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Mechanical Ventilation for severe Asthma
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Mechanical Ventilation for severe Asthma

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Presented at Ninth Pulmonary Medicine Update Course-2009, held at Cairo, Egypt

Presented at Ninth Pulmonary Medicine Update Course-2009, held at Cairo, Egypt

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  • In one study of 21 acute asthmatics with a mean PEFR of 144 L/min, nasal CPAP of 5 or 7.5 cm H2O significantly decreased respiratory rate and dyspnea compared with placebo.
  • If the patient deteriorates or fails to improve despite intensive therapy, intubation and mechanical ventilation must be considered.
  • Since intubation and mechanical ventilation can be life saving but are associated high morbidity and significant mortality

Transcript

  • 1. Mechanical Ventilation for Severe Asthma Niall D. Ferguson, MD, FRCPC, MSc Assistant Professor Interdepartmental Division of Critical Care Medicine University of Toronto
  • 2. Asthma Death Rates Modified from TRENDS IN ASTHMA MORBIDITY AND MORTALITY, ALA • Number of Deaths in 2004 3780 • Age Adjusted Mortality in 1999 1.7 / 100,000 • Age Adjusted Mortality in 2004 1.3 / 100,000 • Reduction in Mortality  18.8% decrease compared to 1999
  • 3. Life Threatening Asthma • Clinical  inability to speak due to severe dyspnea  altered mental status  inter-costal retractions  worsening fatigue  absence of wheezing  bradycardia  absence of pulsus paradoxus
  • 4. Life Threatening Asthma • Physiologic  PCO2 of > 42 µµΗγ  PEF or FEV1 <20 % predicted or personal best
  • 5. Pathophysiology Different patterns of fatal asthma Severe asthma Papiris 2002 Scenario of asthma death Variable Type 1 Type 2 Time course Subacute worsening (days). 'Slow onset – late arrival' Acute deterioration (hours). 'Sudden asphyxic asthma' Frequency 80–85% 15–20% Airways Extensive mucous plugging More or less 'empty' bronchi Inflammation Eosinophils Neutrophils Response to treatment Slow Faster Prevention Possible (?)
  • 6. Cause of Death • Type 1  hypercapnic respiratory failure  mixed acidosis  asphyxia  complications of mechanical ventilation, such as barotrauma and ventilator- associated pneumonia
  • 7. Cause of Death • Type 2  rapidly severe hypercapnic respiratory failure with combined metabolic and respiratory acidosis  asphyxia
  • 8. Risk Factors for Death from Asthma • Asthma history  Prior severe exacerbation (intubation or ICU admission)  Two or more hospitalizations for asthma in the past year  Three or more ED visits for asthma in the past year  Hospitalization or ED visit for asthma in the past month  Using >2 canisters of SABA per month  Difficulty perceiving asthma symptoms or severity of exacerbations  Other risk factors:  lack of a written asthma action plan  Sensitivity to Alternaria
  • 9. Risk Factors: Death from Asthma • Social history  Low socioeconomic status or inner-city residence  Illicit drug use  Major psychosocial problems • Co-morbidities  Cardiovascular disease  Other chronic lung disease  Chronic psychiatric disease
  • 10. Differential Diagnosis • Vocal cord dysfunction • COPD exacerbation • Congestive heart failure • Pulmonary embolism • Mechanical obstruction of the airways (benign and malignant tumors) • Pneumothorax • Pneumonia
  • 11. Asthma Severity Assessment Symptoms Severe Respiratory Arrest Imminent Breathless At rest, sits upright Talks in Words Alertness Usually agitated Drowsy or confused
  • 12. Asthma Severity Assessment Signs Severe Respiratory Arrest Imminent Respiratory rate >30/minute Accessory muscles Usually Paradoxical diaphragmatic movement Wheeze Usually loud Absent Pulse >120 Bradycardia
  • 13. Asthma Severity Assessment Signs Severe Respiratory Arrest Imminent Pulsus paradoxus >25 mmHg Absence re: fatigue PEF/FEV1 <40 percent <25 percent Pa02 / PaCO2 <60 mmHg / >42 mmHg SaO2 <90 percent
  • 14. Medical Management of Life Threatening Asthma • Oxygen  maintain a SaO2 >90 percent • Inhaled short acting B2 agonists (SABA)  4–8 puffs every 20 minutes up to 4 hours, then every 1–4 hours as needed • Ipratropium bromide  8 puffs every 20 minutes as needed up to 3 hours
