Unnecessary interruptions of cardiac massage during simulated cardiac arrests.

BACKGROUND AND OBJECTIVE: Cardiopulmonary resuscitation should not be interrupted until the return of spontaneous circulation or the decision to withhold further treatment. There are no data on how consistent in-hospital cardiopulmonary resuscitation is performed. Accordingly, the aim of the present study was to identify length and type of unnecessary interruptions in simulated cardiac arrests. METHODS: The study was carried out in a patient simulator. A scenario of cardiac arrest due to ventricular fibrillation was used. Resuscitation teams consisted of three nurses, a resident and a staff physician. Using videotapes recorded during simulations, the activities of the teams were coded in 5-s intervals. Unnecessary interruptions were defined as any interruptions in cardiac massage of 10 s or more that were not caused by defibrillation or endotracheal intubation. RESULTS: Twelve teams were studied. The total time of possible cardiac massage was 414 +/- 125 s. In each team at least one unnecessary interruption occurred (range 1-5). Interruptions mounted up to 65 +/- 40 s (range 20-155) or 16 +/- 10% (range 5-41) of the total time of possible cardiac massage. Failure to swiftly resume cardiac massage after an unsuccessful defibrillation accounted for 14 of 39 episodes and for 44 +/- 40% of the time of unnecessary interruptions. The debriefings revealed that participants had generally not noticed the unnecessary interruptions during the simulation. CONCLUSIONS: The present study identified a significant amount of unnecessary interruptions in cardiac massage. These interruptions were not noticed by the health-care workers involved.

Adverse cardiac events in ICU patients with presumptive antidepressant overdose.

BACKGROUND: Antidepressants account for most poison-related admissions to intensive care units. In selected patients with confirmed cyclic antidepressant intoxication a QRS interval <0.1 s in the ECG limb leads during the first six hours excludes adverse cardiac events. However, the incidence of cardiac events and the value of ECG criteria have never been assessed prospectively on patients with presumed antidepressant overdose. AIM: To assess ingested drugs, adverse cardiac events, and ECG findings in ICU patients with a presumptive diagnosis of antidepressant overdose. METHODS: 103 consecutive patients with a presumptive diagnosis of antidepressant overdose were enrolled and prospectively followed. Outcome criteria were arrhythmias, mortality, and duration of the ICU stay. RESULTS: Mixed intoxication was identified in 66 (64%) patients. Tricyclic antidepressants were found in 88 (85%), and serotonin-reuptake inhibitors in 25 (24%) patients. Mean APACHE II score was 9.5 (SD +/- 6.0). Arrhythmias affected 15 (15%) and cardiopulmonary resuscitation was performed on 4 (4%) patients. Three patients (3%) died in the ICU. Median duration of the ICU stay was 1 day (12 hours to 6 days). Adverse cardiac events affected patients with normal and prolonged QRS interval at study entry. CONCLUSIONS: Mixed intoxication is present in most ICU patients with suspected antidepressant overdose. There is a considerable risk for adverse cardiac events, even in the presence of normal ECG recordings within the first six hours after hospital admission.

Design of a new surgical approach for ventricular remodeling to relieve ischemic mitral regurgitation: insights from 3-dimensional echocardiography.

BACKGROUND: Mechanistic insights from 3D echocardiography (echo) can guide therapy. In particular, ischemic mitral regurgitation (MR) is difficult to repair, often persisting despite annular reduction. We hypothesized that (1) in a chronic infarct model of progressive MR, regurgitation parallels 3D changes in the geometry of mitral leaflet attachments, causing increased leaflet tethering and restricting closure; therefore, (2) MR can be reduced by restoring tethering geometry toward normal, using a new ventricular remodeling approach based on 3D echo findings. METHODS AND RESULTS: We studied 10 sheep by 3D echo just after circumflex marginal ligation and 8 weeks later. MR, at first absent, became moderate as the left ventricle (LV) dilated and the papillary muscles shifted posteriorly and mediolaterally, increasing the leaflet tethering distance from papillary muscle tips to the anterior mitral annulus (P<0.0001). To counteract these shifts, the LV was remodeled by plication of the infarct region to reduce myocardial bulging, without muscle excision or cardiopulmonary bypass. Immediately and up to 2 months after plication, MR was reduced to trace-to-mild as tethering distance was decreased (P<0.0001). LV ejection fraction, global LV end-systolic volume, and mitral annular area were relatively unchanged. By multiple regression, the only independent predictor of MR was tethering distance (r(2)=0.81). CONCLUSIONS: Ischemic MR in this model relates strongly to changes in 3D mitral leaflet attachment geometry. These insights from quantitative 3D echo allowed us to design an effective LV remodeling approach to reduce MR by relieving tethering.

Three-dimensional echocardiographic assessment of left ventricular wall motion abnormalities in mouse myocardial infarction.

We applied 3-dimensional echocardiographic reconstruction to assess left ventricular (LV) volumes, function, and the extent of wall motion abnormalities in a murine model of myocardial infarction (MI). Consecutive parasternal short-axis planes were obtained at 1-mm intervals with a 13-MHz linear array probe. End-diastolic and end-systolic LV volumes were calculated by Simpson's rule, and the ejection fraction and cardiac output were derived. Echocardiography-derived cardiac output was validated by an aortic flow probe in 6 mice. Echocardiography was then performed in 9 mice before and after the left anterior descending coronary artery was ligated. Wall motion was assessed, and the ratio of the abnormally to normally contracting myocardium was calculated. After MI occurred, LV end-diastolic volume and LV end-systolic volume increased (33 +/- 10 vs 24 +/- 6 microL, P <.05 and 24 +/- 9 vs 10 +/- 4 microL, P <.001), whereas cardiac output decreased (4.2 +/- 1.5 mL/min vs 6.6 +/- 2.3 mL/min, P <.01). Forty percent of the myocardium was normokinetic, 24% was hypokinetic, and 36% was akinetic. Echocardiography can measure LV volumes and regional and global function in a murine model of myocardial infarction, thereby providing the potential to quantitate and compare the responses of various transgenic mice to MI and its therapies.

