Background Maxillary nerve blocks are often used as part of a multimodal postoperative pain management regimen for children undergoing cleft palate surgery. It has not been demonstrated yet that ultrasound guidance provides superior local anesthetic distribution and better success rates compared with the landmark-based block technique. The aim of the study was to compare the effect of ultrasound guidance for suprazygomatic maxillary nerve blocks on local anesthetic spread to the pterygopalatine fossa. Methods 20 pediatric patients scheduled for cleft palate repair received bilateral suprazygomatic maxillary blocks. Landmark technique was used on one side and ultrasound guidance on the contralateral side according to randomization. After the block procedure, MRI was used to determine the spread of the local anesthetic. Results Local anesthetic spread to the pterygopalatine fossa with contact to the maxillary nerve (defined as successful block) was observed in 13 (65%) of the landmark-based blocks and in 14 (70%) of the ultrasound-guided blocks (p=0.56). No adverse events or complications were observed during or after the block procedures. Conclusion Appropriate pain management for cleft palate repair can be achieved without the availability of imaging guidance. Future studies should focus on improving the success rate of maxillary nerve blocks, both with and without the aid of sonography. Trial registration number NCT05778903 .
BACKGROUND:Ephedrine, phenylephrine, and norepinephrine are commonly used to manage hypotension during the induction of anaesthesia. The objective of this study was to evaluate whether prophylactic administration of assumed equipotent doses of these vasopressors could maintain systolic arterial blood pressure (SAP) and heart rate (HR) within 80% of baseline for the first 5 min following induction of anaesthesia. METHODS:This randomised, double-blind, dose-controlled study was conducted at the Day Surgery Unit of Haugesund Hospital, Norway. One hundred and twenty-eight healthy women scheduled for gynaecological surgery were randomly allocated in a 1:1:1:1 ratio to receive prophylactic administration of ephedrine (0.1 mg/kg), phenylephrine (1 μg/kg), norepinephrine (0.1 mg/kg), or placebo (sodium chloride 9 mg/mL) at a volume of 0.1 mL/kg. Anaesthesia was induced using target-controlled infusion (TCI) of propofol and remifentanil. The initial 2.5 min constituted a sedation phase, after which the targets of propofol and remifentanil were increased, and the assigned vasopressor was administered. Beat-to-beat haemodynamic monitoring was performed using the LiDCOplus system. The primary outcome variables were the maximal decrease in SAP and HR within 5 min following bolus administration. Secondary outcome measures included changes in stroke volume (SV), cardiac output (CO), and systemic vascular resistance (SVR). RESULTS:The absolute changes in SAP (mean ± standard deviation) following vasopressor administration were -27 ± 8.9 (ephedrine), -40 ± 11 (phenylephrine), -41 ± 13 (norepinephrine), and -42 ± 10 (placebo) mmHg. The differences (95% confidence interval [CI]) in the maximal SAP change between placebo and the vasopressors were as follows: ephedrine, -15 (-22, -9.9) mmHg; phenylephrine, -2.3 (-8.8, 4.2) mmHg; and norepinephrine, -1.7 (-8.3, 4.9) mmHg. Relative reductions in SAP from baseline to minimum values were -20% for ephedrine, -30% for phenylephrine, -30% for norepinephrine, and -32% for placebo. The absolute changes (median, interquartile range) in HR with ephedrine, phenylephrine, norepinephrine, and placebo were -10 (-6.2 to -18), -19 (-17 to -26), -23 (-20 to -33), and -15 (-9.5 to -21) bpm, respectively. Relative changes from baseline to minimum values in HR were -17% for ephedrine, -30% for phenylephrine, -37% for norepinephrine, and -22% for placebo. The differences in SV change between groups were small. CO was best preserved with ephedrine (-22% ± 11%), while phenylephrine and norepinephrine were associated with greater reductions (-38% ± 7.8% and -42% ± 9.8%, respectively). SVR increased most markedly in the norepinephrine group, followed by phenylephrine, with the smallest increase observed in the ephedrine group. CONCLUSION:Prophylactic administration of ephedrine effectively maintained SAP, HR, and CO within the first 5 min following bolus injection at induction with propofol and remifentanil. In contrast, bolus administration of norepinephrine and phenylephrine demonstrated a short duration of action, with SAP comparable to placebo at 5 min. Based on these findings, prophylactic administration of a bolus ephedrine is recommended, whereas prophylactic phenylephrine or norepinephrine injections may not be clinically preferable for bolus use in this context. TRIAL REGISTRATION:ClinicalTrials.gov identifier NCT03864094, March 6, 2019 This trial assessed circulatory responses to three different commonly used vasoactive support (vasopressor) drugs given as a single bolus together anesthetic induction propofol and remifentanil, and this in a cardiovascularly healthy adult surgical cohort. Results demonstrated that pharmacodynamic patterns with the three different test drugs, along with a no-prophylactic vasopressor comparitor. Findings showed a favorable profile for ephedrine compared to phenylephrine or noradrenaline if choosing to give a vasopressor in this way.
