BackgroundTo assess changes in right heart flow and pulmonary artery hemodynamics in patients with repaired Tetralogy of Fallot (rTOF) we used whole heart, four dimensional (4D) velocity mapping (VM) cardiovascular magnetic resonance (CMR).MethodsCMR studies were performed in 11 subjects with rTOF (5M/6F; 20.1 ± 12.4 years) and 10 normal volunteers (6M/4F; 34.2 ± 13.4 years) on clinical 1.5T and 3.0T MR scanners. 4D VM-CMR was performed using PC VIPR (Phase Contrast Vastly undersampled Isotropic Projection Reconstruction). Interactive streamline and particle trace visualizations of the superior and inferior vena cava (IVC and SVC, respectively), right atrium (RA), right ventricle (RV), and pulmonary artery (PA) were generated and reviewed by three experienced readers. Main PA net flow, retrograde flow, peak flow, time-to-peak flow, peak acceleration, resistance index and mean wall shear stress were quantified. Differences in flow patterns between the two groups were tested using Fisher's exact test. Differences in quantitative parameters were analyzed with the Kruskal-Wallis rank sum test.Results4D VM-CMR was successfully performed in all volunteers and subjects with TOF. Right heart flow patterns in rTOF subjects were characterized by (a) greater SVC/IVC flow during diastole than systole, (b) increased vortical flow patterns in the RA and in the RV during diastole, and (c) increased helical or vortical flow features in the PA's. Differences in main PA retrograde flow, resistance index, peak flow, time-to-peak flow, peak acceleration and mean wall shear stress were statistically significant.ConclusionsWhole heart 4D VM-CMR with PC VIPR enables detection of both normal and abnormal right heart flow patterns, which may allow for comprehensive studies to evaluate interdependencies of post-surgically altered geometries and hemodynamics.
We used 40-MHz echocardiography to identify key elements of the early mouse embryonic cardiovascular system and for noninvasive dimensional analysis of developing cardiac ventricles. The ability to perform serial measurements and to detect mutant embryos with cardiac defects highlights the usefulness of the technique for investigating normal and abnormal cardiovascular development.
Purpose of review Though fetal arrhythmias account for a small proportion of referrals to a fetal cardiologist, they may be associated with significant morbidity and mortality. The present review outlines the current literature with regard to the diagnosis and, in brief, some management strategies in fetal arrhythmias. Recent findings Advances in echocardiography have resulted in significant improvements in our ability to elucidate the mechanism of arrhythmia at the bedside. At the same time, fetal magnetocardiography is broadening our understanding of mechanisms of arrhythmia especially as it pertains to ventricular arrhythmias and congenital heart block. It provides a unique window to study electrical properties of the fetal heart, unlike what has been available to date. Recent reports of bedside use of fetal ECG make it a promising new technology. The underlying mechanisms resulting in immune-mediated complete heart block in a small subset of ‘at-risk’ fetuses is under investigation. Summary There have been great strides in noninvasive diagnosis of fetal arrhythmias. However, we still need to improve our knowledge of the electromechanical properties of the fetal heart as well as the mechanisms of arrhythmia to further improve outcomes. Multiinstitutional collaborative studies are needed to help answer some of the questions regarding patient, drug selection and management algorithms.
