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

Correspondence Address:
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 Aug 4 ];17:209-210
Available from:

Full Text

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. [1],[2] 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. [3],[4] 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. [5],[6] The effect of phenylephrine is however debatable. [7],[8] 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. [6] 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. [9]

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. [10] 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. [11]

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. [12] 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. [13] Phenylephrine use during CPB has been shown to diminish microcirculatory blood flow and increase shunting. [14] 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. [15],[16]

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. [12] 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.


1Price LC, Wort SJ, Finney SJ, Marino PS, Brett SJ. Pulmonary vascular and right ventricular dysfunction in adult critical care: Current and emerging options for management: A systematic literature review. Crit Care 2010;14:R169.
2Lahm T, McCaslin CA, Wozniak TC, Ghumman W, Fadl YY, Obeidat OS, et al. Medical and surgical treatment of acute right ventricular failure. J Am Coll Cardiol 2010;56:1435-46.
3Suga H, Hisano R, Goto Y, Yamada O, Igarashi Y. Effect of positive inotropic agents on the relation between oxygen consumption and systolic pressure volume area in canine left ventricle. Circ Res 1983;53:306-18.
4Vanoverschelde JL, Wijns W, Essamri B, Bol A, Robert A, Labar D, et al. Hemodynamic and mechanical determinants of myocardial O2 consumption in normal human heart: Effects of dobutamine. Am J Physiol 1993;265:H1884-92.
5Angle MR, Molloy DW, Penner B, Jones D, Prewitt RM. The cardiopulmonary and renal hemodynamic effects of norepinephrine in canine pulmonary embolism. Chest 1989;95:1333-7.
6Ghignone M, Girling L, Prewitt RM. Volume expansion versus norepinephrine in treatment of a low cardiac output complicating an acute increase in right ventricular afterload in dogs. Anesthesiology 1984;60:132-5.
7Rich S, Gubin S, Hart K. The effects of phenylephrine on right ventricular performance in patients with pulmonary hypertension. Chest 1990;98:1102-6.
8Vlahakes GJ, Turley K, Hoffman JI. The pathophysiology of failure in acute right ventricular hypertension: Hemodynamic and biochemical correlations. Circulation 1981;63:87-95.
9Kwak YL, Lee CS, Park YH, Hong YW. The effect of phenylephrine and norepinephrine in patients with chronic pulmonary hypertensionFNx01. Anaesthesia 2002;57:9-14.
10DiNardo JA, Bert A, Schwartz MJ, Johnson RG, Thurer RL, Weintraub RM. Effects of vasoactive drugs on flows through left internal mammary artery and saphenous vein grafts in man. J Thorac Cardiovasc Surg 1991;102:730-5.
11Cannesson M, Jian Z, Chen G, Vu TQ, Hatib F. Effects of phenylephrine on cardiac output and venous return depend on the position of the heart on the Frank-Starling relationship. J Appl Physiol (1985) 2012;113:281-9.
12Mourouzis I, Saranteas T, Ligeret H, Portal C, Perimenis P, Pantos C. Phenylephrine postconditioning increases myocardial injury: Are alpha-1 sympathomimetic agonist cardioprotective? Ann Card Anaesth 2014;17:200-9.
13Murfin D. Phenylephrine: In or out? South Afr J Anaesth Analg 2011;17:200-1.
14Maier S, Hasibeder WR, Hengl C, Pajk W, Schwarz B, Margreiter J, et al. Effects of phenylephrine on the sublingual microcirculation during cardiopulmonary bypass. Br J Anaesth 2009;102:485-91.
15Fedorow C, Grocott HP. Cerebral monitoring to optimize outcomes after cardiac surgery. Curr Opin Anaesthesiol 2010;23:89-94.
16Highton D, Elwell C, Smith M. Noninvasive cerebral oximetry: Is there light at the end of the tunnel? Curr Opin Anaesthesiol 2010;23:576-81.