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Control of cerebral blood flow (CBF) is crucial to the management of neurocritically ill patients. Small studies which have examined the role of cardiac output (CO) as a determinant of CBF have inconsistently demonstrated evidence of cardio-cerebral coupling. Putative physiological mechanisms underpinning such coupling include changes in arterial blood pressure pulsatility, which would produce vasodilation through increased oscillatory wall-shear-stress and baroreceptor mediated reflex sympatholysis, and changes in venous backpressure which may improve cerebral perfusion pressure. We sought to summarize and contextualize the literature on the relationship between CO and CBF and discuss the implications of cardio-cerebral coupling for neurocritical care. A systematic review of the literature yielded 41 studies; all were of low-quality and at high-risk of bias. Results were heterogenous, with evidence for both corroboration and confutation of a relationship between CO and CBF in both normal and abnormal cerebrovascular states. Common limitations of studies were lack of instantaneous CBF measures with reliance on transcranial Doppler-derived blood flow velocity as a surrogate, inability to control for fluctuations in established determinants of CBF (eg, PaCO2), and direct effects on CBF by the interventions used to alter CO. Currently, the literature is insufficiently robust to confirm an independent relationship between CO and CBF. Hypothetically, the presence of cardio-cerebral coupling would have important implications for clinical practice. Manipulation of CBF could occur without the risks associated with extremes of arterial pressure, potentially improving therapy for those with cerebral ischemia of various etiologies. However, current literature is insufficiently robust to confirm an independent relationship between CO and CBF, and further studies with improved methodology are required before therapeutic interventions can be based on cardio-cerebral coupling.Copy

Background: Preterm infants undergoing intensive care often experience painful procedures such as heel lance for blood sampling. Knowledge of the cerebral hemodynamic response to painful stimuli contributes to understanding of cortical pain processing and the neurovascular network in the preterm brain. Previous research has demonstrated cerebral hemodynamic responses using near-infrared spectroscopy (NIRS) after noxious stimuli in infants appropriately grown for age (AGA). But this has not been studied in infants born small for gestational age after fetal growth restriction (FGR). FGR infants differ in brain development due to utero-placental insufficiency leading to the intrauterine growth restriction, and cerebral response to pain may be altered. Objective(s): We aimed to compare the cerebral hemodynamic response to painful stimuli (heel lance) in FGR and AGA infants. Method(s): Preterm FGR infants (n = 20) and AGA infants (n = 15) born at 28-32 weeks' gestation were studied at mean +/- SD postnatal age of 11.5 +/- 2.4 and 10.5 +/- 2.4 days, respectively. Infants had baseline echocardiographic assessment of ductus arteriosus and stroke volume. They were monitored with NIRS for changes in tissue oxygenation index (TOI, %), and oxygenated, deoxygenated, and total hemoglobin (DELTAO2Hb, DELTAHHb, and DELTATHb) in contralateral and ipsilateral cerebral hemispheres, during a heel lance. Result(s): At baseline, FGR infants had significantly lower TOI, higher heart rate, and lower stroke volume compared to AGA infants. Most infants in both groups showed increase in each of the NIRS parameters in the contralateral hemisphere following heel lance. However, more AGA infants (6/15) showed decreased DELTATHb compared to FGR infants (1/20) (p = 0.016). The magnitude of cerebral hemodynamic response and time to response did not differ between FGR and AGA infants. FGR infants showed larger DELTAO2Hb in the contralateral compared to ipsilateral cortex (p = 0.05). Conclusion(s): P

In this retrospective observational study performed in a high-volume hepatobiliary-pancreatic unit, we evaluated the effect of a surgery-specific goal-directed therapy (GDT) physiologic algorithm on complications and length of hospital stay. We compared patients who underwent pancreaticoduodenectomy with either a standardised Enhanced Recovery After Surgery program (usual care group), or a standardised Enhanced Recovery After Surgery program in combination with a surgery-specific cardiac output-guided algorithm (GDT group). We included 145 consecutive patients: 47 in the GDT group and 98 in the usual care group. Multivariable associations between GDT and lengths of stay and complications were investigated using negative binomial regression. Postoperative complications were common and occurred at similar frequencies amongst the GDT and usual care groups: 64% versus 68% respectively, P=0.71; odds ratio 0.82; (95% confidence interval 0.39-1.70). There were fewer cardiorespiratory complications in the GDT group. Median (interquartile range) length of hospital stay was ten days (8.0-14.0) in the GDT group compared to 13 days (8.8-21.3) in the usual care group, P=0.01. Median (interquartile range) total intraoperative fluid was 3,000 ml (2,050-4,175) in the GDT group compared to 4,500 ml (3,275-5,325) in the usual care group, P <0.0001; but by day one, the median (interquartile range) fluid balance was similar (1,198 ml [700-1,729] in the GDT group versus 977 ml [419-2,044] in the usual care group, P=0.96). Use of vasoactive medications was higher in the GDT group. In our patients undergoing pancreaticoduodenectomy, GDT was associated with restrictive intraoperative fluid intervention, fewer cardiorespiratory complications and a shorter hospital length of stay compared to usual care. However, we could not exclude an influence of surgical caseload, which we have previously found to be an important variable. We also could not relate the increased hospital length of stay to

