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Attempting a careful evaluation of the incidence of sudden death (SD) in congestive heart failure is inevitably a complex and imprecise task. In particular, this is due to the difficulties in defining and understanding the baseline mechanisms underlying SD. “Sudden” death is commonly regarded as a synonym of “cardiac arrest due to ventricular fibrillation,” which is in turn considered to be a merely arrhythmic phenomenon occurring during apparent wellbeing, and without any precipitating cause other than an extrasystole or a sustained ventricular tachycardia. Cardiac arrest may also be the terminal event during refractory pulmonary edema and/or cardiogenic shock in a patient with end-stage heart failure, a pulmonary embolism in a patient with severe biventricular dysfunction, bradyarrhythmia due to advanced atrioventricular (AV) block, electrical asystole, ventricular fibrillation secondary to myocardial ischemia or infarction, or secondary to a noncardiac event such as a cerebro vascular accident or a ruptured aortic aneurysm. Pratt et al.[ 1 ] analyzed a population of 834 patients with an automatic implantable cardioverter defibrillator (ICD) implanted for ventricular tachycardia or sustained ventricular tachycardia. During follow-up 109 patients died (17 died “suddenly”). Autopsy findings revealed a nonarrhythmic cause (pulmonary embolism, ruptured aortic aneurysm, stroke, acute myocardial infarction) in 7/17 patients. Postmortem analysis of the ICD memory revealed ventricular tachyarrhythmias preceding death in only 7/17 patients.

In the United States there are 4.9 million people with heart failure, 50% of whom will be dead within 5 years. There are also over 400 000 new cases reported annually [ 1 ], with approximately 43 000 deaths. The number of hospital admissions resulting from heart failure approaches 900 000 per annum and represents 20% of all admissions of patients over 65 years of age. Over the past four decades, the number of deaths caused by heart failure has increased from 10 in 1000 to 50 in 1000 [ 2 ].

Cardiovascular complications of anesthesia and surgery remain, unfortunately, very frequent. In the USA, Mangano and Goldman concluded that approximately 27 million anesthetics were given every year, including 8 million to patients with coronary artery disease. They estimated the number of cardiovascular complications to be approximately 1 million per annum, including 500 000 postoperative myocardial infarctions [ 1 ]. This represents one cardiovascular complication for every 27 anesthetics. The complications considered in this context include myocardial infarction, unstable angina, life-threatening arrhythmias, and acute left ventricular failure.

As persons age, their life styles change, and they become more affluent and obese. If this trend continues, the incidence of associated hypertension (HTN) will continue to increase worldwide [ 1 ]. At the same time, despite widely recognized dangers of uncontrolled HTN, it is still under-treated in most patients. Such inadequate HTN control is seen not only in closely followed populations, but also in closely monitored anti-HTN drug trials [ 1 ]. Moreover, cardiovascular risk remains high in the majority of people with HTN, whether they are treated or not.

Diabetes mellitus is a common disease. The worldwide prevalence of diabetes- especially of the predominant type 2 diabetes mellitus which accounts for about 90% of the adult diabetic population-has increased rapidly and continuously during the last several decades. This phenomenon is a direct consequence of negative lifestyle changes in the population, including a reduction of physical activity and the availability of energydense food rich in saturated fat, leading to an increased prevalence of obesity. The global prevalence of diabetes mellitus in adults is predicted to increase to 5.4% in the year 2025 [ 1 ].

Four basic classes of circulatory shock can be clinically defined: hypovolemic, cardiogenic, obstructive, and distributive. Looking at the physiology of cardiac performance, taking a pathophysiologic approach we can distinguish between hypovolemic shock, distributive shock, systolic cardiogenic shock, diastolic cardiogenic shock, or a mix of them. All these types evolve, if not treated early and adequately, towards end-organ failure (dysoxia, microcirculatory failure). Multi-organ dysfunction syndrome (MODS) accounts for most deaths in the intensive care unit (ICU). Disturbances in systemic hemodynamics and organ perfusion resulting in tissue hypoxia appear to play a key role in the onset and maintenance of MODS.

