The active functions of implantable devices can be broadly divided into two categories—arrhythmia termination and primary pacing. Defibrillation is the primary mode for termination of malignant ventricular tachydysrhythmias, although overdrive pacing may be attempted based on the functionality and programming capabilities of the device. Patients with heart failure are at substantial risk for both atrial and ventricular tachydysrhythmias, with subsequent clinical deterioration. The annual incidence of sudden cardiac death (SCD) in the United States is estimated at 0.2 % [5]. In patients with inducible dysrhythmias and chronic heart failure due to ischemia (the highest-risk subgroup), that incidence climbs to more than 30 %. Other high-risk groups include those with a history of cardiac arrest, ventricular tachycardia/ventricular fibrillation (VT/VF) survivors, those with an LV ejection fraction less than 35 %, and heart failure patients [6]. In the latter group, SCD comprises about 50 % of all deaths [7].

Patients with chronic heart failure who have survived VT/VF or SCD are at high risk for recurrence. Regardless of the degree of underlying structural disease (preserved vs. decreased systolic function) or etiology (ischemic vs. nonischemic cardiomyopathy), a CIED is recommended when quality of life and prognosis are such that sudden cardiac death prevention is a desirable goal [8]. It should be noted that such secondary prevention is not indicated in all survivors, i.e., patients with poor short- to intermediate-term prognoses will likely not benefit from CIED implantation as death is likely regardless of dysrhythmia protection.

Primary prevention, in contrast, refers to fatal dysrhythmia prophylaxis when a sustained VT/VF/SCD event has not yet occurred in a patient who is deemed to be at substantial risk. Multiple trials have demonstrated the superiority of CIED over medical therapy for primary prevention of sudden cardiac death in the heart failure population.

This benefit in patients with reduced EF (LVEF <35 %) has been demonstrated in both ischemic cardiomyopathy (MADIT, MADIT II) [9, 10] and nonischemic cardiomyopathy (SCD-HeFT) [11] in patients with symptomatic heart failure (New York Heart Association (NYHA) classes II–III). Therefore, patients with reduced ejection fraction and symptomatic heart failure should be considered for referral, after stabilization and treatment, for consideration of primary CIED placement.

In addition to arrhythmia management, CIED may be programmed to manage the beat-to-beat conduction of the failing heart. Slowed ventricular contraction can exacerbate preexisting cardiomyopathy, resulting in worsening contractile function as well as leading to unfavorable remodeling. The utilization of cardiac resynchronization therapy (CRT) with biventricular pacing is designed to overcome mechanical dyssynchrony by way of controlled synchronous depolarization of both ventricles. This technology has been demonstrated to enhance quality of life, decrease symptoms, and reverse remodeling [12]. The Multicenter InSync Randomized Clinical Evaluation (MIRACLE) trial enrolled 453 subjects with symptomatic heart failure (NYHA III or IV) with ventricular dyssynchrony (QRS ≥130 ms) and impaired systolic function (LVEF ≤35 %) [13]. All subjects received an implantable cardiac device with CRT capacity and were randomized to either 6 months of CRT or no pacing. At 6 months, the CRT group had demonstrated significant improvement in NYHA class, 6-min walk test, and quality of life metrics. In addition, fewer hospitalizations for heart failure were required in the CRT group (83 hospital patient-days vs. 363 hospital patient-days), although mortality was similar between groups.

The Comparison of Medical Therapy, Pacing, and Defibrillation in Heart Failure (COMPANION) trial randomized 1,520 patients with NYHA III or IV heart failure, reduced EF (≤35 %), and dysfunctional electrical conduction (QRS ≥120 ms and PR interval ≥150 ms) to either CRT with defibrillator (CRT-D), CRT alone, or optimal medical therapy [14]. Although the trial was complicated by a higher than the anticipated withdrawal rate from the medical therapy arm, CRT and CRT-D therapies were associated with a significantly decreased rate of the primary composite end point of death or hospitalization. Additionally, the CRT-D group had a significant reduction in all-cause mortality when compared to the optimal medical therapy group.

