Cardiovascular responses to laryngoscopy and tracheal intubation are not accompanied by ST-segment changes

Editor, The noxious stimuli of laryngoscopy and tracheal intubation are associated with significant increases in plasma catecholamines and cardiovascular changes such as hypertension and tachycardia [1–3]. The aim of the present study was to investigate possible ST-segment changes along with the haemodynamic responses recorded during laryngoscopy and tracheal intubation in a typical mixed surgical population. After institutional approval and informed consent, 100 ASA physical status I–III patients, scheduled for elective surgery under general anaesthesia, were recruited for this prospective open cohort study. Exclusion criteria were indication for rapid sequence induction to anaesthesia, systolic arterial pressure (SAP) on arrival to the operating room of at least 175 mmHg and unexpected difficult intubation requiring more than one attempt at laryngoscopy. Preoperative medication, including calcium-channel blockers and beta-adrenergic blocking agents but except for angiotensin-converting enzyme inhibitors, was continued to the morning of the operation. In the operating room, standard monitoring including bispectral index (BIS) was applied. All patients had an arterial line inserted under local anaesthesia to record SAP, mean arterial pressure (MAP) and diastolic arterial pressure (DAP) (S/5 Anesthesia Monitor, Datex-Ohmeda Inc., Finland). The same monitor was used for the ST-segment analysis. After preoxygenation for 3 min, anaesthesia was induced with thiopental 4.5 mg kg−1. Cisatracurium 0.15 mg kg−1 was administered after loss of the eyelash reflex to facilitate intubation and muscle relaxation. During anaesthetic induction, there was continuous recording of heart rate (HR), blood pressure (BP) and electrocardiogram with automated ST-segment analysis based on leads II, V5 and augmented vector left (aVL). We defined horizontal or downsloping ST-segment depression of at least 2 mm, 60 ms after the J point persisting for at least 1 min, as ischaemia. Sevoflurane in oxygen was supplemented during manual ventilation to ensure an end-tidal concentration of at least 1.5% and a BIS value between 35 and 45 before attempting laryngoscopy. Following intubation, ventilation was controlled with 60% nitrous oxide in oxygen and sevoflurane aiming for normocapnia (end-tidal CO2 between 35 and 40 mmHg) and to an end-tidal sevoflurane concentration of 1.5%. SAP, DAP, HR and respective ST-segment changes were continuously monitored and recorded before anaesthetic induction (baseline), immediately preceding intubation, when the laryngoscope blade had been inserted between the patient' s teeth and firm laryngoscopy was performed, as well as 1, 3, 5 and 10 min after intubation. The ST segment and cardiovascular parameters were analysed for the entire patient population, for those patients receiving and not receiving beta-adrenergic blocking agents and for ASA III high-risk cardiovascular patients separately. Intravenous opioids were given after completion of the study period. Statistical analysis was performed by the use of Sigmastat version 2.03 statistical software (SPSS Inc., Chicago Illinois, USA). Data that followed normal distribution (SAP, DAP and HR) were analysed with one-way analysis of variance (ANOVA) with repeated measures. The ST-segment values did not follow normal distribution and were analysed with Friedman-repeated measures ANOVA on ranks. A P value of less than 0.05 was considered as statistically significant. Twenty out of the 100 patients were excluded from data analysis for various reasons such as need for a rapid-sequence induction due to gastroesophageal reflux or hiatus hernia (five patients), unpredicted difficult intubation (four patients) and SAP at least 175 mmHg upon arrival at the operating room (11 patients). Out of the remaining 80 patients, 33 were ASA III due to cardiovascular disease. Twenty-one of these 33 patients were treated with beta-blockers. SAP decreased after anaesthetic induction as compared with baseline. Conversely, at laryngoscopy and 1 min after intubation, SAP increased when compared with baseline, returned to baseline over the subsequent minutes and decreased below preinduction values 10 min after intubation (Table 1). The same SAP pattern was observed when data were analysed separately for those patients receiving beta-blockers and the patients not treated with beta-blockers. DAP increased at laryngoscopy and 1 min after intubation as compared with baseline. No significant differences were found at 3 and 5 min after intubation, whereas 10 min after intubation DAP was significantly lower than baseline (Table 1). The same pattern was observed when the parameters obtained from patients treated with beta-blockers and patients not receiving beta-blockers were analysed separately. HR increased at laryngoscopy and 1 and 3 min after intubation as compared with baseline. Five minutes