scholarly journals Fractional spinal anesthesia and systemic hemodynamics in frail elderly hip fracture patients

Author(s):  
Fredrik Olsen ◽  
Mathias Hård af Segerstad ◽  
Keti Dalla ◽  
Sven-Erik Ricksten ◽  
Bengt Nellgård

Abstract Background: Aging and frailty make the elderly patients susceptible to hypotension following spinal anesthesia. The systemic hemodynamic effects of spinal anesthesia are not well known. In this study, we examine the systemic hemodynamic effects of fractional spinal anesthesia following intermittent microdosing of a local anesthetic and an opioid.Methods: We included 15 patients aged over 65 with considerable comorbidities, planned for emergency hip fracture repair. Patients received a spinal catheter and cardiac output monitoring using the LiDCOplus system. Invasive mean arterial pressure (MAP), cardiac index, systemic vascular resistance index, heart rate and stroke volume index were registered. Two doses of bupivacaine 2.25 mg and fentanyl 15µg were administered with 25 minutes in between. Hypotension was defined as a fall in MAP by >30% or a MAP <65 mmHgResults: The incidence of hypotension was 30%. Hypotensive patients (n=5) were treated with low doses of norepinephrine (0.003-0.12 µg/kg/min). MAP showed a maximum reduction of 17% at 10 minutes after the first dose. Cardiac index, systemic vascular resistance index and stroke volume index decreased by 10%, 6%, and 7%, respectively, while heart rate was unchanged over time. After the first dose, none of the systemic haemodynamic variables were affected.Conclusion: Fractional spinal anesthesia causes a low incidence of hypotension, induced mainly by a systemic venodilation, causing a decrease in venous return and fall in cardiac output. Our results show that fractional spinal anesthesia is a safe technique from a hemodynamic point of view and is probably underutilized in high-risk, elderly hip fracture patients

2015 ◽  
Vol 101 (2) ◽  
pp. 166-171 ◽  
Author(s):  
Jonathan A Silverman ◽  
Yamikani Chimalizeni ◽  
Stephen E Hawes ◽  
Elizabeth R Wolf ◽  
Maneesh Batra ◽  
...  

ObjectiveCardiac dysfunction may contribute to high mortality in severely malnourished children. Our objective was to assess the effect of malnutrition on cardiac function in hospitalised African children.DesignProspective cross-sectional study.SettingPublic referral hospital in Blantyre, Malawi.PatientsWe enrolled 272 stable, hospitalised children ages 6–59 months, with and without WHO-defined severe acute malnutrition.Main outcome measuresCardiac index, heart rate, mean arterial pressure, stroke volume index and systemic vascular resistance index were measured by the ultrasound cardiac output monitor (USCOM, New South Wales, Australia). We used linear regression with generalised estimating equations controlling for age, sex and anaemia.ResultsOur primary outcome, cardiac index, was similar between those with and without severe malnutrition: difference=0.22 L/min/m2 (95% CI −0.08 to 0.51). No difference was found in heart rate or stroke volume index. However, mean arterial pressure and systemic vascular resistance index were lower in children with severe malnutrition: difference=−8.6 mm Hg (95% CI −12.7 to −4.6) and difference=−200 dyne s/cm5/m2 (95% CI −320 to −80), respectively.ConclusionsIn this largest study to date, we found no significant difference in cardiac function between hospitalised children with and without severe acute malnutrition. Further study is needed to determine if cardiac function is diminished in unstable malnourished children.


Author(s):  
Bernd Saugel ◽  
Elisa-Johanna Bebert ◽  
Luisa Briesenick ◽  
Phillip Hoppe ◽  
Gillis Greiwe ◽  
...  

AbstractIt remains unclear whether reduced myocardial contractility, venous dilation with decreased venous return, or arterial dilation with reduced systemic vascular resistance contribute most to hypotension after induction of general anesthesia. We sought to assess the relative contribution of various hemodynamic mechanisms to hypotension after induction of general anesthesia with sufentanil, propofol, and rocuronium. In this prospective observational study, we continuously recorded hemodynamic variables during anesthetic induction using a finger-cuff method in 92 non-cardiac surgery patients. After sufentanil administration, there was no clinically important change in arterial pressure, but heart rate increased from baseline by 11 (99.89% confidence interval: 7 to 16) bpm (P < 0.001). After administration of propofol, mean arterial pressure decreased by 23 (17 to 28) mmHg and systemic vascular resistance index decreased by 565 (419 to 712) dyn*s*cm−5*m2 (P values < 0.001). Mean arterial pressure was < 65 mmHg in 27 patients (29%). After propofol administration, heart rate returned to baseline, and stroke volume index and cardiac index remained stable. After tracheal intubation, there were no clinically important differences compared to baseline in heart rate, stroke volume index, and cardiac index, but arterial pressure and systemic vascular resistance index remained markedly decreased. Anesthetic induction with sufentanil, propofol, and rocuronium reduced arterial pressure and systemic vascular resistance index. Heart rate, stroke volume index, and cardiac index remained stable. Post-induction hypotension therefore appears to result from arterial dilation with reduced systemic vascular resistance rather than venous dilation or reduced myocardial contractility.


