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Objective: Future automated external defibrillators are being designed to direct rescue efforts (chest compressions first vs. defibrillation) by inferring the duration of ventricular fibrillation based on its waveform characteristics such as frequency content. This approach assumes that the ventricular fibrillation waveform is an appropriate surrogate for ventricular fibrillation duration and is not affected by structural heart disease. We hypothesized that an acute myocardial infarction may alter the frequency content of ventricular fibrillation.Design: Animal intervention study with comparison to control group.Setting: University animal laboratory.Subjects: Twenty-seven swine.Interventions: Acute myocardial infarction was induced by occlusion of the mid-left anterior descending artery. Ventricular fibrillation was induced in swine with acute myocardial infarction and control swine.Measurements and Main Results: Ventricular fibrillation was induced in 11 swine with an acute myocardial infarction and in 16 control swine. Ventricular fibrillation waveforms were analyzed for mean, median, and dominant frequency, as well as bandwidth and amplitude. All frequency characteristics were significantly (p < .001) altered in swine with acute myocardial infarction compared with controls. Specifically, these characteristics were significantly depressed and varied little over time in swine with acute myocardial infarction compared with controls.Conclusions: These data establish that ventricular fibrillation during an acute myocardial infarction has an altered frequency content and time evolution compared with ventricular fibrillation without coronary obstruction. Frequency characteristics such as mean, median, dominant, and bandwidth show little variation in time after an acute myocardial infarction and are not suitable surrogates for ventricular fibrillation duration. These findings have important implications for the development of 'smart' automated external defibrillators designed to determine duration of ventricular fibrillation from the waveform characteristics. [ABSTRACT FROM AUTHOR]

Objective: We report our experience with tele-echocardiography and echocardiograms recorded digitally or on videotape (recorded-echos) at The University of Arizona from August 2006 to December 2010 and compare their quality and diagnostic accuracy., Materials and Methods: Tele-echocardiograms (tele-echos) were transmitted from the Yuma Regional Medical Center to The University of Arizona via a T-1 and aT-3 line at a bandwidth of 768 kilobits per second. Recorded-echos were shipped for interpretation to The University of Arizona by overnight mail. Diagnostic accuracy was assessed by comparing tele- and recorded-echos with electrocardiograms performed by a pediatric cardiologist (PedsCard-echos)., Results: Three hundred forty-six tele-echos in 260 patients and 455 recorded-echos in 406 patients were performed (median age, 6 and 8 days, respectively). Indications included possible congenital heart disease (CHD), patent ductus arteriosus (PDA), and persistent pulmonary hypertension of the newborn. Diagnostic categories included complex CHD, non-critical disease, PDA, and other. PedsCard-echos were available for 27% of the tele-echo and 30% of the recorded-echo patients. Comparisons between tele- and PedsCard-echo yielded no discrepancies in 12 (23%), expected resolution of condition in 26 (49%), and minor in 14 (26%). One (2%) major discrepancy was detected. Comparisons between recorded- and PedsCard-echo showed no discrepancies in 28 (40%), expected resolution of condition in 14 (20%), and minor discrepancies in 28 (40%) patients. No significant difference with respect to discrepancies was detected between tele- and recorded-echos. There was significant (p<0.01) improvement in tele- and recorded-echo study quality by 2010., Conclusions: (1) Tele-echocardiography can be performed successfully with excellent accuracy. (2) The quality of tele- and recorded-echo studies improved toward the end of the analysis period. (3) Although initially tele-echo studies were more accurate than recorded-echo studies, there was no difference between these two types of studies by the fourth year of the study. (4) Both tele- and recorded-echos were indispensible in the remote diagnosis of CHD.

