![Treatment
• The goal of treatment is to re-expand the collapsed lung tissue. If fluid is putting pressure on the lung, removing the
fluid may allow the lung to expand.
• Oxygen therapy
• Clap (percussion) on the chest to loosen mucus plugs in the airway
• Chest physiotherpy
• Perform deep breathing exercises (with the help of incentive spirometry devices)
• Remove or relieve any blockage in the airways by bronchoscopy.
• Tilt the person so the head is lower than the chest (called postural drainage). This allows mucus to drain more
easily.
• Treat a tumor or other condition, if there is one
• Turn the person to lie on the healthy side, allowing the collapsed area of lung to re-expand
• Use aerosolized respiratory treatments (inhaled medications) to open the airway
• Use other devices that help increase positive pressure in the airways and clear fluids (positive expiratory pressure
[PEP] devices)](https://image.slidesharecdn.com/lowerrespiratorydisorder-241207043925-a3e583db/75/LOWER-RESPIRATORY-DISEASES-AND-DISORDER-10-2048.jpg)
![Causes
• Predisposing factors include:
– Stasis, prolonged immobilization.
– Concurrent phlebitis.
– Previous heart (heart failure, myocardial infarction [MI])
or lung disease.
– Injury to vessel wall.
– Coagulation disorders.
– Metabolic, endocrine, vascular, or collagen disorders.
– Malignancy.
– Advancing age, estrogen therapy.](https://image.slidesharecdn.com/lowerrespiratorydisorder-241207043925-a3e583db/75/LOWER-RESPIRATORY-DISEASES-AND-DISORDER-83-2048.jpg)
![• Ventilatory failure is rise in PaCo2 [hypercapnia]that occurs when the
respiratory load can no longer be supported by the strength or activity of
the system.
Causes
– Drug overdose
– Stroke
– Tumors
– Tetanus
– Pneumothorax
– Pneumonia
– Chronic obstructive pulmonary disease (COPD) (chronic bronchitis,
emphysema).
– Severe asthma.
– Cystic fibrosis.](https://image.slidesharecdn.com/lowerrespiratorydisorder-241207043925-a3e583db/75/LOWER-RESPIRATORY-DISEASES-AND-DISORDER-105-2048.jpg)
Uploaded byDR .PALLAVI PATHANIA
LOWER RESPIRATORY DISEASES AND DISORDER
The document provides an overview of various lower respiratory disorders, including atelectasis, pneumonia, pulmonary tuberculosis, lung abscess, and lung cancer, detailing their causes, symptoms, diagnostics, and treatment options. It discusses risks, particularly in relation to surgical procedures, and emphasizes preventive measures such as vaccinations and lifestyle changes. Additionally, it outlines the management of conditions like pulmonary embolism and highlights the importance of nursing diagnoses in patient care.
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LOWER RESPIRATORY DISEASES AND DISORDER
- 1.
- 2. LOWER RESPIRATORY DISORDER •ATELECTASIS 519 • RESPIRATORY INFECTIONS 521 • Acute Tracheobronchitis 521 • Pneumonia 522 • Nursing Process: The Patient With Pneumonia 531 • Pulmonary Tuberculosis 534 • Nursing Process: The Patient With Tuberculosis 538 • Lung Abscess 540 • PLEURAL CONDITIONS 542 • Pleurisy 542 • Pleural Effusion 542 • Empyema 543 • PULMONARY EDEMA 544 • ACUTE RESPIRATORY FAILURE 545 • ACUTE RESPIRATORY DISTRESS SYNDROME 546 • PULMONARY HYPERTENSION 548 • PULMONARY HEART DISEASE (COR PULMONALE) 549 • PULMONARY EMBOLISM 550 • SARCOIDOSIS 554 • OCCUPATIONAL LUNG DISEASES: PNEUMOCONIOSES 554 • Silicosis 555 • Asbestosis 555 • Coal Workers’ Pneumoconiosis 555 • CHEST TUMORS 556 • Lung Cancer (Bronchogenic Carcinoma) 556 • Tumors of the Mediastinum 559 • CHEST TRAUMA 559 • Blunt Trauma 560 • Penetrating Trauma: Gunshot and Stab Wounds 562 • Pneumothorax 563 • Cardiac Tamponade 564 • Subcutaneous Emphysem
- 3.
- 4. • Atelectasis isdefined as the collapse or closure of the lung resulting in reduced or absent gas exchange. It may affect part or all of one lung. • It is the collapse or incomplete expansion of lung or parts of lung. • Atelectasis is caused by blockage of the air passages or absent of gas exchange.
- 5. Causes • Inhalation ofirritants • Chest wall disorders • Atelectasis is caused by a blockage of the air passages (bronchus or bronchioles) or by pressure on the outside of the lung. • Another type of collapsed lung is called pneumothorax. It occurs when air escapes from the lung. The air then fills the space outside of the lung, between the lung and chest wall. • Atelectasis is common after surgery or in patients who were in the hospital.
