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Asthma A chronic inflammatory Disease of the airways that causes airway: • • • • Hyper responsiveness Mucosal edema Mucus production

This inflammation leads to recurrent episodes

Signs and Symptoms • • • • Cough Chest tightness Wheezing Dyspnea

Note: Asthma differs from the other obstructive lung disease in that it is largely reversible, either spontaneously or with treatment patients with asthma may experience symptom free periods alternating with acute exacerbations, which last from minutes to hours or days. • • Most common chronic disease in childhood Occur at any age

Note: a disruptive disease affecting school and work attendance occupational choices, physical activity and general quality of life.


The strongest predisposing factor for asthma chronic exposure to airway irritants or allergens also increase the risk for develop asthma

EG. Grass, Tree, and weed pollens, mold dust, roaches or animal dander. Note: most people who have asthma are sensitive to a variety of triggers a patients asthma condition will change depending upon the environment, activities management practices and other factors.

The 3 most common symptoms of asthma are cough, dyspnea, and wheezing in some instances cough will be the only symptoms • Asthma attacks often occur at night or early morning • There is cough with or without mucus production • There maybe generalized wheezing • Generalized chest tightness and dyspnea occur • Asthma is categorize according to symptoms and objective measures of airflow obstruction

Assessment and Diagnostic Findings • • •
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Complete family, environmental, and occupational history is essential Determine that periodic symptoms of airflow obstruction are present Positive family history and environmental factors including seasonal changes particularly cold air and air pollution are associated with asthma Determines meds. E.g. (Aspirin, antibiotics, piperazine, limetidine) Comorbid conditions such as GERD, Drug induce asthma, and allergic bronchopulmonary aspergillosis Others include Eczema, rashes, and temporary edema During acute episodes, sputum and blood test may disclose eosinophillia elevated levels of eosinophils PaCO2 may rise

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Patients with recurrent asthma should undergo test to identify the substance that precipitate the symptoms The patient is instructed to avoid the causative agents whenever possible Knowledge to the diseases

Complications • Status asthmaticus • Respiratory Failure • Pneumonia • Atelectasis

Medications • •

Corticosteroids Cromolyn NA (intal) and Nedocromic (Tilade) Methylxantines (theophylline) Leukotriene modifiers

Management of asthma Exacerbation • • • •

Best manage by early treatment and education of the patient Beta adrenergic meds. Are first used for prompt relief airflow obstruction Corticosteroids decrease airway inflammation who failed to respond in inhaled beta adrenergic meds. Oxygen supplementation maybe required to relieved hypoxemia Written action plan (guide patient in self mgt.)

Peak flow monitoring

• Peak flow meters measure the highest airflow during a force expiration • Recommended for all patients with moderate or severe asthma • Helps asthma severity and added symptoms monitoring the current degree of asthma control • Monitoring peak flow for 2-3 weeks after receiving optimal asthma therapy Nursing Management • • •

Patient treatment successfully as an out patient if asthma symptoms are relatively mild ICU or hospitalization for acute and severe asthma Dyspnea is present ( calm approach is important) Obtain history of allergy reactions to meds. Fluid administered if the patient is dehydrated Patient with incubation because of acute respiratory failure nurse must assist intubations procedure, continues close monitoring of the patient

Status Asthmaticus • Sever and persistent asthma that does not respond to conventional therapy • Longer than 24 hrs • Infection, anxiety, nebulizer abuse, dehydration may contribute to these episodes • Acute episodes may be precipitated by hypersensitivity to aspirin

Signs and Symptoms • • • • Labored breathing Prolong exhalation Engorge neck veins Wheezing (frequently disappear a sign of impending respiratory failure)

Assessment • Pulmonary functions studies are the most accurate means of assessing acute airway obstruction

Medical Management • • • • Short acting beta adrenergic agonist Corticosteroids Intravenous fluid for hydration O2 therapy to treatment dyspnea, centro cyanosis, and hypoxemia

Note: Death from asthma is associated with several risk factors

Past history of sudden and severe exacerbations Prior endotracheal intubation for asthma Prior admission to ICU for an asthma exacerbation Two or more hospitalization for asthma within past year Excessive used of beta adrenergic inhalers Recent withdrawal form systemic corticosteroids COPD Psychiatric disease Low socio economic Urban residence

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Nursing Management •

Monitor patient for the first 12 to 24 hrs. until status is under control Assess pt. skin turgor Room should be quite and free of respiratory irritants.

