Review and update on inotropes and vasopressors: Evidence-based use in cardiovascular diseases

Abstract

Patients in the intensive care unit frequently develop low-output syndromes due to cardiac dysfunction, myocardial injury and activation of inflammatory cascades. Pharmacological agents, including vasodilators, inotropes and vasopressors, are frequently used in the critical care setting for the management of unstable cardiac patients. These medications are used to elicit varying effects on vascular resistance, myocardial contractility and heart rate to achieve desired hemodynamic and clinical end points. Conventional inotropic agents appear to be useful in restoring hemodynamic parameters and improving peripheral organ perfusion, but they can increase short-term and long-term mortality in these patients. Novel inotropes may be promising in the management of cardiogenic shock patients without serious adverse effects. The present review summarizes the current knowledge about the pathophysiology and evidence-based use of conventional and novel inotropic agents in various clinical scenarios associated with cardiovascular diseases.

Changes in cardiac output with hemodialysis relate to net volume balance and to inferior vena cava ultrasound collapsibility in critically ill patients

“…There was no significant relationship between the frequency of encounters for CO increased or not increased when comparing numbers of encounters with moderate to severe mitral regurgitation to those without moderate to severe mitral regurgitation (p ¼ 0.30 LLR) (Supplemental Table 1). The distribution of the frequency of increased CO or not increased with or without administration of vasopressors/inotropes including dopamine, dobutamine and epinephrine, which may increase CO [42], was not different from random in either the intermittent HD (p ¼ 0.07) or continuous HD encounters (p ¼ 1.0), or for the combined group (p ¼ 0.14) (Supplemental Table 1). Encounter SOFA scores were not significantly related to whether change in CO was increased or not increased.…”

“…Inotropes/vasopressors such as dopamine, dobutamine and/or epinephrine may increase CO [42], and may have played a role in a subset of our patient encounters with relative intravascular overload.…”

“Assessing the hemodynamic impact of various inotropes combination in patients with cardiogenic shock with Non-ST elevation myocardial infarction –the ANAPHOR study”

“…The incidence of cardiogenic shock is approximately 7% (5%–8%) in ST-elevation myocardial infarction and 2.5% in non-ST elevation myocardial infarction patients. 2 Shock results in impaired tissue perfusion, cellular hypoxia, and metabolic derangements that cause cellular injury. Although this early injury is often reversible, persistent hypo perfusion leads to irreversible tissue damage, progressive organ dysfunction and can progress to death.…”

“…The effect varies depending on the interaction with the various receptors in the myocardium and the vascular smooth muscle. 2 Descriptions of the use of inotropes and vasopressors in Shock go back to the 1950s, 5 , 6 but there have been very few clinical trials in these patients and so the choice of which drug combination to be used in this setting remains unclear.…”