INTRODUCTION:Women with cardiovascular disease may be at increased risk of hypertensive disorders of pregnancy (HDP). We aimed to: (1) Investigate the occurrence of HDP in a cohort of pregnant women with cardiovascular disease and compare it with the occurrence in the general population. (2) Assess the association between maternal cardiovascular risk and risk of HDP. MATERIAL AND METHODS:We reviewed clinical data on a cohort of 901 pregnancies among 708 women with cardiovascular disease who were followed at the National Unit for Pregnancy and Heart Disease and gave birth at Oslo University Hospital between 2003 and 2018. The exposure under study was maternal cardiovascular risk, classified as low, moderate, or high based on a modified classification by the World Health Organization. The main outcome of interest was HDP, which included pre-eclampsia and gestational hypertension. The proportion of HDP cases in the general population in the same period was extracted from the Medical Birth Registry of Norway. We used logistic regression to estimate crude and adjusted odds ratios (OR) of HDP, with associated 95% confidence intervals (CIs), for women with moderate- and high cardiovascular risk compared to women with low risk. RESULTS:The occurrence of HDP in the study cohort was 12.1% (95% CI: 10.0%-14.4%) and varied between 8.7% (95% CI: 6.5%-11.3%) in the low-risk group, 15.7% (95% CI: 11.1%-21.4%) in the moderate-risk group, and 22.2% (95% CI: 15.1%-30.8%) in the high-risk group. By contrast, the nationwide occurrence of HDP was 5.1% (95% CI: 5.1%-5.2%). In the study cohort, the proportions of pregnancies with gestational hypertension and pre-eclampsia were similar (6.3% and 5.8%, respectively). Compared to pregnancies with low cardiovascular risk, the adjusted OR of HDP was 2.04 (95% CI: 1.21-3.44) in the moderate-risk group and 2.99 (95% CI: 1.73-5.18) in the high-risk group. CONCLUSIONS:The occurrence of hypertensive disease of pregnancy in the study cohort was more than doubled compared to the general population in Norway. The risk of HDP increased with maternal cardiovascular risk group. We recommend taking into account maternal cardiovascular risk group when assessing risk and prophylaxis of HDP.
BACKGROUND:Remifentanil may have a dose-dependent haemodynamic effect during the induction of general anaesthesia combined with propofol. Our objective was to investigate whether systolic arterial blood pressure (SAP) was reduced to a greater extent when the remifentanil dose was increased. METHODS:This randomised, double-blind, dose-controlled study was conducted at the Day Surgery Unit of Haugesund Hospital, Norway. Ninety-nine healthy women scheduled for gynaecological surgery were randomly allocated in a 1:1:1 ratio to receive remifentanil induction with a low, medium or high dose corresponding to maximum effect-site concentrations (Ce) of 2, 4 and 8 ng/mL. The induction dose of propofol was 1.8 mg/kg, with a Ce of 2.9 μg/mL. Anaesthesia was induced using target-controlled infusion. After 150 s of sedation, a bolus of remifentanil and propofol was administered. Baseline was defined as 55-5 s before the bolus dose, and the total observation time was 450 s. We used beat-to-beat haemodynamic monitoring with LiDCOplus. The primary outcome variable was the maximum decrease in SAP within 5 min after bolus administration of remifentanil and propofol. Absolute and relative changes from baseline to minimal values and the area under the curve (AUC) were used as effect measures. Comparisons of groups were performed using analysis of variance (ANOVA). RESULTS:Median remifentanil doses were 0.75, 1.5 and 3.0 μg/kg in the low-, medium- and high-dose groups, respectively. The absolute changes (mean ± standard deviation) in SAP in the low-, medium- and high-dose groups of remifentanil were -39 ± 9.6 versus -43 ± 9.1, and -41 ± 10 mmHg, respectively. No difference (95% confidence interval) in the absolute change in SAP was observed between the groups (ANOVA, p = .29); medium versus low dose 3.7 (-2.0, 9.4) mmHg, and high versus medium dose -2.2 (-8.0; 3.5) mmHg. The relative changes from baseline to minimum SAP values were -30% versus -32% versus -32% (p = .52). The between-group differences in the AUC were not statistically significant. Relative changes in heart rate (-20% vs. -21% vs. -21%), stroke volume (-19% vs. -16% vs. -16%), cardiac output (-32% vs. -32% vs. -32%), systemic vascular resistance (-24% vs. -27% vs. -28%), and AUC were not statistically significant. CONCLUSION:This trial demonstrated major haemodynamic changes during the induction of anaesthesia with remifentanil and propofol. However, we did not observe any statistically significant differences between low, medium or high doses of remifentanil when using continuous invasive high-accuracy beat-to-beat monitoring.
