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Abc 2011 2012 respiratory disorders part 2

Abc 2011 2012 respiratory disorders part 2






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    Abc 2011 2012 respiratory disorders part 2 Abc 2011 2012 respiratory disorders part 2 Presentation Transcript

    • etiology
      Precipitating conditions
      Previous PE
      CVS disease: HF, RV infarction, cardiomyopathy, corpulmonale
      Surgery: orthopedic, vascular, abdominal
      Cancer: ovarian, pancreatic, stomach, extrahepatic bile duct system
      Trauma (injury or burns): lower extremities, pelvis, hips
      Gynecologic status: pregnancy, postpartum, birth control pills, estrogen replacement therapy
    • Vascular endothelial injury, stasis, hypercoagulability
      Detaches and travels
      Thrombus formation
      Occlusion and blockage of a branch of the pulmonary artery
      Reaches the pulmonary arterial system
      An area of the lung is not being perfused but is being ventilated
      Pulmonary hypertension
      Pulmonary dead space
      Compensatory shunting
      Inflammatory/chemical mediators are released
      No participation in gas exchange
      More bronchoconstriction
      Hypocarbia, hypoxia
      Increased airway resistance
      Increase work of breathing
      Localized bronchoconstriction
    • Assessment and diagnosis
      Impaired gas exchange related to V/Q mismatching or intrapulmonary shunting
      Acute pain related to transmission and perception of cutaneous, visceral, muscular, or ischemic impulses
      Powerlessness related to lack of control over current situation or disease progression
      Deficient knowledge: discharge regimen related to lack of previous exposure to information
    • Assessment and diagnosis
      Tachycardia, tachypnea
      Dyspnea, apprehension, increased pulmonic component of the second heart sound
      Fever, rales, pleuritic chest pain, cough, evidence of DVT, and hemoptysis
      Syncope and hemodynamic instability
    • Assessment and diagnosis
      D-dimer – a fibrin degradation product that is a small protein present in the blood after the clot has undergone fibrinolysis
      Chest radiography
      CT scan
      V/Q scintigraphy
      Pulmonary angiogram
    • Ventilation scintigraphy is a diagnostic procedure that portrays the regional and global distribution of an inhaled radioactive gas or radioaerosol within the lungs’ broncho-alveolar space.   Perfusion scintigraphy is a diagnostic procedure that portrays the regional and global distribution of pulmonary artery blood flow.    In combination V/Q is a useful procedure for the diagnosis of focal vascular, ventilatory or parenchymal pulmonary lesions.
    • • The most common indication: to determine the likelihood of pulmonary embolism• Less common indications: -evaluation of lungs transplantation -pre-operative lungs evaluation -evaluation of right-to-left shunt -tracheobronchialmucociliary escalator function and clearance -evaluation of alveolar function and clearance in patients with endothelial injury such as in AIDS, sarcoidosis, pneumonitis, alveolitis, ARDS
    • Medical management
      Prevention of recurrence
      • Administration of unfractionated or low-molecular-weight heparin and warfarin (Coumadin)
      • Heparin has no effect on existing clot
      • Heparin should be adjusted to maintian the aPTT in a range of 1.5 to 2.3 times the control
      • Warfarin should be started at the same time, and when the INR reaches 3.0, the heparin should be discontinued
      • The patient should remain on warfarin for 3 to 12 months depending on the patient’s risk for thromboembolic disease
    • Medical management
      Prevention of recurrence
      • Interruption of the IVC is reserved for patients in whom anticoagulation is contraindicated
      • The procedure involves placement of a percutaeneous venous filter (e.g., Greenfield filter) into the vena cava, usually below the renal arteries
      • The filter prevents further thrombotic emboli form migrating into the lungs
    • Medical management
      Clot dissolution
      • Thrombolytic agents had limited success, and is reserved for the patient with a massive PE and concomitant hemodynamic instability
      • Either recombinant tissue-type plasminogen activator (rt-PA) or streptokinase may be used
      • Therapeutic window for thrombolytic therapy is 14 days
    • Medical management
      Clot dissolution
      • Pulmonary embolectomy, often considered as a last resort, may be performed to surgically remove the clot
      • Generally it is performed as an open procedure while the pattern is on cardiopulmonary bypass
    • Medical management
      Reversal of pulmonary hypertension
      • Administration of inotropic agents and fluid
      • Fluids should be administered to increase RV preload, which would stretch the RV and increase contractility, thus overcoming the elevated pulmonary arterial pressures
