A small study in Crit Care Med reminds me how it is really hard to anticipate the effects of systemic vasoconstrictors. Norepinephrine/noradrenaline is more likely to reduce cardiac output than maintain it.
A small study including 16 postoperative cardiac elective patients due for coronary bypass or mitral valvuloplasty. The protocol started during the first postoperative hour while the patients where still intubated and sedated. In the hemodynamically stable patients a continuous norepinephrine infusion was started. The infusion rate was increased to induce a MAP increase of 20 mmHg.
MAP, PCV (central venous pressure) , CO and and a host of other parameters were measured. Three sets of measurements were obtained:
Baseline 1 – At hemodynamic stability before norepinephrine infusion.
Baseline 2 – At the 20 mmHG MAP increase
Baseline 3 – After returning to the baseline 1 norad infusion rate.
After MAP increased by 20 mmHg cardiac output increased in only 6 patients. In the remaining ten CO dropped by almost 0,5 L/min.
So, in 10 out of 16 patients CO decreased despite increased MAP. Only 6 patients actually increased CO. This is important. Because when we start norad infusion we do so in order to secure adequate perfusion pressure and at least maintain cardiac output.
It would be nice if we had a way to predict which patients will increase CO. The study notices how patients with high stroke volume variation (SVV) are more likely to increase their CO.
Baseline SVV in the group that increased CO was 14,4% while it was 9,1% in the decreased CO group. Increased SVV is a reasonably reliable predictor of hypovolemia. Does that mean that the CO increasing effect is more likely the more hemodynamically unstable the patient is?
As for what exactly what decides what happens when we start norepinephrine I´m not sure. There is a lengthy explanation in the article that is way beyond my attention span.
Because, at the end of the day….
Angry Birds > Medical Journals
Study lives here.