Despite preserved systemic oxygen transport, septic shock patients frequently die from multiple organ failure or cardiovascular collapse. Typically, death from septic shock is related to the persistence of a hyperdynamic state with progressive and refractory vasodilation.
In this context, myocardial dysfunction may be a contributor to the hemodynamic instability but not the main cause. In addition, cardiac alterations in septic shock comprise systolic and diastolic dysfunction, 41 dynamic left intraventricular obstruction, 42 and acute stress cardiomyopathy.
Therefore, dobutamine will not be useful for most of the cardiac alterations in septic shock. As supported by the results of an observational study, 7 only patients with systolic dysfunction have positive responses in stroke volume. This observation might be an explanation for the heterogeneous responses to dobutamine.
Nevertheless, several other factors might contribute to the variability in responses. Sepsis is characterized by alterations in the adrenergic receptors, which subsequently may modify the response to catecholamines.
Finally, women might have an increased chronotropic response, 53 but the data are inconclusive. Patients with septic shock commonly display varying responses to dobutamine. Frequently, vasodilation and tachycardia are the most prominent effects without evidence of improved cardiac performance. These findings suggest a low profile of efficacy and safety.
In addition, the effects on regional and microcirculatory perfusion are also unpredictable. The presence of echocardiographic systolic dysfunction and severe microvascular disorders could help in the identification of patients who would benefit from the use of dobutamine. Before a definitive therapeutic decision, efficacy of and tolerance to dobutamine should be evaluated during a brief time with close monitoring of its positive and negative effects.
Conflicts of interest: None. Responsible editor: Gilberto Friedman. National Center for Biotechnology Information , U. Rev Bras Ter Intensiva. Find articles by Arnaldo Dubin. Find articles by Bernardo Lattanzio. Find articles by Luis Gatti. Author information Article notes Copyright and License information Disclaimer. E-mail: moc. Received Jan 3; Accepted Mar Copyright notice. This is an Open Access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
This article has been cited by other articles in PMC. Abstract Dobutamine is the inotrope most commonly used in septic shock patients to increase cardiac output and correct hypoperfusion. Open in a separate window. Figure 1. Schematic of the main pharmacodynamic and cardiovascular effects of dobutamine. Figure 2. Effects of levosimendan and dobutamine in experimental acute endotoxemia: a preliminary controlled study.
Intensive Care Med. Figure 3. Systemic and microcirculatory effects of dobutamine in patients with septic shock. J Crit Care. Figure 4. Footnotes Conflicts of interest: None. Crit Care Med. N Engl J Med. Association between inotrope treatment and day mortality in patients with septic shock.
Acta Anaesthesiol Scand. Dobutamine for patients with severe heart failure: a systematic review and meta-analysis of randomised controlled trials.
Heterogeneity and prediction of hemodynamic responses to dobutamine in patients with septic shock. Cardiovascular response to dobutamine stress predicts outcome in severe sepsis and septic shock. Crit Care. Use of dobutamine in the treatment of septic shock. Anesth Analg Paris ; 34 5 — Alpha and beta adrenergic effects of the stereoisomers of dobutamine. J Pharmacol Exp Ther. Vascular effects of the stereoisomers of dobutamine. Eur J Pharmacol. In vivo analysis of adrenergic receptor activity of dobutamine.
Circ Res. Pharmacokinetic-pharmacodynamic relationship of dobutamine and heart rate, stroke volume and cardiac output in healthy volunteers. Clin Drug Investig. Metabolic effects of dobutamine in normal man.
Clin Sci Lond ; 82 1 — Tuttle RR, Mills J. Dobutamine: development of a new catecholamine to selectively increase cardiac contractility. Haemodynamic effects of a new inotropic agent dobutamine in chronic cardiac failure. Br Heart J. Comparison of dobutamine and dopamine in treatment of severe heart failure. Patients who received atropine had significantly higher peak HR and BP values, compared with patients who did not receive atropine.
There were greater SBP changes in younger patients who received atropine and lesser DBP changes in all age groups who received atropine Figure 1. Blood pressure response during DSE, by age and the use of atropine. BP values were higher in younger patients. Complications were rare; 19 patients developed sustained supraventricular tachycardia.
All of these patients went back into sinus rhythm after administration of intravenous metoprolol or esmolol. Another 16 patients developed atrial fibrillation. The other eight patients had HR slowing; at follow-up within 24 h, sinus rhythm had returned spontaneously in seven patients and one patient underwent direct current cardioversion.
