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Canadian Journal of Anesthesia 47:786-791 (2000)
© Canadian Anesthesiologists' Society, 2000
Reports of Investigation

Acute changes in bladder volume produce minimal cardio-respiratory responses in lightly anesthetised humans

Teruhiko Ishikawa , MD, Jiro Sato, MD and Takashi Nishino, MD

From the Department of Anesthesiology, Chiba University School of Medicine, Inohana 1-8-1, Chiba 260-8670, Japan.

Address correspondence to: Teruhiko Ishikawa md. Phone: +81-43-226-2155; Fax: +81-43-226-2156; E-mail: iteru{at}anesth01.m.chiba-u.ac.jp


   Abstract
TOP
 Abstract
Introduction
 Methods
 Results
 Discussion
 References
 
Purpose: To examine whether changes in bladder volume elicit reflex cardiovascular and respiratory responses in humans under general anesthesia with sevoflurane and nitrous oxide.

Methods: Fourteen patients free of autonomic disorders were anesthetized with sevoflurane 0.5% and nitrous oxide 60% in oxygen that were approximately equivalent to 0.9 MAC. Warmed saline (6 ml•kg–1, 37°C) was instilled into the pre-emptied urinary bladder, and then the bladder was kept distended for five minutes. Following the distension, the instilled saline was drained to the pre-instilled volume of the bladder. Arterial blood pressure, respiratory flow, and intra-vesicle pressure were continuously measured, and mean arterial pressure, pulse rate, respiratory rate, tidal volume, and minute ventilation were estimated offline from these signals.

Results: Bladder emptying produced small decreases in mean blood pressure (from 83.4 ± 4.3 to 80.0 ± 4.4 mmHg, mean ± SE, P =0.017) and pulse rate (from 72.2 ± 2.9 to 69.4 ± 2.7 bpm, mean ± SEM, P =0.004). Only minimal respiratory reflexes were invoked by the bladder volume changes.

Conclusion: In lightly anesthetized humans, the acute changes in bladder volume produce only mild cardiovascular and respiratory responses.


   Introduction
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 Abstract
 Introduction
Methods
 Results
 Discussion
 References
 
IN additions to the measurement of urine output, urinary bladder catheterization prevents the bladder from over-distension which may lead to undesirable autonomic reflexes, such as the dramatic increase in blood pressure, especially in patients with high spinal lesions.1–3 Sudden emptying of the bladder may result in severe hypotension.4,5 Attenuation of these responses by spinal or epidural anesthesia2 suggests involvement of afferent input from the urinary bladder in the cardiovascular reflexes. In the absence of block of the afferent pathway, inadequate anesthesia may produce an unstable cardiovascular status when stimuli are applied2,6

In addition to the cardiovascular reflexes, both spontaneous contraction and passive distension of the bladder may produce inhibition of respiratory motor neurone activity in anesthetized or decerebrate cats.7–10 These findings may indicate that changes in bladder volume could produce abnormal breathing during light general anesthesia.

Therefore, we examined whether passive distension and voiding of the bladder caused autonomic responses in cardiovascular and respiratory systems during light general anesthesia in humans.


   Methods
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 Abstract
 Introduction
 Methods
Results
 Discussion
 References
 
Subjects
After obtaining ethics approval and informed consent, patients for elective minor surgery under general anesthesia were recruited. Fourteen patients (six female and eight male; age, 42 ± 14 yr; weight, 60.4 ± 11.5 kg; height, 163.6 ± 10.4 cm) participated in this study. They were undergoing minor surgery of the head & neck,(n=11) plastic,(n=2) or breast surgery.(n=1) All subjects were ASA status I - II. None had any neurological and urological disorders. Patients with possible autonomic dysfunction or diabetes were also excluded.

Anesthesia
Famotidine, 20 mg iv, was administered two hours prior to induction of anesthesia. The subjects received 50 mg hydroxyzine and 0.5 mg atropine im 45 min before induction. After a small dose of vecuronium (0.02 mg•kg–1 iv), anesthesia was induced with 5 mg•kg–1 thiopental (iv) and tracheal intubation was facilitated with 1.5 mg•kg–1 succinylcholine (iv). Anesthesia was maintained with sevoflurane in nitrous oxide and oxygen. A three-lumen balloon tipped silicon catheter (14 Fr.) was inserted via the urethra into the urinary bladder. In addition to routine monitoring, continuous measurement of arterial blood pressure (ABP) was performed via a catheter placed in the radial artery. The concentration of sevoflurane was adjusted to establish an adequate anesthetic depth for the surgical procedures.

Measurements
As well as measurement of ABP, airflow (V.) was measured with a Fleisch type pneumotachograph (#2) placed at the proximal end of the endotracheal tube. We also performed continuous measurement of intra-vesicle pressure (Pvs) through a lumen of the three-lumen bladder catheter. All the signals were lowpass filtered at 50 Hz by a three-pole Butterworth filter (SPA-3, TechnoService, Urayasu, Japan) and digitized at 100 Hz by an analogue to digital converter (DT2801-A, Data Translation, Marlboro, NJ). Data acquisition was performed with a data logging software package (LABDAT 5.2 RHT-InfoDat, Montreal, Quebec, Canada), on an IBM compatible personal computer, and stored on an internal hard disk for offline analysis.