- 6. Risk factors fordeveloping atelectasis include: • Anesthesia • Foreign object in the airway (most common in children) • Lung diseases • Mucus that plugs the airway • Pressure on the lung caused by a buildup of fluid between the ribs and the lungs (called apleural effusion) • Prolonged bed rest with few changes in position • Shallow breathing (may be caused by painful breathing) • Tumors that block an airway
- 8. Signs and symptoms •cough, but not prominent; • chest pain (not common); • breathing difficulty (fast and shallow); • low oxygen saturation; • pleural effusion (transudate type); • cyanosis (late sign); • increased heart rate. • increased temperature.
- 9. Exams and Tests •To confirm if you have atelectasis, the following tests will likely be done: • Bronchoscopy • Chest CT scan • Chest x-ray
- 10. Treatment • The goalof treatment is to re-expand the collapsed lung tissue. If fluid is putting pressure on the lung, removing the fluid may allow the lung to expand. • Oxygen therapy • Clap (percussion) on the chest to loosen mucus plugs in the airway • Chest physiotherpy • Perform deep breathing exercises (with the help of incentive spirometry devices) • Remove or relieve any blockage in the airways by bronchoscopy. • Tilt the person so the head is lower than the chest (called postural drainage). This allows mucus to drain more easily. • Treat a tumor or other condition, if there is one • Turn the person to lie on the healthy side, allowing the collapsed area of lung to re-expand • Use aerosolized respiratory treatments (inhaled medications) to open the airway • Use other devices that help increase positive pressure in the airways and clear fluids (positive expiratory pressure [PEP] devices)
- 11.
- 12. INTRODUCTION • Pneumonia isan inflammation and infection of the lungs. • Inflammation is the immune system normal response to injury or contaminants. • Germs, bacteria and viruses are contaminants and can cause inflammation. • There are more than 50 kinds of pneumonia. • Pneumonia can affect one or both lungs. when it affects both lungs ,it sometimes called double pneumonia.
- 13. PNEUMONIA • Pneumonia isan inflammation of the lung parenchyma that is caused by a microbial agent. • Pneumonia is an inflammatory process, involving the terminal airways and alveoli of the lung, caused by infectious agents. It is classified according to its causative agent
- 14. CAUSES • Bacteria • Viruses •Fungal infections • Aspiration of food, fluids or vomitus • Inhalation of toxins { chemicals, smoke, dust, gases}
- 15. RISK FACTORS • Advancedage • A history of smoking • Upper respiratory infections • Tracheal intubation • Malnutrition • Chronic lung diseases • Renal diseases
- 16. CLASSIFICATION • SITE OFINFECTION – Lober Pneumonia { lobes one or more entire lobe may affected} – Broncho Pneumonia • ORIGION OF INFECTION – Community acquired pneumonia – Nosocomial pneumonia – Aspiration pneumonia – Immunocompromised pneumonia • BASED ON ETIOLOGY – Bacterial, viral, fungal, atypical
- 17.
- 18. Community acquired pneumoniarefers to pneumonia you get, or acquire from your community such as school , work. Hospital acquired pneumonia or nosocomial pneumonia is a serious pneumonia acquired at a hospital or a health care facility it usually effects patients who are • Mechanical ventilators. • I cu unit. • Or having weak immune system.
- 19. Bacterial Pneumonia: occurswhen pneumonia-causing bacteria masses and multiplies in the lungs. The alveoli become inflamed and pus is produced, which spreads around the lungs. The bacteria that caused Bacterial Pneumonia are: • streptococcus pneumonia, • hemophilus influenza, • and staphylococcus aureus.
- 20. Viral Pneumonia: Viral Pneumoniais believed to be the cause of half of all pneumonias. The viruses invade the lungs and then multiply- causing inflammation Aspiration pneumonia happens when any thing other than air gets in to the lungs.
- 21.
- 22. • Due tocausing factor{ when foreign matter such as viruses, bacteria, parasites, or fungus enters the lungs and causes inflammation} • Decrease resistance • Decreases immune system • Inflammation • Decrease cell permiability • Impaired cilliary function • Increase mucus production • Collection of fluid • Bacterial growth • Pneumonia
- 23. SIGN AND SYMPTOMS •Fever • Chills, sweating • Cough, sputum production, • Haemoptysis, Pleuritic chest pain, • Wheezing, difficulty in breathing • Nausea , vomiting • Tactile fermitus increased
- 24. DIAGNOSIS • Clinical historyand Physical exam • Blood & Urine Culture • Chest x ray • Sputum Analysis • Bronchoscopy
- 25. MEDICAL MANAGEMENT • CAP –IV-beta lactum antibiotic plus • NOSOCOMIAL PNEUMONIA – Cephalosporin 2nd generation • ASPIRATION PNEUMONIA – Cephalosporin 2nd generation + metronidazole • ANTIBIOTIC THERAPY • OXYGEN THERAPY • BRONCHODILATORS {SALBUTAMOL} • SUCTIONING • CHEST PHYSIOTHERAPY
- 26. VACCINES • Vaccines help preventpneumococcal pneumonia but cannot prevent all cases of infection. The following vaccines are recommended to help protect you against pneumonia. • Haemophilus influenzae type b (Hib) • Influenza vaccine - • Pneumococcal pneumonia vaccine -.
