Journal of Applied Physiology Fuel your research with LabChart
HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
QUICK SEARCH:   [advanced]


     

J Appl Physiol 70: 454-465, 1991;
8750-7587/91 $5.00
This Article
Right arrow Full Text (PDF)
Right arrow Submit a response
Right arrow Alert me when this article is cited
Right arrow Alert me when eLetters are posted
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Beattie, C.
Right arrow Articles by Robotham, J. L.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Beattie, C.
Right arrow Articles by Robotham, J. L.

Journal of Applied Physiology, Vol 70, Issue 1 454-465, Copyright © 1991 by American Physiological Society

ARTICLES

Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation

C. Beattie, A. D. Guerci, T. Hall, A. M. Borkon, W. Baumgartner, R. S. Stuart, J. Peters, H. Halperin and J. L. Robotham
Department of Anesthesiology and Critical Care Medicine, Johns Hopkins Medical Institutions, Baltimore, Maryland 21205.

Mechanisms of blood flow during cardiopulmonary resuscitation (CPR) were studied in a canine model with implanted mitral and aortic flow probes and by use of cineangiography. Intrathoracic pressure (ITP) fluctuations were induced by a circumferential pneumatic vest, with and without simultaneous ventilation, and by use of positive-pressure ventilation alone. Vascular volume and compression rate were altered with each CPR mode. Antegrade mitral flow was interpreted as left ventricular (LV) inflow, and antegrade aortic flow was interpreted as LV outflow. The pneumatic vest was expected to elevate ITP uniformly and thus produce simultaneous LV inflow and LV outflow throughout compression. This pattern, the passive conduit of "thoracic pump" physiology, was unequivocally demonstrated only during ITP elevation with positive-pressure ventilation alone at slow rates. During vest CPR, LV outflow started promptly with the onset of compression, whereas LV inflow was delayed. At compression rates of 50 times/min and normal vascular filling pressures, the delay was sufficiently long that all LV filling occurred with release of compression. This is the pattern that would be expected with direct LV compression or "cardiac pump" physiology. During the early part of the compression phase, catheter tip transducer LV and left atrial pressure measurements demonstrated gradients necessitating mitral valve closure, while cineangiography showed dye droplets moving from the large pulmonary veins retrograde to the small pulmonary veins. When the compression rate was reduced and/or when intravascular pressures were raised with volume infusion, LV inflow was observed at some point during the compressive phase. Thus, under these conditions, features of both thoracic pump and cardiac pump physiology occurred within the same compression. Our findings are not explained by the conventional conceptions of either thoracic pump or cardiac compression CPR mechanisms alone.


This article has been cited by other articles:


Home page
 ChestHome page
R. Agarwal, D. Gupta, and K. Bendjelid
Is the Decrease in LVEDV the Mechanism of Action of Continuous Positive Airway Pressure in Diastolic Heart Failure?
Chest, September 1, 2005; 128(3): 1891 - 1892.
[Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
K. Bendjelid
Does inhaled nitric oxide support the hemodynamic of spontaneous breathing patients with cardiogenic shock related to right ventricular myocardial infarction?
J. Am. Coll. Cardiol., March 15, 2005; 45(6): 965 - 965.
[Full Text] [PDF]

Home page
 J Am Coll CardiolHome page
G. A. Ewy and J. P. Ornato
Emergency cardiac care: introduction
J. Am. Coll. Cardiol., March 15, 2000; 35(4): 825 - 880.
[Full Text] [PDF]


HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH TABLE OF CONTENTS
Visit Other APS Journals Online