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Ventricular interaction during mechanical ventilation in closed-chest anesthetized dogs
Jamie R Mitchell1, Rozsa Sas, Daniel J Zuege
1Department of Physiology and Biophysics, University of Calgary, Alberta.
The Canadian Journal of Cardiology
|February 3, 2005
Summary
Positive pressure ventilation impacts heart function by altering blood flow and chamber size. Positive end-expiratory pressure further constrains the left ventricle, affecting cardiac output.
Area of Science:
- Cardiovascular Physiology
- Respiratory Mechanics
- Mechanical Ventilation
Background:
- The intricate cardiac effects of positive pressure ventilation (PPV) and positive end-expiratory pressure (PEEP) remain incompletely elucidated.
- Increased intrathoracic pressure during PPV externally constrains the left ventricle, reducing its end-diastolic volume, but effects on venous return and ventricular interaction are less clear.
Purpose of the Study:
- To investigate the phasic cardiac effects of positive pressure ventilation and positive end-expiratory pressure.
- To clarify the impact of PPV and PEEP on venous return, ventricular dimensions, and cardiac output.
Main Methods:
- Measurements of inferior vena caval flow, end-diastolic ventricular dimensions, and cardiac output.
- Utilized seven anesthetized, ventilated normal dogs as the experimental model.
- Analyzed changes during respiratory cycles (inspiration/expiration) and varying levels of PEEP.
Main Results:
- Inspiration decreased right ventricular output and diameter, while increasing left ventricular volume and output due to a rightward septal shift.
- Expiration reversed these effects, with decreased left ventricular volume and output.
- Increased PEEP further reduced left ventricular end-diastolic volume, exacerbated by a leftward septal shift indicating direct ventricular interaction.
Conclusions:
- Positive pressure ventilation dynamically alters right and left ventricular function throughout the respiratory cycle.
- Positive end-expiratory pressure imposes additional constraints on left ventricular filling through external compression and direct ventricular interaction, reducing end-diastolic volume.