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231]

Review Article

Alpha Blockers: A Relook at Phenoxybenzamine

Sambhunath Das, Pankaj Kumar, Usha Kiran, Balram Airan1
Departments of Cardiac Anaesthesia and 1Cardiothoracic and Vascular Surgery, All India Institute of Medical Sciences, New Delhi, India

Abstract
Phenoxybenzamine (PBZ) is an alpha adrenergic antagonist, used for the management of hypertension. PBZ acts by blocking alpha‑adrenergic
receptors, leading to vasodilatation and low systemic vascular resistance. This helps in control of blood pressure in pheochromocytoma,
improvement of systemic oxygen delivery, and optimization of the Qp/Qs in pediatric cardiac surgery such as hypoplastic left heart syndrome
and improving perfusion parameters during open heart surgery. The uses have further extended to causalgia, Raynaud’s phenomenon,
autonomic hyperreflexia, and even for patency of radial artery conduit in coronary artery bypass grafting surgery. However, its prolonged
hypotensive effect limits the regular use. In this review, we discussed the mechanism of action, pharmaco‑physiology of PBZ, perioperative
uses in different clinical setting and controversies for its uses; publications in different scientific journals from the previous years.

Keywords: Cardiovascular disease, hypoplastic left heart syndrome, pheochromocytoma, phenoxybenzamine, pulmonary arterial
hypertension

Introduction • Prazosin
• Tamsulosin
Phenoxybenzamine (PBZ) was initially used in the treatment
• Terazosin
of hypertension, especially that caused by pheochromocytoma.
• Silodosin.
It was also the first alpha blocker to be used for the treatment
of benign prostatic hyperplasia; it has been used in the Selective α2‑adrenergic receptor antagonists include:
treatment of hypoplastic left heart syndrome (HLHS). It is an • Atipamezole
alpha‑receptor blocker. The other alpha receptor blockers are • Idazoxan
listed below. • Mirtazapine
• Yohimbine.
Alpha‑blockers act as antagonists of α‑adrenergic receptors.
The agents carvedilol and labetalol are both α‑ and β‑blockers.
The types include:
• α1‑blockers act on α1‑adrenoceptors PBZ is a potent alpha‑adrenergic blocking agent used routinely
• α2‑blockers act on α2‑adrenoceptors. for the management of hypertension in pheochromocytoma.[1]
The indications of PBZ extend to the management of pulmonary
Examples of non‑selective α‑adrenergic receptor antagonists
hypertension in cardiac disease patients, balancing of systemic
include:
and pulmonary blood flow in HLHS, benign prostatic
• PBZ
hypertrophy, malignant essential hypertension, hypotensive
• Phentolamine
anesthesia, sausage, and so on.[2] However, the side effects,
• Tolazoline
• Trazodone
• Typical and atypical antipsychotics. Address for correspondence: Dr. Sambhunath Das,
Department of Cardiac Anaesthesia, 7th Floor, Cardio Thoracic
Selective α1‑adrenergic receptor antagonists include: Sciences Centre, All India Institute of Medical Sciences, Ansari Nagar,
New Delhi ‑ 110 029, India.
• Alfuzosin E‑mail: sambhunathds833@gmail.com
• Doxazosin

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DOI:
10.4103/jpcs.jpcs_42_16 How to cite this article: Das S, Kumar P, Kiran U, Airan B. Alpha blockers:
A relook at phenoxybenzamine. J Pract Cardiovasc Sci 2017;3:11-7.

