Hyperventilation by positive pressure ventilation can lead to oliguria through a number of different mechanisms:
1) Decreased cardiac output secondary to the increased intrathoracic pressure and an increase in right ventricular afterload – the decrease of cardiac output and BP caused by PPV results in a baroreceptor mediated increase in SNS with subsequent renal vasoconstriction. Volume receptors in the atria respond to decreased filling by decreasing the production of ANP, increasing sympathetic tone, increasing renin activity and ADH production.
2) Increase of IVC pressure → decreased renal perfusion (or an increase of renal venous pressure → decreased renal drainage)
Through the above mechanisms, PPV can lead to a decrease in renal blood flow, GFR, Na excretion and urine flow rate. This impairment of renal function can be prevented or attenuated by preserving normal circulatory status, ie appropriate hydration.
Keep in mind that while hyperventilation caused by PPV can lead to oliguria, there are other situations in the OR in which you may see both hyperventilation and oliguria.
1) Neuroendocrine stress response. Sympathetic outflow from the celiac and renal plexus (T4-L1) result in alpha 1 mediated renal vasoconstriction. Circulating catecholamines also result in a redistribution of renal blood flow to the renal medullary → clinically associated with Na retention. Stress – hyperventilation.
2) Pneumoperitoneum. Oliguria secondary to abdominal compartment like state. Mechanisms include venous compression (IVC and renal veins), renal parenchymal compression, decreased cardiac output and increased levels of renin, aldosterone and ADH. These effects are generally proportional to insufflation pressures. Increased minute ventilation is due to the absorbtion of CO2 from insufflation.
3) Metabolic Acidosis with Respiratory Compensation. Many causes of metabolic acidosis will also be associated with oliguria. For example, lactic acidosis secondary to sepsis or hypovolemia also be associated with oliguria.
Oliguria Caused by Hyperventilation: Mechanisms
- Decreased cardiac output and subsequent SNS response (vasoconstriction)
- Increased IVC pressure (reduced pressure gradient and RBF)