Aims To objectively study cardiorespiratory fitness (CRF) and physical activity (PA) and to evaluate limiting factors of exercise intolerance associated with poor CRF after severe pre-eclampsia. Methods In this single-centre, cross-sectional study, CRF was measured as peak oxygen uptake (VO2peak) during a cardiopulmonary exercise test (CPET) on a treadmill in women 7 years after severe pre-eclampsia. Ninety-six patients and 65 controls were eligible to participate. Cardiac output (CO) was measured by impedance cardiography. PA was measured using accelerometers. Results In 62 patients and 35 controls (mean age 40 & PLUSMN; 3 years), the VO2peak (in mL & BULL;kg-1 & BULL;min-1) values were 31.4 & PLUSMN; 7.2 and 39.1 & PLUSMN; 5.4, respectively (p<0.01). In the patients, the COpeak was (9.6 L & BULL;min-1), 16% lower compared to controls (p<0.01). Twelve patients (19%) had a cardiac limitation to CPET. Twenty-three (37%) patients and one (3%) control were classed as unfit, with no cardiopulmonary limitations. The patients demonstrated 25% lower PA level (in counts per minute; p<0.01) and 14% more time being sedentary (p<0.01), compared with the controls. Twenty-one patients (34%) compared with four (17%) controls did not meet the World Health Organization's recommendations for PA (p=0.02). Body mass index and PA level accounted for 65% of the variability in VO2peak. Conclusion Significantly lower CRF and PA levels were found in patients on long-term follow-up after severe pre-eclampsia. CPET identified cardiovascular limitations in one third of patients. One third appeared unfit, with adiposity and lower PA levels. These findings highlight the need for clinical follow-up and exercise interventions after severe pre-eclampsia.
Aims The aim was to study pregnancy outcomes in women with coarctation of the aorta (CoA) and associations to hypertensive disorders of pregnancy. Maternal morbidity and mortality are higher in women with heart disease and pre-eclampsia. Chronic hypertension, frequently encountered in CoA, is a risk factor for pre-eclampsia. Methods and results Clinical data from the National Unit for Pregnancy and Heart Disease database was reviewed for pregnant women with CoA from 2008 to 2021. The primary outcome was hypertensive pregnancy disorders. The secondary outcomes were other cardiovascular, obstetric, and foetal complications. Seventy-six patients were included, with a total of 87 pregnancies. Seventeen (20%) patients were treated for chronic hypertension before pregnancy. Fifteen (20%) patients developed pre-eclampsia, and 5 (7%) had pregnancy-induced hypertension. Major adverse cardiac events developed in four (5%) patients, with no maternal or foetal mortality. Maternal age at first pregnancy [odds ratio (OR) 1.37], body mass index before first pregnancy (OR 1.77), and using acetylsalicylic acid from the first trimester (OR 0.22) were statistically significantly associated with pre-eclampsia. At follow-up (median) 8 years after pregnancy, 29 (38%) patients had anti-hypertensive treatment, an increase of 16% compared to pre-pregnancy. Five (7%) patients had progression of aorta ascendens dilatation to >40 mm, seven (9%) had an upper to lower systolic blood pressure gradient >20 mmHg, and six (8%) had received CoA re-intervention. Conclusion Pre-eclampsia occurred in 20% of women with CoA in their first pregnancy. All pre-eclamptic patients received adequate anti-hypertensive treatment. All CoA patients were provided multi-disciplinary management, including cardiologic follow-up, to optimize maternal-foetal outcomes.
