Anesthesia: Essays and Researches  Login  | Users Online: 562 Home Print this page Email this page Small font sizeDefault font sizeIncrease font size
Home | About us | Editorial board | Ahead of print | Search | Current Issue | Archives | Submit article | Instructions | Copyright form | Subscribe | Advertise | Contacts


 
Table of Contents  
ORIGINAL ARTICLE
Year : 2018  |  Volume : 12  |  Issue : 2  |  Page : 381-385  

A comparative study of two different intravenous bolus doses of phenylephrine used prophylactically for preventing hypotension after subarachnoid block in cesarean sections


Department of Anaesthesia, Adichunchanagiri Institute of Medical Sciences, Mandya, Karnataka, India

Date of Web Publication14-Jun-2018

Correspondence Address:
Dr. M R Shashank
#1595/1, Sri V G Temple road, 1st Cross, Vidyanagar, Mandya - 571401, Karnataka
India
Login to access the Email id

Source of Support: None, Conflict of Interest: None


DOI: 10.4103/aer.AER_228_17

Rights and Permissions
   Abstract 

Background and Aims: Hypotension occurs in most of the cases following subarachnoid block in for cesarean sections. Studies comparing different bolus doses of phenylephrine for preventing hypotension induced by subarachnoid block in cesarean sections are sparse. Settings and Design: This study was conducted to compare the efficacy of two different bolus doses of phenylephrine for preventing subarachnoid block-induced hypotension in cesarean sections. Materials and Methods: Sixty parturients undergoing cesarean section were allocated into two groups. Group A (n = 30) received 150 mcg phenylephrine intravenously (IV) and Group B (n = 30) received 200 mcg phenylephrine IV prophylactically immediately after subarachnoid block. Then, for every 2 min, systolic blood pressure, diastolic blood pressure, mean arterial pressure (MAP), and heart rate (HR) were measured for 20 min, and APGAR scores were measured. Statistical Analysis: The observations are expressed as mean ± standard deviation and were compared using unpaired t-test. The statistical significance of difference between groups was based on P value. P <0.05 was considered statistically significant. Results: There was no difference in preventing hypotension in both the groups, the incidence in Group A being 16.6% and Group B also 16.6%. However, the rise in systolic pressure in Group B was higher than Group A in the first 2–6 min. The incidence of bradycardia was higher in Group B (43.3%) than Group A (20%). Conclusions: Both the doses of phenylephrine were equally efficient in prevention of hypotension after subarachnoid block. Lower prophylactic bolus phenylephrine 150 mcg IV is better in the prevention of hypotension after subarachnoid block in cesarean sections as the incidence of bradycardia is higher with phenylephrine 200 mcg.

Keywords: Bradycardia, cesarean section, hypotension, phenylephrine, subarachnoid block


How to cite this article:
Prajwal Patel H S, Shashank M R, Shivaramu B T. A comparative study of two different intravenous bolus doses of phenylephrine used prophylactically for preventing hypotension after subarachnoid block in cesarean sections. Anesth Essays Res 2018;12:381-5

How to cite this URL:
Prajwal Patel H S, Shashank M R, Shivaramu B T. A comparative study of two different intravenous bolus doses of phenylephrine used prophylactically for preventing hypotension after subarachnoid block in cesarean sections. Anesth Essays Res [serial online] 2018 [cited 2020 Apr 3];12:381-5. Available from: http://www.aeronline.org/text.asp?2018/12/2/381/225973


   Introduction Top


Subarachnoid block is the preferred anesthetic technique for cesarean sections nowadays [1] to prevent general anesthesia-related complications such as failed intubation, aspiration, and depressant effect of general anesthetics on neonates, etc. However, the incidence of hypotension is 75%–85% with this technique which is detrimental to both mother and fetus.[2] Hypotension is especially associated with nausea and vomiting and in more severe cases there may be risk of decreased consciousness, pulmonary aspiration, respiratory depression, and cardiac arrest in mothers.[3]