Objective: In cardiac arrest resulting from ventricular fibrillation, the ventricular fibrillation waveform may be a clue to its duration and predict the likelihood of shock success. However, ventricular fibrillation occurs in different myocardial substrates such as ischemia, heart failure, and structurally normal hearts. We hypothesized that ventricular fibrillation is altered by myocardial infarction and varies from the acute to postmyocardial infarction periods., Design: An animal intervention study was conducted with comparison to a control group., Setting: This study took place in a university animal laboratory., Subjects: Study subjects included 37 swine., Interventions: Myocardial infarction was induced by occlusion of the midleft anterior descending artery. Ventricular fibrillation was induced in control swine, acute myocardial infarction swine, and in postmyocardial infarction swine after a 2-wk recovery period., Measurements and Main Results: Ventricular fibrillation was recorded in 11 swine with acute myocardial infarction, ten postmyocardial infarction, and 16 controls. Frequency (mean, median, dominant, and bandwidth) and amplitude-related content (slope, slope-amp [slope divided by amplitude], and amplitude-spectrum area) were analyzed. Frequencies at 5 mins of ventricular fibrillation were altered in both acute myocardial infarction (p < .001 for all frequency characteristics) and postmyocardial infarction swine (p = .015 for mean, .002 for median, .002 for dominant frequency, and <.001 for bandwidth). At 5 mins, median frequency was highest in controls, 10.9 +/- .4 Hz; lowest in acute myocardial infarction, 8.4 +/- .5 Hz; and intermediate in postmyocardial infarction, 9.7 +/- .5 Hz (p < .001 for acute myocardial infarction and p = .002 for postmyocardial infarction compared with control). Slope and amplitude-spectrum area were similar among the three groups with a shallow decline after minute 2, whereas slope-amp remained significantly altered for acute myocardial infarction swine at 5 mins (p = .003)., Conclusions: Ventricular fibrillation frequencies depend on myocardial substrate and evolve from the acute through healing phases of myocardial infarction. Amplitude related measures, however, are similar among these groups. It is unknown how defibrillation may be affected by relying on the ventricular fibrillation waveform without considering myocardial substrate.

We noted a dicrotic pulse in several patients following a Ross operation. Although the etiology of this unique arterial waveform is not completely understood, it has been reported as a sign of low cardiac output and a poor prognosis. We reviewed preoperative echocardiograms and postoperative radial arterial pressure tracings in 33 patients who underwent a Ross procedure between 2000 and 2004. We found a dicrotic pulse to occur commonly (20/33; 61%) following a Ross operation. Moderate to severe preoperative aortic insufficiency was present in 19/20 patients (95%) in whom a dicrotic pulse was noted and in only 3/13 (23%) who did not exhibit a postoperative dicrotic pulse (p<0.001). A dicrotic pulse was not associated with an increased use of vasoactive infusions or longer hospitalization following the Ross operation. The dicrotic pulse should be recognized as a common postoperative finding in Ross patients that does not herald a delayed postoperative convalescence. The mechanism for a dicrotic pulse in these patients is speculative but may result from changes in vascular compliance secondary to chronic aortic insufficiency.

Background: For prolonged VF, perfusion of the myocardium by pre-shock chest compressions can improve myocardial readiness for successful defibrillation. Characteristics of the VF waveform correlate with the duration of VF when there is no structural heart disease. A "smart" automated external defibrillator (AED) could therefore analyze the VF waveform, determine if VF has been prolonged, and then direct rescuers to either deliver a shock first or chest compressions first. We hypothesized that ischemic heart failure might alter the waveform content of ventricular fibrillation compared with normal hearts, complicating the determination of VF duration., Methods: Myocardial infarction was induced by ligating the proximal left coronary artery. Six weeks later, VF was then induced in 10 rats with myocardial infarction and heart failure (MI-CHF) and 9 control rats. Waveforms were analyzed for total signal amplitude, median frequency, dominant frequency and bandwidth (the frequency interval containing 50% of the total amplitude about the median frequency)., Results: All of these VF waveform characteristics were altered substantially in MI-CHF rats compared to normal controls. In particular, MI-CHF rats had decreased signal amplitude early in VF (p=0.02), a broader bandwidth (p=0.001) and different frequency characteristics over time (p<0.001)., Conclusions: VF waveforms vary over time in a typical manner among rats with and without ischemic heart failure. However, the time-course and waveform characteristics of ventricular fibrillation are altered in rats with myocardial infarctions and ischemic heart failure compared to normal controls. These findings have important implications regarding the use of waveform analyses to determine the duration of VF.