- 27. PATIENT COUNSELLING • LIFESTYLE MODIFICATIONS: • Eat healthy. • Sleep well. • Avoid smoking. • Exercise. • Reduce stress. • Avoid drinking alcohol excessively
- 29.
- 30. • TB isan infectious disease caused by bacteria (Mycobacterium tuberculosis) that are usually spread from person to person through the air. It usually infects the lung but can occur at virtually any site in the body. HIV-infected patients are especially at risk. Drug-resistant TB is of particular concern in certain parts of the United States
- 33. CAUSES • MYCOBACTERIUM TUBERCULOSIS •Mycobacterium bovis • Mycobacterium africanum • Mycobacterium conctti • Mycobacterium microti
- 38. PATHOPHYSIOLOGY • Due toetiological factor • Decrease immune response • Decrease resistance • Inflammatory reactions occur • Impaired cillary function • Collection of fluid • Macrophages • Phagocytosis • Necrosis • Cavity formation • Cheesy material • WBC’s mycobacterum tuberculii • Symptoms of Primary T.B. • Many infection tuberculi • Hypersensitivity • Reactivation of T.B. • Coughed out with foul smelling • Weak immunity • Secondary T.B.
- 46. PPD: PURIFIED PROTIENDERIVATIVE
- 58. BCG Vaccine Dose Forchildren over one year of age and adults, 0.1 ml of vaccine can be given. A single dose is enough to provide lifetime immunity from TB (tuberculosis) BCG Vaccine Route The BCG vaccine can be administered intradermally. BCG Vaccine for newborn BCG vaccine standard dose at birth is 0.1 mg in 0.1 ml. Few studies show half the dose for newborns. BCG vaccination should be given at birth. Some studies demonstrate increased tuberculin conversion after 1-3 months. BCG Vaccine Scar The BCG vaccine scar can range from 2-8 mm in size. Its measurement has no relation to induced immunity and is usually related to wheal size.
- 63.
- 64. • Lung abscessis a type of liquefactive necrosis of the lung tissue and formation of cavities (more than 2 cm) containing necrotic debris or fluid caused by microbial infection. • This pus-filled cavity is often caused by aspiration, which may occur during altered consciousness. Alcoholism is the most common condition predisposing to lung abscesses. • A lung abscess is a localized, pus-containing, necrotic lesion in the lung characterized by cavity formation. • Lung abscess is defined as necrosis of the pulmonary tissue and formation of cavities containing necrotic debris or fluid caused by microbial infection.
- 65. Causes – Aspiration offoreign body into lung. – Pulmonary embolus. – Trauma. – TB, necrotizing pneumonia. – Bronchial obstruction (usually a tumor) causes obstruction to bronchus, leading to infection distal to the growth. – Necrotizing pneumonia – Necrotizing tumors – Anaerobic bacteria: Actinomyces, Bacteroides, – Aerobicbacteria: Staphylococcus, Klebsiella, , Pseudomonas, Streptococcus, Mycobacteria – Fungi: Candida, – Septic emboli
- 66. Signs and symptoms •Cough, fever, and malaise • Headache, anaemia, weight loss, Dyspnea, weakness. • Pleuritic chest pain • Production of mucopurulent sputum, usually foul- smelling. • Chest may be dull to percussion, decreased or absent breath sounds, intermittent pleural friction rub.
- 67. Diagnosis • Chest X-rayand other imaging studies • Laboratory studies • bronchoscopy aspirates can also be cultured.
- 68. Management • Administration ofappropriate antimicrobial agent, usually by I.V. route, until clinical condition improves; then oral administration. • Chest postural drainage to drain cavity. • Bronchoscopy to drain abscess is controversial. • Nutritional management is usually a high-calorie, high-protein diet. • Pulmonary physiotherapy • postural drainage . • Surgical procedures are required in selective patients for drainage or pulmonary resection.
