[Heart rate control in shock]. / Herzfrequenzkontrolle im Schock.

Heart rate is well established in the diagnosis of shock; however, the mechanisms regulating heart rate, systemic resistance and blood pressure remain unclear. The concept of heart rate control in shock-related tachycardia has been known for about 50 years. Elevated heart rates in septic shock have been identified as an indicator of increasingly inefficient hemodynamics, worsening perfusion and organ function as well as of an unfavourable prognosis. Many drugs used for heart rate control also lower blood pressure. The challenge of this therapeutic concept is achieving optimal heart rate control without provoking critical hypotension. Only in recent years has the development of highly cardioselective, short- and ultrashort-acting ß­blockers such as esmolol and landiolol made it possible to prove the feasibility and usefulness of heart rate control in certain types of shock.

Intra-aortic balloon counterpulsation in the treatment of infarction-related cardiogenic shock--review of the current evidence.

The European ST-elevated myocardial infarction (STEMI) guideline suggested the intra-aortic balloon pump (IABP) with a recommendation level I and a level of evidence C as an effective measure in combination with balloon angioplasty in patients with cardiogenic shock (CS), stent implantation, and inotropic and vasopressor support. Similarly, upon mechanical complication due to myocardial infarction (MI), the guideline suggests that in patients with a ventricular septal defect or in most patients with acute mitral regurgitation, preoperative IABP implantation is indicated for circulatory support. The American College of Cardiology/American Heart Association STEMI guideline recommends the use of the IABP with a recommendation level I and a level of evidence B if CS does not respond rapidly to pharmacological treatment. The guideline notes that the IABP is a stabilizing measure for angiography and early revascularization. Even in MI complications, the use of preoperative IABP is recommended before surgery. Within this overview, we summarize the current evidence on IABP use in patients with CS complicated by MI. From our Cochrane data analysis, we conclude that in CS due to acute MI (AMI) treated with adjuvant systemic fibrinolysis, the IABP should be implanted. In patients with CS following AMI, treated with primary percutaneous coronary intervention (PCI), the IABP can be implanted, although data are not distinctive (i.e., indicating positive and negative effects). In the future, randomized controlled trials are needed to determine the use of IABP in CS patients treated with PCI. When patients with CS are transferred to a PCI center with or without thrombolysis, patients should receive mechanical support with an IABP. To treat mechanical MI complications-in particular ventricular septal defect-patients should be treated with an IABP to stabilize their hemodynamic situation prior to cardiac surgery. Similar recommendations are given in the German Austrian guidelines on treatment of infarction-related CS patients (http://www.awmf.org/leitlinien/detail/ll/019-013.html).

Hemodynamic effects of intra-aortic balloon counterpulsation in patients with acute myocardial infarction complicated by cardiogenic shock: the prospective, randomized IABP shock trial.

We conducted the IABP Cardiogenic Shock Trial (ClinicalTrials.gov ID NCT00469248) as a prospective, randomized, monocentric clinical trial to determine the hemodynamic effects of additional intra-aortic balloon pump (IABP) treatment and its effects on severity of disease in patients with acute myocardial infarction complicated by cardiogenic shock (CS). Intra-aortic balloon pump counterpulsation is recommended in patients with CS complicating myocardial infarction. However, there are only limited randomized controlled trial data available supporting the efficacy of IABP following percutaneous coronary intervention (PCI) and its impact on hemodynamic parameters in patients with CS. Percutaneous coronary intervention of infarct-related artery was performed in 40 patients with acute myocardial infarction complicated by CS, within 12 h of onset of hemodynamic instability. Serial hemodynamic parameters were determined over the next 4 days and compared in patients receiving medical treatment alone with those treated with additional intra-aortic balloon counterpulsation. There were no significant differences among severity of disease (i.e., Acute Physiology and Chronic Health Evaluation II score) initially and no differences among both groups for disease improvement. We observed significant temporal improvements of cardiac output (4.8 ± 0.5 to 6.0 ± 0.5 L/min), systemic vascular resistance (926 ± 73 to 769 ± 101 dyn · s(-1) · cm(-5)), and the prognosis-validated cardiac power output (0.78 ± 0.06 to 1.01 ± 0.2 W) within the IABP group. However, there were no significant differences between the IABP group and the medical-alone group. Additional IABP treatment did not result in a significant hemodynamic improvement compared with medical therapy alone in a randomized prospective trial in patients with CS following PCI. Therefore, the use and recommendation for IABP treatment in CS remain unclear.

Interleukin-6, -7, -8 and -10 predict outcome in acute myocardial infarction complicated by cardiogenic shock.

