Myocardial ischaemia during tracheal intubation and extubation

Abstract

The incidence of myocardial ischaemia during tracheal intubation and extubation was compared using ambulatory ECG monitoring in 60 patients undergoing a variety of different surgical operations. Seven patients had myocardial ischaemia after tracheal intubation and seven patients during tracheal extubation. The patients who developed myocardial ischaemia during tracheal extubation had significantly greater rate-pressure products immediately before tracheal extubation (P < 0.05) and 1 min after tracheal extubation (P < 0.01) compared with those patients who did not develop myocardial ischaemia during extubation.

Attenuation of hemodynamic responses to endotracheal extubation: A prospective randomised controlled study between two different doses of Verapamil

“…7,13,45 Increase in BP, HR and RPP which is a multiple of SBP and HR increases the cardiac workload and the oxygen demand of the myocardium; increasing the risk of developing a fresh episode of myocardial ischemia and infarction in known patients of ischemic heart disease due to a fixed coronary blood flow, along with fall in cardiac index and ejection fraction. [3][4][10][11][12]16 Therefore, perioperative measurement of RPP is of vital importance.…”

“…[7][8][9][10] Acute hemodynamic changes during extubation can lead to dangerous arrhythmias, 2-4 myocardial ischemia, [3][4]7,[10][11][12][13] acute cardiac failure, 2,5,12 pulmonary edema 8 or cerebrovascular haemorrhage 14 in susceptible individuals. These responses can turn catastrophic in several situations like; ocular surgeries leading to dangerous increase in intraocular pressure; 15 patients with cardiac disease [3][4][10][11][12]16 or intracranial surgeries with raised intracranial pressure or for aneurysm surgeries 14 or with essential hypertension who show an exaggerated response to this stressful event.…”

“…[7][8][9][10] Acute hemodynamic changes during extubation can lead to dangerous arrhythmias, 2-4 myocardial ischemia, [3][4]7,[10][11][12][13] acute cardiac failure, 2,5,12 pulmonary edema 8 or cerebrovascular haemorrhage 14 in susceptible individuals. These responses can turn catastrophic in several situations like; ocular surgeries leading to dangerous increase in intraocular pressure; 15 patients with cardiac disease [3][4][10][11][12]16 or intracranial surgeries with raised intracranial pressure or for aneurysm surgeries 14 or with essential hypertension who show an exaggerated response to this stressful event. 13 A number of attempts have been tried to attenuate these cardiovascular responses; such as extubation in deeper planes of anaesthesia, [17][18] avoiding or reducing duration of laryngoscopy before extubation 19 , use of laryngeal mask airway instead of endotracheal tube, [20][21][22] topical airway anaesthesia with lignocaine, [23][24][25][26] intra-cuff or intravenous lignocaine [27][28] .…”

Attenuation of Hemodynamic Response to Direct Laryngoscopy and Intubation Using 10% Lignocaine Spray : A Clinical Study

“…(3) It is a self-limiting in most of the patients however it can leads to morbidity and mortality in patients having coronary artery disease and raised intracranial tension. (4)(5) Hence many attempts have been made to attenuate this presser response. Although this hemodynamic response is due to sympathetic adrenergic reflex to laryngoscopy and intubation, most of the studies or the approach using different agents are aimed at blocking the effect of the reflex rather than preventing the stimulation starting from inducing agents thiopentone, propfol (6) analgesics, (7) different opioids, (8)(9) beta blockers, (10)(11) calcium channel blockers, (12)(13) sodium channel blocker (14) and of late alpha2 agonists.…”

Effect of Dexmedetomidine and Esmolol in Attenuating the Haemodynamic Responses During Laryngoscopy and Endotracheal Intubation in Elective Upper Abdominal Surgeries

“…4 In patients with coronary artery disease (CAD), hypertension, raised intra-cranial pressure it may be associated with myocardial infarction, arrhythmias, cardiac failure or cerebral haemorrhage. 5,6 Methods to attenuate these responses, both pharmacological and physiological, have been extensively studied. 7,8 Treatment modalities include topical lignocaine spray, deeper planes of anaesthesia by inhalation/intravenous agents or narcotics, calcium channel blockers, α-2 agonists, β-2 blockers, vasodilators such as sodium-nitroprusside, nitroglycerine etc.…”