- 69. Nursing Diagnoses • IneffectiveBreathing Pattern related to presence of suppurative lung disease • Acute or Chronic Pain related to infection • Imbalanced Nutrition: Less Than Body Requirements related to catabolic state from chronic infection
- 70. CANCER OF THELUNG (BRONCHOGENIC CANCER)
- 71. • Bronchogenic cancerrefers to a malignant tumor of the lung arising within the wall or epithelial lining of the bronchus. • The lung is also a common site of metastasis by way of venous circulation or lymphatic spread. • Bronchogenic cancer is classified according to cell type: – Epidermoid (squamous cell) most common – Adenocarcinoma – Small cell (oat cell) carcinoma – Large cell (undifferentiated) carcinoma
- 72. Predisposing Factors – Cigarettesmoking amount, frequency, and duration of smoking have positive relationship to cancer of the lung. – Occupational exposure to arsenic, chromium, nickel, iron, radioactive substances, isopropyl oil, coal tar products, petroleum oil mists alone or in combination with tobacco smoke. – Age younger than 50 years – Radiation exposure
- 73. Warning signals oflung cancer – Any change in respiratory pattern – Persistent cough – Sputum streaked with blood – Hemoptysis – Rust color or purulent sputum – Fatigue – Chest, shoulder, back or arm pain – Recurring episodes of pleural effusion, pneumonia or bronchitis. – Unexplained dyspnea
- 74. Staging – Refers toanatomic extent of tumor, lymph node involvement, and metastatic spread. – Staging done by: • Tissue diagnosis • Lymph node biopsy • Mediastinoscopy
- 75. Clinical Manifestations • Usuallyoccur late and are related to size and location of tumor, extent of spread, and involvement of other structures – Cough, especially a new type or changing cough, results from bronchial irritation. – Dyspnea, wheezing (suggests partial bronchial obstruction). – Chest pain (poorly localized and aching) – Excessive sputum production, repeated upper respiratory infections – Haemoptysis – Malaise, fever, weight loss, fatigue, anorexia – Paraneoplastic syndrome metabolic or neurologic disturbances related to the secretion of substances by the neoplasm – Symptoms of metastasis bone pain; abdominal discomfort, nausea and vomiting from liver involvement; pancytopenia from bone marrow involvement; headache from CNS metastasis – Usual sites of metastasis ”lymph nodes, bones, liver
- 76. Diagnostic Evaluation – Computedtomography (CT) scan and positron-emission tomography (PET) scan are indicated because lung cancers may be partly or completely hidden by other structures on chest X-ray. – Cytologic examination of sputum/chest fluids for malignant cells. – Fiber-optic bronchoscopy for observation of location and extent of tumor; for biopsy. – PET scan—sensitive in detecting small nodules and metastatic lesions. – Lymph node biopsy; mediastinoscopy to establish lymphatic spread; to plan treatment. – Pulmonary function tests (PFTs) combined with split-function perfusion scan to determine if patient will have adequate pulmonary reserve to withstand surgical procedure.
- 77. Management • The treatmentdepends on the cell type, stage of disease, and the physiologic status of the patient. It includes a multidisciplinary approach that may be used separately or in combination, including: – Surgical resection. • Lobectomy • pneumonectomy – Radiation therapy. – Chemotherapy. – Immunotherapy.
- 78. Nursing Diagnoses – IneffectiveBreathing Pattern related to obstructive and restrictive respiratory processes associated with lung cancer – Imbalanced Nutrition: Less Than Body Requirements related to hyper metabolic state, taste aversion, anorexia secondary to radiotherapy/chemotherapy – Acute or Chronic Pain related to tumor effects, invasion of adjacent structures, toxicities associated with radiotherapy/chemotherapy – Anxiety related to uncertain outcome and fear of recurrence
- 79.
- 80. • Pulmonary embolism(PE) is a blockage of the lung's main artery or one of its branches by a substance that has traveled from elsewhere in the body through the bloodstream (embolism). • PE results from deep vein thrombosis (commonly a blood clot in a leg) that breaks off and migrates to the lung, a process termed venous thrombo embolism (VTE).
- 82. • Pulmonary embolismrefers to the obstruction of one or more pulmonary arteries by a thrombus (or thrombi) originating usually in the deep veins of the legs, the right side of the heart or, rarely, an upper extremity, which becomes dislodged and is carried to the pulmonary vasculature. • Pulmonary infarction refers to necrosis of lung tissue that can result from interference with blood supply.
- 83. Causes • Predisposing factorsinclude: – Stasis, prolonged immobilization. – Concurrent phlebitis. – Previous heart (heart failure, myocardial infarction [MI]) or lung disease. – Injury to vessel wall. – Coagulation disorders. – Metabolic, endocrine, vascular, or collagen disorders. – Malignancy. – Advancing age, estrogen therapy.
- 84. Pathophysiology – Obstruction, eitherpartial or full, of pulmonary arteries, – which causes decrease or absent blood flow; – there is ventilation but no perfusion – Increased pulmonary vascular resistance – Increased pulmonary artery pressure (PAP) – Increased right ventricular workload to maintain pulmonary blood flow – Decreased cardiac output – Decreased blood pressure – Shock
- 85. Clinical Manifestations • Dyspnea,Pleuritic pain, tachypnea, • Chest pain • Cyanosis, tachyarrhythmia's, syncope, circulatory collapse • Pleural friction rub • cough and hemoptysis (coughing up blood). • More severe cases can include signs such as cyanosis (blue discoloration, usually of the lips and fingers), • collapse, and circulatory instability because of decreased blood flow through the lungs and into the left side of the heart.
- 86. Diagnostic Evaluation • ABGlevels : decreased Pao2 is usually found, due to perfusion abnormality of the lung. • Chest X-ray • Pulmonary angiogram
- 87. Management • Oxygen isadministered to relieve hypoxemia, respiratory distress, and cyanosis. • An infusion is started to open an I.V. route for drugs and fluids. • Vasopressors, inotropic agents such as dopamine (Intropin), and antidysrhythmic agents may be indicated to support circulation if the patient is unstable. • ECG is monitored continuously for right-sided heart failure, which may have a rapid onset. • Small doses of I.V. morphine are given to relieve anxiety, alleviate chest discomfort (which improves ventilation), and ease adaptation to mechanical ventilator, if this is necessary. • Pulmonary angiography, hemodynamic measurements, ABG analysis, and other studies are carried out.
- 88. • Oral anticoagulationwith warfarin (Coumadin) is usually used for follow-up anticoagulant therapy after heparin therapy has been established • Thrombolytic agents, such as streptokinase (Streptase), may be used in patients with massive pulmonary embolism.