There were no cases of sustained ventricular tachycardia, ventricular fibrillation, or myocardial infarction. The HR increased progressively in both groups. The rise was significantly slower in patients who received atropine Figure 2.
Changes from baseline, during each dobutamine stage. Patients who received atropine developed symptoms more frequently than patients who did not receive atropine, including chest pain 17 vs. To facilitate the utilization of these cut-point values in clinical practice, we propose using two unique upper values one systolic and one diastolic and two unique lower values one systolic and one diastolic , obtained from the overall study population.
The proposed normative SBP value at peak stress ranges from 82 to mmHg. The proposed normative DBP value at peak stress ranges from 40 to 96 mmHg. As defined by the peak SBP, 66 patients had a hypertensive response and 51 had a hypotensive response.
Multivariate predictors of a hypertensive response were male sex [odds ratio OR 2. Left ventricular EF at peak stress was not a multivariate predictor of a hypotensive response. BP response is greater in men than in women, and in younger than in older patients, and is most pronounced in patients who receive atropine, regardless of sex and age.
On the basis of these results, we propose novel normative values for BP response to dobutamine stress. In our study population, a predominant dobutamine-induced vasodilating effect was likely the main mechanism for the slight decrease in DBP we observed. This effect is likely counterbalanced in systole by a dobutamine-induced increase in cardiac output, resulting in a slight increase in SBP.
In addition, we observed a significant increase in HR and rate-pressure product. Similarly, in prior animal model studies, rate-pressure product increased but mean aortic pressure did not change significantly with dobutamine infusion. For example, patients who have hypertension often have elevated peripheral vascular resistance; 29 an increase in cardiac output by dobutamine infusion may not be offset by prompt peripheral vasodilation in a subset of these patients.
These findings were consistent with those of a prior study. The precise mechanism underlying these sex differences in BP response during DSE is unclear, but arterial BP dissimilarities between men and women are recognized in the literature.
Age-related changes in adrenergic and baroreflex responsiveness have been demonstrated 33—35 and include a diminished stress-induced HR increase in the elderly. Furthermore, it is known that vascular compliance decreases with age, leading to a lower effectiveness in compensatory BP changes, along with sharp falls in DBP in the elderly.
Atropine use during DSE is safe and enhances the diagnostic accuracy of the test by contributing to an increase in HR and myocardial oxygen demand. Studies on animals demonstrated that atropine has no direct effects on peripheral vasculature.
Peak BP values were especially higher in younger patients, who received atropine more often than older patients. Given the absence of atropine effect on the peripheral vasculature, its effects on BP would have to be due to its positive chronotropic effect. It is also possible that the higher frequency of symptoms that developed in patients receiving atropine contributed to the higher BP values.
Few, but consistent hints of higher BP values in patients who received atropine, compared with patients who did not, have been reported in previous DSE studies. The expected or typical BP responses during DSE have not been systematically defined, and the cut-points used in previous studies to describe abnormal BP responses were arbitrarily established.
These data may help facilitate broad agreement regarding what the definition s of an abnormal BP response to dobutamine stress should be. Moreover, they constitute criteria that can be used for future studies regarding the clinical implications of abnormal BP responses during DSE.
It is unlikely, however, that a study defining the expected or normal BP responses during DSE in healthy adult volunteers of all ages will ever be performed on a large scale. In the present study, it is possible that some patients had coexisting medical conditions that could have affected their BP responses to DSE even though all patients with known cardiovascular disease, those taking vasoactive medications, and those who had abnormal stress echocardiograms were excluded.
A complete explanation of the mechanisms underlying BP pressure variations is beyond the scope of this study. This is the first study to define typical BP responses during DSE in a large population of adult patients of all ages not known to have cardiovascular disease and not taking vasoactive medications.
The existence of cut-off values for normal BP responses, rigorously established in this study, should aid in the recognition of abnormal BP responses during DSE. Moreover, these reference values should serve as a robust foundation for future studies, which could be aimed at answering questions that remain regarding the clinical implications of abnormal BP responses during DSE. American Society of Echocardiography recommendations for performance, interpretation, and application of stress echocardiography.
J Am Soc Echocardiogr ; 20 : — Google Scholar. Eur J Echocardiogr ; 9 : — Seven-year follow-up after dobutamine stress echocardiography: impact of gender on prognosis. J Am Coll Cardiol ; 45 : 93 — 7. Echocardiographic detection of coronary artery disease during dobutamine infusion. Circulation ; 83 : — Am J Cardiol ; 98 : — 3. Symptoms, adverse effects, and complications associated with dobutamine stress echocardiography. Experience in patients. Circulation ; 88 : 15 — 9.
