Literature DB >> 3662153

Intrathoracic pressure fluctuations move blood during CPR: comparison of hemodynamic data with predictions from a mathematical model.

H R Halperin1, J E Tsitlik, R Beyar, N Chandra, A D Guerci.   

Abstract

Whether blood flow during cardiopulmonary resuscitation (CPR) results from intrathoracic pressure fluctuations or direct cardiac compression remains controversial. We developed a mathematical model that predicts that blood flow due to intrathoracic pressure fluctuations should be insensitive to compression rate over a wide range but dependent on the applied force and compression duration. If direct compression of the heart plays a major role, however, the model predicts that flow should be dependent on compression rate and force, but above a threshold, insensitive to compression duration. These differences in hemodynamics produced by changes in rate and duration form a basis for determining whether blood flow during CPR results from intrathoracic pressure fluctuations or from direct cardiac compression. The model was validated for direct cardiac compression by studying the hemodynamics of cyclic cardiac deformation following thoracotomy in four anesthetized, 21-32-kg dogs. As predicted by the model, there was no change in myocardial or cerebral perfusion pressures when the duration of compression was increased from 15% to 45% of the cycle at a constant rate of 60/min. There was, however, a significant increase in perfusion pressures when rate was increased from 60 to 150/min at a constant duration of 45%. The model was validated for intrathoracic pressure changes by studying the hemodynamics produced by a thoracic vest (vest CPR) in eight dogs. The vest contained a bladder that was inflated and deflated. Vest CPR changed intrathoracic pressure without direct cardiac compression, since sternal displacement was less than 0.8 cm. As predicted by the model and opposite to direct cardiac compression, there was no change in perfusion pressures when the rate was increased from 60 to 150/min at a constant duration of 45% of the cycle. Manual CPR was then studied in eight dogs. There was no surgical manipulation of the chest. Myocardial and cerebral blood flows were determined with radioactive microspheres and behaved as predicted from the model of intrathoracic pressure, not direct cardiac compression. At nearly constant peak sternal force (378-426 N), flow was significantly increased when the duration of compression was increased from short (13%-19% of the cycle) to long (40%-47%), at a rate of 60/min. Flow was unchanged, however, for an increase in rate from 60 to 150/min at constant compression duration. In addition, myocardial and cerebral flow correlated with their respective perfusion pressures.(ABSTRACT TRUNCATED AT 400 WORDS)

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Year:  1987        PMID: 3662153     DOI: 10.1007/bf02584292

Source DB:  PubMed          Journal:  Ann Biomed Eng        ISSN: 0090-6964            Impact factor:   3.934


  23 in total

1.  HAEMODYNAMIC EFFECTS OF EXTERNAL CARDIAC COMPRESSION.

Authors:  G J MACKENZIE; S H TAYLOR; A H MCDONALD; K W DONALD
Journal:  Lancet       Date:  1964-06-20       Impact factor: 79.321

2.  Timing of pulmonary and systemic blood flow during intermittent high intrathoracic pressure cardiopulmonary resuscitation in the dog.

Authors:  J M Cohen; N Chandra; P O Alderson; A van AsWegen; J E Tsitlik; M L Weisfeldt
Journal:  Am J Cardiol       Date:  1982-06       Impact factor: 2.778

3.  Augmentation of cerebral perfusion by simultaneous chest compression and lung inflation with abdominal binding after cardiac arrest in dogs.

Authors:  R C Koehler; N Chandra; A D Guerci; J Tsitlik; R J Traystman; M C Rogers; M L Weisfeldt
Journal:  Circulation       Date:  1983-02       Impact factor: 29.690

4.  Role of carotid artery resistance to collapse during high-intrathoracic-pressure CPR.

Authors:  F C Yin; J M Cohen; J Tsitlik; B Zola; M L Weisfeldt
Journal:  Am J Physiol       Date:  1982-08

5.  Pressure-synchronized cineangiography during experimental cardiopulmonary resuscitation.

Authors:  J T Niemann; J P Rosborough; M Hausknecht; D Garner; J M Criley
Journal:  Circulation       Date:  1981-11       Impact factor: 29.690

6.  Mechanisms of blood flow during cardiopulmonary resuscitation.

Authors:  M T Rudikoff; W L Maughan; M Effron; P Freund; M L Weisfeldt
Journal:  Circulation       Date:  1980-02       Impact factor: 29.690

7.  Volumes and compliances measured simultaneously in the right and left ventricles of the dog.

Authors:  M M Laks; D Garner; H J Swan
Journal:  Circ Res       Date:  1967-05       Impact factor: 17.367

8.  Pressure-flow and pressure-volume relations in the entire pulmonary vascular bed of the dog determined by two-port analysis.

Authors:  A A Shoukas
Journal:  Circ Res       Date:  1975-12       Impact factor: 17.367

9.  Mechanisms by which epinephrine augments cerebral and myocardial perfusion during cardiopulmonary resuscitation in dogs.

Authors:  J R Michael; A D Guerci; R C Koehler; A Y Shi; J Tsitlik; N Chandra; E Niedermeyer; M C Rogers; R J Traystman; M L Weisfeldt
Journal:  Circulation       Date:  1984-04       Impact factor: 29.690

10.  Cardiac output during cardiopulmonary resuscitation at various compression rates and durations.

Authors:  K R Fitzgerald; C F Babbs; H A Frissora; R W Davis; D I Silver
Journal:  Am J Physiol       Date:  1981-09
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  2 in total

1.  Modeling the circulation with three-terminal electrical networks containing special nonlinear capacitors.

Authors:  J E Tsitlik; H R Halperin; A S Popel; A A Shoukas; F C Yin; N Westerhof
Journal:  Ann Biomed Eng       Date:  1992       Impact factor: 3.934

2.  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

  2 in total

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