Respiratory Med Surg II

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jbrodie727
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Respiratory Med Surg II
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2011-09-01 18:08:06
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Respiratory Med Surg II
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  1. Air enters the pleural space through a breach of either the parietal or visceral pleura. Most commonly this occurs as air neters the pleural space through the rupture of a bleb or a bronchopleural fistula. May ocur in an apparently healthy person.
    Simple pneumothorax
  2. Occurs when air escapes from a laceration in the lung itself and enters the pleural space or from a wound in the chest wall. May result from blunt trauma, penetrating...May occur during invasive procedures.
    Traumatic pneumothorax
  3. Occurs when air is drawn into the pleural space from a lacerated lung or though a small opeing or wound in the chest wall. Air cannot be expelled during expiration through the air passages and requires emergency interventions.
    Tension pneumothorax
  4. Trachea is midline, expansion of chest is decreased, breath sounds may be diminished, and percussion of the chest may reveal normal sounds or hyperresonance depending on size.
    Simple pneumothorax
  5. Trachea is shifted away from the affected side, chest expansion may be decreased, or fixed in a hyperexpansion state, breath sounds are diminished or abesent, and percussion to the afected side is hyperresonant.
    Tension pneumothorax
  6. For a pneumothorax, a small chest tube is inserted near the _____ intercostal space.
    2nd intercostal space
  7. If a patient has a hemothorax along with a pneumothorax, a large diameter chest tube is inserted usually in the ____ or ____ intercostal space at the midaxillary line.
    4th or 5th intercostal space
  8. This technique involves taking the patient's own blood that has been drained from the chest, filtering it, and then transfusing it back in to the vascular system.
    Autotransfusion
  9. The chest wall is opened surgically (thoracotomy) if more than 1500 mL of blood is aspirated initially by thoracentesis or if chest tube output continues at greater than 200 mL/h.
  10. The patient with a possible tension pneumothrorax should immediately be given a high concentration of O2
  11. In an emergency situation, a tension pneumothorax can be decompressed or quickly converted to a simple pneumothorax by inserting a large bore needle at the second intercostal space, midclavicular line on the affected side. This relieves the pressure and vents the positive pressure to the external environment.
  12. Compression of the heart resulting from fluid or blood within the pericardial sac.
    Cardiac tamponade
  13. Tissues give a crackling sensation when palpated from air entering the tissue planes and passing for some distance under the skin after chest trauma.
    Subcutaneous emphysema
  14. Time is critical in treating chest trauma. It is essential to assess the patient immediately to determine the following:
    • Time elapsed since injury
    • Mechanism of injury
    • Level of responsiveness
    • Specific injuries
    • Estimated blood loss
    • Recent drug or alcohol use
    • Prehospital treatment
  15. Fractures of the first three ribs are rare but can result in a high mortality rate because they are associated with laceration of the subclavian artery or vein. Fractures of the lower ribs are associated with injury to the spleen and liver which may become lacerated
  16. Most rib fractures heal in 3 to six weeks and the pain abates in 5 to 7 days.
  17. Occurs when three or more adjacent ribs are fracutred at two or more sites, resulting in free-floating rib segments. It may also result as a combination fracture of ribs and costal cartilages or sternum. As a result, the chest wall loses stability, causing respiratory impairment and usually severe respiratory distress
    Flail chest
  18. Often cited as the most common potentially life threatening chest injury
    Pulmonary contusion
  19. Damage to the lung tissues resulting in hemorrhage and localized edema. Associated with chest trauma. An abnormal accumulation of fluid in the interstitial and intra-alvelolar spaces.
    Pulmonary contusion
  20. Inflammatory response ours throughout the proximal and peripheral airways, lung parenchyma, and pulmonary vasculature resulting in changes and narrowing in the airways.
    COPD
  21. Constant irritation causes the mucus-secreting glands and goblet cells to increase in number, leading to increased mucus production. Bronchial walls become thickened, further narrowing the bronchial lumen.
    Chronic bronchitis
  22. Alveoli adjacent to the bronchioles may become damaged and fibrosed, resulting in altered function of the alveoloar marophages, which play an important role in destroying bacteria and foreign particles.
    Chronic bronchitis
  23. Impaired oxygen and carbon dioxide exchange results from destruction of the walls of overdistended alveoli. As the walls of the alveoli are destroyed, the alveolar surface area in direct contract with the pulmonary capillaries continually decreases. This causes an increase in dead space and impaired oxygen diffusion, which leads to hypoxemia and eventually respiratory acidosis from impaired CO2 elimination.
    Emphysema
  24. Resistance to pulmonary blood flow is increased, forcing the right ventricle to maintain a higher blood pressure in the pulmonary artery. Hypoxemia may further increase pulmonary artery pressures. For this reason, right sided heart failure (cor pulmonale) is one of the complications of emphysema.
    Emphysema
  25. A deficiency of alpha1-antitrypsin, an enzyme inhibitor that protects the lung parenchyma from injury.
    Risk factor for COPD
  26. Defined by an FEV1/FVC less than 70% and an FEV1 greater than or equal to 80% and the patient may be with or without symptoms of cough and sputum production.
    Stage I of COPD
  27. Defined by an FEV1/FVC less than 70%, an FeV1 50% to 80% predicted, and SOB typically developing upon exertion.
    Stage II of COPD
  28. Defined as an FEV1/FVC less than 70% and an FEV1 less than 30# to 50% predicted. Severe COPD symptoms include increased SOB, reduced exercise capacity, and repeated exacerbations.
    Stage III of COPD
  29. Defined as an FEV1/FVC less than 70%, an FEV1 less than 30% to 50% predicted, and symptoms/signs of chronic respiratory failure.
    Stage IV of COPD
  30. The primary differential dx for COPD is...
    Asthma
  31. Normal ABGs
    ►PH 7.35-7.45

