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The electrocardiographic QT interval duration is a frequently studied ECG parameter. The aim of this study was to compare the quantitative influence of nine QTc formulae and discuss the duration of QT/QTc normal values. The QTc duration was calculated from manually measured QT intervals and heart rate of the Frank XYZ electrocardiograms in 138 white young healthy Slovak women (18-24 years, 690 primary ECG measurements). Dispersion of the QT/QTc interval values was not Gaussian (Shapiro-Wilk test) in most cases. The course of the measured QT regression lines were -1.9186 HR + 511.13 ms or 0.1504RR + 245.72 ms. Median QTc duration in ms was decreasing in this sequence: Bazett 407.04, Fridericia 394.61, Hodges 393.27, Rautaharju and Arrowood 368.79, Framingham-Sagie 368.78, Lecocq 368.70, Sarma 368.66, and Malik 338.70. No QTc value above 440 ms was found after Hodges' correction only. The differences of median QTc values were significant (P < 0.01) in most possible combinations (Kruskal-Wallis test). We recommend using the QTc formula created from observed persons only and updating the QT interval norms. So-called "ideal" QTc models from other not examined persons are methodically incorrect and may produce the misleading results. The frequently used Bazett formula is appropriate for orientation only.

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BACKGROUND: The circa- and ultradians of the single extrasystoles' frequency in patients with chronic respiratory insufficiency (CRI) in lowlands (Kosice 210 m) were studied by the testing of following null hypotheses: their average frequency as well as rhythmicity is the same as at health. METHODS: In 54 elderly males with CRI, mean numbers of supraventricular (SV) and ventricular (VE) extrasystoles were calculated for each 24 hours. The Halberg cosinor regression was used to test the presence of the 24-hour rhythm and its 2nd to 10th harmonics, i.e. ultradians with the period lengths of 12 to 2.4 hours. The resulting approximating function for either extrasystole type included its point, 95% confidence for mean and 95% tolerance for one individual. The results were compared with those obtained at health at alpha = 0.05. RESULTS: The daily mesors in CRI were 20.9 for SV, for VE 17.6 extrasystoles per hour and subject. This was significantly (20.3 (SV) and 17.0 (VE)) higher than at health. Significant periodic harmonic components were 3 in CRI versus 6 at health for SV and 6 in CRI versus 1 at health for VE. The dominating CRI rhythm was the 8 hour ultradian for SV and circadian for VE while at health the circadian rhythm was leading for every type of extrasystoles. CONCLUSION: The most remarkable effect of CRI versus health at lowlands is a marked increase of the frequency of every type of extrasystoles. SV extrasystoles exert more rhythmicity at health while the VE in disease (Tab. 1, Fig. 1, Ref. 20).

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The aim of the study was to determine the dependence of changes in the electrical stability of the heart on the light-dark cycle (LD cycle) in disorders of pulmonary ventilation. The ventricular arrhythmia threshold (VAT) was measured in female Wistar rats (adaptation to the light regime 12:12 h, ketamine/xylazine anesthesia 100 mg/15 mg/kg, i.m., open chest experiments). The conditions of the normal artificial ventilation and reoxygenation were V(T) = 1 ml/100 g, respiratory rate 40 breaths/min, hypoventilation V(T) = 0.5 ml/100 g, respiratory rate 20 breaths/min. The animals (n=11 light group; n=19 dark group) were subjected to 20 min hypoventilation followed by 20 min reoxygenation. The control prehypoventilatory VAT differences were not found between the light (1.90+/-0.84 mA) and dark (1.88+/-0.87 mA) part of the day. Artificial hypoventilation changed the VAT values in light and dark part of the day differently. While during the light period, the average VAT values in most animals (90.9 %) were significantly decreased (1.29+/-0.59 vs. 1.90+/-0.84 mA control, p<0.05), during the dark part these values showed either significant increase (63.2 %) (2.23+/-0.77 vs. 1.48+/-0.39 mA, p<0.005) or a slight non-significant decrease (36.8 %) (2.18+/-0.89 vs. 2.54+/-0.99 mA). Reoxygenation returned the VAT values to the level before hypoventilation by an increase of the VAT (81.8 %) in the light part of day and by decrease of the VAT (68.4 %) in the dark part of the day. It is concluded that 1) in hypoventilation/reoxygenation model, the significant higher average VAT values are in the dark part of the day vs. the light one, 2) rat hearts are more resistant to systemic hypoxia and reoxygenation in the dark part of day, and 3) proarrhythmogenic effect of the systemic hypoxia is only seen in the light part of the day.

