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aproch to patient with dyspnea

  1. 1. introduction cases Asthma and COPD CARDIAC TAMPONADE AND HF p.edema.p. emboli How to deal with dyspnea in emergency DDX management History .exam..investigat ion pathophysio logy
  2. 2. Some definitions Trepopnoea :Breathlessness when lying on one side as a result of ipsilateral pulmonary disease . Causes are dilated cardiomyopathy, pleural effusion. Orthoponea : Breathlessness when lying flat. Ex : Left Ventricular Failure, diaphramatic weakness, massive pleural effusion, huge ascitis, any severe lung disease. Platypnoea : Breathlessness on sitting up. Ex : right to left shunt, ASD, or large intra pulmonary shunt, pericardial effusion, liver cirrhosis. PND : Breathlessness that wakes the patient from sleep. Ex : Left Ventricular failure. Bronchial Asthma
  3. 3. PATIENT FEELING Chest tightness Asthma CHF Air hunger .urge to breath CHF PE,, asthma, pulmonary fibrosis COPD In ability to get a deep breath ASTHMA COPD FIBROSIS Heavy .rapid breath SEDENTARY ANY OTHER CAUSES Increase work or effort to breath COPD ASTHMA CHEST WALL OR NEUROMUS CULAR
  4. 4. pathophysiology • MECHANISMS OF DYSPNEA • Respiratory sensations are the consequence of interactions between the • efferent, or outgoing, motor output from the brain to the ventilatory • muscles (feed-forward) and the afferent, or incoming, sensory input • from receptors throughout the body (feedback) as well as the integrative • processing of this information that we infer must be occurring • in the brain
  5. 5. Sensory Afferents • Chemoreceptors in the carotid bodies and medulla • are activated by hypoxemia, acute hypercapnia, and acidemia. • Stimulation of these receptors and of others that lead to an increase • in ventilation produce a sensation of “air hunger.” Mechanoreceptors • in the lungs, when stimulated by bronchospasm, lead to a sensation of • chest tightness. J-receptors, which are sensitive to interstitial edema, • and pulmonary vascular receptors, which are activated by acute • changes in pulmonary artery pressure, appear to contribute to air • hunger. Hyperinflation is associated with the sensation of increased • work of breathing, an inability to get a deep breath, or an unsatisfying • breath. Metaboreceptors, which are located in skeletal muscle, are • believed to be activated by changes in the local biochemical milieu of • the tissue active during exercise and, when stimulated, contribute to • breathing discomfort.
  6. 6. Receptors involved in mechanism of dyspnea 1) J receptors – alveolo-capillary junction • Stimulated by pulmonary congestion ,oedema, micro emboli. • Responsible for rapid shallow breathing 2) Stretch receptors – thoracic cage & lung 3) Chemoreceptors - carotid arteries, aorta & reticular substance of medulla Stimulated by hypoxia, excess of CO2, decrease in PH 4) Receptors in the respiratory muscle – immediate cause of appreciation of dyspnea
  7. 7. Etiology / Differential Diagnosis
  8. 8. • CHF • CAD • Cardiac tamponade • Cardiomyopathy • Valvular dysfunction • Pericarditis • Arrhythmias
  9. 9. • Asthma • COPD • Pulmonary embolism • Pneumonia • Pneumothorax
  10. 10. • It is a normal symptom of heavy exertion • Normal pregnancy (around 2/3rd ) • Metabolic acidosis • Pain • Trauma • Neuromuscular disorders • Functional (anxiety, panic disorders, hyperventilation) • Chemical exposure • Obesity • Psychogenic
  11. 11. ACUTE SEVERE DDX *Acute pulmonary oedema *Acute severe asthma *Acute exacerbation of COPD *Pneumothorax *Pulmonary embolus * Cardiac tamponade • Inhaled foreign body (especially in the child) • Laryngeal oedema (e.g. anaphylaxis) • Metabolic acidosis (e.g. diabetic ketoacidosis, lactic • acidosis, uraemia, overdose of salicylates, ethylene • glycol poisoning)
