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Acute heart failure and cardiogenic shock


Cardiovascular disease accounts for one quarter of all deaths, and once cancer mortality is excluded, cardiac disease alone accounts for more deaths than all other causes put together. Heart failure (defined as the inability of the heart to pump enough blood to meet the demands of the body) is common, being the primary cause of hospital admission in >1million patients per year in the USA, with 25% readmitted within 1 month, and a 10-20% mortality at 6 months after discharge. In newly diagnosed patients there is a >20% mortality at one year, rising to 50% at two years and >66% at ten years – proving as malignant as many common cancers. The underlying causes include coronary artery disease, hypertension, valve dysfunction, cardiomyopathies (inherited and acquired), congenital heart disease, arrhythmia, toxins (either ‘recreational’ – cocaine and alcohol, or therapeutic – some chemotherapeutic agents), pulmonary embolism and sepsis. Acute heart failure (AHF) may be a new diagnosis in patients with no history of cardiac disease, or occur as a result of acute decompensation in patients with known heart failure. It is the leading cause of hospital admission in people >65 years in the UK. European-wide, approximately 50% of these patients will be readmitted within 12 months, and 30% deceased at the 1-year follow-up.

Key words: cardiogenic shock, heart failure, mechanical circulatory support


AHF is variably defined as the rapid onset/acute worsening of symptoms and signs of heart failure, associated with elevated plasma levels of natriuretic peptides. However, significant diagnostic uncertainty occurs when relying only on clinical findings, and currently a lack of specificity exists in routine investigations for this range of conditions. It is a syndrome rather than a diagnosis per se, caused by a wide array of pathologies, manifesting as a spectrum of disease severity, ranging from dyspnea to cardiogenic shock (CS) or cardiac arrest. At the extreme end of the spectrum, CS reflects the multisystem inflammatory response to profound heart failure. It is highly lethal, and initiation of treatment of the underlying cause as soon as possible (including in the prehospital setting) is potentially beneficial in improving outcomes – the concept of minimizing the ‘time to appropriate therapy’. Although patients may present with a suggestive history, clinical features such as shock (itself variably defined), and pulmonary or peripheral congestion, and/or symptoms related to the underlying cause, these are frequently absent. This diagnostic uncertainty leads to a missed diagnosis in up to 20% of patients. Current guidelines recommend that in AHF and CS, clinical examination and investigations should be integrated to form the diagnosis, including the use of ECG, chest X-ray, urgent echocardiography and biomarkers (natriuretic peptides, troponin and D-dimer) according to the clinical history.


Despite numerous clinical trials to assess optimal treatment and management strategies for patients with CS, little improvement has been made in AHF outcomes in the last 30 years, with management decisions based largely on expert consensus rather than robust evidence. Pivotal to success in management is reversal of the underlying cause of cardiac dysfunction, including urgent revascularisation of the culprit vessel in patients with coronary artery disease and acute myocardial infarction. Treatment of the underlying cause in other aetiologies remains less well evidence-based, however, urgent reversal of associated arrhythmias (tachy- or brady) is included in many resuscitation algorithms. Acute myocarditis may respond to targeted immunotherapy, and in patients with peripartum cardiomyopathy, bromocriptine is included in current guidelines as a potential targeted therapy. In patients with severe valvular disease the emergence of transcatheter interventions (TAVI for critical aortic stenosis, mitraclip for severe mitral regurgitation) may appear to offer lower risk options than conventional surgery in CS patients, however, this is not supported by evidence nor recommended in current valvular heart disease guidelines.

Supportive therapies

Circulatory and respiratory support are frequently required whilst addressing the underlying cause of AHF/CS. This includes pharmacological and mechanical circulatory strategies, as well as standard ventilator support. Inotropic agents are pluripotent molecules that have a range of different biological activities, including increasing myocardial contractility. They affect heart rate, pulmonary and peripheral vasculature, myocardial oxygen consumption, inflammatory cytokines and reactive oxygen species in different ways. To date, none has been shown to improve clinical outcomes in AHF/CS, with concern that some may increase mortality. Current recommendations are that they should be used in the lowest dose, for the shortest possible time. Recent trials in AHF have proven disappointing, all either neutral or demonstrating evidence of cardiac damage (associated troponin rise), and with >210 AHF trials ongoing, the future of randomized controlled trials in AHF/CS is currently being questioned.

Mechanical circulatory support

The IABP has been used to provide left ventricular support for decades, however results of the IABP shock II study mean it is no longer recommended for routine use in patients with myocardial infarction complicated by cardiogenic shock (in the absence of a mechanical complication). Other percutaneous mechanical circulatory support (pMCS) devices provide superior circulatory support when compared with IABP, but to date none has been shown to improve outcomes in high quality studies. Nonetheless, given the significant mortality associated with CS and the lack of demonstrable benefit with alternative forms of support, there has been a significant increase in the use of pMCS in CS. Current recommendations are that in AHF/CS patients who are INTERMACS I (declining despite standard therapies) short-term pMCS may be used to support patients with left or biventricular failure until cardiac and other organ function has recovered. Here the Survival After Veno-arterial ECMO (SAVE) score can be used to help predict survival from cardiogenic shock. Recommendations also include that pMCS (particularly ECMO) can be used as a ‘bridge to decision’ in patients with acute/rapidly deteriorating AHF/CS to stabilize haemodynamics, recover end-organ function and allow for full evaluation regarding the possibility of either a more durable MCS device or heart transplantation. The emergence of pMCS for the right heart (either Impella RP or Protek Duo) provides a promising potential new therapeutic option for patients with severe acute cor pulmonale, but to date there have been only small non-randomised studies addressing their utility. However, given the very high mortality associated with severe, acute RV failure, and their relative ease of use, they may provide an additional option, avoiding the need for systemic cannulation associated with VA-ECMO.


The burden of AHF/CS is substantial, both to individual patients and to society. Despite advances in cardiology, the mortality remains high with reliance on ‘traditional’ critical care supportive techniques. The intuitive attractiveness of early initiation of mechanical support must be balanced by recognition of their high complication rate, the lack of evidence of benefit, and that the key priority must remain to reverse any potentially treatable pathology in patients with AHF before CS supervenes.


Corresponding author:
Susanna Price
Royal Brompton & Harefield NHS Foundation Trust
Royal Brompton Hospital
Sydney Street, London SW3 6NP
United Kingdom
Phone: +44 2073528121 ext: 2611
E-mail: S.Price@rbht.nhs.uk 

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