Modeling and System Identification of Hemodynamic Responses to Vasopressor-Inotropes

Author(s):  
Ramin Bighamian ◽  
Sadaf Soleymani ◽  
Andrew T. Reisner ◽  
Istvan Seri ◽  
Jin-Oh Hahn

In an effort to establish an initial step towards the ultimate goal of developing an analytic tool to optimize the vasopressor-inotrope therapy through individualized dose-response relationships, we propose a phenomenological model intended to reproduce the hemodynamic response to vasopressor-inotropes. The proposed model consists of a cardiovascular model relating blood pressure to cardinal cardiovascular parameters (stroke volume and total peripheral resistance) and the phenomenological relationships between the cardinal cardiovascular parameters and the vasopressor-inotrope dose, in such a way that the model can be adapted to individual patient solely based upon blood pressure and heart rate responses to medication dosing. In this paper, the preliminary validity of the proposed model is shown using the experimental epinephrine dose versus blood pressure and heart rate response data collected from five newborn piglets. Its performance and potential usefulness are discussed. It is anticipated that, potentially, the proposed phenomenological model may offer a meaningful first step towards the automated control of vasopressor-inotrope therapy.

1993 ◽  
Vol 265 (5) ◽  
pp. R1132-R1140 ◽  
Author(s):  
N. B. Olivier ◽  
R. B. Stephenson

Open-loop baroreflex responses were evaluated in eight conscious dogs before and during congestive heart failure to determine the effects of failure on baroreflex control of blood pressure, heart rate, cardiac output, and total peripheral resistance. Heart failure was induced by rapid ventricular pacing. Baroreflex function was determined by calculation of the range and gain of the open-loop stimulus-response relationships for the effect of carotid sinus pressure on blood pressure, heart rate, cardiac output, and total peripheral resistance. The range and gain of blood pressure responses were substantially reduced as early as 3 days after induction of heart failure (161 +/- 6 to 99 +/- 8 mmHg and -2.7 +/- 0.3 to -1.5 +/- 0.1, respectively) and remained depressed for the 21 days of heart failure. This depression in baroreflex control of blood pressure was associated with similar depressions in reflex range and gain for heart rate (125 +/- 9 to 78 +/- 11 beats/min and -2.05 +/- 0.2 to -1.16 +/- 0.2 beats/min, respectively) and cardiac output (1.74 +/- 0.2 to 0.46 +/- 0.2 l/min and -0.81 +/- 0.02 to -0.027 +/- 0.008 l/min, respectively). The group-averaged range and gain for reflex control of vascular resistance were not altered by heart failure. In three dogs, discontinuation of rapid ventricular pacing led to resolution of heart failure within 7 days and partial restoration of the range and gain of reflex control of blood pressure. We conclude that heart failure reversibly depresses baroreflex control of blood pressure principally through a concurrent reduction in reflex control of cardiac output, whereas reflex control of vascular resistance is not consistently affected.


2009 ◽  
Vol 297 (3) ◽  
pp. R769-R774 ◽  
Author(s):  
Steven J. Swoap ◽  
Margaret J. Gutilla

The laboratory mouse is a facultative daily heterotherm in that it experiences bouts of torpor under caloric restriction. Mice are the most frequently studied laboratory mammal, and often, genetically modified mice are used to investigate many physiological functions related to weight loss and caloric intake. As such, research documenting the cardiovascular changes during fasting-induced torpor in mice is warranted. In the current study, C57BL/6 mice were implanted either with EKG/temperature telemeters or blood pressure telemeters. Upon fasting and exposure to an ambient temperature (Ta) of 19°C, mice entered torpor bouts as assessed by core body temperature (Tb). Core Tb fell from 36.6 ± 0.2°C to a minimum of 25.9 ± 0.9°C during the fast, with a concomitant fall in heart rate from 607 ± 12 beats per minute (bpm) to a minimum of 158 ± 20 bpm. Below a core Tb of 31°C, heart rate fell exponentially with Tb, and the Q10 was 2.61 ± 0.18. Further, mice implanted with blood pressure telemeters exhibited similar heart rate and activity profiles as those implanted with EKG/temperature telemeters, and the fall in heart rate and core Tb during entrance into torpor was paralleled by a fall in blood pressure. The minimum systolic, mean, and diastolic blood pressures of torpid mice were 62.3 ± 10.2, 51.9 ± 9.2, 41.0 ± 7.5 mmHg, respectively. Torpid mice had a significantly lower heart rate (25–35%) than when euthermic at mean arterial pressures from 75 to 100 mmHg, suggesting that total peripheral resistance is elevated during torpor. These data provide new and significant insight into the cardiovascular adjustments that occur in torpid mice.


