Reduced Atrial Tachyarrhythmia Susceptibility After Upgrade of Conventional Implanted Pulse Generator to Cardiac Resynchronization Therapy in Patients with Heart Failure

OBJECTIVES: We sought to identify the impact of cardiac resynchronization therapy (CRT) on atrial tachyarrhythmia (AT) susceptibility in patients with left ventricular (LV) systolic dysfunction in whom worsening heart failure (HF) resulted in upgrade from conventional dual-chamber pulse generator to cardiac resynchronization therapy-defibrillator (CRT-D). BACKGROUND: Cardiac resynchronization therapy with a defibrillator improves survival rates and symptoms in patients with LV systolic dysfunction but little is known about its effects on AT incidence in the same patient population. METHODS: Twenty-eight consecutive HF patients who underwent device upgrade to CRT-D were included. Patients had \u3e or =2 device interrogations in the 1 year before upgrade and \u3e or =3 interrogations in the 18- to 24-month follow-up after upgrade. Echocardiographic parameters were assessed before and at 3 to 6 months after CRT-D. Additional observations included number of hospital stays, HF clinical status, and concomitant pharmacological therapy. By virtue of this study design, each patient served as his/her own control. Statistical analysis was performed by 2-tailed paired t test and with nonparametric tests where appropriate. RESULTS: Within 3 months after CRT, the number of HF patients with documented AT decreased significantly from the immediate pre-CRT value and tended to decline with time. At 1-year follow-up, 90% of patients were AT-free compared with 14% of patients 3 months before CRT (p \u3c 0.001). Furthermore, the number of AT episodes/year and their maximum duration decreased after CRT (mean +/- SD; 181 +/- 50 vs. 50 +/- 20.2, p \u3c 0.05, and 220.8 +/- 87 s vs. 28 +/- 21 s, p \u3c 0.05, respectively). Finally, CRT was associated with improved LV ejection fraction (mean +/- SD; from 26 +/- 5.3% to 31 +/- 7%, p \u3c 0.001) and reduced number of HF or arrhythmia hospital stays (p \u3c 0.05). CONCLUSIONS: Our findings support the view that CRT might decrease AT susceptibility in HF patients with LV systolic dysfunctio

Relationship of Paroxysmal Atrial Tachyarrhythmias to Volume Overload

BACKGROUND: Clinical experience suggests that atrial tachyarrhythmias (ATs) are a frequent comorbidity in heart failure patients with left ventricular systolic dysfunction and that volume overload may increase AT susceptibility. However, substantiating this apparent relationship in free-living patients is difficult. Recently, certain implantable cardioverter-defibrillators provide, by measuring transpulmonary electric bioimpedance, an index of intrathoracic fluid status (OptiVol index [OI]). The goal of this study was to determine whether periods of greater intrathoracic fluid congestion (as detected by OI) correspond with increased AT event frequency. METHODS AND RESULTS: This analysis retrospectively assessed the relation between AT events and OI estimate of volume overload in patients with left ventricular systolic dysfunction and OI-capable implantable cardioverter-defibrillators. OI values were stratified into 3 levels: group 1, \u3c40; group 2, 40 to 60; and group 3, \u3e60. An OI threshold-crossing event was defined as OI \u3e or = 60, a value previously associated with clinically significant volume overload. Findings in 59 patients (mean left ventricular ejection fraction, 24%) with 225 follow-up visits (mean, 3.8 visits per patient) were evaluated. AT prevalence was 73%. AT frequency (percent of patients visits with at least 1 episode of AT since previous device interrogation) was greater in group 3 versus group 1 (P=0.0342). Finally, in terms of temporal sequence, AT episodes preceded OI threshold-crossing event in 43% of incidences, followed threshold-crossing event in 29%, and was simultaneous or indeterminate in the remainder. CONCLUSIONS: These findings not only support the view that worsening pulmonary congestion is associated with increased AT frequency in patients with left ventricular dysfunction but also suggest that AT events may be responsible for triggering episodic pulmonary congestion more often than previously suspected