© 2017 Journal of the Practice of Cardiovascular Sciences | Published by Wolters Kluwer - Medknow 11
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Das, et al.: Phenoxybenzamine: Current uses, safety, and limitations
such as persistent hypotension, muscle weakness, and postural
hypotension, limit its use by many physicians. Some physicians
are in favor of using alternative drugs for control of blood
pressure (BP) and systemic vascular resistance (SVR) with
less potency and short acting.[3,4] However, still many centers
use PBZ in situations such as perioperative hemodynamic
management of pheochromocytoma, HLHS, arterial switch
operation (ASO), single‑ventricle physiology, pulmonary
artery hypertension, and congenital cardiac surgery with a
better outcome.[3‑7] The evidence from different studies and
reports in respect to the current uses and limitations of PBZ
necessitates update.
This review article discusses the pharmacological aspects,
mechanism of action, indications, side effects, controversies,
and management of complications related to PBZ. All the
publications and literatures are searched from PubMed and
Google Scholar using the keywords of PBZ, cardiovascular
disease, HLHS, pheochromocytoma, pulmonary arterial
hypertension, and alternate uses of PBZ for the last 16 years.
Pharmacology
PBZ is a haloalkylamine derivative.[1] PBZ is an adrenergic
blocking agent chemically related to nitrogen mustard. The
molecular structure responsible for blockade is the highly
reactive carbonium ion formed by cleavage of the tertiary
amine ring.[8] In consequence of the chemical reactions, a
covalent bond is formed between the drug and the α‑adrenergic
receptor [Figure 1].[8]
Mechanism of Action
PBZ blocks both α1‑ and α2‑adrenergic receptors with more
affinity for α1‑receptor.[1] The presence of a catecholamine or
an α‑adrenergic blocking agent of the competitive type during
the development of blockade by PBZ can reduce the degree
of block.
There is competition for the same population of receptors,
indicating that the initial approximation of the PBZ to its site
of action is due to weak ionic and hydrogen bond involved
Figure 1: Chemical structure of phenoxybenzamine.
12 Journal of the Practice of Cardiovascular Sciences  ¦  Volume 3  ¦  Issue 1  ¦  January-April 2017
in the actions of most other chemical class.[8] Subsequent to
blockade of receptors by PBZ, the conjugate became fixed
and does not allow adrenaline and noradrenalin for binding.
This stage is referred to as nonequilibrium blockade and
is the result of stable covalent bond formation between
the antagonist and the receptors. PBZ increases the rate of
peripheral norepinephrine turnover, which is associated with
increased tyrosine turnover resulting in increased tyrosine
hydroxylase activity.[1]
PBZ and its congeners inhibit the uptake of catecholamines
into both adrenergic nerve terminals and extraneuronal tissues
called uptake 1 and 2, respectively. However, the block of
uptake 2 is probably important in causing potentiation of
responses and augmentation of the outflow of norepinephrine
during the stimulation of sympathetic nerves to an organ. As
a nonselective alpha receptor antagonist, PBZ affects both
postsynaptic α1 and presynaptic α2 receptors in the nervous
system, and hence reduce sympathetic activity. PBZ is used
for the treatment of pheochromocytoma; with extended use, it
establishes a “chemical sympathectomy.” The haloalkylamines
can inhibit responses to 5‑hydroxytryptamine, serotonin,
histamine, and acetylcholine (Ach).[8] Effective blockade of
responses to Ach usually requires relatively high dose.
Pharmacokinetics
PBZ are effectively administered by all routes, but injection
should be given only intravenously because of their irritant
properties.[1] Absorption from the intestine is incomplete
and somewhat unreliable. Approximately 30% of orally
administered PBZ appears to be absorbed in active forms.
PBZ has high lipid solubility at body pH, and accumulation
in fat may occur after large doses. However, a stable bonding
to tissue constituents rather than slow release from fat is
responsible for the prolonged action. Over 50% of the
intravenously administered PBZ is excreted in 12 h and
over 80% in 24 h, but small amounts remain in various tissues
for at least a week. Blockade by PBZ develops relatively slowly,
reaching a peak effect in 1 h, or more after IV administration.
PBZ has a half‑life of approximately 24 h.1 The actual duration
of action depends on fresh PBZ receptor synthesis since the
drug inactivates alpha-adrenergic receptors irreversibly, and
therefore the duration of its effect is dependent not only on its
presence but also on the rate of synthesis of alpha-adrenergic
receptors.
Route of Administration and Dosage
It is available for oral use in 10 mg capsules; ampoule for
intravenous use are available as 100 mg in 2 ml and also
50 mg in 1 ml.[1] The oral dose usually varies between 20 and
200 mg per day and must be increased by small increments.
Pediatric dose ranges from 1 to 2 mg/kg/day in 3–4 divided
doses. Postoperatively, in intensive care unit, a dose of
0.3–0.5mg/kg at 8–12 h interval is used.[4] PBZ must be well
diluted and infused slowly before intravenous administration.
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Das, et al.: Phenoxybenzamine: Current uses, safety, and limitations
Most commonly a dose of 0.25–1 mg/kg is diluted and infused
slowly over a period of at least 30 min.[9]
Pharmacodynamics
Cardiovascular system
