Cardiovascular Responses to Induction of Anaesthesia with Thiopentone and Suxamethonium in Infants and Children

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.

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.


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.


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.


1997 ◽  
Vol 86 (4) ◽  
pp. 797-805 ◽  
Author(s):  
Robert F. Brooker ◽  
John F. IV Butterworth ◽  
Dalane W. Kitzman ◽  
Jeffrey M. Berman ◽  
Hillel I. Kashtan ◽  
...  

Background Despite many advantages, spinal anesthesia often is followed by undesirable decreases in blood pressure, for which the ideal treatment remains controversial. Because spinal anesthesia-induced sympathectomy and management with a pure alpha-adrenergic agonist can separately lead to bradycardia, the authors hypothesized that epinephrine, a mixed alpha- and beta-adrenergic agonist, would more effectively restore arterial blood pressure and cardiac output after spinal anesthesia than phenylephrine, a pure alpha-adrenergic agonist. Methods Using a prospective, double-blind, randomized, cross-over study design, 13 patients received sequential infusions of epinephrine and phenylephrine to manage hypotension after hyperbaric tetracaine (10 mg) spinal anesthesia. Blood pressure, heart rate, and stroke volume (measured by Doppler echocardiography using the transmitral time-velocity integral) were recorded at baseline, 5 min after injection of tetracaine, and before and after management of hypotension with epinephrine and phenylephrine. Cardiac output was calculated by multiplying stroke volume x heart rate. Results Five min after placement of a hyperbaric tetracaine spinal anesthesia, significant decrease in systolic (from 143 +/- 6 mmHg to 125 +/- 5 mmHg; P < 0.001), diastolic (from 81 +/- 3 to 71 +/- 3; P < 0.001), and mean (from 102 +/- 4 to 89 +/- 3; P < 0.001) arterial pressures occurred. Heart rate (75 +/- 4 beats/min to 76 +/- 4 beat/min; P = 0.9), stroke volume (115 +/- 17 to 113 +/- 13; P = 0.9), and cardiac output (8.0 +/- 1 l/m to 8.0 +/- 1l/m; P = 0.8) did not change significantly after spinal anesthesia. Phenylephrine was effective at restoring systolic blood pressure after spinal anesthesia (120 +/- 6 mmHg to 144 +/- 5 mmHg; P < 0.001) but was associated with a decrease in heart rate from 80 +/- 5 beats/min to 60 +/- 4 beats/min (P < 0.001) and in cardiac output from 8.6 +/- 0.7 l/m to 6.2 +/- 0.7 l/m (P < 0.003). Epinephrine was effective at restoring systolic blood pressure after spinal anesthesia (119 +/- 5 mmHg to 139 +/- 6 mmHg; P < 0.001) and was associated with an increase in stroke volume from 114 +/- 12 ml to 142 +/- 17 (P < 0.001) and cardiac output from 7.8 +/- 0.6 l/m to 10.8 +/- 1.1 l/m (P < 0.001). Conclusions Epinephrine management of tetracaine spinal-induced hypotension increases heart rate and cardiac output and restores systolic arterial pressure but does not restore mean and diastolic blood pressure. Phenylephrine management of tetracaine spinal-induced hypotension decreases heart rate and cardiac output while restoring systolic, mean, and diastolic blood pressure.


2000 ◽  
Vol 92 (2) ◽  
pp. 407-407 ◽  
Author(s):  
Jeremy A. Lieberman ◽  
Richard B. Weiskopf ◽  
Scott D. Kelley ◽  
John Feiner ◽  
Mariam Noorani ◽  
...  