    ►PaC02 35-45

    ►Pa02 75-100

    ►Sa02 93-98%

    ►Base Excess +/- 2

    ►HCO3 22-26
  32. Oxygen is a medication. We give oxygen to raise the PaO2 back normal baseline which may vary from 60-95 mm. The blood is saturated at these levels with 80-98% oxygen
  33. Be familiar with FiO2 and the main thing to know about this is that the FiO2 is determined by the PaO2. If the PaO2 is normal then the amount of FiO2 is correct
  34. The venturi mask is the most reliable and accurate for delivering precise concentration of oxygen
  35. The single most cost effective intervention to reduce the risk of COPD and to stop its pregression.
    Smoking cessation
  36. Medication reginmens used to manage COPD are based on disease severity:
    • Stage I (mild): a short-acting bronchodilatory
    • Stage II or III: a short-acting bronchodilator along with regular treatment of one or more long-acting bronchodilators may be used.
    • Stage III or IV: (severe or very severe): medication therapy includes regular treatment with one or more bronchodilators and inhaled cortiosteroids for repeated exacerbations.
  37. The goal of supplemental O2 therapy is to increase the baseline resting partial arterial pressure of O2 (PaO2) to at least 60 mm Hg at sea level and an arterial oxygen saturation (SaO2) at least 90%.
    Long term O2 therapy is usually introduced in very severe COPD and indications usually include a PaO2 of 55 mm Hg or less or evidene of tissue hypoxia and organ damage such as cor pulmonale, secondary polycythemia, edema from right sided heart failure, or impaired mental status.
  38. Oxygen therapy in COPD patients is aimed at achieving an acceptable O2 level without a fall in the pH (increasing hypercapnia)
  39. Enlarged airspaces that do not contribute to ventilation but ocupy space in the thorax; these areas may be surgically excised.
    • Bullae.
    • Bullectomy may help reduce dyspnea and improve lung function.
  40. Involves the removal of a portion of the diseased lung parenchyma.
    Lung Volume Reduction Surgery

