger portion of the lungs. It removes the weight of the heart and abdomen from the lungs, facilitates removal of secretions, improves oxygenation, and enhances recruitment of airways. Nutrition: delivering higher calories to those with ARDS results in an increased likelihood of mortality (withhold feedings for ARDS patients in the most acute phase.)

ARF in COPD (book)

ARF in Chronic Obstructive Pulmonary Disease (COPD): COPD is a progressive and preventable disease characterized by airflow limitations that are not fully reversible. Airflow limitations are from abnormal inflammatory response to noxious particles or gasses* Pathophysiology: It's a disease of the small airways and the lung parenchyma that results in chronic bronchitis and emphysema** -3rd leading cause of death in the U.S (after heart disease and cancer.) -The primary cause of COPD is tobacco smoke (smoking cessation is the most effective intervention to reduce the risk of developing COPD.) -Other contributing factors are air pollution, occupational exposure to dust/checmicals, age, female sex, and the genetic abnormality alpha-antitryspsin deficieny* -COPD causes chronic inflammation which injures the airways - the body repairs the injury though the process of airway remodeling which causes scarring, narrowing, and obstruction of the airways* Causing permanent enlargement of air spaces. -Increased mucus production occurs, cilia are destroyed (pt can't clear thick, tenacious mucus.) -ARF can occur at any time in the patient with COPD - causes include acute exacerbations, heart failure, dysrhythmias, pulmonary edema, pneumonia, dehydration, and electrolyte imbalances. Assessment: the hallmark symptoms of COPD arte progressive dyspnea, chronic cough, and sputum production. Diagnosis is confirmed by post bronchodilator spirometry that documents irreversible airflow limitations. Functional residual capacity is increased from air trapping -The chest is often overexpanded or barrel shaped because the anterior-posterior diameter increases in size. Assess for use of accessory muscles and pursed lip breathing. Finger clubbing indicates long term hypoxemia. -Diminished breath sounds, prolonged exhalation, wheezing and crackles are noted. -ABGs will show mild hypoxemia, over time as a compensatory mechanism, the kidneys increase bicarbonate production and retention (metabolic alkalosis) in an attempt to keep the pH within normal limits. -Wheezing indicates narrowing of the airways. -Pt is usually more comfortable in the upright position -Life-threatening ARF is indicated by tachypnea of more than 30 breaths/min, accessory muscle use, acute decline in mental status, hypoxemia that does not improve with supplemental oxygen via venturi mask -ABGs = at baseline, the pt with COPD usually has an ABG result that shows a normal pH, moderately low PaO2 (60-65 mm Hg,) and elevated PaCO2 in the range of 50-60 mm Hg (compensatory respiratory acidosis.) Interventions for COPD: Influenza and pneumococcal vaccinations* Oxygenation is the most important intervention for an acute exacerbation of COPD (to correct hypoxemia.) O2 is delivered to achieve SaO2 of 88-92% via a Venturi mask (delivers more precise oxygen concentrations.) **COPD patients ventilate based off low O2, giving too much oxygen eliminates their drive to breathe (causing more CO2 retention) - keep between 88-92% Bronchodilator therapy - the use of short acting inhaled beta2-agonists is recommended for treating an acute exacerbation. They cause smooth muscle relaxation that reverses bronchoconstriction. Adverse effects include tachycardia, dysrhythmias, tremors, hypokalemia, anxiety, bronchospasm, and dyspnea. Corticosteroids - administration improves lung function, recovery time, oxygenation, and length of stay. Prednisone 40 mg/day for five days is the recommended regimen. Adverse effects include hyperglycemia, and increased risk of infection. Antibiotics improve survival for those who are moderately to severely ill. Oral route for 5-7 days in pt's with increased dyspnea and increased sputum volume and purulence or if mechanical ventilation is required* -Ventilatory assistance: Patients with ARF from a COPD exacerbation may need positive pressure ventilation with or without intubation - this improves respiratory efforts by delivering positive airways pressure through a nasal, oronasal or full face mask -Intubation and invasive mechanical ventilation are indicated in patients where NPPV have failed

Acute respiratory failure resulting from pneumonia (book)

