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RESPI REVIEW1

RESPI REVIEW1

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Published by: Sheryll Joy Lopez Calayan on Aug 16, 2012
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Sheryll Joy Lopez-Calayan, RN, MSN

MAJOR DISORDERS OF THE RESPIRATORY SYSTEM

PULMONARY EMBOLISM AND INFARCTION
 Etiology and pathophysiology
 Emboli develop from thrombi in peripheral

circulation; associated with venous stasis resulting from immobility, coagulopathy, vascular disease, surgery, aging, oral contraceptives, obesity, and constrictive clothing  When an embolus lodges in the pulmonary artery causing hemorrhage and necrosis of lung tissue it is called a pulmonary infarction

Clinical findings
 Subjective:
       

severe dyspnea that occurs suddenly; anxiety; restlessness; sharp pleuritic pain increased temperature, pulse, and respirations; violent coughing with hemoptysis; diaphoresis

 Objective:

a filter may be implanted in the inferior vena cava preventing the passage of large thrombi .Therapeutic interventions  Anticoagulant therapy  Thrombolytic therapy  Angiography. if the condition is severe. an embolectomy may be indicated  Vena caval interruption.

Nursing Care of Clients with Pulmonary Embolism and Infarction  PLANNING/IMPLEMENTATION  Place in the high-Fowler’s position and     administer oxygen Monitor for hypoxemia and right heart failure Administer thrombolytics/anticoagulants as ordered. monitor for bleeding Maintain calm environment to decrease fear Educate client regarding anticoagulants and prevention of thrombophlebitis .

aspiration of gastric contents. leftventricular failure. circulatory overload. drowning .PULMONARY EDEMA  Etiology and pathophysiology  An acute emergency situation condition characterized by a rapid accumulation of fluid in alveolar spaces resulting from increased pressure within the pulmonary system  Possible causes include valvular disease.

paroxysmal nocturnal dyspnea. wheezing. crackles. acute anxiety. and orthopnea. elevated pulmonary capillary wedge pressure and central venous pressure . wheezing. frothy sputum.PULMONARY EDEMA  Clinical findings  Subjective: history of premonitory symptoms such as shortness            of breath. pink. pallor or cyanosis. low PO2. restlessness Objective: rapid. thready pulse and rapid respirations. apprehension.

diuretics. bronchodilators  Oxygen in high concentration or by PEEP as necessary  Hemodynamic monitoring . Therapeutic interventions  Medications aimed at decreasing cardiac workload and improving cardiac output. vasodilators. digitalis. such as morphine sulphate.

administer morphine sulphate to relieve anxiety Suction as needed to maintain a patent airway Administer and monitor effects of medications to reduce preload and afterload Educate client regarding pharmacology and prevention of heart failure .Nursing Care of Clients with Pulmonary Edema  PLANNING/IMPLEMENTATION  Support client in the orthopneic. high-Fowler’s or      semi-Fowler’s position with legs dependent Observe and record vital signs and monitor cardiac activity and intake and output Provide a reassuring environment to allay anxiety.

other bacterial causes include Klebsiella pneumoniae. or fungal) but may also be caused by inhalation of chemicals and aspiration of gastric contents Pneumonia is commonly spread by respiratory droplets Pnemococcal pneumonia usually caused by Streptococcus pneumoniae. incidence highest in winter.PNEUMONIA  Etiology and pathophysiology        Inflammatory disease usually caused by infectious agent (bacterial. protozoal.g.. is seen in clients with impaired immune function {e. and Staphylococcus aureus Aspiration pneumonia occurs when gastric contents and the normal flora of the upper respiratory tract are aspirated into the lung Pneumocystis carinii pneumonia. AIDS) Viral pneumonia include influenza virus type A and cytomegalovirus May cause a collection of pus (empyema) or fluid (pleural effusion) within the pleural space . a rare protozoal infection. Haemophilus influenzae. Pseudomonas. viral.

rusty sputum Staphylococcal: yellow. chest pain that increases on inspiration  Objective  Elevated temperature. gelatinous sputum Mycoplasmal: non-productive that advances to mucoid sputum . dyspnea. blood-streaked sputum Klebsiella: red.PNEUMONIA  Clinical findings  Subjective: lassitude. increased WBC  Chest x-ray examination shows pulmonary infiltration  Cough with sputum production     Pneumococcal: purulent.

