Drop In Mean Arterial Pressure Research Articles

Efficiency of Percutaneous Stent Angioplasty in Renal Artery Stenosis - 15 Years of Experience at a Single Center.

To determine the therapeutic efficiency of percutaneous revascularization in renal artery stenosis (RAS), as well as the role of comprehensive factors such as patient selection and degree of artery stenosis, on clinical outcome. 101 patients with hemodynamically relevant RAS underwent percutaneous angioplasty (PTA). 65.7 % were male (mean age: 64 years; range: 18-84). The clinical data was retrospectively analyzed. The serum creatinine (Cr), glomerular filtration rate (GFR), and blood pressure (BP) levels pre- and postprocedural, between 6 months and 1year, were retrospectively collected and statistically analyzed. Follow-up data was available in 34 (33.7 %) and 28patients (27.7 %) for Cr and MAP, respectively. A significant drop in mean arterial pressure (MAP) was observed on follow-up (mean -5.27 mmHg). Higher baseline Cr and MAP values showed a more pronounced drop in the follow-up (Cr: p0.002; difference to baseline -0.25 mg/dL, 95 %CI:-0.36, -0.07 and BP p < 0.001; diff. to baseline -0.72 mmHg; 95 %CI: -1.4, -0.40). There was no association between comorbidities, gender, and degree of stenosis with renal and BP outcome. No significant improvement in renal function was observed on follow-up (mean Cr drop: -0.015 mg/dL). The age group 51-60 years showed a significant improvement in BP (p 0.030; diff. to baseline -19.2 mmHg; 95 %CI: -34, -4.3). There was a slight reduction in antihypertensive medication following angioplasty (0.2 fewer). Minor complications were recorded in five procedures (4.9 %). Percutaneous renal artery revascularization in the presence of atherosclerotic RAS is a safe procedure associated with a significant drop in post-procedural BP. No significant improvement in renal function was observed. Further prospective studies focused on patient selection are necessary. · Percutaneous stent angioplasty in renal artery stenosis is associated with a significant improvement in post-procedural blood pressure control.. · There is no improvement in renal function after percutaneous stent angioplasty for renal artery stenosis (RAS).. · Percutaneous stent angioplasty is a safe procedure.. · Guerreiro H, Avanesov M, Dinnies S et al. Efficiency of Percutaneous Stent Angioplasty in Renal Artery Stenosis - 15Years of Experience at a Single Center. Fortschr Röntgenstr 2021; 193: 298 - 304.

Chronic elevation of renal venous pressure induces extensive renal venous collateral formation and modulates renal function and cardiovascular stability in rats.

Acutely increased renal venous pressure (RVP) impairs renal function, but the long-term impact is unknown. We investigated whether chronic RVP elevation impairs baseline renal function and prevents exacerbation of renal dysfunction and cardiovascular instability upon further RVP increase. RVP elevation (20-25 mmHg) or sham operation (sham) was performed in rats. After 1 wk (n = 17) or 3 wk (n = 22), blood pressure, RVP, renal blood flow (RBF), renal vascular conductance (RVC), and glomerular filtration rate (GFR) were measured at baseline and during superimposed RVP increase. Chronic RVP elevation induced extensive renal venous collateral formation. RVP fell to 6 ± 1 mmHg at 1 wk and 3 ± 1 mmHg at 3 wk. Baseline blood pressure and heart rate were unaltered compared with sham. RBF, RVC, and GFR were reduced at 1 wk but normalized by 3 wk. Upon further RVP increase, the drop in mean arterial pressure was attenuated at 3 wk compared with 1 wk (P < 0.05), whereas heart rate fell comparably across all groups; the mean arterial pressure-heart rate relationship was disrupted at 1 and 3 wk. RBF fell to a similar degree as sham at 1 wk (-2.3 ± 0.7 vs. -3.9 ± 1.2 mL/min, P = 0.066); however, at 3 wk, this was attenuated compared with sham (-1.5 ± 0.5 vs. -4.2 ± 0.7 mL/min, P < 0.05). The drop in RVC and GFR was attenuated at 1 and 3 wk (P < 0.05). Thus, chronic RVP elevation induced by partial renal vein ligation elicits extensive renal venous collateral formation, and although baseline renal function is impaired, chronic RVP elevation in this manner induces protective adaptations in kidneys of healthy rats, which attenuates the hemodynamic response to further RVP increase.

Pulse transit time as a proxy for vasoconstriction in younger and older adults.

