Medical Hypotheses 83 (2014) 127–129
Contents lists available at ScienceDirect
Medical Hypotheses journal homepage: www.elsevier.com/locate/mehy
Bilateral femoral artery compression as a technique to increase vital organ perfusion during intraoperative hypotension Taufiek Konrad Rajab a, Jan Dieter Schmitto b,⇑ a b
Department of Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA Department of Cardiothoracic, Transplantation and Vascular Surgery, Hannover Medical School, Hannover, Germany
a r t i c l e
i n f o
Article history: Received 30 October 2013 Accepted 16 March 2014
a b s t r a c t Intraoperative hypotension is associated with adverse outcomes. The preferred treatment for intraoperative hypotension is to address its cause. In the interim the blood pressure can be supported by the anesthesia team with volume resuscitation and vasopressors. Additionally, preferential perfusion of vital organs, such as the myocardium and cerebrum, at the expense of non-vital vascular beds, such as the extremities, is desirable. In the state of shock, the flight or fight response will ensure perfusion of the extremities in order to prepare the organism for a physical confrontation. However, in the context of intraoperative hypotension this response is counter-productive. Therefore we propose bilateral femoral artery compression as a new technique to increase vital organ perfusion during intraoperative hypotension. This results in shunting of blood flow from the legs and towards the vital organs. Bilateral femoral artery compression can be employed by the surgical team to immediately improve blood pressure until other counter-measures against intraoperative hypotension take effect. Ó 2014 Elsevier Ltd. All rights reserved.
Introduction Intraoperative hypotension (IOH) involving systolic blood pressure (SBP) < 80 mmHg occurs in 40% of operations, whereas IOH with SBP < 70 mmHg for at least 5 min occurs in 5% of operations [1]. During this time, organs are at risk for ischemia. The cerebrum and myocardium have a particularly low tolerance for ischemia before irreversible damage occurs. IOH is significantly associated with perioperative stroke as well as cardiac, renal, gastrointestinal and wound complications [2–4]. Every minute of IOH with SBP < 80 mmHg confers a relative risk of 1.044 for mortality within the first year after surgery [5]. The preferred treatment for IOH is to address its cause. In the interim the blood pressure can be supported by the anesthesia team with volume resuscitation and vasopressors [6,7]. Mechanical manipulation of the arterial tree modulates blood pressure Blood pressure (BP) can also be modulated by mechanical manipulation of the arterial tree by the surgical team. The systemic ⇑ Corresponding author. Address: Department of Cardiothoracic, Transplantation and Vascular Surgery, Mechanical Cardiac Circulatory Support and Cardiac Transplantation Program, Hannover Medical School (OE 6210), Carl-Neuberg-Str. 1, 30625 Hannover, Germany. E-mail addresses: [email protected] (T.K. Rajab), Schmitto.Jan@ mh-hannover.de (J.D. Schmitto). http://dx.doi.org/10.1016/j.mehy.2014.03.021 0306-9877/Ó 2014 Elsevier Ltd. All rights reserved.
circulation has multiple parallel circuits that branch from the aorta. This anatomy permits a wide variation in regional blood flow at a given cardiac output (CO). Systemic vascular resistance (SVR) is related to the resistance in each of the parallel circuits (R1, R2 ... 1 ¼ R11 þ R12 þ ::: R1n . Substituting this Rn) according to the equation SVR equation into Ohm’s law yields BP ¼
CO 1 þ 1 þ::: 1 R1 R2 Rn
. Assuming a constant
CO, removal of parallel circuits from the circulation by mechanical compression of the respective arteries will thus increase BP.
Arterial occlusion increases perfusion of proximal organs Modulation of BP by mechanical manipulation of the arterial tree was first observed experimentally by aortic occlusion in dogs, which increased carotid BP [8]. Subsequent animal data showed that clamping of the aorta also results in significantly increased perfusion of organs proximal to the site of arterial compression [9–14]. Furthermore, mixed venous oxygen content is increased [15,16]. Comparable effects are also appreciated in everyday clinical practice. Surgeons have been trained for decades to cross-clamp the aorta during open chest cardiac massage in order to optimize tissue perfusion proximal to the clamp site [17–19]. Furthermore, patients who undergo aortic clamping during aortofemoral reconstruction have significantly increased blood pressure while the aorta is occluded [20,21]. Leriche’s original description of his aortoiliac occlusion syndrome included upper extremity hypertension [22].
