Abstract 11340: Increasing Mean Arterial Pressure or Cardiac Output in Comatose Out-of-Hospital Cardiac Arrest Patients Undergoing Targeted Temperature Management: Effects on Cerebral Tissue Oxygenation

Circulation ◽  
2021 ◽  
Vol 144 (Suppl_2) ◽  
Author(s):  
Johannes Grand ◽  
Sebastian Wiberg ◽  
Jesper Kjaergaard ◽  
Christian Hassager

Introduction: There are few data regarding the effects of norepinephrine-uptitration on global and regional hemodynamics in cardiac intensive care patients. Methods: We prospectively studied 10 OHCA patients at our cardiac intensive care unit. The trial consisted of 5 phases. The first 4 phases were achieved by titrating norepinephrine to reach targets of mean arterial pressure (MAP). First a MAP of 65 mmHg, second 75 mmHg, third 85 mmHg, fourth 65 mmHg again. The fifth phase was with a constant MAP of 65 mmHg but aiming at an increased PaCO2 from 6.5-7.3 kPa to increase cardiac output. During each phase, 20 minutes steady state was achieved before measurements. We measured hemodynamic variables with a Swan-Ganz catheter, arterial and mixed venous blood gases, and near-infrared spectroscopy at the forehead (cerebral oxygen saturation). Results: To obtain a MAP at 85 mmHg, norepinephrine was increased from 0.11±0.02 to 0.18±0.02 μg · kg–1 · min–1 (P < 0.001). Norepinephrine uptitration significantly increased MAP, systemic vascular resistance and pulmonary artery pressure, without affecting cardiac output or heart rate. After phase 3, norepinephrine was decreased to basal values, and all variables returned to baseline. Increasing pCO2, resulted in a significant increase in cardiac output and cerebral oxygen saturation, while decreasing systemic vascular resistance. MAP (and NE dose) was unaffected by increasing pCO2. Conclusions: A short-term increase in MAP with norepinephrine in resuscitated OHCA-patients is associated with increased SVR and PVR without affecting cardiac output or NIRS of the brain. An increase in CO caused by an increase in pCO2 and thereby a decreased SVR increased NIRS potentially improving brain oxygenation.

2008 ◽  
Vol 108 (5) ◽  
pp. 802-811 ◽  
Author(s):  
Robert A. Dyer ◽  
Jenna L. Piercy ◽  
Anthony R. Reed ◽  
Carl J. Lombard ◽  
Leann K. Schoeman ◽  
...  

Background Hemodynamic responses to spinal anesthesia (SA) for cesarean delivery in patients with severe preeclampsia are poorly understood. This study used a beat-by-beat monitor of cardiac output (CO) to characterize the response to SA. The hypothesis was that CO would decrease from baseline values by less than 20%. Methods Fifteen patients with severe preeclampsia consented to an observational study. The monitor employed used pulse wave form analysis to estimate nominal stroke volume. Calibration was by lithium dilution. CO and systemic vascular resistance were derived from the measured stroke volume, heart rate, and mean arterial pressure. In addition, the hemodynamic effects of phenylephrine, the response to delivery and oxytocin, and hemodynamics during recovery from SA were recorded. Hemodynamic values were averaged for defined time intervals before, during, and after SA. Results Cardiac output remained stable from induction of SA until the time of request for analgesia. Mean arterial pressure and systemic vascular resistance decreased significantly from the time of adoption of the supine position until the end of surgery. After oxytocin administration, systemic vascular resistance decreased and heart rate and CO increased. Phenylephrine, 50 mug, increased mean arterial pressure to above target values and did not significantly change CO. At the time of recovery from SA, there were no clinically relevant changes from baseline hemodynamic values. Conclusions Spinal anesthesia in severe preeclampsia was associated with clinically insignificant changes in CO. Phenylephrine restored mean arterial pressure but did not increase maternal CO. Oxytocin caused transient marked hypotension, tachycardia, and increases in CO.