    This type of surgery does not cure the disease or improve life expectancy but it may decrease dyspnea, improve lung function, and improve the patient's overall quality of life.
  41. The breathing pattern of most people with COPD is shallow, rapid, and inefficient; the more severe the disease, the more inefficient the breathing pattern. With practice this type of uper chest breathing can be changed to diaphragmatic breathing, which reduces the respiratory rate, increases alveolar ventilation, and sometimes helps expel as much air as possible during expiration.
  42. If a rapid onset of shortness of breath occurs, the nurse should quickly evaluate the patient for potential pneumothorax by assessing the symmetry of chest movement, differences in breath sounds, and pulse ox.
  43. Pulmonary hypertension may occur as a result of chronic hypoxemia. The pulmonary arteries respond to hypoxemia by constricting, which results in pulmonary hypertension.
    The complication may be prevented by maintaining adequate O2 through an adequate hemoglobin level
  44. Instruct COPD patients to avoid extremes of heat and cold.
    • Heat increases body temp thereby raising O2 requirements
    • Cold tends to promote bronchospasm
  45. Chronic, irreversible dilation of the bronchi and bronchioles. Separate from COPD. Usually localized, affecting a segment or lobe of a lung, most frequently lower lobes.
    • May be caused by a variety of conditions
    • Airway obstruction
    • Diffuse airway injury
    • Pulmonary infection
    • Genetic disorders-CF
  46. The obstruction of the pulmonary artery or one of its branches by a throbus that originates somewhere in the venous system or in the right side of the heart.
    Pulmonary Embolism
  47. When a thrombus completely or partially obstructs a pulmonary artery or its branches, the alveolar dead space is increased. The area, although continuing to be ventilated, receives little or no blood flow. Therefore gas exchange is impaired or absent in this area.
    An increase in pulomary arterial pressure from a PE results in an increase in right ventricular work to maintain pulomary blood flow. When the work requirements of the right ventricle exceed its capacity, right ventricular failure occurs, leading to a decrease in cardiac output followed by a decrease in systemic blood pressure and the development of shock.
  48. Atrial fibrillation also causes PE: An enlarged right atrium in fibrillation causes blood to stagnate and form clots in this area
  49. Dyspnea-most frequent symptom
    Chest pain-common-usually sudden and pleuritic in origin.
    Anxiety
    Fever
    Tachycardia
    Apprehension
    Cough
    Diaphoresis
    Syncope
    Tachypnea-most frequent sign
    S/Sx of PE
  50. Best method to dx PE
    Pulmonary angiography
  51. ECG usually shows sinus tachy, PR interval depression, and nonspecifi T wave changes. ABGs may show hypoxemia and hypoapnia (from tachypnea) however abg may be normal
    PE diagnostic findings
  52. Immediate objective of PE treatment:
    Stabilize the cardiopulmonary system