  12. 12. history • HISTORY • Orthopnea is a common indicator • of congestive heart failure (CHF), • Nocturnal dyspnea suggests CHF or asthma. Acute, intermittent • episodes of dyspnea are more likely to reflect episodes of myocardial • ischemia, bronchospasm, or pulmonary embolism, while chronic • persistent dyspnea is typical of COPD, interstitial lung disease, and • chronic thromboembolic disease. Information on risk factors
  13. 13. ‫سمارة‬
  14. 14. • Minutes • Pneumothorax • Pulmonary oedema • Major pulmonary embolism • Foreign body • Laryngeal oedema Hours • Asthma • Left heart failure • Pneumonia Days 1..Pneumonia 2..ARDS 3..Left heart failure 4…Repeated pulmonary embolism Weeks • Pleural effusion …Anemia…Tumours ONSET OF DYSPNOEA
  15. 15. CHRONIC DYSPNOEA AIRWAYS 1. Obstructive airway disease 2. Asthma 3. Chronic bronchitis 4. Empyema 5. Cystic fibrosis PARENCHYMAL 1. ILD 2. Malignancy -primary -secondaries PLEURAL 1. Effusion 2. Malignancy 3. Fibrosis PULM-VASCULAR DISEASE 1. A-V Malformations 2. Vasculitis 3. Veno-occlusive disease
  16. 16. ORTHOPNOEA •CHF •COPD •asthma • Massive pleural effusion PLATYPNOEA • Left atrial myxoma • Massive p.Embolism • Pulm. AV fistula • Paralysis of intercostal TREPOP OEA • DISEASE OF ON LUNG/ BRONCH
  17. 17. NOCTURNAL ONSET DYSPNOEA  - CHF  - COPD  - BRONCHIAL ASTHMA  - SLEEP APNOEA  - NOCTURNAL ASP. IN GERD
  18. 18. examination • PHYSICAL EXAMINATION • Inability of the patient to speak in full sentences before • stopping to get a deep breath suggests a condition that leads to • stimulation of the controller or impairment of the ventilatory pump • with reduced vital capacity. Evidence of increased work of breathing • (supraclavicular retractions; use of accessory muscles of ventilation; • and the tripod position, characterized by sitting with the hands • braced on the knees) is indicative of increased airway resistance or • stiffness of the lungs and the chest wall. When measuring the vital • signs, the physician should accurately assess the respiratory rate and • measure the pulsus paradoxus); if the systolic pressure • decreases by >10 mmHg, the presence of COPD, acute asthma, or • pericardial disease should be considered.
  19. 19. GENERAL EXAM • During the general examination, • signs of anemia (pale conjunctivae), cyanosis, and cirrhosis • (spider angiomata, gynecomastia) should be sought. Examination • of the chest should focus on symmetry of movement; percussion • (dullness is indicative of pleural effusion; hyperresonance is a sign • of emphysema); and auscultation (wheezes, rhonchi, prolonged • expiratory phase, and diminished breath sounds are clues to disorders • of the airways; rales suggest interstitial edema or fibrosis). • paradoxical movement of the abdomen: inward motion during inspiration is • a sign of diaphragmatic weakness, and rounding of the abdomen • during exhalation is suggestive of pulmonary edema. Clubbing of • the digits may be an indication of interstitial pulmonary fibrosis
  20. 20. Cardiovascular examination Elevated neck veins, extra heart sound (S3 gallop rhythm), and fluid retention - congestive heart failure. Elevated neck veins, pulsus paradoxus, a pericardial knock, pericardial rub, and the Kussmaul's sign - Constrictive pericarditis and effussion An irregular or fast heart beat - a tachyarrhythmia or atrial fibrillation.  A loud S2 -PAH A systolic heart murmur- acute valvular insufficiency, mechanical valve malfunction.