Blood pressure
The usual blocking dose of PBZ is 1 mg/kg given slowly
intravenously. The fall in systemic BP is less in healthy,
recumbent, normovoluemic subjects. Severe hypotension
may occur in a situation involving compensatory sympathetic
vasoconstriction, such as upright posture and hypovolemia. In
addition, impairment of compensatory vasoconstriction sensitizes
to the hypotensive effects of a variety of agents and condition that
tend to produce vasodilatation such as anesthetized patients.[1]
Blood flow
PBZ produces a considerable increase in cardiac output
and decrease of total peripheral resistance in normal
recumbent subjects.[1] Cerebral and coronary resistance are not
significantly altered by adrenergic blockade. Cerebral flow is
less affected unless the BP is greatly reduced, and coronary
flow increases in parallel with reflex cardiac stimulation. PBZ
increases resting muscle blood flow and in a cool environment
enhances cutaneous blood flow. Splanchnic and renal blood
flows are not altered remarkably in the presence of the increased
adrenergic vasoconstrictor tone induced by circumstances such
as hypovolemia or norepinephrine infusion. PBZ increases the
flow to a major degree in both these areas. Pulmonary arteries
and veins are also relaxed, however, because of a greater
systemic vasodilatation; blood volume in the pulmonary circuit
is usually decreased.[1] Pressure responses to epinephrine
and other sympathomimetic amines are blocked or reversed
by PBZ. It effectively blocks pathological effects of infused
epinephrine or norepinephrine, including pulmonary edema,
reduction in plasma volume, accumulation of pericardial fluid,
adrenocortical necrosis, and changes in hepatic cells.[1]
Cardiac effects
The chronotropic and inotropic effects of epinephrine,
norepinephrine, and direct or reflex sympathetic nerve
stimulation on the mammalian myocardium are not inhibited
by the PBZ.[3] PBZ induces reflex tachycardia in response
to peripheral vasodilatation and may be accumulated by
altered norepinephrine release as well as by postjunctional
potentiation. They are used as antihypertensives because they
block alpha‑receptor‑mediated vasoconstriction. The block on
alpha‑2 receptors further potentiates beta‑effects, increasing
cardiac output.[1]
Central nervous system
PBZ stimulates the central nervous system to cause nausea,
vomiting, hyperventilation, motor excitability, and even
convulsions, particularly when large dose is rapidly injected
intravenously. 1In man, a characteristic loss of time perception
may occur. These effects develop and terminate much more
rapidly than does the blockade. Mild‑to‑moderate sedation
Journal of the Practice of Cardiovascular Sciences  ¦  Volume 3 ¦ Issue 1 ¦ January-April 2017
commonly results from the slow intravenous infusion of the
usual blocking dose of PBZ in man and tiredness and lethargy
may accompany oral medication.[1]
Metabolic effects
The receptors involved in metabolic responses to catecholamine
are preferentially β, but important α adrenergic action is also
involved. Inhibitory action of epinephrine on insulin secretion
is blocked by PBZ. It does not antagonize the effects of
catecholamine on glycogenolysis of liver or muscle.[1] It does
not inhibit catecholamine augmented lipolysis.
Other effects
PBZ effectively antagonizes the wide variety of responses
to endogenous and exogenous sympathomimetic amines
that are mediated by α‑adrenergic receptors. These include
contraction of the retractor penis, erector pili, and the uteri.
Salivary secretion of water and electrolyte evoked by cervical
sympathetic nerve stimulation or injected sympathomimetic
drugs is blocked. The volume and enzyme content of pancreatic
exocrine secretion are increased by α and decreased by
β‑adrenergic blockade. The limited adrenergic sweating
observed in man, particularly of the hands and axillae are
also blocked.[1]
Toxicity and Side Effects
Untoward effects of PBZ are largely due to the blockade of
α‑adrenergic receptors.[9] Loss of vasomotor control results
in hypotension and reflex tachycardia. Conditions such as
exercise, eating a large meal, or consuming alcohol precipitate
the side effects [Table 1].
Side effects such as local tissue irritation, sedation, and a
generalized feeling of weakness and tiredness are not related
to α‑blockade. Nausea and vomiting occur after large oral
doses due to local irritation of gastrointestinal tract mucosa,
especially when administered empty stomach.
In patients having carbohydrate intolerance, α‑adrenergic-
receptor blockade may reduce fasting blood sugar levels due to
lack of inhibition of insulin release mediated by α‑adrenergic
receptor stimulation,
Indications
The clinical uses of PBZ are listed [Table 2].
Table 1: Side effects of phenoxybenzamine
Postural hypotension
Reflex tachycardia
Miosis
Nasal stuffiness
Inhibition of ejaculation
GI irritation‑nausea and vomiting
Sedation, generalized feeling of weakness and tiredness
GI: Gastrointestinal
13
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Das, et al.: Phenoxybenzamine: Current uses, safety, and limitations
Table 2: Therapeutic uses
Pheochromocytoma
Pulmonary hypertension
Improved systemic oxygen delivery and stabilization of the
pulmonary‑to‑systemic flow ratio (Qp/Qs) in HLHS
Causalgia
Benign prostate hypertrophy
Raynaud’s phenomenon
Control of autonomic hyperreflexia in patients with spinal cord
transection
Long‑term patency of radial artery graft in CABG patient
Hypotensive anesthesia in children