Cardiorespiratory interactions and blood flow generation during cardiac arrest and other states of low blood flow. Curr Opin Crit Care 9

Purpose of review Recent advances in cardiopulmonary resuscitation have shed light on the importance of cardiorespiratory interactions during shock and cardiac arrest. This review focuses on recently published studies that evaluate factors that determine preload during chest compression, methods that can augment preload, and the detrimental effects of hyperventilation and interrupting chest compressions. Recent findings Refilling of the ventricles, so-called ventricular preload, is diminished during cardiovascular collapse and resuscitation from cardiac arrest. In light of the potential detrimental effects and challenges of large-volume fluid resuscitations, other methods have increasing importance. During cardiac arrest, active decompression of the chest and impedance of inspiratory airflow during the recoil of the chest work by increasing negative intrathoracic pressure and, hence, increase refilling of the ventricles and increase cardiac preload, with improvement in survival. Conversely, increased frequency of ventilation has detrimental effects on coronary perfusion pressure and survival rates in cardiac arrest and severe shock. Prolonged interruption of chest compressions for delivering single-rescuer ventilation or analyzing rhythm before shock delivery is associated with decreased survival rate. Summary Cardiorespiratory interactions are of profound importance in states of cardiovascular collapse in which increased negative intrathoracic pressure during decompression of the chest has a favorable effect and increased intrathoracic pressure with ventilation has a detrimental effect on survival rate. (CPR). Despite this long history, our understanding of how chest compressions during cardiac arrest generate forward blood flow remains incomplete and divided into two schools of thought: the cardiac pump theory and the thoracic pump theory. Initially, the cardiac pump theory predominated. It was thought that pressing the heart between the sternum and spine generated the force to propel the blood from the ventricles to the lungs and systemic circulation, whereas recoiling of the chest promoted flow into the ventricles. It was not until 1976, when Criley et al. [3] described "cough resuscitation," that the theory of a thoracic pump mechanism emerged. Based on the thoracic pump theory, the heart was thought to function more as a passive conduit, while during each chest compression, transmission of blood from the lungs to the systemic circulation occurred because of increased pressure in the intrathoracic arteries. The work of Weisfeldt and Halperin [4] further supported this hypothesis. Echocardiographic observations [5,6] have shown that both the cardiac and thoracic pump mechanisms are operative, but it is still unclear what determines which mechanism predominates. By contrast, it is during the decompression phase that venous blood flow returns to the heart secondary to differences between the extrathoracic and intrathoracic veins. As pressures decrease in the thorax relative to the extrathoracic vasculature, blood moves back to the right heart via the vena cava and, to a lesser extent, back to the left heart via the aorta. In reality, both the thoracic pump and cardiac pump mechanisms play an important role at different times after cardiac arrest. Keywords Factors that might affect the relative roles of the cardiac and thoracic pumps include the time between arrest and CPR, venous return, total body volume status, cardiac chamber blood volume, cardiac valve integrity, vascular compliance, chest compression rate and depth, ability of the chest wall to recoil fully, duration of compression in relation to decompression, chest wall elasticity, airway pressure, ventilation rate, body habitus, hypoxia, hypercarbia, vasoactive medications, and presenting cardiac rhythm. The amount of blood flow to the heart at any given time may be the most important determinant of survival. Indeed, the amount of blood flow that returns to Cardiac Arrhythmia Center, University of Minnesota, Minneapolis, Minnesota, USA. Dr. Lurie is a coinventor of the inspiratory impedance threshold device and active compression/decompression cardiopulmonary resuscitation technology and founded a company, CPRx LLC, to develop this device. There are no other conflicts of interest

Take Heart America: A Comprehensive, Community-Wide, Systems-Based Approach to the Treatment of Cardiac Arrest

