The effect of ventilation on aortic blood gases during left ventricular ejection before separation from cardiopulmonary bypass. Academic Article uri icon

Overview

abstract

  • The time to begin ventilating a cardiac surgical patient recovering from hyperkalemic arrest is controversial. Those who advocate ventilating as soon as the left ventricle begins to eject believe that blood ejected from the left ventricle is likely to be hypoxic since it perfuses collapsed, nonventilated alveoli and that this may be the major blood supply perfusing the coronary arteries. The present study attempts to answer this question by sampling blood gases from the aorta in proximity to the coronary ostia in patients both before and after ventilation. Ten patients undergoing coronary artery bypass grafting using the left internal mammary artery were studied. Each patient served as his own control. Distal anastomoses were placed under hyperkalemic, hypothermic cardiac arrest. The aorta was unclamped, and an intrinsic or paced heart rate of 70 beats per minute was achieved. The heart was allowed to eject to a pulse pressure of 20 to 40 mmHg. Rectal temperatures were between 32 degrees C and 34 degrees C. Blood gases were drawn simultaneously from the proximal aortic root, radial artery, pulmonary artery, and the venous circuit of the cardiopulmonary bypass (CPB) machine. The lungs were then twice inflated with a sustained positive pressure of 30 cm H2O, and the patient was ventilated (10 mL/kg tidal volume, FIO2 1.0, 10 breaths per minute) for two minutes. Another set of blood gases was then obtained. Filling pressures, aortic systolic and diastolic pressures, and CPB flows were kept constant for both sets of samples. There was no significant difference in aortic root PaO2 attributable to ventilation. PCO2 was significantly lower, and pH was significantly higher in the ventilated group.(ABSTRACT TRUNCATED AT 250 WORDS)

publication date

  • June 1, 1989

Research

keywords

  • Aorta
  • Carbon Dioxide
  • Cardiopulmonary Bypass
  • Oxygen
  • Respiration, Artificial
  • Stroke Volume
  • Ventricular Function, Left

Identity

Scopus Document Identifier

  • 0024361899

Digital Object Identifier (DOI)

  • 10.1016/0888-6296(89)90112-9

PubMed ID

  • 2520654

Additional Document Info

volume

  • 3

issue

  • 3