scholarly journals Effect of Levosimendan Compared to Conventional Inotropic Agents on Hemodynamics and Outcome in Patient with Poor LV Function Undergoing Cardiac Surgery

2019 ◽  
Vol 7 (19) ◽  
pp. 3205-3210
Author(s):  
Mahmoud Khaled ◽  
Ahmad Naem Almogy ◽  
Mohamed Shehata ◽  
Fahim Ragab ◽  
Khaled Zeineldein
Keyword(s):  
Heart Rate ◽  
Cardiac Surgery ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Left Ventricular ◽  
Base Deficit ◽  
Inotropic Agents ◽  
Poor Left Ventricular Function ◽  
Mixed Venous

BACKGROUND: Patients undergoing heart surgery involving cardiopulmonary bypass (CPB) experience global myocardial ischemia with subsequent reperfusion which, despite cardioplegic protection, may result in different degrees of transient ventricular dysfunction. Levosimendan is a “calcium sensitisers”, it improves myocardial contractility by sensitising troponin C to calcium without increasing myocardial oxygen consumption and without impairing relaxation and diastolic function. AIM: To evaluate the adding effect of a calcium sensitiser (levosimendan) compared to the conventional inotropic and vasoactive agent used in the patient with poor left ventricular function undergoing cardiac surgery on different measured hemodynamic variables and the effect on the outcome. METHODS: It is prospective observational studies were patients were divided into 2 groups of 30 patients each. The first Group received conventional inotropic and vasoactive treatment at different doses, while the other group received levosimendan additionally at a loading dose of 6-12mic/kg according to mean arterial pressure over 0.5 hr followed by 24 hrs infusion at 0.05 to 0.2 mic/kg/min. Hemodynamic data were collected at the end and 30 minutes after CPB, after that at 6, 12, 24, and 36 hours post CPB. Mean arterial pressure (MAP), central venous pressure (CVP), heart rate (HR), mixed venous saturation (Svo2), and base deficit (BD) were measured. RESULTS: Levosimendan had significantly improved postoperative hemodynamic values as in the mixed venous pressure at different times postoperative (p < 0.05), also the base deficit at different times postoperative (p < 0.05), while there was a significant reduction in systemic vascular resistance as decreased mean arterial pressure in levosimendan group compared to conventional group at 6hrs postoperative mean 77.50 ± 10.81 vs 83.73 ± 10.81 with (p = 0.029), and at 12 hrs postoperative mean 77.37 ± 10.10vs 84.23 ± 13.81 with (p = 0.032), and there was no significant difference in heart rate at different times postoperative between both groups (p > 0.05), while there was no significant effect on mortality between both groups (p = 0.781). CONCLUSION: Levosimendan had improved hemodynamic parameters significantly with no effect on mortality compared to conventional inotropic agents in a patient with poor left ventricular function undergoing cardiac surgery.

Cardiovascular reflexes during abdominal ischemia in cats

1994 ◽  
Vol 267 (1) ◽  
pp. R97-R106 ◽  
Author(s):  
H. S. Huang ◽  
J. C. Longhurst
Keyword(s):  
Blood Pressure ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Femoral Vein ◽  
Venous Pressure ◽  
Vena Cava ◽  
Left Ventricular ◽  
Mesenteric Arteries ◽  
Cardiovascular Reflexes ◽  
Group 3

The cardiovascular effects of regional abdominal ischemia and reperfusion were studied in cats anesthetized with alpha-chloralose. In group 1 (n = 9), central venous pressure was kept constant by a servo-controller while the celiac and superior mesenteric arteries were occluded by loop snares for 10 min. In group 2 (n = 9), a constant-perfusion circuit to the celiac and superior mesenteric arteries that could divert flow to the femoral vein was used to induce abdominal ischemia. In group 3 (n = 7), venous return from the inferior vena cava was controlled, and a constant-perfusion circuit was used to induce abdominal ischemia. Abdominal ischemia significantly (P < 0.05) increased portal venous blood lactate from 4.3 +/- 0.6 to 6.0 +/- 0.6 mM in group 3. The early increases in blood pressure caused by passive volume shifts in groups 1 and 2 were abolished in group 3. The late, i.e., 10 min, response to abdominal ischemia consisted of significant (P < 0.05) increases in mean arterial pressure (29 +/- 7, 24 +/- 7, and 33 +/- 8 mmHg in groups 1, 2, and 3, respectively). Abdominal ischemia also significantly (P < 0.05) increased the first derivative of left ventricular pressure at 40 mmHg developed pressure from 4,355 +/- 377 to 4,839 +/- 407 mmHg/s in group 3. Celiac and superior mesenteric ganglionectomy abolished the late but not the early hemodynamic changes. Ganglionectomy also significantly (P < 0.05) enhanced the decrease in mean arterial pressure during reperfusion in all groups. We conclude that the pressor and contractile responses during 10 min of abdominal ischemia and the relative maintenance of blood pressure during reperfusion after ischemia are reflex in nature.

