Endotracheal intubation (ETI) is a fundamental procedure in emergency, <br />perioperative, and critical care settings. While necessary for securing the <br />airway, ETI is associated with significant haemodynamic alterations due to <br />autonomic nervous system stimulation, mechanical factors, and <br />pharmacologic interventions. The physiological responses to intubation can <br />result in transient or prolonged haemodynamic instability, including <br />hypertension, tachycardia, hypotension, bradycardia, and arrhythmias, which <br />pose a significant risk, particularly in patients with pre-existing cardiovascular <br />disease, sepsis, or neurological conditions. This review provides an extensive<br />analysis of the pathophysiological mechanisms of ETI-induced <br />haemodynamic changes, risk factors, clinical implications, and evidencebased management strategies. A real-world case study and detailed clinical <br />guidelines are also included to aid in optimizing patient safety and outcomes.<br />1. Introduction<br />Endotracheal intubation is a lifesaving intervention used in a variety of clinical<br />settings:<br />Perioperative care for general anesthesia.<br />Emergency medicine for airway protection in trauma, cardiac arrest, or <br />respiratory failure.<br />Intensive care units (ICU) for mechanical ventilation in critically ill patients.<br />Despite its necessity, ETI poses significant risks to haemodynamic stability, <br />particularly in high-risk patients. The haemodynamic response to ETI results <br />from a complex interplay of autonomic nervous system activation, mechanical<br />alterations in intrathoracic pressure, and pharmacologic effects of induction <br />agents and neuromuscular blockers. These effects can lead to profound <br />blood pressure and heart rate fluctuations, necessitating careful preintubation planning and management.<br />2. Physiological Mechanisms of Haemodynamic Changes During <br />ETI<br />2.1 Sympathetic Nervous System Activation and Catecholamine Surge<br />Laryngoscopy and tracheal intubation are potent stimuli for the sympathetic <br />nervous system (SNS). The stress response results in a catecholamine <br />surge, leading to:<br />Hypertension due to increased systemic vascular resistance (SVR).<br />Tachycardia caused by increased beta-adrenergic stimulation.<br />Increased myocardial oxygen demand, posing a risk for ischemia in coronary <br />artery disease<br />(CAD) patients.<br />Dysrhythmias, including atrial fibrillation or ventricular tachycardia.<br />The degree of sympathetic activation depends on:<br />The depth of anesthesia: Inadequate anesthesia increases SNS response.<br />The duration of laryngoscopy: Prolonged attempts exacerbate the response.<br />The use of adjunct medications: Opioids and beta-blockers can attenuate <br />these effects.<br />2.2 Parasympathetic Reflexes and Bradycardia<br />In certain patients, ETI triggers the parasympathetic (vagal) response, leading<br />to:<br />Bradycardia, particularly in pediatric patients and those on beta-blockers.<br />Hypotension due to reduced cardiac output.<br />Asystole in extreme cases due to excessive vagal tone.<br />This response is more common with prolonged airway manipulation, high <br />doses of opioids, and patients with pre-existing high vagal tone.<br />2.3 Mechanical and Intrathoracic Pressure Changes<br />Positive pressure ventilation (PPV) following ETI induces mechanical <br />changes:<br />Decreased venous return, leading to reduced cardiac preload.<br />Increased right ventricular afterload, worsening right heart function in patients<br />with pulmonary<br />hypertension.<br />Reduced coronary perfusion pressure, exacerbating ischemia in vulnerable <br />patients.<br />3. Haemodynamic Effects of Endotracheal Intubation<br />3.1 Blood Pressure Changes<br />Hypertension: Common in response to SNS activation. Dangerous in patients<br />with intracranial hypertension, aneurysms, or cardiovascular disease.