PULMONARY EDEMA -is defined as abnormal accumulation of fluid in the lung tissue or alveolar space. It is a severe, life threatening condition.

PATHOPHYSIOLOGY Pulmonary edema most commonly occurs as a result of increase micro vascular pressure from abnormal cardiac function. The backup of blood into the pulmonary vasculature resulting from inadequate left ventricular function causes an increased micro vascular pressure, and fluid begins to leak into the interstitial space and alveoli. Other causes of pulmonary edema are: a. hypervolemia or a sudden increase in the intravascular pressure in the lung -when one lung has been removed, all the cardiac output then goes to the remaining lung. If the patient’s fluid status is not monitored closely, pulmonary edema can quickly develop in the post operative period as the patient’s pulmonary vasculature attempts to adapt. This type of pulmonary edema is sometimes termed “flash” pulmonary edema. Example: patient who has undergone pneumonectomy b. re-expansion pulmonary edema -this may due to rapid reinflation of the lung after removal of air from pneumothorax or evacuation of fluid from large pleural effusion.

CLINICAL MANIFESTATIONS The patient has: -increasing respiratory, -dyspnea -air hunger -central cyanosis

**The patient is usually very anxious and often agitated. The patient coughs up or the nurse sections out these foamy, frothy and often blood-tinged secretions. The patient has acute respiratory distress and may become confuse or stuporous.

ASSESMENT AND DIAGNOSTIC FINDINGS Auscultation reveals crackles in the lung bases (especially in the posterior bases) that rapidly progressed toward the apaces of the lungs. These crackles are due to the movement of air through the alveolar fluid. The chest x-ray reveals increase interstitial markings. The patient may be tachycardic, the pulse oximetry values begin to fall, and arterial blood gas analysis demonstrates increasing hypoxemia.

MEDICAL MANAGEMENT Management focuses on correcting the underlying disorder. If the pulmonary edema is cardiac in origin, then improvement in left ventricular function is the goal. Vasodilators, inotropic medications, afterload or preload agents, or contractility medications may be given. Additional cardiac measures (e.g. intra-aortic balloon pump) may be indicated if the patient does not respond. If the problem is fluid overload, diuretics are given and the patient is placed on fluid restrictions. Oxygen is administered to correct the hypoxemia; in some circumstances, intubation and mechanical ventilation are necessary. The patient is extremely anxious, and more pain is administered to reduce anxiety and control pain.

NURSING MANAGEMENT Nursing management of the patient with pulmonary edema includes:
1. Assisting with administration of oxygen and intubation and mechanical ventilation if

respiratory failure occurs.
2. The nurse also administers medication (i.e., more pain, vasodilators, inotropic

medications, and preload and afterload agents.) as prescribed and monitors the patient’s response.

ACUTE RESPIRATORY DISTRESS SYNDROME -is a clinical syndrome characterized by a sudden and progressive pulmonary edema, increasing bilateral infiltrates on chest x-ray, hypoxemia refractory to oxygen supplementation, and reduced lung compliance. These signs occur in the absence of left side failure. Patients with ARDS usually require mechanical ventilation with a higher than normal airway pressure.

PATHOPHYSIOLOGY ARDS occurs as a result of inflammatory trigger that initiates the release of cellular and chemical mediators, causing injury to the alveolar capillary membrane. These result in leakage of fluid into the alveolar interstitial spaces and alterations in the capillary bed. Severe ventilation-perfusion mismatching occurs in ARDS. Alveoli collapse because of the inflammatory infiltrate, blood, fluid, and surfactant dysfunction. Small airways are narrowed because of interstitial fluid and bronchial obstruction. The lung compliance becomes markedly decreased (stiff lungs), and the result is a characteristic decrease in functional residual capacity and severe hypoxemia. The blood determines to the lung or gas exchange is pumped through the nonventilated, nonfunctioning areas of the lung, causing a shunt to develop. This means that blood is interfacing with nonfunctioning alveoli and gas exchange is markedly impaired, resulting in severe, refractory hypoxemia.

