|Year : 2012 | Volume
| Issue : 2 | Page : 193-196
A comparison of hypotension and bradycardia following spinal anesthesia in patients on calcium channel blockers and β-blockers
Padmanabha Kaimar1, Narendranath Sanji2, Madhusudan Upadya1, K Riaz Mohammed1
1 Department of Anaesthesiology, Kasturba Medical College, Mangalore, India
2 Department of Pharmacology, J.J.M. Medical College, Davangere, Karnataka, India
|Date of Submission||01-Jun-2011|
|Date of Decision||28-Aug-2011|
|Date of Acceptance||16-Dec-2011|
|Date of Web Publication||16-Mar-2012|
Department of Pharmacology, J.J.M. Medical College, Davangere, Karnataka
Source of Support: None, Conflict of Interest: None
Objectives: Hypotension is a common complication of spinal anesthesia and is frequent in patients with hypertension. Antihypertensive agents decrease this effect by controlling blood pressure. There are conflicting reports on the continuation of antihypertensive drugs on the day of surgery in patients undergoing spinal anesthesia. Sudden hypotension could have detrimental effect on the organ systems. This study was undertaken to compare the variation in blood pressure in hypertensive patients on β-blockers and calcium channel blockers undergoing spinal anesthesia.
Materials and Methods: Ninety patients were enrolled for the study, 30 each in the control, β-blocker and the calcium channel blocker groups.
Results: The incidence of hypotension was not different among the three groups. However, the number of times mephentermine used to treat hypotension was significant in the patients receiving calcium channel blockers while incidence of bradycardia in patients treated with β-blockers was significant (P<0.001).
Conclusion: The incidence of hypotension following spinal anesthesia is not different in patients receiving β-blockers and calcium channel blockers among the three groups.
Keywords: β-blockers, calcium channel blockers, hypotension, spinal anesthesia
|How to cite this article:|
Kaimar P, Sanji N, Upadya M, Mohammed K R. A comparison of hypotension and bradycardia following spinal anesthesia in patients on calcium channel blockers and β-blockers. Indian J Pharmacol 2012;44:193-6
|How to cite this URL:|
Kaimar P, Sanji N, Upadya M, Mohammed K R. A comparison of hypotension and bradycardia following spinal anesthesia in patients on calcium channel blockers and β-blockers. Indian J Pharmacol [serial online] 2012 [cited 2021 Aug 3];44:193-6. Available from: https://www.ijp-online.com/text.asp?2012/44/2/193/93847
| » Introduction|| |
Spinal anesthesia has been widely used and continues to be popular for surgeries involving the lower abdomen, perineum and lower limbs. Hypotension is the most common complication associated with spinal anesthesia. Incidence of hypotension is more common in patients with hypertension.  Although antihypertensive medications decrease this effect by controlling blood pressure, their varying effects on the cardiovascular system can alter the hemodynamics during the initial phase of spinal anesthesia. Better knowledge about these agents will help the anesthesiologists to anticipate the hemodynamic changes associated with its use.
There were conflicting reports on the continuation of angiotensin-converting enzyme inhibitors (ACEI) on the day of surgery in patients undergoing regional anesthesia. , Studies have been done to determine whether it is beneficial to continue calcium channel blockers and β-blockers in patients undergoing general anesthesia. , There is inadequate evidence on the effects of calcium channel blockers and β-blockers on blood pressure in hypertensive patients undergoing spinal anesthesia. Since hypertensive patients can have end organ damage, sudden hypotension could have detrimental effect.