Acute Respiratory Failure Resulting From Pneumonia: -Pneumonia is the leading cause of death from infection in the U.S and a common cause of ARF. -Pneumonia is a lower respiratory tract infection (elderly people are very vulnerable and most often an infected population.) Pathophysiology: for pneumonia to occur, enough organisms must accumulate in the lower respiratory tract to overwhelm the patients defense mechanisms. The lower resp. Tract is usually protected by the upper airway (warming/filtering the air,) closure of the epiglottis, cough and sneeze reflexes, alveolar macrophages. The major cause of entry of these organisms is aspiration of gastric or oropharyngeal secretions (most common). Inflammatory response leads to a ventilation/perfusion mismatch resulting in dyspnea, hypoxemia, fever and leukocytosis The most common cause of community acquired pneumonia is streptococcus or pneumococcal infection; can be prevented by the pneumococcal vaccination. -Influenza is a common cause of viral pneumonia Assessment: Clinical presentation usually begins with fever, cough (productive,) and dyspnea. Older adults may have nonspecific symptoms like changes in mental status with hypothermia. -Order chest CT, WBC, procalcitonin, C-reactive protein, blood/sputum cultures Ventilator-associated pneumonia: VAP is defined as pneumonia that develops in a patient who is intubated and ventilated at the time or within 48 hours prior to the onset of the event. -Patients with ETT are at increased risk for aspiration of oral/gastric secretions. The ETT is inserted into the trachea past the vocal cords (holding the glottis open and compromises the ability to prevent aspiration.) -Interventions are aimed at prevention and treatment; Bundle of care = HOB at least 30 degrees, daily awakening, assessment of needs for continuing mechanical ventilation, etc.

Acute respiratory failure (ARF) is failure of respiration in any of what 3 areas? **Criteria for Respiratory failure? (3)

Acute Respiratory Failure (ARF): Failure of Respiration in any of these 3 areas: 1) Perfusion 2) Oxygenation 3) Ventilation or All of the above = problem in one area leads to problems in other areas (manifested in altered ABGs) Criteria for altered gas exchange (on room air) (of Respiratory Failure)** PaO2 < 60 mm Hg PaCO2 > 50 mm Hg pH ≤ 7.30 Book: Acute respiratory failure (ARF) is the most common admitting diagnosis in critical care units Acute Respiratory Failure (ARF): Is defined as an inability of the respiratory system to provide oxygenation and/or remove carbon dioxide from the body. ARF is classified as 1) oxygenation failure resulting in hypoxemia without a rise in carbon dioxide levels or 2) ventilation failure resulting in hypercapnia and hypoxemia. Type 1 ARF: (oxygenation failure, hypoxemic) - characterized by a partial pressure of arterial oxygen (PaO2) lower than 60 mm Hg with normal to decreased levels of CO2 Type 2 ARF: (ventilation failure, hypercapnic) - Is characterized by a partial pressure of arterial carbon dioxide (PaCo2) greater than 50 mm Hg ARF differs from chronic respiratory failure in that it evolves rapidly over minutes to hours providing little time for physiological compensation. Chronic development over time and allows the body's compensatory mechanisms to activate. Acute Respiratory Failure Pathophysiology: Failure of oxygenation: occurs when PaO2 cannot be adequately maintained (most commonly occurring type of ARF*) Five mechanisms that reduce PaO2 and create a state of hypoxemia = hypoventilation, intrapulmonary shunting, ventilation-perfusion mismatching, diffusion defects, and decreased barometric pressure (occurs at high altitudes) Hypoventilation = decreased RR, increases amount of CO2 Intrapulmonary shunting = in the normally functioning lungs, a small amount of blood returns to the left side of the heart without engaging in gas exchange (called physiological shunt,) when larger amounts return without going through gas exchange, the shunt becomes pathological (Causing a decrease in PaO2) - causes are atelectasis, pneumonia, and pulmonary edema Ventilation-perfusion mismatch: gas exchange in the lungs is dependent on the balance between ventilated areas of the lung (ventilation) receiving blood flow (perfusion.) The rate of ventilation (V) usually equals the rate of perfusion (Q), resulting in a V/Q ratio of 1.0. -If ventilation exceeds blood flow, the V/Q ratio is greater than one -If ventilation is less than blood flow, the V/Q ratio is less than one -V/Q mismatch occurs in pneumonia, pulmonary edema, obstructed airways, pulmonary embolism Diffusion defects: under normal circumstances, O2 and CO2 diffuse across the alveolar capillary membrane in 0.25 seconds; in respiratory failure, the distance between the alveoli and capillaries may be increased by accumulation of fluid in the interstitial space. COPD is an example -As diffusion capacity is reduced, reductions in PaO2 occur first (causing hypoxemia.) Because CO2 is more readily diffusible than O2, hypercapnia is a late sign of diffusion defects Low cardiac output: if the CO decreases, less oxygenated blood is delivered and eventually the cells convert to anaerobic metabolism which causes lactic acid build up and depresses the function of the myocardium and further lowers CO Low hemoglobin level: SaO2 refers to the % of O2 binding sites on each hemoglobin molecule that are filled with O2 (96-100%.) If a person's hemoglobin level is lower than normal, the O2 supply to the tissues may be imparied and tissue hypoxia can occur. (CO2 poisoning, sickle cell disease.) Tissue hypoxia: the final step in oxygenation occurs at the tissues (this is why hypoxemia (blood) occurs before hypoxia.) Anaerobic metabolism occurs when the tissues cannot obtain adequate O2 to meet metabolic demands - resulting in the buildup of lactic acid - leads to cellular death and organ failure. Failure of Ventilation: PaCO2 is the variable used to evaluate ventilation** (PaO2 is used to assess oxygenation)** When ventilation is reduced, PaCO2 is increased (hypercapnia.) When ventilation is increased, PaCO2 is reduced (hypocapnia.) Hypoventilation and V/Q mismatching are the two mechanisms responsible for hypercapnia -Hypoventilation: when CO2 accumulates in the alveoli and is not blown off (decreased RR.) Resp. acidosis occurs rapidly before renal compensation can occur* -Ventilation-perfusion mismatch: the volume of gas that fills the upper and lower airways is called dead space. Dead space increases when an area that is well ventilated has reduced perfusion and no longer participates in gas exchange.