    • Nasal oxygen is admin immediately
    • IV infusion lines are inserted
    • Perfusion scan, hemodynaic measurement, and abg performed
    • Hypotension is treated by a slow infusion of dobutamine (Dobutrex) which has a dilating effect on the pulmonary vessels and bronchi, or dopamine (Intropin)
    • ECG is monitored
    • Small doses of IV morphine or sedatives
    • Digitalis glycosides, IV diuretics, and antiarrhythmic agents are admin when approp.
  53. Heparin-generally recommended for patients who have been dx with PE
    • Half life of heparin is dose dependent
    • Frequent lab testing is necessary
    • Heparin must be continued until the INR is within a therapeutic range: typically 2.0 to 2.5
  54. Thrombolytic therapy is used in treating PE, particularly in pts who are severly compromised.
    • Resolves the thrombi or emboli quickly and restores more normal hemodynamic functioning of the pulmonary circulation.
    • Bleeding is significant side effect
    • Contraindications: CVA within past 2 mos., active bleeding, trauma, severe hypertension
    • INR, PTT, hematocrit, and platelet counts are obtained prior to therapy.
  55. During thrombolytic infusion, while the patient remains on bed rest, vital signs are assessed q2h and invasive procedures are avoided. Tests to determine INR or PTT are performed 3 to 4 hours after the thrombolytic infusion is started
  56. Abnormal accumulation of fluid in the lung tissue, the alveolar space, or both. A severe life-threatening condition.
    Pulmonary edema
  57. Most commonly occurs as a result of increased microvascular pressure from abnormal cardiac function.
    The backup of blood into the pulmonary vasculature resulting from inadequate left ventricular function causes an increased microvascular pressure, and fluid begins to leaks into the interstitial space and the alveoli.
    Pulmonary edema
  58. S/Sx: increasing respiratory distress, characterized by dyspnea, air hunger, and central cyanosis is present.
    Foamy, frothy, blood tinged secretions.
    Pulmonary edema
  59. Auscultation reveals crackles in the lung bases (esp. in the posterior bases) that rapidly progress toward the apices of the lungs.
    Pulmonary edema
  60. If pulmonary edema is cardiac in origin, then improvement in ____ ventricular function is the goal.
    • Left.
    • Vasodilators, inotropic medications, afterload or preload agents, or contractility medications may be admin.
  61. Characterized by a sudden and progressive pulmonary edema, increasing bilateral infiltrates on chest x-ray, hypoxemia unresponsive to o2 regardless of the amount of PEEP, and the absene of an elevated left atrial pressure.
    Acute Respiratory Distress Syndrome (ARDS)
  62. The major cause of death in ARDS is nonpulmonary multiple system organ failure, often with sepsis.
  63. Inflammatory triggers initiate the release of cellular and chemical mediators, causing injury to the alveolar capillary membrane in addition to other structural damage to the lungs. The blood returning to the lung for gas exchange is pumped through the nonventilated, nonfunctioning areas of the lung, causing shunting. This means that blood is interfacing with nonfunctioning alveoli and gas exchange is markedly impaired resulting in severe hypoxemia.
  64. An acute event that typically develops over 4 to 48 hours. Initially resembles severe hemodynamic pulmonary edema.
    • ARDS
    • The acute phase of ARDS is marked by a rapid onset of severe dyspnea that usually occurs 12 to 48 hours after the initiating event.
  65. S/Sx: intercostal retractions and crackles may be present as the fluid begins to leak into the alveolar interstitial space.
    ARDS
  66. Brain natriuretic peptide levels (BNP) is helpful in distinguishing _____ from hemodynami pulmonary edema.
    • ARDS
    • Pulmonary artery catherization is the definitive method to distinguish between hemodynamic (heart failure) and ARDS.
  67. Supportive therapy almost always includes intubation and mechanical ventilation.
    • ARDS
    • PEEP is a critical part of the treatment of ARDS. PEEP usually improves oxygenation, but it does not influence the natural history of the syndrome.
    • The goal is a PaO2 greater than 60 mmHg or an o2 sat level of greater than 90% at the lowest possible FiO2.
  68. Oxygenation in patients with ARDS is sometimes improved in the ____ position.
    Prone
  69. An infectious disease that primarily affects the lung parenchyma. May also be transmitted to other parts of the body, including the meninges, kidneys, bones, and lymph nodes.
    Tuberculosis
  70. Spreads from person to person by airborne transmission.
    • Pulmonary TB
    • Talking, coughing, sneezing, laughing, or singing.
    • Larger droplets settle, smaller droplets remain suspended in the air and are inhaled by a suseptible person.
  71. Initial infection of TB usually occurs _____ after exposure.
    2 to 10 weeks