- 89. Surgery • Used inferiorvena cava filter. • If anticoagulant therapy is contraindicated (e.g. shortly after a major operation), an inferior vena cava filter may be implanted to prevent new emboli from entering the pulmonary artery and combining with an existing blockage. It should be removed as soon as it becomes safe to start using anticoagulation. • (pulmonary thrombectomy).
- 90. Nursing Diagnoses • IneffectiveBreathing Pattern related to acute increase in alveolar dead airspace and possible changes in lung mechanics from embolism • Ineffective Tissue Perfusion (Pulmonary) related to decreased blood circulation • Acute Pain (pleuritic) related to congestion, possible pleural effusion, possible lung infarction • Anxiety related to dyspnea, pain, and seriousness of condition • Risk for Injury related to altered hemodynamic factors and anticoagulant therapy
- 91.
- 92. Respiratory failure • Itis inadequate gas exchange by respiratory system. • It is a broad, non-specific clinical diagnosis indicating that the respiratory system is unable to supply the oxygen necessary to metabolism or can not eliminate sufficient carbon dioxide.
- 93. Classification Acute respiratory failure •It is defined as a partial pressure of arterial oxygen {PaO2} of 55 mmHg or less on room air or PaCo2 of 55 mmHg or more. • It may be classified as : – Hypoxemic respiratory failure – Ventilatory failure
- 94. • Hypoxemic respiratoryfailure / low blood oxygen level : • It may be caused by diffuse problem such as pulmonary edema, ARDS, or localized problem such as pneumonia, bleeding from chest, or lung tumor. • Ventilatory or hypercapnic respiratory failure : • When the client is unable to support adequate gas exchange that can result from CNS depression, inadequate neuromuscular ability to sustain breathing or respiratory system overload.
- 95. • HYPOXEMIC RESPIRATORYFAILURE –Pulmonary edema
- 96.
- 98. Pulmonary Edema • Pulmonaryedema is an abnormal buildup of fluid in the lungs. This buildup of fluid leads to shortness of breath. Pulmonary edema or oedema is fluid accumulation in the air spaces and parenchyma of the lungs. It leads to impaired gas exchange and may cause respiratory failure. • Pulmonary edema is defined as abnormal accumulation of fluid in the lung tissue and/or alveolar space. It is a severe, life threatening condition
- 99. Causes • Bacterial infections •Hypervolemia Or A Sudden Increase In The Intravascular Pressure In The Lung. • Pneumothorax • Pleural Effusion • Inhalation of hot or toxic gases • Pulmonary contusion, i.e., high-energy trauma (e.g. vehicle accidents) • Aspiration, e.g., gastric fluid • thoracocentesis, • removal of endobronchial obstruction • Reperfusion injury, or lung transplantation • Multiple blood transfusions • Pulmonary Hypertension • Other respiratory disease condition
- 100. • Pathophysiology – Dueto etiological factor – Result Of Increased Microvascular Pressure From Abnormal Cardiac Function. – The Backup Of Blood Into The Pulmonary Vasculature Resulting From Inadequate Left Ventricular Function – An Increased Microvascular Pressure, – Fluid Begins To Leak Into The Interstitial Space And The Alveoli. – Impaired gas exchange – Decrease PaO2 & increased Paco2 – Ischemic lung injury – Reduce air flow – Brain stem infarction – Neuro musculer diseases – Muscle weaknes – Decreased Co2 excretion – Increased PaCo2
- 101. Clinical Manifestations Symptoms ofpulmonary edema may include: • Dyspnea • Coughing up blood or bloody froth • Chest pain • Excessive sweating • Anxiety • Pale skin • Pink frothy sputum (which may be coughed up) • Anxiety or restlessness • Decrease in level of alertness (consciousness) • Leg or abdominal swelling
- 102. Diagnostic investigation – Historycollection – Physical examination – Blood chemistries – Blood oxygen levels(oximetry or arterial blood gases) – Chest x-ray – Complete blood count (CBC) – Echocardiogram (ultrasound of the heart) to see if there are problems with the heart muscle – Electrocardiogram (ECG) to look for signs of a heart attack or problems with the heart rhythm
- 103. Treatment • Pulmonary edemais almost always treated in the emergency room or hospital. You may need to be in an intensive care unit (ICU). • Oxygen is given through a face mask or tiny plastic tubes are placed in the nose. • A breathing tube may be placed into the windpipe (trachea) so you can be connected to a breathing machine (ventilator) if you cannot breathe well on your own. • The cause of edema should be identified and treated quickly. For example, if a heart attack has caused the condition, it must be treated right away. • IABP intra aortic balloon pump • Diuretics that remove excess fluid from the body • Medicines that strengthen the heart muscle, control the heartbeat, or relieve pressure on the heart
- 104.
- 105. • Ventilatory failureis rise in PaCo2 [hypercapnia]that occurs when the respiratory load can no longer be supported by the strength or activity of the system. Causes – Drug overdose – Stroke – Tumors – Tetanus – Pneumothorax – Pneumonia – Chronic obstructive pulmonary disease (COPD) (chronic bronchitis, emphysema). – Severe asthma. – Cystic fibrosis.
