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Lower Respiratory Tract Conditions.ppt

Conditions affecting lower respiratory tract

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LOWER RESPIRATORY TRACT CONDITIONS
Lower Respiratory Tract Conditions.ppt
Lower Respiratory Tract Conditions.ppt
Lower Respiratory Tract Conditions.ppt
ATELECTASIS
Definition
• Atelectasis refers to closure or collapse of alveoli.
• It may be acute or chronic and may cover a broad
range of pathophysiologic changes, from micro
atelectasis (which is not detectable on chest x-ray) to
loss of segmental, lobar, or overall lung volume
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Lower Respiratory Tract Conditions.ppt

  • 6. Definition • Atelectasis refers to closure or collapse of alveoli. • It may be acute or chronic and may cover a broad range of pathophysiologic changes, from micro atelectasis (which is not detectable on chest x-ray) to loss of segmental, lobar, or overall lung volume
  • 7. Pathophysiology •Atelectasis may occur in the adult as a result of reduced alveolar ventilation or any type of blockage that impedes the passage of air to and from the alveoli that normally receive air through the bronchi and network of airways. •The trapped alveolar air becomes absorbed into the bloodstream, but outside air cannot replace the absorbed air because of the blockage. •As a result, the isolated portion of the lung becomes airless
  • 11. • Risk factors • The postoperative patient is at high risk for atelectasis because of the numerous respiratory changes that may occur. • A low tidal breathing pattern may cause airway closure and alveolar collapse. • This results from the effects of anesthesia or analgesic agents, supine positioning, splinting of the chest wall because of pain, and abdominal distention. • The postoperative patient may also have secretion retention, airway obstruction, and an impaired cough reflex or may be reluctant to cough because of pain.
  • 12. • Atelectasis may also result from excessive pressure on the lung tissue, which restricts normal lung expansion on inspiration. • Such pressure may be produced by fluid accumulating within the pleural space (pleural effusion), air in the pleural space (pneumothorax), or blood in the pleural space (hemothorax) • Pressure may also be produced by a pericardium distended with fluid (pericardial effusion), tumor growth within the thorax, or an elevated diaphragm.
  • 13. • Musculoskeletal or neurologic disorders or debilitated, bedridden patients, restrictive defects, and specific surgical procedures (eg, upper abdominal, thoracic, or open heart surgery), may lead to bronchial obstruction by secretions and impaired cough mechanisms resulting into atelectasis.
  • 14. Clinical Manifestations •Cough, sputum production, and low-grade fever. •Fever is universally cited as a clinical sign of atelectasis- Infection or inflammation distal to the obstructed airway. •In acute atelectasis involving a large amount of lung tissue(lobar atelectasis), marked respiratory distress may be observed.
  • 15. • Dyspnea, tachycardia, tachypnea, pleural pain, and central cyanosis (a bluish skin hue that is a late sign of hypoxemia). • The patient characteristically has difficulty breathing in the supine position and is anxious. • The signs and symptoms of a pulmonary infection also may be present.
  • 16. Assessment and Diagnostic Findings • Decreased breath sounds and crackles are heard over the affected area. • Chest x-ray findings may reveal patchy infiltrates or consolidated areas. • In the patient who is confined to bed, atelectasis is usually diagnosed by chest x-ray • Depending on the degree of hypoxemia, pulse oximetry (SpO2) may demonstrate a low saturation of hemoglobin with oxygen (less than 90%) or a lower- than-normal partial pressure of arterial oxygen (PaO2).
  • 17. Management •The goal is to improve ventilation and remove secretions. •Before initiating more complex, costly, and labor- intensive therapies, the nurse should ask several questions:
  • 18. • Has the patient been given an adequate trial of deep breathing exercises? I.e. Has the patient received adequate education, supervision, and coaching to carry out the deep-breathing exercises? • Have other factors been evaluated that may impair ventilation or prohibit a good patient effort (eg, lack of turning, mobilization; excessive pain; excessive sedation)? • If the cause of atelectasis is bronchial obstruction from secretions, the secretions must be removed by coughing or suctioning to permit air to re-enter that portion of the lung.
