Heart rate calculating

The second method is by use of the heart rate. The total heart rate is regarded as a sum of several components and, in general, is linearly related to the metabolic heat production for heart rates above 120 beats per minute. Heat stress will, however, also increase the heat rate. The third method is to calculate the metabolic heat production from measures of oxygen consumption, and carbon dioxide production during activity and recovery. 

After 10 days of exposure, reduced social behavior and reduced exploratory behavior were observed in rats exposed to 100 ppm trichloroethylene 6 hours per day 5 days per week for a total of 5 weeks (Silverman and Williams 1975). In rats exposed to 50 or 100 ppm trichloroethylene 8 hours/day, 5 days/week for 6 weeks, effects on sleep patterns were observed (Arito et al. 1994a). At 50 ppm decreased wakefulness was observed during the exposure. Effects remaining at 22 hours after the end of the 6-week exposure included decreased heart rate during sleep at 50 ppm and decreased wakefulness after exposure of 100 ppm (Arito et al. 1994a). Based on the 50-ppm LOAEL identified in the Arito et al. (1994a) study, an intermediate-duration inhalation MRL of 0.1 ppm was calculated as described in the footnote in Table 2-1. 

Using the ECG, the heart rate may be determined by calculating the time from the beginning of one P wave to the beginning of the next P wave, or from peak to peak of the QRS complexes. A normal resting heart rate in adults is approximately 70 beats/min. A heart rate of less than 60 beats/min is referred to as bradycardia and a heart rate of more than 100 beats/min is referred to as tachycardia. 

Heart rate increase was not very great (Fig. 48), even at and above the ID 50 (calculated to be about 12 mcg/kg, based on inspection of the NF results shown above). This signifies a high central/peripheral ratio, which is obviously preferable from a toxicity standpoint, especially in a hot climate. 

Since GABA-ergic synapses are confined to neural tissues, specific inhibition of central nervous functions can be achieved for instance, there is little change in blood pressure, heart rate, and body temperature. The therapeutic index of benzodiazepines, calculated with reference to the toxic dose producing respiratory depression, is greater than 100 and thus exceeds that of barbiturates and other sedative-hypnotics by more than tenfold. Benzodiazepine intoxication can be treated with a specific antidote (see below). 

Data analysis. We use a combination of two movement detection algorithms (23) written in Madab environment (The MathWorks, Inc.) to accurately track movement of the heart edges see Note 10). Measurements of diastolic and systolic diameters as well as diastolic and systolic intervals, % fractional shortening (% PS), arrhythmicity index, and contraction direction and velocity are obtained as output from this analysis program. Heart rate is calculated as the inverse of the heart period where one period corresponds to a single diastolic interval plus subsequent systolic interval. % FS is quantified based on diameter measurements and is calculated as ((diastolic diameter-systolic diameter)/diastolic diameter) x 100 (%). Heart beat rhythmicity is quantified based on the standard deviation of the mean heart period normalized to the median heart period for each fly providing a dimensionless arrhythmicity index. 

The actual length of the QT interval is a representation of its time, or duration, measured in milliseconds. A typical duration is in the order of 400-450 msec. However, in normal circumstances, as the heart beats faster (heart rate increases), the duration of an individual cardiac cycle decreases, since more cardiac cycles now occur in the same time. Therefore, as the cardiac cycle shortens, so do each of the components of the cardiac cycle. This means that the QT interval will naturally be shorter at a higher heart rate. Since it is of interest to examine the QT interval at various heart rates, the interval is corrected for heart rate, i.e., a term called QTc is calculated, by one of several methods. 

The hemodynamic and ECG parameters include systolic, diastolic and mean aortic pressure, peak systolic and end-diastolic left ventricular pressure, LV dP/dt max and dP/dt min, heart rate PQ-, QRS- and QT intervals. NOTOCORD-software (or equivalent) is used for acquisition of data whereas EXCEL (or equivalent) is used for data analysis. Data are summarized at predefined time points by calculating median values+ SD. Whereas all physiological parameters are routinely averaged over predefined time intervals, it has been proposed that for the ECG only a few beats... 

