Cerebral blood flow, cardiac output, cardiac work, mean arterial pressure and right heart pressure during postural syncope

Background The effect of volatile anesthetics on cerebral blood flow depends on the balance between the indirect vasoconstrictive action secondary to flow-metabolism coupling and the agent's intrinsic vasodilatory action. This study compared the direct cerebral vasodilatory actions of 0.5 and 1.5 minimum alveolar concentration (MAC) sevoflurane and isoflurane during an propofol-induced isoelectric electroencephalogram. Methods Twenty patients aged 20-62 yr with American Society of Anesthesiologists physical status I or II requiring general anesthesia for routine spinal surgery were recruited. In addition to routine monitoring, a transcranial Doppler ultrasound was used to measure blood flow velocity in the middle cerebral artery, and an electroencephalograph to measure brain electrical activity. Anesthesia was induced with propofol 2.5 mg/kg, fentanyl 2 micro/g/kg, and atracurium 0.5 mg/kg, and a propofol infusion was used to achieve electroencephalographic isoelectricity. End-tidal carbon dioxide, blood pressure, and temperature were maintained constant throughout the study period. Cerebral blood flow velocity, mean blood pressure, and heart rate were recorded after 20 min of isoelectric encephalogram. Patients were then assigned to receive either age-adjusted 0.5 MAC (0.8-1%) or 1.5 MAC (2.4-3%) end-tidal sevoflurane; or age-adjusted 0.5 MAC (0.5-0.7%) or 1.5 MAC (1.5-2%) end-tidal isoflurane. After 15 min of unchanged end-tidal concentration, the variables were measured again. The concentration of the inhalational agent was increased or decreased as appropriate, and all measurements were repeated again. All measurements were performed before the start of surgery. An infusion of 0.01% phenylephrine was used as necessary to maintain mean arterial pressure at baseline levels. Results Although both agents increased blood flow velocity in the middle cerebral artery at 0.5 and 1.5 MAC, this increase was significantly less during sevoflurane anesthesia (4+/-3 and 17+/-3% at 0.5 and 1.5 MAC sevoflurane; 19+/-3 and 72+/-9% at 0.5 and 1.5 MAC isoflurane [mean +/- SD]; P<0.05). All patients required phenylephrine (100-300 microg) to maintain mean arterial pressure within 20% of baseline during 1.5 MAC anesthesia. Conclusions In common with other volatile anesthetic agents, sevoflurane has an intrinsic dose-dependent cerebral vasodilatory effect. However, this effect is less than that of isoflurane.

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Cerebral blood flow and evoked potentials during Cushing response in sheep

AJP Heart and Circulatory Physiology ◽

10.1152/ajpheart.1989.256.3.h779 ◽

1989 ◽

Vol 256 (3) ◽

pp. H779-H788

Author(s):

R. C. Koehler ◽

J. E. Backofen ◽

R. W. McPherson ◽

M. D. Jones ◽

M. C. Rogers ◽

...

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Cerebral Blood Flow ◽

Intracranial Pressure ◽

Arterial Pressure ◽

Evoked Potentials ◽

Aortic Pressure ◽

Base Line ◽

Auditory Evoked Responses ◽

Cushing Response

We determined how alterations in systemic hemodynamics, characteristic of the Cushing response, are related to changes in cerebral blood flow (CBF), cerebral metabolic rate of O2 (CMRO2), and brain electrical conductive function, as assessed by somatosensory-evoked potentials (SEP) and brain stem auditory-evoked responses (BAER). In three groups of eight pentobarbital-anesthetized sheep, intracranial pressure was gradually elevated to within 50, 25, or 0 mmHg of base-line mean arterial pressure and then held constant for 40 min by intraventricular infusion of mock cerebrospinal fluid. Microsphere-determined CBF fell when cerebral perfusion pressure was less than 50 mmHg. CMRO2 fell when CBF fell greater than 30-40%. Mean aortic pressure and cardiac output increased when CBF fell greater than 40%, i.e., at approximately the level at which CMRO2 fell. Furthermore, the magnitude of the increase in arterial pressure and cardiac output correlated with the reduction of CMRO2. SEP latency did not increase unless CBF fell greater than 55-65%, corresponding to a 20-30% reduction of CMRO2. Increased latency of BAER wave V was associated with a fall in midbrain blood flow of greater than 65-70%. Thus increase in SEP and BAER latencies required reductions of flow greater than those required to elicit a systemic response. This demonstrates that there is a range of intracranial pressure over which the increase in arterial pressure preserves sufficient CBF to sustain minimal electrical conductive function. The best predictor of the onset and magnitude of the Cushing response in adult sheep is the decrease in CMRO2.