2019 ◽  
Author(s):  
Wei Tan ◽  
Dong-chen Qian ◽  
Meng-meng Zheng ◽  
Xuan Lu ◽  
Yuan Han ◽  
...  

Abstract Background: The infusion of magnesium sulfate is well known to reduce arterial pressure and attenuate hemodynamic response to pneumoperitoneum. This study aimed to investigate whether different doses of magnesium sulfate can effectively attenuate the pneumoperitoneum-related hemodynamic changes and the release of vasopressin in patients undergoing laparoscopic gastrointestinal surgery. Methods: Sixty-nine patients undergoing laparoscopic partial gastrectomy were randomized into three groups: group L received magnesium sulfate 30 mg/kg loading dose and 15 mg/kg/h continuous maintenance infusion for 1 h; group H received magnesium sulfate 50 mg/kg followed by 30 mg/kg/h for 1 h; and group S (control group) received same volume 0.9% saline infusion, immediately before the induction of pneumoperitoneum. Systemic vascular resistance (SVR), cardiac output (CO), mean arterial pressure (MAP), heart rate (HR), central venous pressure(CVP), serum vasopressin and magnesium concentrations were measured. The extubation time, visual analogue scale were also assessed. The primary outcome is the difference in SVR between different groups. The secondary outcome is the differences of other indicators between groups, such as CO, MAP, HR, CVP, vasopressin and postoperative pain score. Results: Pneumoperitoneum instantly resulted in a significant reduction of cardiac output and an increase in mean arterial pressure, systemic vascular resistance, central venous pressure and heart rate in the control group (P < 0.01). The mean arterial pressure (T2 – T4), systemic vascular resistance (T2 – T3), central venous pressure(T3-T5) and the level of serum vasopressin were significantly lower (P < 0.05) and the cardiac output (T2 – T3) was significantly higher (P < 0.05) in group H than those in the control group. The mean arterial pressure (T4), systemic vascular resistance (T2), and central venous pressure(T3-T4) were significantly lower in group H than those in group L (P < 0.05). Furthermore, the visual analog scales at 5 min and 20 min, the level of vasopressin, and the dose of remifentanil were significantly decreased in group H compared to the control group and group L (P < 0.01). Conclusion: Magnesium sulfate could safely and effectively attenuate the pneumoperitoneum-related hemodynamic instability during gastrointestinal laparoscopy and improve postoperative pain at serum magnesium concentrations above 2 mmol/L.


2019 ◽  
Author(s):  
Wei Tan ◽  
Dong-chen Qian ◽  
Meng-meng Zheng ◽  
Xuan Lu ◽  
Yuan Han ◽  
...  

Abstract Background: The infusion of magnesium sulfate is well known to reduce arterial pressure and attenuate hemodynamic response to pneumoperitoneum. This study aimed to investigate whether different doses of magnesium sulfate can effectively attenuate the pneumoperitoneum-related hemodynamic changes and the release of vasopressin in patients undergoing laparoscopic gastrointestinal surgery. Methods: Sixty-nine patients undergoing laparoscopic partial gastrectomy were randomized into three groups: group L received magnesium sulfate 30 mg/kg loading dose and 15 mg/kg/h continuous maintenance infusion for 1 h; group H received magnesium sulfate 50 mg/kg followed by 30 mg/kg/h for 1 h; and group S (control group) received same volume 0.9% saline infusion, immediately before the induction of pneumoperitoneum. Systemic vascular resistance (SVR), cardiac output (CO), mean arterial pressure (MAP), heart rate (HR), central venous pressure(CVP), serum vasopressin and magnesium concentrations were measured. The extubation time, visual analogue scale were also assessed. The primary outcome is the difference in SVR between different groups. The secondary outcome is the differences of other indicators between groups, such as CO, MAP, HR, CVP, vasopressin and postoperative pain score. Results: Pneumoperitoneum instantly resulted in a significant reduction of cardiac output and an increase in mean arterial pressure, systemic vascular resistance, central venous pressure and heart rate in the control group (P < 0.01). The mean arterial pressure (T2 – T4), systemic vascular resistance (T2 – T3), central venous pressure(T3-T5) and the level of serum vasopressin were significantly lower (P < 0.05) and the cardiac output (T2 – T3) was significantly higher (P < 0.05) in group H than those in the control group. The mean arterial pressure (T4), systemic vascular resistance (T2), and central venous pressure(T3-T4) were significantly lower in group H than those in group L (P < 0.05). Furthermore, the visual analog scales at 5 min and 20 min, the level of vasopressin, and the dose of remifentanil were significantly decreased in group H compared to the control group and group L (P < 0.01). Conclusion: Magnesium sulfate could safely and effectively attenuate the pneumoperitoneum-related hemodynamic instability during gastrointestinal laparoscopy and improve postoperative pain at serum magnesium concentrations above 2 mmol/L.