Augmented catecholamine uptake by the heart during hemorrhage in the conscious dog

1986 ◽  
Vol 250 (1) ◽  
pp. H76-H81 ◽  
Author(s):  
O. L. Woodman ◽  
J. Amano ◽  
T. H. Hintze ◽  
S. F. Vatner
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Coronary Sinus ◽  
Nerve Stimulation ◽  
Left Ventricular ◽  
Sympathetic Nerve Stimulation ◽  
Net Release

Changes in arterial and coronary sinus concentrations of norepinephrine (NE) and epinephrine (E) in response to hemorrhage were examined in conscious dogs. Hemorrhage (45 +/- 3.2 ml/kg) decreased mean arterial pressure by 47 +/- 6%, left ventricular (LV) dP/dt by 38 +/- 6%, and mean left circumflex coronary blood flow by 47 +/- 6%, while heart rate increased by 44 +/- 13%. Increases in concentrations of arterial NE (5,050 +/- 1,080 from 190 +/- 20 pg/ml) and E (12,700 +/- 3,280 from 110 +/- 20 pg/ml) were far greater than increases in coronary sinus NE (1,700 +/- 780 from 270 +/- 50 pg/ml) and E (4,300 +/- 2,590 from 90 +/- 10 pg/ml). Net release of NE from the heart at rest was converted to a fractional extraction of 66 +/- 9% after hemorrhage. Fractional extraction of E increased from 16 +/- 6% at rest to 73 +/- 8% after hemorrhage. In cardiac-denervated dogs, hemorrhage (46 +/- 2.8 ml/kg) decreased mean arterial pressure by 39 +/- 15%, LV dP/dt by 36 +/- 10%, and mean left circumflex coronary blood flow by 36 +/- 13%, while heart rate increased by 24 +/- 10%. Hemorrhage increased arterial NE (1,740 +/- 150 from 210 +/- 30 pg/ml) and E (3,050 +/- 880 from 140 +/- 20 pg/ml) more than it increased coronary sinus NE (460 +/- 50 from 150 +/- 30 pg/ml) and E (660 +/- 160 from 90 +/- 20 pg/ml) but significantly less (P less than 0.05) than observed in intact dogs. These experiments indicate that hemorrhage, unlike exercise and sympathetic nerve stimulation, does not induce net overflow of NE from the heart.(ABSTRACT TRUNCATED AT 250 WORDS)

Baroreceptor-mediated suppression of osmotically stimulated vasopressin in normal humans

1988 ◽  
Vol 65 (3) ◽  
pp. 1226-1230 ◽  
Author(s):  
S. R. Goldsmith
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Venous Pressure ◽  
Positive Pressure ◽  
Lower Body ◽  
Central Venous ◽  
Lower Body Positive Pressure ◽  
Body Positive

Increases in central venous pressure and arterial pressure have been reported to have variable effects on normal arginine vasopressin (AVP) levels in healthy humans. To test the hypothesis that baroreceptor suppression of AVP secretion might be more likely if AVP were subjected to a prior osmotic stimulus, we investigated the response of plasma AVP to increased central venous pressure and mean arterial pressure after hypertonic saline in six normal volunteers. Plasma AVP, serum osmolality, heart rate, central venous pressure, mean arterial pressure, and pulse pressure were assessed before and after a 0.06 ml.kg-1.min-1-infusion of 5% saline give over 90 min and then after 10 min of 30 degrees head-down tilt and 10 min of head-down tilt plus lower-body positive pressure. Hypertonic saline increased plasma AVP. After head-down tilt, which did not change heart rate, pulse pressure, or mean arterial pressure but did increase central venous pressure, plasma AVP fell. Heart rate, pulse pressure, and central venous pressure were unchanged from head-down tilt values during lower-body positive pressure, whereas mean arterial pressure increased. Plasma AVP during lower-body positive pressure was not different from that during tilt. Osmolality increased during the saline infusion but was stable throughout the remainder of the study. These data therefore suggest that an osmotically stimulated plasma AVP level can be suppressed by baroreflex activation. Either the low-pressure cardiopulmonary receptors (subjected to a rise in central venous pressure during head-down tilt) or the sinoaortic baroreceptors (subjected to hydrostatic effects during head-down tilt) could have been responsible for the suppression of AVP.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiorespiratory response patterns to afferent stimulation of muscle nerves in the rabbit