Changes of vasoconstriction may be measured non-invasively using pulse transit time. This study assessed the sensitivity, test-retest reliability and validity of pulse transit time during vasoconstriction provocation and active standing, and the predictive value of pulse transit time for blood pressure drop. Fifty-five younger (age<65years) and 31 older adults (age>70years) underwent electrocardiography, wrist and finger photoplethysmography and continuous blood pressure and total peripheral resistance measurements during vasoconstriction provocation using a cold pressor test (21 younger adults), or active stand tests (all other participants). Pulse transit time was defined as the time lag between the electrocardiography R-peak and the peak in the photoplethysmography first derivative; sensitivity as a significant decrease relative to baseline; test-retest reliability as the intra class correlation between different repeats of the same test; validity as the association between peripheral resistance and pulse transit time; predictive value as the association between supine resting pulse transit time and mean arterial pressure drop during active standing. Finger pulse transit time was sensitive and reliable (ICC 0.2-0.8) during vasoconstriction provocation, but wrist pulse transit time was poorly reliable (ICC 0-0.5); only finger pulse transit time was sensitive to and reliable (ICC 0.4-0.8) during active standing in both younger and older adults. Finger pulse transit time was not associated with total peripheral resistance. Supine resting pulse transit time had predictive value for blood pressure drop during active standing in older adults (β -0.16; p 0.025). Pulse transit time was sensitive to and reliable during vasoconstriction provocation and active standing, but did not significantly differ between younger and older adults. Pulse transit time could not be demonstrated to particularly reflect vasoconstriction, but it had predictive value for blood pressure drop during active standing.

Effects of Short‐term Warm Water Bathing on Cardiac Baroreflex Sensitivity in Healthy Men

Bath‐related fatal (sudden cardiac arrest) and non‐fatal accident (dizziness and disturbance of consciousness) have been reported frequently in Japan. Cardiac baroreflex sensitivity (BRS) may relate to these symptoms. However, underlying mechanism(s) is poorly understood. With this information as background, we determined the effects of short‐term warm water immersion on cardiac BRS in healthy men. Twelve apparent healthy men underwent the single sit‐stand test (e.g., 5‐min sitting on the floor of bathtub and then standing up and remained standing for 5 min quietly) twice (e.g., without and with 41 °C warm water at the heart level). Beat‐to‐beat blood pressure was continuously recorded through the protocol (via Finometer). BRS was evaluated by the sequence method from heart rate response to the standing‐induced abrupt drop of mean arterial pressure (MAP). Additionally, after the each test, brachial‐ankle pulse wave velocity (baPWV: an index of arterial stiffness) was measured in the supine position. During the bathing, heart rate and cardiac output (estimated by Modelflow method) were significantly increased but MAP, stroke volume, total peripheral resistance, and tympanic temperature did not change significantly (vs. pre‐bathing). Regarding the single sit‐stand test, there were no significant changes in the baseline (sitting) MAP (from 73±16 to 77±16 mmHg, P=0.322) and the standing‐induced decreases in MAP (from −33±12 to −33±13 mmHg, P=0.970) between pre‐ and post‐bathing, but MAP‐HR slope was blunted after the bathing (from −0.47±0.26 to −0.35±0.25 bpm/mmHg, P=0.024, Figure 1). The baPWV was significantly decreased after the bathing (vs. pre‐bathing (from 12.2±1.2 to 11.8±1.2 m/sec, P=0.002). Change in MAP‐HR slope correlated with corresponding change in baPWV (r=0.610, P=0.036, Figure 2). Our results indicate that: (1) even a short‐term warm water bathing deteriorates cardiac BRS although it did not induce greater orthostatic hypotension, and (2) the change in cardiac BRS with the short‐term bathing is associated with the change in arterial stiffness. Further study to determine the impact of prolonged warm water bathing is needed.Support or Funding InformationThis study was supported by Japan Health &amp; Research Institute Research Grant.Cardiac barorefex sensitivity (BRS) gain and brachial‐ankle pulse wave velocity (baPWV) before and after 5‐min warm‐water bathing. Data are mean and SD. Thin lines indicate individual data.Figure 1Relationship between 5‐min bathing induced changes in baPWV and cardiac BRS gain.Figure 2

The impact of fluid optimisation before induction of anaesthesia on hypotension after induction.