  21. 21. Respiratory examination  Pursed lip breathing - COPD.  Stridor -upper airway obstruction  A barrel chest - emphysema and cystic fibrosis.  Hoarseness - in laryngitis, laryngeal tumours, vocal cord paralysis.  The trachea may deviate Unilateral dullness to percussion.  Hyper-resonance  Subcutaneous emphysema - pneumomediastinum B.p  Hypotension, tachycardia, and tachypnea : acute pulmonary edema , ARDS  Hypertension in a dyspnoeic patients: hypertension-related diastolic heart failure with pulmonary oedema, hyperthyroidism, or phaeochromocytoma  Pulsus paradoxus - asthma, COPD, cardiac tamponade
  22. 22. INVESTIGATION • CHEST IMAGING • a chest radiograph should be obtained. The lung volumes should be • assessed: hyperinflation indicates obstructive lung disease, whereas • low lung volumes suggest interstitial edema or fibrosis, diaphragmatic • dysfunction, or impaired chest wall motion. The pulmonary • parenchyma should be examined for evidence of interstitial disease • and emphysema. Prominent pulmonary vasculature in the upper • zones indicates pulmonary venous hypertension, while enlarged • central pulmonary arteries suggest pulmonary arterial hypertension. • An enlarged cardiac silhouette suggests dilated cardiomyopathy • or valvular disease. Bilateral pleural effusions are typical of CHF • and some forms of collagen-vascular disease. Unilateral effusions • raise the specter of carcinoma and pulmonary embolism but may • also occur in heart failure. CT of the chest is generally reserved for • further evaluation of the lung parenchyma (interstitial lung disease) • and possible pulmonary embolism.
  23. 23. INVESTIGATION • LABORATORY STUDIES • electrocardiography to seek evidence of ventricular hypertrophy and prior myocardial infarction. • Echocardiography is indicated when systolic dysfunction, • pulmonary hypertension, or valvular heart disease is suspected. • Bronchoprovocation testing is useful in patients with intermittent • symptoms suggestive of asthma but normal physical examination • and lung function; up to one-third of patients with the clinical • diagnosis of asthma do not have reactive airways disease when • formally tested. Measurement of brain natriuretic peptide levels in • serum is increasingly used to assess for CHF in patients presenting • with acute dyspnea but may be elevated in the presence of right • ventricular strain as well.
  24. 24. GRADE 1 –Dyspnoea only with unusual exertion. GRADE 2 –Dyspnoea on doing ordinary activity GRADE 3 –Dyspnoea on doing less than ordinary activity. GRADE 4 –Dyspnoea at rest. NYHA SCALE
  25. 25. How to deal with Emergent causes emergent p.edema p.emboli c.tamponade Acute asthma Tension pneumot horrax Acute COPD
  26. 26. asthma • Definition. A disease characterized by inflammatory hyperreactivity of the respiratory tree to • various stimuli, resulting in reversible airway obstruction. A combination of mucosal inflammation, • bronchial musculature constriction, and an excessive secretion of viscous mucus-causing • The mediators are histamine, bradykinin, leukotrienes (LTs) C, D, and E, and prostaglandins (PGs) E2, Cells are the mast cells, lymphocytes, and eosinophils. leading to bronchoconstriction and vascular congestion.