1992 ◽  
Vol 73 (1) ◽  
pp. 324-328 ◽  
Author(s):  
J. Meyer ◽  
L. D. Traber ◽  
S. Nelson ◽  
C. W. Lentz ◽  
H. Nakazawa ◽  
...  

Septic shock is characterized by an increase in cardiac output and a fall in systemic vascular resistance index and mean arterial pressure. Endotoxin alters the smooth muscle function of blood vessels, probably by means of an increased production of the potent vasodilator nitric oxide (NO). The present study was accomplished to determine how the inhibition of NO synthesis influences cardiovascular performance in an ovine model of hyperdynamic endotoxemia. Endotoxemia was induced in five range ewes (41 +/- 2 kg) by continuous infusion of Escherichia coli endotoxin (LPS, 10 ng.kg-1.min-1) over the entire study period. After 24 h of LPS infusion, cardiac output increased from 5.2 +/- 0.3 to 7.9 +/- 0.6 (SE) 1/min (P less than 0.05) and mean arterial pressure and systemic vascular resistance index fell from 92 +/- 5 to 79 +/- 6 mmHg (P = 0.08) and from 1,473 +/- 173 to 824 +/- 108 dyn.s.cm-5.m2 (P less than 0.05), respectively. The pulmonary shunt fraction increased from 0.23 +/- 0.03 to 0.32 +/- 0.03 (P less than 0.05). The intravenous administration of the NO synthase inhibitor N omega-nitro-L-arginine methyl ester (25 mg/kg) 24 h after the start of the LPS infusion changed these values to approximately baseline levels over the subsequent 4 h. Although N omega-nitro-L-arginine methyl ester increased pulmonary arterial pressure and pulmonary vascular resistance (P less than 0.05), right and left ventricular stroke volume index showed no significant changes. It is concluded that NO has a major function in cardiovascular performance in endotoxemia.(ABSTRACT TRUNCATED AT 250 WORDS)


2019 ◽  
Author(s):  
Wei Tan ◽  
Dong-chen Qian ◽  
Meng-meng Zheng ◽  
Xuan Lu ◽  
Yuan Han ◽  
...  

