Ultrasonic Cardiac Output Monitoring and Microcirculation: Is It Worthwhile to Consider in Reconstructive Microsurgery?

We read with great interest the report by Dr. Setälä and coworkers focusing the metabolic response in microvascular flaps during partial pedicle obstruction and hypovolemic shock.[1] We believe that this article has touched an important issue of reconstructive microsurgery. That is, how does macrocirculation affect microcirculation in a reconstructive microsurgical environment?

As cited by the authors, Lohman and colleagues investigated the effect of flap flow and cardiac output in an experimental study as early as 1998.[2] They examined five anesthetized pigs following right carotid artery cannulation. Measurements of systemic blood pressure and blood gas analysis were performed. An oximetric Swan-Ganz catheter insertion via the right internal jugular vein was used to measure cardiac output, temperature, and pulmonary artery wedge pressure. In the lateral decubitus position, a right latissimus dorsi muscle flap was elevated in the animal, using standard technique. They found that the hypothesis that flap flow would be preserved in the face of reductions in cardiac output did not prove to be correct in this experiment. Changes in flap flow paralleled changes in cardiac output as the pulmonary artery wedge pressure was reduced.

Another study among 40 patients undergoing cardiopulmonary bypass compared regional tissue oxygenation saturation using near-infrared spectroscopy with standard hemodynamic and biochemical variables.[3] With initiation of cardiopulmonary bypass, tissue oxygen saturation declined by 12.9% with a delayed increase in lactate from 0.9 (interquartile range [IQR], 0.6 to 1.5) mmol/L to 2.3 (IQR, 1.8 to 2.5) mmol/L. The minimum regional tissue oxygen saturation value preceded the maximum lactate level by an average time of 93.9 minutes. Additionally, a decrease in regional tissue oxygen saturation corresponded with an increase in base deficit of 4.8 mEq/L over the same period.

Therefore it is tempting to speculate that the macrocirculatory changes, such as a decreased cardiac output, might influence the microcirculatory environment. Setälä's work supports this theory by stating that during hypovolemic shock, the lactate production increased and the glucose concentration decreased or remained normal, determined by in situ microdialysis technique. The metabolic changes occurring during partial pedicle obstruction and hypovolemic shock are moderate and different from those seen in total pedicle obstruction.

In patients undergoing free-flap transfer, continuous hemodynamic monitoring might help identify phases of deteriorated macrocirculation. Correction of macrocirculatory deficits, such as a deteriorated cardiac output or hypovolemia, might have an impact on the outcome of free-flap surgery. Since the first description of a catheter to measure cardiac output by Swan and Ganz in 1970,[4] several improvements have been accomplished. However, complication rates limit the use of the Swan-Ganz catheter with potential arrhythmias, pulmonary artery perforation, and bronchial hemorrhage.[5] [6] [7] Therefore, the routine use of a Swan-Ganz catheter in patients undergoing free-flap transfer cannot be recommended at this point. However, a noninvasive cardiac output monitoring system might be preferable among patients undergoing free-flap transfer.

A portable ultrasonic cardiac output monitor (USCOM) has been introduced in the clinic primarily for pediatric and adult intensive care units. The validation work has been done versus Swan-Ganz catheters mainly in postcardiac surgery patients with a very good agreement of the USCOM values with the Swan-Ganz values.[8] [9] USCOM allows determining hemodynamic parameters such as stroke volume, cardiac output, cardiac index, and systemic vascular resistance noninvasively by targeting the blood column in the ascending aorta from a suprasternal approach. The learning curve is steep; therefore the additional use of a portable cardiac output monitor on the plastic surgery ward is possible.

Given the preceding observations, further studies might determine the hemodynamic variation following free-flap transfer using the currently freely available methods to determine cardiac output noninvasively. The macrocirculation might well have an impact on the microcirculatory perfusion level, and thus free-flap success rates might be improved by a goal-directed therapy (tailored fluid resuscitation) following microsurgical free-flap transfer.

REFERENCES

• 1 Setälä L, Joukainen S, Uusaro A, Alhava E, Härmä M. Metabolic response in microvascular flaps during partial pedicle obstruction and hypovolemic shock.  J Reconstr Microsurg. 2007;  23(8) 489-496
• 2 Lohman R, Gürlek A, Schusterman M A. Flap flow and cardiac output as functions of pulmonary artery wedge pressure: experimental study in the pig.  J Reconstr Microsurg. 1998;  14 317-321
• 3 Putnam B, Bricker S, Fedorka P et al.. The correlation of near-infrared spectroscopy with changes in oxygen delivery in a controlled model of altered perfusion.  Am Surg. 2007;  73 1017-1022
• 4 Swan H J, Ganz W, Forrster J, Marcus H, Diamond G, Chonette D. Catheterization of the heart in man with use of a flow-directed balloon-tipped catheter.  N Engl J Med. 1970;  283 447-451
• 5 Chun G M, Ellestad M H. Perforation of the pulmonary artery by a Swan-Ganz catheter.  N Engl J Med. 1971;  284 1041-1042
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• 8 Knobloch K, Lichtenberg A, Winterhalter M, Rossner D, Pichlmaier M, Phillips R. Non-invasive cardiac output determination by two-dimensional independent Doppler during and after cardiac surgery.  Ann Thorac Surg. 2005;  80 1479-1483
• 9 Tan H L, Pinder M, Parsons R, Roberts B, van Heerden P V. Clinical evaluation of USCOM ultrasonic cardiac output monitor in cardiac surgical patients in intensive care unit.  Br J Anaesth. 2005;  94 287-291