PNEUMONIA  Therapeutic interventions  If bacterial pneumonia. culture and sensitivity tests will be done on blood and sputum to determine appropriate antibiotic therapy  Oxygen therapy usually via nasal cannula .

balance of activity and rest . notify the physician if organism is resistant to the antibiotic being given Increase fluid intake to 3 liters daily Maintain semi-Fowler’s position Monitor for signs of respiratory distress. such as labored respirations. vaccination against Streptococcus pneumoniae and influenza. PLANNING/IMPLEMENTATION  Encourage coughing and deep breathing after chest         physiotherapy. splinting the chest as necessary Collect sputum specimen for culture and sensitivity tests in sterile container. smoking).g. cool clammy skin.. cyanosis and change in mental status Plan rest periods Instruct client to cover nose and mouth when coughing Administer antibiotics as ordered Teach preventive measures including: role of nutrition and fluids. avoiding respiratory irritants (e.

chronic respiratory infections. exposure to molds and fungi. and allergic reactions . smoking.CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)  Etiology and pathophysiology  Group of diseases that result in chronic airflow limitation (CAL). also called chronic obstructive lung disease (COLD). causes include air pollution.

obstruction of the bronchioles characterized by attacks that occur suddenly and last from 30 to 60 minutes. characterized by a chronic cough  Emphysema: characterized by distended. or destroyed alveoli with bronchiolar obstruction and collapse. an asthmatic attack that is difficult to control is referred to as status asthmaticus  Chronic bronchitis: inflammation of the bronchial walls with hypertrophy of mucous goblet cells. inelastic.CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)  Types  Asthma: reversible bronchospasms and increased secretions that last from 1 to several hours. these alterations greatly impair the diffusion of gases through the alveolar capillary membrane  Bronchiectasis: chronic dilation of the bronchi and bronchioles as a result of infection or obstruction .

UNDERSTANDING ASTHMA .

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1. Histamine attaches to receptor sites in the larger bronchi. where it causes swelling in smooth muscles .

2. . Slow reacting .a substance of anaphylaxis attaches to receptor sites in the smaller bronchi and causes swelling of smooth muscle there.

as show below. further narrowing the bronchial lumen. Histamine stimulates the mucuos membranes to secrete excessive mucus . .3.

On inhalation. . On exhalation . increased intrathoracic pressure closes the bronchial lumen completely. allowing air to reach the alveoli.4. the narrowed bronchial lumen can still expand slightly.

5. inhibiting alveolar ventilation . . Mucus fills the lung bases.

PATHOPHYSIOLOGY Exposure to allergies and irritants Stress Cold Air Exercise STEROIDS Immunoglobulin E Stimula tion .

Mast cells degranulation MAST CELL STAB. Hista mine Anti hist SRSA Pros Ta Glan din Brady kinin Leuko triene .

Broncho dilators Mucus Secretion Inflammation Bronchospasm SOB Wheezing Non Productive Cough .