Familial hypertrophic cardiomyopathy (FHC) is inherited as an autosomal dominant trait that is characterized by unexplained hypertrophy of the ventricular myocardium with histologic evidence of myocyte and myofibrillar disarray. Myocyte loss and replacement fibrosis are often prominent features, which can contribute to arrhythmias and altered myocardial hemodynamics in FHC. Molecular genetic studies have demonstrated that FHC is caused by mutations in genes encoding cardiac sarcomere proteins; these defects are most commonly found in the β cardiac myosin heavy chain (MHC) gene (1, 2). The mechanism(s) by which mutated sarcomere proteins cause the clinical features of FHC is largely unknown.We have developed a mouse model for FHC by introducing a missense mutation identified in humans (β cardiac MHC Arg403Gln; ref. 1) into the murine α cardiac MHC gene using homologous recombination (3). In humans, the Arg403Gln mutation causes marked histopathology, ventricular dysfunction, and a high incidence of sudden death (4). Heterozygous α cardiac MHC mutant mice (α-MHC 403/+ ) develop myocardial histologic abnormalities similar to human FHC by 15 weeks of age. Sedentary α-MHC 403/+ mice have a normal life span. Homozygous α cardiac MHC mice (α-MHC 403/403 ) were generated to examine the consequences of complete replacement of normal myosin by mutant peptide. α-MHC 403/403 pups were liveborn, but, unlike their heterozygous littermates, they all died within one week.We report studies of cardiac structure and function in normal and α-MHC 403/403 mice using a new high-frequency (45 MHz) echocardiographic technique (5, 6). Our data provide the first demonstration that high-quality images can be obtained by 45-MHz echocardiography for in vivo assessment of myocardial size and contractility in neonatal mice. Markedly abnormal physiology and pathology were found in α-MHC 403/403 hearts. These data explain the neonatal lethality of homozygous mutants and provide insights into a potential etiology for myocyte death in human FHC. MethodsAnimals. Details of the targeting construct and homologous recombination procedures used in the generation of α-MHC 403/+ mice have been described previously (3). α-MHC 403/403 , α- Heterozygous mice bearing an Arg403Gln missense mutation in the α cardiac myosin heavy chain gene (α-MHC 403/+ ) exhibit the histopathologic features of human familial hypertrophic cardiomyopathy. Surprisingly, homozygous α-MHC 403/403 mice die by postnatal day 8. Here we report that neonatal lethality is caused by a fulminant dilated cardiomyopathy characterized by myocyte dysfunction and loss. Heart tissues from neonatal wild-type and α-MHC 403/403 mice demonstrate equivalent switching of MHC isoforms; α isoforms in each increase from 30% at birth to 70% by day 6. Cardiac dimensions and function, studied for the first time in neonatal mice by high frequency (45 MHz) echocardiography, were normal at birth. Between days 4 and 6, α-MHC 403/403 mice developed a rapidly progressive cardiomyopathy with left ventricular dilat...
Objective Ventricular kinetic energy measurements may provide a novel imaging biomarker of declining ventricular efficiency in patients with repaired Tetralogy of Fallot (rTOF). Our purpose was to assess differences in ventricular kinetic energy (KE) with four-dimensional (4D) Flow MRI between patients with rTOF and healthy volunteers. Methods Cardiac MR (CMR), including 4D Flow MRI, was performed at rest in 10 subjects with rTOF and nine healthy volunteers using clinical 1.5T and 3T MRI scanners. Right and left ventricular kinetic energy (KERV and KELV), main pulmonary artery flow (QMPA), and aortic flow (QAO) were quantified using 4D Flow MRI data. Right and left ventricular size and function were measured using standard CMR techniques. Differences in peak systolic KERV and KELV in addition to the QMPA/KERV and QAO/KELV ratios between groups were assessed. KE indices were compared to conventional CMR parameters. Results Peak systolic KERV and KELV were higher in rTOF subjects (6.06±2.27mJ and 3.55±2.12mJ, respectively) than healthy volunteers (5.47±2.52mJ and 2.48±0.75mJ, respectively) but not statistically significant (p= .65 and p= .47, respectively). The QMPA/KERV and QAO/KELV ratios were lower in rTOF subjects (7.53±5.37mL/(cycle-mJ) and 9.65±6.61mL/(cycle-mJ), respectively) than healthy volunteers (19.33±18.52mL/(cycle-mJ) and 35.98±7.66mL/(cycle-mJ), respectively; p< .05). QMPA/KERV and QAO/KELV were weakly correlated to ventricular size and function. Conclusions Greater ventricular KE is necessary to generate flow in the pulmonary and aortic circulations in rTOF. Quantification of ventricular KE in patients with rTOF is a new observation. Future studies are needed to determine if changes in ventricular KE can provide earlier evidence of ventricular dysfunction and guide future medical and surgical interventions.