For determination of LVP, a Millar microtip catheter (type PC 350) is inserted via the left A. carotis communis. LVEDP is measured on a high-sensitivity scale. From the pressure curve, dP/dtmax is differentiated and heart rate is calculated. 

Cardiopulmonary parameters and rectal body temperature are determined while the rabbit is in the sling and also at 15 min intervals following induction of anesthesia with the rabbit in lateral recumbency. Heart rate, mean arterial blood pressure, respiratory rate and respiratory pattern are calculated from tracings from the physiological recorder. Arterial blood pH, partial pressure of oxygen (PaQz), and partial pressure of... 

Confidence intervals. The problem with the P value is that it conveys no information on the amount of the differences observed or on the range of possible differences between treatments. A result that a drug produces a uniform 2% reduction in heart rate may well be statistically significant but it is dinicaUy meaningless. What doctors are interested to know is the size of the difference, and what degree of assurance, or confidence, they may have in the precision (reproducibility) of this estimate. To obtain this it is necessary to calculate a confidence interval (see Figs 4.1 and 4.2). ... 

In one careful study EC50 values for certain effects of amiodarone were calculated (269). The respective concentrations of amiodarone and desethylamiodarone that were associated with effects were as follows reduction in heart rate 1.2 and 0.5 mg/ml QTc prolongation 2.6 and 1.4 mg/ml corneal microdeposits 2.2 and 1.1 mg/ml. 

The objective of correcting the QT interval for HR or RR is to obtain a corrected QT interval that is statistically independent of the HR or RR interval. Figure 40.2 shows the dependence of QT on HR. In order to eliminate the dependence of QT on heart rate, numerous HR or RR correction formulas have been proposed in the ECG literature, reflecting the variety of statistical models that have been ht to the data. The reader should be aware that there is no best QT interval correction method for heart rate, but there are some practical methods. The most popular corrections are the Bazett (3) and Fridericia (4) formulas. Both are based on the simple power model QTc = QT/RR that is, calculation of the QTc is equal to the observed QT in milliseconds divided by the term of a root of the RR interval in milliseconds. 

Always reported are the RR, PR, QRS, and QT intervals and the duration, magnitude, and configuration of the P waves, QRS complexes, ST segments, T waves, and U waves. Computer interpretation of the ECG provides a standardized reading and records and calculates basic rhythm patterns, heart rate, and intervals but does not interpret arrhythmias. Independent review of the ECG is necessary for accurate translation of findings. ... 

Qrms = root mean square systolic or diastolic flow rate, cm /s Ap = mean systolic or diastolic pressure drop, mmHg In vitro regurgitation volume (RV) data in the bio-medical engineering literature is generally poorly reported. Only RV data expressed in cm /stroke or data that could be calculated (from the information provided) into such a form were used. In many instances, RV would be expressed in the literature as a percentage, with no information on cardiac output and/or heart rate. The work of Dellsperger et al., (16) and in our laboratory tend to indicate that for a given valve, at a fixed heart rate the value of RV in cm /stroke does not vary (except within experimental error) with cardiac output. 

Once calculated, the drug effect can be used to modify the parameters in the CV model, much hfee the neural and humoral reflexes. Resistances, comphances (including the unstressed volumes) of each segment, neural and humoral feedback gains, heart rate, and contractility are all typically modified by drugs. For example, sodium nitroprusside causes vasodilation and blood pooling therefore it would be made to primarily increase the compliance and unstressed volume of the veins, as well as to decrease arteriolar (peripheral) resistance [Greenway, 1982 Yu et ai, 1990]. 

Turner, J. R., Carroll, D., Hanson, J., Sims, J. (1988). A comparison of additional heart rates during active psychological challenge calculated from upper body and lower body dynamic exercise. P. c/zop/tyito/ogy, 25, 209-216. 

---