2017 ◽  
Vol 26 (2) ◽  
pp. 116-21
Author(s):  
Arif H.M. Marsaban ◽  
Aldy Heriwardito ◽  
I G.N.A.D. Yundha

Background: Increased blood pressure and heart rate are the most frequent response to laryngoscopy which sometimes causes serious complications. Laryngoscopy technique and tools modification lessen the nociceptive stimulation, thus preventing hemodynamic response. BURP maneuver is used to lower Cormack-Lehane level, but it can cause additional pain stimulation during laryngoscopy. The aim of this study was to compare the cardiovascular response and the need of BURP maneuver during laryngoscopy between CMAC® and conventional Macintosh.Methods: A randomized, single blinded, control trial was performed to 139 subjects who underwent general anesthesia with endotracheal tube. Subjects were randomised into a control group (conventional Macintosh) and an intervention group (CMAC®). The cardiovascular parameters (systolic, dyastolic, mean arterial pressure, and heart rate) were measured prior to induction (T1). Midazolam 0.05 mg/kg and Fentanyl 2 micrograms/kg were given 2 minutes before the induction. Moreover, they were given propofol 1 mg/kg followed by propofol infusion of 10 mg/kg/hour and Atracurium 0.8–1 mg/kg. After TOF-0 cardiovascular parameters (T2) were remeasured, it was proceeded to laryngoscopy. When Cormack-Lehane 1–2 was reached (with or without BURP maneuver), cardiovascular parameters were measured again (T3).Results: Unpaired T-test showed that cardiovascular response during laryngoscopy were significantly lower in the intervention group compared to the control group (p<0.05). The need of BURP maneuver was significantly lower in the CMAC® group compared to the Convensional Macintosh group (13.9% vs 40.3%; p<0.05).Conclusion: Cardiovascular response and BURP maneuver during laryngoscopy with CMAC® were significantly lower compared to conventional Macintosh.


2001 ◽  
Vol 281 (3) ◽  
pp. H1040-H1046 ◽  
Author(s):  
J. Kevin Shoemaker ◽  
Debbie D. O'Leary ◽  
Richard L. Hughson

Arterial hypocapnia has been associated with orthostatic intolerance. Therefore, we tested the hypothesis that hypocapnia may be detrimental to increases in muscle sympathetic nerve activity (MSNA) and total peripheral resistance (TPR) during head-up tilt (HUT). Ventilation was increased ∼1.5 times above baseline for each of three conditions, whereas end-tidal Pco 2 (Pet CO2 ) was clamped at normocapnic (Normo), hypercapnic (Hyper; +5 mmHg relative to Normo), and hypocapnic (Hypo; −5 mmHg relative to Normo) conditions. MSNA (microneurography), heart rate, blood pressure (BP, Finapres), and cardiac output (Q, Doppler) were measured continuously during supine rest and 45° HUT. The increase in heart rate when changing from supine to HUT ( P < 0.001) was not different across Pet CO2 conditions. MSNA burst frequency increased similarly with HUT in all conditions ( P < 0.05). However, total MSNA and the increase in total amplitude relative to baseline (%ΔMSNA) increased more when changing to HUT during Hypo compared with Hyper ( P < 0.05). Both BP and Q were higher during Hyper than both Normo and Hypo (main effect; P < 0.05). Therefore, the MSNA response to HUT varied inversely with levels of Pet CO2 . The combined data suggest that augmented cardiac output with hypercapnia sustained blood pressure during HUT leading to a diminished sympathetic response.


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.


1991 ◽  
Vol 260 (1) ◽  
pp. H254-H259
Author(s):  
R. Maass-Moreno ◽  
C. F. Rothe

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.