  • 15. Medical Management of Life Threatening Asthma • Systemic corticosteroids  40–80 mg/day in 1 or 2 divided doses until PEF reaches 70% of predicted or personal best • Subcutaneous epinephrine  0.3–0.5 mg every 20 minutes for 3 doses sq
  • 16. Medical Management of Life Threatening Asthma • Magnesium Sulphate (I.V.)  2 grams in adults and 25–75 mg/kg up to 2 grams in children • Heliox  consider when using nebulizer Rx • Methylxanthines  increases the frequency of adverse effects • Antibiotics  evidence of pneumonia or sinusitis
  • 17. Monitoring during treatment • Serial Measurements of Lung Function  Failure of treatment to improve predicts a more severe course and the need for hospitalization • Lab Studies  Hypercapnia, metabolic acidosis, CBC, electrolytes • Chest Radiography  exclude complications such as lobar atelectasis, pneumothorax, pneumomediastinum, pneumopericardium, or alternate diagnosis such as congestive heart failure and pneumonia • Electrocardiogram  signs of right heart strain
  • 18. Severe Life Threatening Asthma ICU/Mechanical Ventilation
  • 19. Criteria for ICU admission • PaCO2 > 45 mmHg • impaired consciousness • respiratory arrest • significant hypoxia (transcutaneous oxygen saturation <92%) with severe airway obstruction • ICU admission may also be indicated for respiratory arrest, altered mental status, myocardial injury, and when there is need for frequent nebulizer treatments.
  • 20. Pulmonary Hyperinflation • Increase in functional residual capacity  Can be as much as 2x normal • Critical limitation of the expiratory flow:  Reduced driving forces of the expiratory flow  Low pulmonary recoil  High outward recoil of the chest wall generated by the persistent activation of the inspiratory muscles  Increased resistance to airflow  Severely reduced airway caliber  Expiratory narrowing of the glottic aperture
  • 21. Pulmonary Hyperinflation • Increase in the time constant of the respiratory system (prolonged expiration) • Inspiration starts before static equilibrium is reached (PEEPi) • PEEPi depends on:  Vt  Time constant of the respiratory system  RR (shortening of the expiratory time)
  • 22. Non-Invasive Ventilation • Mask CPAP:  Reduce transdiaphragmatic pressure  Improve comfort  Reduce hemodynamic effects (pulsus paradoxus)  May re-expands atelectasis  May decreases airflow obstruction J Crit Care 1993;8:87 Am Rev Respir Dis 1982;126:812 Chest 1996;110:767 Chest 2003;123:1018
  • 23. Non-Invasive Ventilation • Improve gas exchange, alleviate respiratory distress, prevent exhaustion and improve hemodynamics. • In selected patients NIV can shorten the attack, improve lung function and prevent ICU admission. J Crit Care 1993;8:87 Am Rev Respir Dis 1982;126:812 Chest 1996;110:767 Chest 2003;123:1018
  • 24. Mechanical Ventilation • Life saving intervention needed by a small minority of patients! • Fewer deaths with controlled hypoventilation compared with ventilation in which carbon dioxide levels were normalized  historical cohorts and case series have reported mortality rates of 7.5­23%
  • 25. Mechanical Ventilation • Mechanical ventilation is associated with hypotension, barotrauma, infection, and myopathy, especially when prolonged paralysis is required with muscle relaxants and systemic corticosteroids. • Adverse effects reported in one retrospective study of 88 episodes of mechanical ventilation were hypotension (20%), barotrauma (14%), and arrhythmias (10%).
  • 26. Intubation • < 1% of asthmatics require intubation for mechanical ventilation. • Rapid sequence intubation is the method of choice • Crucial objective is to prevent any further increase in lung hyperinflation
  • 27. Intubation • Absolute indications:  Respiratory arrest  Coma • With maximum medical therapy:  Worsening pulmonary function tests  Decreasing PaO2  Increasing PaCO2  Progressive respiratory acidosis  Declining mental status  Increasing agitation
