The Effects of Caffeine Intake on Cardiovascular Parameters in Sleep Deprived Medical Residents

2019 ◽  
Vol 70 (4) ◽  
pp. 1445-1448
Author(s):  
Ioana Raluca Papacocea ◽  
Ioana Anca Badarau ◽  
Mariana Catalina Ciornei ◽  
Sofia Lider Burciulescu ◽  
Marius Toma Papacocea
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Sleep Deprivation ◽  
Medical Residents ◽  
Caffeine Intake ◽  
Caffeine Consumption ◽  
Cardiovascular Parameters ◽  
Arterial Blood

Physicians and medical residents are particularly affected by sleep deprivation are, especially in East European countries. The aim of our study is to analyze the effect of caffeine intake on cardiovascular functions in sleep deprived residents (clinicians in-training) after continuous 24h on-call duty. 26 medical residents aged between 22-33 years old, 12 men and 14 women, who began their activity at 2 pm were included. Each subject consumed coffee or caffeinated drinks such as Coca cola during this period, after 2 am, expressed in caffeine units. We have evaluated their cardiovascular function using impedance cardiography (ICG-M501) and blood pressure measurement using the manometric method, before (at 7 pm) and after caffeine consumption (at 7 am), during one night of on-call duty. Surprisingly, after caffeine consumption, all subjects have had a decrease of the heart rate after one night of sleep deprivation (from mean: 83 b/min before to 69.73 b/min after, p = 0.000), also the mean arterial blood pressure is lower after the overnight call (from mean: 95.3 mmHg before to 88.9 mmHg after). Moreover, cardiac output, stroke volume and cardiac index decreases along with an increase of peripheral vascular resistance. Caffeine intake exerts a paradoxical effect on sleep deprived subjects; acute sleep loss, due to continuously, intense on-call work, modifies several cardiovascular parameters, such as heart rate, blood pressures, stroke volume and cardiac output.

Effect of sympathetic blockade on diurnal variation of hemodynamic patterns

1989 ◽  
Vol 256 (3) ◽  
pp. R778-R785 ◽  
Author(s):  
M. I. Talan ◽  
B. T. Engel
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Peripheral Resistance ◽  
Base Line ◽  
Sympathetic Blockade ◽  
Selective Blockade ◽  
Arterial Blood

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.

Cardiovascular, endocrine, and renal effects of urodilatin in normal humans

1999 ◽  
Vol 276 (3) ◽  
pp. R684-R695 ◽  
Author(s):  
Morten Heiberg Bestle ◽  
Niels Vidiendal Olsen ◽  
Poul Christensen ◽  
Benny Vittrup Jensen ◽  
Peter Bie
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Glomerular Filtration Rate ◽  
Stroke Volume ◽  
Glomerular Filtration ◽  
Filtration Rate ◽  
Excretion Rate ◽  
Renal Tubules ◽  
Arterial Blood

Effects of urodilatin (5, 10, 20, and 40 ng ⋅ kg−1⋅ min−1) infused over 2 h on separate study days were studied in eight normal subjects with use of a randomized, double-blind protocol. All doses decreased renal plasma flow (hippurate clearance, 13–37%) and increased fractional Li+clearance (7–22%) and urinary Na+excretion (by 30, 76, 136, and 99% at 5, 10, 20, and 40 ng ⋅ kg−1⋅ min−1, respectively). Glomerular filtration rate did not increase significantly with any dose. The two lowest doses decreased cardiac output (7 and 16%) and stroke volume (10 and 20%) without changing mean arterial blood pressure and heart rate. The two highest doses elicited larger decreases in stroke volume (17 and 21%) but also decreased blood pressure (6 and 14%) and increased heart rate (15 and 38%), such that cardiac output remained unchanged. Hematocrit and plasma protein concentration increased with the three highest doses. The renin-angiotensin-aldosterone system was inhibited by the three lowest doses but activated by the hypotensive dose of 40 ng ⋅ kg−1⋅ min−1. Plasma vasopressin increased by factors of up to 5 during infusion of the three highest doses. Atrial natriuretic peptide immunoreactivity (including urodilatin) and plasma cGMP increased dose dependently. The urinary excretion rate of albumin was elevated up to 15-fold (37 ± 17 μg/min). Use of a newly developed assay revealed that baseline urinary urodilatin excretion rate was low (<10 pg/min) and that fractional excretion of urodilatin remained below 0.1%. The results indicate that even moderately natriuretic doses of urodilatin exert protracted effects on systemic hemodynamic, endocrine, and renal functions, including decreases in cardiac output and renal blood flow, without changes in arterial pressure or glomerular filtration rate, and that filtered urodilatin is almost completely removed by the renal tubules.