HLHS: Hypoplastic left heart syndrome, CABG: Coronary artery bypass
grafting
Pheochromocytoma
PBZ is mainly recommended for the treatment of
pheochromocytoma, tumors of the adrenal medulla, and
sympathetic neurons‑secreting enormous quantities of
catecholamines. PBZ is used to prepare the patient for
surgical removal of tumor. PBZ restores plasma volume by
counteracting the vasoconstrictive effects of high levels of
catecholamines.[3] Reexpansion of fluid volume may cause
decrease in hematocrit. PBZ initial dose should be 20–30 mg
orally 2–3 times a day.[1] Maximum dose in a day may go up
to 250 mg. The efficacy of therapy should be judged by the
reduction in symptoms, especially sweating and stabilization
of BP.
Preoperatively, PBZ aids in BP control permits the correction
of the contracted plasma volume, and protects against
catecholamine‑induced cardiac damage.[10] The use of PBZ
appeared to produce better attenuation of intraoperative
hypertension but may necessitate vasopressors in the
postoperative period. Preoperative α‑adrenergic receptor
blockade resolved ST‑T changes in electrocardiogram
and clinical manifestation of catecholamine‑induced
myocarditis. [10‑12] Therapy may be limited by postural
hypotension. Prolonged treatment with PBZ may be necessary
in patients with inoperable or malignant pheochromocytoma.
Metyrosine, a competitive inhibitor of tyrosine hydroxylase,
may be a useful adjuvant. Beta‑receptor antagonists also
are used in the treatment pheochromocytoma only after the
administration of α‑receptor antagonist.
Cardiac surgery
The use of PBZ during cardiac surgery facilitates higher
pump flow rate during cardiopulmonary bypass  (CPB) and
is associated with less metabolic acidosis postoperatively.[13]
In addition, PBZ was found to be more effective than sodium
nitroprusside in improving tissue perfusion after CPB, as
measured by smaller peripheral‑to‑core temperature gradients
and lower base deficits in PBZ‑treated patients [Table 3].[14]
After the early neonatal period, there is a progressive increase
in afterload with reduction in the contractility, reaching a
plateau at the age of 4 years. Neonatal heart is more susceptible
14 Journal of the Practice of Cardiovascular Sciences  ¦  Volume 3  ¦  Issue 1  ¦  January-April 2017
to exogenous catecholamines‑induced cardiotoxicity.
Sympathetic innervations, reduced norepinephrine stores, and
less efficient contractile power are the mechanisms involved.
The newborn’s heart is more susceptible to ischemia than
adult’s but recovers faster from short periods of ischemia
<30 min. Hence, vasodilatory therapy can play a key role
in pediatric cardiac surgery, improving cardiac output by
decreasing afterload without affecting the contractility. PBZ
has been tried in infants and children with congenital heart
disease undergoing open cardiac repair, providing a more
balanced pulmonary‑to‑systemic blood flow by lowering
SVR.[5,15] A combination of PBZ and nitroglycerin (NTG) is
a low‑cost alternative for perioperative control of pulmonary
arterial pressure in children with congenital heart disease
undergoing cardiac surgery because PBZ is known for its
pulmonary vasodilating effect, thereby decreasing right
ventricular load [Table 4].[16]
Hypoplastic left heart syndrome
Contractile tissue in neonatal hearts is around 30% of the
myocardial mass and is characterized by a lower velocity of
shortening and a diminished length‑tension relationship.[17]
Thus, the neonatal heart has a reduced compliance, a relatively
fixed stroke volume, and cardiac output is a heart‑rate
dependent. As a result, the neonatal heart has poor response
to increase in afterload.
Neonates undergoing Norwood procedure suffer from the
above intrinsic limitations as well as the factors unique to
HLHS.[7] First, functional limitations of the postoperative
myocardium are further compounded by myocardial depression
from cardioplegia and CPB. Second, the single ventricle must
perform the work of both pulmonary and systemic ventricle in a
setting that may include a low diastolic pressure and alterations
in coronary artery blood flow. Third, sympathetic responses to
stress that result in increases in SVR and subsequent increases in
the Qp/Qs further reduce myocardial performance and systemic
organ perfusion. Consequently, perioperative management
strategies to increase survival have mainly focused on improving
post‑bypass myocardial function and systemic organ perfusion.
PBZ fundamentally decreases SVR by vasodilatation and hence
improves systemic oxygen delivery and stabilizes Qp/Qs.[1,9]
Tweddel et al. studied the effect of PBZ on the oxygen delivery
in patients undergoing Stage 1 palliative repair of HLHS; PBZ
caused a significant improvement in the early postoperative
course of the patients who received the drug.[7]
The authors have been are using PBZ in cardiovascular
disease patients for the last 2 decades. The main uses are
during hypothermic CPB in all neonates, ASO, and Norwood
operation. Cardiac surgery for ventricular septal defect
closure, total anomalous pulmonary venous connection repair,
persistent truncus arteriosus, aortopulmonary window, and total
cavopulmonary connection/Fontan operation receives PBZ
during operation, ICU, and postoperative ward.[16] The use helps
in uniform cooling and rewarming during CPB, improved pump
flow, less acidosis, and higher tissue oxygenation.[6] The SVR is
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Das, et al.: Phenoxybenzamine: Current uses, safety, and limitations

