Bompei Takase

A novel apparatus for non-contact measurement of heart rate variability: a system to prevent secondary exposure of medical personnel to toxic materials under biochemical hazard conditions, in monitoring sepsis or in predicting multiple organ dysfunction syndrome.

Abstract Background. The impaired balance of the low-frequency/high-frequency ratio obtained from spectral components of RR intervals can be a diagnostic test for sepsis. In addition, it is known that a reduction of heart rate variability (HRV) is useful in identifying septic patients at risk of the development of multiple organ dysfunction syndrome (MODS). We have reported a non-contact method using a microwave radar to monitor the heart and respiratory rates of a healthy person placed inside an isolator or of experimental animals exposed to toxic materials. Apparatus design and testing. With the purpose of preventing secondary exposure of medical personnel to toxic materials under biochemical hazard conditions, we designed a novel apparatus for non-contact measurement of HRV using a 1215 MHz microwave radar, a high-pass filter, and a personal computer. The microwave radar monitors only the small reflected waves from the subjects chest wall, which are modulated by the cardiac and respiratory motion. The high-pass filter enhances the cardiac signal and attenuates the respiratory signal. In a human trial, RR intervals derived from the non-contact apparatus significantly correlated with those derived from ECG (r=0.98, P<0.0001). The non-contact apparatus showed a similar power spectrum of RR intervals to that of ECG. Conclusions. Our non-contact HRV measurement apparatus appears promising for future pre-hospital monitoring of septic patients or for predicting MODS patients, inside isolators or in the field for mass casualties under biochemical hazard circumstances.

Non-contact determination of vital sign alterations in hypovolaemic states induced by massive haemorrhage: an experimental attempt to monitor the condition of injured persons behind barriers or under disaster rubble.

To assess a non-contact method to determine the physical alteration of human subjects confined behind a barrier or under disaster rubble, an experimental, non-contact monitoring system was tested on rabbits in a hypovolaemic state. New Zealand male rabbits behind a barrier were subjected to hypovolaemic shock induced by the withdrawal of arterial blood (2ml per 100g body weight). The hypovolaemic state was determined by linear discriminant analysis using non-contact-derived variables: heart rate X1 and respiratory rate X2. Sixteen rabbits were equally divided between the hypovolaemic and control groups. To obtain the heart and respiratory rates simultaneously, the fast Fourier transform (FFT) was performed on the 1215MHz microwave radar analogue output. The linear discriminant function calculated by non-contact-derived variables was negative in the eight hypovolaemic rabbits and positive in the eight controls, so that the linear discriminant function could distinguish the hypovolaemic group from the control group. The Mahalanobis D-square (an index for classification accuracy) was 5908; the classification error rate corresponding to this value was small and negligible. The hypovolaemic rabbits developed metabolic acidosis (HCO3− 18.6±11.1mmoll−1 and pH 7.15±0.18 in arterial blood). The systolic blood pressure of the hypovolaemic group and the control was 56±4 and 83±6 mmHg, respectively (p<0.01). The proposed method appears promising for applications to monitor the condition of human subjects behind barriers or under disaster rubble.

Development of a continuous temperature mapping system using a deep body thermometer

To determine continuous body temperature distribution, an inexpensive temperature mapping system was developed using a deep body thermometer adopting the finite-element method. A stripe with 16 thermocouples was wrapped around the waist of rats to measure body surface temperatures (the boundary conditions). The abdominal deep temperature of the rats was measured from the dorsum using the thermal compensation probe of a deep body thermometer. The abdominal temperature of the rats was mapped by solving a heat conduction equation using surface and deep temperatures obtained in real time. The temperature measured with a thermocouple inserted into the abdominal centre of the rats correlated well with the calculated temperature ( r = 0.93, p < 0.01 ). The system is low cost and simple to use compared with the magnetic resonance temperature mapping system. Our temperature mapping system could potentially result in improved management of patients in critical care medicine.

Effect of betaxolol hydrochloride on heart rate variability indices during exercise stress testing in patients with hypertension

Betaxolol hydrochloride is a beta1-selective antagonist that produces vasodilation in patients with hypertension and ischemic heart disease. The goal of the present study was to characterize the effect of betaxolol on heart rate variability indices (HRV), a well-established prognostic marker. Symptom limited-treadmill exercise testing was performed in 17 hypertensive patients (60.9 +/- 14.8 years-old) before and immediately a 3 weeks course of betaxolol hydrochloride (5 mg daily). Frequency domain HRV (high frequency spectra, HF; 0.15-0.40 Hz: low frequency spectra, LF; 0.04-0.15 Hz) was measured during exercise treadmill testing using MemCalc software. Betaxolol hydrochloride significantly decreased the maximal systolic blood pressure and heart rate (184 +/- 29 vs. 156 +/- 26 mmHg, P < 0.01; 132 +/- 21 vs. 113 +/- 15 bpm, P < 0.01) and significantly increased HF and LF during exercise treadmill testing (HF, 32 +/- 36 vs. 56 +/- 55 men/Hz, P < 0.01; LF, 64 +/- 58 vs. 95 +/- 86 men/Hz, P < 0.01). Thus, treatment with betaxolol hydrochloride resulted in a decrease in blood pressure during exercise treadmill testing and in an increase in HRV. This suggests that this agent could have beneficial effects on long-term prognosis in patients with hypertension.

