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P Picton

Publications and source records attributed to P Picton.

12 recordsLinked to original sources
PubMed2003

Extraction of short-latency evoked potentials using a combination of wavelets and evolutionary algorithms.

Somatosensory evoked potentials, recorded at the spine or scalp of a patient, are contaminated by noise. It is common practice to use ensemble averaging to remove the noise, which usually requires a large number of responses to produce one averaged signal. In this paper a post-processing technique is shown which uses a combination of wavelets and evolutionary algorithms to produce a representative waveform with fewer responses. The most suitable wavelets and a set of weights are selected by an evolutionary algorithm to form a filter bank, which enhances the extraction of evoked potentials from noisy recordings.

Algorithms↗
PubMed2003

Study examining attitudes of staff, patients and relatives to witnessed resuscitation in adult intensive care units.

BACKGROUND: Witnessed resuscitation is widely accepted in paediatric practice and is becoming more common in adult emergency departments, but information on this topic is sparse. METHODS: We gave a questionnaire to 50 intensive care medical and nursing staff and 55 patients and next of kin before elective postoperative admission to the intensive care unit to examine staff opinion about witnessed resuscitation, patient and relatives' demand for witnessed resuscitation, and their perception of the benefits. RESULTS: We found that 56% of doctors and 66% of nurses favoured giving relatives the option to stay. If relatives requested to be present, 70% of doctors and 82% of nurses would allow this if the relatives were escorted. The role of the escort was felt to explain, prevent interference, and to provide emotional support. We found that 29% of patients and 47% of relatives wanted to be together during resuscitation, the commonest reasons being to provide support and to see that everything was done. We found that 95% of patients and 91% of relatives felt their views should be formally sought before ICU admission. CONCLUSIONS: Intensive care staff support witnessed resuscitation. Many intensive care personnel have experienced witnessed resuscitation and the majority felt that relatives gained benefit. Almost all agree that the views of both patient and relatives should be sought formally before admission to intensive care.

Adult↗
PubMed2001

Atrial natriuretic peptide augments the variability of sympathetic nerve activity in human heart failure.

OBJECTIVES: Activation of the sympathetic nervous system, decreased heart rate variability (HRV), and loss of modulation of muscle sympathetic nerve activity (MSNA) within the low frequency (LF, 0.05-0.15 Hz) range are three adverse features of advanced congestive heart failure (CHF). In healthy men, atrial natriuretic peptide (ANP) infusion attenuates reflex increases in MSNA and reduces LF components of HRV spectral power. Sympathoinhibitory actions have also been documented in CHF, but effects on the variability of MSNA and HRV have not been described. DESIGN AND METHODS: Heart rate and MSNA were recorded in 10 men (aged 39 +/- 3 years, mean +/- SE) with dilated cardiomyopathy (mean EF 20 +/- 4%) treated with angiotensin converting enzyme (ACE) inhibitors. Subjects received i.v. ANP (50 microg bolus then 50 ng/kg/min) and nitroglycerin (NTG, 8 mg/min) as a hemodynamic control. Signals at baseline, and 13-20 min into each infusion were submitted to spectral analysis. RESULTS: ANP had no effect on HRV, but increased MSNA LF (from 7.9 +/- 1.5 to 12.1 +/- 2.6 U2; P< 0.02) and total spectral power (from 47.9 +/- 5.4 to 61.9 +/- 6.8 U2; P < 0.05). NTG had no effect on the variability of MSNA or HRV. CONCLUSIONS: In CHF patients receiving ACE inhibitors, ANP (i) does not suppress HRV and (ii) enhances the modulation of MSNA, particularly within the LF range. This latter action is not observed with NTG. These findings suggest beneficial actions of exogenous ANP on neurogenic circulatory control.

Adult↗
PubMed2001

Differential sympathetic nerve and heart rate spectral effects of nonhypotensive lower body negative pressure.

Lower body negative pressure (LBNP; -5 and -15 mmHg) was applied to 14 men (mean age 44 yr) to test the hypothesis that reductions in preload without effect on stroke volume or blood pressure increase selectively muscle sympathetic nerve activity (MSNA), but not the ratio of low- to high-frequency harmonic component of spectral power (P(L)/P(H)), a coarse-graining power spectral estimate of sympathetic heart rate (HR) modulation. LBNP at -5 mmHg lowered central venous pressure and had no effect on stroke volume (Doppler) or systolic blood pressure but reduced vagal HR modulation. This latter finding, a manifestation of arterial baroreceptor unloading, refutes the concept that low levels of LBNP interrogate, selectively, cardiopulmonary reflexes. MSNA increased, whereas P(L)/P(H) and HR were unchanged. This discordance is consistent with selectivity of efferent sympathetic responses to nonhypotensive LBNP and with unloading of tonically active sympathoexcitatory atrial reflexes in some subjects. Hypotensive LBNP (-15 mmHg) increased MSNA and P(L)/P(H), but there was no correlation between these changes within subjects. Therefore, HR variability has limited utility as an estimate of the magnitude of orthostatic changes in sympathetic discharge to muscle.

Adult↗
PubMed2001

Attenuated cardiac baroreflex in men with presyncope evoked by lower body negative pressure.

Mechanisms responsible for presyncope during lower body negative pressure (LBNP) in otherwise healthy subjects are poorly understood. Muscle sympathetic nerve activity (MSNA), blood pressure, heart rate (HR), HR power spectra, central venous pressure (CVP) and stroke volume were determined in 14 healthy men subjected to incremental LBNP. Of these, seven experienced presyncope at LBNP >-15 mmHg. Subjects who tolerated LBNP >-15 mmHg had significantly lower CVP (2.6+/-1.0 versus 7.2+/-1.2 mmHg; means+/-S.E.M., P<0.02), HR (59+/-2 versus 66+/-3 beats/min, P<0.05) and MSNA burst frequency (29.0+/-2.4 versus 39.0+/-3.5 bursts/min, P<0.05) during supine rest. LBNP at -15 mmHg had no effect on blood pressure, but caused similar and significant reductions in stroke volume and cardiac output in both groups. Subjects who tolerated LBNP had significant reflex increases in HR, MSNA burst frequency and burst amplitude with LBNP of -15 mmHg. These responses were absent in those who experienced presyncope. The gain of the cardiac baroreflex regulation of MSNA was markedly attenuated in pre-syncopal subjects (1.2+/-0.6 versus 8.8+/-1.4 bursts/100 heart beats per mmHg; P<0.001). Healthy subjects who experience presyncope in response to LBNP appear more dependent, when supine, upon MSNA to maintain preload, and less able to increase sympathetic vasoconstrictor discharge to skeletal muscle reflexively in response to orthostatic stimuli.

Adult↗