Background The "critical" level of oxygen delivery (DO2) is the value below which DO2 fails to satisfy the metabolic need for oxygen. No prospective data in healthy, conscious humans define this value. The authors reduced DO2 in healthy volunteers in an attempt to determine the critical DO2. Methods With Institutional Review Board approval and informed consent, the authors studied eight healthy, conscious volunteers, aged 19-25 yr. Hemodynamic measurements were obtained at steady state before and after profound acute isovolemic hemodilution with 5% albumin and autologous plasma, and again at the reduced hemoglobin concentration after additional reduction of DO2 by an infusion of a beta-adrenergic antagonist, esmolol. Results Reduction of hemoglobin from 12.5+/-0.8 g/dl to 4.8+/-0.2 g/dl (mean +/- SD) increased heart rate, stroke volume index, and cardiac index, and reduced DO2 (14.0+/-2.9 to 9.9+/-20 ml O2 x kg(-1) x min(-1); all P<0.001). Oxygen consumption (VO2; 3.0+/-0.5 to 3.4+/-0.6 ml O2 x kg(-1) x min(-1); P<0.05) and plasma lactate concentration (0.50+/-0.10 to 0.62+/-0.16 mM; P<0.05; n = 7) increased slightly. Esmolol decreased heart rate, stroke volume index, and cardiac index, and further decreased DO2 (to 7.3+/-1.4 ml O2 x kg(-1) x min(-1); all P<0.01 vs. before esmolol). VO2 (3.2+/-0.6 ml O2 x kg(-1) x min(-1); P>0.05) and plasma lactate (0.66+/-0.14 mM; P>0.05) did not change further. No value of plasma lactate exceeded the normal range. Conclusions A decrease in DO2 to 7.3+/-1.4 ml O2 x kg(-1) min(-1) in resting, healthy, conscious humans does not produce evidence of inadequate systemic oxygenation. The critical DO2 in healthy, resting, conscious humans appears to be less than this value.


1991 ◽  
Vol 261 (3) ◽  
pp. H836-H842 ◽  
Author(s):  
S. E. Litwin ◽  
T. E. Raya ◽  
S. Daugherty ◽  
S. Goldman

Diabetes is believed to be associated with impaired systolic and diastolic function of the heart; however, some investigators have found that diabetic rats have increased cardiac output. We investigated changes in the peripheral circulation that could account for an increased cardiac output in diabetic rats (n = 30), 4 wk after a single tail vein injection of streptozotocin (60 mg/kg), and age-matched control rats (n = 31). Compared with controls, diabetic rats exhibited decreased (P less than 0.05) mean arterial pressure, characteristic aortic impedence, and total peripheral resistance; however, cardiac index and stroke volume index were increased. Aortic compliance, mean circulatory filling pressure, central venous pressure, pressure gradient for venous return, and venous compliance were unchanged in the diabetic rats compared with control. Baseline left ventricular end-diastolic pressure and end-diastolic volume were increased in the diabetic rats. Following a volume load of 30 ml/kg, cardiac index and stroke volume index increased less in the diabetic than in the control rats (35 vs. 102% and 69 vs. 105%, respectively). Thus, even with impaired systolic function, cardiac output is increased or maintained in diabetic rats because of the combination of decreased afterload and maintenance of preload.


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.


1999 ◽  
Vol 84 (7) ◽  
pp. 2308-2313 ◽  
Author(s):  
George J. Kahaly ◽  
Stephan Wagner ◽  
Jana Nieswandt ◽  
Susanne Mohr-Kahaly ◽  
Thomas J. Ryan