Evolution of dobutamine echocardiography protocols and indications: safety and side effects in 3, studies over 5 years. J Am Coll Cardiol ; 29 : — Safety of dobutamine-atropine stress echocardiography: a prospective experience of 4, consecutive studies.
J Am Soc Echocardiogr ; 12 : — Impact of age on the safety and the hemodynamic response pattern during high dose dobutamine echocardiography. Echocardiography ; 16 : — Dobutamine-atropine stress echocardiography in elderly patients unable to perform an exercise test. Hemodynamic characteristics, safety, and prognostic value. Arch Intern Med ; : — 6. Normalwerte fur die dobutamin-stressechokardiographie. Dtsch Med Wochensc ; : — 7.
Hypotension during dobutamine stress echocardiography: initial description and clinical relevance. Am Heart J ; : — 7. Hypertensive response during dobutamine stress echocardiography. Am J Cardiol ; 80 : — 1. Left ventricular outflow tract obstruction as a cause for hypotension and symptoms during dobutamine stress echocardiography. The FDA approveD dobutamine for short-term use in patients with decreased contractility due to heart failure or cardiac surgical procedures leading to cardiac decompensation.
The agent has not been shown to give positive outcomes in the hospitalized or outpatient setting for heart failure patients despite hemodynamically improving the patient's condition. Dobutamine can be used as temporary intravenous inotropic support until resolution of the acute inducing factors or the patient receives more definitive treatment, such as coronary revascularization, mechanical circulatory support, or heart transplant.
Short-term intravenous inotropic support should be given to patients in cardiogenic shock to preserve systemic blood flow and protect from end-organ damage. This activity will highlight the mechanism of action, adverse event profile, pharmacology, monitoring, and relevant interactions of dobutamine, pertinent for members of the interprofessional team in treating patients with cardiac disorders that will respond to such therapy.
Objectives: Identify the various indications for dobutamine. Outline the adverse event profile for dobutamine. Review the mechanism of action of dobutamine that leads to its therapeutic effects. Summarize interprofessional team strategies for improving care coordination and communication to advance diabetes management and improve outcomes by using dobutamine.
They published an article "Dobutamine: development of a new catecholamine to selectively increase cardiac contractility" [1].
Dobutamine is approved by the Food and Drug Administration FDA for short-term use in patients with decreased contractility due to heart failure or cardiac surgical procedures leading to cardiac decompensation. Patients can reasonably receive dobutamine in continuous intravenous form for inotropic support to bridge patients with late-stage heart failure, stage D, that is refractory to guideline-directed medical therapy until patients who are candidates for and awaiting cardiac transplantation or mechanical circulatory support receive the appropriate long-term treatment.
Continuous intravenous inotropic dobutamine support can reasonably be given in the short term for hospitalized patients with severe systolic dysfunction who present with low blood pressure and a significantly decreased cardiac output to preserve systemic blood flow and protect from end-organ damage.
Continuous intravenous inotropic dobutamine support can reasonably be given for the long-term in palliative patients with late-stage heart failure, stage D, who are not candidates for mechanical circulatory support or cardiac transplantation for symptomatic control, regardless of guideline-directed medical therapy.
Intravenous inotropic dobutamine can be given off-label to patients to induce pharmacological stress during stress echocardiography if patients cannot perform an exercise stress test. Dobutamine is used as a pharmacological agent and has both ionotropic and chronotropic effects depending on the dose.
Because of its inotropic effects on the myocardium through binding and activating the beta-1 receptors selectively. Dobutamine's ionotropic effect increases contractility, leading to decreased end-systolic volume and, therefore, increased stroke volume.
The increase in stroke volume leads to an augmentation of the cardiac output of the heart. In addition to the well-known beta-1 activity, dobutamine has been shown to have some beta-2 activity, which contributes to the reduction in the systemic vascular resistance, and alpha-1 activity, to an even lesser extent, whose vasoconstrictive effects are negated by the baroreceptor mediated response and beta-2 activity.
Dobutamine administration is via large intravenous access and infusion pump for inotropic support in decompensated congestive heart failure, stress echocardiogram, and stress nuclear testing. The lower doses of dobutamine can be prescribed at 2. Dobutamine comes in a solution as a racemic mixture of both positive and negative enantiomers for intravenous administration. The positive enantiomer in the solution is predominately selective for the beta sympathetic receptors, mainly beta 1 and 2, whereas the negative enantiomer has been shown in studies to be selective for the alpha one receptors.
Dobutamine administration can lead to possible adverse reactions, mainly due to sympathomimetic activity.
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