Hypotension can have detrimental effects on neonate, which include decrease in utero placental flow, impaired fetal oxygenation with asphyxia and fetal acidosis.[4] Preventive measures for hypotension include adequate preload (10–15 mL/kg), lateral tilt, wedge and use of vasopressors.[5] Ephedrine is the preferred vasopressor in cesarean sections. It has both direct and indirect mechanism of action, stimulating mainly beta receptors (β1 and β2), causing increased cardiac output, heart rate (HR) and systolic blood pressure (SBP) and diastolic blood pressure (DBP). But it can cause supraventricular tachycardia, tachyphylaxis and fetal acidosis.[6]

Phenylephrine, a selective α1 adrenergic agonist, is as effective as ephedrine in the treatment of spinal hypotension with a better neonatal outcome and fetal acid–base status.[7] It elevates the blood pressure without increasing the HR or contractility. Hence, this randomized study was conducted to determine the efficacy of two different bolus doses of phenylephrine in preventing hypotension after subarachnoid block in cesarean sections.


   Materials and Methods Top


After obtaining clearance from the Institutional Ethical Committee and written informed consent from the parturients, a randomized double-blinded prospective study was carried out over a period of 1 year on 60 parturients between the age group of 20–35 years belonging to patients physical status American Society of Anesthesiologists (ASA) classes I and II who were scheduled for elective or emergency cesarean section during the study period under spinal anesthesia.

Singleton full-term pregnant parturients, age 20–35 years, patients physical status ASA classes I and II scheduled for cesarean section under spinal anesthesia were included in the study.

Parturients below 20 years and above 35 years, with height below 150 cm or above 170 cm, weight exceeding 70 kg, resting blood pressure >140/90 mmHg, history of hypertension, preeclampsia/eclampsia, hyperthyroidism, history of any coexisting neurological, cerebrovascular, cardiovascular, renal, metabolic, psychiatric disorder, glaucoma, occlusive vascular disorder, history of hypersensitivity to local anesthetics and any contraindications to spinal anesthesia or having known fetal abnormalities, and fetal distress were excluded from the study.

Parturients were allotted into two groups on the basis of computer-generated random sampling method. In Group A, the parturients received intravenous (IV) prophylactic phenylephrine bolus of 150 mcg after completion of intrathecal injection of 9 mg hyperbaric 0.5% bupivacaine. Then, for every 2 min SBP, DBP, mean arterial pressure (MAP), SPO2, and HR was measured for 20 min. In Group B, the parturients received IV phenylephrine bolus 200 mcg after completion of intrathecal injection. Then, for every 2 min SBP, DBP, MAP, SPO2, and HR was measured for 20 min. Baby APGAR scores were measured in both the groups after the delivery. Double-blinded randomization was achieved where anesthesiologist administering the drug and observer recording the parameters did not know what drugs were being used in the study.

Parameters to be studied

HR, SBP, and DBP every 2 min after the induction of spinal anesthesia up to 20 min, incidence of hemodynamic adverse effects, nausea and vomiting, and APGAR score at 1 and 5 min.

Procedure

After receiving the patient in the left lateral position inside the operation theater, oxygenation through face mask at 4 L/min was done which was continued till delivery of baby, baseline vital signs were recorded using multiparameter monitor. Parturients were preloaded with Ringer lactate solution 10 mL/kg over 15 min after securing IV line with 18 G cannula and continued at 10 mL/min. Under all aseptic precautions, with parturient in lateral position, skin infiltration was done with lidocaine 2%, a 25G Quincke babcocks needle was inserted at the L3–L4 vertebral interspace, and hyperbaric 0.5% bupivacaine 9 mg was injected intrathecally. Parturients were then immediately turned supine with left uterine displacement with the help of a wedge. SBP, DBP, MAP, HR, and SPO2 was measured at 2 min intervals beginning after spinal injection. Immediately after the completion of intrathecal injection, Group A phenylephrine 150 mcg IV bolus was given, whereas for parturients in the Group B, phenylephrine 200 mcg IV bolus was given. For the purposes of the study, we defined hypotension as a fall in SBP of >20% of baseline. Hypotension after 20 min was treated in both the groups by administration of phenylephrine 50 mcg IV bolus. Any incidences of nausea (reported by parturients) or vomiting (observed by investigators) were recorded. We planned to treat nausea or vomiting that was not associated with hypotension with IV ondansetron 0.1 mg/kg and to treat bradycardia defined by an HR <60 beats/min with IV atropine 0.6 mg.

