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Asthma

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Asthma

Aetiology

  • pathogenesis not completely understood
  • immunological mechanisms important
  • airways hyper-reactive to allergens (eg housemites, pollen), non-specific precipitants (eg cold air, exercise, atmospheric and industrial irritants, viral infection) and drugs (eg aspirin, beta-blockers)
  • no precipitant can be identified in over 30%

Clinical presentation

Acute severe asthma

  • more common form
  • F>M
  • occurs in patients with poorly controlled asthma
  • symptoms may be minimal because of underperception of breathlessness, denial and behaviour modification
  • may develop over hours to days
  • predominant airway pathology is chronic inflammation, with oedema and mucous plugging

Hyperacute fulminating asthma

  • young patients
  • M>F
  • relatively normal lung function but high bronchial reactivity
  • previous episodes of severe asthma or evidence of bronchial reactivity (eg diurnal variation)
  • life threatening episode may arise de novo
  • attack usually rapid and may lead to severe respiratory insufficiency within hours (occasionally minutes)
  • response to aggressive therapy usually prompt and may avert mechanical ventilation or shorten duration

Clinical features of severe asthma

  • hypoxaemia invariable. Due to increased V/Q mismatch: roughly proportional to severity of airflow obstruction
  • pulsus paradoxus > 10 mmHg. During vigorous inspiration venous return is augmented with an increase in RV filling early in inspiration. This results in a shift of the intraventricular septum to the left with a resultant decrease in LV filling. This reduction in stroke volume is exacerbated by increased LV afterload by the large negative pleural pressure and by increased RV afterload as a result of hyperinflation. During forced expiration venous return in decreased. Net effect of these cyclical changes is to accentuate the normal inspiratory reduction in stroke volume and hence systolic pressure. NB the fatiguing asthmatic may not be able to generate significant changes in pleural pressure and therefore pulsus paradoxus may decrease
  • can't complete sentences in one breath
  • resp rate > or = 25/min
  • pulse > or = 110/min
  • peak expiratory flow rate (PEFR) <50% of predicted or best

Life-threatening

  • PEFR <33% of predicted or best
  • silent chest, cyanosis or feeble respiratory effort
  • bradycardia or hypotension
  • exhaustion, coma, or confusion

Very severe, life threatening attack

  • normal or raised PaCO2
  • severe hypoxia: Pao2 <8 kPa irrespective of treatment with oxygen
  • low pH

Treatment

Immediate treatment

  • 40-60% oxygen
  • salbutamol 5mg or terbutaline 10mg via oxygen driven nebuliser
  • prednisolone 30-60mg PO or hydrocortisone 200mg IV, or both if patient very ill
  • no sedatives of any kind
  • CXR to exclude pneumothorax or mucous plugging of major airway
  • if life-threatening features are present:
    • add ipratropium 0.5mg to nebulised beta agonist
    • IV aminophylline 250mg over 20 mins (provided patient not already on theophylline) or salbutamol or terbutaline 250 mcg over 10 mins

Inhaled beta agonists

Nebulized beta agonists remain first-line bronchodilator therapy. Minimum reservoir volume of 2-4 ml and oxygen flow rate of 6-8 l/min advocated for optimal nebulizer output. Dose required for MDI and nebulisers is higher in ventilated patients due to deposition in circuit and ETT. Increase dose until there is a 15% fall in airway peak-pause pressure in response. (Peak-pause pressure is a useful measure of airway resistance). Bronchodilators may transiently increase increase hypoxaemia by increasing V/Q mismatch: readily overcome by increasing oxygen. Increasing evidence that administration by metered dose inhaler via a spacer device into inspiratory limb of ventilator circuit may be as effective or more effective than use of a nebulizer

Inhaled anticholinergics

Ipratropium bromide augments response to beta agonists. Preservative in multi-dose preparations of ipratropium may result in dose-dependent paradoxical bronchoconstriction

Intravenous beta agonists

Salbutamol 250 m g over 10 mins in life threatening cases. 5-20 m g/min by infusion.

Theophylline

  • Relaxes bronchial smooth muscle but mode of action not completely understood: probably involves competitive inhibition of adenosine receptors.
  • Inhibition of phosphodiesterase is negligible at therapeutic concentrations
  • Improves diaphragmatic contraction
  • Increases rate and force of cardiac contraction. Increases rate of urine production.
  • No clear evidence to use or not use theophylline in acute severe asthma although is indicated for chronic asthma.
  • Loading: 3mg/kg (half the traditional recommendation) over 20-30 min followed by 0.5 mg/kg. Measure serum concentration 1-2 h after loading and then at 12 and 24 h.
  • NB infusion rate should be reduced in patients with cirrhosis, CCF, COPD, acute fevers or receiving cimetidine, erythromycin or antiviral vaccines.
  • Dose may need to be increased in young patients, smokers without chronic airflow obstruction or regular drinkers without liver disease.

Magnesium

May bronchodilate by blocking Ca mediated bronchoconstriction and inhibiting parasympathetic acetyl choline release. No controlled evidence of benefit but may be tried in severe asthma refractory to standard therapy. Dose: 5-10 mmol over 20 min

Antibiotics

No benefit from routine use

Helium/oxygen mixture

Anecdotal evidence of benefit but use in ventilated patients requires recalibration of blenders and flow meters in ventilator

Inhalation agents

All are bronchodilators. Anecdotal evidence of benefit.

