Management of cardiogenic shock complicating myocardial infarction

Up to 10% of acute coronary syndromes are complicated by cardiogenic shock (CS) with contemporary mortality rates of 40–50%. The extent of ischemic myocardium has a profound impact on the initial, in-hospital, and post-discharge management and prognosis in this patient population. Individualized patient risk assessment plays an important role in determining appropriate revascularization, drug treatment with inotropes and vasopressors, mechanical circulatory support, intensive care support of other organ systems, hospital level of care triage, and allocation of clinical resources. This review will outline the underlying causes and diagnostic criteria, pathophysiology, and treatment of CS complicating acute coronary syndromes with a focus on (a) potential therapeutic issues from the perspective an interventional cardiologist, an emergency physician, and an intensive care physician, (b) the type of revascularization, and (c) new therapeutic advancements in pharmacologic and mechanical percutaneous circulatory support.     

Pathophysiology of cardiogenic shock complicating acute myocardial infarction

Cardiogenic shock is a rapidly progressive, often fatal complication of acute myocardial infarction. A vicious circle of ischemia, decreased cardiac output and reinfarction progress to left ventricular failure and death. The fundamental pathophysiology of this cascade and other mechanisms beyond the classic paradigm of ischemia and dysfunction are discussed in detail.     

Optimal course of treatment in acute cardiogenic shock complicating myocardial infarction

Introduction: About 5% of patients with myocardial infarction suffer from cardiogenic shock as a complication, with a mortality of ≥30%. Primary percutaneous coronary intervention as soon as possible is the most successful therapeutic approach. Prognosis depends not only on the extent of infarction, but also – and even more – on organ hypoperfusion with consequent development of multiple organ dysfunction syndrome.

Areas covered: This review covers diagnostic, monitoring and treatment concepts relevant for caring patients with cardiogenic shock complicating myocardial infarction. All major clinical trials have been selected for review of the recent data.

Expert commentary: For optimal care, not only primary percutaneous intervention of the occluded coronary artery is necessary, but also best intensive care medicine avoiding the development of multiple organ dysfunction syndrome and finally death. On contrary, intra-aortic balloon pump – though used for decades – is unable to reduce mortality of patients with cardiogenic shock complicating myocardial infarction.     

Oxidative stress and antioxidants in patients with cardiogenic shock complicating acute myocardial infarction

BACKGROUND: Lipid peroxidation and derived oxidized products are being intensively investigated because of their potential to cause injury and because of their pathogenic role in several diseases. The view that an excess of lipid peroxidation products is present and is relevant in the pathogenesis of cardiogenic shock-induced damage has still not received definitive support. METHODS: To evaluate the extent of lipid peroxidation, the status of enzymatic and nonenzymatic antioxidants in patients with cardiogenic shock that complicate acute myocardial infarction (AMI) and to compare with normal subjects. RESULTS: Compared with normal subjects, cardiogenic shock patients had higher malondialdehyde, conjugated dienes and reduced activities of erythrocyte antioxidant enzymes such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx) and lower concentrations of reduced glutathione (GSH) in erythrocyte and in plasma GSH, vitamin C, vitamin E and in beta-carotene. CONCLUSIONS: Cardiogenic shock is associated with greater than normal lipid peroxidation and with an imbalance in antioxidants' status. These results indicate that low activities of SOD, CAT, GPx and low concentrations of GSH, vitamin C, vitamin E and beta-carotene in the circulation of patients with cardiogenic shock complicating AMI may be due to increased utilization to scavenge lipid peroxides. Decrease in plasma concentrations of GSH, vitamin E and beta-carotene seems to be responsible for the elevation of lipid peroxidation in cardiogenic shock complicating AMI compared with MI.     

Clinical review: mechanical circulatory support for cardiogenic shock complicating acute myocardial infarction

Acute myocardial infarction is one of the 10 leading reasons for admission to adult critical care units. In-hospital mortality for this condition has remained static in recent years, and this is related primarily to the development of cardiogenic shock. Recent advances in reperfusion therapies have had little impact on the mortality of cardiogenic shock. This may be attributable to the underutilization of life support technology that may assist or completely supplant the patient's own cardiac output until adequate myocardial recovery is established or long-term therapy can be initiated. Clinicians working in the intensive care environment are increasingly likely to be exposed to these technologies. The purpose of this review is to outline the various techniques of mechanical circulatory support and discuss the latest evidence for their use in cardiogenic shock complicating acute myocardial infarction.     

IABP在急性心肌梗死并心源性休克救治中应用现状

急性心肌梗死作为临床上常见的疾病,起病急,易引起并发症,其中,心源性休克死亡率较高。临床上常规应用补液、扩血管、升压及溶栓、血管重建等。近年来,IABP被广泛应用于临床,它作为一种辅助装置可以增加血液灌流,降低心脏后负荷,降低心脏做功,从而快速改善循环灌注不足状态。本综述研究IABP作为血流动力辅助装置,应用于急性心肌梗死并发心源性休克患者的临床现状。     

Cardiogenic shock

Cardiogenic shock remains a significant issue and affects 5% to 10% of patients admitted with an AMI. Mortality remains high despite advances in treatment for AMI. These patients are best treated in centers where they can receive treatment that follows the joint guidelines recommended by ACC and AHA. Rapid reperfusion therapy as well as pharmacologic and mechanical circulatory support provide the best options for survival.     

Cardiogenic shock

Some therapies used to treat cardiogenic shock may actually increase myocardial damage. An aggressive approach to monitoring and managment can help to identify correctable contributing events and evaluate therapies currently in use.     

Cardiogenic shock

Cardiogenic shock is a pathophysiologic cascade that often leads to death. Although there has been a dramatic decrease in the cases of cardiogenic shock since the 1970s, the mortality rate of those patients who are diagnosed with cardiogenic shock remains as high as 50% to 80%. As stated throughout the article, cardiogenic shock in its later stages cannot be reversed, but clinical signs and symptoms of the syndrome may be identified early enough to prevent a patient from developing irreversible end-stage cardiogenic shock. As a prehospital care provider, you must be able to ensure the pre-shock patient has adequate oxygenation of the myocardium and can be effectively treated before it is too late.     

Cardiogenic shock.

Mortality rates in patients with cardiogenic shock remain frustratingly high. Its pathophysiology involves a downward spiral in which ischemia causes myocardial dysfunction, which in turn worsens ischemia. Areas of viable but nonfunctional myocardium can contribute to the development of cardiogenic shock. Rapid diagnosis and prompt initiation of supportive therapy to maintain blood pressure and cardiac output, followed by expeditious coronary revascularization, are crucial. The SHOCK multicenter randomized trial has provided important new data that support a strategy of emergent cardiac catheterization and revascularization with angioplasty or coronary surgery when feasible. This strategy can improve survival and represents standard therapy at this time. In hospitals without direct angioplasty capability, stabilization with IABP and thrombolysis followed by transfer to a tertiary care facility may be the best option.     

Left atrial hematoma complicating inferior myocardial infarction.

Intramyocardial dissecting hematoma after myocardial infarction is a rare condition. Previous reports have documented that these hematomas form almost exclusively in the myocardium adjacent to the culprit coronary lesion. We report a case of coexistent intramyocardial dissecting hematoma and ventricular rupture that arose as a consequence of a distal right coronary artery occlusion. Unusually, there was a very long dissection plane, which crossed the atrioventricular groove, with the hematoma manifesting on the opposite side of the heart (left atrium) to the infarcted myocardium (inferior wall).