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Cardiac rhythm management devices (CRMD) have evolved significantly since the late 1950s, when the first pacemakers (PM) were implanted [ 1 ]. However, transcutaneous electrical cardiac stimulation was used to treat symptomatic advanced second-degree or third-degree atrioventricular (AV) heart block (Stokes-Adams attacks) in the 1920s [ 1 , 2 ]. The first implantable devices were asynchronous ventricular PM (VOO^1) for patients with Stokes-Adams attacks, and then evolved into dual-chamber PMs (DDD) to preserve AV synchrony [ 1 – 4 ].^2 Next, intracardiac sensing was added to avoid competition between paced and intrinsic rhythms in patients with intermittent symptomatic bradycardia due to AV heart block or sinus node dysfunction. The response to sensed events (first ventricular-VVI; then, atrial or dual-chamber sensing-VAT,VDD, DVI, DDD) could be inhibition or the triggering of ventricular pacing stimuli. The next important evolution was adaptive rate pacing (ARP) in the 1980s, whereby a physiologic sensor detected the need for increased paced heart rates with exercise. Physiologic responses that have been investigated and are or might be used clinically in ARP are listed in Table 1.

Cardiac arrest is a dramatic clinical event that can occur suddenly, often without premonitory signs. The condition is characterized by sudden loss of consciousness due to the lack of cerebral blood flow, which occurs when the heart ceases to pump. This phenomenon is potentially reversible if cardiopulmonary resuscitation (CPR) procedures are started early, but it becomes irreversible without interventions or when initiation of CPR is delayed [ 1 ].

Circulatory shock is the clinical picture associated with generalized, acute circulatory insufficiency, which is a frequent complication of many pathological states as diverse as severe sepsis, extensive myocardial infarction, polytrauma, or massive pulmonary embolism. Whatever the cause of the shock, cells no longer possess enough oxygen to function optimally, and this condition is associated with high mortality rates. Even in patients who survive the acute episode of shock, protracted cellular damage frequently results in organ dysfunction. Prompt recognition of shock is essential to enable appropriate therapy to be instituted rapidly and tissue damage limited.

Surgery is analogous to an extreme stress test. It initiates inflammatory, hypercoagulable, stress, and hypoxic states, which may be associated with elevations in troponin levels leading to postoperative myocardial dysfunction and failure [ 1 ]. Cardiac surgery, especially, is associated with the inherent risk of myocardial ischemia and myocardial infarction; and consequently, with postoperative heart failure. The degree of permanent postoperative myocardial injury is determined by the severity and duration of ischemia. A progressive pattern of myocardial dysfunction-apart from ongoing ischemia-suggests that additional underlying mechanisms, which are at least partially different from those of myocardial stunning, may also exist [ 2 ].

Systemic hypertension is a very frequent condition in developed countries and therefore constitutes a common problem in the perioperative period. In the Unites States nearly 29% of adults in 1999 and 2000 were affected by hypertension (age-adjusted prevalence of hypertension): 30% of hypertensive individuals are not aware of their diagnosis, 59% are being treated for hypertension, and only 34% have a blood pressure below 140/90 mmHg [ 1 , 2 ].

Dilated cardiomyopathy (DCM) is heart muscle disease characterized by left ventricular or biventricular dilatation and impaired myocardial contractility [ 1 ]. It is an important cause of morbidity and mortality, and is one of the two most frequent indications for cardiac transplantation. The prevalence of DCM in the United States has been estimated at around 0.04% [ 2 ], with an annual incidence of 0.005–0.006% [ 2 , 3 ].