The benefits of CRT are clearer in patients with milder heart failure (NYHA III) than in patient with severe baseline disease [15]. In addition, CRT has shown little benefit in patients with a narrow QRS complex [16]. It had been suggested that patients with echocardiographic evidence of mechanical dyssynchrony but a narrow QRS complex might benefit from CRT. This hypothesis was tested in the EchoCRT study, which randomized 809 patients with reduced EF, NYHA III or IV heart failure, QRS ≤130 ms, and echocardiographic evidence of mechanical dyssynchrony to sham device or CRT therapy [17]. The trial was stopped early due to an increased rate of death in the CRT group, suggesting that CRT is not helpful and may be harmful in patients with a narrow QRS complex. However, in appropriate patients, multiple clinical trials have consistently demonstrated an improvement in quality of life measures as well as survival [13, 14, 18–22].

It is not our purpose to suggest that the recognition of implantable device indications and specialist referral for such is the standard of care in the ED or short-stay setting. However, the appropriate use of these devices in the evidence-based, guideline-recommended population (i.e., those with a class IA indication) is only about 40–50 % [23]. Even in academic, tertiary centers, standard referral patterns result in missed opportunities to get device-based therapies to at-risk patients; [24] physicians managing heart failure patients in the short-stay setting should be mindful of opportunities and resources that may decrease hospital admission recidivism and improvement in quality of life. Especially in underserved populations, the medical safety net provided by the ED and the subsequent short-stay setting may represent the best opportunity for appropriate referral for postdischarge device therapies.

In order for implantable devices to perform the active functions of defibrillation, cardioversion, or pacing, they must record and interpret the patient’s intrinsic cardiac rhythm data. Different devices store modestly different parameters, although there are some consistent metrics between devices and manufacturers. In addition to devices that record rate, rhythm, and response data, there are an increasing number of devices that collect advanced telemetry data, including physiological information such as heart rate variability, intrathoracic impedance, and patient activity level. Data from both basic and advanced monitoring parameters may be useful during the initial evaluation of the patient as well as to the physician caring for the patient in the short-stay unit.

Atrial fibrillation is the most common dysrhythmia in patients with chronic heart failure; even patients thought to be maintained in sinus rhythm may experience clinically silent paroxysmal atrial fibrillation episodes [25]. New-onset atrial fibrillation may be a worse marker for long-term survival, and many heart failure patients experience worsening symptoms with atrial fibrillation [26]. Conversely, there is an evidence that prolonged volume overload can result in atrial tachydysrhythmias, perhaps as a result of electrical instability due to atrial distension [27]. Discovery of atrial fibrillation as a precipitating event could lead to the consideration of several different medical management options that would not have been immediately apparent choices in the absence of such knowledge, such as initiating rate or rhythm controlling pharmacologic agents, starting long-term anticoagulation for stroke prophylaxis, or changing pacemaker programming parameters.

There is an intrinsic variability in the heart rate of healthy individuals due to both changes in physiologic demand and other diurnal patterns. As physiologic stress increases, this variance decreases due to an increase in sympathetic tone and an attenuation of the parasympathetic nervous system [28]. Implantable cardiac devices that monitor atrial depolarization can record atrial rates and calculate the variability in the intrinsic sinoatrial node function. The association between heart rate variability and heart failure exacerbation was established in a secondary analysis of MIRACLE [13]. Those patients randomized to active CRT functionality experienced a substantial improvement in heart rate variability, regardless of the use of beta-blocker therapy, which was associated with the improvement in multiple echocardiographic indices of cardiac function [29].

Heart rate variability has also been linked as an independent predictor of outcomes, as opposed to a marker of response to therapy. In a prospective observational cohort study of 288 patients receiving a CRT device for NYHA III or IV heart failure coupled with systolic dysfunction (LVEF ≤35 %), heart rate variability was significantly lower in patients experiencing hospitalization or death [30]. The decrease in heart rate variability was notable at a median 16 days prior to hospitalization.

