Threshold for adrenomedullary activation and increased cardiac work during mild core hypothermia

2001 ◽  
Vol 102 (1) ◽  
pp. 119-125 ◽  
Author(s):  
Steven M. FRANK ◽  
Christine G. CATTANEO ◽  
Mary Beth WIENEKE-BRADY ◽  
Hossam EL-RAHMANY ◽  
Neeraj GUPTA ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Normal Saline ◽  
Stress Test ◽  
Left Ventricular ◽  
Control Treatment ◽  
Rate Pressure Product ◽  
Cardiac Events ◽  
Cardiac Work ◽  
Core Cooling

Postoperative hypothermia increases the incidence of ischaemic cardiac events in patients at risk, but the underlying mechanism is unclear. One possibility is increased cardiac work related to the sympathoneural or adrenomedullary hormonal responses. In awake human volunteers, the present study assessed the effects of mild core hypothermia on these responses, and on the associated changes in indices of cardiac work. A total of 11healthy men were studied on two separate days. On one day, core temperature (Tc) was decreased by the intravenous infusion of cold normal saline (4°C; 60ml/kg over 30min) through a central venous catheter. On the other day (normothermic control), warm normal saline (37°C; 60ml/kg over 30min) was given intravenously. Transthoracic echocardiograms, the sympathoneural response (noradrenaline) and the adrenomedullary response (adrenaline) were evaluated before, during and after the intravenous infusions. Echocardiography was used to measure left ventricular function and cardiac output. Compared with the normothermic control treatment, core cooling of 0.7°C was associated with increased plasma noradrenaline (220% increase; P = 0.001), whereas adrenaline, cardiac output, heart rate and the rate-pressure product were unchanged. After core cooling of 1.0°C, increases in noradrenaline (by 230%; P = 0.001), adrenaline (by 68%; P = 0.05), cardiac output (by 23%; P = 0.04), heart rate (by 16%; P = 0.04) and rate-pressure product (by 25%; P = 0.007) were all significant compared with the normothermic control treatment. In conclusion, there is a Tc threshold, below which an adrenomedullary (adrenaline) response is triggered in addition to the sympathoneural (noradrenaline) response. This Tc threshold (≈ 1°C below the normothermic baseline) is also associated with an increase in haemodynamic indices of cardiac work. Mild core hypothermia therefore constitutes a catecholamine-mediated cardiovascular ‘stress test’.

Effects of naloxone on systemic and regional hemodynamic responses to exercise in dogs

1988 ◽  
Vol 64 (4) ◽  
pp. 1493-1499 ◽  
Author(s):  
N. Imai ◽  
C. K. Stone ◽  
P. D. Woolf ◽  
C. S. Liang
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Cardiac Output ◽  
Normal Saline ◽  
Adrenocorticotropic Hormone ◽  
Aortic Pressure ◽  
Left Ventricular ◽  
Moderate Exercise ◽  
Beta Endorphin ◽  
Developed Pressure

To determine whether endogenous opiates have a role in circulatory regulation during mild to moderate exercise, 11 chronically instrumented dogs were exercised on a treadmill up a 6% incline at 2.5 and 5.0 mph, each for 20 min, after treatment with either the opiate receptor antagonist naloxone (1 mg/kg bolus and 20 micrograms.kg-1.min-1 infusion) or normal saline. Naloxone increased plasma beta-endorphin and adrenocorticotropic hormone at rest but had no effect on resting heart rate, aortic pressure, cardiac output, left ventricular time derivative of pressure (dP/dt) and ratio of dP/dt at a developed pressure of 50 mmHg and the developed pressure (dP/dt/P), or plasma catecholamines. Plasma beta-endorphin and adrenocorticotropic hormone increased during exercise. In addition, graded treadmill exercise produced proportional increases in heart rate, cardiac output, aortic pressure, left ventricular dP/dt and dP/dt/P, and blood flow to exercising muscles, right and left ventricular myocardium, and adrenal glands. However, there were no differences in the circulatory responses to exercise between animals receiving naloxone and normal saline. Thus the endogenous opiate system probably does not play an important role in regulating the systemic hemodynamic and blood flow responses to mild and moderate exercise.

