Abstract 2230: Lower Extremity Counterpulsation During The Decompression Phase of CPR Improves Hemodynamics And Provides Continuous Forward Carotid Blood Flow.

Circulation ◽  
2007 ◽  
Vol 116 (suppl_16) ◽  
Author(s):  
Demetris Yannopoulos ◽  
Henry R Halperin ◽  
Johns Hopkins ◽  
Keith G Lurie
Keyword(s):  
Blood Flow ◽  
Lower Extremity ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Fold Increase ◽  
Aortic Pressure ◽  
Hemodynamic Parameters ◽  
Carotid Blood Flow ◽  
Thoracic Decompression

Background: We hypothesize that lower extremity counterpulsations (LECP) during the decompression phase of CPR will increase diastolic aortic pressure without raising the intracranial pressure (ICP) and significantly increase forward carotid blood flow. Methods: In 6 (24±4Kg) pigs, 4 minutes of untreated VF were followed by 2 minutes epochs of standard (STD) CPR, STD +LECP, active compression decompression (ACD) +ITD and ACD + inspiratory impedance threshold device (ITD)+LECP. Compressions and ventilations were performed according to the 2005 AHA guidelines. A large blood pressure cuff that was circumferentially placed around the pig’s thighs avoiding the abdominal cavity was inflated with air to the point that manometer pressure started to rise. Compressions over the cuff were performed manually and synchronized with the thoracic decompression phase. The cuff was compressed up to 200mmHg. Basic hemodynamic parameters and common carotid blood flow (CCBF) (ml/min) were continuously measured. Cerebral perfusion pressure (CerPP) (mean arterial pressure - mean ICP) and CPP (diastolic AoP - diastolic RAP) were calculated at the end of the 2 minute epochs. Statistical analysis was performed with ANOVA. Results: LECP significantly increased diastolic aortic pressure, CPP and CerPP both when added on STD and on ACD+ITD CPR. The largest benefit was observed with ACD+ITD+LECP were there was a 2-fold increase in CPP and CerPP with a 2.5-fold increase in common carotid blood flow compared to STD CPR. LECP did not alter ICP. (Table 1 ). Decompression phase CCBF during ACD+ITD+LECP CPR was positive and reached pre cardiac arrest levels. Conclusion: LECP during thoracic decompression significantly augmented aortic diastolic pressure, CPP and CerPP without increasing the ICP . LECP led to a continuous positive cerebral perfusion pressure gradient during CPR cycles and in combination with ACD + ITD CPR common carotid blood flow reached pre-arrest levels. Hemodynamic Parameters

Effects of graded hypotension on cerebral blood flow, blood volume, and mean transit time in dogs

1992 ◽  
Vol 262 (6) ◽  
pp. H1908-H1914 ◽  
Author(s):  
M. Ferrari ◽  
D. A. Wilson ◽  
D. F. Hanley ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion Pressure ◽  
Blood Volume ◽  
Transit Time ◽  
Cerebral Perfusion ◽  
Pressure Range ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Mean Transit Time

This study tested the hypothesis that cerebral blood flow (CBF) is maintained by vasodilation, which manifests itself as a progressive increase in mean transit time (MTT) and cerebral blood volume (CBV) when cerebral perfusion pressure is reduced. Cerebral perfusion pressure was decreased in 10 pentobarbital-anesthetized dogs by controlled hemorrhage. Microsphere-determined CBF was autoregulated in all tested cerebral regions over the 40- to 130-mmHg cerebral perfusion pressure range but decreased by 50% at approximately 30 mmHg. MTT and CBV progressively and proportionately increased in the right parietal cerebral cortex over the 40- to 130-mmHg cerebral perfusion pressure range. Total hemoglobin content (Hb1), measured in the same area by an optical method, increased in parallel with the increases in CBV computed as the (CBF.MTT) product. At 30 mmHg cerebral perfusion pressure, CBV and Hb were still increased and MTT was disproportionately lengthened (690% of control). We conclude that within the autoregulatory range, CBF constancy is maintained by both increased CBV and MTT. Outside the autoregulatory range, substantial prolongation of the MTT occurs. When CBV is maximal, further reductions in cerebral perfusion pressure produce disproportionate increases in MTT that signal the loss of cerebral vascular dilatory hemodynamic reserve.

Effects of increased intracranial pressure on cerebral blood volume, blood flow, and oxygen utilization in monkeys

1975 ◽  
Vol 43 (4) ◽  
pp. 385-398 ◽  
Author(s):  
Robert L. Grubb ◽  
Marcus E. Raichle ◽  
Michael E. Phelps ◽  
Robert A. Ratcheson
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Metabolic Rate ◽  
Intracranial Hypertension ◽  
Cerebral Perfusion Pressure ◽  
Blood Volume ◽  
Cerebral Perfusion ◽  
Cerebral Blood Volume ◽  
Perfusion Pressure ◽  
Cerebral Metabolic Rate

✓ The relationship of cerebral blood volume (CBV) to cerebral perfusion pressure (CPP), cerebral blood flow (CBF), and the cerebral metabolic rate for oxygen (CMRO2) was examined in rhesus monkeys. In vivo tracer methods employing radioactive oxygen-15 were used to measure CBV, CBF, and CMRO2. Cerebral perfusion pressure was decreased by raising the intracranial pressure (ICP) by infusion of artificial cerebrospinal fluid (CSF) into the cisterna magna. The production of progressive intracranial hypertension to an ICP of 70 torr (CPP of 40 torr) caused a rise in CBV accompanied by a steady CBF. With a further increase in ICP to 94 torr, CBV remained elevated without change while CBF declined significantly. Cerebral metabolic rate for oxygen did not change significantly during intracranial hypertension. For comparison, CPP was lowered by reducing mean arterial blood pressure in a second group of monkeys. Only CBF was measured in this group. In this second group of animals, the lower limit of CBF autoregulation was reached at a higher CPP (CPP ∼ 80 torr) than when an increase in ICP was employed (CPP ∼ 30 torr).