The nurse suspects respiratory failure secondary to hypoventilation in a patient with: a) Anxiety b) Neuromuscular disease c) Pulmonary embolism d) Volume A/C ventilation at rate of 20 breaths/min

B This is a common cause of hypoventilation

Assessment of Respiratory failure? Interventions of ARF? ARF medical management? How can the nurse assist in reducing oxygen demands/decrease WOB?

Assessment of Respiratory Failure: -Respiratory -Cardiovascular -Psychosocial -Chest x-ray -Pulmonary function tests -Arterial blood gases (ABGs) -Pulse oximetry and end-tidal CO2 (End tidal CO2 = the amount of CO2 you are blowing out with each breath (use meter to monitor - nasal cannula.) -Nutrition (anemia from low iron/nutritional problems) -**Neurological signs (anxiety, restless, confusion)- may be earliest signs of hypoxia and hypercapnia Comprehensive assessment helpful in determining etiology of respiratory failure as well as response to treatment. Neurological changes are the earliest signs of respiratory failure. Interventions for ARF: -Maintain a patent airway -Optimize O2 delivery (sniffing/slight sniffing position) -Minimize O2 demand (Promote rest, calm dark room, slight sedatives to calm patient) -Identify and treat the cause of ARF -Prevent complications!! Many interventions are used to treat respiratory failure. Of most importance is to optimize oxygen delivery and minimize oxygen demand. ARF Medical Management: 1. Treat/prevent hypoxia 2. Open bronchi, bronchioles 3. Reduce inflammation 4. Allow rest 5. Increase oxygen carrying capacity 6. Ensure adequate ventilation 7. Decrease work of breathing 8. Promote healing with adequate vitamins and minerals 9. Closely monitor patient's response to therapy 1. Oxygen therapy 2. Bronchodilators* (open airways) 3.Corticosteroids* 4.Sedation (if pt anxious) 5.Transfusions (blood transfusion if not enough hemoglobin or RBCs) 6.Assisted and/or mechanical ventilation 7.Therapeutic paralysis 8.Nutritional support (magnesium helps support the diaphragm muscle) 9.Hemodynamic monitoring What nursing interventions assist in reducing oxygen demands? Decrease WOB via: -Promote rest -Relieve pain (reducing pain decreases oxygen demand) -Alleviate anxiety (paralytics/medications) -Reduce fever -Position patient for optimal management of secretions -Maintain open airways - collaborate with respiratory for suctioning **Hyperoxygenate before and after suctioning** -Don't want to hyperoxygenate for too long. Can cause oxygen toxicity (increases fluid in lungs over time)

What do we need to breathe? (3) Circulation and blood flow = ? Oxygenation and gas exchange = ? Lungs and chest excursion = ?