Unfortunately, a decrease in heart rate variability is not specific to acute heart failure. Other illnesses and comorbidities that manifest with a ramping up of sympathetic tone also present with a decrease in heart rate variability, such as seen in exacerbation of chronic obstructive pulmonary disease or various infectious states [31, 32].

Accelerometers within the implanted device can provide a measurement of hours per day that the patient is moving and presumably physically active, although the actual degree of exertion is not captured with this measurement. As patients become more and more symptomatic with heart failure, exercise intolerance worsens and physical activity decreases [30]. Conversely, a study of patients receiving CRT pacing demonstrated that an increase in daily activity levels corresponded to improvements in NYHA class and exercise tolerance [33]. Patient activity levels have been shown to be less sensitive than decreased heart rate variability in predicting decompensation in the outpatient setting [30], although decreased physical activity levels have been shown to be predictive of subsequent heart failure decompensation within 30 days, when monitored in concert with other CIED monitoring parameters [34].

The measurement of intrathoracic impedance utilizes changes in electrical conduction within the cardiopulmonary structures of the chest to gauge fluid overload. As the total amount of tissue fluid increases, resistance (also known as impedance) to conduction of an electrical impulse between a pulse generator (pacemaker lead) and a sensor (generally the device canister) decreases. Therefore, a low impedance reading is a marker of pulmonic fluid congestion, correlates with wedge pressures and negative fluid balance during hospitalization, and begins to drop several days prior to the overt need for hospitalization [35]. Intrathoracic impedance has been evaluated as a predictor of heart failure decompensation in the outpatient arena in a number of studies [34, 36–39]. For example, in the FAST study [36], intrathoracic impedance monitoring was substantially more sensitive for heart failure decompensation than daily weight monitoring (76 % vs. 23 %) and had fewer false positives (1.9 vs. 4.3 events per patient-year). Unfortunately to date, no prospective studies have been able to successfully use impedance monitoring in the outpatient setting to avoid hospitalizations for acute heart failure.

Of potentially more impact within the acute care setting, Small et al. have demonstrated, in a retrospective analysis of registry data derived from patients with CRT-based intrathoracic impedance monitoring, a low likelihood of hospitalization due to acute heart failure in subjects whose fluid index did not cross the set threshold (0.14 hospitalizations/patient-years vs. 0.76 hospitalizations/patient-years in those patients with multiple threshold crossing events) [40]. It may be that in the absence of decreased impedance, a dyspneic patient being evaluated in the acute setting has an etiology other than acute heart failure due to volume overload for their presenting symptoms.

At the time of this writing, several implantable cardiac devices that directly monitor hemodynamic status are undergoing investigation. The CardioMEMS Heart Failure Sensor (CardioMEMS, Atlanta, Georgia) utilizes a pressure transducer implanted in the pulmonary artery to transmit data wirelessly to a handheld recorder [41]. In the CHAMPION study, a 550-subject prospective randomized trial of protocol-driven modulation of therapy based on daily pulmonary artery pressure readings, heart failure hospitalizations were reduced by 37 % compared to the standard care control group [42]. This was achieved by significantly more frequent dose escalations of both diuretics and vasodilators without an increase in renal failure when compared to the control group [43].

The HeartPOD system (St. Jude Medical, Minneapolis, MN) utilized a wired pressure transducer in the left atrium to record cardiac data [44]. The Hemodynamically Guided Home Self-Therapy in Severe Heart Failure Patients (HOMEOSTASIS) trial evaluated the feasibility of providing this data directly to the patient with recommended changes in medication therapy (diuretics or vasodilators) based on algorithms preprogrammed by the physician [45]. The lack of a control group limited the conclusions that can be drawn from this small study; however, this study led to a controlled trial of patient-facilitated management with the HeartPOD. That study, the Left Atrial Pressure Monitoring to Optimize Heart Failure Therapy (LAPTOP-HF) trial (ClinicalTrials.gov Identifier NCT01121107) [46], was stopped early by the DSMB due to statistical futility of proving the primary end point when compared against the patient risk with device implantation.