BACKGROUND:Hypotension is common after anesthesia induction with propofol and is associated with increased morbidity. It is important to examine the effects of the proposed interventions to limit preventable hypotension, as suggested by the reduction in the dose of propofol. Our objective was to investigate whether a high dose of propofol is inferior to a low dose with respect to changes in systolic arterial blood pressure (SAP). METHODS:This randomized, double-blind, dose-controlled, non-inferiority study included 68 healthy women scheduled for gynecological surgery at the Day Surgery Unit, Haugesund Hospital, Norway. The patients were randomly allocated 1:1 to a low or high dose (1.4 mg/kg total body weight (TBW) versus 2.7 mg/kg TBW of propofol corresponding to maximal effect site concentrations (Ce) of 2.0 μg/mL versus 4.0 μg/mL. The dose of remifentanil was 1.9-2.0 μg/kg TBW, with maximal Ce of 5.0 ng/mL. The patients were observed for 450 s from the start of the infusions. The first 150 s was the sedation period, after which a bolus of propofol and remifentanil was administered. Baseline was defined as 55-5 s before the bolus doses. LiDCOplus was used for invasive beat-to-beat hemodynamic monitoring of changes in SAP, heart rate (HR), cardiac output (CO), stroke volume (SV), and systemic vascular resistance (SVR). A difference of 10 mmHg in the change in SAP was considered to be clinically important. RESULTS:The SAP change difference for low versus high dose was -2.9 mmHg (95% CI -9.0-3.1). The relative changes for low versus high dose were SAP -31% versus -36%, (p < .01); HR -24% versus -20%, (p = .09); SVR -20% versus -31%, (p < .001); SV -16% versus -20%, (p = .04); and CO -35% versus -32%, (p = .33). CONCLUSION:A high dose of propofol was not inferior to a low dose, and a reduction in the dose of propofol did not result in clinically important attenuation of major hemodynamic changes during induction in healthy women. TRIAL REGISTRATION:ClinicalTrials.gov identifier NCT03861364, January 3, 2019.
Objective. To study left ventricular (LV) function and blood pressure (BP) at a long-term follow-up in women after severe pre-eclampsia. Design. In this single-centre, cross-sectional study, 96 patients were eligible for inclusion. LV function was examined by transthoracic echocardiography including tissue Doppler echocardiography and speckle tracking. BP was measured at rest using repeated non-invasive techniques. Results. We compared 36 patients with early-onset and 33 patients with late-onset pre-eclampsia with 28 healthy controls. Mean age (40 +/- 3 years) and median time since delivery (7 +/- 2 years) were similar across the study groups. The patients had 18% higher systolic BP (139 +/- 15 mmHg) and 24% higher diastolic BP (87 +/- 19 mmHg) than controls (p < .01). Hypertension was present in 23 patients (33%), where the estimated LV mass was 16% higher (p = .05) than in controls. The LV ejection fraction was 19% lower in the early-onset group (51 +/- 4%; p = .01) and 14% lower in the late-onset group (54 +/- 6; p = .04) compared with controls. LV global longitudinal strain was 18% lower in the patient group (-17.7 +/- 2.1%) compared with controls (p = .01). Indicative of a more restrictive filling pattern, the diastolic indices showed a lower e ' mean (p < .01) and subsequently higher E/e ' ratio (p < .01). There were no significant differences in BP, systolic or diastolic function indices between the patient groups. Conclusion. We found sustained hypertension, higher LV mass and reduced LV systolic and diastolic function 7 y after severe pre-eclampsia. Our findings emphasize the importance of early risk stratification and clinical counselling, and follow-up for such cases.