Circulation and blood flow → Perfusion Oxygen and gas exchange → Oxygenation Lungs and chest excursion → Ventilation Negative pressure creates vacuum Pulse oximetry (SpO2) provides information about the patient's oxygenation Continuous end-tidal CO2 monitoring provides information about the patient's ventilation **PaO2, the partial pressure of oxygen in the arterial blood, is determined solely by the pressure of inhaled oxygen (the PIO2). SaO2 is the percentage of available binding sites on hemoglobin that are bound with oxygen in arterial blood.** *Hemoglobin = protein in RBCs responsible for transporting oxygen (low levels = anemia) *Hematocrit = % of blood volume that is composed of RBCs

You've determined that "Ineffective Airway Clearance" is a reasonable nursing diagnosis for your patients. A nursing intervention to maximize airway clearance is which of the following? a) Administer supplemental oxygen. b) Elevate the head of bed. c) Provide oral care every 4 hours. d) Reposition patient every 2 hours.

D Will help mobilize secretions Turning pt side to side helps the airway clear itself. Elevating the HOB is also a little helpful but they are probably building up fluid at the base of their lungs

Failure of ventilation -Definition of ventilation? -What things interrupt ventilation?

Definition of ventilation: Exchange of gas (i.e. air) between lungs and the environment Interruption of Ventilation: 1)Hypoventilation 2) Ventilation-perfusion mismatch -Trauma (broken ribs, pneumothorax) -Drug overdose -Neurological disorders -Abdominal or thoracic surgery Many factors can result in hypoventilation and decreased oxygenation and ventilation.

Preventing complications of Mechanical Ventilation (MV) -Dysphagia and Aspiration -GI system complications -Psychosocial complications -Medications

Dysphagia and Aspiration: -Dysphagia common after extubation -Assess swallowing prior to initiating oral feedings -Cardiovascular System Complications: -Hypotension -Decreased cardiac output, especially with PEEP -Assess for dysphagia and reduce risk of aspiration. -Consult speech therapist as needed. GI System Complications: -Complications -Stress ulcers -GI bleeding -Interventions -Stress ulcer prophylaxis -Provide nutritional support -GI side effects are also common Psychosocial Complications: -Stress -Anxiety -Dyssynchrony -Noise -Altered sleep-wake patterns -Dependence -*Nurse must also address psychosocial needs of patient Medications: -Analgesics: morphine -Sedatives: benzodiazepines, neuroleptics, and propofol -Neuromuscular blocking agents (NMBAs): paralytic agents Several medications are used in management of mechanically ventilated patients. Titrate to targets using standardized assessment scales.

Endotracheal intubation -Which route is preferred? -Gold standard?** -Why do we use ETT intubation?

Endotracheal Intubation: Insertion of an endotracheal tube (ETT) through the mouth (or nose) Orotracheal route preferred to reduce infections Endotracheal intubation is often needed to maintain airway and deliver mechanical ventilation. Insertion of an endotracheal tube (ETT) through the mouth (or nose) Orotracheal route preferred to reduce infections** = Gold standard!! (Test) Used to: -Maintain an airway -Remove secretions -Prevent aspiration -Provide mechanical ventilation **ETT tube is the gold standard for keeping the airway open ETT intubation is often needed to maintain airway and deliver mechanical ventilation

Preventing complications of Mechanical Ventilation (MV) -ETT out of position -Laryngeal/Tracheal injury -Damage to oral/nasal mucosa -O2 toxicity

ETT Out of Position: -Right mainstem bronchus -Dislodged -Unplanned extubation -Nurse must protect airway to prevent unplanned extubation -Secruing the tube is important -Tube can dislodge into the right mainstem or esophagus during movement and repositioning. -Important to assess bilateral breath sounds regularly. -Monitor chest x-ray. Laryngeal/Tracheal Injury: -Prevent excessive head movement -Routine monitoring ETT cuff pressure (Keep no higher than 25 to 30 cm H2O) -Damage can occur to the larynx and trachea from the ETT. -Monitoring and managing cuff pressure is one strategy to prevent injury. Damage to Oral and Nasal Mucosa: -Skin breakdown from tape and commercial devices -Carefully monitor patient's skin for breakdown from both tape and commercial devices Book: Airway problems: The Endotracheal tube out of position: may become dislodged during procedures or turning. Symptoms include absent or diminished breath sounds in the left lung and unequal chest excursion. Whenever the ETT is manipulated, assess for bilateral chest excursion, auscultate the chest for bilateral breath sounds after the procedure, and reassess tube position at the lip. If a serious airway problem cannot be resolved, manually ventilate the pt. Laryngeal and tracheal injury can occur. Prevent the pt from excessive head movement, especially flexion and extension which result in the tube moving up and down in the airway causing an abrasive injury* Book: Oxygen toxicity can occur from exposure to FiO2 (Not PaO2), the first signs are tracheobronchitis (caused by irritating effects of oxygen.) Prolonged exposure to high FiO2 can lead to changes in the lungs that mimic ARDS (stiff lungs, decreased compliance.) Nitrogen is used to prevent the collapse of the alveoli** When the FiO2 is 1.0 (100%,) alveolar collapse and atelectasis result from lack of nitrogen in the distal air spaces