Intra-operative hypotension is a known predictor of adverse events and poor outcomes following major surgery. Hypotension often occurs on induction of anaesthesia, typically attributed to hypovolaemia and the haemodynamic effects of anaesthetic agents. We assessed the efficacy of fluid optimisation for reducing the incidence of hypotension on induction of anaesthesia. This prospective trial enrolled 283 patients undergoing radical cystectomy and randomly allocated them to goal-directed fluid therapy (n=142) or standard fluid therapy (n=141). Goal-directed fluid therapy patients received fluid optimisation based on stroke volume response to passive leg raise before induction; those with positive passive leg raise received intravenous crystalloid fluid boluses until stroke volume was optimised. Baseline mean arterial pressure was measured on the morning of surgery and on arriving in the operating theatre. This post-hoc analysis defined haemodynamic instability as either a >30% relative drop in mean arterial pressure compared with baseline or absolute mean arterial pressure <55mmHg, within 15min of induction. Forty-two (30%) goal-directed fluid therapy patients underwent fluid optimisation after finding an intravascular fluid deficit via passive leg raise testing; 106 (75%) goal-directed fluid therapy and 112 (79%) standard fluid therapy patients met criteria for haemodynamic instability. There was no significant difference in the incidence of haemodynamic instability between the goal-directed fluid therapy and standard fluid therapy groups using absolute mean arterial pressure drop below 55mmHg (p=0.58) or using pre-surgical testing or pre-surgical mean arterial pressure values as baseline (p=0.21, p=0.89, respectively); however, the difference in the incidence of haemodynamic instability was significant using the operating theatre baseline mean arterial pressure (p=0.004). We conclude that fluid optimisation before induction of general anaesthesia did not significantly impact haemodynamic instability.

A comparison of time to achieve T5 blockade in lateral versus sitting position during elective cesarean section under spinal anesthesia: A randomized control trial

Context: Spinal anesthesia is the preferred anesthetic technique for cesarean section. Lateral and sitting positions are commonly used for performing subarachnoid block in parturients. Maternal positioning affects the spread of local anesthetic drugs and affects the onset and level of block. Faster onset of block is associated with hemodynamic changes having detrimental effects in parturients. Aims: The aim of our study is to evaluate the effectiveness of two maternal positions – lateral and sitting. Materials and Methods: This prospective randomized control study was conducted on 100 parturients undergoing elective cesarean section under spinal anesthesia. They were randomly assigned into two groups. Group L received spinal anesthesia in lateral and group S in sitting position. Time to achieve T5 blockade, hemodynamics, motor blockade, fetal pH, and Apgar score were noted. Independent sample 't' test, Chi-square test, and paired t test were used for statistical analysis. Results: Time to achieve T5 dermatomal level was less in group L which was statistically significant (2.60 ± 0.535 vs. 4.34 ± 0.745 min, P < 0.001). Number of attempts required and time taken for giving spinal was significantly more in group L. The drop in mean arterial pressure and requirement of phenylephrine was more in lateral position. Conclusion: Adoption of sitting position while performing subarachnoid block for cesarean section was found to be superior to lateral position in view of better hemodynamic stability, need for fewer attempts, and better maternal comfort, though time to achieve T5 block was longer.

Blood pressure measurements during intraoperative pediatric scoliosis surgery.

Background:Intraoperative hypotension is frequently encountered during surgery and it can be associated with adverse outcomes. Blood pressure monitoring is critical during surgery, but there are no universally agreed upon standards for interpreting values of hypotension and no consensus regarding interventions.Material and Methods:We performed a retrospective chart review of pediatric patients who underwent idiopathic scoliosis surgery by a single surgeon. We used the arterial line for all measures. Intraoperative hypotension was defined as 20% decrease of the baseline systolic blood pressure (SBP), 30% decrease of baseline SBP, or mean arterial pressure less than 60 mmHg. Use of vasopressor agents was also recorded and correlated with blood pressure definitions.Results:Seventy idiopathic scoliosis patients were retrospectively evaluated. There was a significant correlation between the three measures of hypotension. Sixty percent of the patients received vasopressors. There was a significant correlation between a drop of mean arterial pressure to less than 60 mmHg and the use of the ephedrine. We did not find any changes on neuromonitoring measures during the case and there were no intraoperative or one-month postoperative complications.Conclusions:Blood pressure is only one of the measures anesthesiologists look to for good perfusion during surgery. Pediatric anesthesiologists and orthopedics agree in trying tight blood pressure control during surgery to decrease blood loss, but what the exact definition of that blood pressure number is, is still unclear. We propose that using mean arterial pressure less than 60 mmHg is perhaps a better definition. We provide recommendations for future studies.

Association of Blood Pressure During Thrombectomy for Acute Ischemic Stroke With Functional Outcome: A Systematic Review.