Background: Derived variables of ventricular fibrillation, such as the frequency distribution by fast Fourier transformation and its evolution over time, have been used to determine the optimum timing for defibrillation. We hypothesized that these frequency variables would differ among neonatal, young child and older child populations due to cardiac developmental and size differences. Such differences may have important implications for developing defibrillation algorithms for pediatric patients and for extrapolating adult defibrillation algorithms to children in VF., Methods: Ventricular fibrillation was induced and recorded for 6 min in 4 kg (n = 11), 14 kg (n = 10), and 24 kg (n = 16) piglets, corresponding to neonatal, young child and older children. Mean, median, and dominant frequencies were computed in 30 s intervals and compared among weight classes., Results: All frequency variables in all weight groups showed first a decline at 1.25-1.75 min, followed by a gradual rise and plateau. There were significant differences for mean, median and dominant frequencies among weight classes. Specifically, 14 kg piglets showed higher frequency variables overall with a time evolution that was different from that of 4 and 24 kg piglets. Mean frequency showed the most stable time evolution with the least moment-to-moment variability., Conclusion: The frequency waveform characteristics and time course are somewhat different in 14 kg piglets compared with 4 and 24 kg piglets. If similar differences are demonstrable among children of different weights and ages, AEDs designed to determine optimal timing of defibrillation shocks in adults by frequency waveform characteristics may require modification for use in children with VF.

The purpose of this study was to determine the hemodynamic and electrophysiologic effects of acute chocolate, and hence theobromine, ingestion on the hearts of young adults. Theobromine was not found to have any cardiovascular effects on subjects in this study.

Background: Although moderate caffeine ingestion has not been shown to be arrhythmogenic, caffeine toxicity can cause severe cardiac arrhythmias, including atrial fibrillation and ventricular tachycardia. Atrial fibrillation and ventricular tachycardia have been associated with prolongation of P-wave and QRS complex durations on signal-averaged electrocardiograms. This study investigated acute effects of caffeine ingestion on signal-averaged P-wave and QRS complexes., Methods and Results: Signal-averaged electrocardiograms were obtained from 12 normal subjects (6 men, 6 women; ages 21 to 26 years) before and after ingestion of caffeine (5 mg/kg body weight) or placebo in a randomized, double-blind, crossover fashion. Electrocardiograms for signal averaging were recorded from electrodes left in a constant location. After bandpass filtering (30 to 300 Hz) and amplification, signals were sampled over 7.2 minutes at 2000 Hz. Signal-averaged P-wave and QRS complex durations did not significantly change after placebo ingestion. After caffeine ingestion QRS duration prolonged in 9 of 11 subjects at 90 minutes (mean +/- SEM = 0.8+/-0.3 ms, P< .02) and in 8 of 9 after 3 hours (1.1+/-0.2 ms, P< .001). No significant change in P-wave duration or heart rate was found after caffeine ingestion at any test interval. Average caffeine level in saliva 90 minutes after ingestion was 6.6+/-1.6 (SD) microg/dL., Conclusions: Although probably not arrhythmogenic in normal subjects, moderate caffeine ingestion does produce a small but statistically significant prolongation of signal-averaged QRS complexes. Further prolongation caused by excessive caffeine intake may be a factor in the genesis of arrhythmias associated with caffeine toxicity.

This study investigated hemodynamic effects of acute caffeine ingestion in young adults 21 to 26 years of age. Data showed an increase in heart rate corrected velocity of circumferential fiber shortening at an indexed afterload up to 4.5 hours following caffeine consumption.