Failure of oxygenation -Definition of oxygenation? -What things interrupt oxygenation?

Failure of Oxygenation Definition of oxygenation: Biological process of providing and adding oxygen, and/or combining other gases with oxygen Interruption of oxygenation: -Tissue hypoxia (clot) -Low hemoglobin level (anemia) -Hypoventilation (CNS depression, trauma, opioids/sedation) -Intrapulmonary shunting (Shunts to R→ L side without being oxygenated) -Ventilation-perfusion mismatch Oxygen decrease can result from a variety of factors

Failure of Oxygenation: tissue hypoxia -Tissue hypoxia causes what? which leads to a build up of ...? -Final step of oxygenation? -Effects of hypoxia?

Failure of Oxygenation: Tissue Hypoxia Some conditions prevent tissues from using oxygen despite availability Cyanide poisoning (oxygen is blocked from going into the tissues) Tissue hypoxia results in anaerobic metabolism (metabolism without oxygen) and causes lactic acidosis (buildup of lactic acid) The final step in oxygenation is use of oxygen at the tissue level. If tissues are hypoxic, anaerobic metabolism and lactic acidosis result** **Look at pic

Failure of perfusion and oxygenation: Intrapulmonary shunting* Causes?

Failure of Perfusion and Oxygenation: Intrapulmonary Shunting*: Blood shunted from right to left side of heart without oxygenation Causes: atrial or ventricular septal defect, atelectasis, pneumonia, pulmonary edema Question: Why does administration of higher levels of oxygen not help in shunt disorders?: = Because shunt represents areas where gas exchange does not occur, 100% inspired oxygen is unable to overcome the hypoxia caused by shunting. ... Although ventilation at that area is unaffected, blood will not be able to flow through that capillary; therefore, at that zone there will be no gas exchange. Shunting occurs when blood is shunted away from the lungs. Pneumonia and pulmonary edema are common causes of shunting in adults. Extra oxygen will not be effective if the blood is shunted*

Failure of perfusion and Oxygenation: Diffusion Defects -Adequate diffusion of O2 and CO2 does not occur if ...? Failure of oxygenation: low hemoglobin -Hemoglobin is necessary for what? -Anemia?

Failure of Perfusion and Oxygenation: Diffusion Defects Adequate diffusion of O2 and CO2 does not occur, if ... Fluid in alveoli -Heart failure -Pneumonia Interstitial lung disease -Pulmonary fibrosis Diffusion means spread or scatter. Perfusion refers to spreading through or diffusing, usually through a liquid, such as blood in the circulatory system Diffusion defects impair gas exchange. Failure of Oxygenation: Low Hemoglobin -Hemoglobin necessary to transport oxygen -95% of oxygen is bound to hemoglobin -For anemia, they could have a pulse ox of 96% but they still don't have enough RBCs...They have less RBCs all together (look at H&H) Hemoglobin is necessary for transport of oxygen. Many critically ill patients have low hemoglobin levels secondary to a variety of factors.

Failure of Perfusion, Oxygenation, and Ventilation: V/Q Mismatch -What is the most common cause of Low O2 and Low V/Q?**

Failure of Perfusion, Oxygenation, and Ventilation: V/Q Mismatch If your body fails to ventilate and/or perfuse, what happens to oxygenation? -Oxygenation decreases This is the most common cause of low O2 and low V/Q = Pulmonary embolism* A mismatch occurs if either: -V is decreased or -Q is decreased Ventilation-perfusion mismatch occurs if either ventilation or perfusion is decreased. A common cause is pulmonary embolism. (heparin is the preventative medication LMWH - SubQ)

Failure of perfusion -Definition of perfusion -Interruption of perfusion from? (4) -Difference between perfusion and diffusion?