Background and Purpose- Optimal blood pressure (BP) targets during mechanical thrombectomy (MT) for acute ischemic stroke (AIS) are unknown, and randomized controlled trials addressing this issue are lacking. We aimed to perform a systematic review of studies evaluating the influence of periprocedural BP on functional outcome after MT. Methods- Studies assessing periprocedural BP effect on functional outcome published after January 1st, 2012 were included in the systematic review. The PRISMA checklist and flow diagram were followed for the design and reporting of this work. Results- Nine studies were included, for a total of 1037 patients. The heterogeneity in findings with respect to BP monitoring and studied parameters precluded a meta-analysis. Mean arterial pressure was the most frequently reported parameter to describe BP variability during MT, and systolic BP was the main parameter used to define periprocedural BP targets. Five studies suggested an association between 3 types of BP drops as predictors of poor functional outcome at 3 months: >40% drop in mean arterial pressure compared with baseline (odds ratio=2.8; [1.09-7.19]; P=0.032), lowest mean arterial pressure before recanalization (odds ratio=1.28; [1.01-1.62] per 10 mm Hg drop below 100 mm Hg; P=0.04), and MAP drops (odds ratio=4.38; [1.53-12.6] for drops >10%). Four studies did not show an association between BP during MT and functional outcome, including 3 studies with strict periprocedural systolic BP targets (within a 140-180 mm Hg). Conclusions- BP drops during MT may be associated with a worse functional outcome. When strict systolic BP targets are achieved, no association between BP and functional outcome was also noted. Both conclusions require further evaluation in randomized studies.

Does Nimodipine Interruption due to High Catecholamine Doses Lead to a Greater Incidence of Delayed Cerebral Ischemia in the Setting of Aneurysmal Subarachnoid Hemorrhage?

Current guidelines recommend the administration of nimodipine for the prevention of delayed cerebral ischemia (DCI) after aneurysmal subarachnoid hemorrhage (aSAH). However, nimodipine can lead to significant drops in mean arterial pressure and cerebral perfusion pressure. Catecholamines are then used to maintain them while nimodipine is reduced and/or held. There is no evidence that nimodipine retains its neuroprotective effect at lower doses. We aimed to investigate the role of nimodipine interruption in the setting of aSAH and its possible impact on the incidence of DCI. We performed a retrospective analysis in patients with aSAH admitted to our center from January 2012 to October 2015. Nimodipine prophylaxis duration and dosage and the incidence of DCI were recorded. Bivariate correlation with Spearman's rho (ρ) and ordinal regression analyses were performed. A total of 170 patients were included in the study. Of these, 165 (97.1%) received nimodipine prophylaxis starting on day 0. Nimodipine was interrupted in 85 of 165 (51.5%), whereas dose was reduced in 47 of 165 (28.5%); full dose was received by only 33 of 165 (20%). DCI was observed in 85 of 170 (50%). Nimodipine interruption correlated in a statistically significant way with a greater incidence of DCI (ρ= 0.431, P < 0.001); receiving full doses of nimodipine showed a statistically significant inverse correlation to DCI (ρ= -0.273, P < 0.001). Ordinal regression analysis revealed nimodipine interruption as a statistically significant independent predictor of DCI (odds ratio 0.194; 95% confidence interval 0.079-0.474, P < 0.001). Our analysis reveals a greater incidence of DCI in patients with aSAH when nimodipine is interrupted.

Impact of bedside percutaneous dilational and open surgical tracheostomy on intracranial pressure, pulmonary gas exchange, and hemodynamics in neurocritical care patients.

Aim was to compare the impact of bedside percutaneous dilational tracheostomy (PDT) and open surgical technique (ST) on intracranial pressure (ICP), pulmonary gas exchange and hemodynamics.We retrospectively analyzed data of 92 neurocritical care patients with invasive ICP monitoring during either PDT (43 patients) or ST (49 patients).Peak ICP levels were higher during PDT (22 [17-38] mm Hg vs 19 [13-27] mm Hg, P = .029). Mean oxygen saturation (SpO2) and end-tidal carbon dioxide partial pressure (etCO2) did not differ. Episodes with relevant desaturation (SpO2 < 90%) or hypercapnia (etCO2 > 50 mm Hg) occurred rarely (5/49 during ST vs 3/43 during PDT for SpO2 < 90%; 2/49 during ST vs 5/43 during PDT for hypercapnia). Drops in mean arterial pressure (MAP) below 60 mm Hg were seen more often during PDT (8/43 vs 2/49, P = .026). Mean infusion rate of norepinephrine did not differ (0.52 mg/h during ST vs 0.45 mg/h during PDT). No fatal complications were observed.Tracheostomy can be performed as ST and PDT safely in neurocritical care patients. The impact on ICP, pulmonary gas exchange and hemodynamics remains within an unproblematic range.