Experimental protocol
At the termination of surgery, end-tidal sevoflurane and nitrous oxide concentrations were set at 0.5 and 60%, respectively, which were confirmed a pre-calibrated infrared gas analyzer (Anesthetic Gas Monitor Type 1304, Brüel & Kjær, Norcross, GA). The depth of anesthesia was approximately equivalent to 0.9 MAC and was considerably lighter than the depth required to inhibit autonomic responses. Roizen et al. showed that about 1.5 times MAC was necessary to prevent cardiovascular responses to skin incision.6 The subjects were allowed to breathe spontaneously in the supine position. The urinary bladder was emptied as much as possible by gentle compression of the lower abdomen. After obtaining stable respiratory and circulatory conditions, the following protocol was started. While measuring Pvs, warmed saline (37°C, 6 ml•kg–1) was infused into the bladder through another lumen of the bladder catheter. The saline was allowed to flow into the bladder with 100 cm hydrostatic pressure gradient. The instillation took approximately five minutes. The volume was chosen according to previous work with suggestion that the maximum bladder volume that was acceptable in awake humans was about 300 to 420 ml.11 At the completion of the infusion, the infusion line was clamped to keep the bladder distended for another five minutes to observe the adaptation to the distension. Following this, the infusion route was reopened for the infused saline to drain freely. Although the fluid was usually voided within two minutes, we continued the measurement for another five minutes from the start of the evacuation to observe the changes during stabilization phase.

Offline analysis
An example of the analysis is shown in Figure 1Go. The ventilatory volume (V) was calculated by numerical integration of V. signals. Respiratory frequency (RR), tidal volume (VT), and minute ventilation (MV) were calculated on a breath-by-breath basis from V. and V signals. Beat-wise trends in mean ABP (MBP) and pulse rate (PR) were calculated from the ABP signals. Signal processing and other numerical analysis were performed by a house made software written in S language (S-Plus 4, MathSoft, Seattle, USA).



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  		FIGURE 1 An example of offline analysis. From the top, panels indicate temporal changes in intra-vesicle pressure (Pvs), tidal volume (VT), minute ventilation (MV), respiratory rate (RR), pulse rate (PR), and mean arterial blood pressure (MBP).

 
Statistics
The effects of bladder volume changes were analyzed by comparing representative values of the cardiovascular (MBP, PR) and respiratory (RR, VT, MV) variables among four different phases: Control, Distension, Adaptation, and Evacuation (Figure 1Go). The phase Control was defined as the period before infusing the saline into the bladder. Distension was a phase during which the saline was instilled into the bladder: the volume of the bladder was increasing. Adaptation was the phase during which the bladder was kept distended but the volume did not change. Evacuation was the phase during voiding of saline from the bladder. The values of the last 30 sec of each phase were averaged as the representative values. Abnormal breaths such as sighs and arrhythmia such as premature contractions were discarded for statistical comparison. Data were analyzed using multivariate ANOVA followed by a contrast analysis to reveal which two specific sets were significantly different. We analyzed circulatory and respiratory variables separately. P < 0.05 was considered significant. Descriptive statistics were expressed as mean ± SD or median (range), unless otherwise stated.


   Results
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 Abstract
 Introduction
 Methods
 Results
Discussion
 References
 
Anesthetic time before the start of the experiment was 205 (110-665) min. The amount of crystalloid administered and bleeding were 6.5 (1.7-12.6) ml•kg–1•hr–1 and 2.3 (0.4-7.9) ml•kg–1 respectively. Although the amount of surgical bleeding was relatively small, it was corrected by administering larger amounts of crystalloid fluids to the patients with greater bleeding. No cardiovascular or respiratory events were reported during the surgery.

Although the bladder distension tended to cause an increase in MBP, it did not reach statistical significance (P =0.169, Control vs Distension). Evacuation of the bladder resulted in a decrease in MBP (P =0.017, Distension vs Evacuation; P =0.013, Adaptation vs Evacuation). Similarly, a small decrease in PR was also observed during adaptation and evacuation (P =0.015, Distension vs Adaptation; P =0.004, Distension vs Evacuation) (Figure 2Go).



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  		FIGURE 2 Changes in cardiovascular variables. Values are presented as mean ± SEM. Square brackets with P values indicate pairs whose difference in means are significant.

 
No consistent response was detected in respiratory variables (Figure 3Go).



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  		FIGURE 3 Changes in respiratory variables. Values are presented as mean ± SEM. No significant changes are observed in respiratory parameters.

 

   Discussion
TOP
 Abstract
 Introduction
 Methods
 Results
 Discussion
References
 
The main findings of this study are that rapid changes in bladder volume 1) produced only minimal cardiovascular reflexes, that 2) did not produce respiratory reflexes in humans lightly anesthetized with nitrous oxide and sevoflurane.