Introduction and aims: Women with heart disease may be at increased risk of hypertensive pregnancy disorders (HPD) due to cardiovascular pathophysiology. We aimed to investigate the risk of HPD and associations to severity of heart disease in a cohort of women with heart disease treated by a multidisciplinary team at a tertiary obstetric center. We compared this occurrence to the occurrence in the Medical Birth Registry of Norway during the same period. Methods: We performed a retrospective cohort study of 902 pregnancies among women with a cardiac ICD-10 diagnosis giving birth in Oslo University Hospital between 2003 and 2018. Primary outcome was HPD as determined by ICD-10. Cases were validated through medical record review. Severity of heart disease was classified into three sub-groups based on a modified World Health Organization risk classification. We estimated risk of HPD in logistic regression models, adjusting for maternal age, parity, and BMI. Results: The proportion of HPD in women with heart disease was 12.1% (95% Confidence Interval (CI) 10.0–14.4) and varied from 8.7% in the low cardiac risk group, 15.7% in the moderate risk group, to 22.2% in the high risk group. In comparison, the nationwide incidence of HPD was 5.1% (CI 5.1–5.2). Proportions of gestational hypertension only and preeclampsia were similar in our group of women with heart disease (6.3% vs 5.8%). Compared to the low cardiac risk group, women in the moderate risk group had a 2-fold increased risk of HPD (odds ratio 2.08, CI 1.28–3.36, p = 0.003), whereas the high risk group had a 3-fold increased risk (odds ratio 3.12, CI 1.84–5.30, p < 0.001). Conclusions: The risk of HPD is doubled in women with heart disease compared to the general population in Norway, and the risk is correlated to severity of heart disease. Close follow-up of this group is mandatory.
Beta-blockers are prescribed for many pregnant women with heart disease, but whether there is a dose-dependent effect on fetal growth remains to be examined. We aimed to investigate if antenatal beta-blocker use and dose were associated with delivering a small-for-gestational-age infant among women with heart disease. Our cohort included women with heart disease who delivered at Oslo University Hospital between 2006 and 2015. Maternal heart disease was classified into modified WHO risk scores. Women with beta-blocker treatment were dichotomized into whether they had been treated with a low or high dose based on clinical factors. We compared the risk of delivering a small-for-gestational-age infant in women exposed to high doses, low doses, or with no exposure to antenatal beta-blockers while adjusting for severity of maternal heart disease in logistic regression models. Of a total of 540 pregnancies among women with heart disease, 163 (30.2%) were exposed to beta-blocker treatment. The majority were treated with metoprolol (86.5%). Almost twice as many babies in the beta-blocker group were small-for-gestational-age, compared with the non-exposed group (19.8 vs 9.5%, P < 0.001). Women using a high-dose beta-blocker had a five-fold increased risk of delivering a small-for-gestational-age infant compared with non-exposure (adjusted odds ratio [aOR] 4.89, 95% confidence interval [CI] 2.22–10.78, P < 0.001). Women using a low dose of beta-blocker had a two-fold increased risk of delivering a small-for-gestational-age infant; however, the confidence interval included the null (aOR 1.75, 95% CI 0.83–3.72, P = 0.143). Results when restricting the analyses to metoprolol showed the same pattern, but with attenuation of risks. We found a five-fold increased risk of delivering a small-for-gestational-age infant in women with heart disease treated with a high dose of beta-blocker, and a two-fold increased risk among those treated with a low dose, showing an apparent dose–response relation. Close monitoring of fetal growth is warranted among women with heart disease treated with beta-blockers. As drug therapy in pregnancy concerns both mother and fetus, an optimum balance for both should be the goal.
Beta‐blockers are prescribed for many pregnant women with heart disease, but whether there is a dose‐dependent effect on fetal growth remains to be examined. We aimed to investigate if antenatal beta‐blocker use and dose were associated with delivering a small‐for‐gestational‐age infant among women with heart disease.
BACKGROUND: Landmark and ultrasound-guided transversus abdominis plane blocks have demonstrated an opioid-sparing effect postoperatively after cesarean delivery. The more posterior quadratus lumborum (QL) might provide superior local anesthetic spread to the thoracolumbar fascia and paravertebral space. The aim of our study was to evaluate the efficacy of the QL block after cesarean delivery. METHODS: A randomized, double-blind, controlled trial was performed. Forty parturients undergoing cesarean delivery received bilateral ultrasound-guided QL blocks with either 2 mg/mL ropivacaine or saline postoperatively. All patients received spinal anesthesia with bupivacaine and sufentanil and a postoperative analgesic regimen of paracetamol, ibuprofen, and ketobemidone administered by a patient-controlled analgesic pump. The ketobemidone consumption and time of each dose administered were recorded. The primary outcome was ketobemidone consumption during the first 24 hours postoperatively. Secondary and exploratory analyses compared repeated measures of pain scores, nausea, and fatigue, and total differences in time until patients were able to stand and able to walk 5 m, and the interaction between the effective analgesic score and time. RESULTS: All 40 patients completed the trial, 20 in each group. The cumulative ketobemidone consumption in 24 hours was reduced in the active group compared with the control group (P = .04; ratio of means = 0.60; 95% confidence interval, 0.37–0.97). The effective analgesic scores were significantly better in the treatment group compared with the placebo group both at rest (P < .01) and during coughing (P < .01). CONCLUSIONS: QL block with ropivacaine reduces the postoperative ketobemidone consumption and pain intensity as a part of a multimodal analgesic regimen that excludes neuraxial morphine.