Hemodynamics effects of ethanol were studied in young adults at specific predetermined ethanol levels of 0.025%, 0.05%, and 0.75%. Findings included a decrease in end-systolic wall stress (afterload) and myocardial contractility following ingestion of ethanol at concentrations found in "social drinking."

We report a case in which residual shunting after a buttoned device occlusion of atrial septal defect (ASD) was eliminated by transcatheter retrieval of a portion of the device, followed by implantation of a second device. This method may be helpful for those patients with residual ASDs who decline surgical device retrieval and defect closure.

A blind study was designed to test the hypothesis that some persons with a relatively rare cardiac malformation, pulmonary atresia with ventriculoseptal defect (PA/VSD), have a recognisable phenotype. Fourteen patients with cyanotic congenital heart lesions were examined by dysmorphologists blinded to the type of cardiac malformation. Six children were judged to have a similar craniofacial appearance; all had PA/VSD. These children were not originally considered to fall within the classic phenotypes of the DiGeorge sequence or the velocardiofacial syndrome, both of which have been shown to be associated with deletions of 22q11. More recently, 22q11 deletions have been documented in the conotruncal anomaly face syndrome and apparently isolated conotruncal heart defects. A new acronym, CATCH 22 syndrome (Cardiac defects, Abnormal facies, Thymic hypoplasia, Cleft palate, and Hypocalcaemia) has been suggested to encompass this very broad phenotypic spectrum. A preliminary molecular study was conducted using the dinucleotide repeat D22S264 located on chromosome 22q11.2. All cases tested with the subtle but recognisable phenotype had deletions, all lacking the maternal contribution at this locus, suggesting there may be a parent of origin effect.

Respiratory syncytial virus (RSV), a common cause of respiratory infections in children, has only rarely been associated with acquired heart disease. We reviewed hospital charts, rhythm strips, and electrocardiograms of 8 infants with abnormal supraventricular tachycardia (SVT), > 250 beats/min, associated with acute RSV infections. Cultures of nasopharyngeal specimens from six of eight infants grew RSV. Two infants with negative viral culture results had symptoms typical of an RSV infection during a documented RSV epidemic. Two infants had congenital heart defects. Seven of the eight infants had an ectopic atrial tachycardia, chaotic atrial tachycardia, or atrial flutter, and five of eight had episodes of nonsustained wide-complex SVT. One patient was initially treated with intravenously administered lidocaine for an incorrect diagnosis of ventricular tachycardia. SVT was unrelated to either beta-agonist therapy or hypoxic episodes. SVT did not recur after discharge in any infant with a structurally normal heart. Both patients with structural heart disease had recurrences of SVT. We conclude that RSV infections in infants may be associated with unusual atrial tachycardias and that the diagnosis may be complicated by episodes of nonsustained, wide-complex tachycardias. In patients with RSV and structurally normal hearts, chaotic and ectopic atrial tachycardias are self-limited and do not require prolonged drug therapy.

Pharmacokinetic and pharmacodynamic data on adrenergic agents in children have revealed wide ranges of plasma clearance rates and hemodynamic responses in patients with critical illnesses or myocardial dysfunction. In order to more clearly elucidate the underlying pharmacologic processes, graded i.v. dobutamine infusions of 0.5, 2.5 and 5.0 micrograms/kg/min were sequentially administered to healthy children and adolescents. Plasma dobutamine concentrations and hemodynamic responses, including echocardiographic measures of systolic and diastolic function, were determined at each infusion rate. Pharmacodynamic data were evaluated by both threshold modeling and mean hemodynamic responses to each infusion rate. Mean plasma dobutamine clearance was 115 +/- 63 ml/kg/min, with an intersubject variability greater than 5-fold. These data establish that the previously published wide variability in dobutamine clearance is not due simply to underlying disease states. Dobutamine clearance was linear over the dosage range evaluated. Dobutamine improved systolic function even at plasma concentrations attained with infusion rates as low as 1 to 2 micrograms/kg/min. The improved systolic function was at least partially due to inotropic effects. In addition, dobutamine improved diastolic function and reduced afterload. Chronotropic effects were observed in only two subjects and only at higher plasma concentrations than the other hemodynamic effects. Individualized threshold modeling effectively described the log-linear relationship between plasma dobutamine concentration and hemodynamic response beyond the threshold concentration.