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The 24-hour periodicity of supraventricular (SVPB) and ventricular (VEB) extrasystoles in healthy elderly men (age 49-69 years) was studied at two altitudes during 24 h Holter ECG monitoring. At the low altitude (200 m, n = 26), SVPB were more frequent than VEB. The highest occurrence of SVPB was at 17:00 h, the lowest at 01:00 and 02:00 h (P<0.001). The highest occurrence of VEB was at 09:00 h, the lowest one at 04:00 h (P<0.001). At 1350 m (n=9) the incidence of both SVPB and VEB was approximately twofold higher compared to that at the low altitude (P<0.001). The highest occurrence of SVPB was at 13:00 h, the lowest at 06:00 h (P<0.001). VEB were the most frequent at 10:00 h and 13:00 h, while the lowest frequency was observed at 06:00 h (P<0.001). Our results indicate that the incidence of SVPB and VEB in healthy persons at the moderate altitude is twofold and its periodicity is shifted compared to the low altitude. The cause of increased occurrence of extrasystoles is probably due to beta-adrenergic activation of the heart at the higher altitude.

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Our aim was to test the hypothesis that the occurrence of extrasystoles in higher decennia is proportional to the altitude. The occurrence of supraventricular (SVPB) and ventricular (VEB) extrasystoles, values of systolic and diastolic blood pressure and the heart rate were studied in 20 healthy elderly men (50-64 years) during cable cabin transportation to a moderate altitude. These values were measured in stations located at 898 m, 1764 m, and 2632 m above sea level during the transportation in both directions. Our records show that the values of blood pressure and heart rate were within normal limits during the whole period of transportation. Both SVPB and VEB were increasing during the ascent and decreasing to the initial values during the descent compared to the values at altitude of 898 m. The highest values (6 to 7-times exceeding the initial ones) were measured at the summit. The results have demonstrated that the occurrence of SVPB and VEB is proportional to the altitude. The increased incidence in the number of extrasystoles is suggested to be mediated by beta-adrenoceptors.

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A 24 h rhythm of the ventricular fibrillation threshold (VFT) was investigated in female Wistar rats under conditions of normal ventilation (NV) (17 animals) and hypoventilation (HV) (10 animals). The animals were adapted to a daily 12:12 h light-dark cycle with the dark period from 18:00 to 06:00 under constant temperature conditions. The experiments were performed in pentobarbital anesthesia (40 mg/kg ip, open chest experiments) during the whole year, and the obtained results were averaged independently of the seasons. During NV, the VFT in female rats showed a significant 24 h rhythm (p < 0.01) with the mesor 2.59 +/- 0.53 mA, amplitude 0.33 +/- 0.11 mA, and acrophase -338 degrees (at 22:53 h) and the confidence intervals from -288 degrees to -7 degrees (from 19:12 to 00:28 h) using the population mean cosinor test. The maximal values of the VFT were measured in the active phase between 24:00 and 03:00 h. During HV, the rhythmicity of the VFT showed a more pronounced biphasic character with a smaller peak between 15:00 h and 18:00 h hours and a higher peak between 24:00 h and 03:00 h of the daily regime. Hypoventilation significantly decreased the VFT (p < 0.001) at each interval of the measurement. It is concluded that the electrical stability of the heart measured by the VFT shows a significant 24 h rhythm in female Wistar rats and that HV decreased the VFT during the whole 24 h period.

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The Frank orthogonal corrected ECG and its first derivation were recorded in 27 healthy volunteers (women aged 19-22 years) during normal ventilation at rest (control group), after voluntary hyperventilation lasting 75 seconds, and during hypoxic-hypercapnic ventilation (through the enlarged dead space) lasting 5 min. The projections of the magnitude and direction of the positive and negative QRS derivation maxima into the horizontal, frontal, left sagittal planes and their spatial distribution were constructed. The magnitude of the positive and negative QRS derivation maxima was significantly decreased during hypoxic-hypercapnic ventilation. A significant alteration in the direction only arose at the positive maximum during hypoxic-hypercapnic ventilation in the frontal plane. The intrinsicoid deflection was not significantly altered. The normal values of the maxima of the first QRS derivation in young healthy women are given. It is supposed that the decrease in amplitude of the maxima of the first QRS derivation is caused by slowed propagation of the depolarization wave under hypoxic-hypercapnic conditions and alteration of the direction of the positive maximum is caused by a greater participation of the right ventricle at the origin of the resulting QRS vector.