  27. 27. pathology
  28. 28.  'cough-variant asthma‘  Nocturnal asthma  triggered by medications. 1...aspirin ????? how 2..β- adrenoceptor antagonists (β-blockers), even when administered topically 3..(NSAIDs 4..oral contraceptive pill, 5..cholinergic agents 6..prostaglandin F2α
  29. 29. Signs and Symptoms and investigation. • In a mild attack, slight tachypnea, tachycardia, prolonged expirations, wheezing. • In a severe attack, use of accessory muscles of respiration, diminished breath sounds, loud wheezing, hyper-resonance Poor prognostic factors include fatigue, diaphoresis, pulsus paradoxus (>20 mm Hg), inaudible breath sounds, decreased wheezing, cyanosis, and bradycardia. Making a diagnosis of asthma clinical history plus FEV1
  30. 30.  Acute severe asthma  •PEF 33-50% predicted (< 200 L/min)  •Respiratory rate ≥ 25/min  •Heart rate ≥ 110/min  •Inability to complete sentences in breath  Life threatening 1•PEF < 33% predicted (< 100 L/min 2•SpO2 < 92% or PaO2 < 8 kPa (60 mmHg)Normal or raised PaCO2  Cliniclly Silent chest ,Cyanosis, Feeble respiratory effort, Bradycardia or arrhythmias Hypotension ,Exhaustion ,Confusion ,Coma   •CPR TO KEEP IT CLINICAL ,,,,RESPIRATORY ARREST ,,,3P ..(PH.PaO2.Paco2)
  31. 31.  COPD is “airflow limitation that is not fully reversible. progressive and associated with an abnormal inflammatory response of the lungs to noxious particles or gases ”  The 'blue bloaters‘ :  low PaO2 & high PaCO2.  They are cyanosed , but not breathless & may develop cor pulmonale  Supplemental O2 should be given with caution  The 'pink puffers‘:  increase in the alveolar ventilation , a near normal PaO2 & normal or low PaCO2 .  breathless but not cyanosed ,,.type 1 respiratory failure
  32. 32.  The diagnosis requires objective demonstration of airflow obstruction by spirometry and is established when the post-bronchodilator FEV1 is less than 80% of the predicted value and accompanied by FEV1/FVC < 70%.  Measurement of lung volumes provides an assessment of hyperinflation  Pulse oximetry may prompt referral for a domiciliary oxygen assessment if less than 93%.  HRCT is likely to play an increasing role in the assessment of COPD, as it allows the detection, characterization and quantification of emphysema and is more sensitive than a chest X-ray at detecting bullae.
  33. 33. Exacerbation (Acute Setting Treatment). considered acute worsening of the patient’s respiratory symptoms (increased dyspnea, increased sputum volume, production of purulent sputum) that necessitates a change in medications. The most common causes of COPD exacerbation are viral lung infections. Other precipitating causes that should be sought out are 1..bacterial infections 2..heart failure, 3..myocardial ischemia, 4..pulmonaryembolism, 5..lung cancer, 6..esophageal reflux disease, 7..and medications (e.g., beta-blockers).
  34. 34. MANAGEMENT • Initial Management • 1. Measure O2 saturation. • 2. ABG determination • 3. Chest x-ray pulmonary • infiltrates = pneumonia • pulmonary edema = heart failure as the cause of the exacerbation. • 4. Spirometry is not helpful in COPD exacerbation not correlate well with the severity of the exacerbation. • 5. theophylline level.Drugs like erythromycin, cimetidine, and ciprofloxacin cause toxicity. • 6..tests of initial evaluation of COPD CBC • (elevated WBCs and polycythemia); ECG atrial fibrillationthat mayexacerbate COPD). • 7. hypercapnia or hypoxemia with severe symptoms, should be hospitalized. • 8.. Assisted ventilition
  35. 35. Specific Therapy • 1. Oxygen supplementation. • 2. Inhaled bronchodilators are the most effective medications (the drugs of choice, use both beta-agonists (albuterol) and anticholinergics (ipratropium) simultaneously. • 3. Systemic corticosteroids ..I.V or orally because the efficacy • is similar. The equivalent of 60 mg prednisone • As starting dose and is usually continued for 2 weeks. • patients who have a severe exacerbation start with IV • methylprednisolone (then change to oral prednisone as they improve. • 4. Antibiotics seem to be beneficial in COPD exacerbations despite “normal” chest Radiograms ..macrolides (clarithromycin, azithromycin fluoroquinolones (levofloxacin, moxifloxacin), cephalosporins and amoxicillin clavulanate. • 5. no benefit to using IV aminophylline. However, if the patient is using • theophylline on a chronic basis it should be continued during the exacerbation because abrupt discontinuation may worsen symptoms. • 6. Always avoid opiates