      • Inotropic agents also cane be sued to increase contractility to facilitate an increase in CO
    • Nursing management
      Optimizing oxygenation
      Monitoring bleeding
      Patient education
    • Collaborative management
      Administer oxygen therapy
      Intubate patient
      Initiate mechanical ventilation
      Administer medications: thrombolytics, anticoagulants, bronchodilators, inotropic agents, sedatives, analgesics
      Administer fluids
      Position patient to optimize V/Q matching
      Maintain surveillance for complications: bleeding and acute lung injury
      Provide comfort and emotional support
    • Patient education
      Pathophysiology of the disease
      Specific etiology
      Precipitating factor modification
      Measures to prevent DVT
      Signs and symptoms of DVT
      Importance of taking medications
      Signs and symptoms of anticoagulant complications
      Measures to prevent bleeding
    • Status asthmaticus
    • Status asthmaticus
      Asthma – a COPD that is characterized by partially reversible airflow obstruction, airway inflammation, and hyperresponsiveness to a variety of stimuli
      Status asthmaticus – a severe asthma attack that fails to respond to conventional therapy with bronchodilators, which may result in acute respiratory failure
    • etiology
      Allergen exposure
      Decreased in antiinflammatory medications
      Overreliance on bronchodilators
      Environmental pollutants
      Lack of access to health care
      Failure to identify worsening airflow obstruction
      Non-compliance with the health care regimen
    • First exposure to allergens (pollen, dust)
      Absorbed into the tissues
      Immune cells are triggerred
      IgE antibodies are produced
      IgE attach to mast cells, which gather in the lungs
    • Second exposure to the same allergen
      Allergens attach to IgE antibodies
      Mast cells degranulate
      Increase capillary permeability
      Inflammatory mediators (histamine) are released
      Bronchial smooth muscles contract
      Edema and inflammation of the bronchial walls
      Increase mucus secretion
      Wheezing and dyspnea
    • Assessment and diagnosis
      Impaired gas exchange related to alveolar hypoventilation
      Ineffective breathing pattern related to musculoskeletal fatigue or neuromuscular impairment
      Ineffective airway clearance related to excessive secretions or abnormal viscosity of mucus
      Anxiety related to threat of biologic, psychologic, and/or social integrity
      Deficient knowledge: discharge regimen related to lack of previous exposure to information
    • Assessment and diagnosis
      Cough, wheezing and dyspnea
      As the attack continues, the patient develops tachypnea, tachycardia, diaphoresis, increased accessory muscle use, and pulsusparadoxus greater than 25 mm Hg
      Decreased LOC, increasing inability to speak, significantly diminished or absent breath sounds, and inability to lie supine herald the onset of acute respiratory failure
    • Assessment and diagnosis
      ABG indicate hypocapnia and respiratory alkalosis caused by hyperventilation
      Hypoxemia and hypercapnia develops as the patient starts to fatigue
      Lactic acidosis may also occur
      Deterioration of PFT despite aggressive bronchodilator therapy is diagnostic of status asthmaticus
    • Assessment and diagnosis
      A PEFR less than 40% of predicted or an FEV1 (maximum volume of gas that the patient can exhale in 1 second) less than 20% of predicted indicates severe airflow obstruction, and the need for intubation with mechanical ventilation may be imminent
    • Medical management
      Bronchodilators – Beta2-agonists and anticholinergics
      Systemic corticosteroids
      Oxygen therapy
      Intubation and mechanical ventilation
    • Bronchodilators – B2-agonists
      Can be administered by nebulizer or metered-dose inhaler (MDI)
      Usually a larger and more frequent doses are given, and the drug is titrated to the patient’s response
      Xanthines are not recommended
      Studies are being focused on the bronchodilating abilities of magnesium
      Magnesium is still inferior to B2-agonists, but may be beneficial to patients who are refractory to conventional therapy
      A bolus of 1 to 4g of IV Mg given over 10 to 40 minutes has been reported to produce desirable effects
    • anticholinergics
      Not very effective by themselves
      Used in conjunction with Beta-agonists (synergistic effect)
      Studies are evaluating the effects of leukotriene inhibitors (zafirlukast, montelukast, and zileuton) in the treatment of status asthmaticus
      Studies have shown that leukotriene inhibitors may be beneficial in those patients who are refractory to B2-agonists
    • Systemic corticosteroids
      IV or oral
      Limit iflammation, decrease mucus production, and potentiate B2-agonists
