Understanding Cardiogenic Shock

This article refers to ‘Clinical picture and risk prediction of short-term mortality in cardiogenic shock’† by Veli-Pekka Harjola et al., published in this issue, European Journal of Heart Failure (2015); 17: 501–509. Cardiogenic shock is the most severe form of acute heart failure.1 It is defined as pump failure despite adequate preload, leading to tissue hypoxia and organ dysfunction. In particular, low mixed venous oxygen saturations and elevated lactate levels are surrogates for tissue hypoxia, while encephalopathy and low urine output indicate organ dysfunction. Using this definition, Harjola and co-workers identified 220 patients with cardiogenic shock in a multicentre observational study.2 Coronary artery disease was the most common underlying cardiac disease, and myocardial ischaemia was the most important trigger for decompensation. In-hospital survival of 63% was better than in other registries, in which mortality was greater than 50%.3 The authors created the CardShock risk score including information on patient characteristics (age), underlying cardiac disease (coronary artery disease), trigger for decompensation (myocardial ischaemia), cardiac function (left ventricular ejection fraction), surrogates of tissue hypoxia (elevated lactate levels), and evidence of organ dysfunction (encephalopathy, renal dysfunction). Not surprisingly, mortality increased with a higher score. Potentially, the CardShock risk score will allow better patient selection for particular therapies, for example early admission to an intensive care unit. It will also help to better characterize patients in future studies on cardiogenic shock. There is one aspect of this study that I would like to highlight, as I think it is of great clinical relevance. Twenty-four per cent of the study patients had shock at presentation to the hospital, whereas 76% developed shock after hospital admission. This information is in line with results from the Swiss AMIS plus registry, in which 72% of patients with acute coronary syndromes complicated by cardiogenic shock developed their haemodynamic instability after hospital admission.4 While shock might evolve from a worsening cardiac disease such as ongoing myocardial ischaemia, haemodynamic deterioration will develop, at least in some patients with acute heart failure, because of inappropriate medical treatment. Tables 1 and 2 list drugs commonly used and interventions frequently performed in patients with acute heart failure, which can potentially contribute to the shock state and promote organ dysfunction. I can recall several patients who rapidly improved from ‘cardiogenic shock’ with fluid administration, as shock was a consequence of insufficient preload resulting from the excessive use of diuretics. Pre-renal kidney dysfunction Arrhythmia (e.g. atrial fibrillation) So, how to best manage patients with cardiogenic shock? First, the underlying cardiac disease and the trigger for decompensation must be identified, as understanding the pathophysiology at play is crucial for the correct treatment. In particular, reversible causes of heart failure must be looked for and treated adequately, which in many circumstances will require prompt interventions (e.g. balloon angioplasty in acute myocardial ischaemia resulting from coronary artery disease) or emergency cardiac surgery (e.g. mitral valve replacement in acute mitral regurgitation caused by papillary muscle rupture). Patients with a treatable underlying disease causing cardiogenic shock usually have a better prognosis than patients without.5 Second, cardiogenic shock must be reversed within hours, which includes optimization of cardiac preload and afterload, control of heart rate and the use of inotropes to increase contractility. While the condition is reversible in the early phase with adequate treatment, prolonged cardiogenic shock will cause multiple organ failure and eventually death (Figure 1). Hence, if cardiogenic shock cannot be reversed with the measures mentioned above, mechanical extracorporeal life support (ECLS) should be evaluated before irreversible organ damage has established.6 The ECLS treatment will buy some time for decision-making. In some patients care will have to be redirected to palliation because of futility of further treatment. In others, ECLS will bridge to recovery (e.g. acute myocarditis) or bridge to other types of assist devices and/or heart transplantation.7 Third, failing organs (kidneys, lungs) must be supported by intensive care with the caveat of first doing no harm.8 As soon as the patient can be stabilized, early rehabilitation must be started. The patient should be enrolled in a specialized heart failure follow-up programme, offering the full spectrum of pharmacological and non-pharmacological treatment options. In summary, a multi-disciplinary (cardiologists, intensivists, cardiac surgeons, and many more) and multi-professional (doctors, nurses, physiotherapists, and many others) approach is necessary to save the lives of critically ill patients with cardiogenic shock.