5. Respiratory Distress in Emergency.pptx

Medical documentation

1. Radwa Muhammad Ashour Lecturer of Emergency Medicine Respiratory Distress in ED

2. Definitions

3. Dyspnea: (described as shortness of breath, breathlessness or not getting enough air) It is a subjective feeling of difficult, labored breathing or uncomfortable awareness of breathing. Respiratory Distress: It is term used by physician. It is combined patient’s subjective sensation of dyspnea é signs indicating difficulty breathing.

4. Exertional Dyspnea (Dyspnea on exertion): in COPD, Heart Failure, or elevation of the diaphragm from ascites, obesity, or pregnancy. Paroxysmal Nocturnal Dyspnea: It is orthopnea that awakens the patient from sleep → prompting an upright posture in order to resolve breathlessness.

5. Orthopnea: It is dyspnea in recumbent position & caused by Left Ventricular Failure or COPD. Platypnea : (opposite of orthopnea) It is dyspnea in upright position. It results from loss of abdominal wall muscular tone. Trepopnea : It is dyspnea associated é lying on one side (diseased lung) but not the other side → ↑ blood flow to diseased lung (gravity) & ↓ to healthy lung.

6. Tachypnea: It is rapid breathing. Hyperpnea: It is essentially hyperventilation (Deep and Rapid). Ventilatory or Respiratory Failure: It occurs when lungs & ventilatory muscles cannot move enough air in & out of alveoli to adequately oxygenate blood & eliminate CO2.

7. Pathophysiology

8. The dyspnea occurs when there is imbalance between: Inspiratory drive. Efferent activity to respiratory muscles. Feedback from these afferent receptors.

9. Dyspnea in ED

10. Goals on dealing with acutely dyspneic patient are to: Determine the need for emergency airway management and ventilatory support (A-B) Initiate treatment and stabilize if critically ill Identify whether a life-threatening condition exists Determine the most likely cause of dyspnea

11. Life Threatening causes of Respiratory Distress Upper Airway Obstruction: Foreign Body, Angioedema, Hemorrhage, Anaphylaxis. Pul monary: Pneumonia – COPD / BA exacerbation - Tension Pneumothorax. Cardiac: ACS – PE - Acute heart failure - Arrhythmia - Pericardial tamponade. Neuromuscular Weakness: Myasthenia Gravis, Guillain-Barré Syndrome.

12. Causes of Respiratory Distress Head & Neck Angioedema Anaphylaxis Foreign body Pharyngeal infections Deep neck infections Neck trauma Chest wall Rib fractures Flail chest Pulmonary COPD exacerbation Asthma exacerbation Pulmonary embolism Pneumothorax Pulmonary infection ARDS Pulmonary contusion Hemorrhage Cardiac ACS Acute Decompensated Heart Failure Pulmonary edema High output failure Cardiomyopathy Arrhythmia Valvular dysfunction Cardiac tamponade Neurologic Stroke Neuromuscular disease Hyperventilation syndrome Primary/psychogenic: panic attack, anxiety Secondary (Metabolic): Acidosis - Anemia - Pain - Hypoxemia - Hypovolemia - Hyperpyrexia - Sepsis - Uremia - DKA - Toxins.

13. How to Deal with Acutely Dyspneic Patient

14. Dyspnea: Onset – Course – Duration - Severity – Associated symptoms “Chest pain – Fever – Hemoptysis – Cough – PND” - Specific triggers or Trauma – Similar attacks. Past Medical History: BA – COPD - VTE – IHD. Family history Medications: noncompliance with medications – new medications Tobacco and drugs Pregnancy: physiological – PE – Pulmonary edema. History

15. Maintain appropriate infection control measures If needed. Signs of airway obstruction: stridor – Crepitations. Provide supplemental oxygen: N. SpO2 ≥ 94%, in Obesity or smoker 92-95%, in COPD 88-92%. Management: Airway Look – Listen –Feel Open AW Oxygen

16. Inspection: Respiratory rate. Auscultation: Rhonchi - Crackles (rales) - ↓ breath sounds Jugular venous distension. Pulse oximetry. Obtain CXR. Management: Breathing IPPA, examine neck Pulse Oximetry Oxygen CXR

17. HR: Irregular Blood Pressure: Pulsus paradoxus → Difference in SBP > 10 mmHg at inspiration. (d.t compromised right heart function e.g. in severe asthma, PE, or cardiac tamponade) Heart murmurs: Acute-onset dyspnea + evidence of cardiac ischemia + new systolic murmur suggests papillary muscle or interventricular septal rupture. Heart Sounds: 3 rd & 4 th heart sounds - Muffled heart sounds “pericardial effusions”. Continuous monitoring. Management: Circulation HR - BP – CRT - UOP Monitor – ECG Cannula – Lab – Fluid - medications

