Analysis of neither steady state conditions nor the single respiratory cycle has been able to resolve the controversies of respiration's effect on left ventricular performance. The use of rapid transient perturbations in pleural pressure is an extremely powerful tool to elucidate the basic mechanisms of cardiopulmonary interactions common to all modes of ventilation or cardiopulmonary resuscitation. The following hypothesis will be tested: Transient alterations in Pleural pressure will favorably affect left ventricular output by increasing Pleural pressure in systole, reducing its afterload and decreased Pleural pressure in diastole, increasing both intrathoracic aortic blood volume and systemic venous return. This hypothesis defines a set of physiologic constructs which explain prior conflicting data and will stimulate the application of a rational set of respiratory maneuvers to diagnose, support and improve myocardial performance in the failing and arrested heart. It will be tested in a series of anesthetized acutely instrumented dogs to measure blood flow with electromagnetic flow probes, cardiac and great vessel dimensions with piezoelectric crystals, along with vascular pressures. Transient perturbations in Pleural pressure within the cardiac cycle will be accomplished with a) phrenic nerve stimulation, and b) positive airway pressure.
The specific aims of this proposal are: 1) to determine the effects on left ventricular performance of transient positive and negative perturbations in Pleural pressure, 2) to compare unique physiologic data, e.g. phasic ventricular inflow and aortic dimensions, to a computer model as both a retrospective and predictive tool to gain insight into the operational elements in the cardiovascular system altered by changes in Pleural pressure. This proposal will provide essential physiologic data applicable to interpretation of studies of cardiorespiratory events during a) spontaneous ventilation with upper or lower airway obstruction, b) positive pressure ventilation at any rate, and c) cardiopulmonary resuscitation.

Agency
National Institute of Health (NIH)
Institute
National Heart, Lung, and Blood Institute (NHLBI)
Type
Research Project (R01)
Project #
1R01HL039138-01
Application #
3355748
Study Section
Cardiovascular Study Section (CVA)
Project Start
1987-08-01
Project End
1990-07-31
Budget Start
1987-08-01
Budget End
1988-07-31
Support Year
1
Fiscal Year
1987
Total Cost
Indirect Cost
Name
Johns Hopkins University
Department
Type
Schools of Medicine
DUNS #
045911138
City
Baltimore
State
MD
Country
United States
Zip Code
21218
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