Objective: Pentobarbital (PB) is a recommended euthanasia drug in doses of 2 to 10 g. Rapid onset of coma and cardio-respiratory arrest occur within 15 to 30 min. We report a case of severe pentobarbital deliberate self-poisoning with full recovery and serial blood concentrations. Case Report: A 45-year-old male, with a history of depression, purchased 10 g of pentobarbital (PB) powder over the Internet 2 years earlier. On the day of presentation, he told his mother 10 min after impulsively ingesting the powder mixed in water. She found him unresponsive and commenced CPR immediately. Within 30 min of the ingestion, EMS arrived and he was in PEA arrest. Advanced life-support and endotracheal intubation were instituted and cardiac output returned after 15 min. In the emergency department: P122/min, BP 117/69 on epinephrine infusion (100 mcg/min). He was hypotonic, hypothermic (33.8 degreeC), with fixed dilated pupils, and no brain stem reflexes. ECG and CT brain were unremarkable. Venous blood gas showed pH 7.02, pCO2 60 mmHg, Bic 15 mmol/L, lactate 11.9 mmol/L. Asingle-dose of activated charcoal was administered and he was admitted to ICU. He developed diabetes insipidus on day 1 treated with DDAVP and required epinephrine infusion for 5 days to support BP. He remained comatose without any supplemental sedation, with absent brain stem reflexes until day 8.Afour-vessel cerebral angiogram on day 3 was normal. He was extubated on day 10. Serum PB concentration 2.5 h post-ingestion was 112 mg/L (therapeutic 1.8-4.7 mg/L), peaking at 116 mg/L, 29 h. PB concentration fell slowly over the next 10 days: 110 mg/L at 42 h, 65 mg/L at 90 h, 20 mg/L at 140 h, 2 mg/L at 190 h. Elimination half-life varied: initially 76 h (42-90 h), then 29 h (90-140 h), and finally 15 h (140-190 h). The patient made a full recovery and confirmed taking pentobarbital 10 g. Conclusion(s): Average PB concentration in fatalities is reported, as 30- 40 mg/L. Previous reports of survival after massive

Background: The best strategy to identify patients in whom fluid loading increases cardiac output (CO) following cardiac surgery remains debated. This study examined the utility of a calculated mean systemic filling pressure analogue (Pmsa) and derived variables to explain the response to a fluid bolus. Method(s): The Pmsa was calculated using retrospective, observational cohort data in the early postoperative period between admission to the intensive care unit and extubation within 6 hours. The venous return pressure gradient (VRdP) was calculated as Pmsa - central venous pressure. Concurrent changes induced by a fluid bolus in the ratio of the VRdP over Pmsa, the volume efficiency (Evol), were studied to assess fluid responsiveness. Changes between Pmsa and derived variables and CO were analysed by Wilcoxon rank-sum test, hierarchial clustering and multiple linear regression. Result(s): Data were analysed for 235 patients who received 489 fluid boluses. The Pmsa increased with consecutive fluid boluses (median difference [range] 1.3 [0.5-2.4] mm Hg, P =.03) with a corresponding increase in VRdP (median difference 0.4 [0.2-0.6] mm Hg, P =.04). Hierarchical cluster analysis only identified Evol and the change in CO within one cluster. The multiple linear regression between Pmsa and its derived variables and the change in CO (overall r2 =.48, P <.001) demonstrated the best partial regression between the continuous change in CO and the concurrent Evol (r =.55, P <.001). Conclusion(s): The mean systemic filling Pmsa enabled a comprehensive interpretation of fluid responsiveness with volume efficiency useful to explain the change in CO as a continuous phenomenon.Copyright © 2020 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd

Objective- The objective of this study was to investigate the effect of intravenous maternal sildenafil citrate (SC) administration on vascular function in growth-restricted fetal sheep. Approach and Results- Fetal growth restriction (FGR) results in cardiovascular adaptations that redistribute cardiac output to optimize suboptimal intrauterine conditions. These adaptations result in structural and functional cardiovascular changes, which may underlie postnatal neurological and cardiovascular sequelae. Evidence suggests SC, a potent vasodilator, may improve FGR. In contrast, recent clinical evidence suggests potential for adverse fetal consequence. Currently, there is limited data on SC effects in the developing fetus. We hypothesized that SC in utero would improve vascular development and function in an ovine model of FGR. Preterm lambs (0.6 gestation) underwent sterile surgery for single umbilical artery ligation or sham (control, appropriately grown) surgery to replicate FGR. Ewes received continuous intravenous SC (36 mg/24 h) or saline from surgery until 0.83 gestation. Fetuses were delivered and immediately euthanized for collection of femoral and middle cerebral artery vessels. Vessel function was assessed via in vitro wire myography. SC exacerbated growth restriction in growth-restricted fetuses and resulted in endothelial dysfunction in the cerebral and femoral vasculature, irrespective of growth status. Dysfunction in the cerebral circulation is endothelial, whereas smooth muscle in the periphery is the origin of the deficit. Conclusions- SC crosses the placenta and alters key fetal vascular development. Extensive studies are required to investigate the effects of SC on fetal development to address safety before additional use of SC as a treatment.

Background: SSC increases physiological stability, reduces bradycardias and desaturations and lowers heart rate variability in preterm infants. This study assessed the impact of SSC on circulatory physiology and organ blood flow. Method(s): Forty self-ventilating infants between 28-36 weeks corrected gestational age (GA) were assessed for cardiac performance and cerebral blood flow by echocardiography within 2 hours prior to SSC and then after 60 minutes of having SSC (while still on parent). Result(s): GA and birthweight of the cohort was 30.5 +/- 0.6 weeks' and 1378 +/- 133 g, respectively. Assessments were done at age 12 (9, 25) days (median (IQR). Significant increases in right ventricular global and longitudinal function was noted (Table 1). This coincided with a reduction in surrogate of pulmonary vascular resistance. On the systemic side, increased cardiac output accompanied ' cerebral blood flow and # middle cerebral artery resistive index (0.81 +/- 0.02 vs 0.74 +/- 0.02, p = 0.0001). Conclusion(s): The findings align with previously documented physiological benefits in cardiorespiratory stability and cardiac rhythm, and could be mediated through modulation of the autonomic nervous system.

Objectives: To ascertain the impact of skin-to-skin care between parents and infants on cardiac function and cerebral blood flow in preterm infants. Study design: We undertook a prospective study of 40 self-ventilating preterm infants at a quaternary center and assessed cardiac performance and cerebral blood flow. Assessments were carried out two hours before skin-to-skin care and then 60 minutes after skin-to-skin care (with the infant still on parent and turned supine). Result(s): Infants were 30.5 +/- 0.6 weeks' gestational age and 1378 +/- 133 g birthweight. Axillary temperature noted a nonsignificant increase during skin-to-skin care from 36.7 +/- 0.07degreeC to 36.9 +/- 0.07degreeC (P =.07). Cardiac contractility (right ventricular fractional area change [26.5% +/- 0.3% vs 27.8% +/- 0.4; P <.001] and tricuspid annular plane systolic excursion [0.73 +/- 0.03 cm vs 0.77 +/- 0.03 cm; P =.02]) increased significantly, coincident with decreased measures of pulmonary vascular resistance. An increase in systemic cardiac output was associated with increased cerebral blood flow and reduced middle cerebral artery resistive index (0.81 +/- 0.02 vs 0.74 +/- 0.02; P =.0001). Conclusion(s): We documented a significant circulatory beneficial adaptation to a common neonatal practice. These findings align with previously documented physiologic benefits in cardiorespiratory stability and cardiac rhythm in preterm infants, and may be mediated through modulation of the autonomic nervous system.Copyright © 2020 Elsevier Inc.