- 106. Clinical Manifestations • Hypoxemiarestlessness, agitation, dyspnea, disorientation, confusion, delirium, loss of consciousness. • Hypercapnia headache, dizziness, confusion. • Tachypnea initially; then when no longer able to compensate, bradypnea • Accessory muscle use • Pulsus paradoxus
- 107. Diagnostic Evaluation – ABGanalysis show changes in Pao2, Paco2, and pH from patient's normal; or Pao2 less than 50 mm Hg, Paco2 greater than 50 mm Hg, pH less than 7.35. – Pulse oxymetery decreasing Sao2. – End tidal CO2 monitoring elevated. – Complete blood count, serum electrolytes, chest X-ray, urinalysis, electrocardiogram (ECG), blood and sputum cultures to determine underlying cause and patient's condition
- 108. Management – Oxygen therapyto correct the hypoxemia. – Chest physical therapy and hydration to mobilize secretions. – Bronchodilators and possibly corticosteroids to reduce bronchospasm and inflammation. – Diuretics for pulmonary congestion. – Mechanical ventilation as indicated. Non-invasive positive-pressure ventilation using a face mask may be a successful option for short-term support of ventilation. – Provide E.T. • Oral- short term • Nasal- long term
- 109.
- 110. Previously known asRDS • RESPIRATORY DISTRESS SYNDROME OR SHOCK LUNG • It is a sudden progressive form of respiratory failure, characterized by severe Dyspnea, hypoxia & diffuse bilateral infiltration. • ARDS is a disease of lung parenchyma that leads to impaired gas exchange.
- 111. Causes • Direct pulmonarytrauma – Viral infection – Bacterial infection – Fungal infection – Pneumonia – Fat emboli – Inhaled toxins • Direct pulmonary trauma – Sepsis shock – Drugs over dose – Radiation therapy
- 112. Phases • Phase -1exudative – It is approximately 24 hours after the initial insult & consist of damage to the capillary endothelium & leakage of fluid into pulmonary interstistium which increases pulmonary artery pressure. – Exudates move or pass slowly as it through a small opening or passages. – Inflammatory responses of parenchyma damage
- 113. • Phase -2proliferative – It begins about 7-10 days. In this phase growing and increasing in number rapidly. – Alveolar cell r ultimately damaged. – Hypoxemia is present & decreased surfactant production which leads to V/Q mismatch.
- 114. • Phase -3fibrotic – It occurs in about 2-3 weeks. There is deposition of fibrin into the lungs than cause lung compliance & worsening hypoxemia, V/Q mismatch.
- 115. Pathophysiology – Lung injury –Release of vasoactive substance – Increased permeability of alveolar membrane – Fluid and proteins move into the alveoli – Altered V/Q – Damage alveolar epithelium – Decrease surfactant production – Atelectasis – Regeneration of alveolar membrane with thick epithelial cell – Scarring & loss of lungs function
- 116. Clinical manifestation • Hypoxemia •Dyspnea • Thick frothy sputum • Atelectasis • Tachypnea • Cough • Crackle sound hear on auscultation
- 117. Diagnostic investigations – Thehallmark sign for ARDS is a shunt; hypoxemia remains despite increasing oxygen therapy. – Decreased lung compliance; increasing pressure required to ventilate patient on mechanical ventilation. – Chest X-ray exhibits bilateral infiltrates. – Pulmonary artery catheter readings: pulmonary artery wedge pressure >18 mm Hg
- 118. Management – The underlyingcause for ARDS must be determined so appropriate treatment can be initiated. – Ventilator support with PEEP will be instituted. PEEP keeps the alveoli open, thereby improving gas exchange. – Fluid management must be maintained – Pulmonary artery catheter monitoring and inotropic medication can be helpful. – Medications are aimed at treating the underlying cause. Corticosteroids are used infrequently due to the controversy regarding benefits of usage. – Adequate nutrition should be initiated early and maintained.
- 119. – Provide nitricoxide to dilate the capillary bed of lungs & help in vasodilatation. – Oxygen therapy – Antibiotic therapy – Steroids
- 120. Specific treatments forrespiratory failure Providers may use medications or procedures to treat respiratory failure, including: • Mechanical ventilation. Providers use a breathing machine and a tube that goes into your airways to move air in and out of your lungs. • Extracorporeal membrane oxygenation (ECMO). Providers use a bypass machine to add oxygen to your blood and remove carbon dioxide. • Oxygen therapy. A machine delivers extra oxygen through a breathing mask or small tube (cannula). You may get oxygen at home or in the hospital. • Fluids. Your provider can give you fluids through an IV (directly to a vein). This can improve the blood flow through your body, bringing more oxygen to your tissues. • Managing underlying conditions. You provider may treat you with other medications or procedures, depending on what’s causing respiratory failure.