A Comparison of the Acute Haemodynamic Effects of Propranolol and Pindolol at Rest and during Supine Exercise in Man

1980 ◽  
Vol 59 (s6) ◽  
pp. 465s-468s ◽  
Author(s):  
T. L. Svendsen ◽  
J. E. Carlsen ◽  
O. Hartling ◽  
A. McNair ◽  
J. Trap-Jensen
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Pulmonary Artery ◽  
Pulmonary Artery Pressure ◽  
Response Curves ◽  
Receptor Blocking ◽  
Artery Pressure ◽  
Arterial Blood ◽  
Β Receptor

1. Dose-response curves for heart rate, cardiac output, arterial blood pressure and pulmonary artery pressure were obtained in 16 male patients after intravenous administration of three increasing doses of pindolol, propranolol or placebo. All patients had an uncomplicated acute myocardial infarction 6–8 months earlier. 2. The dose-response curves were obtained at rest and during repeated bouts of supine bicycle exercise. The cumulative dose amounted to 0.024 mg/kg body weight for pindolol and to 0.192 mg/kg body weight for propranolol. 3. At rest propranolol significantly reduced heart rate and cardiac output by 12% and 15% respectively. Arterial mean blood pressure was reduced by 9.2 mmHg. Mean pulmonary artery pressure increased significantly by 2 mmHg. Statistically significant changes in these variables were not seen after pindolol or placebo. 4. During exercise pindolol and propranolol both reduced cardiac output, heart rate and arterial blood pressure to the same extent. After propranolol mean pulmonary artery pressure was increased significantly by 3.6 mmHg. Pindolol and placebo did not change pulmonary artery pressure significantly. 5. The study suggests that pindolol may offer haemodynamic advantages over β-receptor-blocking agents without intrinsic sympathomimetic activity during low activity of the sympathetic nervous system, and may be preferable in situations where the β-receptor-blocking effect is required only during physical or psychic stress.

Supine exercise restores arterial blood pressure and skin blood flow despite dehydration and hyperthermia

1999 ◽  
Vol 277 (2) ◽  
pp. H576-H583 ◽  
Author(s):  
José González-Alonso ◽  
Ricardo Mora-Rodríguez ◽  
Edward F. Coyle
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Blood Volume ◽  
Plasma Catecholamines ◽  
Central Blood Volume ◽  
Vascular Conductance ◽  
Arterial Blood ◽  
Cutaneous Vascular Conductance

We determined whether the deleterious effects of dehydration and hyperthermia on cardiovascular function during upright exercise were attenuated by elevating central blood volume with supine exercise. Seven trained men [maximal oxygen consumption (V˙o 2 max) 4.7 ± 0.4 l/min (mean ± SE)] cycled for 30 min in the heat (35°C) in the upright and in the supine positions (V˙o 2 2.93 ± 0.27 l/min) while maintaining euhydration by fluid ingestion or while being dehydrated by 5% of body weight after 2 h of upright exercise. When subjects were euhydrated, esophageal temperature (Tes) was 37.8–38.0°C in both body postures. Dehydration caused equal hyperthermia during both upright and supine exercise (Tes = 38.7–38.8°C). During upright exercise, dehydration lowered stroke volume (SV), cardiac output, mean arterial pressure (MAP), and cutaneous vascular conductance and increased heart rate and plasma catecholamines [30 ± 6 ml, 3.0 ± 0.7 l/min, 6 ± 2 mmHg, 22 ± 8%, 14 ± 2 beats/min, and 50–96%, respectively; all P < 0.05]. In contrast, during supine exercise, dehydration did not cause significant alterations in MAP, cutaneous vascular conductance, or plasma catecholamines. Furthermore, supine versus upright exercise attenuated the increases in heart rate (7 ± 2 vs. 9 ± 1%) and the reductions in SV (13 ± 4 vs. 21 ± 3%) and cardiac output (8 ± 3 vs. 14 ± 3%) (all P< 0.05). These results suggest that the decline in cutaneous vascular conductance and the increase in plasma norepinephrine concentration, independent of hyperthermia, are associated with a reduction in central blood volume and a lower arterial blood pressure.

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.

Carotid baroreceptor control of liver and spleen volume in cats

1991 ◽  
Vol 260 (1) ◽  
pp. H254-H259
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Arterial Blood Pressure ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Normal Brain ◽  
Spleen Volume ◽  
Arterial Blood

We tested the hypothesis that the blood volumes of the spleen and liver of cats are reflexly controlled by the carotid sinus (CS) baroreceptors. In pentobarbital-anesthetized cats the CS area was isolated and perfused so that intracarotid pressure (Pcs) could be controlled while maintaining a normal brain blood perfusion. The volume changes of the liver and spleen were estimated by measuring their thickness using ultrasonic techniques. Cardiac output, systemic arterial blood pressure (Psa), central venous pressure, central blood volume, total peripheral resistance, and heart rate were also measured. In vagotomized cats, increasing Pcs by 100 mmHg caused a significant reduction in Psa (-67.8%), cardiac output (-26.6%), total peripheral resistance (-49.5%), and heart rate (-15%) and significantly increased spleen volume (9.7%, corresponding to a 2.1 +/- 0.5 mm increase in thickness). The liver volume decreased, but only by 1.6% (0.6 +/- 0.2 mm decrease in thickness), a change opposite that observed in the spleen. The changes in cardiovascular variables and in spleen volume suggest that the animals had functioning reflexes. These results indicate that in pentobarbital-anesthetized cats the carotid baroreceptors affect the volume of the spleen but not the liver and suggest that, although the spleen has an active role in the control of arterial blood pressure in the cat, the liver does not.