Abstract Background The infusion of magnesium sulfate is well known to reduce arterial pressure and attenuate hemodynamic response to pneumoperitoneum. This study aimed to investigate whether different doses of magnesium sulfate can effectively attenuate the pneumoperitoneum-related hemodynamic changes and the release of vasopressin in patients undergoing laparoscopic gastrointestinal surgery. Methods Sixty-nine patients undergoing laparoscopic partial gastrectomy were randomized into three groups: group L received magnesium sulfate 30 mg/kg loading dose and 15 mg/kg/h continuous maintenance infusion for 1 h; group H received magnesium sulfate 50 mg/kg followed by 30 mg/kg/h for 1 h; and group S (control group) received same volume 0.9% saline infusion, immediately before the induction of pneumoperitoneum. Systemic vascular resistance (SVR), cardiac output (CO), mean arterial pressure (MAP), heart rate (HR), serum vasopressin and magnesium concentrations were measured. The extubation time, visual analogue scale were also assessed. The primary outcome is the difference in SVR between different groups. The secondary outcome is the differences of other indicators between groups, such as CO, MAP, HR, vasopressin and postoperative pain score. Results Pneumoperitoneum instantly resulted in a significant reduction of cardiac output and an increase in mean arterial pressure, systemic vascular resistance, and heart rate in the control group (P < 0.01). The mean arterial pressure (T2 – T4), systemic vascular resistance (T2 – T3) and the level of serum vasopressin were significantly lower (P < 0.05) and the cardiac output (T2 – T3) was significantly higher (P < 0.05) in group H than those in the control group. The mean arterial pressure (T4) and systemic vascular resistance (T2) were significantly lower in group H than those in group L (P < 0.05). Furthermore, the visual analogue scales at 5 min and 20 min, the level of vasopressin, and the dosage of remifentanil were significantly decreased in group H compared to the control group and group L (P < 0.01). Conclusion Magnesium sulfate could safely and effectively attenuate the pneumoperitoneum-related hemodynamic instability during gastrointestinal laparoscopy and improve postoperative pain at serum magnesium concentrations above 2 mmol/L.


2019 ◽  
Vol 19 (1) ◽  
Author(s):  
Wei Tan ◽  
Dong-chen Qian ◽  
Meng-meng Zheng ◽  
Xuan Lu ◽  
Yuan Han ◽  
...  

Abstract Background The infusion of magnesium sulfate is well known to reduce arterial pressure and attenuate hemodynamic response to pneumoperitoneum. This study aimed to investigate whether different doses of magnesium sulfate can effectively attenuate the pneumoperitoneum-related hemodynamic changes and the release of vasopressin in patients undergoing laparoscopic gastrointestinal surgery. Methods Sixty-nine patients undergoing laparoscopic partial gastrectomy were randomized into three groups: group L received magnesium sulfate 30 mg/kg loading dose and 15 mg/kg/h continuous maintenance infusion for 1 h; group H received magnesium sulfate 50 mg/kg followed by 30 mg/kg/h for 1 h; and group S (control group) received same volume 0.9% saline infusion, immediately before the induction of pneumoperitoneum. Systemic vascular resistance (SVR), cardiac output (CO), mean arterial pressure (MAP), heart rate (HR), central venous pressure (CVP), serum vasopressin and magnesium concentrations were measured. The extubation time, visual analogue scale were also assessed. The primary outcome is the difference in SVR between different groups. The secondary outcome is the differences of other indicators between groups, such as CO, MAP, HR, CVP, vasopressin and postoperative pain score. Results Pneumoperitoneum instantly resulted in a significant reduction of cardiac output and an increase in mean arterial pressure, systemic vascular resistance, central venous pressure and heart rate in the control group (P <  0.01). The mean arterial pressure (T2 – T4), systemic vascular resistance (T2 – T3), central venous pressure(T3-T5) and the level of serum vasopressin were significantly lower (P <  0.05) and the cardiac output (T2 – T3) was significantly higher (P <  0.05) in group H than those in the control group. The mean arterial pressure (T4), systemic vascular resistance (T2), and central venous pressure(T3-T4) were significantly lower in group H than those in group L (P <  0.05). Furthermore, the visual analog scales at 5 min and 20 min, the level of vasopressin, and the dose of remifentanil were significantly decreased in group H compared to the control group and group L (P <  0.01). Conclusion Magnesium sulfate could safely and effectively attenuate the pneumoperitoneum-related hemodynamic instability during gastrointestinal laparoscopy and improve postoperative pain at serum magnesium concentrations above 2 mmol/L. Trial registration The study was retrospectively registered at Chinese Clinical Trial Registry; the registration number is ChiCTR-IPD-17011145, principal investigator: D.Y. Q., date of registration: April 13, 2017.


2019 ◽  
Author(s):  
Wei Tan ◽  
Dong-chen Qian ◽  
Meng-meng Zheng ◽  
Xuan Lu ◽  
Yuan Han ◽  
...  