1978 ◽  
Vol 234 (2) ◽  
pp. H152-H156
Author(s):  
G. S. Geis ◽  
G. Barratt ◽  
R. D. Wurster

Resting cardiovascular parameters and the responses to bilateral carotid occlusions (BCO) were monitored in pentobarbital-anesthetized and conscious dogs before and after placing lesions in the dorsolateral funiculi at C7-C8 and after spinal transections at C7. Pre- and postlesion blood pressure (BP) and heart rate (HR) responses to exercise were also monitored. The lesions significantly attenuated the responses to BCO and decreased resting BP in anesthetized dogs. Yet neither resting HR in anesthetized or conscious dogs nor the resting BP in conscious dogs was affected by the lesions. Subsequent spinal transections significantly decreased resting HR and BP and the responses to BCO but did not affect the BP response to BCO in anesthetized dogs as compared with corresponding postlesion parameters. BP responses to exercise were significantly attenuated by the lesions, but HR responses were not affected. Since stimulation and BP studies indicated that the descending pressor pathway had been ablated, the data suggest that the pathway mediates BP and HR responses to BCO in pentobarbital-anesthetized and conscious dogs. It does not maintain resting HR in anesthetized or conscious animals, and the resting BP in conscious dogs. This pathway is important for BP responses to exercise but is not necessary for HR responses. Finally, other spinal pathways are involved in cardiovascular control.


2002 ◽  
Vol 26 (4) ◽  
pp. 309-316 ◽  
Author(s):  
Theresa L. O’Donaughy ◽  
Thomas C. Resta ◽  
Benjimen R. Walker

We have developed a laboratory exercise that demonstrates arterial baroreflex control of heart rate (HR) in the conscious unrestrained rat, incorporating graduate level physiological topics as well as a hands-on exposure to conscious animal research. This demonstration utilizes rats chronically instrumented to measure cardiac output (CO), HR, and arterial blood pressure in response to agents that raise or lower blood pressure. The HR response to progressive increases or decreases in blood pressure is recorded, and a baroreflex curve is generated by plotting mean arterial blood pressure (MABP) vs. HR. Observation of altered CO allows for discussion of the relationship between MAP, CO, HR, stroke volume, and total peripheral resistance. Administration of arginine vasopressin demonstrates the ability of this hormone to alter the sensitivity of the baroreflex. Throughout the demonstration, students answer questions from a handout about general cardiovascular physiology, specific pathways of agonists, and the baroreflex system, encouraging group and individual critical analysis of the results. Interpretation of the data reemphasizes lecture material and allows students to observe the baroreflex response in a physiological setting.


2019 ◽  
Vol 6 (3) ◽  
pp. 623
Author(s):  
Rukmini G. ◽  
Srinivas M. Reddy

Background: During endotracheal intubation, it has been observed that there is evolvement of the responses of the circulatory in nature. These are difficult to control using the IV anesthetic drugs. Hence various agents are tried to overcome this drawback. Objective of research work was to study efficacy of oral clonidine on hemodynamic responses compared to IV fentanyl while patients undergo larngoscopy and endotracheal intubation.Methods: The patients were allocated into two groups of 30 each. i.e. 30 patients in clonidine group and 30 patients in fentanyl group. All the patients received were pre-medicated with glycoprrolate 0.2mg, ondansetron 4mg and tramadol 1mg/kg body weight. Cardiovascular parameters (heart rate, systolic blood pressure, diastolic blood pressure, mean arterial pressure,) were recorded at the following intervals: pre-induction, after induction, at endotracheal intubation, one minute, three minutes and five minutes after intubation.Results: The heart rate was significantly more at various intervals in patients who belonged to fentanyl group and it was significantly lesser in clonidine group. The systolic blood pressure was significantly more at various intervals in patients who belonged to fentanyl group and it was significantly lesser in clonidine group. The diastolic blood pressure was significantly more at various intervals in patients who belonged to fentanyl group and it was significantly lesser in clonidine group. Similar was the case with mean arterial blood pressure.Conclusions: Clonidine has been found to be more effective than IV fentanyl in stabilizing the cardiovascular parameters. Not only that orally it is easier to administer and cost effective.


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