Background: Expansion of the intravascular compartment is common to treat haemodynamic instability in ICU patients. The most useful and accurate variables to guide and evaluate a fluid challenge remain debated and incompletely investigated resulting in significant variability in practice. The analogue mean systemic pressure has been reported as a measure of the intravascular volume state. Method(s): This is a protocol and statistical analysis plan for a review of the application of an analogue of the mean systemic pressure and the use of derived variables to assess the volume state and volume responsiveness. A pulmonary artery catheter was used in 286 postoperative cardiac surgical patients to monitor cardiac output before and after a fluid bolus in addition to arterial and central venous pressures. With otherwise similar monitoring, echocardiography was used in 540 general ICU patients to determine cardiac outputs and indices related to intravascular filling. The responses to a fluid bolus or the passive leg raising manoeuvre will be investigated using continuous and dichotomous definitions of volume responsiveness. The results will be stratified according to the method of monitoring cardiac output. Conclusion(s): This study investigating 2 cohorts that encompass a wide variety of reasons for haemodynamic instability will illustrate the applicability of the analogue mean systemic pressure and derived variables to assess the volume state and responsiveness. The results may guide the rationale and design of interventional studies.Copyright © 2019 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd

Acute ST elevation myocardial infarction (STEMI) is a very rare complication post orthotopic heart transplantation. There are only limited data regarding pathophysiological mechanisms and early occurrence of STEMI in heart transplant recipients. Background(s): We describe a 45-year-old Caucasian man with severe dilated cardiomyopathy, on approximately nine months left ventricular assist device (LVAD), and a temporary right ventricular assist device (RVAD) as a bridge to cardiac transplantation. He received the organ from a 48-year-old male with no cardiac risk factors. The donor's heart had normal left ventricular (LV) ejection fraction, accordingly the presence of coronary heart disease was not tested before transplantation. The total ischaemic time was about 210 minutes. On day one post operation, he suffered left leg compartment syndrome requiring urgent fasciotomy 48 hours post-transplant, he developed a progressive reduction of cardiac output and the incremental need for inotropic support. Electrocardiogram revealed inferolateral ST elevations associated with raised troponin I (93ug/L) and echocardiogram showed severe LV dysfunction with inferolateral and inferior wall akinesia. Result(s): Percutaneous coronary intervention (PCI) and drug eluting stent insertion in the left circumflex coronary artery was successfully performed. (Fig. 1) Subsequent endomyocardial biopsy showed International Society for Heart and Lung Transplantation grade 0R and he survived after a prolonged hospital admission with minor clinical sequelae. [Figure Presented] Conclusion(s): In reviewing the pathophysiology of this case, several reasons for thrombosis were postulated including acute organ rejection, haemostasis imbalance due to Systemic inflammation, immunosuppressive therapy. This case highlights the rarity but the significant early occurrence of STEMI in transplant recipients manifesting as changes in haemody-namic status.

Advances in neonatal care have improved the survival rates of preterm infants, however, the likelihood of brain injury and neurodevelopmental disability remains a significant problem. Whilst the etiology of preterm brain injury is complex, impairments in the cardio- and cerebro-vascular function have been implicated. During infancy, sleep is vital for brain development. However, instabilities in cardio- and cerebro-vascular function are most marked during sleep. Sleeping position is an important part of a safe sleeping environment. Prone sleeping increases the risk of sudden infant death syndrome and is associated with reduced blood pressure, cerebral oxygenation and impaired autonomic cardiovascular control in infants born at term. Importantly, these effects are amplified by preterm birth. Hospitalized preterm infants are often slept in the prone position to improve respiratory function. However, there is little consensus regarding the sustained benefits of prone sleeping in this population. In light of the impaired cardio- and cerebro-vascular function during prone sleeping in term and preterm infants after hospital discharge, the likely adverse effects of prone sleeping in hospitalized preterm infants are concerning. This review examines the cardiovascular and cerebrovascular effects of prone sleeping in infants born at term, those born preterm after term equivalent age and whilst hospitalized.Copyright © 2017 Elsevier Ltd

