Forward blood flow provoked by changing intravascular pressure using an extracorporeal circulation during cardiopulmonary resuscitation

Since both “cardiac pump” and “thoracic pump” theories have been proved during cardiopulmonary resuscitation (CPR), the mechanism of forward blood flow during closed chest compression still remains open to question. The cardiac pump seems to work by the direct compression of the cardiac ventricles between the sternum and vertebral column. A pressure gradient created between the ventricle and aorta generates systemic blood flow. However, the thoracic pump mechanism presumes chest compression causes a rise in intrathoracic pressure which generates a blood flow from the thoracic cavity to the systemic circulation. Retrograde blood flow from the right heart into the systemic veins is prevented by a concomitant collapse of veins at the thoracic inlet. We hypothesize that the intrinsic decrease of vascular resistance from the aorta to peripheral arteries and the existence of competent venous valves enable blood to flow unidirectionally by the fluctuation of intravascular pressures during closed chest compression. The purpose of this study is to prove an antegrade arterial blood flow without cardiac compression and intrathoracic pressure changes in an animal cardiac arrest model. We demonstrate that arterial pulses can be developed by using an extracorporeal circuit, resulting in forward blood flow from the aorta through the systemic vasculature. It can be suggested that changes in intravascular pressure provoked by either cardiac or thoracic pump generate systemic blood flow during closed chest compression, while systemic vascular patency and valve function may be required for successful CPR.

Cardiopulmonary resuscitation; Blood flow; Chest compression; Vascular resistance

[1] Deshmukh HG, Weil MH, Gudipati CV, Trevino RP, Bisera J, Rackow EC. Mechanism of blood flow generated by precordial compression during CPR: I. stuides on closed chest precordial compression. Chest. 1989; 95: 1092-1099.

[2] Niemann JT, Rosborough JP, Hausknecht M, Garner D, Criley JM. Pressure-synchronized cineangiography during experimental cardiopul-monary resuscitation. Circulation. 1981; 64: 985-991.

[3] Criley JM, Blaufuss AH, Kissel Gl. Cough-induced cardiac compression. The Journal of the American Medical Association. 1976; 236: 1246-1250.

[4] Porter TR, Ornate JP, Guard CS, Roy VG, Burns CA, Nixon JV. Transesophageal echocardiography to assess mitral valve function and flow during cardiopulmonary resuscitation. The American Journal of Cardiology. 1992; 70: 1056-1060.

[5] Ma MH, Hwang JJ, Lai LP, Wang SM, Huang GT, Shyu KG, et al. Transesophageal echocardiographic assessment of mitral valve position and pulmonary venous flow during cardiopulmonary resuscitation in humans. Circulation. 1995; 92: 854-861.

[6] Mair P, Kornberger E, Schwarz B, Baubin M, Hoermann C. Forward blood flow during cardiopulmonary resuscitation in patients with severe accidental hypothermia: an echocardiographic study. Acta Anaesthesio-logica Scandinavica. 1998; 42: 1139-1144.

[7] Halperin HR, Weiss JL, Guerci AD, Chandra N, Tsitlik JE, Brower R, et al. Cyclic elevation of intrathoracic pressure can close the mitral valve during cardiac arrest in dogs. Circulation. 1988; 78: 754-760.

[8] Bass CF. New versus old theories of blood flow during CPR. Critical Care Medicine. 1980; 8: 191-196.

[9] Rudikoff MT, Maughan WL, Effron M, Freund P, Weisfeldt ML. Mech-anisms of blood flow during cardiopulmonary resuscitation. Circulation. 1980; 61: 345-352.

[10] Redberg RF, Tucker KJ, Cohen TJ, Dutton JP, Callaham ML, Schiller NB. Cardiopulmonary resuscitation: physiology of blood flow during cardiopulmonary resuscitation: a transesophageal echocardiographic study. Circulation. 1993; 88: 534-542.

[11] Maertens VL, De Smedt LE, Lemoyne S, Huybrechts SA, Wouters K, Kalmar AF, et al. Patients with cardiac arrest are ventilated two times faster than guidelines recommend: an observational prehospital study using tracheal pressure measurement. Resuscitation. 2013; 84: 921-926.

[12] Beattie C, Guerci AD, Hall T, Borkon AM, Baumgartner W, Stuart RS, et al. Mechanisms of blood flow during pneumatic vest cardiopulmonary resuscitation. Journal of Applied Physiology. 1991; 70: 454-465.

[13] Chalkias A , Xanthos T. Timing positive-pressure ventilation during chest compression: the key to improving the thoracic pump? European Heart Journal: Acute Cardiovascular Care. 2015; 4: 24-27.

[14] Dokoumetzidis A, Macheras P. A model for transport and dispersion in the circulatory system based on the vascular fractal tree. Annals of Biomedical Engineering. 2003; 31: 284-293.

[15] Chana CK, Vanhoutte PM. Hypoxia, vascular smooth muscles and endothelium. Acta Pharmaceutica Sinica B. 2013; 3: 1-7.

[16] Peng HL, Ivarsen A, Nilsson H, Aalkjaer C. On the cellular mechanism for the effect of acidosis on vascular tone. Acta Physiologica Scandinav-ica. 1998; 164: 517-525.

[17] Paradis NA, Martin GB, Rivers EP, Goetting MG, Appleton TJ, Feingold M, et al. Coronary perfusion pressure and the return of spontaneous circulation in human cardiopulmonary resuscitation. Journal of the American Medical Association. 1990; 263: 1106-1113.