Use and impact of inotropes and vasodilator therapy in hospitalized patients with severe heart failure

Elkayam, Uri; Tasissa, Gudaye; Binanay, Cynthia; Stevenson, Lynne Warner; Gheorghiade, Mihai; Warnica, J. Wayne; Young, James B.; Rayburn, Barry K.; Rogers, Joseph G.; DeMarco, Teresa; Leier, Carl V.

doi:10.1016/j.ahj.2006.09.005

Cited by 212 publications

(142 citation statements)

References 12 publications

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“…dobutamine, milrinone) is, at least partly, abolished by increased energy consumption at the cellular level [120]. This might explain the lack of favorable long-term outcomes with prolonged use of these drugs in critically ill patients [121]. Hence, novel inotropes are urgently needed.…”

Section: Novel Therapies For the Septic Heartmentioning

confidence: 99%

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Rudiger¹,

Singer²

2013

Current Vascular Pharmacology

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Septic shock is characterized by circulatory compromise, microcirculatory alterations and mitochondrial damage, which all reduce cellular energy production. In order to reduce the risk of major cell death and a diminished likelihood of recovery, adaptive changes appear to be activated. As a result, cells and organs may survive in a non-functioning hibernation-like condition. Sepsis-induced cardiac dysfunction may represent an example of such functional shutdown. Sepsis-induced myocardial dysfunction is common, corresponds to the severity of sepsis, and is reversible in survivors. Its mechanisms include the attenuation of the adrenergic response at the cardiomyocyte level, alterations of intracellular calcium trafficking and blunted calcium sensitivity of contractile proteins. All these changes are mediated by cytokines. Treatment includes preload optimization with sufficient fluids. However, excessive volume loading is harmful. The first line vasopressor recommended at present is norepinephrine, while vasopressin can be started as a salvage therapy for those not responding to catecholamines. During early sepsis, cardiac output can be increased by dobutamine. While early administration of catecholamines might be necessary to restore adequate organ perfusion, prolonged administration might be harmful. Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine reduces myocardial oxygen expenditure and ameliorates diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. All these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice. While early administration of catecholamines might be necessary to restore adequate organ perfusion and pressure, prolonged administration might be harmful.Novel therapies for sepsis-induced cardiac dysfunction are discussed in this article. Cardiac inotropy can be increased by levosimendan, istaroxime or omecamtiv mecarbil without greatly increasing cellular oxygen demands. Heart rate reduction with ivabradine will reduce myocardial oxygen expenditure and ameliorate diastolic filling. Beta-blockers additionally reduce local and systemic inflammation. Advances may also come from metabolic interventions such as pyruvate, succinate or high dose insulin substitutions. However, all these potentially advantageous concepts require rigorous testing before implementation in routine clinical practice.-3 -Alain Rudiger & Mervyn Singer: The heart in sepsis

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Section: Novel Therapies For the Septic Heartmentioning

confidence: 99%

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Rudiger¹,

Singer²

2013

Current Vascular Pharmacology

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“…Due to the potential harm induced by exogenous catecholamine therapy [5][6][7], a less harmful strategy such as GIK may be beneficial. The hyperadrenergic state of heart failure causes plasma free fatty acid (FFA) levels to rise [25][26][27].…”

Section: Discussionmentioning

confidence: 99%

“…Indeed, even adjusting for severity and other factors, these agents are associated with a significantly increased risk of greater morbidity, mortality and rehospitalisation [5][6][7]. Other options for treating low cardiac output states include phosphodiesterase inhibitors such as enoximone or calcium sensitizers such as levosimendan.…”

Section: Introductionmentioning

confidence: 99%

Experience using high-dose glucose-insulin-potassium (GIK) in critically ill patients

Slob

Shulman

Singer

2017

Journal of Critical Care

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Purpose To audit the use of GIK in terms of safety, haemodynamic effects, and impact on catecholamine dosage.Materials and methods A retrospective, descriptive, evaluative audit of GIK use within the adult ICU of a London teaching hospital was conducted. Rescue therapy of GIK (up to 1.0 Units insulin/kg/hour) was administered to improve cardiac function. Outcomes were ICU survival, change in cardiac index (CI) and blood lactate levels, events of hypoglycaemia, hyperglycaemia, hypokalaemia and hyperkalaemia, and discontinuation time of catecholamine inotropes. ResultsOf 85 patients treated with GIK, 13 (15.3%) survived their ICU stay and 9 (10.5%) were discharged home. In patients surviving until 72 hours, a trend of improved CI and lactate levels was seen, often with reductions in catecholamine dosing. Inotropes were discontinued in 35 (54%) patients. Severe hypoglycaemia (<2 mmol/l), hyperglycaemia (>20 mmol/l), hypokalaemia (<2.5 mmol/l) and hyperkalaemia (>7 mmol/l) during GIK affected 1, 6, 8 and 1 patients, respectively. These abnormalities were quickly identified. No measurable harm was noted.Conclusions High-dose GIK can be safely used in critically ill patients, though blood glucose and potassium levels must be monitored frequently. GIK was associated with improved CI and blood lactate levels. Impact on survival requires prospective evaluation.

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“…58 Furthermore, the main determinant of inotrope use in the ESCAPE trial was not the patient's cardiac output, blood pressure, or PCWP, but instead was the hospital to which the patient was admitted. 59 Hospitalists are positioned to play a key role in improving both inpatient care of ADHF patients and the transition to long-term patient management. 60,61 However, specific core competencies are required before hospitalists can effectively undertake this role.…”

Section: Role Of the Hospitalistmentioning

confidence: 99%

Hospitalized patients with acute decompensated heart failure: Recognition, risk stratification, and treatment review

Amin¹

2008

J. Hosp. Med.

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Acute decompensated heart failure (ADHF) has emerged as a major healthcare problem. It causes approximately 3% of all hospitalizations in the United States, with the direct medical cost of these hospitalizations estimated at $18.8 billion per year. Early recognition, risk stratification, and evidence-based treatment are crucial in reducing the morbidity, mortality, and costs associated with this disorder. Classic signs and symptoms of ADHF, such as rales, dyspnea, and peripheral edema, may be absent at hospital presentation and, even when present, are not specific to this disorder. As a result, serum B-type natriuretic peptide level is now used to rapidly and accurately detect ADHF. Multivariate analyses have identified renal dysfunction, hypotension, advanced age, hyponatremia, and comorbidities as significant and independent mortality risk factors. Based on these factors, mortality risk can be stratified from very low to very high using published algorithms that have been validated in independent populations. Evidence-based guidelines for the treatment of ADHF are available from both the European Society of Cardiology and the Heart Failure Society of America. In general, an intravenous loop diuretic, either alone or in combination with a vasodilator, is recommended as initial therapy in patients with volume overload, depending on the patient's clinical status. Use of inotropic agents should be limited to the small subset of patients with low-output syndrome and significant hypotension. In any event, frequent monitoring of clinical response is essential, with subsequent therapy determined by this response. Finally, focused patient education during hospitalization may help reduce readmissions for ADHF. Journal of Hospital Medicine 2008;3(Suppl 6):S16-S24. V

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Use and impact of inotropes and vasodilator therapy in hospitalized patients with severe heart failure

Cited by 212 publications

References 12 publications

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

The Heart in Sepsis: From Basic Mechanisms to Clinical Management

Experience using high-dose glucose-insulin-potassium (GIK) in critically ill patients

Hospitalized patients with acute decompensated heart failure: Recognition, risk stratification, and treatment review

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