Analysis of heart rate-based control of arterial blood pressure

1996 ◽  
Vol 271 (2) ◽  
pp. H812-H822 ◽  
Author(s):  
W. C. Rose ◽  
J. S. Schwaber
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Vascular System ◽  
Reciprocal Relation ◽  
Arterial Baroreflex ◽  
Arterial Blood ◽  
Limited Effectiveness ◽  
Filling Time

Vagal control of the heart is the most rapidly responding limb of the arterial baroreflex. We created a mathematical model of the left heart and vascular system to evaluate the ability of heart rate to influence blood pressure. The results show that arterial pressure depends nonlinearly on rate and that changes in rate are of limited effectiveness, particularly when rate is increased above the basal level. A 10% change in heart rate from rest causes a change of only 2.4% in arterial pressure due to the reciprocal relation between heart rate and stroke volume; at higher rates, insufficient filling time causes stroke volume to fall. These findings agree well with published experimental data and challenge the idea that changes in heart rate alone can strongly and rapidly affect arterial pressure. Possible implications are that vagally mediated alterations in inotropic and dromotropic state, which are not included in this model, play important roles in the fast reflex control of blood pressure or that the vagal limb of the baroreflex is of rather limited effectiveness.

Mechanism of circulatory responses to systemic hypoxia in the anesthetized dog

1965 ◽  
Vol 209 (2) ◽  
pp. 397-403 ◽  
Author(s):  
Hermes A. Kontos ◽  
H. Page Mauck ◽  
David W. Richardson ◽  
John L. Patterson
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Vascular Resistance ◽  
The Other ◽  
Arterial Flow ◽  
Arterial Blood ◽  
Systemic Hypoxia ◽  
Anesthetized Dogs ◽  
Spontaneously Breathing

The possibility that mechanisms secondary to the increased ventilation may contribute significantly to the circulatory responses to systemic hypoxia was explored in anesthetized dogs. In 14 spontaneously breathing dogs systemic hypoxia induced by breathing 7.5% oxygen in nitrogen increased cardiac output, heart rate, mean arterial blood pressure, and femoral arterial flow, and decreased systemic and hindlimb vascular resistances. In 14 dogs whose ventilation was kept constant by means of a respirator pump and intravenous decamethonium, systemic hypoxia did not change cardiac output, femoral arterial flow, or limb vascular resistance; it significantly decreased heart rate and significantly increased systemic vascular resistance. In seven spontaneously breathing dogs arterial blood pCO2 was maintained at the resting level during systemic hypoxia. The increase in heart rate was significantly less pronounced but the other circulatory findings were not different from those found during hypocapnic hypoxia. Thus, mechanisms secondary to increased ventilation contribute significantly to the circulatory responses to systemic hypoxia. Hypocapnia accounts partly for the increased heart rate, but not for the other circulatory responses.

Role of sinoaortic reflexes in hemodynamic patterns of natural defense behaviors in the cat

1981 ◽  
Vol 240 (3) ◽  
pp. H421-H429 ◽  
Author(s):  
G. Baccelli ◽  
R. Albertini ◽  
A. Del Bo ◽  
G. Mancia ◽  
A. Zanchetti
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Cardiac Output ◽  
Carotid Sinus ◽  
Emotional Behavior ◽  
Natural Defense ◽  
Arterial Blood ◽  
Hemodynamic Pattern ◽  
Before And After

To evaluate whether sinoaortic afferents contribute to the hemodynamic pattern of fighting, cardiovascular changes associated with fighting were studied in cats before and after sinoaortic denervation. Sinoaortic denervation exaggerates the decrease in heart rate, cardiac output, and arterial pressure during immobile confrontation (hissing, staring but no movement). During nonsupportive fighting (fighting with forelimbs while lying on one side) and supportive fighting ( fighting while standing on four feet) sinoaortic denervation reduces the increase in heart rate and cardiac output, minimizes the mesenteric vasoconstriction, induces a fall in arterial blood pressure, but does not affect iliac vasoconstriction or vasodilatation. The hemodynamic pattern of fighting is similarly changed by temporary inactivation of carotid sinus baroreflexes by common carotid occlusion as by chronic section of sinoaortic nerves. It is concluded that sinoaortic reflexes play an important role in the cardiovascular patterns accompanying natural fighting. They favor cardiac action and allow a marked visceral vasoconstriction to occur, thus minimizing or preventing a fall in blood pressure during emotional behavior.

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