(Acta Anaesthesiol Scand. 2018. Doi:10.1111/aas.13259) For gynecologic procedures involving the cervix or uterus, long-acting local anesthetics like bupivacaine, administered via paracervical block, can provide a significant reduction in postoperative pain scores. Adrenaline can be added to local anesthetics to reduce toxicity potential. However, there are few data available regarding the frequency and magnitude of hemodynamic changes in patients when adrenaline is added to local anesthetics. In this randomized controlled trial, the authors examined hemodynamic stability after paracervical block in healthy patients given bupivacaine with and without adrenaline.
BackgroundParacervical block is widely used in gynaecological interventions on cervix and uterus. Many surgeons add adrenaline 100 μg or pitressin 3‐5 IU in a total volume of 10‐20 mL to reduce total blood loss. We wanted to examine haemodynamic stability in healthy patients given bupivacaine with and without adrenaline.MethodsIn this randomised, double‐blinded, controlled study, 30 healthy women scheduled for cervical conisation got a paracervical block using bupivacaine 50 mg with adrenaline 100 μg (BA‐group, n = 14) or without adrenaline (B‐group, n = 16) after induction of general anaesthesia. LiDCOplus was used for minimally invasive haemodynamic monitoring. Changes in cardiac output (CO) and systolic blood pressure (SBP) were the primary outcome. Changes in heart rate (HR), stroke volume (SV), and systemic vascular resistance (SVR) were secondary outcome variables. Area under the curve (AUC) ratios and change from baseline to maximal values were used as effect measures comparing the two groups.ResultsThe AUC‐ratio for CO and SBP was 2.50 (P < 0.001) and 1.70 (P = 0.03), respectively. For HR, SV, and SVR the AUC‐ratio was 1.59 (P < 0.01), 1.52 (P < 0.001), and 0.90 (P = 0.14), respectively. CO increased 68% (standard deviation (SD) 42%, P < 0.001), HR increased 41% (SD 26%, P < 0.001), and SV increased 26% (SD 17%, P < 0.001) from baseline to maximal values after 70‐90 seconds in the BA‐group.ConclusionParacervical block with bupivacaine 50 mg and adrenaline 100 μg may give haemodynamic instability in healthy females and is not recommended if haemodynamic side effects are to be avoided.
BACKGROUND:There are few studies on maternal haemodynamic changes during labour. None have used continuous cardiac output monitoring during all labour stages. In this observational study, we monitored haemodynamic variables continuously during the entire course of labour in healthy parturients.METHODS:Continuous haemodynamic monitoring with the LiDCOplus technique was performed in 20 healthy parturients during spontaneous labour, vaginal delivery and for 15minutes postpartum. Cardiac output, stroke volume, heart rate, systemic vascular resistance, and systolic arterial pressure were measured longitudinally at baseline (periods between/without contractions) and during contractions in early and late stage 1, stage 2, during delivery, and postpartum, and were analysed with marginal linear models.RESULTS:Twenty parturients were included. In early stage 1, baseline cardiac output was 6.3L/min (95% CI 5.7 to 6.9). Baseline values were similar across both labour stages and postpartum for all haemodynamic variables. During stage 2 contractions, cardiac output decreased by 32%, stroke volume decreased by 44%, heart rate increased by 52%, systemic vascular resistance increased by 88%, and systolic arterial pressure increased by 36% compared to baseline. During stage 1 contractions, haemodynamic changes were less profound and less uniform than during stage 2.CONCLUSION:Progression of labour had no major effect on haemodynamic baseline values. Haemodynamic stress during contractions was substantial in both labour stages, yet most pronounced during the second stage of labour. The absence of an increase in stroke volume and cardiac output postpartum questions the common belief in an immediate rise in cardiac output after delivery due to autotransfusion from the contracted uterus.