  • 19. •Chest physical therapy(chest percussion and postural drainage) may also be used to mobilize secretions. •Nebulizer treatments with a bronchodilator medication or sodium bicarbonate may be used to assist the patient in the expectoration of secretions. •Deep breathing exercise- Use of spirometer to enhance lung expansion
  • 23. INDICATIONS OF SPIROMETRY • Post operatively to prevent atelectasis • Pneumonia • Restrictive Lung disease associated with dysfunctional diaphragm • Cystic Fibrosis • Those with respiratory capacity of less than 2.5L • COPD
  • 24. • If respiratory care measures fail to remove the obstruction, a bronchoscopy is performed. • Severe or massive atelectasis may lead to acute respiratory failure, especially in a patient with underlying lung disease. • Endotracheal intubation and mechanical ventilation may be necessary. • Prompt treatment reduces the risk for acute respiratory failure or pneumonia.
  • 25. •If atelectasis has resulted from compression of lung tissue, the goal is to decrease the compression. •With a large pleural effusion that is compressing lung tissue and causing alveolar collapse, treatment may include thoracentesis •Management of chronic atelectasis focuses on removing the cause of the obstruction of the airways or the compression of the lung tissue. •The goal is to reopen the airways and provide ventilation to the collapsed area. •In some cases, surgical management may be indicated.
  • 26. Prevention  Change patient’s position frequently, especially from supine to upright position, to promote ventilation and prevent secretions from accumulating. Encourage early mobilization from bed to chair followed by early ambulation.  Encourage appropriate deep breathing and coughing to mobilize secretions and prevent them from accumulating.
  • 27. Teach/reinforce appropriate technique for incentive spirometry. Administer prescribed opioids and sedatives judiciously to prevent respiratory depression. Perform postural drainage and chest percussion, if indicated. Institute suctioning to remove tracheobronchial secretions, if indicated.
  • 28. End
  • 30. Definition • A collection of fluid in the pleural space. • It is rarely a primary disease process but is usually secondary to other diseases. • Normally, the pleural space contains a small amount of fluid (5 to 15 mL), which acts as a lubricant that allows the pleural surfaces to move without friction.
  • 31. • Pleural effusion may be a complication of heart failure, TB, pneumonia, pulmonary infections (particularly viral infections), nephritic syndrome, connective tissue disease, pulmonary embolism, and neoplastic tumors. • Bronchogenic carcinoma is the most common malignancy associated with a pleural effusion.
  • 32. Pathophysiology • The effusion can be composed of a relatively clear fluid, or it can be bloody or purulent. • An effusion of clear fluid may be a transudate or an exudate. • A transudate (filtrates of plasma that move across intact capillary walls) occurs when factors influencing the formation and reabsorption of pleural fluid are altered, usually by imbalances in hydrostatic or oncotic pressures.
  • 33. • The finding of a transudative effusion generally implies that the pleural membranes are not diseased. The most common cause of a transudative effusion is heart failure. • An exudates (extravasation of fluid into tissues or a cavity) usually results from inflammation by bacterial products or tumors involving the pleural surfaces.
  • 34. Clinical Manifestations • Usually the clinical manifestations are those caused by the underlying disease. • Pneumonia causes fever, chills, and pleuritic chest pain, whereas a malignant effusion may result in dyspnea and coughing. • The size of the effusion and the patient’s underlying lung disease determine the severity of symptoms. • A large pleural effusion causes shortness of breath. • When a small to moderate pleural effusion is present, dyspnea may be absent or only minimal.
  • 35. Assessment and Diagnostic Findings • Assessment of the area of the pleural effusion reveals decreased or absent breath sounds, decreased fremitus, and a dull, flat sound when percussed. • In an extremely large pleural effusion, the assessment reveals a patient in acute respiratory distress. • Tracheal deviation away from the affected side may also be noted. • Physical examination, chest x-ray, chest CT scan, and thoracentesis confirm the presence of fluid.