Background: Intra-uterine growth restriction (IUGR) alters cardiac structure and function, but how these changes develop throughout early life is unknown. Moreover, IUGR often leads to prematurity, which is an independent risk factor for cardiovascular disease. Studies disentangling the roles of IUGR and preterm birth are scarce. We aimed to investigate the effects of IUGR and prematurity on the structural and functional properties of the heart during early infancy. Method(s): Echocardiography was performed on 22 preterm IUGR infants and 20 preterm and 17 term appropriately-grownfor- gestational-age infants (pAGA, tAGA, respectively). Preterm infants were studied on postnatal day 1, and all groups were studied at 4 weeks and 6 months post-term age. Result(s): IUGR infants demonstrated increased cardiac sphericity compared to AGA peers on post-natal day 1 (IUGR 0.54 +/- 0.04 vs. pAGA 0.45 +/- 0.03, P<0.05) and at 4 weeks post-term age (IUGR 0.44 +/- 0.02 vs. pAGA 0.37 +/- 0.02 and tAGA 0.38 +/-0.01, P<0.05). Relative wall thickness increased over time in the IUGR group only (P<0.05). No differences were found in myocardial performance index, cardiac output and fractional shortening. E/E' ratio (reflecting diastolic dysfunction) was higher in the preterm groups than the term group at 4 weeks (IUGR 9.8 +/- 0.5 and pAGA 11.3 +/- 1.5 vs. tAGA 7.8 +/- 0.5, P<0.01) and 6months post-term age (IUGR 9.0 +/- 0.8 and pAGA 8.0 +/- 0.5 vs. tAGA 6.8 +/- 0.4, P<0.05). Conclusion(s): IUGR was associated with subtle cardiac structural changes, whereas prematurity was associated with subclinical alterations in diastolic function. These early changes observed within these populations may underpin their increased risk of cardiovascular disease later in life.

Purpose This pilot study aimed to characterise the haemodynamic effect of 1L of IV normal saline (NS) administered as a rapid versus slow infusion on cardiac output (CO), heart rate (HR), systemic blood pressures, and carotid blood flow in six healthy volunteers. Materials and methods Six healthy male volunteers aged 18-65 years were randomized to receive 1L NS given over 30 min or 120 min. On a subsequent study session the alternate fluid regimen was administered. Haemodynamic data was gathered using a non-invasive finger arterial pressure monitor (Nexfin), echocardiography and carotid duplex sonography. Time to micturition and urine volume was also assessed. Results Compared to baseline, rapid infusion of 1 L of saline over 30 min produced a fall in Nexfin-measured CO by 0.62 L/min (p < 0.001), whereas there was a marginal but significant increase during infusion of 1L NS over 120 min of 0.02 L/min (p < 0.001). This effect was mirrored by changes in HR and blood pressure (BP) (p < 0.001). There were no significant changes in carotid blood flow, time to micturition, or urine volume produced. Conclusions Slower infusion of 1L NS in healthy male volunteers produced a greater increase in CO, HR and BP than rapid infusion.Copyright © 2017

Purpose of review Central venous pressure (CVP) alone has so far not found a place in outcome prediction or prediction of fluid responsiveness. Improved understanding of the interaction between mean systemic pressure (Pms) and CVP has major implications for evaluating volume responsiveness, heart performance and potentially patient outcomes. Recent findings The literature review substantiates that CVP plays a decisive role in causation of operative haemorrhage and renal failure. The review details CVP as a variable integral to cardiovascular control in its dual role of distending the diastolic right ventricle and opposing venous return. Summary The implication for practice is in the regulation of the circulation. It is demonstrated that control of the blood pressure and cardiac output/venous return calls upon regulation of the volume state (Pms), the heart performance (Eh) and the systemic vascular resistance. Knowledge of the CVP is required to calculate allthree.© Copyright 2016 Wolters Kluwer Health, Inc. All rights reserved.

Background:Cardiovascular dysfunction at birth may underlie poor outcomes after fetal growth restriction (FGR) in neonates. We compared the cardiovascular transition between FGR and appropriately grown (AG) preterm lambs and examined possible mechanisms underlying any cardiovascular dysfunction in FGR lambs. Method(s):FGR was induced in ewes bearing twins at 0.7 gestation; the twin was used as an internal control (AG). At 0.8 gestation, lambs were delivered and either euthanized with their arteries isolated for in vitro wire myography, or ventilated for 2 h. At 60 min, inhaled nitric oxide (iNO) was administered in a subgroup for 30 min. Molecular assessment of the nitric oxide (NO) pathway within lung tissue was conducted. Result(s):FGR lambs had lower left ventricular output and cerebral blood flow (CBF) and higher systemic vascular resistance compared with AG lambs. INO administration to FGR lambs rapidly improved cardiovascular and systemic hemodynamics but resulted in decreased CBF in AG lambs. Isolated arteries from FGR lambs showed impaired sensitivity to NO donors, but enhanced vasodilation to Sildenafil and Sodium nitroprusside, and altered expression of components of the NO pathway. Conclusion(s):Cardiovascular dysfunction at birth may underlie the increased morbidity and mortality observed in preterm FGR newborns. Impaired NO signaling likely underlies the abnormal vascular reactivity.Copyright © 2016 International Pediatric Research Foundation, Inc.

