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[Heart rate and heart rhythm in healthy infants and children].

Cardiac rate and rhythm in 141 healthy infants, toddlers and schoolchildren during 24 hour ambulatory electrocardiographic monitoring are reported. Maximal and minimal heart rate (1/min) in infants 1 to 5 months of age were 204 +/- 17 and 105 +/- 13, in infants 6 to 12 months of age 187 +/- 19 and 101 +/- 15; in toddlers 177 +/- 17 and 66 +/- 10; in schoolchildren 158 +/- 24 and 54 +/- 6. A sizeable proportion of children of all age groups showed patterns of sinus arrhythmias indistinguishable from second degree sinuatrial block. Supraventricular escape beats and escape rhythms were frequent as well. The longest RR interval was 1.03 +/- 0.16 sec. in infants, 1.20 +/- 0.25 sec. in toddlers, and 1.35 +/- 0.15 sec., respectively, in schoolchildren. Two % of infants, 7% of toddlers, and 6% of schoolchildren had episodes of second degree atrioventricular block type I (Wenckebach) at rest. Supraventricular extrasystoles were found in 38%, 13% and 26%, respectively, and uniform ventricular extrasystoles in 18%, 20% and 16%, respectively, of infants, toddlers and schoolchildren. These data, together with similar information in the literature, can be taken as basis for the evaluation of ambulatory electrocardiograms in children.

Arrhythmias, Cardiac↗

Markers of inflammation in acute coronary syndromes: association with increased heart rate and reductions in heart rate variability.

BACKGROUND: Systemic and vascular inflammation is at the heart of the thrombotic occlusion of coronary arteries. HYPOTHESIS: The study was undertaken to determine the relationship between established inflammatory markers (interleukin-6 [IL-6] and high-sensitivity C-reactive protein [hs-CRP]), neutrophil or white cell count, and concomitant autonomic tone in patients with coronary artery disease soon after occlusive events. METHODS: We tested the linkage between autonomic tone (as defined using both time domain and frequency domain estimates of heart rate variability [HRV]) and circulating markers of inflammation (white cell counts, hs-CRP, and IL-6) in a sample of 100 patients with proven acute coronary syndrome and compared these with healthy controls (n = 49) and the relationships on repeated measures at 4 months in recovery (n = 51). RESULTS: We demonstrated predictable depressed HRV in acute patients who tended to show recovery by 4 months. The acute changes in HRV indices (e.g., triangular index) showed modest negative correlation (r = -0.2-0.3) with the acute elevation of white cell count, IL-6, and hs-CRP. These associations did not persist on multivariate analysis of data gathered at 4 months post event. CONCLUSION: These observational data, while limited, are the first to link autonomic tone and in particular sympathetic tone (as indicated by HRV), to the process of acute leukocytosis and systemic inflammation common in acute coronary syndromes.

Biomarkers↗

Cholinergic stimulation with pyridostigmine reduces ventricular arrhythmia and enhances heart rate variability in heart failure.

BACKGROUND: Increased ventricular arrhythmia density and reduced heart rate variability are associated with risk of death in patients with heart failure. Cholinesterase inhibition with pyridostigmine bromide increases heart rate variability in normal subjects, but its effect on patients with heart failure is unknown. In this study, we tested the hypothesis that short-term administration of pyridostigmine bromide, a cholinesterase inhibitor, reduces ventricular arrhythmia density and increases heart rate variability in patients with congestive heart failure. METHODS: Patients with heart failure and in sinus rhythm participated in a double-blind, cross-over protocol, randomized for placebo and pyridostigmine (30 mg orally 3 times daily for 2 days). Twenty-four hour electrocardiographic recordings were performed for arrhythmia analysis and for the measurement of time domain indices of heart rate variability. Patients were separated into 2 groups, according to their ventricular arrhythmia density. The arrhythmia group (n = 11) included patients with >10 ventricular premature beats (VPBs) per hour (VPBs/h), and the heart rate variability group (n = 12) included patients with a number of VPBs in 24 hours not exceeding 1% of the total number of R-R intervals. RESULTS: For the arrhythmia group, pyridostigmine resulted in a 65% reduction of ventricular ectopic activity (placebo 266 +/- 56 VPBs/h vs pyridostigmine 173 +/- 49 VPBs/h, P =.03). For the heart rate variability group, pyridostigmine administration increased mean R-R interval (placebo 733 +/- 22 ms vs pyridostigmine 790 +/- 33 ms, P =.01), and in the time domain indices of heart rate variability root-mean-square of successive differences (placebo 21 +/- 2 ms vs pyridostigmine 27 +/- 3 ms, P =.01) and percentage of pairs of adjacent R-R intervals differing by >50 ms (placebo 3% +/- 1% vs pyridostigmine 6% +/- 2%, P =.03). CONCLUSION: In patients with heart failure, pyridostigmine reduced ventricular arrhythmia density and increased heart rate variability, most likely due to its cholinomimetic effect. Long-term trials with pyridostigmine in heart failure should be conducted.