Objective: To delineate dobutamine pharmacokinetics and hemodynamic responses in children., Design: Prospective, pharmacokinetic study using sequential, graded dosing of drug., Interventions: Graded intravenous dobutamine infusions of 0.5, 2.5, 5, 10, and 20 micrograms/kg/min were sequentially administered for 25 mins each. Plasma dobutamine concentrations and echocardiographically determined hemodynamic data were obtained at baseline and at 15 and 25 mins during each infusion rate. Hemodynamic responses were evaluated by paired t-test and by computerized evaluation of individual dose-response curves., Setting: Pediatric intensive care unit in a university setting., Patients: Eleven stable, critically ill children previously requiring inotropic support with dobutamine. Seven patients were postcardiac surgical patients; four patients had acute cardiac dysfunction with septic shock and/or adult respiratory distress syndrome., Measurements and Main Results: Mean cardiac index increased from 3.8 to 5.2 L/min/m2 (p < .05). Increasing the infusion rate from 10 to 20 micrograms/kg/min increased cardiac index by 16% (p < .05). Cardiac index increased by > 10% in four of seven patients at a dobutamine infusion rate of 0.5 microgram/kg/min (mean 21%). The relationship of plasma dobutamine concentration to cardiac index, systolic blood pressure, and heart rate fit a threshold model with a log-linear relationship after the threshold in seven of nine, seven of 11, and eight of 11 patients, respectively. As anticipated, in the patients who responded, there were linear increases in hemodynamic responses with exponential increases in plasma dobutamine concentrations. Mean plasma clearance rate was 82 +/- 3 mL/min/kg. First-order kinetics were demonstrated by the direct linear relationship of plasma dobutamine concentration to infusion rate (mean r2 = .95; p < .01 for each patient) and by independence of clearance from dose and duration of each infusion., Conclusions: Dobutamine effectively improves systolic function in critically ill children. Hemodynamic responses to dobutamine generally follow a predicted log-linear dose-response model. Dobutamine clearance in this study was consistent with first-order kinetics. The wide variability in hemodynamic responses and clearance kinetics indicate that dobutamine infusions must be titrated individually.

Central venous pressure measurements in the abdominal inferior vena cava were compared with measurements in the right atrium in 10 infants and 10 children during cardiac catheterization. At end expiration, the mean pressures at these two sites were within 1 mm Hg of each other in all 20 patients, with a mean difference of 0.0 +/- 0.36 mm Hg. The abdominal inferior vena cava is a safe and convenient site for measurement of central venous pressure, and our study confirms that such measurements are accurate.