scholarly journals Absence of left ventricular and arterial adaptations to exercise in octogenarians

2004 ◽  
Vol 97 (5) ◽  
pp. 1654-1659 ◽  
Author(s):  
Robert J. Spina ◽  
Timothy E. Meyer ◽  
Linda R. Peterson ◽  
Dennis T. Villareal ◽  
Morton R. Rinder ◽  
...  
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Exercise Group ◽  
Left Ventricular ◽  
Applanation Tonometry ◽  
Rate Pressure Product ◽  
Control Group ◽  
Modest Improvement ◽  
Dimensional Echocardiography ◽  
And Function

Recent evidence suggests that octogenarians exhibit attenuated adaptations to training with a small increase in peak O2 consumption (V̇o2) that is mediated by a modest improvement in cardiac output without an increase in arteriovenous O2 content difference. This study was designed to determine whether diminished increases in peak V̇o2 and cardiac output in the octogenarians are associated with absence of left ventricular and arterial adaptations to exercise training. We studied 22 octogenarians (81.9 ± 3.7 yr, mean ± SD) randomly assigned a group that exercised at an intensity of 82.5 ± 5% of peak heart rate for 9 mo and 14 (age 83.1 ± 4.1) assigned to a control group. Peak V̇o2 increased 12% in the exercise group but decreased slightly (−7%) in the controls. The exercise group demonstrated significant but small decreases in the heart rate (6%, P = 0.002) and the rate-pressure product (9%, P = 0.004) during submaximal exercise at an absolute work rate. Training induced no significant changes in the left ventricular size, geometry (wall thickness-to-radius ratio), mass, and function assessed with two-dimensional echocardiography or in arterial stiffness evaluated with applanation tonometry. Data suggest that the absence of cardiac and arterial adaptations may in part account for the limited gain in aerobic capacity in response to training in the octogenarians.

In the Loop—Left Ventricular Pressures

2011 ◽  
pp. 42-47
Author(s):  
James R. Munis
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Aortic Valve ◽  
Left Ventricle ◽  
Stroke Volume ◽  
Cardiovascular System ◽  
Aortic Root ◽  
Left Ventricular ◽  
Root Pressure ◽  
The Third

We've already looked at 2 types of pressure that affect physiology (atmospheric and hydrostatic pressure). Now let's consider the third: vascular pressures that result from mechanical events in the cardiovascular system. As you already know, cardiac output can be defined as the product of heart rate times stroke volume. Heart rate is self-explanatory. Stroke volume is determined by 3 factors—preload, afterload, and inotropy—and these determinants are in turn dependent on how the left ventricle handles pressure. In a pressure-volume loop, ‘afterload’ is represented by the pressure at the end of isovolumic contraction—just when the aortic valve opens (because the ventricular pressure is now higher than aortic root pressure). These loops not only are straightforward but are easier to construct just by thinking them through, rather than by memorization.

Effects of nitroglycerin on cardiac function and regional blood flow distribution in conscious dogs

1978 ◽  
Vol 234 (3) ◽  
pp. H244-H252 ◽  
Author(s):  
S. F. Vatner ◽  
M. Pagani ◽  
J. D. Rutherford ◽  
R. W. Millard ◽  
W. T. Manders
Keyword(s):  
Cardiac Output ◽  
Regional Blood Flow ◽  
Flow Distribution ◽  
Left Ventricular ◽  
Conscious Dogs ◽  
Blood Flow Distribution ◽  
Biphasic Response ◽  
Cardiac Work ◽  
Regional Hemodynamics ◽  
Arteriolar Vasodilation