  • 28. Intubation • Post-intubation hypotension  25% to 35% of patients after intubation  loss of vascular tone due to sedation, hypovolemia, tension pneumothorax, or hyperinflation • Barotrauma was found to complicate status asthmaticus in 14 to 27% of patients
  • 29. Mechanical Ventilation • Initial ventilator settings  Low RR (8-12 breaths/min)  Small Vt 6-8 cc/kg of predicted body weight  High peak inspiratory flow (70-100 L/min)  Prolonged expiratory time (I:E 1:2-1:3)  PEEP to compensate for PEEPi if patient is breathing spontaneously (80% of auto- PEEP)  ZEEP if patient is sedated, paralyzed and on controlled mechanical ventilation to maximize exhalation.
  • 30. Permissive Hypercapnia • PaCO2 up to 90 mm Hg • Generally tolerated when adequate oxygenation is achieved • The main contraindication is intracranial disease • Should be avoided in patients who have already suffered an anoxic brain injury and cerebral edema following cardiorespiratory arrest
  • 31. Mechanical Ventilation • Assessing lung inflation  The volume at end-inspiration, termed Vei, is determined by collecting expired gas from total lung capacity to functional residual capacity during 40 to 60 seconds of apnea. A Vei greater than 20 mL/kg has been correlated with barotrauma. • Pplat < 30 • PEEPi Am Rev Respir Dis 1992;146:607.
  • 32. Sedation • Propofol for short term intubation • Midazolam for prolonged ventilation • Morphine or fentanyl depending on hemodynamics  Morphine can cause histamine release
  • 33. Sedation and paralysis • Ketamine  intravenous anesthetic with sedative, analgesic, and bronchodilating properties  indirectly stimulates catecholamine release and, in a dose of up to 2 mg/kg, will produce bronchodilation in the critically ill asthmatic
  • 34. Paralysis • Indication:  When safe and effective mechanical ventilation cannot be achieved by sedation alone • Short-term muscle paralysis
  • 35. Medical Rx with MV • Bronchodilators  Higher drug dosages are required and the dosage should be titrated to achieve a fall in the peak-to-pause airway pressure gradient • General anesthetics  Halothane and enflurane are general anesthetic bronchodilators that can acutely reduce peak pressure and PaCO2 Crit Care Med 2002; 30:477–480 Intensive Care Med 1990; 16:104-107 Chest 1994;106;1401-1406 CHEST 2003; 123:891–896
  • 36. Heliox • Heliox, an 80:20 mixture of helium and oxygen, can be considered in patients with respiratory acidosis who fail conventional therapy. • Helium is a low-density, inert gas that lowers airway resistance and decreases respiratory work. • Significant improvement may be noted within 10- 20 minutes of initiating therapy in the asthmatic with severe bronchospasm.
  • 37. Weaning from MV • Extubation  spontaneous breathing trial once:  PaCO2 normalizes at a minute ventilation that is less than 12 LPM  airway resistance is less than 20 cm H2O/l  the patient follows commands, and  neuromuscular weakness has not been identified
  • 38. Rescue therapies • ECLS  ECMO  NovaLung Am J Emerg Med 1997;15:566-569 Chest 1993;103:1651-54
  • 39. Rescue therapies • Novalung  pumpless low resistance gas exchange membrane reliant on arteriovenous shunt and a sweep flow oxygen for membrane diffusion of oxygen and carbon dioxide.  Arteriovenous and venovenous  Patients: rescue therapy for patients with refractory bronchospasm, who failed all usual interventions, have arterial PaCO2 >110 mmHg and have severe acidosis. Crit Care Med 2007; 35:945–948
  • 40. Novalung • Reasons  Bronchospasm in acute severe asthma is usually reversible, iLA should only be required for short periods of time  Novalung is highly effective at CO2 clearance. Usually Oxygenation is not a major problem  Patients with acute severe asthma have have sufficient cardiac output and blood pressure to maintain arteriovenous shunt across the membrane • Cons  Large bore arterial and venous cannulation  Systemic anticoagulation
  • 41. Life Threatening Asthma • Be on the alert in order to identify high risk patients • Be ready to initiate life saving treatments, possibly even including inhaled anaesthetics and NovaLung • Try your best to prevent complications
  • 42. n.ferguson@utoronto.c a October 20-22, 2009 Metro Toronto Convention Centre