Abstract Background: The infusion of magnesium sulfate is well known to reduce arterial pressure and attenuate hemodynamic response to pneumoperitoneum. This study aimed to investigate whether different doses of magnesium sulfate can effectively attenuate the pneumoperitoneum-related hemodynamic changes and the release of vasopressin in patients undergoing laparoscopic gastrointestinal surgery. Methods: Sixty-nine patients undergoing laparoscopic partial gastrectomy were randomized into three groups: group L received magnesium sulfate 30 mg/kg loading dose and 15 mg/kg/h continuous maintenance infusion for 1 h; group H received magnesium sulfate 50 mg/kg followed by 30 mg/kg/h for 1 h; and group S (control group) received same volume 0.9% saline infusion, immediately before the induction of pneumoperitoneum. Systemic vascular resistance (SVR), cardiac output (CO), mean arterial pressure (MAP), heart rate (HR), central venous pressure(CVP), serum vasopressin and magnesium concentrations were measured. The extubation time, visual analogue scale were also assessed. The primary outcome is the difference in SVR between different groups. The secondary outcome is the differences of other indicators between groups, such as CO, MAP, HR, CVP, vasopressin and postoperative pain score. Results: Pneumoperitoneum instantly resulted in a significant reduction of cardiac output and an increase in mean arterial pressure, systemic vascular resistance, central venous pressure and heart rate in the control group (P < 0.01). The mean arterial pressure (T2 – T4), systemic vascular resistance (T2 – T3), central venous pressure(T3-T5) and the level of serum vasopressin were significantly lower (P < 0.05) and the cardiac output (T2 – T3) was significantly higher (P < 0.05) in group H than those in the control group. The mean arterial pressure (T4) , systemic vascular resistance (T2) and central venous pressure(T3-T4) were significantly lower in group H than those in group L (P < 0.05). Furthermore, the visual analogue scales at 5 min and 20 min, the level of vasopressin, and the dosage of remifentanil were significantly decreased in group H compared to the control group and group L (P < 0.01). Conclusion: Magnesium sulfate could safely and effectively attenuate the pneumoperitoneum-related hemodynamic instability during gastrointestinal laparoscopy and improve postoperative pain at serum magnesium concentrations above 2 mmol/L.


1999 ◽  
Vol 86 (6) ◽  
pp. 1890-1896 ◽  
Author(s):  
D. Slamowitz ◽  
L. Chen ◽  
S. M. Scharf

There are few studies investigating the influence of vagally mediated reflexes on the cardiovascular response to apneas. In 12 sedated preinstrumented pigs, we studied the effects of vagotomy during apneas, controlling for apnea periodicity and thoracic mechanical effects. Nonobstructive apneas were produced by paralyzing and mechanically ventilating the animals, then turning the ventilator off and on every 30 s. Before vagotomy, relative to baseline, apnea caused increased mean arterial pressure (MAP; +19 ± 25%, P < 0.05), systemic vascular resistance (SVR; +33 ± 16%, P < 0.0005), and heart rate (HR; +5 ± 6%, P < 0.05) and decreased cardiac output (CO) and stroke volume (SV; −16 ± 10% P < 0.001). After vagotomy, no significant change occurred in MAP, SVR, and SV during apneas, but CO and HR increased relative to baseline. HR was always greater (∼14%, P < 0.01) during the interapneic interval compared with during apnea. We conclude that vagally mediated reflexes are important mediators of the apneic pressor response. HR increases after apnea termination are related, at least in part, to nonvagally mediated reflexes.