Extracardiac constraint and sensitivity to arterial pressure may be critical factors that limit the functional reserves of the developing fetal heart in utero. We hypothesise that extracardiac constraint is the predominant factor that limits fetal stroke volume (SV). To test this hypothesis we studied six chronically instrumented fetal sheep to determine the relative roles that extracardiac constraint and arterial pressure play in determining left ventricular (LV) function. Pregnant ewes (128-131 days gestation, term = 147 days) were anaesthetised (5 mg kg-1 Propofol I.V., then 1.5 % halothane, 50 % O2, balance N2O by inhalation) and instrumented using sterile surgical techniques to record LV end-diastolic pressure (Plved), aortic pressure (Pao), pericardial pressure (Pper), and LV SV. After a minimum of 72 h recovery, LV function was assessed by altering fetal blood volume to vary Plved. Ventricular function curves were generated using two measures of ventricular function, SV and stroke work index (SWI = SV xPao), and two measures of ventricular filling, Plved and LV end-diastolic transmural pressure (Plved,tm=Plved - Pper). Although decreasing Plved from the resting level decreased SV, increasing Plved from the resting level did not increase SV because the ventricular function curve plateaued. This plateau was not explained solely by an increase in aortic pressure, as the plateau remained present in the SWI versus Plved curve. When extracardiac constraint was accounted for (SV against Plved,tm), the plateau was largely eliminated (=80 %). The remaining portion of the plateau (=20 %) was eliminated when both extracardiac constraint and arterial pressure were accounted for (SWI versus Plved,tm). Thus, the major limitation upon LV function in the near-term fetus results from extracardiac constraint limiting ventricular filling while, at the same time, a much smaller limitation arises from increasing arterial pressure.Copyright © 2001 The Journal of Physiology.

Background & Objectives: The administration of crystalloid fluid therapy for resuscitation, to restore euvolaemia, and/or improve cardiac output (CO) is perhaps the most frequent therapeutic intervention in medicine. Several studies based on mathematical modelling of volume kinetics have suggested that the effect of a fixed volume of intravenous fluid varies considerably with baseline hydration state, rate of fluid infusion and the presence or absence of anaesthesia.[i],[ii],[iii] It has been demonstrated that the degree of plasma expansion produced by the same volume of IV crystalloid is greater with a lower rate of infusion, and more prolonged with longer duration of infusion.[ii] This pilot study aims to characterize the effect of 1L of IV normal saline (NS) administered in a bolus versus continuous infusion on CO, heart rate (HR), and systemic blood pressures in 7 healthy volunteers. We hypothesize that an infusion of 1L of NS given over 120 minutes will produce a more sustained increase in CO when compared to a rapid bolus given over 30 minutes. Material(s) and Method(s): Seven healthy male volunteers between aged 18-65 years participated in 2 experiments each on separate days where 1L NS was given either over 30min or 120min. Haemodynamic data was gathered using a non-invasive finger arterial pressure monitor. Result(s): When compared to baseline, rapid infusion of 1L of saline over 30 min produced a fall in CO by 0.62L/min (p<0.0001), whereas there was a marginal but significant increase in CO during infusion of 1L NS over 120min of 0.02L/min (p<0.0001). The difference in CO between the groups was also significant with a higher CO seen in the infusion group (p<0.0001) (Figure 1). This effect was mirrored by changes in systolic blood pressure (SBP) measurements for each group (p<0.0001). Conclusion(s): Continuous infusion of 1L NS in healthy male volunteers produced a greater increase in both SBP and CO than rapid infusion, which produced a paradoxical fall in