A short chain fatty acid produced by the gut microbiota plays a role in blood pressure regulation and cardiac contractility

Recent studies by our laboratory and others have highlighted the important role played by short chain fatty acids (SCFA) produced by the gut microbiota and their effect on host physiology. Acetate, the most abundant SCFA present in the blood, has been shown to modulate blood pressure control through at least two mechanisms; renin release in the juxtaglomerular apparatus, and changes in vascular tone in peripheral resistance beds (Pluznick, Protzko et al. 2013). Prior studies by our laboratory have shown that intravenous administration of SCFAs causes acute hypotension in anesthetized mice (Pluznick, Protzko et al. 2013). These prior studies suggested that acetate was acting purely on the peripheral vasculature to cause a vasodilatory effect, as treating vessels with acetate ex‐vivo resulted in relaxation (Natarajan, Hori et al. 2016). To expand upon these findings, here we performed IP injections of acetate in mice that were implanted with DSI telemetry transmitters to monitor blood pressure and heart rate (HR) in real time. Sodium acetate was delivered at a 1g/kg dose via IP, a dose which we have previously found to elevate plasma acetate by 3–4 fold over baseline. This resulted in a rapid and reproducible drop in mean arterial pressure (MAP) (−54.32 +/− 14.20 mmHg maximum drop, n=4, p&lt;0.05) when compared to an IP injection of the same volume of saline. The duration, but not the magnitude of the blood pressure drop was dose dependent based on IP injections of sodium acetate at 0.625 g/kg (27.08 +/− 4.80 minutes to ½ recovery vs 15.57 +/− 7.24 minutes, n=4, p&lt;0.05). Surprisingly, in addition to a significant depression of blood pressure, mice injected with acetate also showed a significant depression in heart rate (−233.50 +/− 101.20 bpm maximum drop, n=4, p&lt;0.05). Preliminary data using combinatory injections of acetate and the vasoconstrictor phenylephrine show a potential attenuation of the blood pressure drop caused by acetate, suggesting a strong vascular component to the physiological effects of acetate. However, had acetate purely been acting on the vasculature, we would have expected heart rate to increase. Lower doses of acetate (0.625g/kg) also yielded a drop in heart rate not significantly different from the 1g/kg dose. To further probe the effects of exogenous acetate administration on specific cardiac functions, pressure volume loops were performed in rats and acetate was administered intravenously at a continuous infusion to provide a steady, measurable effect. Rats treated with acetate showed a significant decrease in cardiac stroke work, developed pressure, and dP/dtmax, and a significant increase in dP/dtmin (n=4, p&lt;0.05), indicating a potential effect on contractility. We hypothesize that acetate acts both on the peripheral vasculature and the cardiac muscle, with both components contributing to the blood pressure and heart rate effects seen in whole animals. Together these data hint at a previously unknown and potentially detrimental effect of short chain fatty acids on cardiac function, and efforts are underway to further what role these effects play in whole organism physiology.Support or Funding InformationFunding: F31HL144061, R01HL128512, R01DK107726This abstract is from the Experimental Biology 2019 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Low Copeptin Levels in Patients With Intradialytic Hypotension.

Intradialytic hypotension (IDH) is related to high morbidity and mortality. There is evidence that arginine-vasopressin (AVP) responses could play a role. Copeptin is a reliable biomarker of AVP. In this study, copeptin, aldosterone, epinephrine, and norepinephrine levels in patients with IDH were evaluated throughout a hemodialysis (HD) session and compared with the control group. The study includes 15 patients who were normotensive during HD and 15 patients with IDH with a minimum HD vintage of 1 year. Blood samples were collected before the initiation of an HD session (T0 ), in the mid-session for control group, 30 min after mean arterial pressure drop for IDH patients (T1 ), and at the end of the session (T2 ). Groups had similar demographic features and health parameters, interdialytic weight gains, and ultrafiltration amounts. The IDH group had a mean arterial pressure decline of 39.9 (±6.4) mm Hg. Copeptin levels of the control group increased an average of 79.9 (±97.5) pmol/L at T1 and an additional 24.8 (±33.9) pmol/L at T2 . In the IDH group, copeptin level increases at T1 and T2 were 3.2 (±5.5) pmol/L and 34 (±44.6) pmol/L, respectively. Copeptin levels of the IDH group were significantly lower at T1 (P < 0.001) and at the T0 -T2 interval than control group (P = 0.05). In the control group, aldosterone levels distinctly decreased, and in the IDH group, aldosterone levels were elevated (P < 0.001). Small changes were detected in epinephrine and norepinephrine levels for both groups but did not reach significance (P = 0.6 and P = 0.3, respectively). Lower copeptin level alterations suggest inadequate AVP responses in patients with IDH.

