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RESPIRATORY EMERGENCIES

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  1. RESPIRATORY EMERGENCIES Intermediate Lecture – Respiratory Emergencies

  2. Respiratory EmergenciesObjectives Upon completion the student will be able to: • Identify the historical factors to elicit when evaluating the respiratory system • Identify specific observations and physical findings to evaluate in the patient with a respiratory complaint • Describe the techniques of inspection, auscultation, and palpation of the chest • Review the basic principles of respiratory management Intermediate Lecture – Respiratory Emergencies

  3. Respiratory EmergenciesObjectives • Define the following terms: • Snoring • Stridor • Wheezing • Rhonchi • Rales • Friction rub Intermediate Lecture – Respiratory Emergencies

  4. Respiratory EmergenciesObjectives • Describe the difference between the normal respiratory drive and the respiratory drive of the patient with chronic obstructive pulmonary disease (COPD). • Discuss the pathophysiology, assessment, and management of the following conditions: • Emphysema • Chronic bronchitis • Asthma • Pneumonia Intermediate Lecture – Respiratory Emergencies

  5. Respiratory EmergenciesObjectives • Toxic inhalation • Pulmonary embolism • Hyperventilation syndrome • Central nervous system dysfunctions Intermediate Lecture – Respiratory Emergencies

  6. COPDOverview • More common in men than women • More common in urban than rural environments • Most significant contributing factor is cigarette smoking • Minor Role: air pollution/industrial inhalants • Widespread TB can damage enough lung tissue to result in COPD Intermediate Lecture – Respiratory Emergencies

  7. Overview • All patients with COPD have the following: • Increased airway resistance, with a resultant increase in the work of breathing • Inefficiency of inspiratory muscles due to chronic thoracic hyperinflation • Ventilation-perfusion mismatching leading to impaired gas exchange Intermediate Lecture – Respiratory Emergencies

  8. Overview • Two most common forms of COPD: • EMPHYSEMA • CHRONIC BRONCHITIS Intermediate Lecture – Respiratory Emergencies

  9. EMPHYSEMAPathophysiology • Destruction of the alveolar walls, causing the following: • Increased ration of air to lung tissue • Weakening of the walls of the small bronchioles • Decreased alveolar membrane area, which lessens the area available for gas exchange • Decreased number of pulmonary capillaries in the lung, which increases the resistance to the pulmonary blood flow Intermediate Lecture – Respiratory Emergencies

  10. Pathophysiology • Loss of elastic recoil in the lung and a marked decrease in expiratory airflow • Residual air volume increases • Vital capacity (volume of air that can be expelled from the lungs from a position of full respiration) remains near normal • As the disease advances, arterial pO2 decreases, which may lead to increased red blood cell production. Intermediate Lecture – Respiratory Emergencies

  11. Pathophysiology • Carbon dioxide retention occurs • Increased resistance to blood flow leads to right heart failure • Other complications include acute respiratory infection and cardiac dysrhythmia Intermediate Lecture – Respiratory Emergencies

  12. Pathophysiology • Paramedics are most commonly called to patients who are in advanced stages of the disease. Be aware of the patients hypoxic drive, but this is not a justification to deprive the patient of oxygen therapy, for he may die without it!!!!! • Sometime referred to as “pink puffers” Intermediate Lecture – Respiratory Emergencies

  13. Assessment • History • May have recent loss of appetite and weight loss • Increasing shortness of breath on exertion • Progressive limitation of physical activity • Coughing – not usually a prominent complaint – can produce small amounts of whitish-gray, mucous-like sputum Intermediate Lecture – Respiratory Emergencies

  14. Assessment • Physical Exam • Chest is barrel-shaped and hyperresonant to percussion • May have decreased chest excursion • Hypertrophied accessory respiratory muscles • Expiration of breath takes place through pursed lips • May have clubbing of the fingers • Decreased breath and heart sounds • Expiration time is lengthened Intermediate Lecture – Respiratory Emergencies

  15. Assessment • May have signs of right heart failure: distended neck veins and pedal edema • Cyanosis may be present • Tachycardia is often present Intermediate Lecture – Respiratory Emergencies

  16. Intermediate Lecture – Respiratory Emergencies

  17. CHRONIC BRONCHITISPathophysiology • An increased number of mucous-secreting cells in the respiratory epithelium produce characteristically large amounts of sputum • Alveoli are not seriously affected; diffusion of oxygen remains normal • Alveoli hypoventilation affects respiratory gas exchange • Arterial hypoxemia (decreased pO2) and hypercarbia (elevated pCO2) occur Intermediate Lecture – Respiratory Emergencies

  18. CHRONIC BRONCHITISPathophysiology • Hypoxia may cause increased red blood cell production • Increased pCO2 levels constrict the pulmonary circulation, possible leading to right heart failure • Increased pCO2 levels may lead to irritability, decreased intellectual abilities, headaches, and personality changes • Acute and chronic infections produce scarring in the lungs Intermediate Lecture – Respiratory Emergencies