  • 36. Medical Management The objectives of treatment are to: •Discover the underlying cause, •Prevent reaccumulation of fluid, •Relieve discomfort, dyspnea, and respiratory compromise. •Specific treatment is directed at the underlying cause (eg, heart failure, pneumonia, lung cancer, cirrhosis
  • 37. • If the pleural fluid is an exudate, more extensive diagnostic procedures are performed to determine the cause. • Treatment for the primary cause is then instituted. • Thoracentesis is performed to remove fluid, to obtain a specimen for analysis, and to relieve dyspnea and respiratory compromise. • Thoracentesis may be performed under ultrasound guidance.
  • 38. • • Depending on the size of the pleural effusion, the patient may be treated by removing the fluid during the thoracentesis procedure or by inserting a chest tube connected to a water-seal drainage system or suction to evacuate the pleural space and re-expand the lung.
  • 39. • If the underlying cause is a malignancy, however, the effusion tends to recur within a few days or weeks. • Repeated thoracentesis result in pain, depletion of protein and electrolytes, and sometimes pneumothorax. • Once the pleural space is adequately drained, a chemical pleurodesis may be performed to obliterate the pleural space and prevent reaccumulation of fluid. • Pleurodesis may be performed using a thoracoscopic approach or via a chest tube. Chemically irritating agents (eg.,bleomycin or talc) are instilled in the pleural space.
  • 40. • With the chest tube insertion approach, after the agent is instilled, the chest tube is clamped for 60 to 90 minutes and the patient is assisted to assume various positions to promote uniform distribution of the agent and to maximize its contact with the pleural surfaces. • The tube is unclamped as prescribed, and chest drainage may be continued several days longer to prevent reaccumulation of fluid and to promote the formation of adhesions between the visceral and parietal pleurae. • Other treatments for malignant pleural effusions include surgical pleurectomy,
  • 41. Nursing Management • The nurse’s role in the care of the patient with a pleural effusion includes implementing the medical regimen. • The nurse prepares and positions the patient for thoracentesis and offers support throughout the procedure. • Pain management is a priority, and the nurse assists the patient to assume positions that are the least painful. • However, frequent turning and ambulation are important to facilitate drainage. • The nurse administers prescribed analgesics and as needed.
  • 42. • If a chest tube drainage and water-seal system is used, the nurse is responsible for monitoring the system’s function and recording the amount of drainage at prescribed intervals. • Nursing care related to the underlying cause of the pleural effusion is specific to the underlying condition. • If the patient is to be managed as an outpatient with a pleural catheter for drainage, the nurse is responsible for educating the patient and family regarding management and care of the catheter and drainage system.
  • 43. END
  • 45. Definition • Air within the pleural cavity • The air enters via a defect in the visceral pleura (e.g. ruptured bulla) or the parietal pleura (e.g. puncture following rib fracture)
  • 46. Types of Pneumothorax • Simple Pneumothorax This occurs as air enters the pleural space through a ruptured bleb/blister on the surface of the lungs or a bronchopleural fistula Clinical condition stable Can wait for CXR to confirm diagnosis
  • 47. • Traumatic pneumothorax Occurs when air escapes from a laceration in the lungs and enters the pleural space or from a wound in the chest wall May be caused by a blunt trauma, penetrating chest or abdominal trauma or diaphragmatic tears It may also occur during invasive procedures in which the pleura is punctured-Thoracentesis
  • 48. • Open traumatic Pneumothorax – Wound in chest wall is large enough to allow free movement of air to and from the pleural space • In such the lungs collapse and there is a shift of the mediastinum towards the uninjured side with each inspiration and in the opposite direction with expiration