      Usually takes 6 to 8 hours for the effects to become evident
    • Oxygen therapy
      Supplemental oxygen for initial treatment of hypoxemia
      High-flow oxygen therapy to keep the patient’s SpO2 greater than 92%
    • Intubation and mechanical ventilation
      Indications for mechanical ventilation:
      Cardiac or respiratory arrest
      Failure to respond to bronchodilator therapy
      Avoid high inflation pressures because they can result in barotrauma
      PEEP monitoring is important because the patient is prone to air trapping
      Patient-ventilator asynchrony also can occur and can be a major problem
      Sedation and neuromuscular paralysis may be necessary to allow for adequate ventilation
    • Nursing management
      Optimizing oxygenation and ventilation
      Providing comfort and emotional support
      Maintaining surveillance for complications
    • Patient education
      Pathophysiology of the disease
      Specific etiology
      Early warning signs of worsening airflow obstruction
      treatment of attacks
      Importance of taking prescribed medications and avoidance of OTC asthma medications
      Correct use of an inhaler (with and without spacer)
    • Patient education
      Correct use of peak flow meter
      Removal or avoidance of environmental triggers
      Measures to prevent pulmonary infections
      Signs and symptoms of pulmonary infections
      Importance of participating in pulmonary rehabilitation program
    • Acute respiratory distress syndrome
    • ards
      • A form of pulmonary edema that can quickly lead to acute respiratory failure
      • Also known as shock or stiff, white or Da Nang lung
      • Difficult to diagnose and can be fatal within 48 hours
      • Severe form of Acute Lung Injury
    • Phase 1
      Phase 2
      Phase 3
      Phase 4
      Phase 5
      Phase 6
    • H5N1 and A(H1N1)
      H – hemagglutinin
      N - enzyme on the surface of influenza viruses that enables the virus to be released from the host cell.
      Drugs that inhibit neuraminidase are used to treat influenza.
    • Phase 1 – injury reduces normal blood flow to the lungs
      Platelets aggregate
      Release of histamine, serotonin and bradykinin
      Interstitial osmotic pressure increases
      Phase 2 – inflammation of alveolocapillary membrane
      Phase 3 - Leakage of protein and more fluids
      Fluid shifts from intravascular space into the interstitial space
      Capillary membrane permeability is increased
    • Pulmonary edema
      Interstitial osmotic pressure increases
      Phase 4 - decrease blood flow to the lungs
      Decreasing lung compliance
      Increase fluid in the alveoli
      Impeding gas exchange
      Surfactant is damaged
      Alveoli collapse
      Impairs type 2 pneumocytes to produce more surfactant
    • Decreasing lung compliance
      Phase 5 – oxygen cannot cross the alveolocapillary membrane but carbon dioxide can
      Phase 6 – pulmonary edema worsens
      Carbon dioxide is lost through exhalation
      Oxygen and carbon dioxide levels decrease in the blood
    • Causes of ARDS
      Trauma-related factors: fat emboli, pulmonary contusions, and multiple transfusions may increase the likelihood that microemboli will develop
    • Assessment and diagnosis
      Impaired gas exchange related to V/Q mismatching or intrapulmonary shunting
      Decreased cardiac output related to alterations in preload
      Imbalanced nutrition: less than body requirements related to lack of exogenous nutrients or increased metabolic demand
      Anxiety related to threat to biologic, psychologic, and/or social integrity
      Compromised family coping related to critically ill family member
    • Assessment and diagnosis
      Tachypnea, restlessness, apprehension, and moderate increase in accessory muscle use – exudativepahse
      Agitation, dyspnea, fatigue, excessive accessory muscle use, and fine crackles as respiratory failure – fibrinolytic phase
      Low PaO2 despite increases in supplemental O2 (refractory hypoxemia)
      Low PaCO2 initially, but eventually increases as the patient fatigues
      The pH is high initially but decreases as respiratory acidosis develops
    • Assessment and diagnosis
      Chest x-ray
      Initially, it is normal
      After 48 hours: diffuse patchy interstitial and alveolar infiltrates appear
      Progression to multifocal consolidation of the lungs, which as a “white out” on the chest x-ray film
    • Management
      A – antibiotics
      R – respiratory support
      D – diuretics
      S – situate in the prone position
    • Medical management
      Low tidal volume
      Permissive hypercapnia
      Pressure control ventilation
      Inverse ratio ventilation
      Oxygen therapy
      Tissue perfusion
    • Nursing management
      Optimizing oxygenation and ventilation
      Providing comfort and emotional support
      Maintaining surveillance for complications