Phenoxybenzamine in Septic Shock

Anderson, Robert; James, Paul M.; Bredenberg, Carl E.; Hardaway, Robert M.

doi:10.1097/00000658-196703000-00002

Cited by 22 publications

(4 citation statements)

References 11 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…A positive inotropic effect of phenoxybenzamine has also been suggested. 34 The use of IPPR or CP AP in the presence of raised intracranial pressure is also undesirable. Peripheral vasodilatation may make these measures unnecessary especially if initiated promptly as redistribution of central blood volume back to the systemic circulation will occur.…”

Section: Discussionmentioning

confidence: 99%

Neurogenic Pulmonary Oedema in Man: Aetiology and Management with Vasodilators based on Haemodynamic Studies

Loughnan

Brown

Edis

et al. 1980

Anaesth Intensive Care

View full text Add to dashboard Cite

Acute pulmonary oedema is a rare complication of head injury. A case is reported in which the pulmonary oedema was treated initially by tracheal intubation, constant positive airway pressure, ventilation and isoprenaline. Subsequent treatment was by vasodilatation with sodium nitroprusside and phenoxybenzamine and the patient made a good recovery. The findings are discussed in relation to reported experimental work. The aetiology appears to be related to a massive sympathetic discharge leading to systemic vasoconstriction, shift of blood to the pulmonary circulation with left ventricular failure and pulmonary oedema.

show abstract

Section: Discussionmentioning

confidence: 99%

Neurogenic Pulmonary Oedema in Man: Aetiology and Management with Vasodilators based on Haemodynamic Studies

Loughnan

Brown

Edis

et al. 1980

Anaesth Intensive Care

View full text Add to dashboard Cite

show abstract

“…Firstly, heart failure due to a primary depressant effect of endotoxin on the myocardium occurs in some cases of septic shock (MacLean et al, 1965;McGowan and Walters, 1966;Anderson et al, 1967;Siegel and Fabian, 1967;Starzecki and Spink, 1968). This view, however, is not universally accepted (Vaughn et al, 1968).…”

Section: Discussionmentioning

confidence: 99%

Intravenous Isoprenaline in Treatment of Septic Shock in Man

Wosornu¹,

Easmon²

1970

BMJ

View full text Add to dashboard Cite

“…Counterintuitively, in the setting of experimental septic shock and following sympathetic inhibition with a neuroleptic or an alpha-antagonist, BP and survival improved (respectively, chlorpromazine vs. phentolamine (Regitine ® ) or phenoxybenzamine (Dibenzyline ® ) [ 6 , 150 ]. The translation to humans [ 5 , 151 , 152 ] was met with skepticism [ 6 ]. The supposedly beneficial effects of sympathetic activation [ 96 ] prevail in physicians’ minds.…”

Section: How To Decrease Administration Of Exogenous Catecholamines In Septic Shock?mentioning

confidence: 99%

“…The beneficial effects of vasodilators in the setting of cardiogenic shock and beta-blockers in the setting of congestive cardiomyopathy [ 153 ] renewed the interest in sympathetic deactivation in septic patients. The use of antihypertensive drugs in hypotensive sepsis is counterintuitive but beneficial (“inverted therapy” [ 154 ]: ergotoxine [ 115 ], chlorpromazine [ 6 , 16 , 106 ], phenoxybenzamine [ 5 , 151 , 152 ], beta-blockers [ 155 , 156 , 157 , 158 , 159 , 160 , 161 ], and alpha-2 agonists [ 111 , 162 , 163 , 164 , 165 , 166 , 167 , 168 , 169 , 170 , 171 ]). On the other hand, a metanalysis [ 172 ] concluded an absence of effect of alpha-2 agonists on outcome.…”

Section: How To Decrease Administration Of Exogenous Catecholamines In Septic Shock?mentioning

confidence: 99%

Is the Sympathetic System Detrimental in the Setting of Septic Shock, with Antihypertensive Agents as a Counterintuitive Approach? A Clinical Proposition

Petitjeans

Géloën

Pichot

et al. 2021

JCM

View full text Add to dashboard Cite

Mortality in the setting of septic shock varies between 20% and 100%. Refractory septic shock leads to early circulatory failure and carries the worst prognosis. The pathophysiology is poorly understood despite studies of the microcirculatory defects and the immuno-paralysis. The acute circulatory distress is treated with volume expansion, administration of vasopressors (usually noradrenaline: NA), and inotropes. Ventilation and anti-infectious strategy shall not be discussed here. When circulation is considered, the literature is segregated between interventions directed to the systemic circulation vs. interventions directed to the micro-circulation. Our thesis is that, after stabilization of the acute cardioventilatory distress, the prolonged sympathetic hyperactivity is detrimental in the setting of septic shock. Our hypothesis is that the sympathetic hyperactivity observed in septic shock being normalized towards baseline activity will improve the microcirculation by recoupling the capillaries and the systemic circulation. Therefore, counterintuitively, antihypertensive agents such as beta-blockers or alpha-2 adrenergic agonists (clonidine, dexmedetomidine) are useful. They would reduce the noradrenaline requirements. Adjuncts (vitamins, steroids, NO donors/inhibitors, etc.) proposed to normalize the sepsis-evoked vasodilation are not reviewed. This itemized approach (systemic vs. microcirculation) requires physiological and epidemiological studies to look for reduced mortality.

show abstract

Phenoxybenzamine in Septic Shock

Cited by 22 publications

References 11 publications

Neurogenic Pulmonary Oedema in Man: Aetiology and Management with Vasodilators based on Haemodynamic Studies

Neurogenic Pulmonary Oedema in Man: Aetiology and Management with Vasodilators based on Haemodynamic Studies

Intravenous Isoprenaline in Treatment of Septic Shock in Man

Is the Sympathetic System Detrimental in the Setting of Septic Shock, with Antihypertensive Agents as a Counterintuitive Approach? A Clinical Proposition

Contact Info

Product

Resources

About