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The circadian rhythm of ventricular fibrillation threshold (VFT) and its relation to the heart rate (HR) and the rectal temperature (RT) was studied in female Wistar rats. The animals were exposed to daily light-dark cycles of 12 h of light alternating with 12 h of darkness and were under pentobarbital anaesthesia (40 mg/kg i.p.). The experiments were performed on open chest animals and VFT was measured by direct stimulation of the myocardium. VFT in female rats showed a circadian rhythm with the acrophase -338 degrees (at 22.53 h), with the mesor 2.58 mA and the amplitude 0.33 mA. HR was not significantly changed during the experiments and no dependence was found between VFT and HR during the whole 24-hour period (r = 0.08). The acrophase of the circadian rhythm of HR (on -47 degrees, i.e. at 03.08 h) was shifted to the acrophase of VFT. The circadian rhythms of RT before the application of the anaesthetic agent and under general anaesthesia before the operative interventions had a very similar course with the nearly corresponding acrophases as the circadian rhythm of VFT. It is concluded that the electrical stability of the rat heart measured by VFT shows the significant circadian rhythm in a parallel with the circadian rhythm of RT and probably without dependence on the changes of HR.

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Hemodynamic and respiratory changes were studied during embolization of the pulmonary arterial bed in 20 rabbits after pentobarbital anesthesia. Air was insufflated into the auricular vein in the amount necessary to induce circulatory and respiratory changes. Circulatory changes were manifested by decreased arterial blood pressure, increased blood pressure in the right atrium, and aortal and pulmonary blood flow reduced to zero. The respiratory rate was diminished. A series of deep inspirations was followed by apnoe and death of the animal. (Fig. 5, Ref. 9.)

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The influence of some pulmonary ventilation alterations (the normal ventilation at rest = control), the hyperventilation (HV) lasting 75 s, the hypoxic-hypercapnic ventilation (HXV) lasting 3 and 6 min) on the instantaneous QRS vectors was investigated in 42 young healthy women (19-24 years old). The magnitude and the direction of instantaneous QRS vectors in the 10th to the 70th ms and in QRS max were constructed from the Frank lead ECG. The significant alterations of the direction (angle) were found in the 30th ms and QRS max at HXV and in the 60th ms at HV. A significant decrease in the magnitude of instantaneous vectors was found in the 10th to 50th ms after 6 min of HXV, in the 30th to 50th ms at 3 min of HXV, in the 40th to 50th ms at HV. These alterations were the most marked in the horizontal plane. We suggest that the alterations of the instantaneous QRS vectors were caused by the influence of the autonomic nervous system or humoral agents, but not by heart position, Brody's effect or lung hyperinflation.

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Changes in the duration and size of the vulnerable period of the myocardium in the presence of respiratory changes were studied in acute experiments on rats. The limits of the vulnerable period were determined by directly stimulating the heart during ventilation via the enlarged respiratory dead space, during hyperventilation and during heart failure. In the control group (normal ventilation without enlargement of the dead space), the vulnerable period lasted 5.7 +/- 0.76 ms. During ventilation via the enlarged dead space, hypercapnic hypoxaemia developed and the vulnerable period was markedly prolonged (18.55 +/- 5.29 ms) by a shift of its inner limit to the left. Hyperventilation caused normoxic to hyperoxic hypocapnia and markedly reduced the duration of the vulnerable period (8.17 +/- 2.21 and 9.31 +/- 2.38 ms respectively). The vulnerable period lengthened the most in heart failure (25.46 +/- 3.93), mainly as a result of a shift of its outer limit. In all the experimental groups there was a shift of the vulnerable period to the right, which was fastest in hypercapnic hypoxaemia and slowest in hyperoxic hypocapnia. The administration of Inderal (3 mg/kg i.p.) or Arfonad (50 mg/kg i.p.) markedly shortened the vulnerable period during hypercapnic hypoxaemia (9.87 +/- 2.78 and 9.32 +/- 2.16 ms respectively), but did not block the shift. Lengthening of the vulnerable period during hypercapnic hypoxaemia was probably due to activation of sympathetic nerves via beta-adrenergic receptors.

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