18. Skin inspection: cyanosis, pallor, mottling Extremities: Peripheral edema “heart failure” - Clubbing “chronic hypoxemia” Abdominal examination: abdominal distension - Peritoneal signs – Ascites. Obesity: Risk factor for OSA and obesity hypoventilation syndrome. Obtain ECG Establish intravenous (IV) access and obtain blood for laboratory measurements. Management: Circulation HR - BP – CRT - UOP Monitor – ECG Cannula – Lab – Fluid - medications

19. DCL Management: Disability GCS – Pupil - RBS Management: Exposure Complete exposure - Temperature

20. Signs of imminent respiratory arrest include: DCL - Poor respiratory effort: bradypnea or agonal respirations - Cyanosis Signs of severe respiratory distress include: Accessory muscles use Significant tachypnea - Brief, fragmented speech Sitting in a tripod position - Inability to lie supine Audible stridor or wheezing Agitation – Anxious - Profound diaphoresis Clinical Danger Signs

21. Management of Acute Asthma

22. Peak Expiratory Flow Rate (PEFR): the maximum flow rate [L/min] generated during a forceful exhalation, starting from full inspiration.

23. PEF: 33–50% of best (use % predicted if recent best unknown). Can't complete sentences in one breath. RR ≥ 25 breaths/minute. HR ≥ 110 beats/minute. Features of Acute Severe Asthma

24. PEF < 33% of best or predicted. SpO2 < 92% Silent chest, cyanosis, or feeble respiratory effort. Arrhythmia or hypotension.  Exhaustion, altered consciousness.  Features of Life-Threatening Asthma

25. PEF < 33% of best or predicted. SpO2 < 92% Silent chest, cyanosis, or feeble respiratory effort. Arrhythmia or hypotension.  Exhaustion, altered consciousness.  Features of Life-Threatening Asthma

26. Raised PaCO2 Requiring mechanical ventilation  Features of Near Fatal Asthma

27. Oxygen: maintain SpO2 94–98%. B-adrenergic Agents: Salbutamol 5mg or terbutaline 10mg via oxygen-driven nebulizer. Anticholinergics: Ipratropium bromide 0.5mg via oxygen-driven nebulizer. Corticosteroids: Prednisolone 40–50mg PO or hydrocortisone 100mg IV. Immediate Management Medications No sedatives of any kind.

28. Discuss with senior clinician and ICU team. Magnesium Sulphate: IV 1.2–2g infusion over 20 minutes (unless already given). B-adrenergic Agents: nebulized salbutamol 5mg /15–30 minutes or (if special nebulizer available for continuous nebulization) 10mg/hour. Immediate Management If Life-Threatening

29. Oxygen: maintain SpO2 94–98%. Corticosteroids: Prednisolone 40–50mg/d PO or hydrocortisone 100mg/6h IV. Nebulized ẞ2 agonist and ipratropium /4–6h. Subsequent Management If Improving

30. Continue oxygen and steroids. B-adrenergic Agents: nebulized salbutamol 5mg /15–30 minutes or (if special nebulizer available for continuous nebulization) 5-10mg/hour. Anticholinergics: Ipratropium 0.5mg /4–6h until patient is improving. Subsequent Management If not Improving after 15-30 min

31. Discuss patient with senior clinician and ICU team. Magnesium Sulphate: IV 1.2–2g infusion over 20 minutes (unless already given). Senior clinician may consider use of IV salbutamol or IV aminophylline or progression to mechanical ventilation. Subsequent Management If still not Improving

32. Oxygen: maintain SpO2 94–98%. PEF / 15-30 min. Chart PEF before and after giving ẞ2 agonist and at least 4 times / d during hospital stay. CXR : only if pneumothorax or consolidation are suspected or patient requires mechanical ventilation. Monitoring & Investigation

33. Blood Gas: ABG if life-threatening asthma. Repeat blood gas within 1 hour of starting treatment if: Initial PaO2 < 60mmHg unless subsequent SpO2 >92%. PaCO2 normal or raised. Patient deteriorates. Monitoring & Investigation

34. Deteriorating PEF Worsening or persisting hypoxia or hypercapnia. Exhaustion, altered consciousness Poor respiratory effort or respiratory arrest. Indications of ICU/intubation

