Direct laryngoscopy and tracheal intubation are potent noxious stimuli that activate airway mechanoreceptors and provoke sympathetic discharge with catecholamine release, resulting in transient increases in heart rate and arterial blood pressure.¹⁻³ Although often well tolerated in healthy individuals, this response can precipitate myocardial ischemia, arrhythmias, cerebral hemorrhage, or worsening shock in susceptible patients.¹⁻⁴ The magnitude of this hemodynamic response is influenced by multiple factors, including depth of anesthesia, duration/force of laryngoscopy, choice and timing of induction agents, use of opioids or alpha-2 agonists, and patient baseline physiology.²⁻⁵

General surgery practice includes both elective and emergency procedures, but emergency cases carry unique airway and physiologic risks. Emergency general surgery patients frequently present with acute pain, heightened stress hormone levels, relative hypovolemia from poor intake/third spacing, sepsis, anemia, electrolyte derangements, and incomplete fasting—often necessitating rapid sequence induction (RSI).⁶⁻⁸ Contemporary RSI guidance emphasizes minimizing aspiration risk while maintaining oxygenation and hemodynamic stability, yet acknowledges that critically ill or under-resuscitated patients may deteriorate during or immediately after induction and intubation.⁶⁻⁹ The concept of the “physiologically difficult airway” further highlights that even with anatomically straightforward airways, severe derangements in oxygenation or circulation can convert intubation into a high-risk event due to peri-intubation collapse.⁵,¹⁰

Large international cohorts and emergency registries consistently demonstrate that peri-intubation adverse events—particularly new hemodynamic instability—are common during emergency intubation and are associated with poor outcomes.⁷,¹¹ In one multicenter emergency department registry, major peri-intubation adverse events occurred in approximately one-third of emergency intubations, with hemodynamic instability among the most frequent complications.¹¹ Similarly, the INTUBE study (29 countries) reported high rates of peri-intubation adverse events in critically ill patients, reinforcing the need for standardized strategies and first-pass success to reduce complications.⁷

In elective general surgery, patients are usually optimized preoperatively with controlled fasting status, pre-induction stabilization, and predictable anesthetic conditions. In contrast, emergency surgery may involve limited time for optimization, hemodynamic lability, and RSI-driven airway approaches—factors that may change both the direction and magnitude of hemodynamic perturbations.⁶,⁸,⁹ Pharmacologic approaches to blunt the pressor response (e.g., dexmedetomidine, esmolol, fentanyl, lidocaine) are well studied in elective settings, and systematic reviews suggest measurable attenuation of tachycardia/hypertension, but these agents can also worsen hypotension and bradycardia in vulnerable physiology.¹²⁻¹⁶ Therefore, comparing the hemodynamic response between emergency and elective general surgery patients provides clinically relevant insight for tailoring induction and airway management to patient context.

This study aimed to evaluate differences in peri-intubation hemodynamic changes between emergency and elective general surgery under general anesthesia with endotracheal intubation, and to quantify clinically significant hemodynamic events in both groups.

Prospective observational comparative study conducted in the Department of Anaesthesiology in collaboration with General Surgery at a tertiary care teaching hospital over 12 months.

Study population and sampling

Adult patients scheduled for general surgery under general anesthesia requiring orotracheal intubation were enrolled consecutively into two groups:

• Emergency group: emergency general surgery requiring anesthesia within 24 hours of surgical decision.
• Elective group: planned elective general surgery with standard preoperative evaluation.

A total sample of 200 patients (100 per group) was targeted for comparative precision of hemodynamic outcomes.

Inclusion criteria

1. Age 18–70 years.
2. ASA physical status I–III.
3. General surgery procedures requiring endotracheal intubation under general anesthesia.
4. Written informed consent from patient/attendant (as per institutional policy for emergency cases).

Exclusion criteria

1. Anticipated difficult airway requiring awake intubation (planned).
2.  
3. Known severe valvular heart disease, EF <35%, severe pulmonary hypertension.
4. Uncontrolled arrhythmias or ongoing myocardial ischemia.
5. Patients on chronic high-dose beta-blockers/antiarrhythmics where HR response interpretation would be confounded (unless dose stable and documented; such patients were excluded for uniformity).
6. Multiple intubation attempts (>2) or change in technique (excluded from primary analysis due to prolonged stimulation).

Standardized anesthetic technique (protocolized as feasible)

• Monitoring: ECG, NIBP/IBP (as indicated), SpO₂, EtCO₂.
• Preoxygenation: 3 minutes with 100% oxygen.
• Induction: propofol (titrated) or ketamine/etomidate when clinically indicated; opioid (fentanyl 1–2 µg/kg) and muscle relaxant (rocuronium/succinylcholine) per standard practice. RSI was used for emergency cases where aspiration risk was high as per departmental protocol.⁶
• Laryngoscopy: Macintosh blade by an anesthesiologist with ≥2 years experience; attempt duration aimed <20 seconds.
• Maintenance: volatile anesthetic with oxygen/air mixture; ventilation to normocapnia.

Data collection and outcome measures

Hemodynamic variables (HR, SBP, DBP, MAP) were recorded at:

• Tbaseline: pre-induction (after 5 min rest)
• Tpre-L: post-induction immediately before laryngoscopy
• T0: immediately after intubation confirmation
• T1, T3, T5, T10: 1, 3, 5, and 10 minutes post-intubation

Primary outcome: peak change in MAP from Tpre-L to T1.