OBJECTIVES: To determine out-of-hospital cardiac arrest survival rates before and after implementation of the Take Heart America program (a community-based initiative that sequentially deployed all of the most highly recommended 2005 American Heart Association resuscitation guidelines in an effort to increase out-of-hospital cardiac arrest survival). PATIENTS: Out-of-hospital cardiac arrest patients in Anoka County, MN, and greater St. Cloud, MN, from November 2005 to June 2009. INTERVENTIONS: Two sites in Minnesota with a combined population of 439,692 people (greater St. Cloud and Anoka County) implemented: 1) widespread cardiopulmonary resuscitation and automated external defibrillator skills training in schools and businesses; 2) retraining of all emergency medical services personnel in methods to enhance circulation, including minimizing cardiopulmonary resuscitation interruptions, performing cardiopulmonary resuscitation before and after single-shock defibrillation, and use of an impedance threshold device; 3) additional deployment of automated external defibrillators in schools and public places; and 4) protocols for transport to and treatment by cardiac arrest centers for therapeutic hypothermia, coronary artery evaluation and treatment, and electrophysiological evaluation. MEASUREMENTS AND MAIN RESULTS: More than 28,000 people were trained in cardiopulmonary resuscitation and automated external defibrillator use in the two sites. Bystander cardiopulmonary resuscitation rates increased from 20% to 29% (p = .086, odds ratio 1.7, 95% confidence interval 0.96-2.89). Three cardiac arrest centers were established, and hypothermia therapy for admitted out-of-hospital cardiac arrest victims increased from 0% to 45%. Survival to hospital discharge for all patients after out-of-hospital cardiac arrest in these two sites improved from 8.5% (nine of 106, historical control) to 19% (48 of 247, intervention phase) (p = .011, odds ratio 2.60, confidence interval 1.19-6.26). A financial analysis revealed that the cardiac arrest centers concept was financially feasible, despite the costs associated with high-quality postresuscitation care. CONCLUSIONS: The Take Heart America program doubled cardiac arrest survival when compared with historical controls. Study of the feasibility of generalizing this approach to larger cities, states, and regions is underway

Awakening After Cardiac Arrest and Post Resuscitation Hypothermia: Are We Pulling the Plug Too Early?

BACKGROUND: Time to awakening after out-of-hospital cardiac arrest (OHCA) and post-resuscitation therapeutic hypothermia (TH) varies widely. We examined the time interval from when comatose OHCA patients were rewarmed to 37°C to when they showed definitive signs of neurological recovery and tried to identify potential predictors of awakening. METHODS: With IRB approval, a retrospective case study was performed in OHCA patients who were comatose upon presentation to a community hospital during 2006-2010. They were treated with TH (target of 33°C) for 24h, rewarmed, and discharged alive. Comatose patients were generally treated medically after TH for at least 48h before any decision to withdraw supportive care was made. Pre-hospital TH was not used. Data are expressed as medians and interquartile range. RESULTS: The 89 patients treated with TH in this analysis were divided into three groups based upon the time between rewarming to 37°C and regaining consciousness. The 69 patients that regained consciousness in ≤48h after rewarming were termed early-awakeners . Ten patients regained consciousness 48-72h after rewarming and were termed intermediate-awakeners . Ten patients remained comatose and apneic \u3e72h after rewarming but eventually regained consciousness; they were termed late-awakeners . The ages for the early, intermediate and late awakeners were 56 [49,65], 62 [48,74], and 58 [55,65] years, respectively. Nearly 67% were male. Following rewarming, the time required to regain consciousness for the early, intermediate and late awakeners was 9 [2,18] (range 0-47), 60.5 [56,64.5] (range 49-71), and 126 [104,151]h (range 73-259), respectively. Within 90 days of hospital admission, favorable neurological function based on a Cerebral Performance Category (CPC) score of 1 or 2 was reported in 67/69 early, 10/10 intermediate, and 8/10 late awakeners. CONCLUSION: Following OHCA and TH, arbitrary withdrawal of life support \u3c48h after rewarming may prematurely terminate life in many patients with the potential for full neurological recovery. Additional clinical markers that correlate with late awakening are needed to better determine when withdrawal of support is appropriate in OHCA patients who remain comatose \u3e48h after rewarmin