  • 49. • Tension Pneumothorax –Progressive build up of air in the pleural space, causing a shift of the heart and mediastinal structures away from side of pneumothorax –The air that enters the pleural cavity with each inspiration is trapped and cannot be expelled –With each breath pressure increases in the pleural cavity
  • 50. –The lungs collapse and there is a mediastinum shift to the unaffected side –Both respiration and circulatory functions are compromised due to increased intrathoracic pressure that decreases venous return to the heart and decreased cardiac output –Clinical condition unstable –Do not wait for CXR to confirm
  • 51. Causes of Pneumothorax • Spontaneous –Rupture of an apical bleb • Traumatic –With rib fractures –Penetrating chest trauma • Pre-existing lung abnormality –Pulmonary fibrosis –Asthma –Vasculitis –Pulmonary metastases close to edge of lung
  • 52. Clinical Manifestations • Depend on the size and cause • Sudden pain that is pleuritic • Acute respiratory distress in severe pneumothorax • Anxiety • Dypsnea • Air hunger • Central cyanosis • Diminished breath sounds
  • 53. • In tension pneumothorax; • Trachea shifts to the unaffected side • Decreased chest expansion • Hyperresonant on percussion
  • 54. MANAGEMENT • Depends on its cause and severity • The goal is to evacuate the air from the pleural cavity • A chest tube is inserted to remove the air and any fluid in the cavity • Treatment of the underlying cause
  • 57. Definition •Inflammation of lung parenchyma and caused by different microorganisms •Bacteria, fungi, viruses mycobacteria •Pneumonitis- The inflammatory process of the lung tissue that predisposes the patient to microbial invasion •Most common type of infectious disease of the lung
  • 58. Pneumonia Risk Factors • History of nosocomial pneumonia within the last 6 to 12 months • Diagnosed lung disease (COPD) • Recent hospitalization • Nursing home residence • Smoking • Alcoholism • Neurologic disease
  • 59. Pneumonia Risk Factors Immunosuppression Severe protein-calorie malnutrition Heart failure Antibiotic therapy during the previous month Enteral feeding by nasogastric tube.
  • 60. Microbial pathogens enter the lung by: Aspiration of organisms from oropharynx More common in patients with impaired level of consciousness , Alcoholics, stroke, anesthesia, swallowing disorders, NG tubes, EndoTrachealTubes (ETT)
  • 61. Inhalation of Infectious Aerosols Influenza, Legionella, Psittacosis, Histoplasmosis, TB Hematogenous : Dissemination Staph aureus Direct inoculation and Spread Tracheal intubation, stab wounds
  • 62. PATHOPHYSIOLOGY  The streptococci reach the alveoli and lead to inflammation and pouring of an exudates into the air spaces.  WBCs migrates to alveoli, the alveoli become more thick due to its filling and consolidation  The inflamed areas are not adequately ventilated, due to secretion and edema.  This will lead to partial occlusion of alveoli and bronchi causing a decrease in alveolar oxygen content.
  • 63.  Venous blood goes to affected areas without being oxygenated and returns to the heart.  This will lead to arterial hypoxemia and even death due to interference with ventilation.  If substantial portion of one or more lobes is involved- Lobar pneumonia  Pneumonia originating from the bronchi and extending to the lungs- Bronchopneumonia  More common than lobar pneumonia
  • 64. Signs and Symptoms  Varies depending on the type, causal organism and presence of underlying diseases  Those with streptococcal pneumonia have:  Cough-Sputum production  Sudden onset of chills  Rapidly raising Fever  Chest pain that increases with deep breathing and coughing  Changes in function, appetite  Orthopnia
  • 65.  Patient is severely ill with marked tachypnea and general respiratory distress- shortness of breath, use of accessory muscles  Rapid and bounding heart rate – usually increases by 10bpm for every degree Celsius of temperature elevation  Diaphoresis and tires easily
  • 66. Pneumonia Diagnosis  History taking  PE  Chest X-ray  Blood culture  Sputum specimen  Pulse oximetry  Blood chemistry analysis
  • 67. Classification  Community acquired  Hospital acquired  Pneumonia in the immunocompromised host  Aspiration pneumonia
