Literature DB >> 3608124

Sequence of mitral valve motion and transmitral blood flow during manual cardiopulmonary resuscitation in dogs.

M P Feneley, G W Maier, J W Gaynor, S A Gall, J A Kisslo, J W Davis, J S Rankin.   

Abstract

According to the thoracic pump model of cardiopulmonary resuscitation (CPR), the heart serves as a passive conduit for blood flow from the pulmonary to the systemic vasculature, necessitating an open mitral valve and anterograde transmitral blood flow during chest compression. To assess the applicability of this model to manual CPR techniques, two-dimensional echocardiograms were recorded from the right chest wall and/or the esophagus in nine dogs (18 to 26 kg) during manual CPR. The aortic valve opened with chest compression and closed with release, while the pulmonary and tricuspid valve leaflets closed with compression and opened during release. The mitral valve remained open during ventilation alone and during abdominal compressions. With the onset of brief, high-velocity (high-impulse) chest compressions, the mitral valve closed rapidly and the left ventricle was deformed, whether compressions were applied to the sternum or the left mid-chest wall. The mitral valve reopened with release of each compression. Left atrial echocardiographic contrast injections confirmed the absence of anterograde transmitral blood flow during high-impulse compression and its presence during release. Failure of mitral leaflet approximation during chest compression was observed only when a very low-velocity, prolonged (low-impulse) compression technique was used, or when regions that did not directly overlie the heart were compressed. Consistent with these observations, simultaneous recordings of the left ventricular and left atrial pressures during high-impulse sternal compressions in five dogs (19 to 25 kg) demonstrated peak and mean left ventriculoatrial pressure gradients of 38.5 +/- 4.0 and 13.5 +/- 2.9 mm Hg, respectively, and these pressure gradients declined with less impulsive compressions. The observations made during all but low-impulse chest compressions are inconsistent with the thoracic pump model, and support direct cardiac compression as the primary mechanism of forward blood flow with more impulsive manual chest compression techniques.

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Year:  1987        PMID: 3608124     DOI: 10.1161/01.cir.76.2.363

Source DB:  PubMed          Journal:  Circulation        ISSN: 0009-7322            Impact factor:   29.690


  6 in total

1.  Mechanics of the circulation during cardiopulmonary resuscitation. Pathophysiology and techniques (Part II).

Authors:  J Peters; P Ihle
Journal:  Intensive Care Med       Date:  1990       Impact factor: 17.440

Review 2.  The physiology of cerebral blood flow during cardiopulmonary resuscitation.

Authors:  I D Berkowitz; M C Rogers
Journal:  Can J Anaesth       Date:  1988-05       Impact factor: 5.063

3.  Mechanism of closed chest cardiopulmonary resuscitation investigated by transoesophageal echocardiography.

Authors:  A C Pell; U M Guly; G R Sutherland; D J Steedman; P Bloomfield; C Robertson
Journal:  J Accid Emerg Med       Date:  1994-09

4.  Outcomes of severe hyperkalemia in cardiopulmonary resuscitation with concomitant hemodialysis.

Authors:  J L Lin; P S Lim; M L Leu; C C Huang
Journal:  Intensive Care Med       Date:  1994       Impact factor: 17.440

5.  Resuscitation training in small-group setting--gender matters.

Authors:  Saša Sopka; Henning Biermann; Rolf Rossaint; Steffen Rex; Michael Jäger; Max Skorning; Nicole Heussen; Stefan K Beckers
Journal:  Scand J Trauma Resusc Emerg Med       Date:  2013-04-16       Impact factor: 2.953

6.  Correlation between end-tidal carbon dioxide and the degree of compression of heart cavities measured by transthoracic echocardiography during cardiopulmonary resuscitation for out-of-hospital cardiac arrest.

Authors:  Roman Skulec; Petr Vojtisek; Vladimir Cerny
Journal:  Crit Care       Date:  2019-10-29       Impact factor: 9.097

  6 in total

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