Failure of Perfusion: Definition of perfusion: Biological process of delivering blood to a capillary bed in order to reach an organ or tissue* Interruption of perfusion from: 1) Low cardiac output (A-fib, many dysrhythmias, supra-v-tach, HF*, intrapulmonary shunting - blood goes to R → L of heart w/o being oxygenated) 2) Intrapulmonary shunting 3) Diffusion defects - disruption in spreading through the system 4) Ventilation/perfusion mismatch* What's the difference between perfusion and diffusion? -Ventilating at a different rate than the blood being perfused our circulatory system Diffusion: passive movement of molecules or particles from one region to another (high to low concentration) Perfusion: volume of blood flowing into a region of an organ or tissue

Failure of perfusion: Low cardiac output -What is the normal delivery of oxygen per min? -CO vs SV?

Failure of Perfusion: Low Cardiac Output Cardiac output must be adequate to maintain tissue perfusion (distribute oxygen throughout the bloodstream) Normal delivery of oxygen is 4 to 8 L/min of oxygen* CO = HR x SV (SV = ejection fraction - amount of blood expelled with each heartbeat) **CO = over 1 min **SV/Ejection fraction = one BEAT Many conditions result in decreased cardiac output, which will impair oxygenation.

Failure of Ventilation -- Hypoventilation & Hypercapnia

Hypoventilation -Sleep Apnea (obstructive is when we are blocking the airway - 85%, central sleep apnea relates to the central part of the brain - 15%) Hypercapnia -Alveolar hypoventilation -decrease in ventilation and hypoxemia V/Q mismatch What is V/Q? (ventilation/perfusiom) V = Ventilation Q = Perfusion When ventilation is impaired, PaCO2 increases, resulting in hypercapnia* Hypoventilation is one common cause. Ventilation-perfusion mismatch is another cause.

Preventing complications of Mechanical Ventilation (MV) -Infection -Ventilator associated pneumonia (VAP) Ventilator bundle?

Infection: -Normal protective mechanisms bypassed by ETT tube -Ventilator-associated pneumonia (VAP) Ventilator bundle: -Head of bed 30 degrees -Awaken daily and assess readiness to wean -Stress ulcer prophylaxis -DVT prophylaxis -Oral care (chlorhexidine in some bundles) -VAP is common, but the incidence of VAP is being reduced by effective implementation of the ventilator bundle, which includes oral care. Research-Based: Ventilator-Associated Pneumonia (VAP) Prevention: -Elevate head of bed 30 to 45 degrees -Prevent drainage of condensate back to patient -Hand hygiene -ETT with subglottic suction capability -Aspirate secretions from above ETT -Oral hygiene program -Noninvasive ventilation as possible -*Several strategies are effective in reducing VAP Ventilator-Associated Events: -New concept of identifying ventilator-associated events rather than just VAP -Determined by worsening oxygenation or higher PEEP needs after patient has shown improvement -May indicate infection or other respiratory complication -Ventilator-associated events are a new concept introduced by the CDC. -As content is evolving at time of publication, monitor the CDC Web site for updates.

Within 2 hours of NPPV, Mrs. J. is getting worse. Her SpO2 is only 85% despite oxygen delivery with NPPV at 80%. Her chest x-ray shows bilateral "white out." What treatment is indicated?

Intubation and mechanical ventilation are urgently needed. What are bilateral infiltrates? -Fluid/blood/puss in lungs (secondary to non-cariogenic pulmonary edema) What is "white out"? -White on the scan from fluid

What are bilateral infiltrates?

Left = normal Right = White out from ARDS (bilateral infiltrates) which is fluid Bilateral pulmonary infiltrates secondary to noncardiogenic pulmonary edema, refractory hypoxia, and decreased lung compliance. Acute respiratory distress syndrome occurs most frequently in the setting of sepsis, aspiration of gastric contents, trauma, or multiple transfusions.

Adjunct treatments for ARDS -Maintain: -Be alert for:

Maintain: -Fluid and electrolyte balance -Adequate nutrition -Psychosocial support Nutrition and fluid management must be provided in the patient with ARDS. Due to the critical nature of the patient, psychosocial support of the family is another important intervention. Patient may receive non-traditional modes of ventilation, oscillatory ventilation, or proning—all of these can increase family stress. ARDS: Be alert for complications: -Multiple organ dysfunction syndrome -Renal failure -Disseminated intravascular coagulation -Long-term pulmonary effects associated with high oxygen and other therapies Many complications can result from ARDS. Multiple organ dysfunction syndrome can have many negative sequelae, including renal failure and DIC.

