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Anesth Analg 2002;94:1652-1655 © 2002 International Anesthesia Research Society
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Abstract |
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In this clinical study, we tested the hypothesis that a marked systolic blood pressure decrease >35% (
SBP >35%) from preanesthetic baseline during the induction and maintenance of anesthesia is associated with more postoperative nausea and vomiting (PONV). In 300 ASA physical status I and II women undergoing elective gynecological surgery with general anesthesia, the maximum SBP during the induction as well as maintenance of general anesthesia were calculated. Observers blinded to hemodynamic variables assessed the incidence of PONV. The overall incidence of nausea (visual analog scale >4) and vomiting within the immediate observation period (0–2 h) was 39% and 25%, respectively. Frequency of nausea and vomiting in the late observation period was 21% and 9%, respectively. Women with a SBP >35% during the induction of anesthesia suffered from a more frequent incidence of PONV within the immediate (57% versus 35% and 41% versus 22%, respectively; P < 0.01) and within the late observation period (33% versus 18% and 19% versus 7%, respectively; P 
0.01). In women with a SBP >35% during maintenance of anesthesia, a more frequent incidence of nausea within the immediate observation period (53% versus 36%; P < 0.05) was found. We conclude that a maximum SBP >35% during the anesthetic induction is associated with an increased incidence of PONV after gynecological surgery during general anesthesia.
IMPLICATIONS: A prospective clinical investigation revealed that a marked systolic blood pressure decrease >35% (SBP >35%) during the induction of general anesthesia is associated with an increased incidence of postoperative nausea and vomiting (PONV). The association between a SBP >35% during maintenance of general anesthesia and PONV is less pronounced.
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Introduction |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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Postoperative nausea and vomiting (PONV) is not a uniform phenomenon in either appearance or causality. The influence of hemodynamic variables on PONV has been repeatedly considered. Sympathomimetic drugs, such as ephedrine, and parasympatholytics, such as atropine and scopolamine, have proven effective for the treatment of PONV (1,2). Furthermore, an infrequent incidence of postoperative nausea has been observed in patients with adequate perioperative hydration (3). Blood pressure abnormalities, autonomic nervous system disturbance, and orthostatic hypotension are of major importance for the occurrence of vertigo and dizziness (4) and may contribute to PONV. Intraoperative hypotension is caused either by anesthetics (5), surgery-associated variables, cardiovascular diseases, or by disturbances of the autonomic nervous system. Functions of the vestibular apparatus and blood circulation to the intestine and the brainstem, with its emetic center, may be altered by a marked blood pressure decrease. However, hemodynamic variables and PONV-promoting factors may influence each other. The present study has therefore been designed to determine the association between a marked decrease in systolic blood pressure of >35% (
SBP >35%) from the preoperative baseline value during the induction as well as maintenance of general anesthesia and the incidence and risk factors of PONV. |
Methods |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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This study was performed after review by the institutional ethics commission and obtaining patients’ written informed consent. We studied 300 adult female patients with ASA physical status I or II who were scheduled for elective gynecological surgery. Only nonpregnant women independent of their menstrual cycle phase were recruited. Women presenting with significant cardiac disease (New York Health Association class >1) or dysfunction of their vestibular system were excluded per closed questionnaire.
On the day before surgery, women were interviewed during routine preoperative medical and physical assessment for details of previous anesthesia, PONV, and history of motion sickness (6). Age, weight, and the date of their last menstruation were recorded. No women received prophylactic antiemetics.
Women were premedicated with 7.5 mg of midazolam given orally 1 h before the transport to the operating room. In the operating room, standard monitoring consisting of electrocardiogram, noninvasive blood pressure (NIBP), pulsplethysmography, oxygen-saturation, and end-tidal CO2 was applied. Immediately before the anesthesia induction, an infusion of Ringer’s lactate solution was started, and all patients received intraoperative 10 mL · kg-1 · h-1. Anesthesia was induced with fentanyl (2–3 µg/kg) and IV propofol 2 mg/kg. Muscle relaxation was achieved using rocuronium 0.6 mg/kg and was continuously monitored using a peripheral nerve stimulator. Anesthesia was maintained with nitrous oxide (70%), oxygen (30%), and sevoflurane as a volatile anesthetic up to end-tidal values of 1.5% dependent on the anesthesiologists’ discretion. Normoventilation (end-tidal CO2, 32–36 mm Hg) was assured. A nasogastric tube was inserted to drain gases or gastric contents from the stomach. Before tracheal extubation, the nasogastric tube was suctioned and removed. Atropine 0.02 mg/kg and neostigmine 0.04 mg/kg were administered IV for reversal of muscle relaxation. Women received either the nonsteroidal analgesic drug, 75 mg of diclofenac, or bolus doses of 3 mg of piritramide, a synthetic opioid, both administered IV for postoperative analgesia as required.
