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

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

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

Role of Epinephrine and Extracorporeal Membrane Oxygenation in the Management of Ischemic Refractory Ventricular Fibrillation

Summary: Extracorporeal membrane oxygenation (ECMO) is used in cardiopulmonary resuscitation (CPR) of refractory cardiac arrest. The authors used a 2 à 2 study design to compare ECMO versus CPR and epinephrine versus placebo in a porcine model of ischemic refractory ventricular fibrillation (VF). Pigs underwent 5 min of untreated VF and 10 min of CPR, and were randomized to receive epinephrine versus placebo for another 35 min. Animals were further randomized to left anterior descending artery (LAD) reperfusion at minute 45 with ongoing CPR versus venoarterial ECMO cannulation at minute 45 of CPR and subsequent LAD reperfusion. Four-hour survival was improved with ECMO whereas epinephrine showed no effect. Key Words: advanced cardiopulmonary life support, cardiac arrest, cardiopulmonary resuscitation, ECMO, extracorporeal membrane oxygenation, ischemic refractory ventricular fibrillation, ST-segment elevation myocardial infarction, ventricular fibrillatio

Intracoronary Poloxamer 188 Prevents Reperfusion Injury in a Porcine Model of ST-Segment Elevation Myocardial Infarction

Poloxamer 188 (P188) is a nonionic triblock copolymer believed to prevent cellular injury after ischemia and reperfusion. This study compared intracoronary (IC) infusion of P188 immediately after reperfusion with delayed infusion through a peripheral intravenous catheter in a porcine model of ST-segment elevation myocardial infarction (STEMI). STEMI was induced in 55 pigs using 45 min of endovascular coronary artery occlusion. Pigs were then randomized to 4 groups: control, immediate IC P188, delayed peripheral P188, and polyethylene glycol infusion. Heart tissue was collected after 4 h of reperfusion. Assessment of mitochondrial function or infarct size was performed. Mitochondrial yield improved significantly with IC P188 treatment compared with control animals (0.25% vs. 0.13%), suggesting improved mitochondrial morphology and survival. Mitochondrial respiration and calcium retention were also significantly improved with immediate IC P188 compared with control animals (complex I respiratory control index: 7.4 vs. 3.7; calcium retention: 1,152 nmol vs. 386 nmol). This benefit was only observed with activation of complex I of the mitochondrial respiratory chain, suggesting a specific effect from ischemia and reperfusion on this complex. Infarct size and serum troponin I were significantly reduced by immediate IC P188 infusion (infarct size: 13.9% vs. 41.1%; troponin I: 19.2 μg/l vs. 77.4 μg/l). Delayed P188 and polyethylene glycol infusion did not provide a significant benefit. These results demonstrate that intracoronary infusion of P188 immediately upon reperfusion significantly reduces cellular and mitochondrial injury after ischemia and reperfusion in this clinically relevant porcine model of STEMI. The timing and route of delivery were critical to achieve the benefit