The effects of intravenous infusion of nitroglycerin (NTG), 8 and 32 microgram/kg.min for 7 min, and of sublingual NTG, 1.2 mg, were examined on direct and continuous measurements of systemic, coronary, and regional hemodynamics, left ventricular (LV) dimensions, pressures, and myocardial contractility in conscious dogs. NTG induced sustained reductions in LV dimensions and transient increases in heart rate and dP/dt, and decreases in mean arterial pressure. Initially NTG increased cardiac output and flows to the coronary, mesenteric, renal, and iliac beds, while systemic and regional vascular resistances fell. Later, cardiac output, cardiac work, and mesenteric and iliac flows fell significantly below control, and significant vasoconstriction in the systemic as well as mesenteric, iliac, and coronary beds was observed at a time when LV end-diastolic dimensions were still significantly reduced. Peripheral vasoconstriction was not observed with systemic NTG in deafferented dogs or when NTG, 1 microgram/kg.min, was infused intra-arterially into the iliac bed. Thus, systemic NTG induces a biphasic response consisting of initial arteriolar vasodilation followed by vasoconstriction in the mesenteric, iliac, coronary and systemic beds, which is presumably due to longer lasting effects on preload and to secondary reflex responses to the drug.

Atrial natriuretic peptide reverses angiotensin-induced venoconstriction in dogs

1989 ◽  
Vol 257 (4) ◽  
pp. H1062-H1067 ◽  
Author(s):  
R. W. Lee ◽  
R. G. Gay ◽  
S. Goldman
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Atrial Natriuretic Peptide ◽  
Natriuretic Peptide ◽  
Blood Volume ◽  
Left Ventricular ◽  
Ang Ii ◽  
Central Blood Volume ◽  
Venous Compliance ◽  
Induced Hypertension

To determine whether atrial natriuretic peptide (ANP) can reverse angiotensin (ANG II)-induced venoconstriction, ANP was infused (0.3 micrograms.kg-1.min-1) in the presence of ANG II-induced hypertension in six ganglion-blocked dogs. ANG II was initially administered to increase mean arterial blood pressure (MAP) 50% above control. ANG II did not change heart rate or left ventricular rate of pressure development (LV dP/dt) but increased total peripheral vascular resistance (TPVR) and left ventricular end-diastolic pressure (LVEDP). Mean circulatory filling pressure (MCFP) increased, whereas cardiac output and venous compliance decreased. Unstressed vascular volume did not change, but central blood volume increased. ANP infusion during ANG II-induced hypertension resulted in a decrease in MAP, but TPVR did not change. There were no changes in heart rate or LV dP/dt. ANP decreased cardiac output further. LVEDP returned to base line with ANP. ANP also decreased MCFP and normalized venous compliance. There was no significant change in total blood volume, but central blood volume decreased. In summary, ANP can reverse the venoconstriction but not the arterial vasoconstriction produced by ANG II. The decrease in MAP was due to a decrease in cardiac output that resulted from venodilatation and aggravation of the preload-afterload mismatch produced by ANG II alone. Because TPVR did not change when MAP fell, we conclude that the interaction between ANG II and ANP occurs primarily in the venous circulation.

Adrenal contribution to cardiac responses elicited by acute hypoxia in piglets

1980 ◽  
Vol 239 (6) ◽  
pp. H751-H755 ◽  
Author(s):  
J. C. Lee ◽  
J. C. Werner ◽  
S. E. Downing
Keyword(s):  
Heart Rate ◽  
Adrenal Glands ◽  
Acute Hypoxia ◽  
Cardiac Contractility ◽  
Sympathetic Nerves ◽  
Left Ventricular ◽  
Cardiac Work ◽  
Ganglionic Blockade ◽  
Cardiac Responses

