Maintenance Of Mean Arterial Pressure Research Articles

Anaesthesia in a Pregnant Female with Infective Spondylodiscitis Posted for Laminectomy with Posterior Instrumentation

Introduction: Spondylodiscitis in pregnancy is an uncommon entity that can inadvertently hamper the pregnancy. Case presentation: A 25-year-old primigravida in the middle of her third trimester presented with new-onset ascending paralysis due to infective spondylodiscitis. The compression of the spinal cord by virtue of spondylodiscitis demanded immediate surgical decompression. The indirect decompression of the spinal cord was successfully accomplished by performing laminectomy with posterior instrumentation while the anesthesiologists provided general anaesthesia, monitored, and maintained maternal and foetal safety. Anaesthetic methods employed include perioperative tocolytic cover, an induction of rapid sequence, aspiration prophylaxis, balanced analgesia, and appropriate maintenance of Mean Arterial Pressure, thereby ensuring maternal and foetal well-being. Conclusion: A prompt surgical intervention and appropriate anaesthesia management resulted in successful decompression of the spinal cord with excellent recovery of paraplegia while avoiding maternal and foetal morbidity and mortality. Keywords: Pregnancy, Laminectomy, Foetal monitoring, Patient positioning, Uteroplacental blood flow.

A double-blind randomised feasibility trial of angiotensin-2 in cardiac surgery.

SummaryAcute kidney injury is common after cardiac surgery. Vasoplegic hypotension may contribute to kidney injury, and different vasopressors may have variable effects on kidney function. We conducted a double‐blind, randomised feasibility trial comparing peri‐operative angiotensin‐2 with noradrenaline. We randomly allocated 60 patients at two centres to a blinded equipotent angiotensin‐2 or noradrenaline infusion intra‐operatively and for up to 48 h postoperatively, titrated to mean arterial pressure of 70–80 mmHg. Primary feasibility outcomes included consent rate, protocol adherence, infusion duration, mean arterial pressure maintenance in the target range and major adverse outcomes. Secondary outcomes included kidney injury rate. The consent rate was 47%. Protocol adherence was 100% in the angiotensin‐2 group and 94% in the noradrenaline group. Study drug duration was median (IQR [range]) 217 (160–270 [30–315]) vs. 185 (135–301 [0–480]) min (p = 0.78) min intra‐operatively, and 5 (0–16 [0–48]) vs. 14.5 (4.8–29 [0–48]) hours (p = 0.075) postoperatively for angiotensin‐2 and noradrenaline, respectively. The mean arterial pressure target was achieved postoperatively in 25 of 28 (89%) of the angiotensin‐2 group and 27 of 32 (84%) of the noradrenaline group. One participant had a stroke, one required extracorporeal support and three required renal replacement therapy, all in the noradrenaline group (p = 0.99, p = 0.99 and p = 0.1). Acute kidney injury occurred in 7 of 28 in the angiotensin‐2 group vs. 12 of 32 patients in the noradrenaline group (p = 0.31). This pilot study suggests that a trial comparing angiotensin‐2 with noradrenaline is feasible. Its findings justify further investigations of angiotensin‐2 in cardiac surgery.

Evaluation of the Addition of Angiotensin II in Patients With Shock After Cardiac Surgery at a Veterans Affairs Medical Center.

Vasoplegic shock occurs in up to 37% of cardiac surgery patients. We investigated the use of angiotensin II for treating vasoplegic shock in these patients. We assessed clinical outcomes and mortality in patients undergoing cardiac surgery at our center between March 1, 2018 and October 31, 2020 who developed vasoplegic shock, comparing those who received angiotensin II with those who did not. This was a retrospective chart review. Response to angiotensin II was defined as increase in or maintenance of mean arterial pressure (MAP) and decrease in background vasopressor dosage. Angiotensin II was administered to 7 patients (postoperatively in 4 patients [57.1%]) with vasoplegic shock and baseline norepinephrine equivalent (NEE) of 0.49 ± 0.08 μg/kg/min; 12 patients with vasoplegic shock did not receive angiotensin II. Within 3 hours of angiotensin II administration, NEE decreased by 38.0 ± 33.1%. Angiotensin patients were more likely to newly require renal replacement therapy (66.7% vs 9.1%, P = 0.03) and had a longer, although not statistically significant, postoperative stay (23.1 vs 14.0 days, P = 0.16). Despite higher NEE requirements at baseline (0.49 vs 0.30, P = 0.03) and over the next 48 hours in the angiotensin group, no between-group differences in 7-day mortality (14.3% vs 0.0%, P = 0.37) or 30-day mortality (28.6% vs 8.3%, P = 0.52) were noted. In patients who developed vasoplegic shock after cardiac surgery, angiotensin II administration allowed immediate dosage reductions of other vasopressors while maintaining MAP. Despite its small sample size, this study adds to the paucity of data in these patients and highlights future research needs.