Management of cardiovascular instability resulting from calcium channel antagonist (CCB) or beta-adrenergic receptor antagonist (BB) poisoning follows similar principles. Significant myocardial depression, bradycardia and hypotension result in both cases. CCBs can also produce vasodilatory shock. Additionally, CCBs, such as verapamil and diltiazem, are commonly ingested in sustained-release formulations. This can also be the case for some BBs. Peak toxicity can be delayed by several hours. Provision of early gastrointestinal decontamination with activated charcoal and whole-bowel irrigation might mitigate this. Treatment of shock requires a multimodal approach to inotropic therapy that can be guided by echocardiographic or invasive haemodynamic assessment of myocardial function. High-dose insulin euglycaemia is commonly recommended as a first-line treatment in these poisonings, to improve myocardial contractility, and should be instituted early when myocardial dysfunction is suspected. Catecholamine infusions are complementary to this therapy for both inotropic and chronotropic support. Catecholamine vasopressors and vasopressin are used in the treatment of vasodilatory shock. Optimizing serum calcium concentration can confer some benefit to improving myocardial function and vascular tone after CCB poisoning. High-dose glucagon infusions have provided moderate chronotropic and inotropic benefits in BB poisoning. Phosphodiesterase inhibitors and levosimendan have positive inotropic effects but also produce peripheral vasodilation, which can limit blood pressure improvement. In cases of severe cardiogenic shock and/or cardiac arrest post-poisoning, extracorporeal cardiac assist devices have resulted in successful recovery. Other treatments used in refractory hypotension include intravenous lipid emulsion for lipophilic CCB and BB poisoning and methylene blue for refractory vasodilatory shock.Copyright © 2015 The British Pharmacological Society.

1 Five lambs (19-27 days old) were studied to determine the effects of feeding on cardiorespiratory function. 2 Each lamb was instrumented to record cardiac output, aortic and pulmonary artery pressure and arterial and mixed venous oxyhaemoglobin saturations (Sa,O2 and Sv,O2). 3 During feeding, arterial haemoglobin desaturated and resaturated sequentially during the periods of sucking and non-sucking. The nadir of these Sa,O2 desaturations (83 +/- 2%, mean +/-s.e.m.) was significantly lower than the baseline value (92 +/- 2%, P<= 0.05, ANOVA). Sa,O2 returned to the baseline level between periods of sucking. Sv,O2 also decreased (55 +/- 3% baseline, 46 +/- 3% sucking, P<= 0.05) but, in contrast to Sa,O2, it remained significantly lower than baseline levels in the pauses between periods of sucking. 4 Arterial pressure increased during feeding (94 +/- 4 mmHg baseline, 113 +/- 6 mmHg feeding, P<= 0.05), while heart rate and cardiac index did not change. 5 Total body oxygen consumption rose during the pauses between sucking periods (10.9 +/- 1.1 ml O2 min-1 kg-1 baseline, 13.9 +/- 1.2 ml O2 min-1 kg-1 non-sucking, P<= 0.05) and was provided for by a significant increase in total body oxygen extraction as systemic oxygen transport was unchanged. 6 Our results reveal that during feeding in young lambs oxygen consumption increases and body stores of oxygen (e.g. Sv,O2) become depleted; this combination may promote rapid arterial desaturation and cyanosis during feeding.Copyright © 1997 The Physiological Society.

Introduction. Transpulmonary thermodilution (TD) is the most used method for cardiac output (CO) monitoring during cardiac surgery. Although 2D transoesophageal (TOE) measurement of CO using spectral Doppler correlates with TD, 3D TOE more accurately measures left ventricular outflow tract (LVOT) and aortic valve (AV) area, which are used to calculate CO. The aim of this study is to compare the precision of CO measurement between 2D and 3D TOE against TD. Method. After ethics approval, 50 patients aged over 18 years scheduled for on-bypass cardiac surgery were recruited prospectively at two institutions. Exclusion criteria included more than mild valvular regurgitation, and atrial fibrillation. CO was measured simultaneously by TD and TOE before sternotomy and after cardiopulmonary bypass. CO was calculated using TOE by the product of either the LVOT or AV area, the velocity-time integral (VTI) of flow at the same site and heart rate. The LVOT area was assumed circular and calculated using the LVOT diameter for 2D but with planimetry using 3D TOE. The AV area was estimated with planimetry by both 2D and 3D TOE, and VTI with continuous wave Doppler. Both modal and outer edge traces of LVOT VTI were performed with the cursor 0.5 cm from the annulus. Measurements were averaged from 3 consecutive beats by 2 observers. Deming model II regression was used to assess fixed and proportional bias of agreement with TD. Bland-Altman technique was used to assess closeness of fit. Results. CO was measured at 94 time-points (50 before sternotomy, 44 after chest closure) in 50 patients. The 3D methods had better agreement than 2D with TD, with the best agreement with 3D planimetry of the AV (bias -0.04 Lmin-1, SD of difference between the mean 1.37 Lmin-1), followed by 3D LVOT area planimetry (0.14, 1.41), 2D AV area planimetry (0.28, 1.3) and 2D LVOT VTI outer edge trace (-0.59, 1.29). 3D LVOT area planimetry had the best correlation (slope 1.39, 95%CI 0.97-1.82), followed by 2D A