  • 68. Community Acquired  Occur either in a community setting or within 48 hours after hospitalization  Most commonly caused by: S pneumonia (most Common) , H. influenza, Pseudomonas aeruginosa  S. pneumonia (most Common) in people less than 60 years without comorbidity and older with comorbidity  May follow a recent respiratory illness  H. influenza cause pneumonia in elderly people and those with co morbidity (COPD), alcoholism, DM,
  • 69.  Viruses are most common cause in children  Cytomegalovirus in immunocompromised adults  The acute stage of a viral respiratory infection occurs within the ciliated cells of the airway, then the tracheobronchial tree  With pneumonia the inflammatory process extents to the alveolar leading to edema and exudation
  • 70. HOSPITAL ACQUIRED PNEUMONIA  Onset of s n s occur more than 48 hours post admission in pts with no evidence of infection at the time of admission  Incidence is 4-7/1000 hospitalization  Ventilator associated pneumonia- Occur in patients with acute respiratory failure under mechanical ventilation for at least 48 hours  Most pts have a multiple organism colonization
  • 71. PREDISPOSING FACTORS  Comorbidity  Supine positioning and aspiration  Coma  Malnutrition  Prolonged hospitalization  Hypotension  Poor IPC measures  Numerous intervention related factors  Impaired clearance of secretions
  • 72. Clinical manifestations  Commonly caused by: E coli, H. influenza MRSA, S. pneumoniae  Most patients with HAP are colonized by multiple organisms -New infiltration on CXR  Evidence of infection- Fever, respiratory symptoms, purulent sputum, leukocytosis, Bacteremia  Cough, GBM, pleural effusion, Tachycardia
  • 73. PNEUMONIA IN IMMUNOCOMPROMISED HOST  Include Pneumocystcic Pneumonia(PCP), Fungal pneumonia, Mycobacterium Tuberculosis  PCP is caused by Pneumocystis jirovecii (carinii)  Those at RISK  Immunosuppresants use – Corticosteroids  Chemotherapy  Malnutrition  Use of broad spectrum antimicrobial agents  HIV / AIDS  Congenital immune disorders
  • 74. ASPIRATION PNEUMONIA  Due to entry of endogenous or exogenous substances in the lower airway  Most common form is bacterial due to aspiration of bacteria from the upper airway  Substances may also be aspirated into the lower airway eg Stomach content, chemicals and irritating gases  The aspiration may impair lung defense leading to the inflammatory process, bacterial growth and pneumonia
  • 75. CLINICAL MANIFESTATION  Varies depending on the type, causative organism and presence of comorbidity  S pneumonia-  Sudden onset of chills  Rapidly rising fever 38.5-40.5 degrees  Pleuritic chest pain aggravated by deep breathing and coughing  Patient is severely ill with tachypnea and other signs of respiratory distress  Rapid bounding pulse and increases by 10bpm for every degree of temp elevation
  • 76.  A relative bradycardia- Pulse temp deficit may suggest viral or mycoplasma infection  Upper respiration infections – Nasal congestion, sore throat and symptoms of pneumonia are gradual n non specific
  • 77.  Rapidly rising fever ( 39.5 to 40.5 degree)  Stabbing chest pain aggravated by inspiration and coughing  Tachypnea, nasal flaring  Patient is very ill and lies on the affected side to decrease pain  Use of accessory muscles of respiration e.g. abdomen and intercostal muscles  Cough with purulent, blood tinged, rusty sputum  Shortness of breath  Flushed cheeks  Loss of appetite, low energy, and fatigue  Cyanosed lips and nail beds
  • 78. Diagnosis  History taking  Physical examination  Chest x-ray  Blood test  Sputum culture
  • 79. Management  Antibiotic,depending on sputum and blood culture  Macrolide-Erythromycin,azithromycine, clarithromycin  Vancomycine for MRSA  Ceftriaxone, Ampicillin, Levofloxacin- For hospital acquired pneumonia  Antipyretics  Hydration  Antitussives  Warm moist inhalation
  • 80.  Antihistamine in viral infection-Sneezing and rhinorrhea  Bed rest  Oxygen therapy – use pulse oximetry  Chest physiotherapy
  • 81. Nursing management  Maintain a patent airway and adequate oxygenation- May need oxygen adminstration  Obtain sputum specimens as needed.  Use suction if the patient can’t produce a specimen.  Perform chest physiotherapy.  Provide a high calorie, high protein diet of soft foods.