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Cerebrovascular effects of hypocapnia during adenosine-induced arterial hypotension

Journal of Neurosurgery ◽

10.3171/jns.1985.63.6.0937 ◽

1985 ◽

Vol 63 (6) ◽

pp. 937-943 ◽

Cited By ~ 7

Author(s):

David J. Boarini ◽

Neal F. Kassell ◽

James A. Sprowell ◽

Julie J. Olin ◽

Hans C. Coester

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Arterial Hypotension ◽

Content Type ◽

Blood Flows ◽

Before And After ◽

Regional Blood Flows ◽

Fine Print

✓ Profound arterial hypotension is à commonly used adjunct in surgery for aneurysms and arteriovenous malformations. Hyperventilation with hypocapnia is also used in these patients to increase brain slackness. Both measures reduce cerebral blood flow (CBF). Of concern is whether CBF is reduced below ischemic thresholds when both techniques are employed together. To determine this, 12 mongrel dogs were anesthetized with morphine, nitrous oxide, and oxygen, and then paralyzed with pancuronium and hyperventilated. Arterial pCO2 was controlled by adding CO2 to the inspired gas mixture. Cerebral blood flow was measured at arterial pCO2 levels of 40 and 20 mm Hg both before and after mean arterial pressure was lowered to 40 mm Hg with adenosine enhanced by dipyridamole. In animals where PaCO2 was reduced to 20 mm Hg and mean arterial pressure was reduced to 40 mm Hg, cardiac index decreased 42% from control and total brain blood flow decreased 45% from control while the cerebral metabolic rate of oxygen was unchanged. Hypocapnia with hypotension resulted in small but statistically significant reductions in all regional blood flows, most notably in the brain stem. The reported effects of hypocapnia on CBF during arterial hypotension vary depending on the hypotensive agents used. Profound hypotension induced with adenosine does not eliminate CO2 reactivity, nor does it lower blood flow to ischemic levels in this model, even in the presence of severe hypocapnia.

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Impact of blood pressure changes in cerebral blood perfusion of patients with ischemic Moyamoya disease evaluated by SPECT

Journal of Cerebral Blood Flow & Metabolism ◽

10.1177/0271678x20967458 ◽

2020 ◽

pp. 0271678X2096745

Author(s):

Zhao Liming ◽

Sun Weiliang ◽

Jia Jia ◽

Liang Hao ◽

Liu Yang ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cerebral Blood Flow ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Moyamoya Disease ◽

Emission Computed Tomography ◽

Study Cohort ◽

Pressure Changes ◽

The Impact

Our aim was to determine the impact of targeted blood pressure modifications on cerebral blood flow in ischemic moyamoya disease patients assessed by single-photon emission computed tomography (SPECT). From March to September 2018, we prospectively collected data of 154 moyamoya disease patients and selected 40 patients with ischemic moyamoya disease. All patients underwent in-hospital blood pressure monitoring to determine the mean arterial pressure baseline values. The study cohort was subdivided into two subgroups: (1) Group A or relative high blood pressure (RHBP) with an induced mean arterial pressure 10–20% higher than baseline and (2) Group B or relative low blood pressure (RLBP) including patients with mean arterial pressure 10–20% lower than baseline. All patients underwent initial SPECT study on admission-day, and on the following day, every subgroup underwent a second SPECT study under their respective targeted blood pressure values. In general, RHBP patients showed an increment in perfusion of 10.13% (SD 2.94%), whereas RLBP patients showed a reduction of perfusion of 12.19% (SD 2.68%). Cerebral blood flow of moyamoya disease patients is susceptible to small blood pressure changes, and cerebral autoregulation might be affected due to short dynamic blood pressure modifications.

