Phenylephrine and cardiac output
We enjoyed reading the article by Oliver Rebet et al.1 The authors demonstrated that haemodynamic response to a dose of phenylephrine may be affected by preload dependency.
The authors offered the ‘geometrical’ explanation for their finding, namely, they depict the points of intersection between stroke volume/cardiac output and venous return curves and suggested that depending on the position of the heart on the Frank Starling curve the response to phenylephrine may increase or decrease the cardiac output. The graphs are hypothetical, they are not constructed on actual data and therefore might not reflect the physiological reality.
Some data might need additional explanation. Table 3 showed that phenylephrine decreased pulse pressure variations in the preload-dependent group whereas cardiac output did not change. In a normal functioning heart any decrease in respiratory-induced arterial variability should be associated with an increase in stroke volume.2 This did not happen in this study.
One of the possible explanations for such unexpected physiological response is the inaccuracy of the oesophageal Doppler method in determining cardiac output during the phenylephrine therapy. The discrepancy between oesophageal Doppler cardiac output and thermodilution measurements of cardiac output following vasodilatation or catecholamine therapy has been shown repeatedly.3,4
Some data are interesting. For example, what is the physiological explanation for the decrease in stroke volume in preload-independent (presumably normovolaemic) patients?
Were the doses used in these two groups of patients different? The authors used the dose of phenylephrine 50 to 150 μg (a three-fold difference). They do not say whether the doses were different in the two groups of patients. The density of α1-adrenergic receptors is much higher in the veins than in arteries;5,6 therefore, veins are much more sensitive to α1-adrenergic agonists than arteries.5–7 Could such a difference play a role in the observed event?
Finally, what is the physiological explanation for these findings? Our guess is that one of the two (or both) events occurred: arterial constriction in the fast compartment developed, associated with a decrease in flow through the arteries that decreased mean circulatory filling pressure and cardiac output;7 hepatic vein constriction slows flow from the splanchnic system into the systemic circulation (from slow into the fast compartment), decreasing preload and cardiac output.