2021 ◽  
Vol 74 (8) ◽  
pp. 1809-1815
Author(s):  
Ulbolhan A. Fesenko ◽  
Ivan Myhal

The aim of the study was to analyze cardiac function during Nuss procedure under the combination of general anesthesia with different variants of the regional block. Materials and methods: The observative prospective study included 60 adolescents (boys/girls=47/13) undergone Nuss procedure for pectus excavatum correction under the combination of general anaesthesia and regional blocks. The patients were randomized into three groups (n=20 in each) according to the perioperative regional analgesia technique: standart epidural anaesthesia (SEA), high epidural anaesthesia (HEA) and bilateral paravertebral anaesthesia (PVA). The following parameters of cardiac function were analyzed: heart rate, estimated cardiac output (esCCO), cardiac index (esCCI), stroke volume (esSV) and stroke volume index (esSVI) using non-invasive monitoring. Results: Induction of anesthesia and regional blocks led to a significant decrease in esCCO (-9.4%) and esCCI (-9.8%), while esSV and esSVI remained almost unchanged in all groups (H=4.9; p=0.09). At this stage, the decrease in cardiac output was mainly due to decreased heart rate. At the stage of sternal elevation we found an increase in esSV, which was more pronounced in the groups of epidural blocks (+23.1% in HEA and +18.5% in SEA). After awakening from anesthesia and tracheal extubation esSV was by 11% higher than before surgery without ingergroup difference. Conclusions: The Nuss procedure for pectus excavatum correction lead to improved cardiac function. increase in stroke volume and its index were more informative than cardiac output and cardiac index which are dependent on heart rate that is under the influence of anaesthesia technique.


1992 ◽  
Vol 73 (1) ◽  
pp. 324-328 ◽  
Author(s):  
J. Meyer ◽  
L. D. Traber ◽  
S. Nelson ◽  
C. W. Lentz ◽  
H. Nakazawa ◽  
...  

Septic shock is characterized by an increase in cardiac output and a fall in systemic vascular resistance index and mean arterial pressure. Endotoxin alters the smooth muscle function of blood vessels, probably by means of an increased production of the potent vasodilator nitric oxide (NO). The present study was accomplished to determine how the inhibition of NO synthesis influences cardiovascular performance in an ovine model of hyperdynamic endotoxemia. Endotoxemia was induced in five range ewes (41 +/- 2 kg) by continuous infusion of Escherichia coli endotoxin (LPS, 10 ng.kg-1.min-1) over the entire study period. After 24 h of LPS infusion, cardiac output increased from 5.2 +/- 0.3 to 7.9 +/- 0.6 (SE) 1/min (P less than 0.05) and mean arterial pressure and systemic vascular resistance index fell from 92 +/- 5 to 79 +/- 6 mmHg (P = 0.08) and from 1,473 +/- 173 to 824 +/- 108 dyn.s.cm-5.m2 (P less than 0.05), respectively. The pulmonary shunt fraction increased from 0.23 +/- 0.03 to 0.32 +/- 0.03 (P less than 0.05). The intravenous administration of the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (25 mg/kg) 24 h after the start of the LPS infusion changed these values to approximately baseline levels over the subsequent 4 h. Although N omega-nitro-L-arginine methyl ester increased pulmonary arterial pressure and pulmonary vascular resistance (P less than 0.05), right and left ventricular stroke volume index showed no significant changes. It is concluded that NO has a major function in cardiovascular performance in endotoxemia.(ABSTRACT TRUNCATED AT 250 WORDS)


1964 ◽  
Vol 207 (4) ◽  
pp. 753-758 ◽  
Author(s):  
Gerald Glick ◽  
William H. Plauth ◽  
Eugene Braunwald

The generally held view that acute hypoxia stimulates the cardiovascular system was reinvestigated in ten normal, trained, unanesthetized dogs and in six dogs which had previously been subjected to total cardiac denervation. In the normal dogs, no significant or consistent changes were noted in cardiac output, stroke volume index, or in systemic arterial pressure 5 and 15 min after the onset of 8% O2 inhalation. Heart rate, however, rose significantly. The dogs which had been subjected to cardiac denervation responded with small elevations of cardiac output and heart rate during the late hypoxic period. Thus, these findings are contrary to the classical concept that hypoxia elevates the cardiac output. Moreover, despite the absence of both the sympathetic and parasympathetic innervations of the heart, subjecting the denervated animals to severe hypoxia revealed that they were at no apparent hemodynamic disadvantage in comparison to the intact animals.