After intrathecal injection of local anesthetic bupivacaine, the upper sensory level of anesthesia was measured by assessing the loss of pinprick discrimination and the level was maintained at T5–T6 in almost all the cases. After delivery, oxytocin 10 IU in 500 mL lactated Ringers solution was given by slow IV infusion. APGAR scores were assessed 1 and 5 min after delivery.

Statistical analysis

The observations are expressed as mean ± standard deviation. The baseline hemodynamic values and the postspinal hemodynamic changes at various time intervals were compared using unpaired t-test.

The statistical significance of the difference between Group A and Group B were based on P value. P <0.05 was considered to be statistically significant, P < 0.01 was considered to be highly significant, P < 0.001 was considered to be very highly significant, and P > 0.05 was considered to be not significant.


   Results Top


Maternal characteristics

Age, weight, and height characteristics of two groups in our study were comparable and were found to be not significant (P > 0.05).

Systolic blood pressure variations

The variations in mean SBP in Group A, Group B after SAB were in the range of 115.2–128.5 mm Hg, and 112.9–142.7 mm Hg, respectively, as shown in [Table 1].
Table 1: Systolic blood pressure

Click here to view


Both the groups had similar basal SBP; however, the mean SBP was higher in Group B and was statistically significant at 2–6 min after study drug administration.

Diastolic blood pressure variations

The mean DBP of the two groups was in the range of 72.83–62.83 and 84.5–67.63 mm of Hg, respectively, as shown in [Table 2].
Table 2: Diastolic blood pressure

Click here to view


Both the groups had similar basal DBP; however, the mean DBP in Group B was higher and statistically significant at 2–6 min after the study drug administration.

Mean arterial pressure variations

The MAP variations in Group A and Group B were in the range of 91.43–79.03 and 102.7–80.33 mm of Hg, respectively, as shown in [Table 3].
Table 3: Mean arterial pressure

Click here to view


Both the groups had similar basal MAP; however, the mean MAP was higher in Group B and was statistically significant at 2–6 min after study drug administration.

Heart rate variations

The mean basal HRs in Group A and Group B were 89.46 and 90, respectively, and not statistically significant. The mean HRs in Group A and Group B were in the range of 72.5–89.46 and 90.53–67.5, respectively. The mean HR in Group B was less and statistically significant at 4th min after study drug administration as shown in [Table 4].
Table 4: Heart rate

Click here to view


Incidence of bradycardia

The incidence of bradycardia in Group A and Group B was 20% and 43.33%, respectively. A number of episodes of bradycardia in Group A and Group B were 6 out of 30 cases and 13 out of 30 cases, respectively.

Apgar scores

The mean APGAR scores of Group A and Group B at 1st min were 7.53 and 7.73, respectively, and were not statistically significant.