1996 ◽  
Vol 81 (1) ◽  
pp. 266-273 ◽  
Author(s):  
G. Raimondi ◽  
J. M. Legramante ◽  
F. Iellamo ◽  
S. Cassarino ◽  
G. Peruzzi
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Venous Pressure ◽  
Response Patterns ◽  
Central Venous ◽  
Frequency Stimulation ◽  
End Tidal ◽  
Stimulation Of

The aim of this study was to test the hypothesis that stimulation of thin fiber muscle afferents is capable of matching the cardiovascular and ventilatory responses. In 46 anesthetized rabbits, the central end of the gastrocnemius nerves was electrically stimulated at 3 [low-frequency stimulation (LFS)] and 100 Hz [high-frequency stimulation (HFS)]. Intensities up to 200 times motor threshold were used. LFS induced a decrease in both mean arterial pressure (-19.9 +/- 2.9%) and systemic vascular resistance (-23.9 +/- 3.2%) an increase in cardiac output (CO) (6.4 +/- 1.7%), stroke volume (7.3 +/- 3.0%) and pulmonary ventilation (VE) (26.7 +/- 2.3%); heart rate and central venous pressure were not changed significantly. HFS induced an increase in mean arterial pressure (11.1 +/- 4.9%), CO (15.8 +/- 5.4%), stroke volume (13.4 +/- 5.4%), and VE but no significant changes in heart rate, systemic vascular resistance and central venous pressure. In both response patterns, arterial and end-tidal CO2 did not change significantly. The patterns of cardiorespiratory responses to both LFS and HFS were characterized by an increase in Co and VE without concomitant decreases in arterial and end-tidal PCO2 (isocapnic hyperpnea).

Cardiovascular Effects of Moxibustion at Jen Chung (Go-26) during Halothane Anesthesia in Dogs

1975 ◽  
Vol 03 (03) ◽  
pp. 245-261 ◽  
Author(s):  
Do Chil Lee ◽  
Myung O. Lee ◽  
Donald H. Clifford
Keyword(s):  
Heart Rate ◽  
Cardiac Output ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Stroke Volume ◽  
Total Peripheral Resistance ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Cardiovascular Effects ◽  
Halothane Anesthesia

The cardiovascular effects of moxibustion at Jen Chung (Go-26) in 10 dogs under halothane anesthesia were compared to 5 dogs under halothane anesthesia without moxibustion and 5 dogs under halothane anesthesia in which moxibustion was effected at a neutral or non-acupuncture site. Cardiac output, stroke volume, heart rate, mean arterial pressure, central venous pressure, total peripheral resistance, pH, PaCO2, PaO2 and base deficit were measured over a two-hour period. A significant increase in cardiac output and stroke volume and a significant decrease in the total peripheral resistance were observed in the group which was stimulated by moxibustion at Jen Chun (Go-26). Heart rate, mean arterial pressure and pulse pressure were significantly increase during the early part of the two-hour period in the same group. The cardiovascular effects of moxibustion at Jen Chung (Go-26) which were observed at the end of the two hours were also present in two dogs in which measurements were continued for two additional hours.

Effects of the Second (Ethanol) Extract of Ginseng on the Cardiovascular Dynamics of Dogs During Halothane Anesthesia

1978 ◽  
Vol 06 (03) ◽  
pp. 247-252 ◽  
Author(s):  
DO CHIL LEE ◽  
CHON YUL KIM ◽  
MYUNG O. LEE ◽  
DONALD H. CLIFFORD
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Pressure Pulse ◽  
Venous Pressure ◽  
Peripheral Resistance ◽  
Electromagnetic Flowmeter ◽  
Ethanol Extract ◽  
Halothane Anesthesia ◽  
Cardiovascular Variables

An electromagnetic flowmeter probe was chronically implanted around the ascending aorta in a group of dogs. Subsequently, ten dogs were lightly anesthetized with halothane (0.75%), and a second (ethanol) extract of ginseng (40 mg/kg) was administered intravenously. Five dogs were anesthesized without the administration of ginseng. Eleven cardiovascular variables including cardiac output, stroke volume, heart rate, mean arterial pressure, pulse pressure, central venous pressure, total peripheral resistance, pH, PaCo2, Pa2, and base deficit were compared for two hours. Then heart rate and mean arterial pressure were significantly decreased following ginseng. There were no other meaningful changes in either group.