Vagus Nerve Stimulation Protects Enterocyte Glycocalyx After Hemorrhagic Shock Via the Cholinergic Anti-Inflammatory Pathway.

ABSTRACTIntroduction:Electrical vagal nerve stimulation is known to decrease gut permeability and alleviate gut injury caused by traumatic hemorrhagic shock. However, the specific mechanism of action remains unclear. Glycocalyx, located on the surface of the intestinal epithelium, is associated with the buildup of the intestinal barrier. Therefore, the goal of our study was to explore whether vagal nerve stimulation affects enterocyte glycocalyx, gut permeability, gut injury, and remote lung injury.Materials and methods:Male Sprague Dawley rats were anesthetized and their cervical nerves were exposed. The rats underwent traumatic hemorrhagic shock (with maintenance of mean arterial pressure of 30–35 mmHg for 60 min) with fluid resuscitation. Vagal nerve stimulation was added to two cohorts of animals before fluid resuscitation, and one of them was injected with methyllycaconitine to block the cholinergic anti-inflammatory pathway. Intestinal epithelial glycocalyx was detected using immunofluorescence. Intestinal permeability, the degree of gut and lung injury, and inflammation factors were also assessed.Results:Vagal nerve stimulation alleviated the damage to the intestinal epithelial glycocalyx and decreased intestinal permeability by 43% compared with the shock/resuscitation phase (P < 0.05). Methyllycaconitine partly eliminated the effects of vagal nerve stimulation on the intestinal epithelial glycocalyx (P < 0.05). Vagal nerve stimulation protected against traumatic hemorrhagic shock/fluid resuscitation-induced gut and lung injury, and some inflammatory factor levels in the gut and lung tissue were downregulated after vagal nerve stimulation (P < 0.05).Conclusions:Vagal nerve stimulation could relieve traumatic hemorrhagic shock/fluid resuscitation-induced intestinal epithelial glycocalyx damage via the cholinergic anti-inflammatory pathway.

Mean arterial pressure maintenance following spinal cord injury: does meeting the target matter?

The American Association of Neurological Surgeons recommends maintaining a mean arterial pressure (MAP) of 85 or greater after spinal cord injury (SCI), despite relatively weak evidence. This target can be difficult to meet and often puts significant burden of cost and attention on the healthcare system.

The reliance on α-adrenergic receptor stimuli for blood pressure regulation in the chronically hypoxaemic fetus is not dependent on post-ganglionic activation.

