European Journal of Cardiovascular Medicine

Laryngoscopy and endotracheal intubation remain the most stimulating moments of routine general anesthesia. Mechanical stimulation of the epipharynx, larynx, and trachea activates sympatho-adrenal reflexes, leading to abrupt increases in heart rate and arterial pressure.[1,4] These changes can be clinically visible within seconds and typically peak around the time the tracheal tube is placed.[5] Although the response is transient, the short interval of marked tachycardia and hypertension can be clinically important when cardiovascular reserve is limited.

Early clinical observations described acute hypertension occurring during induction and intubation in patients without pre-existing hypertension, emphasizing the reflex nature of the response.[1] Subsequent reports linked the pressor response to peri-intubation complications such as dysrhythmias, myocardial ischemia, and cerebrovascular events, particularly when tachycardia accompanies the rise in blood pressure.[2] The biological basis is supported by studies showing substantial increases in circulating catecholamines during laryngoscopy and intubation.[4] Shribman and colleagues further demonstrated that laryngoscopy alone produces significant catecholamine and blood pressure rises, while tracheal intubation adds a distinct chronotropic component.[5]

Patients with systemic hypertension and coronary artery disease (CAD) are especially vulnerable. Hypertension is associated with increased afterload and vascular stiffness, which can amplify peri-intubation blood pressure surges.[6,7] In CAD, the imbalance between myocardial oxygen supply and demand becomes critical when heart rate and systolic pressure rise abruptly, and intraoperative ischemia can appear as ST-segment changes on continuous ECG monitoring.[3] Classic work in patients with CAD demonstrated that ischemic episodes can occur during anesthesia and that enhanced lead monitoring improves detection.[3] Because airway instrumentation is brief, ischemia is often silent and transient, yet it signals a high-risk physiologic stress.

Multiple strategies have been evaluated to attenuate these responses, including opioids, lidocaine, beta-blockers, alpha-2 agonists, vasodilators, and technical refinements aimed at minimizing airway stimulation.[6] Alternative intubation devices that improve glottic visualization with less force have also been studied. Comparative studies in hypertensive and cardiac populations show heterogeneous findings, with some reporting reduced hemodynamic swings and others noting comparable responses despite better views and longer intubation times.[7-13] Because hypertension and CAD frequently coexist in surgical patients, real-world observational data remain valuable for quantifying the magnitude and time course of peri-intubation changes in high-risk settings.

Objectives: This prospective observational study aimed (1) to quantify changes in heart rate and blood pressure during laryngoscopy and endotracheal intubation in adults with hypertension and/or CAD and (2) to document peri-intubation electrocardiographic changes, including transient arrhythmias and ST-segment deviations, in a tertiary care teaching hospital setting.

Study design and setting: A prospective observational study was conducted in the Department of Anaesthesiology at Government Medical College (GMC) Ananthapuramu, Andhra Pradesh, India, from March 2024 to May 2024.

Participants: Adults aged 18-75 years with established systemic hypertension and/or documented coronary artery disease (history of angina or myocardial infarction, prior coronary intervention, or treatment with anti-anginal medication) scheduled for elective surgery under general anesthesia were screened. Patients were included if classified as American Society of Anesthesiologists (ASA) physical status II or III.

Exclusion criteria were anticipated difficult airway (Mallampati III/IV, restricted mouth opening, or limited neck extension), emergency procedures, severe valvular heart disease, significant arrhythmias at baseline, heart failure with poor functional capacity, pregnancy, or refusal of consent.

Perioperative protocol: Antihypertensive and anti-anginal medications were continued as per institutional practice. Standard fasting guidelines were followed. In the operating room, monitoring included pulse oximetry, non-invasive blood pressure, and continuous ECG with lead II and V5 display to improve ischemia detection.[3] Baseline values were recorded after a 5-minute rest in the supine position prior to induction. Anesthesia was administered using a uniform institutional protocol that included an opioid, an intravenous induction agent, and a non-depolarizing neuromuscular blocker, followed by maintenance with inhalational anesthesia and controlled ventilation. Laryngoscopy was performed using a standard Macintosh blade, and endotracheal intubation was completed by an experienced anesthesiologist. Efforts were taken to avoid prolonged laryngoscopy and repeated attempts; patients requiring more than one attempt were not included in the final analysis.

Data collection and outcomes: Hemodynamic parameters - heart rate (HR), systolic blood pressure (SBP), diastolic blood pressure (DBP), and mean arterial pressure (MAP) - were recorded at the following time points: baseline (T0), during laryngoscopy (T1), immediately after endotracheal intubation (T2), 3 minutes after intubation (T3), and 5 minutes after intubation (T4). Maximum percentage change from baseline for each parameter was calculated. A rise greater than 20% from baseline was considered clinically significant, as such increases have been associated with adverse cardiovascular stress in prior peri-intubation literature.[2,6] ECG changes were documented during and immediately after intubation, including sinus tachycardia, ST-segment depression (>1 mm), and premature ventricular complexes. ST-segment depression was assessed on the displayed leads (II and V5) and interpreted in conjunction with hemodynamic changes.[3]

Statistical analysis: Data were entered in a spreadsheet and analyzed using descriptive statistics. Continuous variables are presented as mean ± standard deviation (SD) and categorical variables as frequency and percentage. Changes across time points are summarized tabularly, and clinically significant (>20%) rises are presented as proportions.

Ethical considerations: Institutional Ethics Committee approval was obtained prior to recruitment. Written informed consent was obtained from all participants.

A total of 80 adult patients with established hypertension and/or coronary artery disease (CAD) undergoing elective surgery under general anesthesia were included in this prospective observational study. Hemodynamic and electrocardiographic parameters were recorded at baseline, during laryngoscopy, immediately after endotracheal intubation, and at predefined intervals thereafter.

