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Hemodynamic changes during prolonged laparoscopic surgery

U Windberger1, H Siegl, R Woisetschläger

  • 1Center for Biomedical Research, Ludwig Boltzmann-Institute for Cardiac Surgery, University of Vienna, Austria.

European Surgical Research. Europaische Chirurgische Forschung. Recherches Chirurgicales Europeennes
|January 1, 1994
PubMed
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Pneumoperitoneum during laparoscopic surgery increases systemic and pulmonary arterial pressures, affecting cardiac function. Sustained hemodynamic changes may involve complex regulatory mechanisms, posing risks for cardiac patients.

Area of Science:

  • Cardiovascular Physiology
  • Surgical Anesthesia

Background:

  • Laparoscopic surgery utilizes pneumoperitoneum, involving CO2 insufflation to elevate intra-abdominal pressure.
  • Understanding the hemodynamic effects of pneumoperitoneum is crucial for patient safety, especially those with pre-existing cardiac conditions.

Purpose of the Study:

  • To investigate the acute hemodynamic and respiratory effects of carbon dioxide (CO2) pneumoperitoneum in pigs during laparoscopic surgery.
  • To analyze the impact of sustained intra-abdominal pressure on systemic and pulmonary circulation, cardiac function, and blood gases.

Main Methods:

  • Seven healthy pigs underwent laparoscopic anterior resection of the descending colon under anesthesia (ketamine/azaperone/thiopentone) and mechanical ventilation.
  • Carbon dioxide pneumoperitoneum was established to an abdominal pressure of 14 mm Hg.

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  • Systemic and pulmonary arterial pressures, left ventricular (LV) pressure, LV dp/dt, peak inspiratory pressure, central venous pressure, and blood gases were monitored.

    • Main Results:

    • Systemic and pulmonary arterial pressures acutely increased upon CO2 insufflation.
    • Pulmonary artery pressure decreased after 10 minutes, while systemic arterial pressure remained elevated.
    • Left ventricular pressure and dp/dt increased with systemic arterial pressure; peak inspiratory and central venous pressures rose with abdominal pressure.
    • Increased pCO2 and mild acidosis were observed; arterial pO2 remained stable, indicating preserved oxygenation.
    • Pulmonary pO2 and oxygen saturation increased, suggesting enhanced cardiac output or reduced oxygen extraction.

    Conclusions:

    • The initial rise in arterial pressures is likely mechanical, while sustained alterations involve regulatory mechanisms (sympathetic activity, baroreceptor control, acidosis response).
    • The acute and stable increase in ventricular afterload necessitates consideration in patients with cardiac diseases or those on interfering medications.