  • 82. To prevent aspiration during nasogastric tube feedings, check the position of tube, and administer feeds slowly. To control the spread of infection, dispose secretions properly.
  • 83.  Provide a quiet, calm environment, with frequent rest periods.  Monitor the patient’s ABG levels, especially if he’s hypoxic.  Assess the patient’s respiratory status. Auscultate breath sounds at least every 4 hours.  Monitor fluid intake and output.  Evaluate the effectiveness of administered medications.  Explain all procedures to the patient and family.
  • 84. Complications  Septic shock  Respiratory Failure  Pleural effusion  Confusion- Hypoxemia
  • 85. Prevention  Pneumococcal Vaccine • - 65 years & above • Immunocompromised pts • Those with chronic illnesses  Staff education and adherence to IPC measures  Infection and microbiologic surveillance
  • 86.  Frequent turning of bed ridden patients and early ambulation as much as possible.  Coughing and breathing techniques.  Sterilization of respiratory therapy equipment  Suctioning of secretion in the unconscious who have poor cough and swallowing reflexes, to prevent aspiration of secretions and its accumulation.
  • 87. End
  • 89. Pulmonary Embolism Def An occlusion of a portion of the pulmonary vascular bed by an embolus consisting of a thrombus, an air bubble, or a fragment of tissue or lipids Results in shortness of breath, heart failure, or death
  • 90.  A common disorder and usually associated with trauma, surgery, pregnancy, heart failure, hypercoagulable states and prolonged immobility
  • 91. PATHOPHYSIOLOGY  Mostly due to blood clot or thrombus  When a thrombi or blood clot partially obstructs the pulmonary artery or its branches, the alveolar dead space increases  The area though continues to be ventilated receives little or no blood flow  Gas exchange is impaired or absent in this space  In addition various substances are released from the clot that causes regional blood vessels and bronchioles to constrict- ventilation –perfusion imbalance
  • 94.  The hemodynamic consequences are:  Increased pulmonary vascular resistance  Increased pulmonary arterial pressure  Increase in right ventricular work to maintain pulmonary blood flow  This may lead to right ventricular failure and shock due to decreased cardiac output
  • 95. CLINICAL MANIFESTATION  Dyspnea  Tachypnea  Chest pain – Sudden  Anxiety  Fever  Tarchycardia  Cough  Diaphoresis  Hemoptysis  Syncope
  • 96. DIAGNOSIS  Chest xray  ABGs  Ventilation perfusion scan  Pulmonary angiography  D-Dimer assay for evidence of blood clot
  • 97. Pulmonary Embolism Risk Factors  Clotting disorders  Immobility  Dehydration  Recent surgery  Atherosclerotic changes in the circulatory system  Obesity
  • 98. Pulmonary Embolism Treatment Anticoagulant therapy  Intravenous administration of heparin  Other anticoagulant therapy  Warfarin therapy may be continued 3 to 6 months after discharge to prevent the formation of another pulmonary embolus
  • 99.  Thrombolytic Therapy- Urokinase, streptokinase,Tissue plasminogen activator. • Resolves the thrombi or emboli quickly and restores normal hemodynamic functioning, improving perfusion, oxygenation and cardiac output  Surgical management- Surgical embolectomy- Removal of the actual clot with the patient on cardiopulmonary bypass  For those who do not respond to thrombolytic
  • 100. Nursing care  Minimizing the risk of pulmonary embolism  Preventing thrombi formation  Assessing potential for pulmonary embolism  Monitoring thrombolytic therapy  Managing pain  Managing oxygen therapy  Relieving anxiety  Monitoring for complications  Post op care  Promoting HCBC
  • 101. Prevention Prevent DVT- Active leg exercise, Early ambulation, Anti embolism socks
  • 104. RESPIRATORY FAILURE • “Inability of the lung to meet the metabolic demands of the body. • This can be from failure of tissue oxygenation and/or failure of CO2 homeostasis.”