Cardiovascular Effects of Spinal Anesthesia
The cardiovascular effects of neuraxial blocks are similar in some ways to the combined use of intravenous α -1 and β-adrenergic blockers i.e., decreased heart rate and arterial blood pressure.  The sympathectomy that accompanies the spinal anesthesia depends on the level of the block, extending for two to six dermatomes above the sensory level with spinal anesthesia and at the same level with epidural anesthesia. This causes venous and arterial vasodilatation, but because of large amount of blood in the venous system (approximately 75% of total blood volume) the venodilatation effect predominates whereas the vascular smooth muscle on the arterial side of the circulation retains a considerable degree of autonomous tone. If normal cardiac output is maintained, total peripheral resistance should decrease by 15-18% in normovolemic healthy patients even with near total sympathectomy. In elderly patients with cardiac disease, systemic vascular resistance may decrease almost 65%, whereas cardiac output decreases only 10%. Heart rate during high neuraxial block typically decreases as a result of blockade of the cardio accelerator fibres arising from T1 to T4. The heart rate may also decrease as a result of a fall in right atrial filling.
As arterial blood pressure decreases to a level for which treatment is believed necessary, ephedrine, a mixed adrenergic agonist, provides more appropriate therapy for the noncardiac circulatory sequelae of neuraxial block than a pure α-adrenergic agonist unless the patient has a specific and defined blood pressure requirement.
It has long been taught that the decrease in blood pressure after neuraxial block can be minimized by administration of crystalloids intravenously before the block; however, this logic needs rethinking. When all data are considered, it appears that 250-2000 ml preblock hydration regimens appear to temporarily increase preload and cardiac output without consistently increasing arterial pressure or preventing hypotension.
The study was undertaken to observe the variation in blood pressure and heart rate in controls and in patients taking antihypertensive medications -β-blockers and calcium channel blockers undergoing surgery on spinal anesthesia.
| » Materials and Methods|| |
The study was conducted in the Department of Anaesthesia of an urban, tertiary care teaching hospital during Dec 2007-May 2009. After obtaining Institutional Ethics Committee approval and written informed consent from the patients, 30 American society of Anaesthesiologists (ASA) category I - II patients were enrolled into three groups, as per their antihypertensive treatment with calcium channel blockers, β-blockers and the control group.
- Patients diagnosed to have essential hypertension receiving anti-hypertensive medications (calcium channel blockers or β-blockers).
- Patients scheduled for elective surgeries of lower abdomen, lower limbs and perineum under spinal anesthesia.
- Patients with other coexisting diseases like diabetes, coronary artery disease, cardiac diseases, severe hypovolemia, sepsis.
- Pregnant women.
- Patients less than 18 years of age.
At the preanesthetic clinic, patients were assessed, explained about the procedure, anesthesia and consent was obtained. Detailed history regarding the antihypertensive medications, duration of treatment and other coexistent diseases, and other medications, if any, was also obtained.
On arrival in the operating room, 18-G IVcannula was inserted in the nondominant hand. All patients were preloaded with 10 ml/kg of Hartmann's solution. Standard monitoring included continuous ECG, pulse rate, SPO 2 and automated noninvasive blood pressure (systolic blood pressure, diastolic blood pressure and mean arterial pressure) was carried out. Baseline values were taken as the reading during rest period after infusion of fluids.
The patients were allotted into three groups of 30 each as per their antihypertensive treatment. The patients received calcium channel blockers was group I, β-blockers was group II and the control group comprised ASA I undergoing any lower limb, urological or perineal surgeries.
Lumbar puncture was performed in the left lateral position with all aseptic precautions using 25-GQuincke - Babcock spinal needle in the L3-L4 space. When free flow of CSF was established, 3 ml of 0.5% hyperbaric bupivacaine was administered over 10-second period. The level of sensory blockade was determined with pinprick at 5 minutes and 15 minutes after the blockade. Noninvasive blood pressure and heart rate were recorded every 2 minutes for the first 10 minutes and then every 5 minutes till the end of the procedure.