The comparison between propofol and dexmedetomidine infusion on perioperative anxiety during regional anesthesia

Regional anesthesia for surgery is associated with increased anxiety for patients. This study aimed to compare the effect of propofol and dexmedetomidine infusion on perioperative anxiety during regional anesthesia. Eighty-four patients were randomly divided into two groups receiving either study drug infusion. Anxiety score, level of sedation using the Bispectral Index and Observer’s Assessment of Alertness and Sedation, hemodynamic stability, and overall patient’s feedback on anxiolysis were assessed. Both groups showed a significant drop in mean anxiety score at 10 and 30 min after starting surgery. Difference in median anxiety scores showed a significant reduction in anxiety score at the end of the surgery in the dexmedetomidine group compared to the propofol group. Dexmedetomidine and propofol showed a significant drop in mean arterial pressure in the first 30 min and first 10 min respectively. Both drugs demonstrated a significant drop in heart rate in the first 20 min from baseline after starting the drug infusion. Patients in the dexmedetomidine group (76.20%) expressed statistically excellent feedback on anxiolysis compared to patients in the propofol group (45.20%). Dexmedetomidine infusion was found to significantly reduce anxiety levels at the end of surgery compared to propofol during regional anesthesia.

Efficacy of fluid loading as a countermeasure to the hemodynamic and hormonal changes of 28-h head-down bed rest.

After exposure to microgravity, or head‐down bed rest (HDBR), fluid loading is often used with the intent of increasing plasma volume and maintaining mean arterial pressure during orthostatic stress. Nine men (aged 18–32 years) underwent three randomized trials with lower body negative pressure (LBNP) before and after: (1) 4‐h of sitting with fluid loading (1 g sodium chloride/125 mL of water starting 2.5‐h before LBNP), (2) 28‐h of 6‐degree HDBR without fluid loading, and (3) 28‐h of 6‐degree HDBR with fluid loading. LBNP was progressive from 0 to −40 mmHg. After 28‐h HDBR, fluid loading did not protect against the loss of plasma volume (−280 ± 64 mL without fluid loading, −207 ± 86 with fluid loading, P = 0.472) nor did it protect against a drop of mean arterial pressure (P = 0.017) during LBNP (Post‐28 h HDBR response from 0 to −40 mmHg LBNP: 88 ± 4 to 85 ± 4 mmHg without fluid loading and 93 ± 4 to 88 ± 5 mmHg with fluid loading, P = 0.557 between trials). However, fluid loading did protect against the loss of stroke volume index and central venous pressure observed after 28‐h HDBR. Fluid loading also attenuated the increase of angiotensin II seen after 28‐h HDBR and throughout the LBNP protocol (Post‐28 h HDBR response from 0 to −40 mmHg LBNP: 16.6 ± 3.4 to 23.7 ± 5.0 pg/mL without fluid loading and 6.1 ± 0.8 to 12.2 ± 2.3 pg/mL with fluid loading, P < 0.001 between trials). Our results indicate that fluid loading did not protect against plasma volume loss due to HDBR or change blood pressure responses to LBNP. However, changes in central venous pressure, stroke volume and fluid regulatory hormones could potentially influence longer duration studies and those with more severe orthostatic stress.

Hypertensive Disorders of Pregnancy and Future Maternal Cardiovascular Risk.

Hypertensive disorders of pregnancy (HDP) complicate 5% to 10% of pregnancies and are increasing with the rising prevalence of cardiometabolic diseases in younger women.1 Normal pregnancy is marked by an initial drop in mean arterial pressure, with an eventual rise in blood pressure (BP) to prepregnancy levels.2 The development of HDP involves a number of factors that result in volume and hemodynamic alterations that fail to adapt to the changes accompanying pregnancy. There are well established associations between HDP and the development of maternal cardiovascular disease (CVD) later in life. Although the associations between preeclampsia and future CVD have long been known, newer evidence suggests that there are also long‐term CVD risks associated with gestational hypertension (GH), although the etiology of GH is thought to be distinct from that of preeclampsia. Whether preeclampsia and GH result as manifestations of already preexisting CVD risk or whether they contribute to the pathogenesis of later CVD development is unclear. A history of HDP has the unique potential to identify women at higher risk of future CVD, for whom targeted risk‐reduction interventions may be particularly helpful. In this review, we discuss the evidence for the long‐ and short‐term risks of maternal CVD associated with HDP, with a focus on preeclampsia and GH. We also outline current recommendations for screening and prevention of CVD in women with a history of HDP and highlight important areas in which additional research is needed.