The adrenal contribution to cardiac responses elicited by acute hypoxia was assessed in 16 piglets, 1-12 wks old, anesthetized with pentobarbital (30 mg/kg). External cardiac work was held constant and parasympathetic blockade was produced in each animal with atropine (1 mg). Hypoxia was produced by addition of N2 to the respirator. In a sham-adrenalectomy group (n = 6) left ventricular (LV) dP/dtmax increased significantly during hypoxia (PaO2 approximately 30 mmHg) to 3,680 +/- 414 mmHg/s from control values of 2,686 +/- 317 mmHg/s (P < 0.01). Heart rate rose from 171 +/- 6 to 186 +/- 7 beats/min (P < 0.02). These responses were not significantly altered by ganglionic blockade with trimethaphan camsylate (0.5 mg x kg-1 x min-1). Equally large increases of LV dP/dtmax appeared when heart rate was held constant by pacing. beta-Adrenoreceptor blockade with practolol (4 mg/kg) sharply reduced but did not eliminate the response. In contrast, no changes in LV dP/dtmax or heart rate were observed during hypoxia in adrenalectomized piglets (n = 6). These findings indicate that the increased cardiac contractility during acute hypoxia in piglets is dependent on the integrity of the adrenal glands and that there is minimal contribution from cardiac sympathetic nerves.

Effects of isoproterenol on the cardiovascular system of fetal sheep exposed to long-term high-altitude hypoxemia

1995 ◽  
Vol 78 (5) ◽  
pp. 1793-1799 ◽  
Author(s):  
M. Kamitomo ◽  
T. Ohtsuka ◽  
R. D. Gilbert
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Right Ventricular ◽  
High Altitude ◽  
Arterial Blood Pressure ◽  
Left Ventricular ◽  
Arterial Blood ◽  
Isoproterenol Infusion

We exposed fetuses to high-altitude (3,820 m) hypoxemia from 30 to 130 days gestation, when we measured fetal heart rate, right and left ventricular outputs with electromagnetic flow probes, and arterial blood pressure during an isoproterenol dose-response infusion. We also measured the distribution of cardiac output with radiolabeled microspheres during the maximal isoproterenol dose. Baseline fetal arterial blood pressure was higher in long-term hypoxemic fetuses (50.1 +/- 1.3 vs. 43.4 +/- 1.0 mmHg) but fell during the isoproterenol infusion to 41.3 +/- 1.4 and 37.5 +/- 1.4 mmHg, respectively, at the highest dose. Heart rate was the same in both groups and did not differ during isoproterenol infusion. Baseline fetal cardiac output was lower in the hypoxemic group (339 +/- 18 vs. 436 +/- 19 ml.min-1.kg-1) due mainly to a reduction in right ventricular output. During the isoproterenol infusion, right ventricular output increased to the same extent in both hypoxemic and normoxic fetuses (approximately 35%); however, left ventricular output increased only approximately 15% in the hypoxemic group compared with approximately 40% in the normoxic group. The percent change in individual organ blood flows during isoproterenol infusion in the hypoxemic groups was not significantly different from the normoxic group. All of the mechanisms that might be responsible for the differential response of the fetal left and right ventricles to long-term hypoxia are not understood and need further exploration.

scholarly journals Muscle metaboreflex-induced coronary vasoconstriction functionally limits increases in ventricular contractility

2010 ◽  
Vol 109 (2) ◽  
pp. 271-278 ◽  
Author(s):  
Matthew Coutsos ◽  
Javier A. Sala-Mercado ◽  
Masashi Ichinose ◽  
ZhenHua Li ◽  
Elizabeth J. Dawe ◽  
...  
Keyword(s):  
Blood Flow ◽  
Cardiac Output ◽  
Left Ventricular ◽  
Ventricular Contractility ◽  
Left Ventricular Contractility ◽  
Coronary Vasodilation ◽  
Cardiac Work ◽  
Vascular Conductance ◽  
Muscle Metaboreflex ◽  
Coronary Vasoconstriction