35. Inhaler technique checked and recorded. “educate if needed” PEF >75% of best or predicted and PEF diurnal variability <25%. Treatment: Own Peak Flow Meter and written asthma action plan. Oral corticosteroids: Prednisolone 40-50mg minimum of 5 d Inhaled steroids in addition to bronchodilators. GP follow up within 2 working days - respiratory clinic within 4 weeks. Discharge instructions

36. Management of COPD Exacerbation

37. Dyspnea at rest or on exertion. Cough with or without sputum production. Progressive limitation of activity. Triggers of COPD (e.g., tobacco smoke “smoking >20 pack years”, occupational dust) COPD Symptoms COPD Exacerbation Symptoms Worsening Dyspnea Increasing Severity or frequency of Cough. Increasing volume or changing character of sputum .

38. Advanced age Comorbid disease. (IHD – HF – DM) Longer duration of COPD. Productive cough or Chronic mucous hypersecretion. History of antibiotic use or prior exacerbations “best predictor” Blood eosinophil count > 0.34 x 10 9 cells/L. Risk factors for exacerbations of COPD

39. Respiratory infections: (70%) Viral (most commonly): Rhinovirus. Bacterial: Haemophilus influenzae “13-50%” Environmental pollution. Pulmonary Embolism. Unknown etiology. Triggers for exacerbations of COPD

40. COPD Exacerbation Severity GOLD: Severity of airflow limitation (based on postbronchodilator FEV 1 ) “In patients with FEV 1 /FVC <0.7” Stage Severity FEV 1  (% of predicted) GOLD 1 Mild ≥80 GOLD 2 Moderate 50 to 79 GOLD 3 Severe 30 to 49 GOLD 4 Very severe <30

41. COPD Exacerbation Severity Severity Clinical Signs No respiratory failure   RR: 20-30 bpm No change in mental status. SpO 2 : 88-92% with Venturi mask 24-35% FiO2 No hypercapnia. Acute nonlife-threatening respiratory failure   RR >30 bpm. No change in mental status. SpO 2 : 88-92% with Venturi mask 24-35% FiO2 Use of accessory muscles of respiration PaCO2: 50-60 mmHg or increased over baseline. Acute life-threatening respiratory   failure   RR >30 bpm. Acute change in mental status. SpO 2 : 88-92% with ≥ 40% FiO2 Use of accessory muscles of respiration PaCO2: > 60 mmHg or increased over baseline or associated with acidosis (pH ≤7.25).

42. Spirometry. ECG: for DD Laboratory: CBC - ABG Radiological: CXR Investigation

43. Ensuring appropriate oxygenation: SpO2 88-92% or PaO2 60-70 mmHg Avoiding intubation and mechanical ventilation. Reversing airflow limitation: inhaled short-acting bronchodilators and systemic glucocorticoids. Treating infection. COPD exacerbation Management Aim

44. Inhaled ẞ agonist: Nebulized Salbutamol 2.5 mg or 2-4 inhalations MDI / h for 2-3 doses. Anticholinergic agent: Nebulized Ipratropium 0.5 mg or 2-4 inhalations MDI / h for 2-3 doses. Corticosteroids: Prednisolone 40-50mg/d PO or Methylprednisolone 60-125mg/6-12h IV. Reversing Airflow Limitation

45. Antiviral: Oseltamivir 75 mg / 12 h PO Antibiotics: No Pseudomonas risk factor(s): Ceftriaxone or cefotaxime 1-2 gm IV or levofloxacin 500 mg IV/PO or moxifloxacin 400 mg IV/PO Pseudomonas risk factor(s): Piperacillin-tazobactam 4.5 gm or cefepime 2 gm or ceftazidime 2 gm. (IV) Treating Infection Pseudomonas risk factors: Broad spectrum antibiotic use in the past 3 months - chronic colonization or previous isolation of Pseudomonas aeruginosa from sputum (particularly in past 12 months) - very severe underlying COPD - chronic systemic glucocorticoid use

46. Mechanical Ventilation Noninvasive ventilation (NIV):  Severe exacerbations of COPD unless immediate intubation is needed or NIV is otherwise contraindicated. Invasive mechanical ventilation: NIV is contraindicated - fail to improve with NIV – severe acidosis or hypoxemia – respiratory arrest.