Mrs. J. is placed on volume assist/control (V-A/C) control ventilation: rate 16 breaths/min, VT 8 mL/kg, FiO2 0.80, and PEEP 10 cm. What is the rationale for these settings, including PEEP?

Mrs. J. needs adequate oxygenation and ventilation. The V-A/C mode will provide ventilation. Since she is severely hypoxemic, a high level of oxygen is required. The PEEP is used to maximize oxygenation by increasing the functional residual capacity, i.e. the functional component of he lung volume (FRC). The amount of air left in the lungs at the end of expiration, and available for gas exchange. Positive end-expiratory pressure (PEEP) is the pressure in the lungs (alveolar pressure) above atmospheric pressure(the pressure outside of the body) that exists at the end of expiration The two types of PEEP are extrinsic PEEP (PEEP applied by a ventilator) and intrinsic PEEP (PEEP caused by a non-complete exhalation)

Mechanical ventilation: -Nasogastric tube -Endotracheal tube -Mechanical ventilation -Air flowing to the patient -Exhaled air flowing _____

Nasogastric tube: goes through the pt's nose and into the stomach to delivery nutrients Endotracheal tube: goes through the patient's mouth and into the windpipe Mechanical ventilation: Blows air or air with increased oxygen through tubes into the patients airways Air flowing to the patient: passes through a humidifier which warms and moistens the air Exhaled air flowing away from the patient

How to calculate the PaO2/FiO2 ratio?**

PaO2 divided by FiO2 PaO2 (O2 in arterial blood) / FiO2 (Oxygen being delivered) ex: Mrs.J's condition worsens; SpO2 is 85% on Venturi mask at 0.50. ABGs show a PaO2 of 50 mm Hg. Her chest x-ray is showing infiltrates. = PaO2/FiO2 (venturi mask) 50 / .50 = 100 (ans = ratio of 100) **ARDS is anything less than 200

Purpose of noninvasive positive pressure ventilation (NPPV) as a first step before more invasive options?

Provides patient with a trial of assisted ventilation and extra oxygen without the need for invasive tracheal intubation and mechanical ventilation A trail of NPPV may be done to avoid the need for intubation and mechanical ventilation

Mrs. J.'s condition does not improve. -SpO2 is 85%, and the FiO2 is increased to 0.90 to maintain this. -A decision is made to increase the PEEP to 20 cm H2O. -About 10 minutes after the PEEP is increased, Mrs. J.'s blood pressure drops to 80/50 mm Hg. -Breath sounds are equal bilaterally. What is the likely rationale for the drop in Mrs. J.'s blood pressure? What is the significance of the bilateral breath sounds?

Several complications can occur from high levels of PEEP, including pneumothorax and tension pneumothorax. The bilateral breath sounds would likely rule out a pneumothorax. At high levels, PEEP decreases venous return and can reduce cardiac output. Optimum PEEP that maximizes oxygenation without decreasing cardiac output must be determined. Mrs. J. is in critical condition.

Preventing complications of Mechanical Ventilation (MV) -Spontaneous breathing trial -Weaning methods -Stop the weaning process if? -Extubation and return to spontaneous breathing

Spontaneous Breathing Trial: -Weaning trial or spontaneous breathing trial (SBT) -Trial is important* Weaning Methods: -Pressure support - May be used to facilitate spontaneous respirations) -T-piece trials -Continuous positive airway pressure (CPAP) -Synchronized intermittent mandatory ventilation (SIMV) - Delivers minimum number of assisted breaths/minute, synchronized with the patient's respiratory effort (like AC). May see used in patients' with history of difficult weaning (in long-term vent unit). -Review Table 9-5. -SIMV - SIMV may increase work of breathing and cause respiratory muscle fatigue that may thwart weaning and extubation. -Ventilatory mode as the process by which the mechanical ventilator determines, either partially or fully, when the mechanical breaths are to be provided to the patient, thus determining the breathing pattern of the patient during mechanical ventilation. -Still a need for an international consensus or standardization as there remains non-standardized and confusing terminology. Stop the Weaning Process if: -Respiratory rate > 35 or < 8 breaths/min -Low spontaneous VT < 5 mL/kg -Labored respirations -Use of accessory muscles -Low oxygen saturation < 90% -HR or BP changes > 20% from baseline -Dysrhythmias (e.g., PVCs) -ST-segment elevation -Decreased level of consciousness -Anxiety -Several assessments indicate that patient is not tolerating the weaning process (see Box 9-11). -In this case, return patient to mechanical ventilation at previous settings. -Collaborate with team. Extubation & Return to Spontaneous Breathing: -Determine need for secretion management -Assess -Stridor -Hoarseness -Change in vital signs -Low oxygen saturation -Non-invasive positive pressure ventilation (NPPV) may help prevent need for re-intubation -Assess for complications post-extubation* Book: Extubation: Is the pt demonstrates tolerance to the weaning procedure and can sustain spontaneous breathing for 90-120 min, the next step is to consider removing the ETT tube (extubate) Prior to extubation, evaluate the need for airway secrete clearance; the pt must have a good cough and require suctioning no more than every 2 hours* When the decision is made to extubate, suction the ETT thoroughly before removal. Once extubated, ask the patient to cough and speak and assess for stridor, hoarseness, changes in vital signs, low SpO2 (may indicate complications.) Noninvasive ventilation may be used to avert reintubation in some patients as needed*