Administration, Oral↗

Intrapartum fetal heart rate monitoring. V. Fetal heart rate patterns in the second stage of labor.

A total of 1,755 fetal heart rate (FHR) tracings of the second stage of labor was analyzed. The FHR patterns were classified according to the behavior of the baseline FHR and are listed in decreasing order of benignity: normocardia, transitory bradycardia, tachycardia, persistent bradycardia, and progressive bradycardia. Each category was further subdivided into four groups on the basis of association or nonassociation with early, variable, or late decelerations. Cord compression pattern were noted in over 50% of the FHR tracings and account for the majority of low Apgar scores and fetal acidosis. FHR abnormalities occurred in 91% of second-stage labor patterns, and were mild in most cases or of too short duration to influence fetal outcome. An effort was made to establish therapeutic guidelines based on the morphologic features, prognostic grading, and the etiology of the FHR patterns in the second stage of labor.

Bradycardia↗

Ability of new heart rate monitors to measure normal and abnormal heart rate.

BACKGROUND: The extended use of heart rate monitors to non sportive people, and older ones increases the risk to be facing heart rate troubles. Questions exist upon the ability of this devices to detect such abnormalities. The purpose of the investigation was to evaluate the accuracy of two third generation heart rate monitors, Accurex Plus and Vantage NV and to compared these data with those of an older one, PE 4000. Then we investigate responses of this monitors to abnormal heart rate. METHODS EXPERIMENTAL DESIGN: The three heart rate monitors were tested in the laboratory, wired in parallel to an ECG simulator under two modes: a normal heart rate program (7 stable heart rate stages with two marked transitions) and an automatic arrhythmia one. MEASURES: 1st program: Values generated by the ECG simulator were compared to the values produced by the three devices. Particular attention was paid to the transition phases (heart rate drop and heart rate fall). Results of heart rate monitors accuracy were expressed at the exact value (devices value=simulator value) and at approximated value of +/-3 beats x min(-1) (devices value=simulator value +/-3 beats x min(-1)); 2nd program: Abnormal rhythms were analysed using an ambulatory ECG recorder (Synésis) as control data, and compared to the data from the three devices. STATISTICS: Correlation between simulator generated true values and HRMs read values were calculated. RESULTS: In the 1st normal heart rate program, with an accuracy of exact value, Accurex Plus and Vantage NV, were more accurate than the PE 4000 (94% and 89% of values respectively versus 33% for the PE4000). At +/-3 beats x min(-1), the three devices gave good results: over 98% of total values. In transition phases: the three devices showed a smoothing effect, which was stronger in decelerating heart rate than in accelerating heart rate. In the 2nd program: isolated heart rhythm troubles (missing beat, pause <4 sec, supra-ventricular ectopic activity, and ventricular ectopic activity) were either not detected or were rejected. Signal changes such as changes in QRS (ventricular bigeminy) may cause detection losses, and so modify calculated heart rate. The HR signal rising/dropping slopes caused by sudden heart rhythm disorders, were notably attenuated, with a consequent loss of HR accuracy. CONCLUSIONS: In laboratory stable heart rate conditions, third generation HRMs are more accurate than earlier ones. Heart rate monitors are less accurate in transient phases and have not been improved in that domain. The three HRMs ignore isolated heart rate troubles. As expected, the usefulness of HRMs in detecting HR disorders is limited. Nevertheless, these devices have some value with serious troubles, like pause, bradycardia or tachycardia, lasting longer than 4 sec, and especially if they coincide with functional symptoms. The use of such even more accurate devices may consequently be recommended to healthy public for which they were built.

Arrhythmias, Cardiac↗

The influence of mean heart rate on measures of heart rate variability as markers of autonomic function: a model study.