Damage control of caval injuries in a porcine model using a retrievable Rescue stent

ObjectiveEarly hemorrhage control before the operating room is essential to reduce the significant mortality associated with traumatic injuries of the vena cava. Conventional approaches present logistical challenges on the battlefield or in the trauma bay. A retrievable stent graft would allow rapid hemorrhage control in the preoperative setting when endovascular expertise is not immediately available and without committing a patient to the limitations of current permanent stents. This study details a refined retrievable Rescue stent for percutaneous delivery that was examined in a porcine survival model of penetrating caval hemorrhage. MethodsA retrievable caval stent was reduced in delivery profile to a 9F sheath using finite element analysis. The final stent was constructed with a “petal and stem” design using nitinol wire followed by covering with polytetrafluoroethylene. Seven Yorkshire pigs (79-86 kg) underwent 22F injury of the infrarenal vena cava with intentional class II hemorrhage (1200 mL). Percutaneous deployment of the Rescue stent was used to temporize hemorrhage for 60 minutes, followed by resuscitation with cell saver blood and permanent caval repair. Hemorrhage control was documented with photography and angiography. Vital signs were recorded and laboratory values were measured out to 48 hours postoperatively. Data were examined with a repeated-measures analysis of variance. ResultsThe profile of the caval Rescue stent was successfully reduced from 16F to 9F while remaining within fracture and shape memory limits for nitinol. In addition, both rapid deployment and recapture were preserved. Following intentional hemorrhage after caval injury, animals revealed a significant drop in mean arterial pressure (average, 30 mm Hg), acidosis, and elevated lactate level compared with before injury. Compared with uncontrolled hemorrhage, which resulted in death in <9 minutes, the Rescue stent achieved hemorrhage control in <1 minute after venous access in all seven animals. All animals were successfully recovered after permanent repair. There was no significant change in levels of transaminases, bilirubin, creatinine, or hemoglobin at 48 hours compared with preinjury baseline. ConclusionsA retrievable Rescue stent achieved rapid percutaneous hemorrhage control after a significant traumatic injury of the vena cava and allowed successful recovery of all injured animals. Further development of this approach may have utility in preoperative damage control of caval injuries.

Bispectral index to guide induction of anesthesia: a randomized controlled study

BackgroundIt is unknown to what extent hypotension frequently observed following administration of propofol for induction of general anesthesia is caused by overdosing propofol. Unlike clinical signs, electroencephalon-based cerebral monitoring allows to detect and quantify an overdose of hypnotics. Therefore, we tested whether the use of an electroencephalon-based cerebral monitoring will cause less hypotension following induction with propofol.MethodsSubjects were randomly assigned to a bispectral index (BIS)-guided (target range 40–60) or to a weight-related (2 mg.kg− 1) manual administration of propofol for induction of general anesthesia. The primary endpoint was the incidence of hypotension following the administration of propofol. Secondary endpoints included the degree of hypotension and correlations between BIS and drop in mean arterial pressure (MAP). Incidences were analyzed with Fisher’s Exact-test.ResultsOf the 240 patients enrolled into this study, 235 predominantly non-geriatric (median 48 years, 25th – 75th percentile 35–61 years) patients without severe concomitant disease (88% American Society of Anesthesiology physical status 1–2) undergoing ear, nose and throat surgery, ophthalmic surgery, and dermatologic surgery were analyzed. Patients who were manually administered propofol guided by BIS (n = 120) compared to those who were given propofol by weight (n = 115) did not differ concerning the incidence of hypotension (44% vs. 45%; p = 0.87). Study groups were also similar regarding the maximal drop in MAP compared to baseline (33% vs. 30%) and the proportion of hypotensive events related to all measurements (17% vs. 19%). Final propofol induction doses in BIS group and NON-BIS group were similar (1.93 mg/kg vs. 2 mg/kg). There was no linear correlation between BIS and the drop in MAP at all times (r < 0.2 for all) except for a weak one at 6 min (r = 0.221).ConclusionResults of our study suggest that a BIS-guided compared to a weight-adjusted manual administration of propofol for induction of general anesthesia in non-geriatric patients will not lower the incidence and degree of arterial hypotension.Trial registrationGerman Registry of Clinical Trials (DRKS00010544), retrospectively registered on August 4, 2016.

Differential Effects of Brain Death on Rat Microcirculation and Intestinal Inflammation: Female Versus Male.