The mean APGAR scores of the two groups at 5th min were 9.43 and 9.4, respectively and were not statistically significant as shown in [Table 5].
Table 5: APGAR scores

Click here to view



   Discussion Top


General anesthesia for cesarean sections poses complications such as failed endotracheal intubation, failed ventilation, aspiration pneumonitis, dental trauma, postoperative nausea and vomiting, delayed breastfeeding, and sedation of the baby. Epidural or spinal anesthesia avoid these risks, allow the mother to be awake at the baby's birth and may reduce the need for systemic opioid administration postoperatively. However, a spinal anesthetic technique has the advantage of simplicity, rapid onset, low failure rate, minimal drug dose, and the provision of excellent muscle relaxation during surgery. This frequently makes it the anesthetic technique of choice for both elective and emergency cesarean delivery.[1]

Spinal anesthesia to the level of T5–T6 is necessary to provide an adequate block for cesarean section. As a consequence, an almost inevitable complete sympathetic block occurs and decreased venous return to the heart exacerbated by a degree of inferior vena caval compression results in hypotension and decreased cardiac output. Despite all regional techniques being associated with maternal hypotension, the slower onset and lower incidence of this complication during epidural anesthesia may make the need for prophylactic medications unnecessary. In contrast, the frequent occurrence 75%–85%[2] and rapid onset of hypotension during spinal anesthesia has encouraged anesthesiologists to try and prevent or minimize the associated maternal symptoms of vomiting, nausea, impaired consciousness, pulmonary aspiration, respiratory depression, and cardiac arrest [3] and detrimental effects on neonate, which include decrease in utero placental flow, impaired fetal oxygenation with asphyxia, and fetal acidosis.[4]

Conventionally, ephedrine was the preferred vasopressor, but it can cause supraventricular tachycardia, tachyphylaxis, and fetal acidosis.[5] One possible mechanism of fetal acidemia is not related to the uteroplacental or fetoplacental circulation, but to the ephedrine-induced fetal β-adrenergic stimulation, as it crosses the placenta and increases fetal catecholamine levels and HR. A meta-analysis of four randomized clinical trials by Ngan Kee et al. showed that ephedrine could not be used for prophylaxis against hypotension. This is because it cannot prevent hypotension in low doses, and in high doses, it may cause hypertension that per se might be problematic.[6]

Phenylephrine claims better neonatal outcome and fetal acid-base status.[7] It can be used in case where tachycardia is undesirable. Das et al.[8] compared infusions of phenylephrine, ephedrine, and their combination with lower doses for prophylaxis against maternal hypotension following spinal anesthesia and found that phenylephrine alone is a better choice than ephedrine or combined. A combination of the drugs (half of the usual dosage) had no additional advantage over phenylephrine but was better than ephedrine alone. Ngan Kee et al.[9],[10] showed that prophylactic infusion of phenylephrine was more effective than other methods in the prevention of spinal anesthesia-induced hypotension. They also found that phenylephrine with crystalloid infusion is better than administration of each alone.[11]

In view of the above studies, we used prophylactic IV bolus dose of phenylephrine to prevent maternal hypotension after subarachnoid block in cesarean sections. Hypotension was defined as fall in systolic pressure of >20% from the baseline value or a value <90 mm Hg.[12] It has been shown that the percentage decrease in placental perfusion is related to the percentage reduction in maternal arterial pressure and not to the absolute reduction in pressure.

Observations

Blood pressure

In our study, the SBP, DBP, and MAP were higher in Group B and were statistically significant at 2–6 min after study drug administration. The incidence of hypotension in Group A and Group B was 16.66% and 16.66%, respectively. This shows a stable management of blood pressure in both the groups. This is due to α1 agonistic action of phenylephrine causing venoconstriction and thereby increasing the preload. Bhattarai et al.[13] compared phenylephrine 25 mcg, ephedrine 5 mg, and mephentermine 6 mg as bolus for maintaining arterial pressure and found that all three drugs maintained hemodynamics within 20% of baseline values on IV administration. Ngan Kee et al.[9] compared phenylephrine infusion of 100 μg/min with bolus administration of it and showed that infusion of phenylephrine can decrease the incidence and severity of hypotension as effective as bolus injections. These studies were consistent with our study.

