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

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