Echocardiographic determination of risk area size in a murine model of myocardial ischemia.

Genetically altered mice are useful to understand cardiac physiology. Myocardial contrast echocardiography (MCE) assesses myocardial perfusion in humans. We hypothesized it could evaluate murine myocardial perfusion before and after acute coronary ligation. MCE was performed before and after this experimental myocardial infarction (MI) in anesthetized mice by intravenous injection of contrast microbubbles and transthoracic echo imaging. Time-video intensity curves were obtained for the anterior, lateral, and septal myocardial walls. After MI, MCE defects were compared with the area of no perfusion measured by Evans blue staining. In healthy animals, intramyocardial contrast was visualized in all the cardiac walls. The anterior wall had a higher baseline video intensity (53 +/- 17 arbitrary units) than the lateral (34 +/- 13) and septal (27 +/- 13) walls (P < 0.001) and a lower increase in video intensity after contrast injection [50 +/- 17 vs. 60 +/- 24 (lateral) and 65 +/- 29 (septum), P < 0.01]. After MI, left ventricular (LV) dimensions were enlarged, and the shortening fraction was decreased. A perfusion defect was imaged with MCE in every mouse, with a correlation between MCE perfusion defect size (35 +/- 13%) and the nonperfused area by Evans blue (37 +/- 16%, y = 0.77x + 6.1, r = 0.93, P < 0. 001). Transthoracic MCE is feasible in the mouse and can accurately detect coronary occlusions and quantitate nonperfused myocardium.

Regional wall motion assessment in stress echocardiography by tissue Doppler bull's-eyes.

Quantification of regional myocardial wall velocities is needed in stress echocardiography for transition from subjective to quantitative assessment. Tissue Doppler allows quantitation of wall velocities, but interpretation is difficult and angle-dependent. Calculating the ratios of velocities with similar angles to the beam may overcome angle dependency. We measured left ventricular wall velocities during stress echocardiography with tissue Doppler. Regional peak systolic and early (E) and late (A) diastolic velocities were constructed in a "bull's-eye" format. Regional stress/rest and E/A ratios were calculated. Bull's-eye map construction demanded only minimal manual interaction, and the maps showed the left ventricular velocity distribution, simplifying wall motion reading markedly. Still, apical velocities appeared lower as a result of Doppler angle-dependency. With velocity ratios, angle-dependency was no longer noted. In stress echocardiography, wall motion abnormalities at rest and contractility changes with dobutamine became readily apparent. Bull's-eye display of quantitative tissue Doppler velocity allows rapid assessment of regional wall motion. Calculating the ratio of regional velocities circumvents the angle-dependency of Doppler. This novel technique has the potential for simplified and automated quantitative analysis in stress echocardiography.

Determination of right ventricular structure and function in normoxic and hypoxic mice: a transesophageal echocardiographic study.

BACKGROUND: Noninvasive cardiac evaluation is of great importance in transgenic mice. Transthoracic echocardiography can visualize the left ventricle well but has not been as successful for the right ventricle (RV). We developed a method of transesophageal echocardiography (TEE) to evaluate murine RV size and function. METHODS AND RESULTS: Normoxic and chronically hypoxic mice (F(IO2)=0.11, 3 weeks) and agarose RV casts were scanned with a rotating 3.5F/30-MHz intravascular ultrasound probe. In vivo, the probe was inserted in the mouse esophagus and withdrawn to obtain contiguous horizontal planes at 1-mm intervals. In vitro, the probe was withdrawn along the left ventricular posterior wall of excised hearts. The borders of the RV were traced on each plane, allowing calculation of diastolic and systolic volumes, RV mass, RV ejection fraction, stroke volume, and cardiac output. RV wall thickness was measured. Echo volumes obtained in vitro were compared with cast volumes. Echo-derived cardiac output was compared with measurements of an ascending aortic Doppler flow probe. Echo-derived RV free wall mass was compared with true RV free wall weight. There was excellent agreement between cast and TEE volumes (y=0.82x+6.03, r=0.88, P<0.01) and flow-probe and echo cardiac output (y=1.00x+0.45, r=0.99, P<0.0001). Although echo-derived RV mass and wall thickness were well correlated with true RV weight, echo-derived RV mass underestimated true weight (y=0.53x+2.29, r=0.81, P<0.0001). RV mass and wall thickness were greater in hypoxic mice than in normoxic mice (0.78+/-0.19 versus 0.51+/-0.14 mg/g, P<0.03, 0.50+/-0.03 versus 0.38+/-0.03 mm, P<0.04). CONCLUSIONS: TEE with an intravascular ultrasound catheter is a simple, accurate, and reproducible method to study RV size and function in mice.

Improved myocardial ischemia detection by combined physical and mental stress testing.

The hypothesis that addition of mental stress to physical exercise would modify the circulation response to stress and improve noninvasive detection of myocardial ischemia was tested in a randomized, crossover radionuclide angiocardiographic study. Compared with physical exercise or mental stress alone, combined stress led to higher heart rates and rate-pressure products in early stress stages, to more pronounced symptoms, and to a better discrimination of subjects with and without coronary artery disease by radionuclide angiography.