Chronic hypoxaemia is associated with intrauterine growth restriction (IUGR) and a predisposition to the development of hypertension in adult life. IUGR fetuses exhibit a greater reliance on α-adrenergic activation for blood pressure regulation. The fetal blood pressure response to post-ganglionic blockade is not different between control and IUGR fetuses. The decrease in mean arterial pressure is greater in the IUGR sheep fetus after α-adrenergic receptor blockade at the level of the vasculature and this is inversely related to fetal . The increased reliance that the IUGR fetus has on α-adrenergic activation for maintenance of mean arterial pressure is not a result of increased post-ganglionic sympathetic activation. Intrauterine growth restriction (IUGR) is associated with an increased risk of cardiovascular disease in adult life. Placental restriction (PR) in sheep results in chronic hypoxaemia and early onset IUGR with increased circulating plasma noradrenaline concentrations. These IUGR fetuses exhibit a greater decrease in mean arterial pressure (MAP) during α-adrenergic blockade. We aimed to determine the role of post-ganglionic sympathetic activation with respect to regulating MAP in IUGR fetal sheep. PR was induced by carunclectomy surgery prior to conception. Fetal vascular catheterization was performed at 110-126days gestational age (GA) (term, 150 days) in nine control and seven PR-IUGR fetuses. The fetal blood pressure response to both a post-ganglionic and an α-adrenergic receptor blocker was assessed at 116-120days GA and/or 129-131days GA. The effect of both post ganglionic and α-adrenergic blockade on fetal blood pressure was then compared between control and IUGR fetuses at both GAs. There was no difference in the effect of post-ganglionic blockade on MAP in control and IUGR fetal sheep at either 116-120days GA or 129-131days GA. α-adrenergic receptor blockade decreased MAP to the same extent in both control and IUGR fetuses at 116-120days GA. At 129-131days GA, the drop in MAP in response to α-adrenergic receptor blockade was greater in IUGR fetuses than controls. There was a significant inverse relationship between the drop in MAP in response to α-adrenergic receptor blockade at both GAs with fetal . Thus, the increased dependence on α-adrenergic activation for blood pressure regulation in the chronically hypoxaemic IUGR fetus is not a result of increased post-ganglionic sympathetic activation.

Mean arterial pressure maintenance following spinal cord injury: Does meeting the target matter?

Neurosurgical guidelines recommend maintaining mean arterial pressure (MAP) between 85 and 90 mm Hg following acute spinal cord injury (SCI). In our hospital, SCI patients receive orders for MAP targeting for 72 hours following admission, but it is unclear how often the patient's MAP meets the target and whether or not this affects outcome. We hypothesized that the proportion of MAP measurements ≥85 mm Hg would be associated with neurologic recovery. Spinal cord injury patients with blunt mechanism of injury admitted between 2014 and 2019 were identified from the registry of a level 1 trauma center. Proportion of MAP values ≥85 mm Hg was calculated for each patient. Neurologic improvement, as measured by positive change in American Spinal Injury Association (ASIA) impairment scale by ≥1 level from admission to discharge was evaluated with respect to proportion of elevated MAP values. A total of 136 SCI patients were evaluated. Average proportion of elevated MAP values was 75%. Admission ASIA grades were as follows: A, 30 (22.1%); B, 20 (14.7%); C, 28 (20.6%); and D, 58 (42.6%). One hundred six patients (77.9%) required vasopressors to elevate MAP (ASIA A, 86.7%; B, 95.0%; C, 92.9%; D, 60.3%). Forty patients (29.4%) were observed to have improvement in ASIA grade by discharge (admission ASIA A, 15%; B, 33%; C, 40%; D, 13%). The proportion of elevated MAP values was higher for patients with neurologic improvement (0.81 ± 0.15 vs. 0.72 ± 0.25, p = 0.014). Multivariate modeling demonstrated a significant association between proportion of elevated MAP values and neurologic improvement (p = 0.028). An interaction revealed this association to be moderated by vasopressor dose (p = 0.032). The proportion of MAP measurements ≥85 mm Hg was determined to be an independent predictor of neurologic improvement. Increased vigilance regarding MAP maintenance above 85 mm Hg is warranted to optimize neurologic recovery following SCI. Therapeutic/care management, level IV.

Peripheral Chemoreceptors Hemodynamic Responses During Simulated Hemorrhage Under Hypoxia Conditions

