Haemodynamic responses to intubation: what more do we have to know?

THE influence of airway manipulation on heart rate and blood pressure was recognized more than 50years ago, and the magnitude of the changes was observed to depend on the depth of anaesthesia (1, 2). In 1951, King and co-workers described in detail what we now know as the haemodynamic response to laryngoscopy and intubation. In patients anaesthetized with thiopental, a mean rise of 53mmHg in systolic arterial pressure and of 23 beats per minute in heart rate were recorded after tracheal intubation. The changes appeared during laryngoscopy, and levelled off within 5min of intubation (2). The results of these early studies have not been challenged. However, in the decades that followed, hundreds of studies aiming tomodify the cardiovascular response have been published in the anaesthesia literature. Among the first ones, Wycoff (3) showed attenuation of the haemodynamic response to laryngoscopy and intubation with topical anaesthesia of the airway, and similarly, Kautto and Heinonen demonstrated attenuation but not inhibition of the pressor response by aerosol spray or gargling with viscous lidocaine before the induction of anaesthesia (4). Since the earliest studies, the favourable effect of topical anaesthesia has been questioned, until in 2001 when Takita and others suggested that it is effective only if applied at least 2min before the laryngoscopy (5). Laryngoscopy and tracheal intubation contribute to the responses separately as shown by King et al. and Shribman and others (1, 6). Also, the duration of laryngosopy has a significant effect on the magnitude of the pressor response, during a 60-s laryngoscopy, mean arterial pressure increased until 45 s; thereafter, no further increase was seen until tracheal intubation (7). It is generally accepted that the increases in blood pressure and heart rate occur within 30 s of the stimuli, and can last up to 5min. Consequently, when the attenuation of these responses is studied, direct arterial blood pressure measurement should be a standard practice. On the other hand, inserting an arterial cannula in healthy patients undergoing minor surgery for research purposes has been considered unethical by some institutional committees, which limits the selection of patients for these studies. Furthermore, to obtain reliable results, only patients without anticipated difficulties in airway management should be included, and the duration of laryngoscopy and intubation needs to be recorded. The anaesthetic agents may be considered to be the most appropriate choice in controlling the changes in haemodynamic parameters at induction of anesthesia. In a double-blind and placebo-controlled trial, Kautto demonstrated that fentanyl 2mg/kg attenuated and fentanyl 6mg/kg inhibited the pressor response (8). The relatively high doses of fentanyl can delay recovery, but the more short-acting opioids, alfentanil 15—45mg/kg (9) or remifentanil 0.5—1mg/kg followed by an infusion, are also effective in this respect (10). Also, the laryngoscopy and intubation-related increases in the concentrations of catecholamines (11—13) can be attenuated by opioids (9, 14). On the other hand, inhalation anaesthetics blunt the increase in arterial pressure, but at the same time may result in elevated concentrations of plasma catecholamines (15). Of the intravenous induction agents, thiopentone and propofol modulate the haemodynamic response, but do not abolish it at commonly used doses (16, 17). Either one of them with a muscle relaxant has been given to patients in control groups in studies evaluating the effectiveness of other drugs in the attenuation of cardiovascular responses to airway manipulation. Beyond these approaches, intravenous lidocaine, beta blocking drugs, alpha-2 agonists, and vasodilators among others have been studied in this context. The results on the efficacy are highly variable even within the specific drug groups, and most of the studied agents have blunted either the tachycardic or the hypertensive component of the haemodynamic Acta Anaesthesiol Scand 2004; 48: 393—395 Copyright # Acta Anaesthesiol Scand 2004 Printed in Denmark. All rights reserved ACTA ANAESTHESIOLOGICA SCANDINAVICA