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Decreased cardiac output at the onset of diabetes: renal mechanisms and peripheral vasoconstriction

AJP Endocrinology and Metabolism ◽

10.1152/ajpendo.2000.278.5.e917 ◽

2000 ◽

Vol 278 (5) ◽

pp. E917-E924 ◽

Cited By ~ 12

Author(s):

Michael W. Brands ◽

Sharyn M. Fitzgerald ◽

William H. Hewitt ◽

Allison E. Hailman

Keyword(s):

Blood Flow ◽

Type 1 Diabetes ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Replacement Therapy ◽

Sodium Intake ◽

Sodium Balance ◽

Insulin Replacement

Recently we reported that hindquarter blood flow, measured 24 h/day, decreased progressively over the first 6 days of type 1 diabetes in rats. That response, coupled with the tendency of mean arterial pressure to increase, suggested a vasoconstrictor response. The purpose of this study was to measure the changes in cardiac output together with the renal hemodynamic and excretory responses to allow integrative determination of whether vasoconstriction likely accompanies the onset of type 1 diabetes. Rats were instrumented with a Transonic flow probe on the ascending aorta and with artery and vein catheters, and cardiac output and mean arterial pressure were measured continuously, 24 h/day, throughout the study. The induction of diabetes, by withdrawing intravenous insulin-replacement therapy in streptozotocin-treated rats, caused a progressive decrease in cardiac output that was 85 ± 5% of control levels by day 7. This was associated with significant increases in glomerular filtration rate, renal blood flow, and microalbuminuria as well as urinary fluid and sodium losses, with a negative cumulative sodium balance averaging 15.7 ± 1.6 meq by day 7. Restoring insulin-replacement therapy reversed the renal excretory responses but did not correct the negative sodium balance, yet cardiac output returned rapidly to control values. Increasing sodium intake during the diabetic and recovery periods also did not significantly affect the cardiac output response during any period. These results indicate that cardiac output decreases significantly at the onset of type 1 diabetes without glycemic control, and although volume loss may contribute to this response, there also is a component that is not volume or sodium dependent. We suggest this may be due to vasoconstriction, but to what extent local blood flow autoregulation or active vasoconstriction may have mediated that response is not known.

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Relationship between Cardiopulmonary Bypass Flow Rate and Cerebral Embolization in Dogs

Anesthesiology ◽

10.1097/00000542-199911000-00031 ◽

1999 ◽

Vol 91 (5) ◽

pp. 1387-1387 ◽

Cited By ~ 11

Author(s):

Hulya Sungurtekin ◽

Walter Plöchl ◽

David J. Cook

Keyword(s):

Blood Flow ◽

Cerebral Blood Flow ◽

Cardiopulmonary Bypass ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Rank Order ◽

Brain Regions ◽

Pump Flow ◽

Cerebral Embolization ◽

The Brain

Background Cerebral embolization is a primary cause of cardiac surgical neurologic morbidity. During cardiopulmonary bypass (CPB), there are well-defined periods of embolic risk. In theory, cerebral embolization might be reduced by an increase in pump flow during these periods. The purpose of this study was to determine the CPB flow-embolization relation in a canine model. Methods Twenty mongrel dogs underwent CPB at 35 degrees C with alpha-stat management and a fentanyl-midazolam anesthetic. In each animal, CPB flow was adjusted to achieve a mean arterial pressure of 65-75 mmHg. During CPB, an embolic load of 1.2 x 10(5) 67 microm fluorescent microspheres was injected into the arterial inflow line. Before and after embolization, cerebral blood flow was determined using 15-microm microspheres. Tissue was taken from 12 brain regions and microspheres were recovered. The relation between pump flow and embolization/g of brain was determined. Results The mean arterial pressure at embolization was 67 +/-4 mmHg, and the range of pump flow was 0.9-3.5 l x min(-1)x m(-2). Cerebral blood flow was independent of pump flow. At lower pump flow, the percentage of that flow delivered to the brain increased. There was a strong inverse relation between pump flow and cerebral embolization (r = -0.708, P < 0.000 by Spearman rank order correlation). Conclusions Cerebral embolization is determined by the CPB flow. At an unchanged mean arterial pressure, as pump flow is reduced, a progressively greater proportion of that flow is delivered to the brain.

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Blood Pressure Deviations From Optimal Mean Arterial Pressure During Cardiac Surgery Measured With a Novel Monitor of Cerebral Blood Flow and Risk for Perioperative Delirium: A Pilot Study

Journal of Cardiothoracic and Vascular Anesthesia ◽

10.1053/j.jvca.2016.01.012 ◽

2016 ◽

Vol 30 (3) ◽

pp. 606-612 ◽

Cited By ~ 24

Author(s):

Daijiro Hori ◽

Laura Max ◽

Andrew Laflam ◽

Charles Brown ◽

Karin J. Neufeld ◽

...