<br />Hypotension: More common in critically ill patients due to vasodilation, <br />reduced venous return, and myocardial depression from anesthetic agents.<br />3.2 Heart Rate Alterations<br />Tachycardia: Increases myocardial oxygen demand and risk of ischemia.<br />Bradycardia: Seen in vagal stimulation, high-dose opioids, or hypoxia.<br />3.3 Cardiac Output and Myocardial Oxygen Demand<br />Transient increase in cardiac output due to catecholamine surge.<br />Decreased cardiac output in hypovolemic or septic patients due to impaired <br />preload.<br />4. Case Study: Haemodynamic Instability During ETI in a Septic <br />Patient<br />Patient Profile:<br />Age: 65-year-old male<br />Medical History: Hypertension, Type 2 diabetes, ischemic heart disease<br />Diagnosis: Septic shock secondary to pneumonia<br />Clinical Course:<br />Patient presented with respiratory distress and hypotension (MAP 55 mmHg).<br />Decision for intubation was made due to worsening hypoxemia.<br />Pre-intubation: Given fluid bolus (500mL lactated Ringer's) and started on <br />norepinephrine<br />infusion (5 mcg/min).<br />Induction agents: Etomidate 0.3 mg/kg, fentanyl 1 mcg/kg, and rocuronium 1 <br />mg/kg.<br />Intubation: Successful on the first attempt with video laryngoscopy.<br />Post-intubation: Blood pressure dropped to MAP 45 mmHg, requiring an <br />increase in<br />norepinephrine infusion.<br />Outcome: Stabilized with additional fluid resuscitation and vasopressor <br />titration.<br />Discussion:<br />This case highlights the risk of post-intubation hypotension in sepsis, <br />emphasizing the importance of fluid resuscitation and vasopressor support <br />before ETI. The choice of etomidate minimized haemodynamic depression, <br />and fentanyl blunted the sympathetic response.<br />5. Clinical Guidelines for Managing Haemodynamic Instability <br />During ETI<br />5.1 Pre-Intubation Optimization<br />Fluid resuscitation in hypovolemic or septic patients.<br />Vasopressors (norepinephrine, phenylephrine) for hemodynamic support.<br />Preoxygenation with high-flow oxygen to avoid hypoxia-induced hypotension.<br />5.2 Medication Selection<br />Etomidate: Preferred for unstable patients due to minimal BP effects.<br />Ketamine: Useful in shock but avoided in hypertension or CAD.<br />Opioids (fentanyl, remifentanil): Blunt SNS response but can cause <br />bradycardia.<br />5.3 Procedural Modifications<br />Use of video laryngoscopy to reduce intubation duration.<br />Minimizing airway manipulation to prevent exaggerated SNS stimulation.<br />Using lower tidal volumes to prevent increased intrathoracic pressure.<br />6. Conclusion<br />ETI induces significant haemodynamic alterations, primarily due to autonomic<br />nervous system activation, mechanical effects, and pharmacologic influences.<br />Patients at high risk, such as those with sepsis, cardiovascular disease, or <br />intracranial pathology, require meticulous pre-intubation optimization, <br />including fluid resuscitation, vasopressor support, and careful drug selection. <br />Implementing evidence- based clinical guidelines can significantly improve <br />patient safety and reduce complications.<br />7. References<br />1. Teong, C. Y., Huang, C. C., & Sun, F. J. (2020). The Haemodynamic <br />Response to Endotracheal Intubation at Different Time of Fentanyl Given <br />During Induction: A Randomised Controlled Trial. Scientific Reports, 10, 8829.<br />2. Shribman, A. J., Smith, G., & Achola, K. J. (1987). Cardiovascular and <br />catecholamine responses to laryngoscopy with and without tracheal <br />intubation. British Journal of Anaesthesia, 59(3), 295-299.<br />3. Kovac, A. L. (2009). Controlling the haemodynamic response to <br />laryngoscopy and endotracheal intubation. Journal of Clinical Anesthesia, <br />21(1), 81-97<br /><br />م.محمد خضير عباس<br /><br />Al-Mustaqbal University is the first university in Iraq