BackgroundMaintaining baroreflex sensitivity is integral to ensuring blood pressure maintenance and end‐organ perfusion during hemorrhage. This is especially true under conditions of hypoxemia, where decreased tolerance to central hypovolemia is commonly observed. Hypoxia activates peripheral chemoreceptors and reduces baroreceptor‐vascular resistance reflex sensitivity. However, a direct role for the peripheral chemoreceptors in the hemodynamic response to hemorrhage in hypoxia remains unclear.ObjectiveWe tested the hypothesis that attenuation of peripheral chemoreceptor activity (low‐dose dopamine; 1–2 μg/kg/min) during acute hypoxia would promote maintenance of mean arterial pressure, pulse pressure, and other hemodynamic markers [heart rate (HR), stroke volume (SV), cardiac output (CO), total peripheral resistance (TPR)] during simulated hemorrhage.MethodsTen healthy men (35±3 years, BMI 25±1 kg/m2) participated in a randomized, double‐blind, placebo controlled study. Participants completed two experimental visits (saline and low‐dose dopamine) at which lower body negative pressure (LBNP) was conducted during hypoxia (SpO2 ~85%; PaO2 ~52 mmHg) delivered via a non‐rebreather mask. Ventilation [V̇ (turbine transducer)], arterial blood pressure (brachial artery catheter), HR (ECG), and central venous pressure (peripherally inserted central catheter) were measured continuously and SV, CO, and TPR were calculated. Following a 5‐min rest, participants underwent LBNP for 5‐min at 3 intervals (−15, −30, and −45 mmHg). Outcome values were analyzed and compared using a mixed linear model (SAS PROC MIXED) with a direct product AR(1) covariance structure using indicator variables for saline vs. dopamine. Data from the mixed linear model are reported as an estimated change per 15 mmHg of LBNP.ResultsDopamine had no effect on hypoxia PaO2, PaCO2, V̇ or respiratory rate (all P&gt;0.05) and this relationship persisted throughout all LBNP stages. The mixed linear model showed no effect of dopamine vs. saline on changes in: central venous pressure (−1.1±0.4 vs −1.3±0.3 mmHg, P=0.15), mean arterial pressure (−4.7±2.3 vs −5.3±1.4 mmHg, P=0.25), pulse pressure (−6.7±1.5 vs −8.3±1.4 mmHg, P=0.50), HR (7.8±1.5 vs 6.1±1.5 bpm, P=0.41), SV (−10.9±1.9 vs −11.6±3.3 mL, P=0.41), CO (−0.3±0.2 vs −0.4±0.4 L · min−1, P=0.31) or TPR (0.2±0.4 vs 0.7±0.6 mmHg · L · min−1P=0.27).DiscussionIntravenous infusion of low‐dose dopamine designed to attenuate peripheral chemoreflex activity during acute hypoxia did not alter the integrated hemodynamic response to simulated hemorrhage. Our data suggests that peripheral chemoreceptors have a limited role during hypoxic central hypovolemia. More research is needed to understand the sensitivity and cross‐talk between chemoreceptors and baroreceptors during hemorrhage.Support or Funding InformationFunding: W81XWH‐13‐2‐0038 (DOD), DK90541 (NIH), UL1 TR000135 (NIH).

Electrical stimulation of the vagus nerve improves intestinal blood flow after trauma and hemorrhagic shock

BackgroundGut damage after trauma/hemorrhagic shock contributes to multiple organ dysfunction syndrome. Electrical vagal nerve stimulation is known to prevent gut damage in animal models of trauma/hemorrhagic shock by altering the gut inflammatory response; however, the effect of vagal nerve stimulation on intestinal blood flow, which is an essential function of the vagus nerve, is unknown. This study aimed to determine whether vagal nerve stimulation influences the abdominal vagus nerve activity, intestinal blood flow, gut injury, and the levels of autonomic neuropeptides. MethodsMale Sprague Dawley rats were anesthetized, and the cervical and abdominal vagus nerves were exposed. One pair of bipolar electrodes was attached to the cervical vagus nerve to stimulate it; another pair of bipolar electrodes were attached to the abdominal vagus nerve to measure action potentials. The rats underwent trauma/hemorrhagic shock (with maintenance of mean arterial pressure of 25 mmHg for 30 min) without fluid resuscitation and received cervical vagal nerve stimulation post-injury. A separate cohort of animals were subjected to transection of the abdominal vagus nerve (vagotomy) just before the start of cervical vagal nerve stimulation. Intestinal blood flow was measured by laser Doppler flowmetry. Gut injury and noradrenaline level in the portal venous plasma were also assessed. ResultsVagal nerve stimulation evoked action potentials in the abdominal vagus nerve and caused a 2-fold increase in intestinal blood flow compared to the shock phase (P < .05). Abdominal vagotomy eliminated the effect of vagal nerve stimulation on intestinal blood flow (P < .05). Vagal nerve stimulation protected against trauma/hemorrhagic shock -induced gut injury (P < .05), and circulating noradrenaline levels were decreased after vagal nerve stimulation (P < .05). ConclusionCervical vagal nerve stimulation evoked abdominal vagal nerve activity and relieved the trauma/hemorrhagic shock–induced impairment in intestinal blood flow by modulating the vasoconstriction effect of noradrenaline, which provides new insight into the protective effect of vagal nerve stimulation.