Exertion symptoms occur frequently in subjects with hyperthyroidism. Using stress echocardiography, exercise capacity and global left ventricular function can be assessed noninvasively. To evaluate stress-induced changes in cardiovascular function, 42 patients with untreated thyrotoxicosis were examined using exercise echocardiography. Studies were performed during hyperthyroidism, after treatment with propranolol, and after restoration of euthyroidism. Twenty- two healthy subjects served as controls. Ergometry was performed with patients in a semisupine position using a continuous ramp protocol starting at 20 watts/min. In contrast to control and euthyroidism, the change in end-systolic volume index from rest to maximal exercise was lower in hyperthyroidism. At rest, the stroke volume index, ejection fraction, and cardiac index were significantly increased in hyperthyroidism, but exhibited a blunted response to exercise, which normalized after restoration of euthyroidism. Propranolol treatment also led to a significant increase of delta (Δ) stroke volume index. Maximal work load and Δ heart rate were markedly lower in hyper- vs. euthyroidism. Compared to the control value, systemic vascular resistance was lowered by 36% in hyperthyroidism at rest, but no further decline was noted at maximal exercise. The Δ stroke volume index, Δ ejection fraction, Δ heart rate, and maximal work load were significantly reduced in severe hyperthyroidism. Negative correlations between free T3 and diastolic blood pressure, maximal work load, Δ heart rate, and Δ ejection fraction were noted. Thus, in hyperthyroidism, stress echocardiography revealed impaired chronotropic, contractile, and vasodilatatory cardiovascular reserves, which were reversible when euthyroidism was restored.


1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel

Heart rate, stroke volume, and intra-arterial blood pressure were monitored continuously in each of four monkeys, 18 consecutive h/day for several weeks. The mean heart rate, stroke volume, cardiac output, systolic and diastolic blood pressure, and total peripheral resistance were calculated for each minute and reduced to hourly means. After base-line data were collected for approximately 20 days, observation was continued for equal periods of time under conditions of alpha-sympathetic blockade, beta-sympathetic blockade, and double sympathetic blockade. This was achieved by intra-arterial infusion of prazosin, atenolol, or a combination of both in concentration sufficient for at least 75% reduction of response to injection of agonists. The results confirmed previous findings of a diurnal pattern characterized by a fall in cardiac output and a rise in total peripheral resistance throughout the night. This pattern was not eliminated by selective blockade, of alpha- or beta-sympathetic receptors or by double sympathetic blockade; in fact, it was exacerbated by sympathetic blockade, indicating that the sympathetic nervous system attenuates these events. Because these findings indicate that blood volume redistribution is probably not the mechanism mediating the observed effects, we have hypothesized that a diurnal loss in plasma volume may mediate the fall in cardiac output and that the rise in total peripheral resistance reflects a homeostatic regulation of arterial pressure.


2015 ◽  
Vol 122 (4) ◽  
pp. 736-745 ◽  
Author(s):  
Warwick D. Ngan Kee ◽  
Shara W. Y. Lee ◽  
Floria F. Ng ◽  
Perpetua E. Tan ◽  
Kim S. Khaw

Abstract Background: During spinal anesthesia for cesarean delivery, phenylephrine can cause reflexive decreases in maternal heart rate and cardiac output. Norepinephrine has weak β-adrenergic receptor agonist activity in addition to potent α-adrenergic receptor activity and therefore may be suitable for maintaining blood pressure with less negative effects on heart rate and cardiac output compared with phenylephrine. Methods: In a randomized, double-blinded study, 104 healthy patients having cesarean delivery under spinal anesthesia were randomized to have systolic blood pressure maintained with a computer-controlled infusion of norepinephrine 5 μg/ml or phenylephrine 100 μg/ml. The primary outcome compared was cardiac output. Blood pressure heart rate and neonatal outcome were also compared. Results: Normalized cardiac output 5 min after induction was greater in the norepinephrine group versus the phenylephrine group (median 102.7% [interquartile range, 94.3 to 116.7%] versus 93.8% [85.0 to 103.1%], P = 0.004, median difference 9.8%, 95% CI of difference between medians 2.8 to 16.1%). From induction until uterine incision, for norepinephrine versus phenylephrine, systolic blood pressure and stroke volume were similar, heart rate and cardiac output were greater, systemic vascular resistance was lower, and the incidence of bradycardia was smaller. Neonatal outcome was similar between groups. Conclusions: When given by computer-controlled infusion during spinal anesthesia for cesarean delivery, norepinephrine was effective for maintaining blood pressure and was associated with greater heart rate and cardiac output compared with phenylephrine. Further work would be of interest to confirm the safety and efficacy of norepinephrine as a vasopressor in obstetric patients.


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