1988 ◽  
Vol 16 (3) ◽  
pp. 285-291 ◽  
Author(s):  
J. Tibballs ◽  
S. Malbezin

Cardiac output, blood pressure and heart rate were measured with noninvasive techniques before, during and after induction of anaesthesia with halothane and after intubation in unpremedicated infants and in diazepam-atropine premedicated children presenting for elective surgery. Cardiac output was measured with pulsed doppler echocardiography. Left ventricular shortening fraction was estimated with M-mode echocardiography during induction. Induction with halothane in infants caused significant decrements in blood pressure, cardiac index, stroke volume index and significant depression of left ventricular shortening fraction. Induction with halothane in diazepam-atropine premedicated children caused a significant increase in heart rate but significant decreases in blood pressure, stroke volume index and left ventricular shortening fraction while cardiac index decreased slightly. Intubation in infants caused a mild increase in heart rate compared with pre-induction values but blood pressure, cardiac index and stroke volume index remained below pre-induction values. Intubation in diazepam-atropine premedicated children caused significant increases in heart rate and cardiac index, and a nonsignificant increase in blood pressure but stroke volume index remained significantly below pre-induction values. Healthy infants and children tolerate induction of anaesthesia with halothane to a depth to permit intubation but large reductions in cardiac output and myocardial contractility are expected with subsequent reductions in blood pressure.


Author(s):  
Anish Bhatt ◽  
Laura Flink ◽  
Dai-Yin Lu ◽  
Qizhi Fang ◽  
Dwight Bibby ◽  
...  

While the phases of left atrial (LA) function at rest have been studied, the physiological response of the LA to exercise is undefined. This study defines the exercise behavior of the normal left atrium by quantitating its volumetric response to graded effort. Healthy subjects (n=131) were enrolled from the Health eHeart cohort. Echocardiograms were obtained at baseline and during ramped supine bicycle exercise. Left ventricular volume index, stroke volume index (LVSVI), left atrial end-systolic volume index (LAESVI), end-diastolic volume index (LAEDVI), emptying fraction (LAEF), reservoir and conduit fraction were analyzed. The LVSVI increased with low exercise, but did not increase further with peak exercise; cardiac output increased through the agency of heart rate. The LAESVI and LAEDVI decreased and the LAEF increased with exercise. As a result, LA reservoir volume index was static throughout exercise. The reservoir fraction decreased from 46% at rest to 40% with low exercise (p<0.001) in association with increased LVSVI, and remained similar at peak exercise. The conduit volume index increased from 20 mL/m2 at rest to 24 mL/m2 at low exercise and stayed the same at peak exercise. Similarly, the conduit fraction increased from 54% at rest to 60% at low exercise (p<0.001) and did not change further with peak exercise. Although atrial function increased with exercise, the major contribution to the augmentation of LV SV is LA conduit fraction, a marker of active ventricular relaxation. Furthermore, the major determinant of raising cardiac output during high level exercise is heart rate.


1988 ◽  
Vol 16 (3) ◽  
pp. 278-284 ◽  
Author(s):  
J. Tibballs ◽  
S. Malbezin

Cardiac output, systolic blood pressure and heart rate were measured with non-invasive techniques before, during and after induction of anaesthesia with thiopentone (7.5–8.5 mg/kg) and suxamethonium (1.4–1.7 mg/kg), and after intubation in unpremedicated infants and diazepam-atropine premedicated children. Cardiac output was measured with a combination of M-mode and pulsed doppler echocardiography. Significant decreases in systolic blood pressure, cardiac index and stroke volume index were observed during induction in both infants and children. Intubation caused increases above pre-induction levels of heart rate, blood pressure and cardiac index in both infants and children. Stroke volume index increased marginally in infants but remained depressed in children after intubation. Left ventricular shortening fraction decreased significantly in five other children during induction. It is concluded that thiopentone causes significant reduction in cardiac output by depression of myocardial contractility manifested by depression of blood pressure and stroke volume. Premedication with atropine may ameliorate reduction in cardiac output by permitting an increase in heart rate during induction. Induction of anaesthesia with thiopentone and premedication with diazepam does not prevent hypertension and tachycardia occurring with intubation.


EP Europace ◽  
2019 ◽  
Vol 21 (11) ◽  
pp. 1733-1741 ◽  
Author(s):  
Robert S Sheldon ◽  
Lucy Lei ◽  
Juan C Guzman ◽  
Teresa Kus ◽  
Felix A Ayala-Paredes ◽  
...  