Hypotension was defined as a decrease of mean arterial blood pressure of more than 30% from baseline within a 20-min interval, and relevance was defined as a therapeutic intervention with fluids or pressors within 20 min.  Incidence of hypotension was denoted as, 0=No hypotension or 1=Incidence of hypotension in first 20 minutes. Hypotensive patients were treated with rescue IV boluses of mephentermine 6 mg/dose and IV fluids 5 ml/kg until both SAP and MAP increased above the threshold level. The number of times mephentermine used was noted as 0=No Vasopressor used, 1=one dose, 2=two doses and so on. The time to the first rescue dose and the total dose of mephentermine required was recorded.
Bradycardia was defined as heart rate less than 50 beats per minute. Patients not responding to treatment with IV fluids were treated with injection atropine 0.6 mg IV. Maintenance infusion of ringer lactate was continued throughout the surgery. Side effects like nausea and vomiting was treated accordingly. Patient characteristics and hemodynamic data were compared by ANOVA test. The sensory level of block, administration of I.V. fluids and vasopressors in the three groups was analyzed by χ2 test. P<0.05 was considered statistically significant.
| » Results|| |
The demographic details of patients included in the all three groups were comparable [Table 1]. There was no difference in the level of sensory block and adequate analgesia was achieved.
The commonly used drug in calcium channel blocker group was amlodipine 5 mg (28), followed by nifedipine 10 mg (2). In the β-blocker group, 23 patients received atenolol 50 mg, five 25 mg and two metoprolol 25 mg. The mean duration of treatment was 579 days in the calcium channel blocker group and 560 days in the β-blocker group.
The pattern of fall in systolic, diastolic and mean arterial pressure was comparable in between the three groups. Moreover, the incidence of hypotension was not significant when compared among the three groups. Fifteen patients in the control group had a decrease in blood pressure more than 20%. In the calcium channel blocker group, 20 patients had hypotension and 16 in the β-blocker group. When compared with control group, the P value was 0.387 (not significant).
The frequency of administration of mephentermine was significant (P <0.05) in calcium channel blocker group compared to the control [Table 2]. There was also significant bradycardia in β-blocker treated group (P <0.001) compared to calcium channel blockers and control group [Table 3].
|Table 2: Comparison of frequency of administration of mephentermine following spinal anesthesia in patients receiving antihypertensive treatment|
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|Table 3: Comparison of adverse effects and treatment received following spinal anesthesia in patients eceiving antihypertensive treatment (n=30 each)|
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| » Discussion|| |
Fall in blood pressure is an invariable accompaniment of spinal anesthesia. However, clear distinction between physiological effects of an anesthetic technique and complications that imply some harm to the patient is essential.  Rooke et al., found out that exaggerated decrease in blood pressure occurs in elderly patients and those with cardiovascular disease mainly due to a decrease in systemic vascular resistance by 25% and cardiac by 10%.  Dinesh et al., found out that incidence of early hypotension is not associated with age, gender, body mass index >30 kg/m 2 , history of hypertension, diabetes mellitus, anemia, baseline heart rate, systolic and diastolic blood pressure, pulse pressure, rate pressure product, vascular overload index, sensory level of blockade higher than or equal to T6.  But a fall in blood pressure more than 25% may be hazardous in patients with compromised arterial supply to coronary and cerebral circulation.
The present study observed that there was no significant difference in the fall of systolic and/or diastolic blood pressure following spinal anesthesia in patients treated with calcium channel blockers and β-blockers. But the number of times mephentermine used was significant in the patients treated with calcium channel blockers.
Sear et al., reported that the pressor responses to laryngoscopy and intubation are unaffected by concurrent medication in mild-moderate hypertensive patients and changes of a similar magnitude are observed also in untreated hypertensive patients.  Butthere were reports of exaggerated hypotension in patients on ACEIs and continued on day of surgery. Coriat et al., reported that in hypertensive patients chronically treated with ACEIs, maintenance of therapy until the day of surgery may increase the probability of hypotension at induction.  The effects on these drugs on spinal anesthesia were however inadequately studied.