The mean age of the participants was 56.8 ± 9.4 years, with a male predominance (65%). Hypertension alone constituted 47.5% of the cohort, while 22.5% had CAD alone and 30.0% had both hypertension and CAD. Most participants belonged to ASA physical status II (57.5%) (Table 1).

Table 1. Baseline demographic and clinical characteristics of study participants (n = 80)

A marked and transient rise in heart rate and blood pressure was observed during laryngoscopy and peaked immediately after endotracheal intubation. Although values gradually declined, they remained above baseline at 3 minutes and approached pre-induction levels by 5 minutes (Table 2).

Table 2. Changes in hemodynamic parameters at different time points (n = 80)

Figure 1: Hemodynamic responses to laryngoscopy and endotracheal intubation

More than half of the participants experienced a rise greater than 20% in heart rate and systolic blood pressure, indicating a pronounced pressor response in this high-risk population. Clinically significant rises were also frequent for diastolic pressure and mean arterial pressure (Table 3).

Table 3. Maximum percentage change in hemodynamic parameters from baseline (n = 80)

Figure 2: Maximum percentage change from baseline and proportion with> 20% rise

Transient ECG changes were noted in 22.5% of patients, predominantly sinus tachycardia. ST-segment depression suggestive of myocardial ischemia was observed in a small subset (7.5%), mainly among patients with known coronary artery disease. No life-threatening arrhythmias or adverse cardiac events were recorded (Table 4).

Table 4. Electrocardiographic changes observed during and after intubation (n = 80)

This prospective observational study demonstrates that adults with hypertension and/or coronary artery disease experience a pronounced but short-lived sympathetic response during airway instrumentation. Heart rate and arterial pressures increased substantially during laryngoscopy and peaked immediately after endotracheal intubation, followed by a gradual decline toward baseline within five minutes. This time course is consistent with early reports describing acute hypertension during induction and intubation and later work emphasizing the clinical relevance of the pressor response.[1,2]

The magnitude of tachycardia and hypertension observed is biologically plausible given the catecholamine surge documented during laryngoscopy and intubation.[4,5] Derbyshire et al. demonstrated marked plasma catecholamine elevations after tracheal instrumentation, supporting a reflex sympatho-adrenal mechanism.[4] Shribman and colleagues showed that laryngoscopy alone produces significant catecholamine and blood pressure increases, while tracheal intubation adds a further increase in heart rate.[5] In patients with hypertension, impaired vascular compliance and higher baseline afterload can amplify the blood pressure rise, while chronotropic responses directly increase myocardial oxygen demand.[6]

Device and technique-related factors can modulate the intensity of airway stimulation. In hypertensive patients, Meshram et al. compared Macintosh direct laryngoscopy with GlideScope videolaryngoscopy and evaluated hemodynamic responses during intubation, reporting clinically evident responses in both arms.[13] Kihara et al. evaluated multiple intubation devices in normotensive and hypertensive individuals and found that hemodynamic responses persisted across devices, suggesting that stimulus reduction is not uniform and that patient physiology remains a major determinant.[7] In cardiac surgical populations, comparisons between direct and indirect laryngoscopy have shown broadly similar hemodynamic profiles, even when videolaryngoscopy improves laryngeal view.[12] These data support the practical focus on ensuring adequate anesthetic depth, minimizing laryngoscopy duration, and avoiding repeated attempts rather than relying on device choice alone.

Electrocardiographic changes in our cohort were predominantly sinus tachycardia, while ST-segment depression was infrequent and transient. Roy et al. highlighted that ischemic episodes during anesthesia can be common in patients with CAD and that lead selection (notably V5) improves detection.[3] Our lower frequency of ST depression could reflect optimized baseline medical therapy, elective surgical scheduling, and the brief nature of the stimulus in controlled operating room conditions. Similarly, Theodoraki and Fassoulaki reported that typical cardiovascular responses to laryngoscopy and intubation are not necessarily accompanied by ST-segment changes in all settings.[10,14] In patients with established CAD, however, even transient ST changes warrant attention because they signal a supply-demand imbalance.

Overall, the present findings reinforce the need to anticipate a pressor response in hypertensive and CAD patients, monitor continuously, and apply attenuation measures tailored to individual risk. Reviews on controlling the hemodynamic response emphasize the roles of opioids, local anesthetics, and short-acting sympatholytic agents, alongside careful airway technique. Observational quantification of these responses in routine practice provides a pragmatic basis for risk communication and for designing targeted interventional studies in high-risk groups.

Limitations

This single-centre study was conducted over a short period and used an observational design, limiting causal inference. Anesthetic drugs, laryngoscopy duration, and depth of anesthesia were standardized by protocol but were not objectively quantified with BIS or drug concentration monitoring. Invasive arterial pressure monitoring was not used, so beat-to-beat changes were not captured. ECG assessment relied on surface leads and did not include cardiac biomarkers or postoperative Holter monitoring.

In adults with hypertension and/or coronary artery disease undergoing elective surgery, laryngoscopy and endotracheal intubation produced a clear pressor response. Heart rate, systolic and diastolic blood pressure, and mean arterial pressure rose sharply during laryngoscopy and peaked immediately after tube placement, with values approaching baseline within five minutes. More than half of patients experienced a clinically significant (>20%) rise in heart rate and systolic pressure. Electrocardiographic changes were usually limited to sinus tachycardia; ST-segment depression occurred in a small subset and resolved without sustained arrhythmia or hemodynamic collapse. These findings underline the need for vigilant peri-intubation monitoring and proactive attenuation strategies in high-risk patients at tertiary care centres during induction.

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