WHAT TO LOOK FOR!!!!  Dyspneic  Marked respiratory effort  Marked respiratory effort  Wheezing upon auscultation .

cor pulmonale.CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)  Clients with COPD become accustomed to an elevated residual carbon dioxide level and do not respond to high CO2 concentrations as the normal respiratory stimulant. they respond instead to a drop in oxygen concentration in the blood  May precipitate pulmonary hypertension. and right ventricular heart failure .

sterious breathing sounds. clubbing of fingers. polycythemia  Distended neck veins. cyanosis. cough  Barrel chest. peripheral edema (with right heart failure) .CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)  Clinical findings  Subjective: fatigue and weakness. headache. impaired sensorium  Objective  Orthopnea. pursed lip breathing  Increased PCO2 and decreased PO2 of arterial blood gases. expiratory wheezing. dyspnea. use of accessory muscles.

and exercise  High-protein soft diet in small.CHRONIC OBSTRUCTIVE PULMONARY DISEASE (COPD)  Therapeutic interventions     Steroids to prevent and reduce inflammation Antibiotics to prevent/treat infection Bronchodilators to reduce muscular spasm Mucolytics and expectorants to liquefy secretions and to facilitate their removal  Oxygen at 1 to 2 L even if hypoxia is severe  Respiratory therapy program to include nebulizer therapy. frequent feedings is most easily tolerated . postural drainage.

spacer) Carefully observe for symptoms of hypoxia and carbon dioxide intoxication (CO2 narcosis) if oxygen is being administered Teach client to adjust activities to avoid overexertion Teach clients to avoid people with respiratory infections Teach the client to avoid the use of sedatives or hypnotics.g.Nursing Care of Clients with Chronic Obstructive  PLANNING/IMPLEMENTATION  Advise the elimination of smoking and other Pulmonarydust. such as pursed      lip or diaphragmatic breathing Teach proper use of inhalers and other special equipment (e. such as  Supervise the client’s respiratory exercises. which could compromise respirations .. as much as possible external Disease irritants.

properly for weather      receiving vaccinations against S. hypercapnea.Diseasefood. or adverse response to medications Encourage client to continue with close medical supervision. hypoxia. maintaining fluid intake. dressing eating nutritious Pulmonary conditions. pneumoniae and influenza Teach client to be alert to early symptoms of infection.Nursing Care of Clients with Chronic Obstructive  Teach client to maintain the highest resistance possible by getting adequate rest. monitor compliance Encourage client to express feelings about disease and therapy Accept feelings about life-long restrictions in activity Encourage client and family to take an active role in planning therapy .

may be associated with fractured ribs  Reduces the surface area for gaseous exchange and leads to hypoxia and retention of carbon dioxide (hypercarbia) .PNEUMOTHORAX/CHEST INJURY  Etiology and pathophysiology  Collapse of a lung resulting from disruption of the negative pressure that normally exists within the intrapleural space caused by the presence of air in the pleural cavity.

air then moves from the lung to the intrapleural space causing collapse. heart. this involves the trachea.g. highest incidence is in men 20 to 40 years of age Open: laceration (e. esophagus.. the pressure increase is likely to induce a mediastinal shift Mediastinal shift may occur toward the uninvolved side as a result of increased pressure within the pleural space. caused by crushing chest injuries . Types  Spontaneous: thought to occur when a weakened area of the       lung (bleb) ruptures. a stab wound) through the chest wall into the intrapleural space Hemothorax: collection of blood within the pleural cavity Hydrothorax: accumulation of fluid in the pleural cavity Tension: buildup of pressure as air accumulates within the pleural space. and great vessels Flail chest: instability of chest wall related to fractures of the ribs or detached sternum.

How open pneumothorax occurs ? Complete Collapse Knife wound .

SPONTANEOUS PNEUMOTHORAX Partial collapse Rupture bleb .

UNDERSTANDING TENSION On Expiration. the mediastinal shift distorts PNEUMOTHORAX the vena cava and reduces venous return .

impairing ventilation . the mediastinum shifts toward the unaffected lung.On inspiration.

shallow respirations (nonsymmetric)  Flail chest: loose chest segment moves inward during inspiration and outward during expiration (paradoxical respiration)  Breath sounds on the affected side will be diminished or absent  Chest x-ray examination will reveal extent of the pneumothorax . drowsiness  Objective  Tachycardia.PNEUMOTHORAX/CHEST INJURY  Clinical findings  Subjective: chest pain. rapid. usually described as sharp and increasing on exertion. hypotension. dyspnea.