During the first postoperative hour, all women received oxygen therapy at a rate of approximately 2–3 L/min. Within the first 2 postoperative h, all patients received 5 mL · kg-1 · h-1 of Ringer’s lactate solution. Women were allowed to drink after the first 2 h. The SBP measured immediately before the induction of anesthesia was determined as the baseline value. Maximum SBP during the induction of general anesthesia was calculated as the difference between the preanesthetic baseline value and the lowest value of SBP within 15 min after the start of the anesthesia induction. During maintenance of anesthesia, SBP was defined as the difference between preanesthetic baseline value and the lowest value of SBP measured between the end of the induction (15 min) and the end of anesthesia. NIBP was measured during the induction and maintenance in 1- and 5-min intervals, respectively. Women with severe hypotension, i.e., a SBP >35%, assessed by a single measurement received a bolus dose of etilefrine 0.03 mg/kg.
According to our data from a pilot study, we set cutoff values for marked SBP at 35%. Throughout the immediate postoperative observation period (0–2 h), an anesthesiologist, and during the late observation period (2–24 h), trained nurses, both blinded to the hemodynamic variables, assessed PONV. Women presenting with nausea (visual analog scale [VAS] >4), vomiting, or both received 2 mg of tropisetron IV as rescue medication (7). The VAS consisted of a 10-cm-long line. The left end corresponded to no symptom and the right to unbearable symptoms. On the backside of the scale, which was invisible to the patient, the corresponding value from zero to 10 was recorded. The incidence of PONV symptoms within the postoperative 24 h were compared among women with and without a maximum SBP >35% from baseline.
All data are presented as mean ± SD and frequencies. Normality of distribution was assessed by the Kolmogorov-Smirnov test. Unpaired t-test was calculated for comparison of continuous data between groups. For comparison of proportional data, 
2 tests were performed. A P value < 0.05 was considered significant.
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Results |
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Three hundred women recruited to the investigation completed the protocol. Descriptive data for age, weight, height, body mass index, and types of surgery are shown in Table 1. Duration of anesthesia (112 min [55 min] versus 91 min [70 min], respectively; P < 0.01) and surgery (81 min [51 min] versus 66 min [59 min], respectively; P < 0.05) was longer in women who suffered from PONV anytime during the study period. The overall incidence of nausea (VAS >4) and vomiting within the immediate observation period was 118 (39%) and 75 (25%), respectively. The incidence of nausea and vomiting in the late observation period was 62 (21%) and 28 (9%), respectively. Mean maximum
SBP during the induction and maintenance were 25% (sd 10%) and 24% (sd 11%), respectively. SBP >35% were found during the induction and maintenance of general anesthesia in 54 (18%) and 55 (18%) women, respectively.
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Within the entire study period, a significantly more frequent incidence of PONV was found in women with a
SBP >35% during the induction of anesthesia (Table 2). In women with a SBP >35% during maintenance of anesthesia, only a more frequent rate of nausea in the immediate observation period was observed (Table 2). In women with a SBP >35% during the induction, more frequent rates of previous PONV were found (Table 2).
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Discussion |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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The main result of this prospective clinical investigation is that a marked
SBP >35% during the induction of general anesthesia is associated with significantly more nausea and vomiting (Table 2), whereas the effect of a SBP >35% during the maintenance of general anesthesia on PONV is less pronounced.
Several mechanisms may account for the different effects of SBP during the induction and maintenance of anesthesia. Induction with cardiodepressant and vasodilating anesthetics may lead to a more rapid SBP compared with those occurring during maintenance of general anesthesia. Compensatory mechanisms may be insufficient for fast restoration of an adequate cardiovascular stability after the anesthesia induction. A temporary decrease in splanchnic perfusion may result (8). Intestinal tissues are highly metabolically active and have a poor tolerance for even brief periods of ischemia. One consequence of isch-emia is the release of 5-hydroxytryptamine from the intestine where it acts as a local vasodilator. Large serotonin concentrations are frequently associated with PONV (9). Rapid SBP during the induction of anesthesia may also reduce the blood flow to the brainstem and influence the chemoreceptor trigger zone. This may intensify adverse effects of anesthetics such as dizziness, disturbance of the vestibular system, nausea, and vomiting (4). From our data, effects of blood pressure decreases during maintenance of anesthesia on PONV cannot be convincingly demonstrated. Power analyses performed with regard to the results of this study and in consideration of the infrequent incidence of PONV revealed a minimum number of 2500 women to confirm an effect of a SBP >35% during maintenance of general anesthesia on PONV (statistical power of 80% for a 20% difference at P < 0.05). Those patients exhibiting marked SBP >35% during the anesthesia induction more often suffered from PONV during former anesthetic procedures (Table 1).
