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Ventilatory support in asthma and COPD

Ventilatory support in asthma and COPD. By HP Shum 3 Mar 2006. Definitions. COPD: disease due to emphysema or chronic bronchitis characterized by airflow limitation that is not fully reversible. Definitions.

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Ventilatory support in asthma and COPD

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  1. Ventilatory support in asthma and COPD By HP Shum 3 Mar 2006

  2. Definitions • COPD: disease due to emphysema or chronic bronchitis characterized by airflow limitation that is not fully reversible

  3. Definitions • Asthma: an inflammatory condition in which complex cellular, chemical, and nervous system (sympathetic, cholinergic and nonadrenergic-noncholinergic) mediators lead to heightened bronchial responsiveness and episodic, variable and reversible airflow obstruction

  4. Dynamic pulmonary hyperinflation • Common findings in patient with acute exacerbation of asthma / COPD

  5. Dynamic pulmonary hyperinflation • Why this occur? • Increased ventilatory requirement • Prolong expiratory time constant due to increased airway obstruction by inflammation, mucus plug, bronchospasm, with or without reduced elastic recoil • Shortening of expiratory time Am Rev Respir Dis 1989, 139:242–246 Eur Respir J 1997, 10:1663–1674

  6. Dynamic pulmonary hyperinflation • Resulting in: • Increased inspiratorythreshold load for breath initiation • Increased work ofbreathing Intensive Care Med 2001, 27:166–178

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  8. Other factors • The capacity of the respiratory muscles to generate inspiratorypressure is limited by decreased operatinglength and impaired geometric arrangement Clin Chest Med 2000, 21:679–692 • Long-term steroid use and/or malnutrition contributesto strength impairment in many patients with severechronic disease Am Rev Respir Dis 1996;153:610–615 • Blunted respiratory drivedecrease responsivenessto hypoxia and hypercapnia N Engl J Med 1994,330:1329–1334

  9. Pharmacological Management • Bronchodilator • 2-adrenergic receptor agonists causes bronchodilation via cAMP-mediated relaxation of bronchial smooth muscle (Albuterol, Terbutaline) • Anticholinergics mediated by blocking formation of cGMP (Ipratropium bromide, tiotropium)

  10. Pharmacological Management • Corticosteroids • Reduce airway inflammation, airway responsiveness, mucus secretion and airway edema. Also enhance -adrenergic responsiveness and relax bronchial smooth muscle (beclomethasone, budesonide, hydrocortisone, methylprednisolone)

  11. Pharmacological Management • Methylxanthines • Improve respiratory drive and muscle function, weak bronchodilator. Act by non-specific inhibition of phosphodiesterase to increase intracellular cAMP, blockage of adenosine and release of endogenous catecholamines (theophylline, aminophylline)

  12. Pharmacological Management • Antibiotics • COPD • Airway colonization with potential pathogens • High risk of progress to more severe bronchitis / pneumonia which is poorly tolerated in those critically ill COPD • Antibiotic use recommended Expert Rev Anti Infect Ther. 2006 Feb;4(1):101-24 Treat Respir Med. 2005;4(3):153-67 • Asthma • Usually no chronic bacterial colonization • Use of antibiotic should based on clear evidence of infection only

  13. Benefits of mechanical ventilation • Assist orsupport impaired ventilatory function • Reduce the workof breathing • Allow muscle resting • Facilitate sleeping • Improve gas exchange • Allowing time for restorationof ventilatory function through treatment of eitherthe underlying disease or the precipitating causes ofacute decompensation

  14. Ventilation in COPD and Asthma • Even though the pathogenesis and clinical course of COPD and asthma differ, their management is similar in many aspects and this is especially true on the ventilatory support

  15. NIPPV for COPD exacerbation • Consensus statement from the American Association for Respiratory Care Respir Care 1997; 42:361 • Suggest early use of NIPPV in setting when at least 2 of the following occur: • Respiratory distress with moderate to severe dyspnea • Arterial pH less than 7.35 with PaCO2 above 45 mmHg (6 kPa) • Respiratory rate of 25/minute or greater

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  17. NIPPV for COPD exacerbation • Keenan SP et al: Crit Care Med 1997 Oct;25(10):1685-92 • Meta-analysis of use of NIPPV in those with acute resp. failure • 7 RCTs