Our study shows that some exaggerated hypotension does occur in patients on calcium channel blockers. This could be partly explained by the vasodilator property of the drug which could have had an added effect after spinal anesthesia induced hypotension. One interesting finding in the calcium channel blocker group was that patients who required treatment with mephentermine more than twice had been on therapy less than 20 days. Those who were on chronic treatment (>1 year) required either no vasopressors or one dose of mephentermine during the first 20 minutes. Whether this difference is related to the effect of chronic treatment on the vasomotor tone has to be studied further.
Bradycardia following spinal anesthesia was entirely limited to the β-blocker group. Cardiac arrest and bradycardia following β-blocker therapy has been reported.  But these occur infrequently and do not warrant discontinuation of the drug before surgery. On the other hand, it has been proved to be beneficial to continue β-blockers perioperatively. 
Although the effect of antihypertensive medications on spinal anesthesia based on the duration of treatment could not be studied, we think our study was able to figure out the difference in the hemodynamic pattern among the two drug classes. Better anticipation of the complications following spinal anesthesia can help the anesthesiologist for early treatment of hypotension in frail patients who cannot afford to tolerate a decrease in blood pressure.
| » References|| |
|1.||Hartmann B, Junger A, Klasen J, Benson M, Jost A, Banzhaf A, et al. The incidence and risk factors for hypotension after spinal anaesthesia induction: An analysis with automated data collection. Anesth Analg 2002;94:1521-9. |
|2.||Cozanitis DA. The importance of interrupting angiotensin converting enzyme inhibitor treatment before spinal anaesthesia - A controlled case report. Anaesthesiol Reanim 2004;29:16-8. |
|3.||Höhne C, Meier L, Boemke W, Kaczmarczyk G. ACE inhibition does not exaggerate the blood pressure decrease in the early phase phase of spinal anaesthesia. Acta Anaesthesiol Scand 2003;47:891-6. |
|4.||Sear JW, Jewkes C, Tellez JC, Foex P. Does the choice of antihypertensive therapy influence haemodynamic responses to induction, laryngoscopy and intubation. Br J Anaesth 1994;73:303-8. |
|5.||Samad K, Khan F, Azam I. Haemodynamic effects of anaesthetic induction in patients treated with beta and calcium channel blockers. Middle East J Anaesthesiol 2008;19:1111-28. |
|6.||Brown DL. Spinal, Epidural and Caudal Anaesthesia. Miller's Anaesthesia. Philadelphia: Elsevier; 2010. p. 1612-37. |
|7.||Mackey DC. Physiologic effects of regional blocks. In: Brown DL, editor. Regional Anaesthesia and Analgesia. Philadelphia: W B Saunders; 1996. p. 397. |
|8.||Rooke GA, Freund PR, Jacobson AF. Haemodynamic response and change in organ blood volume during spinal anaesthesia in elderly men with cardiac disease. Anaesth Analg 1997;85:99. |
|9.||Singla D, Kathuria S, Singh A, Kaul TK, Gupta S, Mamta. Risk factors for development of early hypotension during spinal anaesthesia. J Anaesthesiol Clin Pharmacol 2006;22:387-93. |
|10.||Coriat P, Richer C, Douraki T, Gomez C, Hendricks K, Giudicelli JF, et al. Influence of chronic angiotensin - converting enzyme inhibition on anaesthetic induction. Anaesthsiology 1994;81:299-307. |
|11.||Pollard JB. Cardiac arrest during spinal anaesthesia: Common mechanisms and strategies for prevention. Anaesth Analg 2001;92:252-6. |
|12.||Ponten J, Biber B, Bjuro T, Henriksson BA, Hjalmarson A, Lundberg D. Beta-receptor blockade and spinal anaesthesia. Withdrawal versus continuation of long term therapy. Acta Anaesthesiol Scand Suppl 1982;76:62-9. |
[Table 1], [Table 2], [Table 3]
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