CONTINUOUS COMPUTERIZED TRACKING DEFINES RELATIONSHIP BETWEEN CEREBRAL BLOOD FLOW, CEREBRAL PERFUSION PRESSURE AND TIME

1995 ◽  
Vol 23 (Supplement) ◽  
pp. A79
Author(s):  
George Chovanes ◽  
Michael Pasquale ◽  
Mark Cipolle ◽  
Rafael Richards ◽  
Michael Rhodes
Keyword(s):  
Blood Flow ◽  
Cerebral Blood Flow ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure

scholarly journals Comparison of static and dynamic cerebral autoregulation under anesthesia influence in a controlled animal model

PLoS ONE ◽  
2021 ◽  
Vol 16 (1) ◽  
pp. e0245291
Author(s):  
Alexander Ruesch ◽  
Deepshikha Acharya ◽  
Samantha Schmitt ◽  
Jason Yang ◽  
Matthew A. Smith ◽  
...  
Keyword(s):  
Blood Pressure ◽  
Animal Model ◽  
Blood Flow ◽  
Intracranial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Autoregulation ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Phase Lag ◽  
Arterial Blood

The brain’s ability to maintain cerebral blood flow approximately constant despite cerebral perfusion pressure changes is known as cerebral autoregulation (CA) and is governed by vasoconstriction and vasodilation. Cerebral perfusion pressure is defined as the pressure gradient between arterial blood pressure and intracranial pressure. Measuring CA is a challenging task and has created a variety of evaluation methods, which are often categorized as static and dynamic CA assessments. Because CA is quantified as the performance of a regulatory system and no physical ground truth can be measured, conflicting results are reported. The conflict further arises from a lack of healthy volunteer data with respect to cerebral perfusion pressure measurements and the variety of diseases in which CA ability is impaired, including stroke, traumatic brain injury and hydrocephalus. To overcome these differences, we present a healthy non-human primate model in which we can control the ability to autoregulate blood flow through the type of anesthesia (isoflurane vs fentanyl). We show how three different assessment methods can be used to measure CA impairment, and how static and dynamic autoregulation compare under challenges in intracranial pressure and blood pressure. We reconstructed Lassen’s curve for two groups of anesthesia, where only the fentanyl anesthetized group yielded the canonical shape. Cerebral perfusion pressure allowed for the best distinction between the fentanyl and isoflurane anesthetized groups. The autoregulatory response time to induced oscillations in intracranial pressure and blood pressure, measured as the phase lag between intracranial pressure and blood pressure, was able to determine autoregulatory impairment in agreement with static autoregulation. Static and dynamic CA both show impairment in high dose isoflurane anesthesia, while low isoflurane in combination with fentanyl anesthesia maintains CA, offering a repeatable animal model for CA studies.

Effect of hypoxemia on the cardiovascular response to intracranial hypertension in postnatal lambs

1993 ◽  
Vol 265 (5) ◽  
pp. H1557-H1563 ◽  
Author(s):  
M. L. Kearney ◽  
J. E. Backofen ◽  
R. C. Koehler ◽  
M. D. Jones ◽  
R. J. Traystman
Keyword(s):  
Blood Flow ◽  
Intracranial Pressure ◽  
Arterial Pressure ◽  
Cerebral Perfusion Pressure ◽  
Cerebral Perfusion ◽  
Perfusion Pressure ◽  
Cardiovascular Response ◽  
Fetal Sheep ◽  
Peripheral Vasoconstriction ◽  
Significant Difference

Large increases in intracranial pressure in fetal sheep result in more potent peripheral vasoconstriction and better maintenance of cerebral O2 consumption (CMRO2) than in postnatal sheep. The fetus is exposed to a lower PO2. We tested the hypothesis that low PO2 in postnatal lambs potentiates peripheral vasoconstriction and better maintains cerebral perfusion pressure and CMRO2. Pentobarbital-anesthetized lambs, 2-7 days old, were ventilated with either room air (n = 7) or a low O2 mixture to reduce arterial O2 saturation to 50% (n = 7). Elevation of intracranial pressure to within 3-5 mmHg of baseline mean arterial pressure for 30 min by ventricular fluid infusion initially caused a similar increase in arterial pressure in the normoxic [11 +/- 3 (SE) mmHg] and hypoxic (14 +/- 2 mmHg) groups. Plasma catecholamines increased more rapidly in the hypoxic group. However, plasma vasopressin levels were substantially elevated by hypoxia alone and failed to increase further with elevated intracranial pressure. Moreover, there was no significant difference between groups in the steady-state increase in arterial pressure, and microsphere-determined blood flow to intestines, kidney, skin, and muscle did not decrease in either group. Consequently, cerebral perfusion pressure, regional cerebral blood flow, and CMRO2 were reduced similarly in both groups. Therefore, hypoxemia failed to potentiate the postnatal pressor response. Low PO2 is unlikely to be the major mechanism for the potent Cushing response in the fetus.

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