ETHOLOGIC FACTORS RELATED TO ARDS: • • • • • • • Aspiration (gastric secretions, drowning, hydrocarbons) Drug ingestion and over dose Hematological disorders (disseminated intravascular massive transfusions, cardiopulmonary bypass) coagulopathy [DIC],

Prolonged inhalation of high concentrations of oxygen, smoke or corrosive substances. Localized infection (bacterial, fungal, viral pneumonia) Metabolic disorders (pancreatitis, uremia) Shock

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Trauma (pulmonary contusion, multiple fractures, head injury) Major surgery Fat or air embolism Systemic sepsis

CLINICAL MANIFESTATIONS Clinically, the acute phase of ARDS is marked by a rapid offset of severe dyspnea that usually occurs 12-48 hours after the initiating event. A characteristic feature is arterial hypoxemia that does not respond to supplemental oxygen. On chest x-ray, the findings are similar to those seen with cardiogenic pulmonary edema and present as bilateral infiltrates that quickly worsen. The acute lung injury then progresses to fibrosing alveolitis with persistent, sever hypoxemia. The patient also has increased alveolar dead space (ventilation to alveoli, but poor perfusion) and decrease pulmonary compliance (“stiff lungs”, which are difficult to ventilate). Clinically, a patient is thought to be in the recovery phase if the hypoxemia gradually resolves, the chest x-ray improves, and the lungs become more compliant.

ASSESSMENT AND DIAGNOSTIC FINDINGS Intercostals retractions and crackles, as the fluid begins to leak into the alveolar interstitial space, are evident on physical examination. A diagnosis of ARDS maybe made based on the following criteria: • • • •

a history of systemic or pulmonary risk factors acute onset of respiratory distress bilateral pulmonary infiltrates clinical absence of left sided heart failure ratio of partial pressure of oxygen of arterial blood to fraction of inspired oxygen (PaO2/FiO2) less than 200 mmHg (severe factory hypoxemia)

MEDICAL MANAGEMENT The primary focus in the management of ARDS includes identification and treatment of the underlying condition. Aggressive, supportive care must be provided to compensate for the severe respiratory dysfunction. This supportive therapy almost always includes intubation and mechanical ventilation. In addition, circulatory support, adequate fluid volume, and nutritional support are important. Supplemental oxygen is used as the patient begins the initial spiral of hypoxemia. As the hypoxemia progresses, intubation and mechanical ventilation are instituted. The concentration of oxygen and ventilator settings and modes are determined by patient’s status. This is monitored by arterial blood gas analysis, pulse oximetry, and bedside pulmonary function testing.

Positive end-expiratory pressure (PEEP) is a critical part of the treatment of ARDS. PEEP usually improves oxygenation, that it does not influence the natural history of the syndrome. Use of PEEP helps to increase functional residual capacity and reverse alveolar collapse by keeping the alveoli open, resulting in improved arterial oxygenation and a reduction in the severity of the ventilationprofusion and balance. Systemic hypotension may occur in ARDS as a result of hypovolemia secondary to leakage of fluid into the interstitial spaces and depressed cardiac output from high levels of PEEP therapy. Hypovolemia must be carefully treated without causing further overload. Intravenous crystalloid solutions are administered with careful monitoring of pulmonary status. Inotropic or vasopressor agents may be required. Pulmonary artery pressure catheters are used to monitor patient’s fluid status and the severe and progressive pulmonary hypertension sometimes observed in ARDS.

NURSING MANAGEMENT • • Positioning is important. The nurse should turn the patient frequently to improve ventilation and profusion in the lungs and enhance secretion drainage. The nurse must closely monitor the patient for deterioration in oxygenation with changes in position.

