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etiology
• Precipitating conditions• Previous PE• CVS disease: HF, RV infarction, cardiomyopathy, cor
pulmonale• 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
Thrombus formation Detaches and travels Embolus
Reaches the pulmonary arterial
system
Occlusion and blockage of a branch
of the pulmonary artery
An area of the lung is not being
perfused but is being ventilated
Pulmonary dead space
No participation in gas exchange
Increase work of breathing
Localized bronchoconstriction
Inflammatory/chemical mediators are released
Hypocarbia, hypoxia
Increased airway resistance
More bronchoconstriction
Compensatory shunting
hypoxemia
atelectasisPulmonary hypertension
vasoconstrictors
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
• ABG• D-dimer – a fibrin degradation product that is a small
protein present in the blood after the clot has undergone fibrinolysis
• ECG• Chest radiography• Echocardiography• 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 -tracheobronchial mucociliary 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
• URTI• 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
Inflammatory mediators (histamine) are released Bronchial smooth
muscles contract
Increase capillary permeability
Increase mucus secretion
Edema and inflammation of the bronchial walls
Bronchospasm
ObstructionWheezing 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 pulsus paradoxus 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:1. Cardiac or respiratory arrest2. Disorientation3. Failure to respond to bronchodilator therapy4. Exhaustion• 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 5Phase 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
Phase 2 – inflammation of alveolocapillary membrane
Capillary membrane permeability is increased
Fluid shifts from intravascular space into the interstitial space
Phase 3 - Leakage of protein and more fluids
Interstitial osmotic pressure increases
Pulmonary edema
Phase 4 - decrease blood flow to the lungs
Increase fluid in the alveoli
Surfactant is damaged
Impairs type 2 pneumocytes to produce more surfactant
Alveoli collapse
Interstitial osmotic pressure increases
Impeding gas exchange
Decreasing lung compliance
Phase 5 – oxygen cannot cross the alveolocapillary membrane but carbon dioxide can
Carbon dioxide is lost through exhalation
Oxygen and carbon dioxide levels decrease in the blood
Fibrosis
Phase 6 – pulmonary edema worsens
Decreasing lung compliance
Causes of ARDS
• Shock• Sepsis• Trauma• 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 – exudative pahse
• Agitation, dyspnea, fatigue, excessive accessory muscle use, and fine crackles as respiratory failure – fibrinolytic phase
• ABG1. Low PaO2 despite increases in supplemental O2 (refractory
hypoxemia)2. Low PaCO2 initially, but eventually increases as the patient
fatigues3. The pH is high initially but decreases as respiratory acidosis
develops
Assessment and diagnosis
• Chest x-ray1. Initially, it is normal2. After 48 hours: diffuse patchy interstitial and
alveolar infiltrates appear3. 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
• Ventilation 1. Low tidal volume2. Permissive hypercapnia3. Pressure control ventilation4. Inverse ratio ventilation5. Oxygen therapy6. PEEP7. Tissue perfusion
Nursing management
• Optimizing oxygenation and ventilation• Providing comfort and emotional support• Maintaining surveillance for complications