1993 ◽  
Vol 85 (2) ◽  
pp. 157-163 ◽  
Author(s):  
R. J. MacFadyen ◽  
M. Tree ◽  
A. F. Lever ◽  
J. L. Reid

1. Haemodynamic and hormonal responses to infused angiotensin II were studied in conscious salt-deplete dogs during infusion of D-glucose or losartan (DuP753/MK954). 2. Mean arterial pressure (118±13mmHg) fell rapidly after losartan (60 min 106±18 mmHg) with a rise in heart rate (107±16 beats/min) from baseline (98±17 beats/min). Pressor responses to angiotensin II during D-glucose infusion (6 ng min−1 kg−1, 99±10 mmHg; 18 ng min−1 kg−1, 140±15 mmHg; 54 ng min−1 kg−1, 157±12 mmHg; 162 ng min−1 kg−1, 178±14 mmHg) showed a parallel shift during losartan infusion with very similar pressures in response to higher rates of angiotensin II infusion (54 ng min−1 kg−1,108 ± 17 mmHg;162 ng min−1 kg−1 138±14 mmHg; 486 ng min−1 kg−1, 155±14 mmHg; 1458 ng min−1 kg−1, 177 ± 12 mmHg). Losartan caused a fall in baseline systemic vascular resistance. Despite the similar mean arterial pressure, the rise in systemic vascular resistance after angiotensin II during D-glucose infusion (162 ng min−1 kg−1, 8065± 1967 dyn s cm−5) was reduced during losartan infusion (1458 ng min−1 kg−1, 6645 ±1720 dyn s cm−5. Losartan caused a small rise in cardiac output related to a rise in heart rate and increased stroke volume. Pressure infusions of angiotensin II caused a fall in cardiac output during D-glucose infusion, which was blocked during losartan infusion. The rise in heart rate in response to angiotensin II was similar during both D-glucose and losartan infusion, but with higher absolute values during losartan alone. There was a linear relationship between heart rate and the plasma concentration of angiotensin II, which was unaffected by losartan. Pulmonary pressure was marginally elevated by losartan, related to the rise in cardiac output, and was much less sensitive to angiotensin II infusion, rising only at the highest rate of infusion during both D-glucose and losartan infusion. 3. Losartan infusion alone caused a rise in plasma angiotensin II concentration with a fall in aldosterone concentration. During pressor infusions the measured angiotensin II concentrations suggested that losartan increased the clearance of angiotensin II. 4. Losartan has complex effects on cardiovascular function. The pressor response of mean arterial pressure to angiotensin II shows competitive inhibition, but this marks subtle effects on cardiac output and heart rate, in addition to systemic vascular resistance. In addition to elevating endogenous angiotensin II and suppressing aldosterone, losartan may enhance clearance of infused angiotensin II.


1982 ◽  
Vol 243 (5) ◽  
pp. H748-H753 ◽  
Author(s):  
J. C. Longhurst ◽  
J. Ibarra

There is presently little information on the efferent mechanisms responsible for the reflex cardiovascular activation during passive gastric distension. Therefore, 40 cats anesthetized with alpha-chloralose were studied with passive gastric balloon distention before and during 1) two repeated gastric distensions, 2) beta-adrenergic blockade with propranolol, 3) alpha-adrenergic blockade with phentolamine, or 4) bilateral adrenalectomy. Before and during each distension mean arterial pressure, heart rate, cardiac output, rate of rise of left ventricular pressure (dP/dt) at 40 mmHg developed pressure and calculated systemic vascular resistance were determined. Repeated gastric distension caused similar hemodynamic responses without tachyphylaxis. beta-Blockade significantly reduced the increase in dP/dt from 893 +/- 362 to 150 +/- 63 mmHg/s. alpha-Blockade significantly altered the changes in mean arterial pressure from 33 +/- 5.0 to -2 +/- 4.7 mmHg and systemic vascular resistance from 0.114 +/- 0.019 to 0.004 +/- 0.031 peripheral resistance units. Bilateral adrenalectomy significantly diminished the contractile response from 525 +/- 107 to 50 +/- 85 mmHg/s but did not significantly alter the pressor and vasoconstrictor responses. We conclude that, during passive gastric distension in cats, the increase in myocardial contractility is mediated by beta-adrenergic-receptor stimulation, whereas the arterial vasoconstrictor and pressor responses are mediated by alpha-adrenergic receptor stimulation. Additionally, during gastric distension a substantial portion of the contractile response is dependent on the integrity of the adrenal glands.


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