Muscle metaboreflex activation during dynamic exercise induces a substantial increase in cardiac work and oxygen demand via a significant increase in heart rate, ventricular contractility, and afterload. This increase in cardiac work should cause coronary metabolic vasodilation. However, little if any coronary vasodilation is observed due to concomitant sympathetically induced coronary vasoconstriction. The purpose of the present study is to determine whether the restraint of coronary vasodilation functionally limits increases in left ventricular contractility. Using chronically instrumented, conscious dogs ( n = 9), we measured mean arterial pressure, cardiac output, and circumflex blood flow and calculated coronary vascular conductance, maximal derivative of ventricular pressure (dp/d tmax), and preload recruitable stroke work (PRSW) at rest and during mild exercise (2 mph) before and during activation of the muscle metaboreflex. Experiments were repeated after systemic α1-adrenergic blockade (∼50 μg/kg prazosin). During prazosin administration, we observed significantly greater increases in coronary vascular conductance (0.64 ± 0.06 vs. 0.46 ± 0.03 ml·min−1·mmHg−1; P < 0.05), circumflex blood flow (77.9 ± 6.6 vs. 63.0 ± 4.5 ml/min; P < 0.05), cardiac output (7.38 ± 0.52 vs. 6.02 ± 0.42 l/min; P < 0.05), dP/d tmax (5,449 ± 339 vs. 3,888 ± 243 mmHg/s; P < 0.05), and PRSW (160.1 ± 10.3 vs. 183.8 ± 9.2 erg·103/ml; P < 0.05) with metaboreflex activation vs. those seen in control experiments. We conclude that the sympathetic restraint of coronary vasodilation functionally limits further reflex increases in left ventricular contractility.

scholarly journals Hemodynamic Consequence of Different Pacing Modes after Aortic Valve Replacement

2018 ◽  
Vol 21 (2) ◽  
pp. 090
Author(s):  
Arndt H Kiessling
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Aortic Valve ◽  
Left Ventricular Hypertrophy ◽  
Aortic Valve Replacement ◽  
Diastolic Function ◽  
Valve Replacement ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Heart Rates

Objectives: Ventricular pacemaker stimulation may cause deterioration of hemodynamics in patients with left-ventricular hypertrophy following aortic valve replacement. Since the diastolic function is often impaired, it remains unclear which heart rate best optimizes cardiac output. Low heart rates are suggested to treat impaired diastolic function chronically, but it is possible that cardiac output may be augmented by increasing the heart rate in patients with a fixed stroke volume (SV). The aim of this study is the identification of the best pacing mode and heart rate for the surrogate parameter SV and cardiac index(CI) in patients with left ventricular hypertrophy.Methods: Various pacemaker stimulation modes and different heart rates, as well as their influence on hemodynamics, were tested following aortic valve replacement in 48 patients with severe left-ventricular hypertrophy (Intraventricular septum (IVS)>1.5 cm) and aortic stenosis. SV and cardiac output were recorded by pulse curve analysis. Four modes of stimulation (right ventricular pacemaker stimulation (DDDright), left ventricular pacemaker stimulation (DDDleft), biventricular pacemaker stimulation (DDDbi), atrial pacemaker stimulation (AAI)) were documented at five different rates (60, 80, 100, 120, 140 beats/min) and three different postoperative time points (intraoperatively, 3h and 24h postoperatively).Results: The highest CI was found at linear rates between 60 to 140bpm. AAI was the best mode of stimulation in the majority of cases (35%), but in others, either left, right and/or biventricular stimulation was found to be better (15%). SV showed a u-shaped trend with a peak at 100 beats/min.Conclusion: An increase in the heart rate does not lead to a notable drop in SV postoperatively in left-ventricular hypertrophy; hence a rise in cardiac output can be anticipated up to a rate of 100 beats/min. A standardized response in terms of an ideal pacemaker stimulation mode could not be identified.

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