Principles of cerebral hemodynamics when intracranial pressure is raised: lessons from the peripheral circulation.

BACKGROUND: The brain is highly vascular and richly perfused, and dependent on continuous flow for normal function. Although confined within the skull, pressure within the brain is usually less than 15 mmHg, and shows small pulsations related to arterial pulse under normal circumstances. Pulsatile arterial hemodynamics in the brain have been studied before, but are still inadequately understood, especially during changes of intracranial pressure (ICP) after head injury. METHOD: In seeking cohesive explanations, we measured ICP and radial artery pressure (RAP) invasively with high-fidelity manometer systems, together with middle cerebral artery flow velocity (MCAFV) (transcranial Doppler) and central aortic pressure (CAP) generated from RAP, using a generalized transfer function technique, in eight young unconscious, ventilated adults following closed head trauma. We focused on vascular effects of spontaneous rises of ICP ('plateau waves'). RESULTS: A rise in mean ICP from 29 to 53 mmHg caused no consistent change in pressure outside the cranium, or in heart rate, but ICP pulsations increased in amplitude from 8 to 20 mmHg, and ICP waveform came to resemble that in the aorta. Cerebral perfusion pressure (=central aortic pressure - ICP), which equates with transmural pressure, fell from 61 to 36 mmHg. Mean MCAFV fell from 53 to 40 cm/s, whereas pulsatile MCAFV increased from 77 to 98 cm/s. These significant changes (all P < 0.01) may be explained using the Monro-Kellie doctrine, because of compression of the brain, as occurs in a limb when external pressure is applied. CONCLUSION: The findings emphasize importance of reducing ICP, when raised, and on the additional benefits of reducing wave reflection from the lower body.This study was supported by the National Institute of Health Research, the Biomedical Research Centre (Neuroscience Theme), and the Medical Research Council (Grants G0600986 and G9439390). J.D.P. has received the NIHR Investigator Awards. M.O.K. is sponsored by an Australian Postgraduate Awards Industrial Linkage Grant from the Australian Research Council (LP0884094), with AtCor Medical Australia as the collaborating organization.This is the final version of the article. It first appeared from Wolters Kluwer via http://dx.doi.org/10.1097/HJH.000000000000053

Central pressure and pulse wave amplification in the upper limb

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Non-invasive characterisation of age-related changes in ascending aortic blood pressure and blood flow: from old concept to novel approach

Thesis by publication.Bibliography: pages 449-472.Chapter 1. Introduction -- Chapter 2. Literature review -- Chapter 3. Accuracy of distance measurement in the measurement of “aortic” pulse wave velocity -- Chapter 4. Non-invasive central aortic pressure measurements : calibration and clinical value -- Chapter 5. Characterisation of age-related changes in aortic pressure and flow -- Chapter 6. Relationship of cerebral arterial pressure and flow with aortic pressure and flow -- Chapter 7. Published reviews, editorials and commentaries pertaining to the thesis topic -- Chapter 8. Conclusion.The elucidation of mechanisms whereby arterial stiffness with increasing age alters the propagation of pressure (and flow ejection) waves generated by each heart beat is still evolving and sometimes debated. The research described in this thesis aims to better characterise the age-related changes in ascending aortic blood pressure and blood flow non-invasively.This thesis investigates four key areas:- (i) measurement of aortic stiffness with pulse wave velocity; (ii) non-invasive central arterial pressure measurements; (iii) characterisation of age-related changes in central aortic pressure and flow with non-invasive methodology; (iv) relationship of cerebral arterial pressure and flow with central aortic pressure and flow.Findings of this investigation highlight the clinical importance of non-invasive measurement of central aortic pressure and aortic flow to determine ascending aortic impedance as a measure of cardiac load. The physical relationship between aortic pressure, flow and arterial impedance is quantified in terms of age-related changes. Changes in aortic flow pattern and means to derive aortic flow waveform from aortic pressure waveform non-invasively are compared with other methods. Results show that changes in the cardiac ejection pattern with age are better determined using magnetic resonance imaging compared to Doppler ultrasound techniques. Initial investigation of the effect of arterial stiffening, as occurs with age, shows that there is a relationship between the higher pressure pulsations from the heart and the damage in the brain due to the higher flow pulsations being transferred to the cerebral circulation.This investigation confirmed the changes in central aortic blood pressure and flow ejection with aging. Derivation of the aortic flow pattern from central aortic pressure is feasible, through their relationship with aortic impedance. Increased pulsatility of arterial pressure and flow may cause damage to the microvasculature in the brain and may relate to the cognitive decline with aging and disease.Mode of access: World wide web1 online resource (xx, 489 pages) illustrations (some colour

Noninvasive generation of aortic pressure from radial pressure waveform by applanation tonometry, brachial cuff calibration, and generalized transfer function

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Reply : misclassification of studies in 'Brachial artery tonometry and the Popeye phenomenon'

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Brachial artery tonometry and the Popeye phenomenon : explanation of anomalies in generating central from upper limb pressure waveforms

Background: Noninvasive applanation tonometry studies of the brachial and radial artery pressure waves show that the arterial pulse is substantially amplified between the brachial and radial sites. Brachial tonometry waveforms have also been used to calibrate carotid tonometry waves as a measure of central pressure in major clinical trials. These trials assume identity of mean and of DBP in calculation of central (carotid) SBP. None of these trials showed superiority of central over brachial pressure in predicting outcome, but all showed equivalence of SBP and pulse pressure at brachial and carotid sites! Method: We tested this method by measuring pressure waves at brachial, radial and carotid sites by applanation tonometry in 100 patients, with attention to any subtle difference between brachial and radial waveforms, and with both calibrated to cuff SBP and DBP. Results: The results confirmed no proximal and strong distal amplification in the arm. However, this was accompanied by blunting of the brachial compared with radial waveform with brachial pressure 2.7 mmHg higher during most of the cardiac cycle. Form factor of the ensemble-averaged brachial wave [39.1 standard deviation (SD) 4.9%] was similar to the carotid (40.2 SD 4.1%) but different to the radial wave (34.8 SD 3.7%; P<0.01). Conclusions: All findings were explained by inability to applanate the brachial artery, and resulting systematic error in generating brachial waveforms. I n estimation of central pressure with applanation tonometry, the radial pressure wave, which can be accurately applanated, should be used, and calibrated to the brachial cuff.12 page(s

Determination of central aortic systolic and pulse pressure from the radial artery pressure waveform

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Reply : isolated systolic hypertension in the young : a need for clarity

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