Non-invasive estimation of arterial blood pH using exhaled CO/CO2 analyser, microwave radar and infrared thermography for patients after massive haemorrhage

In order to conduct non-contact estimation of arterial blood pH after massive haemorrhage, we calculated the arterial pH based on linear-regression analysis of exhaled gas concentrations (CO and CO2) and vital signs (heart rate, respiratory rate, and surface temperature) measured using non-contact methods in hypovolemic animals.

Recombinant interferon alpha treatment decreases heart rate variability indices and impairs exercise tolerance in patients with chronic hepatitis.

Complications of interferon (IFN) therapy include cardiac arrhythmias, impaired cardiac function and myocardial ischemia. Decreased heart rate variability (HRV) indices, impaired exercise tolerance and decreased left ventricular (LV) function are related to unfavorable outcome of heart disease. To investigate the effect of IFN therapy on HRV, exercise tolerance and cardiac function, 24-h ambulatory electrocardiographic monitoring (AECG), two-dimensional echocardiography, and exercise treadmill testing (ETT) was performed in 9 patients (age 56 +/- 9 years-old) with chronic hepatitis and without underlying heart disease before and after treatment with IFN (recombinant alpha 2b; 10 x 10(6) U/day for 4 weeks). HRV parameters consisted of standard deviation of RR interval (sdNN, ms), SDANN (ms), S.D. index (ms), rMSSD (ms), pNN50 (%) and frequency analysis of heart rate spectrum resulted in low (ms, 0.04-0.15 Hz), high (ms, 0.15-0.40 Hz) and total (ms, 0.01-1.00 Hz) frequency components. Ischemia was not detected by AECG or ETT, and LV function was normal after INF treatment in all patients. However, INF treatment resulted in a decrease in exercise tolerance time (449 +/- 94 s vs. 329 +/- 67 s, P < 0.05) and a decrease in several HRV parameters (S.D. index, 42 +/- 5 ms vs. 37 +/- 9 ms; rMSSD, 22 +/- 5 ms vs. 19 +/- 4 ms; pNN50, 4 +/- 3% vs. 2 +/- 1%; P < 0.05). Further, patients treated with INF tended to have a lower sdNN and total frequency spectra, although this difference did not reach the level of statistical significance. These data suggest that the arrhythmogenic effect of INF may be mediated by decreases in HRV and impairment of exercise tolerance even in patients without overt heart diseases. Further, INF therapy may be contraindicated in patients with predisposing severe cardiac disorders, including arrhythmias, ischemia and decreased LV function.

Effect of antiarrhythmic agents on heart rate variability indices after myocardial infarction: comparative experimental study of aprindine and procainamide

The cardiac arrhythmic suppression trial (CAST) reported that antiarrhythmic treatments in post-myocardial infarction (MI) patients resulted in poor outcome and decreased in heart rate variability indices (HRV). The goal of the present study was to determine whether aprindine and procainamide, antiarrhythmic agents that increase HRV, result in beneficial effects in post-MI rabbits. Four weeks before experiment, MI was induced in four rabbits by ligating the major branch of left coronary artery. A total of eight rabbits (four post-MI and four normal rabbits) were randomly assigned to treatment with either intravenous aprindine (1 mg/kg) or intravenous procainamide (15 mg/kg). Frequency domain HRV (low frequency spectra, LF, 0.04-0.15 Hz; high frequency spectra, HF, 0.15-0.40 Hz) were assessed by MemCalc software. Aprindine significantly increased HF and LF in both MI and normal rabbits, whereas procainamide tended to decrease HF and LF in MI and normal rabbits (in total rabbits; aprindine, LF, from 6.3 +/- 7.9 to 16.5 +/- 15.0 ms(2)/Hz, P < 0.05; HF, from 8.0 +/- 11.7 to 17.5 +/- 15.0 ms(2)/Hz, P < 0.05; procainamide, LF, from 4.9 +/- 7.4 to 4.8 +/- 8.5 ms(2)/Hz, NS; HF, from 11.1 +/- 23.0 to 5.1 +/- 10.6 ms(2)/Hz, NS). Under pharmacological denervation with propranolol (0.1 mg/kg) and atropine (0.04 mg/kg), aprindine increased LF and HF (LF, from 0.2 +/- 0.2 to 0.8 +/- 0.7 ms(2)/Hz, P < 0.05; HF, from 0.1 +/- 0.0 to 0.2 +/- 0.0 ms(2)/Hz, P < 0.05). These data suggest that aprindine can increase HRV in post-MI rabbits. Further experiments in human subjects would be of benefit.