Profound hypotension after atenolol in severe hypertension.

Abstract

deterioration in lung function, which has been described after nebulised asthma treatment in infancy, did not occur."4 Ipratropium bromide acts on the nose by decreasing secretions but has not been shown to alter resistance in the nasal airway. As two infants with complete nasal blockage showed a 20% improvement in specific conductance we assume that the improvement seen after ipratropium bromide was due to bronchodilatation.A Nebuhaler has been shown to be effective in giving inhaled budesonide to young children.' We used this delivery system to give budesonide and fP2 agonists to asthmatic children aged under 2 and obtained dramatic improvement in many cases (unpublished results).Though this method of delivery does not replace nebulisers in severe attacks of asthma in young children, it may enable many children without access to a nebuliser to be treated successfully at home. Handicapped patients who cannot use other inhalation devices may also benefit.

'First dose' hypotension and venodilatation [letter]

“…Although these 'first dose' hypotensive reactions may be asymptomatic, in some patients myocardial ischaemia, transient hemiparesis, dysphasias or coma have developed (Cleland et al, 1985;Hodsman et al, 1983;Packer et al, 1986;Todd & Heel, 1986;Webster, 1987); deaths have also occurred. Similar 'first dose' reactions have been described with phentolamine (Galloway et al, 1975), prazosin (Graham et al, 1976), ketanserin (Waller et al, 1987), labetalol (Maronde, 1983), renin inhibitors (Semple et al, 1988;Zusman et al, 1983), ,-adrenoceptor blockers and adrenergic neurone blockers (Kholeif & Isles, 1989;Webster, 1987). Although the underlying mechanism was originally assumed to be arterial vasodilatation, often enhanced by bradycardia (Cleland et al, 1983;Semple et al, 1988;Webster, 1987), recent evidence suggests that venous dilatation may also be important.…”

“…The patients at greatest risk of 'first dose' reactions when commencing ACE inhibitors are now well recognised, and include those with heart failure, hyponatraemia, salt depletion, high renin or aldosterone II levels, those with renovascular or severe hypertension and the elderly (Cleland et al, 1985;Kholeif & Isles, 1989;Todd & Heel, 1986;Webster, 1987). Practical measures to avoid or minimise 'first dose' reactions should therefore include identification of 'high risk' patients, prior correction of salt and water depletion with strict bed rest and close observation when commencing therapy in such individuals.…”