Respiratory failure concerns: Respiratory muscle fatigue -Symptoms? -Nursing actions to improve O2 delivery and decrease O2 demand

Symptoms = diaphoresis, nasal flaring, tachycardia, muscle relations, central cyanosis Improve O2 delivery = administer O2, ensure adequate CO and BP, correct low hemoglobin (administer blood as needed), administer bronchodilators Decrease O2 demand = provide rest, reduce fever, relieve pain/anxiety, decrease WOB, position pt for optimal gas exchange and perfusion, prepare for possible intubation and mechanical ventilation

Symptoms of ARDS? Treatment of ARDS?

Symptoms of ARDS -Dyspnea and tachypnea -Hyperventilation with normal breath sounds -Respiratory alkalosis -Increased temperature and pulse -Worsening chest x-rays that progress to: → White out* -Increased positive inspiratory pressure (PIP), if on ventilation -Eventual severe hypoxemia -ARDS has many symptoms. -Deterioration occurs. -Need to monitor ABGs and serial chest x-rays. -Calculate PaO2/FiO2 ratio daily to trend the value. Treatment of ARDS: -Treat the cause -Oxygenation and ventilation -Possible non-traditional modes of ventilation: high-frequency, pressure-control, and inverse-ratio -Positive end-expiratory pressure (PEEP) Additional treatments in ARDS: Comfort -Sedation -Pain relief -Neuromuscular blockade -Decrease O2 consumption -Positioning -Prone positioning -Continuous lateral rotation therapy Comfort is an important intervention in managing the patient with ARDS. Prone positioning may be required. Research findings are mixed regarding proning, so each patient must be assessed for response. Discuss nursing interventions if the patient is proned to protect the airway and prevent skin breakdown.

What is the PaCo2/FiO2 ratio that is considered the cut-off diagnosis of ARDS?

The cut-off is less than 200. Anything less than 200 for ARDs!

ARDS medical management, Medications used for the following: -Treat hypoxia; prevent further hypoxia -Open bronchi, bronchioles -Reduce inflammation -Allow rest -Increase oxygen carrying capacity -Ensure adequate ventilation -Decrease work of breathing -Promote healing adequate vitamins and minerals -Closely monitor patient's response to therapy

Treat hypoxia; prevent further hypoxia = Oxygen supplementation Open bronchi, bronchioles = Bronchodilators Reduce inflammation = Corticosteroids Allow rest = Sedation Increase oxygen carrying capacity = Blood transfusions Ensure adequate ventilation =Assisted and/or mechanical ventilation Decrease work of breathing = Therapeutic paralysis Promote healing adequate vitamins and minerals = Nutritional support Closely monitor patient's response to therapy = Hemodynamic monitoring

Ventilation/Perfusion** (test) What is a normal V/Q?

What is normal V/Q? Normal ventilation (V) is 4 L/min Normal perfusion (Q) is 5 L/min Normal V/Q ratio is 4/5 or 0.8-1 range (this is an approximation, there's a range)

What is the "50/50" club?

What's the "50/50 club"? Referring to people who often have COPD PaO2 ~ 50 mm Hg (pretty low oxygen) PaCO2 ~ 50 mm Hg (pretty high) pH 7.35 -7.45 (within normal range) Failure of Perfusion What conditions may present typically with these arterial blood gas measurements? -COPD