47. Spontaneous Pneumothorax

48. Spontaneous pneumothorax: (Not Traumatic) Primary: No clinically apparent lung disease - usually tall, thin males. Secondary: occurring in patients with underlying lung disease. Traumatic pneumothorax: Iatrogenic or non-iatrogenic. Causes/Types

49. Unilateral chest pain (either sharp or steady pressure or pleuritic) and acute shortness of breath . In secondary pneumothorax: may present with significant distress , even with a small pneumothorax. Presentation

50. Physical examination: may be normal if pneumothorax is small. Inspection, Palpation “↓ chest movement” – Percussion “hyper-resonance” , Auscultation “↓ breath sounds”. Tension Pneumothorax: Tachycardia, hypotension, and tracheal deviation. Presentation

51. CXR Erect/Supine: Signs of pneumothorax in CXR Deep Sulcus Sign. (Supine) Investigation

52. CXR Erect/Supine: Signs of pneumothorax in CXR Pleural line. Investigation

53. CXR Erect/Supine: Signs of pneumothorax in CXR Loss of lung marking in periphery. Investigation

54. CXR Erect/Supine: Signs of pneumothorax in CXR Low diaphragm on affected side. Investigation

55. CXR Erect/Supine: Size of pneumothorax in CXR Investigation Small pneumothorax if interpleural distance < 2 cm or from apex of lung to copula < 3 cm.

56. CT Chest: Investigation Lung Ultrasound. ABG

57. Small Pneumothorax Management Observation for >3 h on oxygen. Repeat chest radiograph. Discharge if no symptoms. Return for evaluation if symptoms recur or in 2 wk. Small-size catheter aspiration with immediate catheter removal. Then as above

58. Small Pneumothorax Management Small-size catheter aspiration or Small-size chest tube insertion. Under water seal. Admission.

59. Large Pneumothorax Management Moderate-size chest tube. Under water seal. Admission Large-size chest tube if fluid or hemothorax present. Under water seal. Admission

60. Tension Pneumothorax Management Immediate decompression followed by, Moderate or large-size chest tube insertion. Under water seal. Admission. Immediate chest tube placement ideal.

61. Cardiogenic Pulmonary Edema

62. Pulmonary Edema is characterized by the presence of excess fluid within the pulmonary interstitium and, at its most severe, within the alveoli. Cardiogenic pulmonary edema is due to a primary cardiac or circulatory cause. 

63. Acute Heart Failure Decompensated Chronic HF Volume overload – stopping diuretics – infection – Renal impairment – Asthma/COPD Acute Arrhythmia HTN IHD Circulatory Failure: Sepsis – anemia – Thyrotoxicosis - PE Myopathy: myocarditis – postpartum cardiomyopathy Valvular: stenosis – regurgitation - endocarditis - AD

64. Airway: Usually intact except if DCL - In extreme cases blood stained frothy sputum may be present Breathing: Tachypnoea – Dyspnea – SpO2 < 90% - bibasal inspiratory crepitations which extend higher up the chest as the condition worsens - wheeze (In some cases). Presentation

65. Circulation: diaphoretic pale, cold and clammy skin - Sinus tachycardia – blood pressure “high/low in cardiogenic shock” - gallop rhythm – Murmurs - peripheral oedema and hepatomegaly “right heart failure”. Disability: alert and anxious → agitated → DCL (hypercapnic) Exposure: Afebrile with cold and clammy skin Presentation

66. ECG: T achycardia. LVH. Cause: ACS - arrhythmia. Investigations

67. CXR: Investigations

68. CXR: Butterfly pattern Or batwing opacity . Investigations

69. Echocardiography Laboratory investigation: ABG . CBC. Investigations for the cause: troponin Investigations

70. Airway & Breathing: Upright position for airway and breathing. Oxygen: aim SpO2 94-98% (COPD 88-92%) Non-invasive Ventilation (NIV): CPAP if hypoxia only – BiPAP if hypercapnia. Management

71. Circulation : Vasodilators: venous and/or arteriolar VD → ↓ pre-load and/or after-load. (contraindicated in SBP < 90 mmHg) Nitrates: SL till IV access → start with 10-20 μ g/min → increasing by 5-10 μ g/min /3-5 min as needed → maximum of 200 μ g/min. Nitroprusside: particularly useful in extreme HTN precipitating CPO. “0.3 mcg/Kg/min IVI up to 5 mcg/Kg/min. Management

72. Circulation : Loop Diuretics: ↓ preload by preventing Na Cl reabsorption - by vasodilatory action. (dose: 20-40mg) Inotropes: in hypotension. Disability: Morphine: if agitated - distressed - complaining of chest pain. “ 2.5-5mg”. Management

73. Thank You