  • 105. • Clinically Respiratory failure is defined as PaO2 <50 mmHg while breathing air, Or a PaCO2 >50 mmHg with an arterial pH of less than 7.35
  • 106. • Acute respiratory failure occurs when: –pulmonary system is no longer able to meet the metabolic demands of the body • Hypoxaemic respiratory failure: –PaO2  50 mm Hg when breathing room air • Associated with acute lung disease eg. Pulmonary edema, pneumonia, pulmonary collapse • Hypercapnic respiratory failure: –PaCO2  50 mm Hg.
  • 107. Pathophysiology • The ventilation or perfusion mechanisms in the lungs are impaired
  • 108. Pathophysiologic causes of Acute Respiratory failure • Hypoventilation • Ventilation/Perfusion mismatch-  Ventilation without perfusion  Perfusion without ventilation • Shunt • Diffusion abnormality
  • 111. Respiratory Failure Symptoms Restlessness, fatigue ,tachycardia, increased BP, central cyanosis Headache Visual Disturbances Anxiety Confusion Memory Loss Weakness Decreased Functional Performance
  • 112. Decreased breath sounds Acute respiratory distress- use of accessory muscles Cough Diaphoresis Respiratory arrest
  • 114. HYPOXEMIC RESPIRATORY FAILURE(TYPE 1) • PaO2 <50mmHg with normal or low PaCO2  normal or high pH • Most common form of respiratory failure • Caused by disorders of the lungs, heart or blood • Lung disease is severe to interfere with pulmonary O2 exchange, but over all ventilation is maintained • Physiologic causes: V/Q mismatch and shunt
  • 115. HYPOXEMIC RESPIRATORY FAILURE CAUSES OF ARTERIAL HYPOXEMIA 1. FlowO2 2. Hypoventilation ( PaCO2) 3. V/Q mismatch 4. Diffusion limitation 5. Intrapulmonary shunt - pneumonia - Atelectasis - Congestive Heart Failure(CHF)
  • 116. Hypercapnic Respiratory Failure (Type II) • PaCO2 >50 mmHg • Hypoxemia is always present • pH depends on level of Bicarbonate (HCO3) • Renal response occurs over days to weeks
  • 117. Acute Hypercapnic Respiratory Failure (Type II) • Acute • Arterial pH is low • Causes - Sedative drug over dose - Acute muscle weakness such as myasthenia gravis - Severe lung disease-alveolar ventilation can not be maintained (i.e. Asthma or pneumonia)
  • 118. Causes of Hypercapnic Respiratory failure • Respiratory centre (medulla) dysfunction • Drug over dose, CVA, tumor, hypothyroidism • Neuromuscular disease eg Guillain-Barre, Myasthenia Gravis, polio, spinal injuries • Chest wall/Pleural diseases - pneumothorax, massive pleural effusion • Upper airways obstruction-tumor, foreign body, laryngeal edema • Peripheral airway disorder - asthma, COPD
  • 119. Clinical & Laboratory Manifestations • Circulatory changes - tachycardia, hypertension, hypotension • Polycythemia - chronic hypoxemia - erythropoietin synthesis • Pulmonary hypertension leading to Cor-pulmonale or right ventricular failure
  • 120. Management of Respiratory Failure Principles • Hypoxemia may cause death • Primary objective is to reverse and prevent hypoxemia • Secondary objective is to control PaCO2 and respiratory acidosis • Treatment of underlying disease • Patient’s CNS and CVS must be monitored and treated
  • 121. • Airway management-Intubation • Oxygen therapy • Mechanical ventilation • Treatment of underlying cause- antibiotics, bronchodilators, physiotherapy,

Editor's Notes

  1. This slide illustrates the various pathophysiological mechanisms which cause respiratory failure.
  2. Hypoventilation can be caused by disease at any of the anatomical sites involved in ventilation. Brainstem injury or disease may result in impaired functioning of the respiratory centre, which may also be suppressed by depressant drugs