Anesth Analg 2001;93:787-790
© 2001 International Anesthesia Research Society
GENERAL ARTICLES
The Pressor Response and Airway Effects of Cricoid Pressure During Induction of General Anesthesia
Mahmood Saghaei, MD, and
Mehrdad Masoodifar, MD
Department of Anesthesia and Critical Care, Isfahan University of Medical Sciences, Isfahan, Iran
Address correspondence and reprint requests to Dr. Mahmood Saghaei, PO Box 931, Al-Zahra Medical Center, Isfahan, Iran.
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Abstract
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Cricoid pressure (CP) has been used to protect the patient from regurgitation and gastric insufflation. Because the hemodynamic effects of CP have not been evaluated independently, we designed this prospective study. Eighty ASA I adult patients were prospectively included in the study. Patients were randomly divided into Cricoid and Placebo groups. In the Cricoid group, after the induction of anesthesia, bimanual CP was performed, and in the Control group, simple placement of hands without exerting pressure was performed. Peak inspiratory pressure and exhaled tidal volume were recorded before and during the application of CP. Arterial blood pressure and heart rate were recorded before and after application of CP. The data were compared between and within groups by using the mixed-design analysis of variance. Peak inspiratory pressure increased and tidal volume decreased significantly after the application of CP compared with the Control group and baseline values. Arterial blood pressure and heart rate increased significantly after the application of CP compared with the baseline values and with those of the Control group. The result of this study shows that CP can cause a relatively strong pressor response.
IMPLICATIONS: Cricoid pressure is used for prevention of gastric regurgitation under general anesthesia. We found that cricoid pressure can increase the blood pressure and heart rate significantly.
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Introduction
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Cricoid pressure (CP) was first used as a protective measure against gastric regurgitation during the rapid-sequence induction of general anesthesia in patients suspected to have a full stomach (1). This maneuver was also later used for the prevention of gastric insufflation during cardiopulmonary resuscitation (2). The beneficial effects of CP seem to be due to an occlusion of the upper esophageal sphincter by the force of external CP (3–8).
Since its advent into the clinical practice of anesthesia, CP has been investigated for its efficacy and safety (9–11). Complications attributed to the application of CP include partial or even complete airway obstruction, difficulty in placement of the laryngoscope blade, deteriorating effect on the visualization of the glottis during laryngoscopy, and difficulty with tracheal intubation (12).
The hemodynamic effects of CP have rarely been assessed in studies related to the rapid-sequence induction of anesthesia (13,14). Although the development of a relatively strong hemodynamic pressor response after laryngoscopy and tracheal intubation has been attributed to the rapid-sequence induction of anesthesia, the lack of a control group with only CP (without rapid-sequence induction of anesthesia) has made study results questionable. In fact, no previous studies have been performed to specifically evaluate the hemodynamic effects of CP independently of the rapid-sequence induction of anesthesia. To assess the pressor response after application of CP, we designed a study of adult patients during the routine induction of general anesthesia.
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Methods
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After institutional approval and patient consent, 80 ASA I consecutive adult patients without a history of cardiovascular or renal diseases and who were scheduled for elective operation with general anesthesia were prospectively included in the study. Patients with difficult mask ventilation and gas leak around the face mask, and those with abnormal hemodynamic responses immediately after the administration of the drugs needed for the induction of anesthesia, were excluded from the study.
Lactated Ringer’s solution 7 mL/kg was infused before the induction of anesthesia. Anesthesia was induced with thiopental 5 mg/kg, atracurium 0.5 mg/kg, and fentanyl 1 µg/kg, followed by controlled mechanical ventilation (tidal volume = 10 mL/kg, respiratory rate = 10 breaths/min, inspiratory/expiratory ratio 1:2, and zero plateau time) (Ventilator Unit of Cicero anesthesia machine; Dräger, Lübeck, Germany) with a tight-fitting face mask by using halothane 1% in oxygen. Atracurium injection was performed in a 60-s period to prevent histamine release. Laryngoscopy and tracheal intubation were performed 4 min after the induction of anesthesia.
Patients were randomly divided into Cricoid and Placebo groups by use of a computer-generated sequence of 80 (2 x 40) shuffled allocations. In the Cricoid group, 2 min after the induction of anesthesia, bimanual CP was performed by using the palm of the left hand at the back of the neck and by using the thumb, index finger, and middle finger of the right hand to press the cricoid cartilage with a force of approximately 4.5 kg for a period of 1 min (12). The pressure was applied directly and precisely on cricoid cartilage in a backward direction against the C5 and C6 vertebra. In the Control group, a simple placement of hands without exerting pressure was performed. To blind the observer, either real CP or its simulation was performed under a covering.
Peak inspiratory pressure (Ppk) and exhaled tidal volume (VT) were recorded before the application and also 30 s after the initiation of CP or placebo maneuver. One minute after termination of CP, laryngoscopy and tracheal intubation were performed. Arterial blood pressure and heart rate were recorded at the following events (all at 1-min intervals): before the induction of anesthesia; 1 min after the induction of anesthesia; before application of CP; after termination of CP; before laryngoscopy and intubation; and every minute after tracheal intubation until 4 min. Pressor response was defined as the occurrence of hypertension, tachycardia, or both (
20% increase in blood pressure or heart rate compared with the baseline value) at any time after the application of CP or placebo maneuver. After the completion of the procedure and return of consciousness, the patients were asked about the presence of a sore throat.