Heart rate

The mean HR in both the groups for 20 min was comparable except at 4th min after study drug administration where it was significantly less in Group B. The incidence of bradycardia (<60 bpm) was more in Group B (43.33%) than Group A (20%). These episodes were treatable with atropine 0.6 mg IV. This is probably due to reflex bradycardia caused by the phenylephrine which lowered the HR. Thomas et al.[5] found that >50% of women given phenylephrine developed significant bradycardia compared to the ephedrine group. As cardiac output is the product of HR and stroke volume, this suggests that phenylephrine restored a greater stroke volume than ephedrine. Because phenylephrine (but not ephedrine) is virtually devoid of β inotropic effect, the better stroke volume produced by phenylephrine probably reflects a much better preload than with ephedrine, i.e., a better control of venous pooling caused by venoconstriction. However, in ephedrine group, cardiac sympathetic denervation was masked by the chronotropic effect of this β adrenergic agonist. Hall et al.[2] also recorded two cases of bradycardia in phenylephrine group which was <40 beats/min which was corrected with a bolus dose of atropine and both these episodes occurred after multiple doses of phenylephrine. No other patient had developed bradycardia. These findings were consistent with our study and suggest that phenylephrine causes reflex bradycardia.

Side effects

In our study group, none of the patients who received phenylephrine had nausea or vomiting. Cooper et al.[7] suggest that the possible explanation for nausea and vomiting is an increase in vagal tone following reduction of preload. Saravanan et al.[1] found that among the patients with ineffective blood pressure control, phenylephrine was significantly better compared to ephedrine in the prevention of vomiting.

All the above-mentioned studies demonstrated lower incidence of nausea and vomiting in patients receiving phenylephrine which is in accordance with our study.

Neonatal outcome

The APGAR score was similar in both the groups and was above 9 at 5 min. Previous studies have also shown that phenylephrine either in the form of bolus or infusion has no neonatal adverse effects.[14]

Limitations

Difficulties in standardizing the speed of administration of intrathecal drugs, time taken to lay the patients flat from left lateral position, speed of onset of sympathetic blockade, adjusting the left uterine displacement by wedge. Since phenylephrine is a very short-acting vasopressor, hypotension recurs after the effect of the prophylactic IV bolus wears off necessitating repeated boluses which was also a main limitation for our study. Among the weakness of our study, design was the differences in the timing of baby extraction and not assessing the neonatal outcome in terms of umbilical artery pH. Sample size may have affected the true clinical significance.


   Conclusions Top


As in both the groups, the maternal blood pressures were maintained in a stable range throughout the study and incidence of hypotension was same in both the groups, both the doses were equally efficient to prevent hypotension in cesarean sections after subarachnoid block with no adverse effects on neonatal outcome. However, the incidence of bradycardia was more with the higher bolus dose of phenylephrine, i.e., 200 mcg. Hence, we conclude that prophylactic IV bolus dose of phenylephrine 150 mcg is better than 200 mcg in preventing hypotension after subarachnoid block in cesarean sections.

Financial support and sponsorship

Nil.

Conflicts of interest

There are no conflicts of interest.

 
   References Top

1.
Saravanan S, Kocarev M, Wilson RC, Watkins E, Columb MO, Lyons G, et al. Equivalent dose of ephedrine and phenylephrine in the prevention of post-spinal hypotension in caesarean section. Br J Anaesth 2006;96:95-9.  Back to cited text no. 1
    