Oxygenation in the ARDS patient is sometimes improved in the prone position and may be used in special circumstances; studies to asses the benefits and problems of such positioning are on going. The patient is extremely anxious and agitated because of the increasing hypoxemia and dyspnea. The nurse should explain all procedures and provide care in calm, reassuring manner. It is important to reduce the patient’s anxiety because anxiety prevents rest and increase oxygen expenditure. Rest is essential to reduce oxygen consumption, thereby reducing oxygen needs.

Pulmonary Embolism (PE)
 Refers to the obstruction of the pulmonary artery or one of its branches by

thrombus (Thrombi) that originates in the venous system or in the right side of the heart.  TYPES OF EMBOLI a. Blood clot – Most common b. Air c. Fat d. Amniotic Fluid e. Septic – from bacterial invasion of the thrombus 1. Risk factor for pulmonary emboli a. Venous stasis – slowing of blood flow in veins - Prolonged immobilization - Prolonged periods of sitting/ traveling - Varicose veins - Spinal cord injury b. Hypercoagulability – due to release of tissue thromboplastin after surgery. - Injury - Tumor – pancreatic, GU, GI, breast , lung - Increased platelet count – polycythemia, splenectomy. c. Venous Endothelial Disease - Thrombophlebitis - Vascular disease - Foreign bodies – IV/ central venous catheter d. Certain Disease State – combination of stasis coagulation alteration and venous injury - Heart Disease - Trauma – fracture of the hip, pelvic, vertebrae, lower extremities - Post operative state/ postpartum period - DM - COPD e. Other Predisposing Conditions - Advanced age

- Obesity - Pregnancy - Oral contraceptive use - History of previous thrombophlebitis, pulmonary embolism - Constrictive clothing 2. most thrombi originate in the deep veins of the legs, other sites include the pelvic veins and the right atrium of the heart 3. venous thrombosis can result from slowing of blood flow (stasis), secondary to damage to the blood vessel wall ( Endothelial lining) or changes in the blood coagulation mechanism 4. Atrial Fibrillation causes pulmonary embolism. An enlarged right atrium in fibrillation causes blood to stagnate and form clot in this area. This clots are prone to travel into the pulmonary circulation PATHOPHYSIOLOGY 5. When a thrombus completely or partially obstructs a pulmonary artery or its branches, the alveolar dead space is increased. Area though continue to ventilate, receives little or no blood flow. Thus gas exchange is impaired or absent in this area. 6. The hemodynamic increased pulmonary vascular resistance from the regional vasoconstriction and reduced size of the pulmonary vascular bed. This result in an increase in pulmonary arterial pressure and an increased in right ventricular requirements of the right ventricle exceed its capacity, right ventricular failure occurs leading to a decrease in cardiac output followed by decreased in systemic blood pressure and development of shock. CLINICAL MANIFESTATION -




dyspnea tachypnea chest pain Anxiety Fever Tachycardia Apprehension Cough Diaphoresis Hemoptysis Syncope Rapid weak pulse Shock Sudden onset of pain or warmth/ swelling of the proximal or distal extremity skin discoloration superficial vein distention Pain is relieve when elevated


death is common in PE if not detected early Chest x ray usually normal but may show infiltrate, atelectasis, elevation of the diaphragm on the affected side. ECG shows sinus tachycardia, PR interval depression and nonspecific T wave changes Peripheral Vascular Studies – Doppler, ultrasonography, venosenography Arterial Blood Gas – show hypoxemia and hypocapnia Ventilation Perfusion Scan test choice in patients with suspected PE Pulmonary Angiography – gold standard for the diagnosis of PE

2. 3. 4. 5. 6. PREVENTION -


To prevent PE is to prevent Deep Venous Thrombosis Active exercise to avoid venous stasis Early ambulation Use of elastic compression stockings Low dose of heparin before the surgery to reduce the risk of post operative deep venous thrombus Low dose of heparin is thought to enhance the activity of antithrombin III a major plasma inhibitor of clotting factor X. this regimen is not recommended for patients with active thrombotic process, major orthopedic surgery, open prostatectomy Low molecular weight heparin is alternative Intermittent pneumatic leg compression device is useful in preventing thromboembolism