  36. 36. Pulmonary edema
  37. 37. Spontaneous Primary No evidence of overt lung disease. Air escapes from the lung into the pleural space through rupture of a small subpleural emphysematous bulla or pleural bleb, or a pleural adhesion Secondary Underlying lung disease, most commonly COPD and TB; also seen in asthma, lung abscess, pulmonary infarcts, bronchogenic carcinoma, all forms of fibrotic and cystic lung disease Traumatic Iatrogenic (e.g. following thoracic surgery or biopsy) or chest wall injury
  38. 38. • If the rim of air is < 2cm and the patient is not short of breath then discharge should be considered & CXR after 2 weeks. • Otherwise aspiration should be attempted • if this fails (defined as > 2 cm or still short of breath) then a chest drain should be inserted Primary Pneumothorax
  39. 39. Secondary Pneumothorax All patients should be admitted for at least 24 hours • if the pneumothorax is less the 1cm then the BTS guidelines suggest: giving oxygen (high flow O2) and admitting for 24 hours • If the patient is 50 years old and the rim of air is > 2cm and/or The patient is short of breath then o A chest drain should be inserted.
  40. 40. • Surgical pleurodesis is recommended in all patients following a second pneumothorax and should be considered following the first episode of secondary pneumothorax if low respiratory reserve makes recurrence hazardous
  41. 41. Cardiac Tamponade Definition Cardiac tamponade occurs when fluid accumulation in the finite serous pericardial space causes an increase in pressure, with subsequent cardiac compression and hemodynamic compromise.
  42. 42. Treatment : Aspiration of a pericardial effusion is indicated for diagnostic purposes or for the treatment of cardiac tamponade. A few millilitres of fluid aspirated through the needle may be sufficient for diagnostic purposes but pericardial drainage is needed for symptom relief.
  43. 43. Contraindication • Tamponade due to Aortic dissection • Cardiac injury
  44. 44. Pulmonary embolism triad of pleuritic chest pain, dyspnea and haemoptysis. Pulmonary embolism can be difficult to diagnose as it can present with virtually any cardiorespiratory symptom/sign depending on its location and size. So, which features make pulmonary embolism more likely? The relative frequency of common clinical signs is shown below: Tachypnea (RR>16/min) - 96% Crackles - 58% Tachycardia (HR>100/min) - 44% Fever (>37.8C) - 43% It is interesting to note that the Well's criteria for diagnosing a PE use tachycardia rather than tachypnea
  45. 45. LMWH or fondaparinux should be given initially after a PE is diagnosed. An exception to this is for: Patients with a massive PE where thrombolysis is being considered. In such a situation unfractionated heparin should be used • A vitamin K antagonist (i.e. warfarin) should be given within 24 hours of the diagnosis the LMWH or fondaparinux should be continued for at least 5 days or until INR is 2.0 or above for at least 24 hours, whichever is longer, i.e. LMWH or fondaparinux is given at the same time as warfarin until the INR is in the therapeutic range Warfarin should be continued for at least 3 months. treatment
  46. 46. Psychogenic cause of dyspnea (signs: no cyanosis, no heart or lung signs, carpopedal spasm) Treatment: anxiolytics, paper bag technique (increases needed CO2 and reduces symptoms, but may worsen the condition sometimes)
  47. 47. In children, the possibility of inhalation of a foreign body or acute epiglottitis should always be considered.
