Acute heart failure (AHF) encompasses a wide range of clinical presentations, from acute hypertensive heart failure (HF) to low cardiac output hypoperfusion syndromes with cardiogenic shock at the extreme end of this side. Inotropes are pharmacologic agents that enhance cardiac contractility, thereby augmenting cardiac output. Currently, there are three classes of inotropes available in clinical practice with distinct mechanisms of action: beta-adrenergic agonists, phosphodiesterase III inhibitors, and the calcium-sensitizer levosimendan. Inotropes are indicated as short-term therapy in low cardiac output AHF and cardiogenic shock (usually with coadministration of a vasoconstrictor) to increase cardiac output, restore peripheral perfusion, and prevent end-organ dysfunction. Inotropes can cause serious cardiovascular adverse effects, most commonly tachyarrhythmias and myocardial ischemia and are associated with increased medium- and long-term mortality in HF. Therefore, intense monitoring is necessary during their administration, while long-term infusion is contraindicated with the exception of advanced HF patients in whom inotropes may be used as a bridge to a definitive therapy (transplantation or ventricular assist device implantation) or as palliative treatment. Emerging inotropes acting through novel pathways independent of those targeted by conventional agents may overcome safety limitations of currently available agents.
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Liver involvement in chronic heart failure has long been recognized and reflects the systemic hemodynamic changes that occur during the evolution of heart failure syndrome. Apart from venous congestion and backward failure, other fundamental mechanisms also exist such as decreased hepatic blood flow, decreased arterial saturation, and sinusoidal thrombosis. In the acute setting, the decrease in cardiac output, accompanied by severe and profound hypotension is the main cause of acute liver injury, whereas increased venous pressure also plays an important role. The biochemical dominance of a cholestatic profile is rather related to congestion and increased systemic venous pressures, whereas the hepatotoxic profile is rather related to hypoperfusion.
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Acute heart failure (AHF) is defined as the rapid development or change in symptoms and signs of heart failure that requires urgent medical attention and usually hospitalization. AHF is the first reason for hospital admission in individuals aged 65 or more. Despite therapeutic advances, it remains a syndrome with particularly ominous prognosis, with an in-hospital mortality rate of 4–7%, a 2- to 3-month postdischarge mortality of 7–11% and a 2- to 3-month readmission rate of 25–30%. In addition, AHF is the single most important determinant of the huge healthcare expenditure related to heart failure, as it accounts for nearly 70% of the total heart failure-related cost.
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Acute heart failure (AHF) in the elderly is becoming an increasingly common clinical problem, associated with very high in-hospital and long-term mortality rates. Elderly AHF patients, as opposed to younger ones, may have a different demographic, pathophysiological, clinical, and prognostic profile, and therefore, some carefully considered therapeutic adjustments may be warranted for their treatment. Patients with older age, shock, diabetes, renal failure, infection, confusion, and severe non-cardiac comorbidities may be at the highest mortality risk.
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Acute heart failure (AHF) represents a potentially fatal disease that needs immediate hospital care. In-hospital management can be divided into three consecutive phases: an early phase of intensive management of symptoms, an intermediate phase of stabilization and transition from intravenous to oral medication, and a late phase of discharge and outpatient management. However, despite its life-threatening features (increased mortality and readmission rates), many treatment decisions are opinion based and only few are evidence based. The present paper describes in-hospital treating modalities and attempts to provide clinical and laboratory criteria for patient evaluation that will help doctors determine readiness and safety of discharge. In addition, it highlights some unresolved issues that need to be addressed by future research.
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Cardiogenic shock (CS) is the most severe form of acute heart failure, characterized by low cardiac output, hypotension, and systemic hypoperfusion. CS is the leading cause of death in acute coronary syndrome (ACS) that accounts for about 80% of CS cases. In addition to acute cardiac cause, the diagnostic criteria for CS include persistent hypotension (systolic blood pressure < 90 mmHg) and clinical signs of hypoperfusion. Mortality rates in CS remain as high as 35–50%. Severe left ventricular dysfunction usually triggers the shock and leads to the activation of systemic inflammatory response and hypothalamic-pituitary-adrenal axis. Immediately after detection of the shock, electrocardiography and echocardiography should be performed to determine the etiology of CS and to rule out mechanical complications. Urgent revascularization by percutaneous coronary intervention, or less often by coronary artery bypass graft, is the most important treatment in CS caused by ACS. In the case of mechanical complication, immediate surgical treatment is essential. Regardless of the etiology, the basic treatment strategy includes fluid challenge that aims at obtaining euvolemia and relieving tissue hypoperfusion. Inotropes and vasopressors are often needed to improve cardiac performance and to maintain sufficient blood pressure. Ventilation is often supported mechanically and CS patients are best treated in intensive cardiac care unit. Continuous invasive blood pressure monitoring, electrocardiography, and repeated echocardiography are required. In CS refractory to other treatments, mechanical circulatory support may be considered to maintain adequate perfusion pressure and to prevent multiorgan failure.
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There is a relationship between patients with chronic kidney disease and coronary artery disease. These two entities share both common etiologies and risk factors. Management of different patients with coronary artery disease in the aspect of renal insufficiency and certain medications such as contrast media is thus of high importance. Treatment nihilism is a major problem though and healthcare providers must make efforts to maintain a stable kidney function in all coronary artery disease patients.
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Cardiovascular magnetic resonance imaging (CMR) offers a broader assessment of cardiac structure and function than any other single imaging modality. In patients with known or suspected ischemic heart disease (IHD), a comprehensive CMR protocol provides an assessment of left ventricular function, myocardial perfusion, edema, and viability in a single sitting. There are applications for this technology in both the acute and chronic IHD settings. CMR is also a valuable tool in the assessment of patients presenting with chest pain, raised troponin levels, and unobstructed coronaries.
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