MEDICAL MANAGEMENT a. Emergency Management - Massive PE is a life threatening emergency. - Objective is to stabilize the cardiopulmonary system. Because a sudden rise in pulmonary resistance increases the work of the right ventricle which causes acute right sided heart failure with cardiogenic shock. - Patients die in the 1st 1 hour to 2 hours after the embolic event. The following are some of the emergency management a. Nasal Oxygen- to relieve hypoxemia, respiratory distress and central cyanosis b. Intravenous infusion lines- to establish routes for medication or fluids that will be needed c. Perfusion Scan, hemodynamic measurements and arterial blood gas d. Slow infusion of dobutamine for hypotension

e. ECG- monitor for dysrrhythmias and right ventricular failure

f. Digitalis glycosides- diuretics and antiarrhythmic agents g. Blood- for serum electrolyte, CBC, HCT h. Indwelling catheter- to monitor urinary output if the pt. has suffered massive embolism i. Small dose of morphine and sedatives- to relieve the patient’s anxiety, to alleviate chest discomfort, to improve the endotracheal tube, to ease adaptation to the mechanical ventilator. b. General Management- Oxygen therapy to correct hypoxemia, relieve the pulmonary vascular vasoconstriction and reduce the pulmonary hypertension. - Using Elastic compression - Elevate the leg to increase venous flow b. Pharmacologic Therapy - Anticoagulation Therapy (heparin and warfarin sodium) are primary method in managing acute deep vein thrombosis and PE - Heparin to prevent the recurrence of Emboli but no effect on emboli that are already present. - Goal is to keep the partial thromboplastin time 1.5-2.5 times normal - Warfarin administration is start within 24 hrs after the start of heparin because the onset of action of 4 to 5 days - Prothrombin time is maintained at 1.5 to 2.5 times the normal - Anticoagulation therapy is contraindicated in pt. who are at risk for bleeding

Thrombolytic therapy anistreplase, reteplase)





Patients who are severely compromised hypotension and hypoxemia despite oxygenation therapy This therapy resolves the thrombi or emboli more quickly and restore more than hemodynamic functioning of the pulmonary circulation reducing pulmonary hypertension and improve perfusion, oxygenation and cardiac output, bleeding Before thrombolytic therapy obtained prothrombin time and partial thromboplastin time, HCT, Platelet counts Heparin is stopped prior to the administration of thrombolytic agents.





All but essential invasive procedures are avoided because of potential bleeding Contraindicated to thrombolytic therapy CVA within 2 mo. Active ICP, Active bleeding, surgery within the past 10 days of the thrombotic events, recent labor and delivery, trauma or severe hypertension


c. Surgical Management - Embolectomy indicated if the p. has massive PE - Transvenous catheter embolectomy is a technique in which a vacuum cupped catheter is introduced transvenously into the affected pulmonary artery. - Pulmonary embolectomy requires a thoracotomy with cardiopulmonary bypass. NURSING MANAGEMENT 1. Minimizing the risk of pulmonary Embolism 2. Preventing thrombus Formation- encourages early ambulation, active and passive exercise, don’t wear constrictive clothes. 3. Assessing Potential for Pulmonary Embolism- monitor for positive homan’s sign 4. Monitoring Thrombolytric Therapy 5. Managing Pain- Semi fowlers position, turn and reposition the pt. to improve ventilation perfusion ratio. Administer analgesics for severe pain 6. Managing oxygen therapy- deep breathing and incentive spirometry are indicated for all patients to minimize or prevent atelectasis and improve ventilation 7. Relieving Anxiety8. Monitor for complication – cardiogenic shock and Right ventricular failure. 9. Providing Post operative nursing care- After the surgery measure the pt. pulmonary arterial pressure and urinary output.