Norwegian Guidelines within our field include Guidelines in General Gynecology, in Gynecological Oncology, and in Obstetrics. The work with the last updated version of the Guidelines in Obstetrics started in 2012, when the Norwegian Society of Obstetrics and Gynecology (Norsk Gynekologisk Forening: NGF) decided to revise the previous NGF Guidelines published in 2008. The NGF Guideline in Obstetrics includes around 50 chapters. A responsible author was appointed by the NGF for each chapter, as well as coauthors.
BACKGROUND:Phenylephrine infusion is the current first-line choice for prevention of spinal hypotension during cesarean delivery. The optimal dosage regimen is still undetermined. A mechanical alternative, lower limb wrapping, has been examined in a few small studies showing moderate success. In this trial, we compared the effect of leg wrapping with low-dose phenylephrine infusion and with placebo treatment on systolic arterial blood pressure during spinal anesthesia for cesarean delivery. METHODS:In this randomized, double-blinded, placebo-controlled study, healthy women received either phenylephrine (n = 38; initial bolus of 0.25 &mgr;g kg−1 and infusion of 0.25 &mgr;g kg−1 min−1), leg wrapping (n = 38), or no treatment (control; n = 36) during spinal anesthesia for elective cesarean delivery. LiDCOplus was used for continuous minimally invasive hemodynamic monitoring. The extent of decrease in systolic arterial blood pressure (for 13 minutes after spinal induction) was the primary outcome. Cardiac output, systemic vascular resistance, stroke volume, heart rate, neonatal acid–base status, and Apgar score were secondary outcome variables. Mixed model analysis of continuous hemodynamic trends during the first 13 minutes after induction of spinal anesthesia was performed. RESULTS:In the phenylephrine group, the decrease in systolic arterial blood pressure was significantly less (difference in rate of change, 0.09 mm Hg 5 s−1; 95% confidence interval, 0.02–0.16; P = 0.013); systemic vascular resistance (P < 0.001) was significantly higher; stroke volume (P = 0.41) was similar; and heart rate (P = 0.002) and cardiac output (P < 0.001) were significantly lower compared with the leg wrapping group. Compared with control, the leg wrapping group had a significantly smaller decrease in systolic arterial blood pressure (0.39 mm Hg 5 s−1; 95% confidence interval, 0.32–0.46; P < 0.001), higher stroke volume (P < 0.001), and higher cardiac output (P = 0.001). CONCLUSIONS:An initial bolus of phenylephrine followed by a low-dose phenylephrine infusion was superior to leg wrapping and no intervention for the prevention of hypotension during spinal anesthesia for cesarean delivery. Phenylephrine prevented hypotension primarily by restoring systemic vascular resistance and did not cause hypertension or a clinically relevant reduction in cardiac output. Leg wrapping prevented hypotension compared with no intervention by limiting modest early spinal anesthesia-mediated venodilation.
PURPOSE OF REVIEW:Haemodynamic monitoring in obstetric patients has evolved during the last decade, with the development of minimally invasive and noninvasive continuous cardiac output (CO) monitors. This review focuses on recent articles that improve our understanding of physiology and haemodynamic changes during spinal anaesthesia in healthy pregnant women, and pathophysiology in women with preeclampsia and other cardiovascular disease.RECENT FINDINGS:Recent research findings in healthy women focus on the haemodynamic changes due to aortocaval compression, fluid administration, vasopressor therapy, and oxytocin during spinal anaesthesia for caesarean delivery. In preeclampsia, the haemodynamics of early versus late-onset disease and fluid management have been the subject of considerable investigation. Case reports suggest that invasive monitoring in combination with echocardiography is preferable for clinical management of high-risk obstetrics cases with unstable haemodynamics.SUMMARY:In healthy women, left lateral tilt remains an important clinical intervention during caesarean delivery, and phenylephrine is an essential early adjunct to fluid therapy. Noradrenaline may have a clinical benefit in selected patients. Carbetocin has similar haemodynamic effects to oxytocin. Haemodynamic changes associated with delivery per se may be minor compared with those due to oxytocin. Uncomplicated severe preeclampsia is usually associated with a normal to raised CO. Early-onset preeclampsia may be associated with more vasoconstriction and lower CO than late-onset disease. Passive leg raising may be useful to judge fluid responsiveness, and lung ultrasound may predict pulmonary oedema in preeclampsia. Further research is warranted to study the area of circulatory changes during delivery and the postpartum period, in healthy and preeclamptic women.