Early goal directed therapy: where do we stand after the individual patient’s meta-analysis?

In the recent years, the issue of early goal directed therapy (EGDT) has led to many debate. EGDT became popular after the Rivers’ trial (1). In that single center trial including 263 patients with septic shock, EGDT application in the emergency department (ED) resulted in an important decrease in 28-day mortality from 46.5% to 30.5% (P<0.01). Even though the main difference in hemodynamic goal was the target of central venous oxygen saturation (ScvO2) that has to be maintained above 70%, the entire package, including maintenance of mean arterial pressure (MAP) ≥65 mmHg, central venous pressure (CVP) between 8-12 mmHg and urine output ≥0.5 mL/kg.h, was adopted in resuscitation guidelines (2). The trial was heavily criticized. Many of the criticisms were directed to the targets, and especially CVP as CVP is not an excellent indicator of fluid responsiveness, as well as to some of the interventions used to increase ScvO2 and in particular to the frequent use of red blood cell transfusions. Also the incidence of low ScvO2 at baseline was higher than in subsequent observational trials. All these factors raised the issue of the external validity of the trial.

Update on critical care for acute spinal cord injury in the setting of polytrauma.

Traumatic spinal cord injury (SCI) often occurs in patients with concurrent traumatic injuries in other body systems. These patients with polytrauma pose unique challenges to clinicians. The current review evaluates existing guidelines and updates the evidence for prehospital transport, immobilization, initial resuscitation, critical care, hemodynamic stability, diagnostic imaging, surgical techniques, and timing appropriate for the patient with SCI who has multisystem trauma. Initial management should be systematic, with focus on spinal immobilization, timely transport, and optimizing perfusion to the spinal cord. There is general evidence for the maintenance of mean arterial pressure of > 85 mm Hg during immediate and acute care to optimize neurological outcome; however, the selection of vasopressor type and duration should be judicious, with considerations for level of injury and risks of increased cardiogenic complications in the elderly. Level II recommendations exist for early decompression, and additional time points of neurological assessment within the first 24 hours and during acute care are warranted to determine the temporality of benefits attributable to early surgery. Venous thromboembolism prophylaxis using low-molecular-weight heparin is recommended by current guidelines for SCI. For these patients, titration of tidal volumes is important to balance the association of earlier weaning off the ventilator, with its risk of atelectasis, against the risk for lung damage from mechanical overinflation that can occur with prolonged ventilation. Careful evaluation of infection risk is a priority following multisystem trauma for patients with relative immunosuppression or compromise. Although patients with polytrauma may experience longer rehabilitation courses, long-term neurological recovery is generally comparable to that in patients with isolated SCI after controlling for demographics. Bowel and bladder disorders are common following SCI, significantly reduce quality of life, and constitute a focus of targeted therapies. Emerging biomarkers including glial fibrillary acidic protein, S100β, and microRNAs for traumatic SCIs are presented. Systematic management approaches to minimize sources of secondary injury are discussed, and areas requiring further research, implementation, and validation are identified.