after intubation, HR did not differ from baseline (Table 1). In patients on beta-blockers though, HR increased only at laryngoscopy and at 1 min after intubation but not 3 min after intubation.Table 1: Mean ± SD values of systolic arterial pressure, diastolic arterial pressure and heart rate in response to laryngoscopy and intubation (n = 80)The ST segment did not change significantly from baseline in any of the leads displayed (Fig. 1). None of the patients had a more than 2 mm change in the ST segment. In the subgroup of patients not treated with beta-blockers, we did not observe significant ST changes. Furthermore, we analysed separately the ST-segment results for the 33 high-risk cardiovascular patients and found no significant ST elevation or depression in this group of patients. None of the patients included in the study presented any clinical indication of an ischaemic insult, myocardial infarction (MI) or both during their hospital stay.Fig. 1The cardiovascular changes induced by laryngoscopy and tracheal intubation have been extensively investigated [1–4]. Nonetheless, to our knowledge, the impact of tachycardia and hypertension on the myocardium as assessed by ST-segment analysis during and early after intubation has not been investigated by means of a clinical controlled study. In our study, we investigated SAP, DAP and HR changes during the induction period with simultaneous recording of the ST segment in leads II, V5 and aVL, the first two being the most sensitive ones for detecting ischaemic changes in the inferior and lateral walls, respectively. The haemodynamic changes recorded in our patients are consistent with results reported previously [1,2,4]. We demonstrated significant increases in SAP and DAP at laryngoscopy persisting as long as 1 min after intubation. In the entire patient population, HR increased significantly at laryngoscopy and 1 and 3 min after intubation but, in the 21 patients receiving beta-blockers, the increase persisted for only 1 min. Under the present study design, the significant increases in SAP and DAP and HR were not accompanied by significant ST-segment changes from baseline. We did not observe ST-segment changes in the 33 high-risk cardiovascular patients with ischaemic heart disease (IHD) or with high-risk factors for its development. Moreover, no difference was detected when ST segments in patients without the ‘cardioprotective’ effects of beta-blockade were analysed separately. Our results showed that the haemodynamic response to laryngoscopy and intubation might not evoke ischaemic insult as assessed by ST-segment analysis. Therefore, measures obtunding this response might not prove the technique of choice in ambulatory cases without significant cardiac risk factors. However, in specific patient populations such as those with known intracranial hypertension, large aortic or cerebral aneurysms, cardiac ischaemia or recent MI, anaesthetic techniques attenuating the circulatory responses to laryngoscopy and intubation are desirable [4]. Our findings suggest that haemodynamic derangements accompanying laryngoscopy and tracheal intubation do not necessarily lead to postoperative ischaemic episodes. Postoperative myocardial ischaemia is multifactorial in origin and reflects unmet increases in myocardial oxygen demand brought about by complex situations not necessarily related to airway instrumentation [5,6]. Our results are based on the ST recording, which is not the most sensitive monitor of subendocardial ischaemia. This may be considered a limitation of the study. Assessment of the effect of laryngoscopy and intubation on subendocardial ischaemia needs more sensitive monitoring such as echocardiography imaging [7]. Another limitation is that we did not examine ST-segment changes in patients with very high baseline values of SAP. Data were not collected for the aforementioned patients because opioids, intravenous vasodilators or both were administered before intubation and these patients were withdrawn as determined by the study protocol. As we considered it unethical to proceed to laryngoscopy and tracheal intubation in these patients without treating the high arterial BP, our results should not be extrapolated to hypertensive patients with potentially underlying IHD. It could also be argued that we studied a rather heterogeneous group of adult patients. However, this is the population that the anaesthesiologist comes across routinely. Furthermore, no evidence of ischaemia was demonstrated even in the subgroup of patients with high cardiac risk. In conclusion, under the present study protocol, the haemodynamic responses to laryngoscopy and tracheal intubation were not associated with ischaemia, as assessed by ST-segment monitoring. Further studies are required using more sensitive modalities (such as transoesophageal echocardiography) in typical surgical populations, including high-risk cardiovascular patients under treatment, as occurs in routine clinical practice.