- 123. • Respiratory arrest(and impaired respiration that can progress to respiratory arrest) can be caused by • Airway obstruction • Decreased respiratory effort • Respiratory muscle weakness
- 126. Management Respiratory arrest isa life-threatening medical emergency that requires immediate medical attention. The goal of management is to restore adequate ventilation and prevent further damage. Some interventions for respiratory arrest include • Oxygen: Provide oxygen to the patient. The recommended oxygen saturation is 94% SpO2 or higher, but 100% SpO2 is the goal. • Airway: Open the airway and maintain it with advanced airways like an endotracheal tube (ETT), laryngeal mask airway (LMA), or laryngeal tube. • Ventilation: Provide basic ventilation or use a bag-valve mask to deliver breaths. The patient's chest should rise and fall with each breath. • Suction the mouth and oropharynx to remove secretions and maintain a clear airway. • Administer medications to address the underlying causes of the respiratory arrest. • Effective CPR requires a team, led by a senior attending physician who directs resuscitation.
- 127.
- 128. • IT isinjury of the thoracic cage & can restrict the heart ability to pump blood or the lungs ability to exchange air & oxygenated blood. • Major danger associated with chest injuries r: – Interstitial bleeding – Punctured organs
- 129. CHEST INJURIES BLUNT INJURIESPENETRATING INJURIES
- 130. • BLUNT INJURIES:r most commonly deceleration injuries associated with motor vehicle, crashes. It may result from falls or blows of the chest. • PENETRATING INJURIES: it is an open chest wound permitting atmospheric air into the pleural space & disrupting the normal vacuum ventilation mechanism.
- 131. BLUNT • RIB FRACTURE •FRACTURED STERNUM • FLAIL CHEST PENETRATING • PNEUMOTHORAX • TRAUMATIC PNEUMOTHORAX • TENSION PNEUMPTHORAX • HEMOTHORAX
- 132. Rib Fracture – Mostcommon chest injury. – May interfere with ventilation and may lacerate underlying lung. – Causes pain at fracture site; painful, shallow respirations; localized tenderness and crepitus (crackling) over fracture site
- 133. • Fracture inribs associated with any kind of blunt injury. The 5 -9th r most commonly affected. • It is associated with blunt injury such as a fall, etc. S/S – Localized pain & tenderness over the fracture area on inspiration & expiration. – Dislocation, protruding bone – Shallow respiration – Click sound sensation on inspiration – Ineffective cough – Dyspnea – Weak lungs – Abnormal V/Q – Infection
- 134. Management • Rapid mobilizationto hospital. • Pain control • Give analgesics (usually nonopioid) to assist in effective coughing and deep breathing. • Encourage deep breathing with strong inspiration; give local support to injured area by splinting with hands. • Assist with intercostal nerve block to relieve pain so coughing and deep breathing may be accomplished. An intercostal nerve block is the injection of a local anesthetic into the area around the intercostal nerves to relieve pain temporarily after rib fractures, chest wall injury, or thoracotomy. • For multiple rib fractures, epidural anesthesia may be used. • Pulmonary physiotherapy
- 135. FRACTURED STERNUM • ITIs usually result from blunt deceleration injuries such as impact from a steering wheel. C/M: -- sharp, stabbing pain, swelling & discoloration over the fractured site & creptius Management -Analgesics -Intercostals nerve blocks -Surgical fixation
- 137. Flail Chest{ portionof the rib cage is seprated from the rest of chest} – Loss of stability of chest wall as a result of multiple rib fractures, or combined rib and sternum fractures. – When this occurs, one portion of the chest has lost its bony connection to the rest of the rib cage. – During respiration, the detached part of the chest will be pulled in on inspiration and blown out on expiration (paradoxical movement) – Normal mechanics of breathing are impaired to a degree that seriously jeopardizes ventilation, causing Dyspnea and cyanosis,creptius, hypoxia, – Hypercapnia, abnormalV/Q. – Generally associated with other serious chest injuries; lung contusion, lung laceration, diffuse alveolar damage
- 139. Management – Stabilize theflail portion of the chest with hands; apply a pressure dressing and turn the patient on injured side, or place 10-lb sandbag at site of flail. – Thoracic epidural analgesia may be used for some patients to relieve pain and improve ventilation. – If respiratory failure is present, prepare for immediate ET intubation and mechanical ventilation—treats underlying pulmonary contusion and serves to stabilize the thoracic cage for healing of fractures, improves alveolar ventilation, and restores thoracic cage stability and intrathoracic volume by decreasing work of breathing. – Prepare for operative stabilization of chest wall in select patients.
- 140.
- 141. • It isthe presence of air in the pleural space that prohibits complete lung expansion. • It is an abnormal collection of air or gas in the pleural space that separate the lung from the chest wall. • It is often called collapsed lung.