  48. 48. Foreign body---- Heimlich maneuver, supportive measures(oxygen, pulse oximetry), racemic epinephrine as temporary measure until bronchoscopy can be done, bronchoscopy Acute epiglottitis---- intubation (difficult if laryngeal edema present) , antibiotics. treatment
  49. 49. A.Immediate ABC Management : Emergency Airway Management Emergency Breathing Management Emergency Circulation Management B. Obtain initial vital signs : Temperature, Blood Pressure, and Pulse Respiratory Rate and Oxygen Saturation
  50. 50. Immediately triage unstable patients :if 1. Hypotension 2. Altered Level of Consciousness 3. Hypoxia (decreased Oxygen Saturation) 4. Arrhythmia 5. Stridor or other signs of upper airway obstruction 6. Unilateral breath sounds or other Pneumothorax signs 7. Respiratory Rate >40 breaths per minute 8. Accessory muscle use with retractions 9. Cyanosis
  51. 51. D. Initial management of acute distress 1. Obtain Intravenous Access (when appropriate) 2. Administer High Flow Oxygen 3. Evaluate and treat Hypoxia if present 4. Consider Pulmonary Embolism Diagnosis E. Initiate disease specific management 1. Emergency Management of Acute severe Asthma 2. COPD Exacerbation Management 3. Acute Pulmonary Edema Management 4. Tension Pneumothorax -Needle Thoracentesis
  52. 52. A 24-year-old man presents to the Emergency department with a two hour history of pleuritic chest pain. He denies feeling breathless, with oxygen saturations of 96% on air. A chest x ray is performed and an observant CT1 recognises a small apical pneumothorax, which when measured is 1.8 cm. Accordingly to current guidelines, what intervention should be undertaken? What`s your action ??
  53. 53. This patient has a small pneumothorax with no known underlying lung disease and as such can be classed as a spontaneous pneumothorax. According to current BTS guidelines, if the patient is not breathless and the rim of air is less than 2 cm they can be considered for early discharge and repeat chest x ray in two weeks.
  54. 54. A 19-year-old man with recurrent admissions to hospital for exacerbations of his asthma attends the Emergency department with a short history of increasing breathlessness and cough. On examination he is obviously dyspnoeic and wheezy and becoming exhausted. His respiratory rate is 16 breaths per minute, his HR is 125 bpm (sinus tachycardia) and his PEF is 30% predicted. An arterial blood gas is taken and the results are as follows: pH 7.43 (7.36 - 7.44) pO2 7.3 kPa (11.3 - 12.6) pCO2 5.2 kPa (4.7 - 6.0) What`s the severity of asthma in this case ?
  55. 55. A life threatening exacerbation of asthma can be diagnosed based on one of the following: • PEF <33% best or predicted • SpO2 <92% • PaO2 <8 kPa • Normal PaCO2 (4.6-6.0 kPa) • Silent chest • Cyanosis • Poor respiratory effort • Arrhythmia • Exhaustion, altered conscious level.
  56. 56. An 87-year-old man was admitted to the Emergency department with a two hour history of sharp central chest pain and breathlessness. One week ago he noticed his left leg had become swollen, but had decided not to consult medical advice. Apart from essential hypertension, for which he was taking bendroflumethiazide, he had no other medical conditions. He was a lifelong nonsmoker. On clinical examination he was dyspnoeic at rest with a respiratory rate of 28 breaths per minute. His blood pressure was 90/60 mmHg, pulse 110 beats per minute and regular with oxygen saturations of 86% on room air. Auscultation of his chest revealed a loud second heart sound over the right second intercostal space. What`s the diagnostic test you shoud send the patient for? What`s your treatment ?
  57. 57. A 14-year-old boy with a known nut allergy was admitted to the Emergency department following the accidental ingestion of a pistachio nut biscuit. On examination he had audible stridor and looked peripherally shut down. His blood pressure was 70/50 mmHg, oxygen saturations 86% on room air and respiratory rate of 26 breaths per minute. His pulse was feeble What is the most appropriate immediate management?
  58. 58. Anaphylactic shock requires urgent treatment with adrenaline, which is absorbed at a faster rate intramuscularly than subcutaneously.

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