Circulatory response to hypoxia in unanesthetized dogs with and without cardiac denervation

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.

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.


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.


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.


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.


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.


1963 ◽  
Vol 205 (2) ◽  
pp. 393-400 ◽  
Author(s):  
David E. Donald ◽  
John T. Shepherd

Dogs with chronic cardiac denervation by the technic of regional neural ablation showed an unchanged capacity for work as measured by oxygen consumption. The relation of cardiac output to oxygen consumption during exercise remained unchanged from preoperational values. When the dogs started to run, the heart rate rose slowly over 1.5 min to reach a steady value proportional to the work performed. When exercise was stopped, the heart rate declined slowly. With mild exercise, the increase in cardiac output was mainly through stroke volume; with more severe exercise, increase in stroke volume and heart rate contributed equally, in contrast to the normal dog where the increase in rate predominates. Neither the pattern of the change in heart rate nor the plateau values were altered by adrenalectomy. The change in rate was not attributable to change in intravascular temperature. In an equivalent dose of base, norepinephrine caused tachycardia but little or no change in cardiac output, whereas epinephrine resulted in an increase in cardiac output with but a modest increase in heart rate.


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&lt;0.001). Oxygen consumption (VO2; 3.0+/-0.5 to 3.4+/-0.6 ml O2 x kg(-1) x min(-1); P&lt;0.05) and plasma lactate concentration (0.50+/-0.10 to 0.62+/-0.16 mM; P&lt;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&lt;0.01 vs. before esmolol). VO2 (3.2+/-0.6 ml O2 x kg(-1) x min(-1); P&gt;0.05) and plasma lactate (0.66+/-0.14 mM; P&gt;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.


1996 ◽  
Vol 271 (4) ◽  
pp. R912-R917 ◽  
Author(s):  
R. Fritsche ◽  
W. Burggren

Cardiovascular responses (blood pressure, heart rate, stroke volume, cardiac output, and peripheral vascular resistance) to acute hypoxia (Po2 = 70 mmHg) in developing larvae of Xenopus laevis from Nieuwkoop-Faber (NF) stage 45 and up to newly metamorphosed froglets were investigated. The results revealed two distinct response patterns to acute hypoxia in "early" (NF stages 45-48 and 49-51) and "late" (NF stages 52-53, 54-57, and 58-62) larval Xenopus. The early larvae responded to acute hypoxia with a significantly decreased stroke volume, cardiac output, and blood pressure. Peripheral resistance increased, whereas no change in heart rate occurred. In late larvae, stroke volume and blood pressure increased during acute hypoxia, but an offsetting bradycardia prevented major changes in cardiac output. We conclude that, up to stage 51 of development, hypoxia exerts a direct inhibitory effect on the heart and smooth muscle of the blood vessels, with no Frank-Starling relationship apparent. Older larvae show evidence of both intrinsic and extrinsic regulation of the cardiovascular system in response to acute hypoxia, suggesting that there is a specific point in larval development when cardiovascular regulation during hypoxia is expressed.


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.


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.


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