- 142. PNEUMOTHORAX CLASSIFICATION • ASPONTANEOUS PNEUMOTHORAX: it may be idiopathic. A spontaneous Pneumothorax onset of air in the pleural space with deflation of the affected lung in the absence of trauma. • OPEN PNEUMOTHORAX: (sucking wound of chest) implies an opening in the chest wall large enough to allow air to pass freely in and out of thoracic cavity with each attempted respiration. • TRAUMATIC PNEUMOTHORAX : is a collapse lung resulting from either blunt force trauma to the chest wall or the creation of an open sucking chest wound caused by motor-vehicle accidents etc. • TENSION PNEUMOTHORAX: build up of air under pressure in the pleural space resulting in interference with filling of both the heart and lungs
- 143. CAUSES Spontaneous Pneumothorax • Blebor bulla • Emphysema • AIDs • T.B. • Cocaine use Traumatic Pneumothorax • Chest surgery • Thoracentsis • Gun shot wound • Knife wound • Motor vehicle accidents • Fractured Rib
- 144. Clinical manifestation – Hyperresonance; diminished breath sounds. – Reduced mobility of affected half of thorax. – Tracheal deviation away from affected side in tension Pneumothorax – Clinical picture of open or tension Pneumothorax is one of air hunger, agitation, hypotension, and cyanosis – Mild to moderate Dyspnea and chest discomfort may be present with spontaneous Pneumothorax – Decreased tactile fermitus
- 145. Diagnostic Evaluation • ChestX-ray confirms presence of air in pleural space.
- 146. Management Spontaneous Pneumothorax • Treatmentis generally non operative if Pneumothorax is not too extensive. – Observe and allow for spontaneous resolution for less than 50% Pneumothorax in otherwise healthy person. – Needle aspiration or chest tube drainage may be necessary to achieve re expansion of collapsed lung if greater than 50% Pneumothorax. • Surgical intervention by pleurodesis or thoracotomy with resection of apical blebs is advised for patients with recurrent spontaneous Pneumothorax.
- 149. Tension Pneumothorax – Immediatedecompression to prevent cardiovascular collapse by Thoracentsis or chest tube insertion to let air escape. – Chest tube drainage with underwater-seal suction to allow for full lung expansion and healing
- 151. Open Pneumothorax – Closethe chest wound immediately to restore adequate ventilation and respiration. • Patient is instructed to inhale and exhale gently against a closed glottis (Valsalva maneuver) as a pressure dressing (petroleum gauze secured with elastic adhesive) is applied. This maneuver helps to expand collapsed lung. – Chest tube is inserted and water-seal drainage set up to permit evacuation of fluid/air and produce reexpansion of the lung. – Surgical intervention may be necessary to repair trauma.
- 152. Hemothorax – Blood inpleural space as a result of penetrating or blunt chest trauma. – Accompanies a high percentage of chest injuries. – Can result in hidden blood loss – Patient may be asymptomatic, dyspneic, apprehensive, or in shock
- 153. HEMOTHORAX • It maybe present in client with chest injuries. • A small amount of blood more than 300 ml in the pleural space may cause no clinical manifestation and may require no intervention with the blood being reabsorbed spontaneously. • Severe Hemothorax {1400-2500ml} may be life threatening becoz of resultant hypovolemia & tension.
- 154. Clinical manifestation – Respiratorydistress – Shock – Dullness upon percussion of the affected side.
- 155. Management – Assist withThoracentsis to aspirate blood from pleural space, if being done before a chest tube insertion.( 7th & 8th intercostal space) – Assist with chest tube insertion and set up drainage system for complete and continuous removal of blood and air. • Auscultate lungs and monitor for relief of dyspnea. • Monitor amount of blood loss in drainage. – Replace volume with I.V. fluids or blood products.
- 158. PULMONARY HEART DISEASE /CORPULMONALE
- 160. COR PULMONALE • Pulmonaryheart disease (cor pulmonale) is an alteration in the structure or function of the right ventricle resulting from disease of lung structure or function or its vasculature (except when this alteration results from disease of the left side of the heart or from congenital heart disease). It is heart disease caused by lung disease.
- 161. Pathophysiology and Etiology –Condition that deprives lungs of oxygen: hypoxemia, hypercapnia, acidosis, circulatory complications, pulmonary hypertension, right heart enlargement, right- sided heart failure. – Etiology includes: • Pulmonary vascular disease. • Pulmonary embolism. • COPD.
- 162. Clinical Manifestations – Increasingdyspnea and fatigue; progressive dyspnea (orthopnoea, paroxysmal nocturnal dyspnea), chronic cough. – Distended jugular veins, peripheral edema, hepatomegaly. – Bibasilar crackles and split second heart sound on (auscultation of chest , lung sound on the base of right and left lung) – Manifestations of CO2 narcosis headache, confusion, somnolence{ strong desire for sleep bcoz of drowsiness), coma
- 163. Diagnostic Evaluation – ABGlevels decreased Pao2 and pH, increased Paco2. – PFTs may show airway obstruction. – ECG changes are consistent with right ventricular hypertrophy. – Chest X-ray shows right heart enlargement. – Echocardiogram shows right heart enlargement.
- 165.
- 168. Management • Goal: treatmentof underlying lung disease and management of heart disease. – Long-term, low-flow oxygen to improve oxygen delivery to peripheral tissues, thus decreasing cardiac work and lessening sympathetic vasoconstriction. Liter flow individualized during activities, rest, and sleep. – Diuretics to lower PAP by reducing total blood volume and excess fluid in lungs. – Pulmonary vasodilators such as nitroprusside (Nitropress); hydralazine (Apresoline); calcium channel blockers to dilate pulmonary vascular bed and reduce pulmonary vascular resistance; use is controversial. – Bronchodilators to improve lung function. – Mechanical ventilation, if patient in respiratory failure. – Sodium restriction to reduce edema.