Purpose: To evaluate an analogue of mean systemic filling pressure (Pmsa) and derived variables to quantitatively assess the effectiveness of volume expansion in increasing cardiac output. Methods: Sixty-one cardiac post-surgical patients were studied and 107 fluid boluses were captured. Cardiac output, mean arterial pressure and right atrial pressure were recorded with Pmsa before and after a bolus fluid. An increase in cardiac output greater than 10 % following a fluid bolus defined a patient as a responder. Cardiac power (i.e. the product of arterial pressure and cardiac output) and Pmsa to right atrial pressure gradient (i.e. the driving pressure for venous return and hence cardiac output) were evaluated to assess the efficiency of volume expansion to increase cardiac output. Cardiac power relative to Pmsa (CPvol), its dynamic changes and the dynamic changes in Pmsa-right atrial pressure gradient relative to the Pmsa change (Evol) were investigated. Results: CPvol was lower and Evol was higher in responders vs. non-responders. Furthermore, in patients receiving a second fluid bolus, Evol correlated with the degree of increase in cardiac output. Multivariate regression analysis identified both CPvol and Evol as independent variables associated with volume responsiveness. Conclusions: Using an algorithm to derive a mean systemic filling pressure analogue, cardiac power and dynamic measures of the venous return pressure gradient relative to the mean systemic filling pressure provided an assessment of the efficiency of volume expansion in post-surgical cardiac patients.Copyright © 2014, Springer-Verlag Berlin Heidelberg and ESICM.

Previous studies suggest that high airway pressure may compromise cardiac output. We investigated the effect of 3 nasal continuous positive airway pressure levels on cardiac output in preterm infants with evolving chronic lung disease. We found that brief changes in continuous positive airway pressure did not affect cardiac output.Copyright © 2015 Elsevier Inc.

Background The place of central venous pressure (CVP) measurement in acute care has been questioned during the past decade. We reviewed its physiological importance, utility and clinical use among anaesthetists and intensivists. Methods A literature search using the PubMed, Cochrane, Scopus and Web of Science databases was performed in regard to details of the physiology, measurement and interpretation of CVP. A questionnaire was conducted among members of the European Society of Intensive Care Medicine concerning knowledge and uses of CVP. Results Aligning pressure transducers to the phlebostatic axis was handled inadequately. The unsuitability of CVP to assess the intravascular volume state was generally recognised by clinicians. Still, many used CVP to guide volume resuscitation in the absence of a cardiac output monitor, while the literature positioned CVP as a useful haemodynamic variable only in the expanded context of being one determinant of the driving pressure for venous return and hence cardiac output. Conclusion The correct measurement of CVP is pivotal to its proper clinical application. This relates to defining the pressure gradient for venous return and heart efficiency. The clinical appreciation of CVP should be restored by educational efforts of its physiological context.Copyright © 2015 The Acta Anaesthesiologica Scandinavica Foundation. Published by John Wiley & Sons Ltd.

Aim: Arteriovenous fistula-formation remains critical for the provision of hemodialysis in end-stage renal failure patients. Its creation results in a significant increase in cardiac output, with resultant alterations in cardiac stroke volume, systemic blood flow, and vascular resistance. The impact of fistula-formation on cardiac and vascular structure and function has not yet been evaluated via "gold standard" imaging techniques in the modern era of end-stage renal failure care. Methods: A total of 24 patients with stage 5 chronic kidney disease undergoing fistula-creation were studied in a single-arm pilot study. Cardiovascular magnetic resonance imaging was undertaken at baseline, and prior to and 6 months following fistula-creation. This gold standard imaging modality was used to evaluate, via standard brachial flow-mediated techniques, cardiac structure and function, aortic distensibility, and endothelial function. Results: At follow up, left ventricular ejection fraction remained unchanged, while mean cardiac output increased by 25.0% (P<0.0001). Significant increases in left and right ventricular end-systolic volumes (21% [P=0.014] and 18% [P<0.01]), left and right atrial area (11% [P<0.01] and 9% [P<0.01]), and left ventricular mass were observed (12.7% increase) (P<0.01). Endothelial-dependent vasodilation was significantly decreased at follow up (9.0%+/-9% vs 3.0%+/-6%) (P=0.01). No significant change in aortic distensibility was identified. Conclusion: In patients with end-stage renal failure, fistula-formation is associated with an increase in cardiac output, dilation of all cardiac chambers and deterioration in endothelial function.Copyright © 2014 Dundon et al.