Chronic elevation of renal venous pressure induces extensive renal venous collateral formation and modulates renal function and cardiovascular stability in rats

2020 ◽  
Vol 319 (1) ◽  
pp. F76-F83
Author(s):  
Shereen M. Hamza ◽  
Xiaohua Huang ◽  
Tayyaba Zehra ◽  
Wenqing Zhuang ◽  
William A. Cupples ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Heart Rate ◽  
Renal Function ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Venous Pressure ◽  
Similar Degree ◽  
Sham Operation ◽  
Baseline Renal Function ◽  
Collateral Formation

Acutely increased renal venous pressure (RVP) impairs renal function, but the long-term impact is unknown. We investigated whether chronic RVP elevation impairs baseline renal function and prevents exacerbation of renal dysfunction and cardiovascular instability upon further RVP increase. RVP elevation (20–25 mmHg) or sham operation (sham) was performed in rats. After 1 wk ( n = 17) or 3 wk ( n = 22), blood pressure, RVP, renal blood flow (RBF), renal vascular conductance (RVC), and glomerular filtration rate (GFR) were measured at baseline and during superimposed RVP increase. Chronic RVP elevation induced extensive renal venous collateral formation. RVP fell to 6 ± 1 mmHg at 1 wk and 3 ± 1 mmHg at 3 wk. Baseline blood pressure and heart rate were unaltered compared with sham. RBF, RVC, and GFR were reduced at 1 wk but normalized by 3 wk. Upon further RVP increase, the drop in mean arterial pressure was attenuated at 3 wk compared with 1 wk ( P < 0.05), whereas heart rate fell comparably across all groups; the mean arterial pressure-heart rate relationship was disrupted at 1 and 3 wk. RBF fell to a similar degree as sham at 1 wk (−2.3 ± 0.7 vs. −3.9 ± 1.2 mL/min, P = 0.066); however, at 3 wk, this was attenuated compared with sham (−1.5 ± 0.5 vs. −4.2 ± 0.7 mL/min, P < 0.05). The drop in RVC and GFR was attenuated at 1 and 3 wk ( P < 0.05). Thus, chronic RVP elevation induced by partial renal vein ligation elicits extensive renal venous collateral formation, and although baseline renal function is impaired, chronic RVP elevation in this manner induces protective adaptations in kidneys of healthy rats, which attenuates the hemodynamic response to further RVP increase.

Neurocirculatory Responses to Sevoflurane in Humans

1995 ◽  
Vol 83 (1) ◽  
pp. 88-95. ◽  
Author(s):  
Thomas J. Ebert ◽  
Michael Muzi ◽  
Craig W. Lopatka
Keyword(s):  
Heart Rate ◽  
Steady State ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Central Venous Pressure ◽  
Sympathetic Nerve ◽  
Sympathetic Nerve Activity ◽  
Venous Pressure ◽  
Central Venous ◽  
Nerve Activity

Background Sevoflurane and desflurane are new volatile anesthetics with low blood solubilities that confer properties of rapid anesthetic induction and emergence. Desflurane has been associated with neurocirculatory excitation after the rapid increase in inspired concentrations. The current study evaluated and compared the sympathetic and hemodynamic responses associated with the administration of sevoflurane to those associated with administration of desflurane in humans. Methods After Institutional Review Board approval, 21 healthy, young (19-32 yr) volunteers were randomly selected for participation. Arterial and central venous pressures were measured directly, and heart rate, forearm blood flow, and plasma norepinephrine concentrations were determined indirectly. Efferent muscle sympathetic nerve activity was recorded by microneurography. After neurocirculatory recordings at conscious baseline, measurements were repeated beginning 2 min after 2 mg/kg propofol while the anesthetic was increased incrementally by mask over a 10-min period at 1%, 2%, and 3% sevoflurane (n = 12) or 3%, 6%, and 9% desflurane (n = 9). Responses to intubation were recorded and, 20 min later, recordings were evaluated during steady-state periods of 0.41, 0.83, and 1.24 MAC. Data also were obtained after steady-state 0.83 MAC measurements when the inspired gas concentration was rapidly increased to either 3% sevoflurane or 9% desflurane ("transition" to 1.24 MAC). Results Neurocirculatory variables did not differ between the two groups at conscious baseline. During the period of administration via mask and during the "transition" period, the significant increases in sympathetic nerve activity, heart rate, mean arterial pressure, and central venous pressure associated with desflurane were not observed with sevoflurane. Ten minutes after induction, mean arterial pressure and heart rate responses to intubation did not differ between groups. With increasing anesthetic concentration, there were progressive and similar decreases in mean arterial pressure in both groups and no changes in heart rate. Central venous pressure, sympathetic nerve activity, and plasma norepinephrine increased with the greater minimum alveolar concentration multiple of desflurane but not with that of sevoflurane. Conclusions The neurocirculatory excitation seen with rapid increases in desflurane did not occur with sevoflurane. At steady-state, increasing the concentration of sevoflurane was associated with lower sympathetic nerve activity and central venous pressure and similar mean arterial pressure and heart rate with that of desflurane.