Secondary outcomes: peak HR change, incidence of:

• Hypertension (SBP ≥160 mmHg or ≥20% rise from baseline)
• Tachycardia (HR ≥110/min or ≥20% rise)
• Hypotension (MAP <65 mmHg within 10 min), need for vasopressor bolus.

Statistical analysis

Continuous variables were expressed as mean ± SD and compared using Student’s t-test (or Mann–Whitney U where appropriate). Categorical variables were expressed as n (%) and compared using chi-square/Fisher’s exact test. Multivariable linear regression was used to adjust peak MAP response for potential confounders (age, ASA, baseline MAP, induction agent). p<0.05 was considered significant.

Table 1. Baseline demographic characteristics

Groups were comparable in age, sex, and BMI. Emergency cases had a higher proportion of ASA III patients (p=0.01), indicating greater baseline physiological risk.

Table 2. Surgical and anesthetic characteristics

Emergency cases more frequently underwent RSI and more often required hemodynamically “supportive” induction agents (ketamine/etomidate), consistent with emergency physiology and aspiration risk.⁶,¹⁰,¹¹

Table 3. Baseline hemodynamics before induction (Tbaseline)

Emergency patients began with significantly higher HR and BP, consistent with stress response, pain, and acute illness burden.

Table 4. Hemodynamic response over time (mean values)

                                                     HR (beats/min)

MAP (mmHg)

Both HR and MAP peaked at 1 minute post-intubation, with consistently higher values in emergency patients and slower return toward baseline.

Table 5. Primary/secondary peak response metrics

The pressor response (MAP/SBP) was significantly greater in emergency cases, while peak HR change was numerically higher but not statistically different. Emergency cases also took longer to recover toward pre-laryngoscopy values.

Table 6. Clinically significant events within 10 minutes post-intubation

Emergency patients experienced a “double burden”—more hypertension/tachycardia from stress response and more hypotension/vasopressor requirement, aligning with the vulnerability of emergency physiology and the recognized risk of peri-intubation instability in urgent settings.⁷,¹¹

This study demonstrates that emergency general surgery patients have significantly higher baseline heart rate and blood pressure and experience a greater pressor response (MAP/SBP) to laryngoscopy and endotracheal intubation compared with elective patients. The findings align with established physiology: airway instrumentation triggers sympathetic stimulation and catecholamine release, causing transient tachycardia and hypertension.¹⁻³ The magnitude of this response is influenced by baseline sympathetic tone and the force/duration of laryngoscopy—both likely increased in emergency patients due to pain, anxiety, systemic inflammation, and incomplete physiologic optimization.⁵,⁶

The observed higher incidence of clinically significant hypertension and tachycardia in the emergency cohort is consistent with literature emphasizing that pressor responses may be more pronounced when anesthetic depth is constrained by hemodynamic concerns or when induction is tailored to preserve blood pressure (e.g., ketamine/etomidate use).⁶,¹⁰ At the same time, emergency cases in our study had a higher rate of peri-intubation hypotension and vasopressor bolus requirement. This seemingly paradoxical pattern—simultaneous susceptibility to both hypertensive surges and hypotensive collapse—reflects the concept of the “physiologically difficult airway,” where critically ill patients can respond unpredictably to induction agents, positive pressure ventilation, and the transition from compensatory sympathetic tone to anesthetic-induced vasodilation.⁵,¹⁰

Large observational datasets reinforce the clinical importance of peri-intubation hemodynamic instability in emergency contexts. The INTUBE study reported substantial peri-intubation adverse events in critically ill patients across multiple countries, highlighting that complications remain common despite widespread expertise.⁷ Similarly, the BARCO emergency department registry documented major peri-intubation adverse events in roughly one-third of emergency intubations, with new hemodynamic instability a leading component and associated with worse outcomes.¹¹ These studies support our finding that emergency airway management carries high hemodynamic risk and underlines the need for mitigation strategies.

Pharmacologic attenuation of the pressor response is well described. Beta-blockade with esmolol has demonstrated superior reduction in post-intubation tachycardia compared with lidocaine in randomized trials, though careful selection is required in patients at risk of hypotension.¹⁴ Alpha-2 agonists such as dexmedetomidine show benefits in reducing tachycardia compared with fentanyl in meta-analyses, but may increase bradycardia/hypotension risk if not titrated.¹² Opioid timing also matters: fentanyl administered at an optimal interval before intubation can yield more stable hemodynamics.¹³ In emergency surgery, however, the priority is often not only blunting hypertension/tachycardia but also preventing hypotension through pre-induction resuscitation, vasopressor readiness, and agent selection consistent with shock physiology.⁶,¹⁰

Practically, our results support a structured approach in emergency general surgery: aggressive optimization (analgesia, fluids/blood as indicated), selection of induction drugs that balance stress response and perfusion, minimizing laryngoscopy duration, maximizing first-pass success, and early vasopressor support when indicated.⁶,⁷,¹¹ Additionally, difficult airway frameworks and RSI guidance emphasize checklist-based preparation and anticipating physiologic collapse.⁶,⁹,¹⁷ Collectively, these strategies may reduce both extremes of hemodynamic instability observed around intubation in emergency patients.

Emergency general surgery patients exhibit significantly greater pressor responses to laryngoscopy and endotracheal intubation than elective patients and also have higher rates of peri-intubation hypotension and vasopressor requirement. Emergency airway management should prioritize physiologic optimization, first-pass success, vigilant monitoring, and proactive hemodynamic control to minimize complications.

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