Some studies have demonstrated that the assessments of autonomic activities from the alterations of heart rate variations (HRVs) after autonomic blockade and during exercise of high intensity by the spectral analysis of HRV seemed inconsistent with actual situation. The inconsistency is probably caused by the contributions of fluctuating magnitudes and mean levels of autonomic activities on HRV having not been clarified. The alterations of HRV after autonomic blockade and during exercise of high intensity using a mathematical model were simulated. The autonomic activity in normal condition was assumed first according to some experimental evidence. Then autonomic activities after sympathetic blockade, vagal blockade and during exercise of high intensity were appropriately adjusted accordingly. The HRVs in response to these given autonomic activities were simulated. We found that the effect on HRV influenced by the mean level of autonomic activity is helpful to explain alterations of HRV in these conditions. After vagal blockade, a largely reduced low frequency (LF) power could be caused by the reduced mean heartbeat interval induced by a decreased mean level of vagal activity. Increased low and high frequency powers after sympathetic blockade could be caused by the increased mean heartbeat interval induced by a decreased mean level of sympathetic activity. A decreased LF power during exercise of high intensity, in addition to the withdrawal of vagal activity, could also be caused by the decreased mean heartbeat interval induced by an increased mean level of sympathetic activity.

Animals↗

Heart rate and blood pressure during placebo-associated panic attacks.

Increases in the anxiety ratings, heart rate, and systolic and diastolic blood pressure were compared in eight panicking and 57 nonpanicking panic disorder patients during placebo (dextrose) infusions. Heart rate and systolic and diastolic blood pressure increased significantly in placebo-infused panickers, but these increases did not correlate well with increases in anxiety.

Adult↗

Investigation of altered heart rate variability, nonlinear properties of heart rate signals, and organ dysfunction longitudinally over time in intensive care unit patients.

PURPOSE: To investigate longitudinally over time heart rate dynamics and relation with mortality and organ dysfunction alterations in patients admitted to a multidisciplinary intensive care unit. METHODS: Data from 53 patients were used, with heart rate recorded from monitors and analyzed on a daily basis (every morning) for 600 seconds and sampling rate at 250 Hz, from admission to the intensive care unit until final discharge from the unit. Variance, which is a measure of heart rate variability; exponent alpha2; and approximate entropy (ApEn), which assess long-range correlations and periodicity within a signal, respectively; were measured and compared with every day Sequential Organ Failure Assessment Score (SOFA) and mortality. RESULTS: Nonsurvivors had lower ApEn mean (greater periodicity in their signals) and minimum values compared to survivors (0.53 +/- 0.25 vs 0.62 +/- 0.23, P = .04; 0.24 +/- 0.23 vs 0.48 +/- 0.23, P = .01, respectively). Patients in better conditions with SOFA of less than 7 (mean value) had higher variance and ApEn (more variable, less periodic signals) than those with SOFA of 7 or higher (0.47 +/- 0.51 vs 0.10 +/- 0.65, P < .001; 0.67 +/- 0.28 vs 0.49 +/- 0.24, P < .001, respectively). The alpha2 exponent and variance were correlated with length of stay (r = 0.55, P = .02, and r = 0.53, P = .02, respectively) and minimum ApEn with mortality (r = 0.41, P = .01). CONCLUSIONS: Loss of variability and increase in periodicity in heart rate of critically ill patients are linked with parallel deterioration of organ dysfunction and high mortality.

Analysis of Variance↗

Intrathecal kynurenate reduces arterial pressure, heart rate and baroreceptor-heart rate reflex in conscious rats.

In the present study, an excitatory amino acid (EAA) pathway in the spinal cord which maintains sympathetic vasomotor tone in conscious rats has been investigated. To this end, the cardiovascular effects of an intrathecally administered EAA antagonist, kynurenate (KYN), were studied in conscious rats. KYN (0.5 mumol in 10 microliters) caused a dramatic reduction in mean arterial pressure (MAP) and heart rate (HR) that persisted for 2-3 h, and also resulted in extensor paralysis of the hindlimbs. The time courses of fall in MAP and HR and hindlimb paralysis were similar. Baroreceptor-HR reflex activity was also markedly impaired after KYN, suggesting functional diminution of sympathetic outflow at the level of the spinal cord after blockade of EAA receptors by KYN. Xanthurenate, a metabolite of KYN without EAA antagonistic properties, produced negligible effects at the same dose of KYN. While these findings do not identify the putative EAA pathway, they do provide the first demonstration that this system is tonically active in conscious rats.

Animals↗