BACKGROUND: The IABP-SHOCK-trial was a morbidity-based randomized controlled trial in patients with infarction-related cardiogenic shock (CS), which used the change of the quantified degree of multiorgan failure as determined by APACHE II score over a 4-day period as primary outcome measure. The prospective hypothesis was that adding IABP therapy to "standard care" would improve CS-triggered multi organ dysfunction syndrome (MODS). The primary endpoint showed no difference between conventionally managed cardiogenic shock patients and those with IABP support. In an inflammatory marker substudy, we analysed the prognostic value of interleukin (IL)-1ß, -6, -7, -8, and -10 in patients with acute myocardial infarction complicated by cardiogenic shock. DESIGN: Inflammatory marker substudy of the prospective, randomized, controlled, open label IABP-SHOCK-trial (ClinicalTrials.gov ID-NCT00469248). SETTING AND METHODS: A single-center study was performed in a 12-bed Intensive-Care-Unit in an university hospital in which 40 consecutive patients were enrolled with an observational period of 96 h. RESULTS: The pro- and anti-inflammatory markers IL-6, -7, -8 and -10 showed a predictive power for mortality of infarct-related CS patients, while IL-1ß did not discriminate. The maximal values during the observational period, in case of IL-7 the minimal value, showed the best power to predict mortality. Both, ROC and multivariate analyses confirmed these suggestions (area under the curve: IL-8, 0.80 ± 0.08; IL-6, 0.79 ± 0.08; IL-10, 0.76 ± 0.08; IL-7, 0.69 ± 0.08). Inflammatory markers were not affected by the presence of IABP support. CONCLUSION: The inflammatory response in patients with myocardial infarction complicated by cardiogenic shock, as reflected by the inflammatory markers IL-6, IL-7, IL-8 and IL-10, demonstrates a clinically relevant prognostic contribution to clinical outcome.

Intra-aortic balloon counterpulsation in patients with acute myocardial infarction complicated by cardiogenic shock: the prospective, randomized IABP SHOCK Trial for attenuation of multiorgan dysfunction syndrome.

OBJECTIVE: Patients undergoing percutaneous coronary intervention (PCI) for acute myocardial infarction with cardiogenic shock (CS) are often treated with intra-aortic balloon pump counterpulsation (IABP), even though the evidence to support this is limited. We determined whether IABP as an addition to PCI-centered therapy ameliorates multiorgan dysfunction syndrome (MODS) in patients with acute myocardial infarction complicated by CS. DESIGN: A prospective, randomized, controlled, open-label clinical trial recruiting patients between March 2003 and June 2004 (ClinicalTrials.gov ID NCT00469248). SETTING: Tertiary care university hospital. PATIENTS AND INTERVENTIONS: Forty-five consecutive patients with AMI and CS undergoing PCI were randomized to treatment with or without IABP. MEASUREMENTS AND MAIN RESULTS: Acute Physiology and Chronic Health Evaluation (APACHE) II scores (primary outcome measure), hemodynamic values, inflammatory markers, and plasma brain natriuretic peptide (BNP) levels (secondary outcomes) were collected over 4 days from randomization. The prospective hypothesis was that adding IABP therapy to "standard care" would improve CS-triggered MODS. The addition of IABP to standard therapy did not result in a significant improvement in MODS (measured by serial APACHE II scoring over 4 days). IABP use had no significant effect on cardiac index or systemic inflammatory activation, although BNP levels were significantly lower in IABP-treated patients. Initial and serial APACHE II scoring correlated with mortality better than cardiac index, systemic inflammatory state, and BNP levels in this group of patients. Nonsurvivors had significantly higher initial APACHE II scores (29.9 +/- 2.88) than survivors (18.1 +/- 1.66, p < .05). Nevertheless, discrepancies among patients within the groups cannot be ruled out and might interfere with our results. CONCLUSIONS: In this randomized trial addressing addition of IABP in CS patients, mechanical support was associated only with modest effects on reduction of APACHE II score as a marker of severity of disease, improvement of cardiac index, reduction of inflammatory state, or reduction of BNP biomarker status compared with medical therapy alone. However, the limitations of our present trial preclude any definitive conclusion, but request for a larger prospective, randomized, multicentered trial with mortality as primary end point.

Right ventricular function in myocardial infarction complicated by cardiogenic shock: Improvement with levosimendan.