Cardiovascular events are considered the main cause of death in the perioperative period. The most important events are acute myocardial infarction (MI), unstable angina, cardiac failure, severe arrhythmias, nonfatal cardiac arrest, and death. Patients experiencing an MI after noncardiac surgery have a hospital mortality rate of 15–25% [ 1 , 2 ], and nonfatal perioperative MI is an independent risk factor for cardiovascular death and nonfatal MI during the 6 months following surgery. Patients who have a cardiac arrest after noncardiac surgery have a hospital mortality rate of 65%, and nonfatal perioperative cardiac arrest is a risk factor for cardiac death during the 5 years following surgery [ 3 , 4 ]. The objectives of preoperative evaluation are: (a) performing an evaluation of the patient’s current medical status; (b) making recommendations concerning the evaluation, management, and risk of cardiac problems over the entire perioperative period; and (c) providing a clinical risk profile that the patient, primary physician, anesthesiologist, and surgeon can use in making treatment decisions that may influence short- and long-term outcomes. No test should be performed unless it is likely to influence patient treatment [ 5 ]. The cost of risk stratification cannot be ignored. Accurate estimation of a patient’s risk for postoperative cardiac events (MI, unstable angina, ventricular tachycardia, pulmonary edema, and death) after surgery can guide allocation of clinical resources, use of preventive therapies, and priorities for future research.

Acute heart failure has been defined simply as “the rapid onset of symptoms and signs secondary to abnormal cardiac function” [ 1 ]. Acute heart failure can present de novo with no prior history of heart disease (although asymptomatic cardiac disease may well have been present), or on a background of decompensated chronic cardiac failure. Acute heart failure is, therefore, a syndrome with varying etiologies and ranging in severity from relatively mild dyspnea, through severe pulmonary edema with acute respiratory distress, to full-blown cardiogenic shock, where tissue perfusion is compromised. Whatever the etiology, the result is an inability of the heart to maintain cardiac output, and hence oxygen supply, sufficient to meet the needs of the peripheral tissues.

While this chapter addresses the electrocardiographic (ECG) features of heart failure (HF) and physiologically significant arrhythmias in patients with HF, neither ECG findings nor specific arrhythmias establish the diagnosis of HF, regardless of its origin. The diagnosis of HF is established by the patient’s symptoms and physical signs, along with confirmatory evidence of mechanical heart dysfunction (e.g., by echocardiography or cardiac catheterization). HF can be due to systolic and/or diastolic dysfunction affecting one or both ventricles. Regardless of which, because of ventricular interdependence, HF ultimately leads to compromise of both systemic and pulmonary hemodynamics. Unchecked, the end result is multiorgan system failure and death, whether HF results from congenital or acquired heart disease. This chapter highlights the ECG features of HF and arrhythmias in patients with HF.

With an aging population and improved therapeutic strategies in patients with coronary artery disease, hypertension, and diabetes mellitus, the prevalence of patients with chronically impaired myocardial performance is constantly increasing [ 1 ]. As a consequence, physicians are also frequently faced with the diagnosis and treatment of a rapid onset of symptoms and signs secondary to abnormal cardiac function. This clinical syndrome of acute heart failure (AHF) in general requires rapid diagnosis and is associated with challenging treatment and a high mortality. Unfortunately, steady improvements in the care of these patients have not been able to change the fact that heart failure is still a major cause of death in the intensive medicine setting. Because of the urgency and challenge of treatment, the number of randomized controlled clinical trials that include these patients is currently low, and therefore empirical rather than evidence-based therapeutic approaches dominate. In 2005, the European Society of Cardiology and the European Society of Intensive Care Medicine published guidelines on the diagnosis and treatment of AHF [ 2 ], in which clinical trials are reviewed and treatment algorithms are proposed. In this chapter the recommendations for diagnosis and treatment are summarized and new publications incorporated.