In this study, all CPs and placebo maneuvers were applied by the same anesthesiologist, who was tested before the study by a scale instrument to ensure his level of force for correct application of CP. Another anesthesiologist working in all cases performed other tasks (including mask ventilation) except for measurement of vital signs, VT, and Ppk. An independent observer, who was blinded for the type of intervention, performed the latter tasks. This observer activated and recorded the automatic device for blood pressure measurement and also recorded the display values on the monitor for heart rate, VT, and Ppk every minute. Ppk and VT were measured by the respiratory unit of the Cicero anesthesia machine, and the blood pressure was measured by using a noninvasive blood pressure measurement (Datex Cardiocap II; Datex/Division of Instrumentarium Corp., Helsinki, Finland).
Data were presented as mean ± SD. Percentages were reported with their 95% confidence intervals (CIs). Repeatedly measured variables (Ppk, VT, blood pressure, and heart rate) were compared between and within groups by using the mixed-design analysis of variance (15). Other quantitative variables were compared by using Student’s t-test. Count data were compared between the two groups by use of an appropriate 
2 method. All comparisons were two sided, and a P value <0.05 was considered statistically significant. Statistical analysis was performed with SPSS 10.0 software (SPSS, Inc., Chicago, IL).
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Results
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A total of 81 patients were included in the study. A female patient who developed complete airway obstruction after the application of CP was excluded from the study. No significant differences between the two groups were found regarding age, sex distribution, weight, and height (Table 1). Baseline measurements of blood pressure, heart rate, VT, and Ppk were comparable between the two groups (Table 1).
After the application of CP, Ppk increased and VT decreased compared with the Control group and baseline values (P < 0.001) (Table 2).
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Table 2. Comparison of Ppk, Vt, and Cdyn Before and During the Application of Cricoid Pressure or Placebo Maneuver Between Two Groups
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Blood pressure and heart rate increased significantly after the application of CP compared with the baseline values and with those of the Control group (P < 0.001) (Table 3, Fig. 1). The incidence of pressor response was 65% (95% CI, 50%–80%) in Cricoid group compared with 7.5% (95% CI, 0%–15%) in the Control group (P = 0.005, Fisher’s exact test). The incidence of postextubation sore throat was not significantly different between the two groups (45% in the Cricoid group versus 47% in the Control group).
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Table 3. Comparison of Systolic, and Diastolic Blood Pressure and Heart Rate Before and After the Application of Cricoid Pressure or Placebo Maneuver Between Two Groups
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Figure 1. Comparison of percentage systolic blood pressure (A), diastolic blood pressure (B), and heart rate (C) changes between and within groups. ATRA = atracurium injection; CP = cricoid pressure application; LTI = laryngoscopy and tracheal intubation. The values at 4 min were taken immediately before tracheal intubation.
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Discussion
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This study shows that application of CP may lead to increases in blood pressure and heart rate in addition to partial obstruction of the upper airway. We found that the application of CP for a period of one minute after the induction of anesthesia in otherwise healthy subjects caused a significant increase in arterial blood pressure and heart rate. Also, the Ppk was increased and VT decreased during the application of CP. The reason for blood pressure and heart rate increase after application of CP seems to involve stimulation of the autonomic nervous system due to compression of sensitive laryngeal and perilaryngeal structures (12,16).
No previous studies have specifically addressed the hemodynamic effects of CP independently of rapid-sequence induction of anesthesia, and studies on the hemodynamic effects of rapid-sequence induction of anesthesia have focused mainly on these effects after laryngoscopy and intubation (13,14). Mills et al. (13) reported a significantly increased pressor response to tracheal intubation during rapid-sequence induction of anesthesia. They found that the application of CP did not augment this pressor response. They suggested that the stimulus by laryngoscopy and intubation is already nearly maximal and that a combination of laryngoscopy and CP tends to decrease the pressor response, especially on heart rate (13,17). Although these explanations are plausible, close examination of their results reveals that a 30% increase in heart rate, concomitant with a 10% decrease in systolic blood pressure at 30 seconds after CP (before tracheal intubation), may be due to a confounding factor such as hypovolemia. O’Hare et al. (14) studied the effects of remifentanil for control of hemodynamic response to tracheal intubation during rapid-sequence induction of anesthesia. Data from their control group can be used for comparative purposes. It shows a small but significant increase in systolic blood pressure and heart rate (8% and 7%, respectively) and a moderate increase in diastolic blood pressure (24%) after the application of CP (before laryngoscopy). These changes in blood pressure and heart rate are comparable to those of this study at one minute after the application of CP (before laryngoscopy) (Fig. 1). Unfortunately, the data of O’Hare et al. have not been further analyzed to clarify the incidence of hypertension, tachycardia, or both of these after the application of CP.
Neither the level of force used for CP nor the effects on the airway are described in the study by O’Hare et al. (14). The amount of reduction in dynamic compliance can be used as an indirect indication of the level of force that has been applied to cricoid cartilage. In our study, the amount of reduction in dynamic compliance during application of CP shows that the CP is administered by an appropriate level of force. The reduction in VT and increase of Ppk in this study were comparable to those in the study by Allman (10), except for the relatively frequent incidence of complete airway obstruction in that study (11% compared with 2.5% in our study).
As can be seen in Figure 1, the pressor response caused only by laryngoscopy and tracheal intubation was minimal in both groups because the trachea was intubated after four minutes of controlled ventilation, when the patients were completely relaxed and the alveolar concentration of anesthetic was large enough to suppress the pressor response.
We conclude that the application of CP alone, and in combination with laryngoscopy and intubation, increases the incidence of hypertensive or tachycardic episodes during the induction of anesthesia.
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Acknowledgments
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Supported in part by the Research Department, Isfahan University of Medical Sciences, Isfahan, Iran.
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References
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Accepted for publication May 11, 2001.
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Abstract
Introduction