Doxorubicin is an effective anticancer chemotherapeutic agent known to cause acute and chronic cardiomyopathy. To develop a more sensitive echocardiographic screening test for cardiac damage due to doxorubicin, a cohort study was performed using dobutamine infusion to differentiate asymptomatic long-term survivors of childhood cancer treated with doxorubicin from healthy control subjects. Echocardiographic data from the experimental group of 21 patients (mean age 16 +/- 5 years) treated from 1.6 to 14.3 years (median 5.3) before this study with 27 to 532 mg/m2 of doxorubicin (mean 196) were compared with echocardiographic data from 12 normal age-matched control subjects. Graded dobutamine infusions of 0.5, 2.5, 5 and 10 micrograms/kg per min were administered. Echocardiographic Doppler studies were performed before infusion and after 15 min of infusion at each rate. Dobutamine infusion at 10 micrograms/kg per min was discontinued after six studies secondary to a 50% incidence rate of adverse symptoms. The most important findings were that compared with values in control subjects, end-systolic left ventricular posterior wall dimension and percent of left ventricular posterior wall thickening in doxorubicin-treated patients were decreased at baseline study and these findings were more clearly delineated with dobutamine stimulation. End-systolic left ventricular posterior wall dimension at baseline for the doxorubicin-treated group was 11 +/- 1.9 mm versus 13.1 +/- 1.5 mm for control subjects (p less than 0.01). End-systolic left ventricular posterior wall dimension at the 5-micrograms/kg per min dobutamine infusion for the doxorubicin-treated group was 14.1 +/- 2.4 mm versus 19.3 +/- 2.6 mm for control subjects (p less than 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Study Objective: To test the hypotheses that in multiple pathophysiologic settings (1) end-expiratory central venous pressure measurements in the intraabdominal inferior vena cava accurately reflect those in the superior vena cava and (2) mean central venous pressure monitoring is as reliable in the inferior vena cava as it is in the superior vena cava., Design: Simultaneous inferior vena caval and superior vena caval pressures were measured during five ventilatory phases: apnea, end-expiratory mechanical ventilation, maximal inspiratory mechanical ventilation, end-expiratory spontaneous ventilation, and maximal inspiratory spontaneous ventilation. Measurements were repeated after progressive intravascular volume depletion., Subjects: Eight puppies., Measurements and Results: Simultaneous inferior vena caval and superior vena caval end-expiratory pressures did not differ significantly (mean differences 0 to 0.1 mm Hg) and the limits of agreement of these measurements were within 2 mm Hg. Differences between mean maximal inspiratory pressures in the inferior vena cava and superior vena cava during mechanical and spontaneous ventilation were -0.7 and 3.6 mm Hg, respectively (p less than 0.01), and the limits of agreement extended beyond 2 mm Hg. Furthermore, mean maximal inspiratory pressures in the superior vena cava differed from end-expiratory pressures in the superior vena cava (1.1 and -3.6 mm Hg, p less than 0.01), whereas those in the inferior vena cava did not differ from end-expiratory superior vena caval pressures., Conclusions: Under the experimental conditions studied (1) end-expiratory intraabdominal inferior vena caval pressures accurately reflected end-expiratory superior vena caval pressures and (2) mean central venous pressure monitoring was as reliable in the inferior vena cava as in the superior vena cava.

Previous investigations of mechanical valve sounds have shown that (1) frequency spectra of sounds produced by abnormal valves differ from those of properly functioning valves and (2) leaflets of normally functioning bileaflet valves do not close synchronously. This investigation studied effects of mechanical valve size, environment, and hemodynamic state on closing sounds. A single 25 mm bileaflet mitral mechanical valve was implanted in six sheep and a single 27 mm valve in four sheep. With digital signal processing, asynchronous leaflet closure and frequency spectra were assessed after alterations in animal position, respiratory phase, heart rate, afterload, contractility, and preload. Both asynchronous leaflet closure and frequency spectra varied among animals, and, except for a decrease in asynchrony with increasing contractility, were largely independent of valve size and hemodynamics. Baseline asynchrony ranged from 0.5 to 4.2 msec. Frequency spectra were characterized by the first three resonant peaks. Lowest resonant peaks ranged from 2.5 to 3.4 kHz, middle from 4.7 to 6.8 kHz, and highest from 7.2 to 9.6 kHz. These results indicate that accurate assessment of mechanical valve function with acoustic analysis requires baseline studies in all patients by means of a system with a frequency response of more than 10 kHz.