OBJECTIVES: Levosimendan improves left ventricular hemodynamic function in patients with cardiogenic shock. However, its impact on right ventricular performance has not been determined. We compared the hemodynamic effects of levosimendan on left and right ventricular function in patients with intractable cardiogenic shock following myocardial infarction. DESIGN: Observational hemodynamic study. SETTING: Tertiary care center university hospital. PATIENTS: Fifty-six patients with cardiogenic shock secondary to myocardial infarction were treated with percutaneous revascularization (including intra-aortic balloon pump when appropriate) and commenced on conventional inotropic therapy. INTERVENTION: Twenty-five consecutive patients with cardiogenic shock due to myocardial infarction who had not improved sufficiently with conventional therapy (including dobutamine and norepinephrine) received levosimendan (as a bolus of 12 microg/kg per minute for 10 mins then 0.1 microg/kg per minute--0.2 mug/kg per minute) as "bail-out" therapy for 24 hrs while invasive hemodynamic parameters were recorded. MEASUREMENTS AND MAIN RESULTS: Levosimendan therapy was associated with a significant increase in cardiac index from 2.1 +/- 0.1 to 3.0 +/- 0.2 L x min x m (p < .01). In addition, levosimendan enhanced right ventricular cardiac power index (0.14 +/- 0.19 to 0.18W +/- 0.12, p < .001), while pulmonary vascular resistance fell from 227.7 +/- 94.5 to 178.1 +/- 62.3 dyne x s x cm (p = .002). No significant change in central venous pressure or mean pulmonary artery pressure was observed. The observed hemodynamic improvement was sustained after the levosimendan infusion was stopped. CONCLUSIONS: Levosimendan infusion for cardiogenic shock following acute myocardial infarction improved hemodynamic parameters of right ventricular performance. Furthermore, we describe the use of right ventricular cardiac power index as a hemodynamic parameter of right ventricular performance.

Early and sustained haemodynamic improvement with levosimendan compared to intraaortic balloon counterpulsation (IABP) in cardiogenic shock complicating acute myocardial infarction.

OBJECTIVE: To investigate the haemodynamic effects of levosimendan in patients with cardiogenic shock (CS) complicating acute myocardial infarction in comparison to the effects of intra-aortic balloon counterpulsation (IABP). METHODS: 10 patients with intractable CS under standard therapy (including the use of PCI, inotropes, and vasopressors) received i.v. infusion of levosimendan (bolus 12 microg/kg i.v., followed by continuous infusion 0.1 microg/kg/min for 24 h). Haemodynamic effects were compared to the effects of IABP-placement added to standard care in 12 patients with CS. RESULTS: Within 24 h, both levosimendan and IABP produced a significant increase in cardiac index (CI) and cardiac power index and a decrease in systemic vascular resistance (SVR) (CI [l/min/m2] baseline 1.97+/-0.15, at 24 h 2.82+/-0.22 for levosimendan; baseline 1.98+/-0.17, at 24 h 2.66+/-0.08 for IABP; SVR [dyn*s*cm-5] baseline 1353+/-106, at 24 h 846+/-69 for levosimendan; baseline 1311+/-214, at 24 h 853+/-63 for IABP, respectively). After 3 h of treatment, CI and SVR had significantly improved in patients treated with levosimendan but not in the IABP-group (CI [l/min/m2] at 3 h 2.72+/-0.28 (+38%) for levosimendan versus 2.18+/-0.15 (+10%) for IABP). CONCLUSION: Infusion of levosimendan in acute CS results in early and sustained haemodynamic improvement. Short-term haemodynamic effects compare favourably with those seen after invasive IABP placement.

Hemodynamic improvement following levosimendan treatment in patients with acute myocardial infarction and cardiogenic shock.

OBJECTIVES: Levosimendan, a novel inodilator, has been shown to improve hemodynamic function in patients with acute exacerbation of congestive heart failure. We wanted to determine the hemodynamic effects of levosimendan following ineffective conventional therapy (with catecholamines) in patients with cardiogenic shock following myocardial infarction. DESIGN: Observational hemodynamic study. SETTING: Tertiary care center university hospital. PATIENTS: Fifty-six patients with cardiogenic shock secondary to myocardial infarction were treated with percutaneous revascularization (intra-aortic balloon pump where appropriate) and commenced on conventional inotropic therapy. INTERVENTIONS: Patients with persisting cardiogenic shock 24 hrs after revascularization were additionally treated with levosimendan (rapid bolus of 12 microg/kg for 10 mins, then 0.05-0.2 mug/kg/min for 24 hrs) (n = 25). MEASUREMENTS AND MAIN RESULTS: With conventional catecholamine therapy (norepinephrine and dobutamine), we observed only marginal improvement in mean arterial pressure or cardiac index. In contrast, the addition of levosimendan produced a significant increase in cardiac index (2.1 +/- 0.56 to 3.0 +/- 1.11 L/min/m2, p < .01) and cardiac power index (0.32 +/- 0.08 to 0.44 +/- 0.18 W, p < .01), whereas systemic vascular resistance decreased significantly (1208 +/- 333 to 858 +/- 299 dyne.sec.cm(-5), p < .01). There was no significant change in blood pressure during levosimendan treatment. Hemodynamic improvement was sustained after levosimendan infusion was stopped. CONCLUSIONS: Levosimendan infusion in cardiogenic shock following acute myocardial infarction improved cardiovascular hemodynamics without leading to hypotension.