Effects of Dopamine and Norepinephrine on Systemic and Hepatosplanchnic Hemodynamics, Oxygen Exchange, and Energy Balance in Vasoplegic Septic Patients

Guérin, J.-P.; Levraut, J.; Samat-Long, Corine; Leverve, Xavier; Grimaud, D.; Ichaï, Carole

doi:10.1097/01.shk.0000150549.45338.6c

Cited by 60 publications

(30 citation statements)

References 44 publications

(115 reference statements)

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“…Norepinephrine and dopamine have a similar impact on hepatosplanchnic blood flow in septic patients but have differing effects on hepatic energy balance Vasoplegic patients were randomized to either drug in this crossover study to maintain a MAP greater than 80 mmHg [10 ]. Patients had similar rates of hepatosplanchnic blood flow in each group.…”

Section: Norepinephrinementioning

confidence: 99%

Vasoactive drugs and the gut: is there anything new?

Woolsey

Coopersmith

2006

Current Opinion in Critical Care

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Purpose of reviewSystemic changes in blood pressure and cardiac output induced by pressors and inotropes do not always correlate to improvements in regional perfusion. Since the gut is often referred to as the 'motor' of the systemic inflammatory response syndrome, the impact of vasoactive agents on splanchnic perfusion has theoretical importance. This review will highlight recent studies examining secondary effects of vasoactive agents on intestinal perfusion, metabolism, and barrier function. Recent findingsNorepinephrine has minimal impact on mesenteric blood flow although the combination of norepinephrine and dobutamine increases splanchnic blood flow in sepsis. Dopamine also increases mesenteric blood flow although this may be associated with negative hepatic energy balance at high does. Vasopressin and epinephrine both have negative effects on splanchnic blood flow. Newer inodilators levosimendan and olprinone preferentially improve mesenteric perfusion in animal models. Summary Secondary effects of norepinephrine and dopamine on splanchnic perfusion are minor compared with their systemic effects. While vasopressin usage is increasing in the intensive care unit, caution should be used because of its adverse effects on gut perfusion. Experimental agents for the treatment of heart failure have beneficial gut-specific effects although the clinical significance of this is currently limited by their availability.

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Section: Norepinephrinementioning

confidence: 99%

Vasoactive drugs and the gut: is there anything new?

Woolsey

Coopersmith

2006

Current Opinion in Critical Care

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“…Published data in sepsis suggest that dopamine may impair hepatosplanchnic perfusion and metabolism (9,12,13). Tachycardia, another adverse effect of dopamine, together with vasoconstriction can lead to increased cardiac oxygen demand and decreased oxygen delivery and may trigger myocardial ischemia and arrhythmias.…”

Section: Dopaminementioning

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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“…In the selection of drugs for increasing the blood pressure about shock in recent years, norepinephrine has shown to be effective for improving blood fl ow of the viscera. [8,9] So we used norepinephrine to increase the blood pressure and found that in the hypertransfusion group, CO and HR were significantly increased after blood pressure increased, resulting in DO 2 in this group much higher than that in the control group, then improving tissue oxygen supply. Although VO 2 was increased simultaneously in the hypertransfusion group, ERO 2 was lower than that in the control group, indicating that hypertransfusion was effective to improve the oxygen metabolism.…”

Section: Discussionmentioning

confidence: 99%