Bradykinin contributes to the exercise pressor reflex: mechanism of action

1993 ◽  
Vol 75 (5) ◽  
pp. 2061-2068 ◽  
Author(s):  
H. L. Pan ◽  
C. L. Stebbins ◽  
J. C. Longhurst
Keyword(s):  
Heart Rate ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Left Ventricular Pressure ◽  
Muscle Afferents ◽  
Left Ventricular ◽  
Receptor Blockade ◽  
Exercise Pressor Reflex ◽  
Pressor Reflex ◽  
Over Time

This study determined the receptors responsible for mediating bradykinin's effect on skeletal muscle afferents that cause the pressor reflex in anesthetized cats. In eight cats, 1 microgram of bradykinin was injected intra-arterially into the gracilis muscle before and after intravenous injection of a kinin B2-receptor antagonist (NPC 17731, 20 micrograms/kg). Initial injection of bradykinin reflexly increased mean arterial pressure by 23 +/- 7 mmHg, maximal change in pressure over time by 439 +/- 272 mmHg/s, and heart rate by 11 +/- 4 beats/min. The hemodynamic response to bradykinin was abolished by kinin B2-receptor blockade. Similar injection of the kinin B1-receptor agonist des-Arg9-bradykinin caused no cardiovascular responses (n = 6). In eight different animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses to 30 s of electrically stimulated hindlimb contraction were attenuated by 50 +/- 6, 55 +/- 7, and 41 +/- 8%, respectively, after kinin B2-receptor blockade. In eight other animals, mean arterial pressure, maximal change in left ventricular pressure over time, and heart rate responses were reduced by 58 +/- 8, 66 +/- 6, and 40 +/- 12%, respectively, after inhibition of prostaglandin synthesis with indomethacin (2.5–3 mg/kg iv) and were then abolished by subsequent B2-receptor blockade. These data suggest that bradykinin contributes to the exercise pressor reflex through its action on kinin B2 receptors located on the nerve endings of the muscle afferents.(ABSTRACT TRUNCATED AT 250 WORDS)

Effects of calcium entry blockade on left ventricular dynamics in exercising dogs

1986 ◽  
Vol 251 (3) ◽  
pp. H656-H663
Author(s):  
R. A. Walsh ◽  
F. X. Cleary ◽  
R. A. O'Rourke
Keyword(s):  
Heart Rate ◽  
Blood Flow ◽  
Mean Arterial Pressure ◽  
Arterial Pressure ◽  
Coronary Blood Flow ◽  
Left Ventricular ◽  
Calcium Entry ◽  
Peak Exercise ◽  
Beta Blockade ◽  
Lv Function

To study the previously undefined effects of calcium entry blockade on left ventricular (LV) function and coronary blood flow during dynamic exercise we gave intravenous equihypotensive infusions of nifedipine (10 +/- 4 SE micrograms X kg-1 X min-1), diltiazem (60 +/- 8 micrograms X kg-1 X min-1), and verapamil (52 +/- 7 micrograms X kg-1 X min-1) before and after intravenous propranolol (2 mg/kg) to chronically instrumented dogs at rest and while running on a treadmill at 4 and 10 km/h. Prior to beta-blockade, each agent significantly and equivalently (P = NS among drugs) reduced mean arterial pressure during exercise (-13% nifedipine, -8% diltiazem, -15% verapamil at 4 km/h, each P less than or equal to 0.01 vs. exercise alone) but did not significantly alter LV end-diastolic dimension (EDD), heart rate, or cardiac output compared with exercise alone. Only verapamil blunted the positive inotropic response to exercise (LV dP/dtmax decreased 20% at 4 km/h, P less than 0.01 vs. exercise alone). Coronary blood flow was significantly and equivalently increased at rest and during submaximal exercise with each calcium blocker, but this effect was largely offset by propranolol. During exercise after beta-blockade each agent produced significant additional reductions in mean arterial pressure and dP/dtmax at peak exercise but did not alter LVEDD or heart rate compared with results obtained with propranolol alone. Combined beta-blockade and verapamil uniquely diminished myocardial contractility to a greater extent at peak exercise than at rest (dP/dtmax 1,260 +/- 410 peak exercise vs. 1,775 +/- 431 mmHg/s rest, P less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)

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