2.
Hall PA, Bennett A, Wilkes MP, Lewis M. Spinal anaesthesia for caesarean section: Comparison of infusions of phenylephrine and ephedrine. Br J Anaesth 1994;73:471-4.  Back to cited text no. 2
[PUBMED]    
3.
Balki M, Carvalho JC. Intraoperative nausea and vomiting during cesarean section under regional anesthesia. Int J Obstet Anesth 2005;14:230-41.  Back to cited text no. 3
[PUBMED]    
4.
Corke BC, Datta S, Ostheimer GW, Weiss JB, Alper MH. Spinal anaesthesia for caesarean section. The influence of hypotension on neonatal outcome. Anaesthesia 1982;37:658-62.  Back to cited text no. 4
[PUBMED]    
5.
Thomas DG, Robson SC, Redfern N, Hughes D, Boys RJ. Randomized trial of bolus phenylephrine or ephedrine for maintenance of arterial pressure during spinal anaesthesia for caesarean section. Br J Anaesth 1996;76:61-5.  Back to cited text no. 5
[PUBMED]    
6.
Ngan Kee WD, Khaw KS, Lee BB, Lau TK, Gin T. A dose-response study of prophylactic intravenous ephedrine for the prevention of hypotension during spinal anesthesia for cesarean delivery. Anesth Analg 2000;90:1390-5.  Back to cited text no. 6
[PUBMED]    
7.
Cooper DW, Carpenter M, Mowbray P, Desira WR, Ryall DM, Kokri MS, et al. Fetal and maternal effects of phenylephrine and ephedrine during spinal anesthesia for cesarean delivery. Anesthesiology 2002;97:1582-90.  Back to cited text no. 7
    
8.
Das S, Mukhopadhyay S, Mandal M, Mandal S, Basu SR. A comparative study of infusions of phenylephrine, ephedrine and phenylephrine plus ephedrine on maternal haemodynamics in elective caesarean section. Indian J Anaesth 2011;55:578-83.  Back to cited text no. 8
[PUBMED]  [Full text]  
9.
Ngan Kee WD, Khaw KS, Ng FF, Lee BB. Prophylactic phenylephrine infusion for preventing hypotension during spinal anesthesia for cesarean delivery. Anesth Analg 2004;98:815-21.  Back to cited text no. 9
[PUBMED]    
10.
Ngan Kee WD, Khaw KS, Ng FF. Comparison of phenylephrine infusion regimens for maintaining maternal blood pressure during spinal anaesthesia for caesarean section. Br J Anaesth 2004;92:469-74.  Back to cited text no. 10
[PUBMED]    
11.
Ngan Kee WD, Khaw KS, Ng FF. Prevention of hypotension during spinal anesthesia for cesarean delivery: An effective technique using combination phenylephrine infusion and crystalloid cohydration. Anesthesiology 2005;103:744-50.  Back to cited text no. 11
[PUBMED]    
12.
Greene NM, Brull SJ. Pulmonary ventilation and hemodynamics. Physiology of Spinal Anaesthesia. 4th ed., Ch. 3. Baltimore: Williams and Wilkins; 1993. p. 201-24.  Back to cited text no. 12
    
13.
Bhattarai B, Bhat SY, Upadya M. Comparison of bolus phenylephrine, ephedrine and mephentermine for maintenance of arterial pressure during spinal anesthesia in cesarean section. JNMA J Nepal Med Assoc 2010;49:23-8.  Back to cited text no. 13
[PUBMED]    
14.
Moran DH, Perillo M, LaPorta RF, Bader AM, Datta S. Phenylephrine in the prevention of hypotension following spinal anesthesia for cesarean delivery. J Clin Anesth 1991;3:301-5.  Back to cited text no. 14
[PUBMED]    



 
 
    Tables

  [Table 1], [Table 2], [Table 3], [Table 4], [Table 5]



 

Top
 
  Search
 
    Similar in PUBMED
   Search Pubmed for
   Search in Google Scholar for
 Related articles
    Access Statistics
    Email Alert *
    Add to My List *
* Registration required (free)  

 
  In this article
    Abstract
   Introduction
    Materials and Me...
   Results
   Discussion
   Conclusions
    References
    Article Tables

 Article Access Statistics
    Viewed1169    
    Printed27    
    Emailed0    
    PDF Downloaded93    
    Comments [Add]    

Recommend this journal