  18. NIPPV for COPD exacerbation • randomized to early use of NIPPV versus standard care • In COPD groups • lower rate of intubation (odds ratio 0.20; 95% CI 0.11-0.36) • lower risk of death (odds ratio 0.29; 95 percent Cl 0.15 to 0.59) Risk of death Risk of intubation

  19. NIPPV in asthma exacerbation • Cochrane Database Syst Rev. 2005 Jul 20;(3):CD004360 • Only RCT for adult included, those with features of COPD were excluded • Up till 4/2004, only 1 RCT obtained • The application of NPPV in patients suffering from status asthmaticus, despite some interesting and very promising preliminary results, still remains controversial. Large, prospective, randomised controlled trials are therefore needed to determine the role of NPPV in status asthmaticus

  20. NIPPV in asthma exacerbation • Soroksky A et al: Chest 2003;123:1018-1025 • Randomised double-blind, placebo controlled trial conducted in the emergency department of the Asaf Harofe Medical Center, Zerifin, Israel • Inclusion criteria: FEV1 < 60% of predicted; respiratory rate > 30 breaths/min; Hx of asthma >= 1 year; duration of current asthma attack of > 7 days • Exclusion criteria: smoking history of > 10 years; known chronic pulmonary disease other than asthma; intubation for CPR; haemodynamic instability (HR>=150bpm / SBP <=90mmHg), decreased GCS, CHF, IHD, pregnancy, facial deformity, lung infiltration due to APO / pneumonia

  21. NIPPV in asthma exacerbation • Soroksky A et al: Chest 2003;123:1018-1025 • NIPPV: control (nebulized salbutamol / ipratropium + IV steroid) = 17: 16 • Duration of tx: 3 –4 hrs • NPPV was applied through a nasal mask (BiPAP model ST; Respironics) • IPAP start at 8 cmH2O, increasedgradually by 2 cmH2O q15min to max15 cmH2O, or until RR< 25 breaths/min (mean:13) • EPAP set at 3 cmH2O, increased gradually by 1cmH2O q15min to max 5cmH2O (mean: 4) • Primary end point: increase of FEV1 >50% baseline • Secondary end point: hospitalization rate

  22. NIPPV in asthma exacerbation • Soroksky A et al: Chest 2003;123:1018-1025 • 80% in NIPPV group vs 20% in control group reach primary end point (p<0.004)

  23. NIPPV in asthma exacerbation • Hospitalization was required for 3 of 17 patients (17.6%) in the NIPPV group, as compared with 10 of 16 patients (62.5%) in the control group (p = 0.0134). • Concluded that: In selected patients with a severe asthma attack, the addition of NIPPV to conventional treatment can improve lung function, and significantly reduce the need for hospitalization

  24. NIPPV in asthma exacerbation • No clear guideline for use of NIPPV in asthma • Selection criteria may include: • Moderate to severe dyspnea • RR >=25 • Accessary muscle use or paradoxical breathing • Presence of hypercapnic acidosis Am J Respir Crit Care Med 2001; 163: 540-77

  25. Intubation in asthma • Rapid sequence intubation should be performed by the most experienced operator • Manipulation of the airway in the asthmatic can worsen the bronchospasm or provoke a laryngospasm

  26. Intubation in asthma • Pretreatment with atropine and/or topical anesthetics at the level of the hypopharynx and glottis • The largest endotracheal tube possible should be chosen to lower airflow resistance and permit suctioning of thick mucosal secretions • A cuffed endotracheal tube is sometimes useful even in small children (<5 years) when insufflation pressures become very high

  27. Inducehypotension through a combination of directvasodilation, histaminerelease, and vagally-mediated bradycardia.

  28. Post-intubation • Hypotension very common in severe asthmatic after intubation • Sedative use • Hypovolemia (increased sweating and decreased water intake) • Pneumothorax • Use of PEEPe • Dynamic hyperinflation (gas trapping) • delivering of 2–3 breaths/min of 100% oxygen for few minutes or disconnect from ambu-bag / ventilator • in the absence of pneumothorax, the mean intrathoracic pressure will fall, systemic blood pressure will rise, pulse pressure will increase, and pulse rate will fall Am J Respir Crit Care Med1995, 151:1296-1316

  29. Principles of ventilation • Minimization of dynamic pulmonary hyperinflation • Controlled hypoventilation / permissive hypercapnic ventilation • Prolonged expiratory time • Unload breathing effort • Promote synchrony between patient and ventilator