  19. CHRONIC BRONCHITISPathophysiology • Vital capacity is decreased • Residual volume of air is normal or decreased • Referred to as a “blue bloater” Intermediate Lecture – Respiratory Emergencies

  20. CHRONIC BRONCHITISAssessment • History • Heavy cigarette smoking • Frequent respiratory tract infections • Between infections, there is a productive cough that produces at least 10 cc’s of green or yellow sputum daily Intermediate Lecture – Respiratory Emergencies

  21. CHRONIC BRONCHITISAssessment • Physical Examination • The patient is overweight and cyanotic • Respiratory rate is normal or slightly increased • Dyspnea at rest is uncommon • Signs of right heart failure • Rales, rhonchi, and wheezes can be heard in the chest Intermediate Lecture – Respiratory Emergencies

  22. Intermediate Lecture – Respiratory Emergencies

  23. ACUTE DECOMPENSATIONOverview • Patients with established COPD are prone to episodes of acute decompensation leading to respiratory failure. • Such episodes are often triggered by respiratory infection. • Notice a change in his sputum, which becomes more purulent and may increase in volume • Dyspnea increases, often to the point that it disturbs sleep Intermediate Lecture – Respiratory Emergencies

  24. Overview • Increasing degrees of hypoxemia lead to cyanosis, confusion, agitation, and sometimes muscular twitching • Right heart failure may develop Intermediate Lecture – Respiratory Emergencies

  25. COPD TREATMENT • Establish an open airway • Administer oxygen: • Monitor rate and depth • Supplemental oxygen may decrease respiratory drive (hypoxic drive), be prepared to assist in ventilating the patient • NEVER, NEVER, NEVER, WITHHOLD OXYGEN THERAPY FROM ANY PATIENT IN RESPIRATORY DISTRESS, EVEN A PATIENT WITH COPD!!!!!!!!!! Intermediate Lecture – Respiratory Emergencies

  26. COPD TREATMENT • Place the patient in a position of comfort • Sitting • Semi-sitting • Start an IV of crystalloid of choice at a KVO rate • Administer Beta-2 selective adrenergic • Do not give sedatives or tranquilizers • Depress respirations further Intermediate Lecture – Respiratory Emergencies

  27. COPD TREATMENT • Monitor cardiac rhythm/pulse oximetry • Encourage the patient to cough up his secretions Intermediate Lecture – Respiratory Emergencies

  28. ASTHMADescription/Definition • Common chronic disease, affecting nearly 9 million individuals in this country • More common in children and young adults, onset of symptoms can occur in any decade of life • Childhood asthma often dissipates with age • Adult-onset disease is usually persistent Intermediate Lecture – Respiratory Emergencies

  29. ASTHMADescription/Definition • Asthma is reversible airflow obstruction, associated with a state of increased responsiveness of the tracheobronchial tree to many different stimuli • The bronchospasm characteristic of the acute asthmatic attack is typically reversible: it improves spontaneously or within minutes or hours of treatment Intermediate Lecture – Respiratory Emergencies

  30. ASTHMADescription/Definition • Patients experience dyspnea, cough, and wheezing as the major complaints • Provocation of the Asthmatic Response: • Immunologic reaction (exposure to antigen with mediator release) • Viral respiratory infections (upper and lower respiratory tract) • Changes in temperature and humidity (especially cold air) Intermediate Lecture – Respiratory Emergencies

  31. ASTHMADescription/Definition • Strong odors (perfumes, etc.) • Pollutants, dusts, fumes and other irritants (including occupational exposures) • Certain drugs and chemicals: • Aspirin • Nonsteroidal anti-inflammatory drugs • Tartrazine dye (yellow dye #5) • Sulfiting agents • Beta-adrenergic blocking drugs Intermediate Lecture – Respiratory Emergencies

  32. ASTHMADescription/Definition • Sinus infections • Exercise • Strong emotions, laughing, coughing • Deep inspiration or forceful expiration • Gastroesophageal reflux Intermediate Lecture – Respiratory Emergencies

  33. ASTHMAPathophysiology • Due mainly to bronchial smooth muscle contraction • The asthmatic attack is frequently associated with mucus hypersecretion and inflammatory changes in the bronchial walls; these two processes result in mucosal edema Intermediate Lecture – Respiratory Emergencies

  34. ASTHMAPathophysiology • Focus of therapy usually centers around pharmacologic manipulation of airway smooth muscle • Bronchospasm can be reversed within minutes, but the airflow obstruction due to mucous plugging and inflammatory changes in bronchial walls does not resolve for many days or weeks Intermediate Lecture – Respiratory Emergencies

  35. ASTHMAPathophysiology • In addition to contributing to airflow obstruction, mucous plugging may lead to: • Atelectasis • Infectious bronchitis • Pneumonitis Intermediate Lecture – Respiratory Emergencies