Table 3: Studies related to cardiac surgery and use of phenoxybenzamine

Reference Study design Patients Intervention Outcome
Bisoi Retrospective 55 primary ASO in PBZ was used 1 mg/kg during CPB, Successful weaning from CPB and ECMO.
et al. 2010[5] observational children with d‑TGA and 0.3 mg/kg used 8 hourly in ICU PBZ is helpful for reducing SVR and
and IVS presenting improves LV function
beyond 6 weeks age
Das et al.[6] Prospective 45 infants undergoing 3 groups 15 patients in each. Group 1 PBZ during CPB produces lower aortic line
observational ASO and 2 received PBZ 1 mg/kg and and facilitates for higher pump flow; resulting
study 0.5 mg/kg, respectively, during CPB in higher venous and cerebral oxygenation,
and Group 3 was the control group faster cooling and re‑warming, and less base
who did not receive PBZ deficit. PBZ in a dose of 1 mg/kg was more
effective than 0.5 mg/kg
Tweddell Prospective, 15 patients undergone Oximetric catheters were placed in PBZ appeared to improve systemic oxygen
et al.1999[7] nonrandomized the Norwood the superior vena cava for continuous delivery during the early postoperative period
study procedure monitoring of systemic venous
oxygen saturation. Postoperative
hemodynamic variables were
compared between 7 control patients
and 8 patients who received PBZ
Mossad Retrospective 75 pediatric patients Patients were selected in three The effect of PBZ on SVRI, cooling, and
et al. 2008[13] chart review undergoing surgical age groups: younger than 1 month rewarming on CPB varies with age as
repair of congenital (n=25), 1-12 months (n=25), and shown by more profound vasodilatation and
heart defects 1-5 years (n=25). All patients narrower temperature gradients
received a full dose of PBZ 1 mg/kg
Motta Prospective, 60 infants scheduled Patients received either sodium The use of PBZ can maintain organ perfusion
et al. 2005[14] multicenter, for elective congenital nitroprusside 2-5 µg/kg/min on CPB and improve peripheral circulation
observational cardiac surgery infusion intraoperatively and in the as shown by less base deficit and smaller
study repair requiring ICU (n=30 patients) or received PBZ temperature gradients intraoperatively and in
cardiopulmonary 1 mg/kg slowly intravenously at the the ICU better than nitroprusside
onset of CPB (n=30 patients)
Tweddell 115 patients Prospective Comparison of survival after use of Use of PBZ as a factor favoring survival
et al. 2002[15] undergoing Stage observational POB for the current era, July 1996 from Stage 1 to Stage 2 Norwood operation.
1 palliation for (case series) study to October 2001, hospital survival Improved survival following S1P can be
hypoplastic left was 93% (75/81) compared with achieved with strategies that allow for early
heart syndrome 53% (18/34) for the period, January identification of decreased systemic output
1992 to June 1996, P<0.001 and the use of afterload reduction to stabilize
SVR and therefore the pulmonary to systemic
flow ratio
Kiran Letter to editor Children undergoing Combination of PBZ and Effective control of pulmonary artery
et al. 2005[16] intracardiac repair nitroglycerin during surgery and ICU pressures in children undergoing cardiac
with pulmonary surgery
hypertension
IVS: Intact ventricular septum, CPB: Cardiopulmonary bypass, PBZ: Phenoxybenzamine, ICU: Intensive Care Unit, ECMO: Extracorporeal membrane
oxygenator, SVR: Systemic vascular resistance, LV: Left ventricular, SVRI: Systemic vascular resistance index, ASO: Arterial switch operation