  72. S/Sx: Fever, anorexia, weight loss, night sweats, fatigue, cough, and sputum production
    Pulmonary TB
  73. Used to determine whether a person has been infected with the TB bacillus.
    • The Mantoux method (TB skin test)
    • Purified protein derivative (PPD) is injected into the intradermal layer of the inner aspet of the forearm approx. 4 inches below the elbow.
    • Bevel facing up
    • 0.1 mL of PPD is injeted creating an elevation in the skin, a well demarcated wheal 6 to 10 mm in diameter.
    • Test is read 48 to 72 hours after injection
  74. PPD test results:
    • A reaction of 0-4 mm is considered non significant
    • A reaction of 5 mm or greater may be significant in people who are considered to be at risk. (HIV, in contact with TB, or chest x ray consistent with TB)
    • An induration of 10 mm or greater is usually considered significant in people who have normal or mildly impaired immunity.
  75. The ____ vaccine is given to produce a greater resistance to development of TB
    • BCG
    • Effective in up to 76% of people who receive it.
    • Used in Europe and Latin America but not in US.
  76. TB may have atypical manifestations in elderly patients whose symptoms may include unusual behavior and altered mental status, fever, anorexia, and weight loss.
  77. The initial phase of TB consists of multiple medication regimen of INH, rifampin, pyrazinamide, and ethambutol. This initial intensive treatmenent regimen is admin daily for 8 weeks after which options for the continuation phase of treatment include INH and rifampin or INH and rifapentine. The continuation regimen lasts for an additional 4 or 7 mos.
    • People are considered non-infectious after 2 to 3 weeks of continuous medication therapy.
    • Vitamin B (pyridoxine) is usually administered with INH to prevent INH associated peripheral neuropathy.
  78. Prophylactic INH treatment involves taking daily doses for 6 to 12 mons. Liver
  79. What risk factors can a patient have that will increase
    the probability of developing atelectasis?
    • COPD, Length of procedure, length of incision, level of
    • consciousness, immobility, duration of anesthesia, increase age, obesity,
    • supine position, general anesthesia, smoking, pain, NG Tube, aspiration
  80. What
    organism do you think is most likely to cause pnuemonia?
    • Streptococcus
    • which is pneumococcus. Hemopholus influenzae affects alcoholics,
    • elderly, patients in chronic care nursing homes, diabetes, COPD. Legionnaires’
    • disease which is caused by legionella pneumophila. Viral pnuemonia is also considered
    • CAP, mycoplasma, and chalmydial
  81. Hospital acquired pneumonia is caused most frequently by
    which organism-pseudomonas occurs in those with lung cancer, leukemia, burns,
    debilitated patients, patients receiving antimicrobial therapy. Stapholococcal occurs in those with
    occurs in IV drug users, complication of epidemic influenza. Klebsiella occurs in the
    elderly, alcoholics, those with chronic diseases, COPD, diabetes,
  82. Pnuemonia
    in the Immunocompromised patient is caused by
    pneumocystis, fungal pneumonia,
    and TB. What other term to we use for hospital acquired diseases? Nosocomial. It is defined as occuring after 48 hours of
    admission to the hospital. MRSA, E coli, Kebsiella,
    Proteus are common organisms responsible for HAP.
  83. the
    patient with streptococcoal pnuemonia may have a sudden
    onset of chills, shaking, the patient is severely ill, has tachypnea, chest pain, and
    high fever, shortness of breath, respiratory distress, tachycardic for the amount of
    fever. A bradycardic pulse may accompany
    a viral pneumonia or legionairres disease. Usually the
    patient has orthopnea which is (SOB when
    reclining). The S&S also depend on the underlying chronic condition such as
    lung cancer, they may have fever, crackles. Purulent sputum or slight changes
    in respiratory distress may be the only symptoms of those with COPD.
  84. Offer the pneumonia vaccine once every 5 years
  85. Pulmonary edema is generally caused by abnormal cardiac function. What happens is there a backup of
    blood into the pulmonary vasculature due to left ventricular function
  86. Acute Respiratory failure is life threatening. It is defined when the arterial PaO2
    falls below 50 mm Hg and arterial PaCO2 rises to greater than 50 mm Hg. We
    confirm this with blood gases
  87. Primary pulmonary hypertension is rare and the exact cause is not known. Secondary
    pulmonary hypertension is more common and occurs from an existing cardiac or
    pulmonary condition. It is defined as an increase in the pulmonary arterial
    pressure exceeding 30 mm Hg which are measured through right sided heart
    catheterization.
    Treatment includes fluid restriction, digoxin, calcium channel blockers to improve the cardiac function.

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