Dopexamine and its role in the protection of hepatosplanchnic and renal perfusion in high-risk surgical and critically ill patients

Renton, Mary; Snowden, Chris

doi:10.1093/bja/aei072

Cited by 30 publications

(5 citation statements)

References 43 publications

(39 reference statements)

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“…Dopexamine results in improved or impaired visceral microperfusion by its general, ␤ 1 receptor-mediated, and mesenteric DA 1 receptor-mediated vasodilation (16 -18). Most data, however, suggest increased blood flow in major visceral arteries by dopexamine, which is not passed down to the microcirculation, possibly as a result of shunting (16 -18); therefore, the proposed improvement of hepatosplanchnic microperfusion by dopexamine is questionable, as previously reviewed (5,19). In contrast to dopamine, dopexamine does not suppress pituitary function (20).…”

Section: Dopexaminementioning

confidence: 99%

Approach to Hemodynamic Shock and Vasopressors

Herget–Rosenthal¹,

Saner²,

Chawla³

2008

Clinical Journal of the American Society of Nephrology

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H emodynamic shock (HS) is a clinical syndrome that is commonly observed in hospitalized patients. Prompt recognition and intervention are the cornerstones of mitigating the dire consequences of HS. Untreated HS usually leads to death. Unlike other types of clinical syndromes (e.g., chest pain), for which a clinical diagnosis is made before treatment is initiated in earnest, the treatment of shock often occurs concurrently or ahead of the diagnostic process. The maintenance of end-organ perfusion is critical to prevent irreversible organ injury and failure, and this frequently requires the use of fluid resuscitation and vasopressors. A complete review of all of the signs and symptoms, diagnosis, and treatment of HS has been reviewed in detail elsewhere (1). This article provides a concise summary of how to approach the patient in HS, diagnostic and therapeutic decision making, and the use of vasopressors. In addition, the effects of vasopressors on end organs with particular focus on renal hemodynamics is reviewed. Clinical Manifestations and Recognition of Hemodynamic ShockHS is classically described as "an acute clinical syndrome initiated by ineffective perfusion, resulting in severe dysfunction of organs vital to survival" (1). As clinicians, we take great pains to teach our trainees that shock is not just hypotension, but that shock represents hypoperfusion of end organs. This rationale leads to the common refrain: "Normotensive patients can often suffer from shock." The clinical manifestations of HS are related directly to the end organs that are not receiving adequate perfusion and can be categorized on the basis of the organ affected. Besides hypotension, the classic signs and symptoms of HS are tachycardia, relative hypotension (a decrease in baseline BP of 40 mmHg), tachypnea, cool and clammy extremities, oliguria, dysglycemia, and delirium (1). Patients who are hypotensive (systolic BP Ͻ90 mmHg in patients whose baseline BP is usually low) but show no signs or symptoms of shock should have their BP rechecked. An indwelling arterial catheter or Doppler may be necessary to resolve a false low BP reading (1). In the absence of hypotension, the diagnosis of HS can be more challenging and will require the clinician to increase his or her scrutiny of the patient and either rule in or rule out HS with further clinical investigations. For patients who are normotensive, the measurement of serum lactate will often reveal the presence of HS in a patient whose clinical evaluation is equivocal. This entity of a normotensive patient with some clinical signs of HS with an elevated lactate is often referred to as "cryptic shock." In this condition, the patient is not yet in critical condition but cannot meet their body's oxygen demand, resulting in evidence of significant anaerobic metabolism. Previous trials showed that presence of HS and a serum lactate concentration of Ͼ4.0 mmol/L are associated with a mortality of 30 to 45% (2).Once HS is recognized, interventions to restore tissue perfusion are mandatory. Three ...

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Section: Dopexaminementioning

confidence: 99%

Approach to Hemodynamic Shock and Vasopressors

Herget–Rosenthal¹,

Saner²,

Chawla³

2008

Clinical Journal of the American Society of Nephrology

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“…Phenylephrine also reduces splanchnic blood flow when compared with noradrenaline in septic shock (Reinelt et al ., 1999). Although dopexamine may improve tissue oxygenation and microvascular flow (Jhanji et al ., 2010), the evidence for this in the hepatosplanchnic bed is equivocal and may only occur in some patient groups (Renton and Snowden, 2005). Vasopressin analogues also decrease hepatosplanchnic blood flow, but have unique effects on intrarenal haemodynamics in shock (Albert et al ., 2004).…”