Objective Bedside ultrasound, as performed by the intensivist, is gaining in popularity and has become a powerful tool to understand the physiological state of the critically ill patient and to decrease procedural risks. This review assesses clinical applications of bedside ultrasound in the pediatric intensive care unit. Design A literature review was conducted to identify English language studies in Pubmed as of June, 2010, using combinations of the following search terms: ‘pediatric,’ ‘ultrasound,’ ‘critical care,’ and ‘intensive care.’ Examination of reference lists of these studies yielded additional studies. Studies were reviewed by both authors. Setting Intensive care unit, emergency department, or operating rooms, as relevant to application of bedside ultrasound in the pediatric intensive care unit. Patients/Subjects Pediatric patients (age 0 –18 yrs) with adult patients (>18 yrs) in relevant studies utilizing bedside ultrasound by the treating clinician. Interventions Bedside ultrasound by treating clinician. Measurements Variable, per individual studies. Main Results/Conclusions Bedside ultrasound, as practiced by the pediatric intensivist, has the potential to improve pediatric critical care medicine, but data supporting its use is limited. Further studies are needed to explore applications, with specific emphasis on the training and experience of ultrasound operators. There is a need for a standardized educational curriculum, and questions remain as to the optimal mode of education and quality assurance of ultrasound operators.
Altered total cavopulmonary connection (TCPC) hemodynamics can cause long-term complications. Patient-specific anatomy hinders generalized solutions. 4D Flow MRI allows in vivo assessment, but not predictions under varying conditions and surgical approaches. Computational fluid dynamics (CFD) improves understanding and explores varying physiological conditions. This study investigated a combination of 4D Flow MRI and CFD to assess TCPC hemodynamics, accompanied with in vitro measurements as CFD validation. 4D Flow MRI was performed in extracardiac and atriopulmonary TCPC subjects. Data was processed for visualization and quantification of velocity and flow. Three-dimensional (3D) geometries were generated from angiography scans and used for CFD and physical model construction through additive manufacturing. These models were connected to a perfusion system, circulating water through the vena cavae and exiting through the pulmonary arteries at two flow rates. Models underwent 4D Flow MRI and image processing. CFD simulated the in vitro system, applying two different inlet conditions from in vitro 4D Flow MRI measurements; no-slip was implemented at rigid walls. Velocity and flow were obtained and analyzed. The three approaches showed similar velocities, increasing proportionally with high inflow. Atriopulmonary TCPC presented higher vorticity compared to extracardiac at both inflow rates. Increased inflow balanced flow distribution in both TCPC cases. Atriopulmonary IVC flow participated in atrium recirculation, contributing to RPA outflow; at baseline, IVC flow preferentially travelled through the LPA. The combination of patient-specific in vitro and CFD allows hemodynamic parameter control, impossible in vivo. Physical models serve as CFD verification and fine-tuning tools.
Background: Multi-institutional, international practice variation of pediatric anaphylaxis management by healthcare providers has not been reported.Objective: Characterize variability in epinephrine administration for pediatric anaphylaxis across institutions, including frequency and types of medication errors. Methods:A prospective, observational, study using a standardized in situ simulated anaphylaxis scenario was performed across 28 healthcare institutions in six countries. The on-duty healthcare team was called for a child (patient simulator) in anaphylaxis. Real medications and supplies were obtained from their actual locations. Demographic data about team members, institutional protocols for anaphylaxis, timing of epinephrine delivery, medication errors, and systems safety issues discovered during the simulation were collected.Results: Thirty-seven in situ simulations were performed. Anaphylaxis guidelines existed in 41% (15/37) of institutions. Teams used a cognitive aid for medication dosing 41% (15/37) of the time and 32% (12/37) for preparation. Epinephrine auto injectors (EAIs) were not available in 54% (20/37) of institutions and were used in only 14% (5/37) simulations. Median time to epinephrine administration was 95 seconds (IQR 77, 252) for EAI and 263 seconds (IQR 146, 407.5) for manually prepared epinephrine (p=.12). At least one medication error occurred in 68% (25/37) of simulations. Prior nursing experience with epinephrine administration for anaphylaxis was associated with fewer preparation (p=.04) and administration (p=.01) errors.Latent safety threats (LSTs) were reported by 30% (11/37) of institutions, more than half of these (6/11) involved a cognitive aid. Conclusion and Relevance:A multicenter, international study of simulated pediatric anaphylaxis reveals: 1) variation in management between institutions in usage of protocols,
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