PNEUMOTHORAX/CHEST INJURY  Therapeutic interventions  Bed rest initially  Analgesics and antibiotics  Negative pressure is returned to the intrapleural space by the insertion of chest tubes attached to underwater drainage  Restoration of blood volume loss as a result of trauma  Volume controlled ventilation .

Nursing Care of Clients with Pneumothorax  PLANNING/IMPLEMENTATION  Maintain constant supervision until stable  Maintain patency of chest tubes  Place in high-Fowler’s position  Offer fluids frequently  Monitor vital signs. particularly respirations  EVALUATION/OUTCOMES  Maintains adequate gas exchange  Verifies reduction or absence of chest pain .

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8. examine the entire system to ensure airtightness and absence of obstruction from kinks or dependent loops of tubing 3. If drainage ceases and system is not blocked. always keep drainage system lower than the level of the client’s chest 7. 6. note oscillation of the fluid level within the water-seal tube. If oscillation stops and system is intact. amount and characteristics of the drainage. prepare the unit for use and connect the chest catheter to the drainage tubing 2. Hold the proximal part of tubing with one hand and squeeze the distal portion in a downward direction 5. keep Vaseline gauze at bedside at all times in case chest tube falls out. check the color. It will rise on inspiration and fall on expiration due to changes in the intrapleural pressure. provide ROM exercises . notify the physician 4. assess for signs of respiratory distress from fluid / air accumulation.Nursing care: without suction          1. milk the chest tubes and drainage tubing every 1-2 hours as ordered to dislodge mucus and blood clots. encourage coughing and deep breathing to facilitate removal of air and drainage from pleural cavity 9.

encourage coughing and deep breathing. K if the water seal bottle should break immediately obtain some type of fluidfilled container to create an emergency water seal until a new unit can be obtained . I. attach suction tubing to suction apparatus and chest catheter to drainage tubing 2. provide Rom exercises as noted above. keep Vaseline gauze at bedside. apply a Vaseline pressure dressing to the site. There should be continuous bubbling in this chamber and intermittent bubbling in the water seal. J. Check for an air leak in the system if bubbling in water seal is constant. removal of the chest tube: instruct the client to perform Valsalva maneuver. Clamping the chest tube’s of a client with air in the pleural space will cause increased pressure build up and possible tension pneumothorax. open suction slowly until a stream of bubbles is seen in the suction chamber. notify physician if no air leak 3. keep drainage system below level of client’s chest. never clamp chest tubes unless a specific order is written by the physician.Nursing care: with suction       1. check drainage.

collapse of alveoli  Atelectasis resulting in labored and inefficient respiration . fat emboli. severe infection. shock  Involves:  Pulmonary capillary damage with loss of fluid and interstitial edema  Impaired alveolar gas exchange and tissue hypoxia resulting from pulmonary edema  Alteration in surfactant production. aspiration. open-heart surgery. prolonged mechanical ventilation.ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)  Etiology and pathophysiology  Respiratory failure as a complication of trauma.

CAUSES OF ARDS  Fat emboli  Sepsis  Shock  Pulmonary contusions  Multiple transfusions .

Control Complications Improve General health .

PLATELETS AGGREGATE AND RELEASE ( H). (S) & ( B) .

increasing capillary per.Fluid shifts to interstitial space .(H ) Inflame and damage the alveolocapillary mem.

Increases. Protein leak out.Inc. PULMONARY EDEMA .Capillary perm. Interstitial osmotic pressure.

Decreased bld. Flow ALVEOLI COLLAPSE IMPAIRING GAS EXCHANGE .

BUT CO2 CAN .SUFFICIENT OXYGEN CAN’T CROSS THE ALVELOCAPI. MEMBRANE.