mentioning

confidence: 99%

Use of inotropes and vasopressor agents in critically ill patients

Bangash

Kong

Pearse

2012

British J Pharmacology

164

138

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Inotropes and vasopressors are biologically and clinically important compounds that originate from different pharmacological groups and act at some of the most fundamental receptor and signal transduction systems in the body. More than 20 such agents are in common clinical use, yet few reviews of their pharmacology exist outside of physiology and pharmacology textbooks. Despite widespread use in critically ill patients, understanding of the clinical effects of these drugs in pathological states is poor. The purpose of this article is to describe the pharmacology and clinical applications of inotropic and vasopressor agents in critically ill patients. LINKED ARTICLESThis article is commented on by Bracht et al., pp. 2009 and De Backer and Scolletta, pp. 2012-2014 ]i, Intracellular calcium concentration; ATP, adenosine triphosphate; cAMP, cyclic adenosine monophosphate; CPR, cardiopulmonary resuscitation; DO2, systemic oxygen delivery; GPCR, G-protein coupled receptor; GTP/GDP, guanosine triphosphate/diphosphate; PKA/PKC, protein kinase A/C; PLC, phospholipase C; SvO2, mixed/central venous oxygen saturation; TNF-a, tumour necrosis factor alpha; VO2, oxygen consumption IntroductionInotropes are agents administered to increase myocardial contractility whereas vasopressor agents are administered to increase vascular tone. The use of these potent agents is largely confined to critically ill patients with profound haemodynamic impairment such that tissue blood flow is not sufficient to meet metabolic requirements. Examples include patients with severe heart failure and septic or cardiogenic shock, as well as patients undergoing major surgery and victims of major trauma. They are generally administered via a large central vein and, in some specific situations, via a peripheral vein. These agents have a diverse range of actions including metabolic and immune effects, many of which are poorly understood. The objective of this review is to describe the underlying cardiovascular mechanisms that clinicians seek to influence through the use of inotropic agents, to describe the basic pharmacology of those drugs in common use and, finally, to explore the evidence base for specific approaches to inotrope and vasopressor therapy in clinical practice. As many of the commonly used agents exert both inotropic and vasopressor effects, the term 'inotrope' will be generally used in this review to describe agents with a spectrum of actions. The physiological basis for the actions of inotropic agentsMyocyte excitation and contraction. Cardiac muscle fibres contract through the sliding filament mechanism. Actin and myosin filaments are propelled past each other through repeated cross-bridge linking and unlinking. Each cardiac action potential results in the opening of voltage-gated myocyte calcium channels and a rise in intracellular calcium concentration ([Ca 2+ ]i). This triggers a further release of calcium from the sarcoplasmic reticulum, which accounts for around three quarters of the total increase in [Ca 2+ ]i (Levick, 2003...

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“…Perioperative use of dopexamine does not provide renal protection for cardiac or vascular surgical patients. 12 Fenoldopam increases renal blood flow by its selective action on dopamine-1 receptors. At present, there is conflicting evidence regarding its usefulness as a potential renal protective agent.…”

Section: Dopamine Agonistsmentioning

confidence: 99%

Perioperative renal protection

Webb

Allen

2008

Continuing Education in Anaesthesia Critical Care & Pain

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Acute renal failure (ARF) occurring around the time of surgery is a serious complication associated with considerable morbidity and mortality. Appropriate perioperative strategies are required to protect renal function to optimize patient outcome. Perioperative ARF accounts for 20-25% of cases of hospital-acquired renal failure. The incidence varies between 1 and 25% depending on the type of surgery and on the definition of renal failure. Renal dysfunction after surgery is often associated with multiple organ dysfunction syndrome and may result in a mortality of up to 60%. It is also associated with a high risk of infection, prolonged intensive care unit (ICU) and hospital stay, progression to chronic renal failure (CRF), and dialysis-dependent end-stage renal disease (ESRD). The chance of full recovery from an episode of ARF in the surgical setting is only 15%-many patients progress to develop varying degrees of chronic renal dysfunction. Patients undergoing cardiac and vascular surgery are at particular risk of developing ARF. ARF related to major surgery in patients with significant co-morbidity commonly results in a poor outcome. A large multi-centre cohort study demonstrated that ARF requiring dialysis occurred in 1.1% of cardiac surgical patients and was associated with an operative mortality of 63.7%. 1 This study confirmed that ARF was an independent predictor of mortality in this group of patients, resulting in a 7.9-fold increase in risk of death. ARF after open abdominal aortic surgery is similarly associated with a high mortality. 2

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Dopexamine and its role in the protection of hepatosplanchnic and renal perfusion in high-risk surgical and critically ill patients

Cited by 30 publications

References 43 publications

Approach to Hemodynamic Shock and Vasopressors

Approach to Hemodynamic Shock and Vasopressors

Use of inotropes and vasopressor agents in critically ill patients

Perioperative renal protection

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