Table 4: Beneficial effects of phenoxybenzamine in Miscellaneous uses

cardiac surgery
Facilitates higher pump flow with lower arterial line pressure during CPB
Less metabolic acidosis by improved tissue perfusion postoperatively
Improves cardiac output by decreasing the afterload without affecting the
contractility
Balanced pulmonary‑to‑systemic blood flow by lowering SVR
CPB: Cardiopulmonary bypass, SVR: Systemic vascular resistance
managed perfectly in ASO and Norwood patients and helps in
improving LV function of regressed LV.[5] The balance in Qp/
Qs ratio by PBZ facilitates to reduce and manage pulmonary
hypertension.[16] The combination of PBZ, NTG, and sildenafil
in perioperative period helps to treat hypertensive crisis and
successful weaning from CPB and extracorporeal membrane
oxygenator.
PBZ may be useful in the treatment of Raynaud’s phenomenon,
but their side effects often curtail extended use.[18] PBZ has
been found to be alternative treatment for causalgia.[19] There
is less morbidity in comparison to surgical sympathectomy. It
was found useful in the first 3 months after diagnosis. Sudeck’s
atrophy, characterized by severe trophic changes, skin changes,
and osteoporosis might occur after the onset of causalgia. PBZ
occasionally has been used for this. PBZ has been reported to
be used for hypotensive anesthesia in children.[20] Due to its
5‑HT2A receptor antagonism, PBZ is useful in the treatment
of carcinoid tumor, a neoplasm that secretes large amounts of
serotonin.[21]
Lower doses of PBZ was found to be beneficial for endothelial
viability and potentially the long‑term patency of the graft

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Das, et al.: Phenoxybenzamine: Current uses, safety, and limitations
after coronary artery bypass graft surgery along with
nitrates, phosphodiesterase inhibitors, or calcium channel
blockers.[22,23] It has been found useful in peripheral vascular
disease.[1]
The combined use of PBZ with dopamine was recommended
because PBZ will block α‑adrenergic action of dopamine,
whereas peripheral perfusion is improved with intact
beta‑adrenergic stimulation.[24] The combination of dobutamine
and PBZ is as effective as newer drugs such as enoximone,
an inotrope/vasodilator after cardiac surgery in children.[25]
Management of side effects
When exogenous sympathomimetics are administered after α
receptor blockade, their vasoconstrictive effects are inhibited.
The effect of phenylephrine is completely blocked. Despite
its irreversible binding to the receptor, the recommended
treatment of PBZ‑induced hypotension is norepinephrine
infusion because some of the receptors remain free of the
drug. Vasopressin is an effective antidote to this vasodilation.
Vasopressin acts on smooth muscle V1 receptors, which
have preserved activity even in the presence of PBZ, and can
overcome its effect.[26] Epinephrine administrations after the
use of PBZ cause severe hypotension and tachycardia because
of refractory α‑receptor blockade and unopposed ß receptor
activity.[1] This is known as vasomotor reversal of Dale or
Dale’s phenomena.
Conclusion
PBZ has a promising therapeutic option for the treatment
of hypertension in pheochromocytoma, control of SVR in
HLHS and pulmonary hypertension of varied origin. The
improvement in perfusion parameters during CPB in neonatal
and pediatric cardiac surgery by PBZ therapy is established
by different studies. It offers convenient and versatile dosing
because of the oral and parenteral administration. The
intraoperative, postoperative, and intensive care setting use
is safer with hemodynamic monitoring and delivers the best
results with excellent patient outcome. The therapeutic use
should be decided rationale considering the benefits and risks.
The potent hypotensive effects alarm the judicious and titrated
use of PBZ. However, rigorous, blinded, placebo‑controlled,
multicenter, randomized studies are required to confirm the
efficacy of PBZ for single or as a combination therapy with
other drugs. Noncardiac uses based on different evidence also
need further study for establishing the efficacy and safety of
PBZ.
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
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Journal of the Practice of Cardiovascular Sciences  ¦  Volume 3 ¦ Issue 1 ¦ January-April 2017 17