INFLAMMATION LEADS TO FIBROSIS .PULMONARY EDEMA WORSENS.

What to look for !!!!  Rapid .shallow breathing and dypnea  Hypoxemia  Crackles and rhonchi .

WHAT TESTS TELL YOU !!!
 Arterial Blood Gas- respiratory alkalosis   Pulmonary Artery Catheterization- capillary

wedge pressure  Chest X ray- bilateral infiltration  “Whiteouts “ of both lung fields

ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)
 Clinical findings
       

Subjective: restlessness; anxiety; dyspnea Objective: tachycardia; grunting respirations; intercostals retractions; cyanosis; PCO2 initially decreased and later increased, and decreased PO2 arterial blood gases;  chest x-ray examination reveals pulmonary edema

ADULT RESPIRATORY DISTRESS SYNDROME (ARDS)
 Therapeutic interventions  Relieve the underlying cause  Mechanical ventilation with positive end

expiratory pressure (PEEP): this setting on a mechanical ventilator maintains positive pressure within the lungs at the end of expiration, which increases the residual capacity, reducing hypoxia  Corticosteroids may be used

sedation is contraindicated       because of its depressant effect on respirations Observe behavioural changes and vital signs because confusion and hypertension may indicate cerebral hypoxia Auscultate breath sounds to observe for signs of pneumothorax when the client is on PEEP (lung tissue that is frail may not withstand increased intrathoracic pressure. as ordered. supportive environment. and pneumothorax occurs) Monitor arterial blood gases. Nursing Care of Clients with ADULT RESPIRATORY DISTRESS SYNDROME (ARDS) PLANNING/IMPLEMENTATION  Allow frequent rest periods between therapeutic interventions  Provide tranquil. use a heparinized syringe Maintain a patent airway Care for the client on mechanical ventilation Measure central venous and pulmonary artery pressures .

loss of consciousness. cyanotic. resulting in tissue anoxia. caused by inadequately vented combustion devices  Clinical findings  Subjective: headache. faintness. paralysis.CARBON MONOXIDE POISONING  Etiology and pathophysiology:  carbon monoxide combines with haemoglobin more readily than does oxygen. or flushed but usually cherry pink. tinnitus  Objective: color normal. ECG changes . vertigo.

PLEURISY  Inflammation of the visceral and parietal membranes  These membranes rub together during respiration and         cause pain May be caused by pulmonary infarction or pneumonia It usually occurs on one side of the chest. usually in lower lateral portions in the chest wall Assessment Knife like pain that is aggravated on deep breathing and coughing Dyspnea Pleural friction rub on auscultation Apprehension Pleurisy .

Implementation  Identify and treat the cause  Monitor lung sounds  Analgesics as prescribed  Hot and cold applications  Coughing and deep breathing  Lie on affected side to splint chest .

CARBON MONOXIDE POISONING  Therapeutic interventions  Mechanical ventilation with 100% oxygen until carboxyhemoglobin is reduced to less than 5% and respirations are normal  Hyperbaric pressure chamber to increase oxygen concentration and accelerate formation of carbon dioxide which can be exhaled .

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Nursing Care of Clients with  ASSESSMENT  History to determine extent of exposure  Color of skin  Level of consciousness  ANALYSIS/NURSING DIAGNOSIS  Impaired gas exchange related to chemical imbalance  Alteration in thought processes related to hypoxia .

with special concern for respirations .CARBON MONOXIDE POISONING  PLANNING/IMPLEMENTATION  Remove the individual from the immediate area     of poisoning Evaluate for cardiopulmonary resuscitation if necessary and maintain until additional help arrives Administer oxygen as prescribed Maintain respirations with assistance if needed Monitor vital signs.

CARBON MONOXIDE POISONING  EVALUATION/OUTCOMES  Maintains adequate oxygen levels  Remains conscious and alert .

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