The cardiovascular responses observed in this study were similar to the results of previous studies conducted either in anesthetized animals12,13 or in awake human subjects.14 However, the magnitude of responses seen in this study was smaller than that in previous studies. Our results indicate that acute changes in bladder volume do not evoke serious cardiovascular instability in humans during light general anesthesia. Nevertheless, we observed unstable circulatory profiles in several subjects (Figure 4Go) indicating variable autonomic responsiveness among subjects. Kao et al. also reported a case who exhibited loss of consciousness probably due to hemodynamic decompensation associated with micturition.4 The variability might be explained by the large variation in bladder capacity and a relatively small distension volume used in this study.



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  		FIGURE 4 A subject who had clear responses both in cardiovascular and respiratory variables. Note the clear responses associated with changes in the bladder volume.

 
Several studies in anesthetized or decerebrate cats reported respiratory inhibition produced by bladder volume changes.7,9,10 We did not observe any consistent responses in respiration. The discrepancy is probably due to the differences in species and experimental conditions. The magnitude of the respiratory reflex responses generally varies among species.15 In some studies on cats,7,10 the vagi were sectioned. The vagus nerve may act as ‘a buffer’ which would blunt the respiratory responses as in the hemodynamic response.16 Decerebration performed in the animal studies,7,10 may also account for the discrepancy, since it can eliminate the influence of anesthesia, thus augments reflexes. With larger distension volume, we might have consistent responses in respiratory parameters, however, we imposed limits on the distension volume to avoid injury of the bladder due to over distension.

In conclusion, in lightly anesthetized humans, bladder distension and voiding produced minimal cardiovascular reflexes. These volume changes did not invoke respiratory reflexes. During light general anesthesia, as may seen during emergence from anesthesia, changes in the bladder volume are unlikely to produce appreciable cardiovascular and respiratory reflexes.


   Footnotes
 
This work was supported by Grant-in-Aid for Encouragement of Young Scientists 11770836, from the Ministry of Education, Japan.

Accepted for publication May 6, 2000.


   References
TOP
 Abstract
 Introduction
 Methods
 Results
 Discussion
 References
 
1 Krum H, Louis WJ, Brown DJ, Clarke SJ, Fleming JA, Howes LG. Cardiovascular and vasoactive hormone responses to bladder distension in spinal and normal man. Paraplegia 1992; 30: 348–54.[Medline]

2 Moss J, Craigo PA. The autonomic nervous system. In: Miller RD (Ed.). Anesthesia, 4th ed. New York: Churchill Livingstone, 1994: 523–75.

3 Wurster RD, Randall WC. Cardiovascular responses to bladder distension in patients with spinal transection. Am J Physiol 1975; 228: 1288–92.[Abstract/Free Full Text]

4 Kao YJ, Racz GB. Loss of consciousness after emergence from anaesthesia. A case of suspected micturition syncope. Anaesthesia 1990; 45: 738–40.[Medline]

5 Watkins AL. Reflex response of the nictitating membrane and the blood pressure to distention of the bladder and rectum. Am J Physiol 1938; 121: 32–9.

6 Roizen MF, Horrigan RW, Frazer BM. Anesthetic doses blocking adrenergic (stress) and cardiovascular responses to incision - MAC BAR. Anesthesiology 1981; 54: 390–8.[Medline]

7 Gdovin MJ, Knuth SL, Bartlett D Jr. Respiratory motor nerve activities during spontaneous bladder contractions. J Appl Physiol 1994; 77: 1349–54.[Abstract/Free Full Text]

8 Gdovin M J, Knuth SL, Bartlett D Jr. Roles of the pontine pneumotaxic and micturition centers in respiratory inhibition during bladder contractions. Respir Physiol 1997; 107: 15–25.[Medline]

9 Gdovin M J, Knuth SL, Bartlett D. Influence of lung volume on respiratory responses to spontaneous bladder contractions. Respir Physiol 1997; 107: 137–48.[Medline]

10 Schondorf R, Polosa C. Effects of urinary bladder afferents on respiration. J Appl Physiol 1980; 48: 826–32.[Abstract/Free Full Text]

11 Axelsson K, Möllefors K, Olsson JO, Lingårdh G, Widman B. Bladder function in spinal anaesthesia. Acta Anaesthesiol Scand 1985; 29: 315–21.[Medline]

12 Medda B K, Koley J, Koley B. Sympathetic efferent activity in the viscerovascular reflexes induced by urinary bladder distension. Jpn J Physiol 1995; 45: 265–77.[Medline]

13 Tsuchida S, Kumagai I. Effect of urinary bladder distension on renal blood flow, blood pressure and plasma renin activity. Tohoku J Exp Med 1978; 126: 335–41.[Medline]

14 Fagius J, Karhuvaara S. Sympathetic activity and blood pressure increases with bladder distension in humans. Hypertension 1989; 14: 511–7.[Abstract]

15 Widdicombe JG. Respiratory reflexes in man and other mammalian species. Clin Sci 1961; 21: 163–70.[Medline]

16 Mukherjee SR. Effect of bladder distension on arterial blood pressure and renal circulation: role of splanchnic and buffer nerves. J Physiol 1957; 138: 307–25.





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