  36. AsthmaBronchial Hyperreactivity • Hallmark of the asthmatic condition is bronchial hyperreactivity (an extreme sensitivity of the airway to a multiplicity of stimuli), this sensitivity results in a greater degree of bronchoconstriction than is seen in normal individuals Intermediate Lecture – Respiratory Emergencies

  37. AsthmaBronchial Hyperreactivity • The parasympathetic nervous system has an abundance of vagal efferent fibers ending in airway smooth muscle. Vagus nerve stimulation releases acetylcholine at post-ganglionic nerve endings, thus causing bronchospasm Intermediate Lecture – Respiratory Emergencies

  38. AsthmaConsequences of Airflow Obstruction • The initial abnormality is increased airway resistance, stemming from a combination of bronchoconstriction, mucosal edema, and mucus hypersecretion • These conditions result in a reduction in maximum expiration flow rates Intermediate Lecture – Respiratory Emergencies

  39. AsthmaConsequences of Airflow Obstruction • As impairment of the expiratory phase of ventilation progresses the complete tidal volume is not exhaled, and air trapping ensues => reflected in elevation of the residual volume and functional residual capacity of the lungs Intermediate Lecture – Respiratory Emergencies

  40. AsthmaConsequences of Airflow Obstruction • Increased airway resistance and air trapping combine to produce increased airway pressures, which may result in barotrauma (subcutaneous emphysema, pneumomediastinum, or pneumothorax) Intermediate Lecture – Respiratory Emergencies

  41. AsthmaConsequences of Airflow Obstruction • The acute asthmatic attack also results in an uneven distribution of ventilation, which in turn results in ventilation-perfusion imbalance. • Hypercarbia may be seen in extreme cases, hypoxemia is more commonly observed. Intermediate Lecture – Respiratory Emergencies

  42. AsthmaConsequences of Airflow Obstruction • These factors lead to greater demands on the muscles of inspiration. Excessive contractions of these muscles (during inspiration and, for unknown reasons, during expiration also) and an increased workload contribute to the patient’s sensation of dyspnea Intermediate Lecture – Respiratory Emergencies

  43. AsthmaConsequences of Airflow Obstruction • When the energy supply to these muscles fails to match the energy requirements, lactic acidosis ensues, followed by overt ventilatory failure. • When the major muscles of inspiration, the diaphragm, begins to tire, accessory inspiratory muscles assume a greater proportion of the ventilatory work • An abnormal pulsus paradoxus (>20 mm Hg) is associated with severe asthma Intermediate Lecture – Respiratory Emergencies

  44. Clinical Presentation - AsthmaHistory • History of previous attacks • Progressive dyspnea, chest tightness, wheezing, and cough; persistent cough is often the major complaint • Is the cough productive, color of sputum, amount of sputum and consistency of sputum • Duration of acute symptomatology is important because episodes lasting more than several days are likely to be associated with significant mucosal edema and mucous plugging Intermediate Lecture – Respiratory Emergencies

  45. Clinical Presentation - AsthmaHistory- Physical Examination • Presenting with a severe asthmatic attack, the patient is in obvious distress, with rapid, loud breathing; wheezing may be audible • Use of accessory muscles of inspiration (neck muscles are most prominent) indicates diaphragmatic fatigue while the appearance of paradoxical respiratory (inward movement of the upper abdominal wall due to inspiratory ascent of the diaphragms) reflects impending ventilatory failure Intermediate Lecture – Respiratory Emergencies

  46. Clinical Presentation - AsthmaHistory – Physical Examination • Alteration in the mental status => lethargy, exhaustion, agitation, or confusion => also heralds respiratory arrest • Hyperresonance to percussion • Decreased intensity of breath sounds • Prolongation of the expiratory phase, usually with wheezing Intermediate Lecture – Respiratory Emergencies

  47. Clinical Presentation - AsthmaHistory – Physical Examination • “Quiet Chest” reflects very severe airflow obstruction with air movement insufficient to promote wheeze • Pulsus paradoxus above 20 mm Hg is also indicative of severe asthma Intermediate Lecture – Respiratory Emergencies

  48. Intermediate Lecture – Respiratory Emergencies

  49. Congestive Heart Failure Upper airway obstruction Aspiration of foreign body or gastric acid Bronchogenic carcinoma with endobronchial obstruction Vocal-cord dysfunction ASTHMA MIMICKERS Intermediate Lecture – Respiratory Emergencies

  50. Assessing the Severity of an Asthma Attack:Status Asthmaticus • Status Asthmaticus (severe asthma) • No responses with objective improvement in airflow obstruction to initial treatment consisting of: 1. Nebulized beta-adrenergic drugs 2. Injectible beta-adrenergic drugs 3. Corticosteroids 4. Nebulized anticholinergics Intermediate Lecture – Respiratory Emergencies