Keyword(s):

Blood Pressure ◽

Blood Flow ◽

Cardiac Surgery ◽

Cerebral Blood Flow ◽

Mean Arterial Pressure ◽

Pilot Study ◽

Arterial Pressure

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Cardiac output and peripheral blood flow during occlusion of carotid arteries

American Journal of Physiology-Legacy Content ◽

10.1152/ajplegacy.1961.200.6.1185 ◽

1961 ◽

Vol 200 (6) ◽

pp. 1185-1190 ◽

Cited By ~ 19

Author(s):

C. Polosa ◽

G. Rossi

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Arterial Pressure ◽

Pressor Response ◽

Pressure Rise ◽

Blocking Agent ◽

Carotid Occlusion ◽

Peripheral Blood Flow ◽

Cardiac Work ◽

Anesthetized Dogs

Cardiac output and blood flow to the kidney, hind limb, and splanchnic area were studied in anesthetized dogs during the arterial pressure rise due to carotid occlusion. All the vascular beds studied exhibited an increased resistance to flow. Cardiac output was maintained constant through an increased cardiac work in spite of the increased arterial pressure. This increased cardiac work was reflexly produced as evidenced by the action of the adrenergic blocking agent dichloroisoproterenol (DCI). This drug allowed the reflex vasoconstriction and the consequent pressure rise, but preventing the reflex chronotropic and inotropic sympathetic effects on the heart resulted in a fall of cardiac output during carotid occlusion. It is concluded a) that the reflex increase in vasomotor tone is the main factor in the pressor response to carotid occlusion and b) that the reflex effect on the myocardium is an important factor in regulating cardiac output in this situation.

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Effects of Sodium Nitroprusside and Phenylephrine on Blood Flow in Free Musculocutaneous Flaps during General Anesthesia

Anesthesiology ◽

10.1097/00000542-199901000-00020 ◽

1999 ◽

Vol 90 (1) ◽

pp. 147-155 ◽

Cited By ~ 56

Author(s):

Andrej Banic ◽

Vladimir Krejci ◽

Dominique Erni ◽

Anthony M. Wheatley ◽

Gisli H. Sigurdsson

Keyword(s):

Blood Flow ◽

Cardiac Output ◽

Mean Arterial Pressure ◽

Arterial Pressure ◽

Sodium Nitroprusside ◽

Free Flaps ◽

Total Blood ◽

Musculocutaneous Flaps ◽

Microcirculatory Flow ◽

Total Blood Flow

Background Hypoperfusion and necrosis in free flaps used to correct tissue defects remain important clinical problems. The authors studied the effects of two vasoactive drugs, sodium nitroprusside and phenylephrine, which are used frequently in anesthetic practice, on total blood flow and microcirculatory flow in free musculocutaneous flaps during general anesthesia. Methods In a porcine model (n = 9) in which clinical conditions for anesthesia and microvascular surgery were simulated, latissimus dorsi free flaps were transferred to the lower extremity. Total blood flow in the flaps was measured using ultrasound flowmetry and microcirculatory flow was measured using laser Doppler flowmetry. The effects of sodium nitroprusside and phenylephrine were studied during local infusion through the feeding artery of the flap and during systemic administration. Results Systemic sodium nitroprusside caused a 30% decrease in mean arterial pressure, but cardiac output did not change. The total flow in the flap decreased by 40% (P < 0.01), and microcirculatory flow decreased by 23% in the skin (P < 0.01) and by 30% in the muscle (P < 0.01) of the flap. Sodium nitroprusside infused locally into the flap artery increased the total flap flow by 20% (P < 0.01). Systemic phenylephrine caused a 30% increase in mean arterial pressure, whereas heart rate, cardiac output, and flap blood flow did not change. Local phenylephrine caused a 30% decrease (P < 0.01) in the total flap flow. Conclusions Systemic phenylephrine in a dose increasing the systemic vascular resistance and arterial pressure by 30% appears to have no adverse effects on blood flow in free musculocutaneous flaps. Sodium nitroprusside, however, in a dose causing a 30% decrease in systemic vascular resistance and arterial pressure, causes a severe reduction in free flap blood flow despite maintaining cardiac output.

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