Ketamine

Decreases airway resistance. No established role

Epinephrine

  • No advantage in practice to giving beta2 agonists instead of epinephrine or vice versa.
  • Exception is the pregnant patient. Epinephrine has been associated with congenital malformations and may decrease uterine blood flow. Beta2 agonists may inhibit labour.
  • Terbutaline may result in greater tachycardia for the same degree of bronchoconstriction than epinephrine.
  • Theoretical advantage of epinephrine is that its alpha effects of vasoconstriction and mucosal shrinkage may increase airway diameter in addition to beta effects.
  • Epinephrine should be given with extreme caution and with ECG monitoring. Initial dose of 0.2-1 mg over 3-5 min followed by a continuous infusion of 1-20m g/min

Hydration

Patients with prolonged severe attacks prior to presentation may be dehydrated because of poor fluid intake. Take care not to overload patient. Role of fluids in decreasing sputum tenacity unclear

Bronchoalveolar lavage

May have a role in ventilated patients without critical hyperinflation whose recovery is delayed by resistant mucus impaction

Mechanical ventilation

Non-invasive ventilation

  • insufficient data to recommend this form of ventilation in acute asthma
  • available data suggests that it is probably safe

Invasive ventilation

When to ventilate

  • complex decision which needs to be based on a number of factors:
    • rate of deterioration
      • monitor pH and PaCO2
      • respiratory rate
      • clinical signs of exhaustion
    • likely response to treatment

- neuromuscular block. Indicated in patients who, in spite of sedation, continue to breath in a desynchronized manner. Vecuronium seems to be associated with a higher incidence of myopathy and neuropathy. Theoretical risk of histamine release following administration of atracurium. Clinical significance of this is unknown. Effects of pancuronium on heart rate make it less suitable
- initial settings: tidal volume 8 ml/kg, rate 10-14, (minute volume 115 ml/kg), inspiratory flow rate 80-100 L/min
- set ventilator to minimize hyperinflation by maximizing expiratory time. Lung hyperinflation best estimated using volume of gas at end-inspiration above FRC (Vei). Latter can be measured by measuring total exhaled volume during 20-60 secs of apnoea. Vei>20ml/kg has been shown to predict hypotension and barotrauma. Suggested that ventilator settings are altered to keep VEI < 20 ml/kg

Maximizing expiratory time necessitates use of a high inspiratory flow rate and resultant high peak airway pressure which has in past been shown to be associated with barotrauma. However recent data has failed to show this relationship, possibly because peak airway pressure does not predict alveolar pressure or the degree of lung hyperinflation. Plateau pressure better indicator of alveolar pressure.

Benefit from this ventilatory strategy in terms of outcome have yet to be convincingly demonstrated.

Note that it is very difficult to distinguish clinically between tension pneumothorax and severe hyperinflation and therefore if a trial of hypoventilation does not improve haemodynamics rapidly insertion of bilateral chest drains should be considered. Conversely chest drains should not be inserted without clear evidence of pneumothorax until a trial of hypoventilation has failed to produce improvement.
- use of pressure control ventilation illogical as resistive component is high resulting in use of low alveolar pressures. Use of SIMV in the patient who is making no respiratory effort allows the use of longer expiratory times than is possible in other volume preset modes
- hypotension in the ventilated patient may be due to sedation, dynamic hyperinflation or pneumothorax. Resolution of hypotension during apnoea is strongly suggestive that dynamic hyperinflation is the cause.

Monitoring ventilation

  • plateau airway pressure during 0.5 s end-inspiratory exhale occlusion. Represents alveolar pressure at end inspiration - directly proportional to degree of hyperinflation. Keep < 20 cm H2O
  • PEEPi represents alveolar pressure at end of expiration. Proportional to trapped gas volume. May underestimate degree of hyperinflation and does not take into account the tidal volume which also determines risk of barotrauma. Not recommended but if measured should be done with small constant tidal volume. Keep < 12 cmH2O
  • End-inspiratory volume (VEI) above FRC. This is difficult to measure in clinical practice.
  • CVP or oesophageal balloon pressures. Extent of fall in CVP and rise in BP during a period of apnoea indicates degree of circulatory tamponade due to hyperinflation

Asthma in children

- maximal therapy should be introduced early
- nebulised salbutamol 2.5-5mg/dose depending on severity. In severe cases continuous nebulisation of undiluted 0.5% solution
- children < 9 yrs metabolize theophylline more rapidly and require higher doses: aminophylline 1.1mg/kg/h. Measure serum levels. Theophylline may override pulmonary hypoxic vasoconstrictor response and worsen hypoxia
- continuous infusion of salbutamol has been shown to reduce need for CMV. Early use improves outcome. Add when PaCO2 rising or >8 kPa as infusion of 1 m g/kg/min increasing every 20 min until PaCO2 falls by about 10% to maximum of 14 m g/kg/min
- ??? bicarbonate for metabolic acidosis to improve cardiovascular function and bronchomotor responsiveness to theophylline

Asthma in pregnancy

- treatment of severe asthma little different from that in non-pregnant
- larger doses of theophylline may be required due to larger volume of distribution

Further reading

Duncan AW. Acute respiratory failure in children. In Oh TE (ed), Intensive Care Manual, 4th Ed., Butterworth Heinemann, Oxford, 1997, pp 888-900

British Thoracic Society and others, Guidelines for the management of asthma: a summary. Br Med J 1993; 306:776-82

Tuxen DV. Permissive hypercapnic ventilation. Am J Respir Crit Care Med, 1994; 150:870-4

Tuxen DV, Oh TE. Acute severe asthma. In Oh TE (ed), Intensive Care Manual, 4th Ed., Butterworth Heinemann, Oxford, 1997, pp 297-307

 


Charles Gomersall December 1999

 

Charles Gomersall, April, 2014 unless otherwise stated. The author, editor and The Chinese University of Hong Kong take no responsibility for any adverse event resulting from the use of this webpage.
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