PubMed HealthSearch

PubMed · 1751113

Electrohydraulic ventricular assist device development.

Abstract

A 64 ml (effective stroke volume) in vitro electrohydraulic ventricular assist device (VAD) prototype has been built. The energy converter is an axial flow pump driven by a brushless direct current (DC) motor. Systole begins as silicone oil is pumped from the volume displacement chamber (VDC) into the ventricle, displacing the flexing diaphragm separating the oil and the blood. In diastole, the motor reverses, providing active filling by pumping oil from the ventricle into the VDC. The surface mount electronic internal controller provides motor commutator, energy management, telemetry, and physiologic control functions. Energy is supplied externally by either a 12 V DC power supply or a 12 V DC rechargeable battery and is transmitted through the skin by a transcutaneous energy transformer (TET). Energy can also be supplied by a 12 V DC rechargeable internal battery. Bidirectional infrared telemetry is used to transmit information between the internal and external controllers.

Explore related subjects

Keep this discovery

Explore connections, maps & timelines

BibTeXRIS

P D Diegel, T Mussivand, J W Holfert, D Nahon, J Miller, G K Maclean, J P Santerre, G B Bearnson, J Juretich, A C Hansen. Electrohydraulic ventricular assist device development.. https://pubmed.ncbi.nlm.nih.gov/1751113/

Cite the original work for its findings. Save a collection to share your selection of sources.

KEEP EXPLORING

Related citations

A noninvasive method of predicting pulmonary-capillary wedge pressure.

BACKGROUND: The noninvasive prediction of pulmonary-capillary wedge pressure (PCWP) is important for the recognition and treatment of a variety of cardiovascular disorders. The response of the arterial pressure to the Valsalva maneuver has been shown to correlate with the PCWP. We therefore devised a noninvasive method to measure this pressure response at the bedside and correlated these measurements with the PCWP measured directly with a pulmonary-artery catheter. METHODS: Simultaneous, blinded, noninvasive measurements of the ratio of the final amplitude to the initial amplitude of the pulse wave form during the stress phase of the Valsalva maneuver (pulse-amplitude ratio) and direct measurements of the PCWP were obtained in 20 clinically stable patients and in 14 clinically unstable patients who were receiving vasoactive agents, 12 of whom also had endotracheal tubes in place. RESULTS: Using linear regression analysis, we found that the pulse-amplitude ratio strongly correlated with the measured PCWP over a range of base-line values from 4 to 32 mm Hg for the 20 clinically stable patients (R2 = 0.80) and the 14 clinically unstable patients (R2 = 0.85). The method also correctly predicted changes in the PCWP after the administration of nitroglycerin or furosemide and after expansion of the intravascular volume (R2 = 0.79). CONCLUSIONS: These preliminary data indicate that a simple noninvasive method can accurately predict the PCWP and changes in the PCWP in response to medical therapy.

Blood Pressure

Exercise-induced S-wave prolongation in left anterior descending coronary artery stenosis.

Myocardial ischemia may decrease conduction velocity and produce QRS prolongation in the surface electrocardiogram. In cases with normal intraventricular conduction, areas of the myocardium contributing to the development of the S wave receive blood from all 3 major coronary arteries, whereas in left anterior hemiblock or right bundle branch block, most of the blood supply to the areas of the myocardium contributing to the development of the S wave is from the left anterior descending (LAD) coronary artery. To test the hypothesis that the S wave will be prolonged with exercise only in patients with LAD coronary artery stenosis and left anterior hemiblock or right bundle branch block, 88 patients with normal intraventricular conduction, 66 with left anterior hemiblock and 36 with right bundle branch block were studied. Sixty-four, 32 and 21 patients had LAD, right and left circumflex coronary artery stenoses, respectively. In patients with normal coronary arteries, S-wave duration decreased with exercise regardless of the status of ventricular conduction. In patients with coronary artery disease and normal intraventricular conduction, the S wave was prolonged slightly with exercise, but in those with left anterior hemiblock and right bundle branch block, it was prolonged significantly (12.5 +/- 6 and 10.4 ms, respectively) only in those with LAD, but not in those with circumflex or right coronary artery stenosis. S-wave prolongation in patients with LAD coronary artery stenosis and left anterior hemiblock or right bundle branch block most likely is related to exercise-induced ischemia in the areas of the myocardium contributing to the development of the S wave.

Blood Pressure