Abstract Aims There are few effective therapies for vasovagal syncope (VVS). Pharmacological norepinephrine transporter (NET) inhibition increases sympathetic tone and decreases tilt-induced syncope in healthy subjects. Atomoxetine is a potent and highly selective NET inhibitor. We tested the hypothesis that atomoxetine prevents tilt-induced syncope. Methods and results Vasovagal syncope patients were given two doses of study drug [randomized to atomoxetine 40 mg (n = 27) or matched placebo (n = 29)] 12 h apart, followed by a 60-min drug-free head-up tilt table test. Beat-to-beat heart rate (HR), blood pressure (BP), and cardiac haemodynamics were recorded using non-invasive techniques and stroke volume modelling. Patients were 35 ± 14 years (73% female) with medians of 12 lifetime and 3 prior year faints. Fewer subjects fainted with atomoxetine than with placebo [10/29 vs. 19/27; P = 0.003; risk ratio 0.49 (confidence interval 0.28–0.86)], but equal numbers of patients developed presyncope or syncope (23/29 vs. 21/27). Of patients who developed only presyncope, 87% (13/15) had received atomoxetine. Patients with syncope had lower nadir mean arterial pressure than subjects with only presyncope (39 ± 18 vs. 69 ± 18 mmHg, P < 0.0001), and this was due to lower trough HRs in subjects with syncope (67 ± 30 vs. 103 ± 32 b.p.m., P = 0.006) and insignificantly lower cardiac index (2.20 ± 1.36 vs. 2.84 ± 1.05 L/min/m2, P = 0.075). There were no significant differences in stroke volume index (32 ± 6 vs. 35 ± 5 mL/m2, P = 0.29) or systemic vascular resistance index (2156 ± 602 vs. 1790 ± 793 dynes*s/cm5*m2, P = 0.72). Conclusion Norepinephrine transporter inhibition significantly decreased the risk of tilt-induced syncope in VVS subjects, mainly by blunting reflex bradycardia, thereby preventing final falls in cardiac index and BP.


2021 ◽  
Vol 20 (1) ◽  
Author(s):  
Matthias Rau ◽  
Kirsten Thiele ◽  
Niels-Ulrik Korbinian Hartmann ◽  
Alexander Schuh ◽  
Ertunc Altiok ◽  
...  

Abstract Background In the EMPA-REG OUTCOME trial (Empagliflozin Cardiovascular Outcome Event Trial) treatment with the sodium-glucose cotransporter-2 (SGLT2) inhibitor empagliflozin significantly reduced heart failure hospitalization (HHF) in patients with type 2 diabetes mellitus (T2D) and established cardiovascular disease. The early separation of the HHF event curves within the first 3 months of the trial suggest that immediate hemodynamic effects may play a role. However, hitherto no data exist on early effects of SGLT2 inhibitors on hemodynamic parameters and cardiac function. Thus, this study examined early and delayed effects of empagliflozin treatment on hemodynamic parameters including systemic vascular resistance index, cardiac index, and stroke volume index, as well as echocardiographic measures of cardiac function. Methods In this placebo-controlled, randomized, double blind, exploratory study patients with T2D were randomized to empagliflozin 10 mg or placebo for a period of 3 months. Hemodynamic and echocardiographic parameters were assessed after 1 day, 3 days and 3 months of treatment. Results Baseline characteristics were not different in the empagliflozin (n = 22) and placebo (n = 20) group. Empagliflozin led to a significant increase in urinary glucose excretion (baseline: 7.3 ± 22.7 g/24 h; day 1: 48.4 ± 34.7 g/24 h; p < 0.001) as well as urinary volume (1740 ± 601 mL/24 h to 2112 ± 837 mL/24 h; p = 0.011) already after one day compared to placebo. Treatment with empagliflozin had no effect on the primary endpoint of systemic vascular resistance index, nor on cardiac index, stroke volume index or pulse rate at any time point. In addition, echocardiography showed no difference in left ventricular systolic function as assessed by left ventricular ejections fraction and strain analysis. However, empagliflozin significantly improved left ventricular filling pressure as assessed by a reduction of early mitral inflow velocity relative to early diastolic left ventricular relaxation (E/eʹ) which became significant at day 1 of treatment (baseline: 9.2 ± 2.6; day 1: 8.5 ± 2.2; p = 0.005) and remained apparent throughout the study. This was primarily attributable to reduced early mitral inflow velocity E (baseline: 0.8 ± 0.2 m/s; day 1: 0.73 ± 0.2 m/sec; p = 0.003). Conclusions Empagliflozin treatment of patients with T2D has no significant effect on hemodynamic parameters after 1 or 3 days, nor after 3 months, but leads to rapid and sustained significant improvement of diastolic function. Trial registration EudraCT Number: 2016-000172-19; date of registration: 2017-02-20 (clinicaltrialregister.eu)


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