Because PONV is a repetitive phenomenon, many authors report the effects of preventive measures on its incidence. Interestingly, many of those antiemetic measures somehow interfere with cardiovascular variables. The incidence of adverse outcome variables such as nausea, vomiting, dizziness, and speed of recovery after general anesthesia even depends on the fluid status of the patient. Hypovolemia leads to increased response to anesthetics and analgesics, which potentiates the hypotensive effects of anesthetics (10). Hypovolemia may in turn increase the risk of nausea and vomiting (3). Studies have shown that ephedrine, administered IM at the end of abdominal hysterectomy, protects against PONV during the first three postoperative hours. Ephedrine has a sympathomimetic action and is antiemetic, probably because it counteracts emetic vagal stimuli (1). Ephedrine has a specific antiemetic effect on PONV, partly by reducing the incidence of hypotension (1). Sympathomimetics are effective in preventing motion sickness and increasing the rate of gastric emptying after motion sickness has been established (11). A high degree of vagal tone in the perioperative period may also add to the incidence of PONV (12). Ephedrine may minimize these symptoms by increasing sympathetic tone.
In a rabbit model, the 5-hydroxytryptamine-3-receptor antagonist, granisetron, approved for prevention of PONV and chemotherapy-induced nausea and vomiting, attenuates both the hypotension and inappropriate heart rate slowing (Bezold-Jarisch reflex) after acute blood loss. Granisetron has been effective in preventing bradycardia and preventing the rate of SBP caused by bleeding and may prevent vasovagal syncope in humans as well (13). The hemodynamic effects of granisetron may partly explain its preventive effect on PONV.
In conclusion, our study demonstrates that a SBP >35% may be associated with PONV. Whether the blood pressure decrease triggers PONV or PONV symptoms influence hemodynamic variables is not clear. Our results suggest that the initial hemodynamic instability during the anesthesia induction may play a role in the development of PONV.
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References |
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TopAbstractIntroductionMethodsResultsDiscussionReferences |
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- Hagemann E, Halvorsen A, Holgersen O, et al. Intramuscular ephedrine reduces emesis during the first three hours after abdominal hysterectomy. Acta Anaesthesiol Scand 2000; 4: 107–11.
- Honkavaara P, Pyykkö I. Effects of atropine and scopolamine on bradycardia and emetic symptoms in otoplasty. Laryngoscope 1999; 109: 108–12.[Web of Science][Medline]
- Yogendran S, Asokumar B, Cheng DCH, Chung F. A prospective randomized double-blinded study of the effect of intravenous fluid therapy on adverse outcomes on outpatient surgery. Anesth Analg 1995; 80: 682–6.[Abstract]
- Nakagawa H, Ohashi N, Kanda K, Watanabe Y. Autonomic nervous system disturbance as etiological background of vertigo and dizziness. Acta Otolaryngol Suppl 1993; 504: 130–3.[Medline]
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Fairfield JE, Dritsas A, Beale RJ. Haemodynamic effects of propofol: induction with 2.5 mg kg-1. Br J Anaesth 1991; 67: 618–20.
[Abstract/Free Full Text] - Apfel CC, Läärä E, Koivuranta M, et al. A simplified risk score for predicting postoperative nausea and vomiting. Anesthesiology 1999; 91: 693–700.[Web of Science][Medline]
- Boogaerts JG, Vanacker E, Seidel L, et al. Assessment of postoperative nausea using a visual analogue scale. Acta Anaesthesiol Scand 2000; 44: 470–4.[Web of Science][Medline]
- Piriou V, Chiari P, Lehot JJ, et al. Effects of propofol on haemodynamics and on regional blood flows in dogs submitted or not to a volaemic expansion. Eur J Anaesthesiol 1999; 16: 615–21.[Web of Science][Medline]
- Greif R, Laciny S, Rapf B, et al. Supplemental oxygen reduces the incidence of postoperative nausea and vomiting. Anesthesiology 1999; 91: 1246–52.[Web of Science][Medline]
- De Paepe P, Belpaire FM, Rosseel MT, et al. Influence of hypovolemia on the pharmacokinetics and the electroencephalographic effect of propofol in the rat. Anesthesiology 2000; 93: 1482–90.[Web of Science][Medline]
- Wood CD, Stewart JJ, Wood MJ, et al. Therapeutic effects of antimotion sickness medications on the secondary symptoms of motion sickness. Aviat Space Environ Med 1990; 61: 157–61.[Medline]
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Rothenberg DM, Parnass SM, Litwack K, et al. Efficacy of ephedrine in the prevention of postoperative nausea and vomiting. Anesth Analg 1991; 72: 58–61.
[Abstract/Free Full Text] - White CM, Chow MSS, Fan C, et al. Efficacy of intravenous granisetron in suppressing the bradycardia and hypotension associated with a rabbit model of the Bezold-Jarisch reflex. J Clin Pharmacol 1998; 38: 172–7.[Abstract]
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