Adrenomedullin and galanin responses to orthostasis in older persons

Neuroendocrine responses to orthostasis may be critical in the maintenance of mean arterial pressure in healthy individuals. A greater reduction in orthostatic tolerance with age may relate to modulation of hormonal responses such as adrenomedullin and galanin. Thus, we investigated (i) whether adrenomedullin and galanin concentrations increase during orthostatic challenge in older subjects, (ii) whether adrenomedullin and galanin concentrations are higher in older females compared with older males when seated and during orthostatic challenge, and (iii) whether postural changes in plasma concentrations of galanin are correlated with levels of adrenomedullin in either older females or males. Subjects (n = 18; 12 ♀; 55-80 years old) performed a sit-to-stand test in a 25°C sensory-minimised environment, with blood samples collected after 4 min of being seated and then when standing. Plasma adrenomedullin and galanin concentrations were determined. Baseline plasma concentration of adrenomedullin (5·35 ± 0·74 (n = 12, females) vs. 7·40 ± 1·06 pg/mL (n = 5, males)) and galanin (64·07 ± 9·05 vs. 98·99 ± 16·90 pg/mL, respectively) did not significantly differ between genders. Furthermore, plasma adrenomedullin and galanin concentrations were not significantly affected by adoption of the upright posture in either gender and were not correlated in females or males. Adrenomedullin and galanin concentrations were similar between genders and did not change following adoption of the standing posture. To further clarify the roles, these hormones play in orthostatic intolerance, adrenomedullin and galanin concentrations should be assessed in participants who show presyncopal symptoms during an orthostatic challenge.

Failure of Mean Arterial Pressure Goals to Improve Outcomes Following Penetrating Spinal Cord Injury.

Increased spinal cord perfusion and blood pressure goals have been recommended for spinal cord injury (SCI). Penetrating SCI is associated with poor prognosis, but there is a paucity of literature examining the role of vasopressor administration for the maintenance of mean arterial pressure (MAP) goals in this patient population. To elucidate this topic and to determine the efficacy of vasopressor administration in penetrating SCI by examining a case series of consecutive penetrating SCIs. We reviewed consecutive patients with complete penetrating SCI who met inclusion and exclusion criteria, including the administration of vasopressors to maintain MAP goals. We identified 14 patients with complete penetrating SCIs with an admission American Spinal Injury Association grade of A from 2005 to 2011. The neurological recovery, complications, interventions, and vasopressor administration strategies were reviewed and compared with those of a cohort with complete blunt SCI. In our patient population, only 1 patient with penetrating SCI (7.1%) experienced neurological recovery, as determined by improvement in the American Spinal Injury Association grade, despite the administration of vasopressors for supraphysiological MAP goals for an average of 101.07 ± 34.96 hours. Furthermore, 71.43% of patients with penetrating SCI treated with vasopressors experienced associated cardiogenic complications. Given the decreased likelihood of neurological improvement in penetrating injuries, it may be important to re-examine intervention strategies in this population. Specifically, the use of vasopressors, in particular dopamine, with their associated complications is more likely to cause complications than to result in neurological improvement. Our experience shows that patients with acute penetrating SCI are unlikely to recover, despite aggressive cardiopulmonary management. ASIA, American Spinal Injury AssociationMAP, mean arterial pressureSCI, spinal cord injury.

Stroke volume variation compared with pulse pressure variation and cardiac index changes for prediction of fluid responsiveness in mechanically ventilated patients

IntroductionAdequate volume resuscitation is very important for a favorable outcome of critically ill patients. Both over and under filling of intravascular volume could be deleterious. Static indices including central venous pressure, pulmonary capillary wedge pressure, left ventricular end-diastolic area, mean arterial pressure (MAP) and tachycardia are commonly used and are known to be of little value in discriminating responders from non-responders. On the other hand dynamic indices such as pulse pressure variation (PPV), inferior vena cava diameter, superior vena cava diameter, aortic blood flow, which are based on variation on the left ventricular stoke volume, have been shown to be more accurate predictors of fluid responsiveness in mechanically ventilated patients. In this study we are evaluating the ability of stroke volume variation (SVV) obtained by Vigileo–FloTrac device to predict fluid responsiveness in patients with acute circulatory failure under complete passive, volume controlled mechanical ventilation and correlating it to manually calculated PPV. Materials and methodsTwenty five patients aged above 18years, with acute circulatory failure and at least one sign of tissue hypoperfusion requiring fluid resuscitation and mechanical ventilation were included. Excluded are patients with cardiogenic shock, acute pulmonary edema, LVEF <50%, atrial fibrillation, frequent ectopics, significant aortic or mitral valve abnormalities or renal failure. Candidates were subjected to thorough clinical evaluation, lab investigation and ECG. Following sedation, muscle relaxation and maintenance of mean arterial pressure >65mmHg by norepinephrine, 500ml of Hes-steril were administered over 10min. Static and dynamic hemodynamic parameters were taken in supine position before and after fluid challenge. Patients who had an increase of cardiac index measured by trans-thoracic echocardiography ⩾15% of baseline measurement were considered responders. ResultsFourteen patients were fluid responders. Before fluid challenge SVV and PPV were significantly higher in responders than non-responders (p=0.0001 for each). SVV⩾8.15% predicted responders with a sensitivity of 100% and specificity 81.1% (AUC 0.906). PPV⩾10.2 also predicted responders with a sensitivity of 92.9% and specificity of 90.9% (AUC 0.974). The higher the SVV before fluid challenge the higher the percentage of increase of CI following fluid challenge (r=0.733, p=0.00). PPV showed the same correlation pattern with percentage increase of CI (r=0.798, p=0.00). ConclusionsBaseline stroke volume variation ⩾8.15% predicted fluid responsiveness in mechanically ventilated patients with acute circulatory failure. The study also confirmed the ability of pulse pressure variation to predict fluid responsiveness.