Signal averaged atrial activity recorded from the body surface is finding increased use in assessing atrial arrhythmias. The process of signal averaging is critically dependent upon precise alignment of the waveform of interest. The alignment accuracy of wide (0.01-300 Hz) and narrow (10-300 Hz) bandpass filtered P waves recorded from the body surface were compared to atrial electrograms recorded from temporary pacing wires. The locations of the filtered P waves relative to the atrial electrogram were calculated beat-by-beat for 100 beats in 15 patients aged 1 month to 71 years. The standard deviation of the alignment error for the wide filtered surface P wave averaged 1.7 +/- 0.8 msec and for the narrow filtered P waves was 0.8 +/- 0.4 ms. These results demonstrate that high pass filtering will improve alignment accuracy, and therefore, improve frequency resolution for the analysis of signal averaged P waves.

By means of real-time--directed M-mode ultrasound, the hearts of normal and abnormal fetuses were evaluated for evidence of a pericardial effusion. Because of its limited potential space, the pericardial sac appears to become distended with fluid prior to ultrasound evidence of ascites, pleural effusions, or soft tissue edema. Fetal echocardiography, therefore, appears to be useful in the assessment of fetuses at risk for developing hydrops.

The prenatal diagnosis of fetal cardiac disease has become increasingly accurate as the technology of ultrasound has improved. Although two-dimensional real-time ultrasound remains the primary method of diagnosis, Doppler blood flow velocity estimates can provide valuable pathophysiologic information to support the anatomic diagnosis. We present six cases in which Doppler studies contributed to the accuracy of the diagnosis of fetal heart disease, including tetralogy of Fallot, right and left ventricular hypoplasia, atrioventricular canal defect, double-outlet right ventricle, and pulmonic stenosis. Velocities in these cases are compared with those in normal fetuses. If Doppler flow velocities are not consistent with the observed morphologic changes, further observations are indicated. Inasmuch as most anatomical heart lesions result in altered flow patterns, Doppler investigations of intracardiac and extracardiac flow should be a routine component of the fetal echocardiogram when structural abnormalities are found.

Fetal echocardiographic studies were performed in 71 patients referred for evaluation of cardiac rhythm disturbances at 24 to 40 weeks' gestation. After 2-dimensional echocardiographic study of cardiac structure was performed, M-mode echocardiograms were analyzed for measurement of cardiac rate, atrioventricular contraction sequence, atrioventricular valve motion, and duration of postectopic pauses. Arrhythmias were diagnosed in 59 patients. In 34 patients with isolated ectopic beats, the arrhythmia resolved during later pregnancy in 26 or within the first 5 days of life in 8. Six patients had mild sinus bradycardia and 8 had frequent sinus pauses; all 14 had resolution of the arrhythmia during pregnancy. Sustained arrhythmias occurred in 11 patients. Deaths occurred when there was associated fetal congestive heart failure (hydrops fetalis), structural heart disease, or both. M-mode echocardiography diagnosed supraventricular tachycardia in 3 fetuses. The echocardiogram was used thereafter for monitoring transplacental digoxin therapy.

Thirteen fetuses with nonimmune hydrops (22 to 39 weeks of gestation) were evaluated with two-dimensional and M-mode echocardiography. Ten fetuses had cardiovascular abnormalities resulting in heart failure, and three had noncardiac causes of hydrops. In three cases, hydrops was caused by supraventricular tachycardia. One of these fetuses responded to cardioversion at birth, another responded to transplacental digoxin therapy, and the third died with atrial flutter and high-grade atrioventricular block before delivery. There were no cases of "idiopathic" hydrops. Our results show that fetal echocardiography is useful in determining cardiac causes of in utero heart failure resulting in hydrops fetalis. The fetal echocardiogram may also be used in monitoring transplacental therapy of heart failure.

