Year : 2014 | Volume
: 17 | Issue : 3 | Page : 209--210
Phenylephrine in cardiac surgery: Will it have a place?
Mukul Chandra Kapoor
Department of Anaesthesiology, Saket City Hospital, Saket, Delhi, India
Mukul Chandra Kapoor
6 Dayanand Vihar, Delhi - 110 092
|How to cite this article:|
Kapoor MC. Phenylephrine in cardiac surgery: Will it have a place?.Ann Card Anaesth 2014;17:209-210
|How to cite this URL:|
Kapoor MC. Phenylephrine in cardiac surgery: Will it have a place?. Ann Card Anaesth [serial online] 2014 [cited 2020 Jan 23 ];17:209-210
Available from: http://www.annals.in/text.asp?2014/17/3/209/135851
Cardiac surgery and cardio-pulmonary bypass (CPB) are associated with hypoperfusion, arterio-venous shunting, and ischemia and reperfusion due to various factors. The effects of these alterations may extend well into the postsurgical recovery period. Off-pump coronary artery bypass (OPCAB) surgery is associated with hypoperfusion, coronary occlusion, and reperfusion resulting from heart displacement, cardiac dysfunction, and surgical compulsions. Vasopressor drugs are routinely used to overcome the effects of these changes. Vasopressors are also needed to maintain perfusion pressures during CPB; for the management of vasoplegic shock postCPB; and to manage right ventricular (RV) failure, when low systemic pressures threaten RV coronary perfusion.
Use of a vasoconstrictor to increase coronary perfusion pressure has been advocated by a number of studies. Vasoconstrictors have a definite role in maintaining adequate diastolic coronary perfusion pressures and thereby prevent ischemic myocardial dysfunction. , Vasoconstrictor use is particularly recommended in the management of patients with acute pulmonary hypertension accompanied by RV failure. Phenylephrine, adrenaline and nor-adrenaline (and in recent times vasopressin) have been used in adult cardiac-surgical patients to maintain adequate organ perfusion pressures.
Sympathomimetic agents improve hemodynamics in low output states but they may worsen the myocardial oxygen demand/supply balance and induce calcium overload, particularly in the setting of ischemia-reperfusion. , In clinical and animal studies of acute pulmonary hypertension, pulmonary artery pressure (PAP), and pulmonary vascular resistance (PVR) decreased when systemic arterial pressure (SAP) was raised with noradrenaline because subsequent increase in coronary perfusion pressure improved RV function and increased cardiac output. , The effect of phenylephrine is however debatable. , In a canine experiment, comparing the effect of phenylephrine and norepinephrine in dogs with acute RV failure, only noradrenaline reduced PVR and increased coronary blood flow and consequently improved RV function and systemic hemodynamics.  Another study too found that noradrenaline increased SAP to a greater extent, with less increase in PAP compared to phenylephrine in patients with chronic pulmonary hypertension. 
Phenylephrine is a synthetic selective α1-adrenergic agonist sympathomimetic amine with a strong vasoconstrictive, but minimal inotropic and chronotropic effect. The ability of phenylephrine to raise blood pressure in acute hypotensive states has been consistently demonstrated. It increases total systemic vascular resistance. The increase in blood pressure commonly results in baroreceptor activation and causes a reflex decrease in heart rate. It has a rapid onset and a quick offset of action. The increase in SAP and PAP augments the coronary artery blood flow. These increases in pressures are not accompanied by changes in pulmonary capillary wedge pressure, heart rate, central venous pressure or cardiac index.  Impact of phenylephrine bolus on cardiac output is preload and dose dependent. When the heart is working on the plateau of the Frank-Starling relationship, phenylephrine bolus induces a decrease in cardiac output. When the heart is working on the steep portion of the Frank-Starling relationship, phenylephrine bolus induces an increase in cardiac output. 
The effects of phenylephrine, when used for cardiac surgery, have been under scrutiny. However, studies have focused on its effects on the sympathetic receptors, the resultant hemodynamic changes and their impact on organ performance, mainly the heart. The direct effects of phenylephrine on the myocardium have not been investigated much. In this issue of Annals of Cardiac Anesthesia, Mourouzis et al. present a very interesting study on the effects phenylephrine on an isolated ischemia-reperfusion rat-heart model.  The authors have demonstrated phenylephrine induced myocardial injury during reperfusion. Phenylephrine failed to significantly increase postischemic contractile function and the authors propose that this myocardial injury could have offset its effect on contractile function. The study data provides no evidence of severe coronary vasoconstriction and the authors propose that phenylephrine may have a direct effect on the myocardium and induce apoptosis and cell death.
Although some patients may benefit from higher mean arterial pressure on CPB, phenylephrine has been implicated to worsen microcirculatory oxygen and nutrient delivery.  Phenylephrine use during CPB has been shown to diminish microcirculatory blood flow and increase shunting.  It has been suggested that the effects of these microcirculatory effects need to be studied by a protocol-based interventional approach using near-infrared cerebral oxymetry monitoring to detect possible cerebral desaturation with its use. ,
Phenylephrine is often used in cardiac surgery, particularly in OPCAB surgery, to maintain systemic hemodynamics and coronary perfusion. The result of the study by Mourouzis et al. raises questions on the safety of its use in OPCAB as well as cardiac surgery on CPB.  The findings of this study (and earlier studies showing evidence reduction in microcirculatory blood flow) place a shadow on its use as the myocardium is exposed to multiple periods of ischemia-reperfusion during cardiac surgery.
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