Brain death (BD) affects organs by multiple mechanisms related to hemodynamic effects, hormonal changes, and the systemic inflammatory response, which reduce organ function and viability. BD reduces microcirculatory perfusion in rat mesentery; this disturbance is also observed in the pancreas and lungs. Sex hormones can affect microcirculatory function, altering tissue perfusion and influencing the inflammatory process. Here, we present differences between sexes in the microcirculatory alterations generated by BD and in inflammatory infiltrate. Male, female, and ovariectomized-female Wistar rats were submitted to BD by intracranial balloon catheter sudden inflation. BD was confirmed by maximally dilated and fixed pupils, apnea, absence of reflexes, and a drop in mean arterial pressure. Perfusion and flow of the mesenteric microcirculation were analyzed. Intestinal myeloperoxidase activity and leukocyte infiltration were quantified. ELISA quantified serum estradiol, corticosterone, and inflammatory mediators, whereas expression of eNOS, endothelin, and endothelial adhesion molecule was measured by immunohistochemistry. Male rats presented lower percentages of mesenteric perfused microvessels and reduced blood flow compared to females. The female group presented higher eNOS and endothelin expression. Leukocyte infiltration into intestinal walls was higher in females in comparison to that in males. Moreover, the female group showed higher mesenteric vessel ICAM-1 expression than males, whereas serum TNF-α, IL-1β, and IL-10 levels did not differ between sexes. The high estradiol concentration before BD and high eNOS expression apparently favored the maintenance of microvascular perfusion/flow; however, BD caused an acute reduction of female sex hormone concentration and higher ICAM-1 level; thus, the proinflammatory organ status after BD is favored.

Role of baroreflex during endotoxemic shock

Septic shock is a prevalent and life‐threatening condition which is often associated with major hypotension, resulting in multiple organs failure. The infusion of high doses of endotoxin lipopolysaccharide (LPS) is a well‐accepted experimental model of septic shock. Considering that baroreflex is a mandatory mechanism involved in the beat‐to‐beat hemodynamic regulation, we hypothesized herein that baroreflex plays a role buffering endotoxin‐induced hypothension in conscious freely moving rats. Thus, in the present study, we evaluated the cardiovascular outcomes of iv injection of endotoxin (1.5 mg.kg−1 or 2.5 mg.kg−1) or saline in male Wistar rats (280–350g, CEUA #2017.1.585.58.9). The baseline levels of mean arterial pressure and heart rate were not different among all groups. As expected, endotoxin induced hypotension (P&lt;0.001) and tachycardia (P &lt; 0.001). These effects were independent of dose. Interestingly, the drop of mean arterial pressure was significantly higher in rats previously submitted to baroreceptors afferents removal (4 days before recordings) than in (sham) rats with intact baroreceptor afferents (P&lt;0.001). The present data are consistent with the notion that baroreflex is key lessening endotoxin‐induced hypothension. The neural mechanisms involved in this control deserve further investigation aiming new strategic therapeutic tools to revert this critical condition.Support or Funding InformationFinancial support: FAPESP, CAPES and CNPqThis abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.

Haemodynamic stability during anaesthesia induction with propofol – impact of phenylephrine. A double-blind, randomised clinical trial

Background. We studied the effects of a parallel phenylephrine infusion during bispectral index guided anaesthesia in-duction with propofol on haemodynamic parameters. We hypothesised that mean ar-terial pressure and cardiac index would be better maintained in the group of patients receiving the phenylephrine infusion dur-ing induction.Methods. We studied ASA I-III patients scheduled for oncological abdominal sur-gery. Forty patients randomly received ei-ther a 0.9% NaCl or a phenylephrine (0.5 μg/kg/min) infusion during the induction of anaesthesia with propofol to a bispectral index value of 60. Mean arterial pressure, stroke volume index and systemic vascular resistance index were recorded, starting at one minute before induction for 20 min-utes, at one-minute intervals.Results. After induction of anaesthesia before intubation mean arterial pressure and stroke volume index decreased sig-nificantly compared to baseline in both groups, while the systemic vascular resist-ance index increased slightly. At the end of measurements, mean arterial pressure (66 ± 11 vs. 94 ± 14 mmHg; 0.9% NaCl vs. phenylephrine group p<0.01) and stroke volume index (34.2 ± 9.1 vs. 44.0 ± 9.7 ml/m2; 0.9% NaCl vs. phenylephrine group p<0.01) were lower in both groups in com-parison to baseline values, but were better maintained in the phenylephrine group, whereas systemic vascular resistance index was higher than at baseline (2308 ± 656 vs. 3198 ± 825 dynes s/cm5/m2; 0.9% NaCl vs. phenylephrine group p<0.01) with signifi-cant differences between groups. Conclusion. Our study shows that a con-tinuous phenylephrine infusion can atten-uate the drop in mean arterial pressure and stroke volume index during anaesthesia induction with propofol.