Severity of stenotic heart lesions affects timing, quality and pitch of associated heart murmurs. This quantitative study investigated the relation between instantaneous sound frequencies contained in heart murmurs and magnitudes of Doppler jet velocities measured distal to associated obstructions. Heart murmurs were recorded from 18 patients, ages 1 day to 23 years, with 21 separate murmurs resulting from abnormal valves (18 studies) or left-to-right shunts (3 studies). Recorded murmurs were digitized and divided into 12.3-ms time segments for computer frequency analysis using the maximum entropy method. Murmur spectra were plotted in gray scale against time. All murmurs contained dominant frequencies that varied with time. Dominant murmur frequencies and associated Doppler jet velocities at equivalent points in time were measured at 50-ms intervals. For 88 points analyzed, instantaneous dominant frequencies ranged from 130 to 410 Hz (mean +/- standard deviation 282 +/- 70 Hz) and instantaneous jet velocities ranged from 110 to 460 cm/s (290 +/- 80 cm/s). For the 21 murmurs studied, peak murmur frequencies ranged from 200 to 410 Hz (308 +/- 70 Hz) and peak jet velocities ranged from 165 to 460 cm/s (320 +/- 78 cm/s). Instantaneous dominant frequency correlated to instantaneous jet velocity (r = 0.85) and peak dominant frequency correlated to peak jet velocity (r = 0.89). This in vivo study demonstrates that dominant frequencies contained in heart murmurs are related to instantaneous jet velocities distal to associated obstructions.

Echocardiography may provide information concerning the structural development of the fetal human heart. The information available from such studies, when interpreted in light of existing knowledge of developmental cardiac physiology, may give insight concerning in utero cardiac pump function. The quantitation of cardiac structural growth in utero has been used to provide growth curves for the chambers of the fetal heart. Disparity in the ratio of right ventricular/left ventricular size (normally 1.0 to 1.2) may suggest acute ventricular failure and dilation. Electromechanical analysis using M-mode techniques may be used to analyze and monitor the treatment of fetal cardiac arrhythmias and provide systolic time interval analysis. Doppler waveform analysis provides information concerning directional flow and vascular impedance and Doppler flowmetry has promise for the measurement of fetal aortic and umbilical venous blood flows. Such studies have increased our understanding of fetal circulatory function and have practical implications for the establishment of fetal cardiac diagnosis and treatment programs.

With current ultrasound technology, it is now possible to obtain accurate real-time and M-mode information from the fetal heart with the use of real-time--directed M-mode echocardiography. With this method, the M-mode cursor is directed to the fetal cardiac structures of interest while the image is obtained in the real-time mode. This enables M-mode echocardiograms to be obtained in an accurate, reproducible manner. The most useful imaging planes for cardiac evaluation are the long axis four-chamber plane, the short axis plane through the atrioventricular valves, and the short axis plane through the aortic and pulmonic outflow tracts. Once normal fetal cardiac anatomy is understood, structural defects and/or alterations of function can be evaluated accurately antenatally.

Doppler echocardiography enables the possibility of determining pulmonary to systemic flow ratios in patients with left to right shunts. Volume flow is calculated as the product of mean velocity over time, as evaluated by pulsed Doppler, and the cross-sectional area through which the flow passes. Appropriate sites for measurement of velocity and cross-sectional area of flow are the ascending aorta, right ventricular outflow tract and pulmonary artery as well as the tricuspid and mitral valve orifices. Velocity is always recorded as parallel as possible to the direction of flow. Echocardiographic measurements of the area of flow are carried out at the level of the sample volume. In the presence of an atrial or ventricular septal defect, the flow in the ascending aorta normally serves as systemic flow; alternatively, mitral or tricuspid flow may be used to cross-check these values. The latter serves for calculation of systemic flow in patent ductus arteriosus. In atrial or ventricular septal defect, the pulmonary flow is normally derived in the region of the pulmonary artery; in patent ductus arteriosus, however, in the region of the ascending aorta. As an alternative, or for confirmative use, in atrial septal defect the tricuspid flow and in ventricular septal defect and patent ductus arteriosus the mitral flow, can be taken into consideration. Studies we performed in 31 patients with atrial septal defect showed a close correlation between Doppler echocardiographic measurements and data obtained by cardiac catheterization and radionuclide studies.(ABSTRACT TRUNCATED AT 250 WORDS)