Perspectives: Microcirculation in hypertension and cardiovascular disease

The microcirculation of terminal vascular beds represents the ‘business end’ of the circulation, which supplies oxygen and nutrients to the tissue, controls inflammation and repair as well as fluid exchange with the tissue.1 The microcirculation comprising vessels ranging from small arteries or arterioles with diameters below 100–300 µm to corresponding venules is also the site of regulation for flow resistance and perfusion.2–4 In relation to hypertension, the establishment and regulation of flow resistance and perfusion is of special importance. The high flow resistance in the arteriolar part of microvascular networks leads to a strong reduction in intravascular pressure, before the blood enters the capillary section of the network. The maintenance of mean arterial pressure (and low capillary pressures) for different functional conditions and with increasing or decreasing tissue mass requires a fine-tuned set of regulatory controls of microvascular flow resistance. Hypertension can be interpreted as the result of an …

Medetomidine can selectively activate cardiac vagal nerve without vagal activation in gastrointestinal tract

Purpose: Vagal activation therapy has recently become a new therapeutic option for heart failure (HF). However, electrical cervical vagal nerve stimulation (VNS) may activate the whole vagal system and cause unfavorable side-effects in non-target organs, e.g. gastrointestinal tract. We have recently reported that an α2-adrenergic agonist, medetomidine, can activate cardiac vagal nerve. Using microdialysis technique, we investigated whether medetomidine were able to selectively activate cardiac vagal nerve. Methods: In anesthetized rabbits, microdialysis probes were implanted into the right atrial wall and the anterior wall of the stomach, and were perfused by Ringer's solution containing eserine. Acetylcholine (ACh) concentrations in dialysate samples were measured by high-performance liquid chromatography. (1) Under maintenance of mean arterial pressure (MAP) using intravenous infusion of phenylephrine, we examined the effects of electrical VNS (10 Hz, 1ms, 10V) at efferent sides on both cardiac and gastric ACh releases, and investigated the effects of medetomidine on VNS-induced ACh releases. (2) We examined the effects of 100 μg/kg of intravenous medetomidine on both cardiac and gastric vagal ACh releases. Results: (1) Electrical VNS significantly decreased heart rate from 265±10 bpm at baseline to 138±12 bpm (P<0.01), and increased ACh releases to both the heart (6.7±1.2 to 14.8±1.8 nM, P<0.01) and stomach (3.8±0.8 to 181.3±65.6 nM, P<0.01). 100 μg/kg of intravenous medetomidine did not alter these increases in VNS-induced ACh releases. (2) 100 μg/kg of intravenous medetomidine significantly decreased heart rate from 273±5 bpm at baseline to 185±6 bpm (P<0.01), and MAP from 87±3 mmHg to 52±2 mmHg (P<0.01). Then, medetomidine significantly increased cardiac vagal ACh release (4.7±1.1 to 7.8±0.9 nM, P<0.05), but suppressed gastric vagal ACh release (8.0±2.6 to 3.5±1.5 nM, P<0.01). The maintenance of MAP using phenylephrine brought a further decrease in heart rate (132±7 bpm, P<0.01) and a further increase in cardiac vagal ACh release (22.3±3.6 nM, P<0.01), but suppressed gastric vagal ACh release (3.5±1.1 nM) as well as medetomidine alone. Conclusions: Electrical VNS increased vagal ACh releases to both the heart and stomach. This may cause unfavorable side-effects in non-target organs. On the other hand, medetomidine activates cardiac vagal nerve without gastric vagal activation. Selective vagal activation of medetomidine may be beneficial for vagal activation therapy in the HF patients.