  30. Controlled hypoventilation • Minute volume, expiratory time fraction, and severity ofairway narrowing are primary determinants of dynamichyperinflation • Decrease minute ventilation • lessens the expiratory flow requirement • allowing the lung to decompress • peak static lung pressures (plateau pressures) to decline

  31. Controlled hypoventilation • Aimed to achieve plateau pressure <=30cmH2O, moderate hypercapnia (aim PaCO2<=90mmHg / 12 KPa) and acidosis (aim pH >=7.2) Curr OpinPulm Med 1998, 4:4–8 Crit Care Clin 1998, 14:685–705

  32. Prolonged expiratory time • Achieved by: • shorter inspiratory time fraction • using a higher peak inspiratory flowsetting (70–100 L/min) • eliminating inspiratory pause time • However, lengthening of the expiratory periodis only modestly effective if minute ventilation remainsthe same

  33. Unload breath effort • Gas trapped at the end of expiration exerts a positive pressure on the alveoli – PEEPi or auto-PEEP • 41% of inspiratorymuscle effort was expended to overcomePEEPiin patients with COPD duringspontaneousbreathing Am J Respir Crit Care Med 1996, 54:1301–1309

  34. Unload breath effort • Adding PEEPe in COPD may attenuate the inspiratory muscle effort needed to trigger inspirationand improving patient-ventilator interaction • If PEEPe is set higher thanPEEPi, it mayworsen the dynamichyperinflation (esp. true in those asthmatics) • Aim 85% PEEPi

  35. Promote synchrony between patient and ventilator • Most patients take shallowquick breaths and become agitated shortly after intubationbecause of dyspnea and the discomfort of invasiveventilation Clin Chest Med 1996, 17:577–590 • Controlled hypoventilation also required good sedation +/- NMB to achieve • NMB + high dose steroid   risk of myopathy • NMB should be used only for short periods (<24hr) and only as absolutely necessary Chest 1999, 115:1627–1631

  36. Correction of hypoxemia is first priority • In status asthmaticus, low V/Q ratio mainly due to mechanical problem and true shunt does not contribute significantly to the hypoxemia • Low FiO2 (0.3-0.5) usually need to raise PaO2 >60mmHg • High FiO2 needs may indicates some kind of complication e.g. mucoid impaction, atelectasis, pneumonia, or pneumothorax • Complete correctionof the respiratory acidosis is not an urgent priority

  37. Alternative technique in difficult patients • Severe bronchospasm worsen ventilation, oxygenation and increase DHI • Ketamine • cause bronchodilatation by both sympathomimetic potentiation and direct effect on airway smooth muscle Pediatr Emerg Care 1996; 12: 294-7 • Some case reports showed beneficial effects Pharmacotherapy. 2001 Sep;21(9):1100-6 J Asthma. 2001 Dec;38(8):657-64 • no clinical benefit in children with moderately severe asthmatic attacks Ann Emerg Med. 2005 Jul;46(1):43-50

  38. Alternative technique in difficult patients • Volatile inhalational agents (isoflurane, halothane): at 0.5-2% induce bronchodilation and sedative effect decreased bronchospasm Crit Care Med 1986;14: 832-833 Intensive Care Med 1990; 16:104-107 Pediatr Crit Care Med. 2000 Jul;1(1):55-9 Arerugi. 2005 Jan;54(1):18-23. Japanese • All are cases reports only and no RCT a/v

  39. Alternative technique in difficult patients • Heliox: inert gas, 1/4 the density of air and mixtures of helium and oxygen (60% / 40%) decrease the work of breathing by decreasing inspiratory and expiratory resistance Crit Care Med2000, 28:2721–2728 • The Cochrane Database of Systematic Reviews 2003, Issue 2. Art. No.: CD002884 • 6 RCTs, 369 asthmatics • Heliox use did not improve pulmonary functions compared to standard care

  40. Alternative technique in difficult patients • The Cochrane Database of Systematic Reviews 2001, Issue 1. Art. No.: CD003571 • 4 RCTs, about 200 COPD patients • Heliox vs standard medical care • no significant differences in the change of FEV1 and FVC between

  41. Alternative technique in difficult patients • MgSO4: block Ca channels thereby mediating smooth muscle relaxation and bronchodilation JAMA 1989; 262: 1210-3 • The Cochrane Database of Systematic Reviews 2000, Issue 1. Art. No.: CD001490 • 7 RCTs, 665 patients • Non-significant improvement of PFR • Admission rate decreased in severe subgroup but not in overall asthmatics

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