Fixing Hearts and Protecting Minds

Ischemic heart disease is a significant cause of mortality and morbidity in Western populations. Consistent with this, coronary artery bypass graft (CABG) surgery remains one of the most frequently performed major surgeries. Improved survival rates mean that our research focus now extends beyond surgical technique to include quality of postoperative outcome. Postoperative cognitive dysfunction (POCD) has emerged as one of the most challenging and hotly debated issues, with increasing impetus to answer the unresolved question: does fixing the heart come at a cost to the brain? CABG surgery is associated with neurological events including stroke in 1.6%1 and delirium in 5.8%2 of patients. Beyond these severe and marked alterations to neurological function, there has been a widely held belief that CABG surgery is associated with POCD, which may presage a decline toward dementia. Research has been influenced by the 1995 Consensus Statement3 into the study of POCD in patients undergoing CABG surgery. Although the methods of investigation set forth by the Consensus Statement achieved widespread acknowledgment, its specific recommendations have not always been followed.4 Despite significant methodological issues, it seems that the balance of interpretation has historically been in favor of CABG surgery as a cause of significant POCD. More recently, however, a review of a series of publications from a well-controlled longitudinal cohort study conducted at Johns Hopkins5 and a meta-analysis6 suggested that cognition is in fact stable or may even show some improvement after CABG surgery in the majority of patients, at least within the first year (Figures 1 and 2). There is little doubt that POCD affects some patients in the short term, but the pathophysiological mechanisms underlying this and the influence on longer-term cognitive function remain uncertain. For research to progress, we require a paradigmatic shift in our focus from …

Case Scenario: Hemodynamic Management of Postoperative Acute Kidney Injury

Case Scenario: Hemodynamic Management of Postoperative Acute Kidney Injury

The effect of induced hypotension on the perioperative bleeding and transfusion in the bipolar hemiarthroplasty of hip: retrospective study for four years

The effect of induced hypotension on the perioperative bleeding and transfusion in the bipolar hemiarthroplasty of hip: retrospective study for four years

Temporary Percutaneous Left Ventricular Support for Ablation of Untolerated Ventricular Tachycardias

Catheter ablation is increasingly recognized as an important option for the treatment of ventricular tachycardia (VT) in the serious clinical settings of frequent implantable cardioverter defibrillator shocks, and arrhythmia storms, in a variety of structural heart diseases.1 The high incidence of VTs that are not hemodynamically tolerated forces challenges to the traditional approaches of using activation and entrainment mapping to localize the ablation target area, in favor of a strategy of substrate modification that can be performed during sinus rhythm. In some patients, however, a clear target cannot be detected during sinus rhythm; this frequently occurs in some forms of nonischemic cardiomyopathies. More recently, interest is growing in the possibility of making VT tolerable through cardiopulmonary support. Article see p 1202 In this issue of Circulation: Arrythmia and Electrophysiology , Ostadal et al2 provide experimental data on the different capabilities offered by 3 commercially available support systems. It should be kept in mind, however, that these systems are Food and Drug Administration–approved only to support temporary high-risk situations. The data offered in this study are limited in that they provide only information related to systemic arterial pressure in healthy animals and do not allow any evaluation of the different levels of perfusion attained at individual critical organs, ie, brain or kidney. The study does, however, offer a comparative evaluation of the performances of these different systems and offers the opportunity to discuss advantages and limitation of their use. Percutaneous left ventricular assist devices (pLVAD) are increasingly used in few high-volume and skilled centers around the world in an attempt to achieve hemodynamic support during previously nontolerated ventricular arrhythmias to allow use of electrophysiological maneuvers to identify the critical isthmus of the circuit where an effective ablation will produce a permanent interruption of the VT. It is hoped that …