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T.K. Rajab, J.D. Schmitto / Medical Hypotheses 83 (2014) 127–129
Similar effects also occur during occlusion of peripheral arteries. There is an increase in SBP after femoral artery clamping during femoral reconstruction and conversely releasing femoral clamps to re-establish lower extremity blood flow after aortofemoral reconstruction is notoriously associated with hypotension [19,23–25]. Vascular surgeons are also familiar with the increased waterhammer pulse that is found proximal to the site of an embolic occlusion of peripheral arteries such as the femoral arteries [26]. Bilateral femoral artery occlusion optimizes organ perfusion Based on these principles, systemic blood pressure and vital organ perfusion could be optimized during episodes of IOH by exclusion of non-vital vascular beds from the circulation. The largest caliber arteries that can be occluded non-invasively by compression during routine surgery are the femoral arteries. Blood flow in each femoral artery is approximately 350 ml/min. This is approximately 6% of the total cardiac output [27]. Consequently occlusion of both femoral arteries by external compression in a normal individual will shunt approximately 690 ml/min of additional blood flow towards the proximal vascular beds. This amounts to 12% of total cardiac output. In the case of a hypotensive individual, a sympathetic response termed the ‘‘flight or fight response’’ is activated [28]. This sympathetic response will result in constriction of the peripheral circulation. However, perfusion of the extremity skeletal musculature is conserved to prepare the organism for a physical confrontation and to allow rapid escape from danger. In the case of intra-operative hypotension this is counter-productive since the lower extremity skeletal musculature is not necessary for fighting or fleeing. Therefore compression of both femoral arteries during intra-operative hypotension is expected to shunt additional blood flow amounting to approximately 10% of total cardiac output towards the proximal vascular beds, which include the vital organs. Compression of the femoral arteries also prevents resuscitative crystalloids, colloids and pharmaceuticals from running off into the lower extremities and concentrates them in the vascular beds that supply the vital organs. A theoretical draw-back of bilateral femoral artery compression during IOH is incidental occlusion of the femoral veins. This would sequester blood in the lower extremity venous compartment and exclude it from the circulation. However, this blood can still return to the heart via collaterals such as the gluteal, obturator and hypogastric veins. Consequently there is a re-distribution of blood volume from the extremities into the proximal vascular beds [14]. This increases pre-load and further augments SBP by activating the Frank–Starling mechanism [12,14]. Bilateral femoral artery compression is a temporizing technique to increase organ perfusion during intraoperative hypotension Occlusion of the femoral arteries by external compression is technically straight-forward. The relation of the common femoral artery (CFA) to the surface landmarks of the groin are well characterized since vascular surgeons routinely access this artery percutaneously. The CFA originates under the inguinal ligament at the midpoint between the anterior superior iliac spine and the pubic symphysis. Palpation of the point with maximal pulse indicates the location where the CFA can be readily occluded by compression against the femoral head [29]. Femoral artery compression can be achieved manually or via a specially designed compression device that is secured to a fixed retractor frame. This should immediately increase perfusion of proximal vascular beds including the vital organs by approximately 10%.
Based on the literature for pneumatic tourniquets used in lower extremity surgery we recommend maximum lower extremity ischemic times of 45 min [30]. While the femoral artery can be occluded for six hours before tissue necrosis occurs, re-perfusion has a measurable detrimental systemic effect after less than one hour ischemic time [30,31]. Therefore we advocate that femoral artery compression only be used as a short-term maneuver until other measures to support BP take effect. In summary, we propose bilateral femoral artery compression as a temporizing technique for IOH that can be employed by the surgical to immediately improve BP until other counter-measures taken by the anesthesia team take effect.
Conflicts of interest We have no conflicts of interest to disclose. References [1] Bijker JB, van Klei WA, Kappen TH, van Wolfswinkel L, Moons KG, Kalkman CJ. Incidence of intraoperative hypotension as a function of the chosen definition: literature definitions applied to a retrospective cohort using automated data collection. Anesthesiology 2007;107(2):213–20. [2] Bijker JB, Persoon S, Peelen LM, et al. Intraoperative hypotension and perioperative ischemic stroke after general surgery: a nested case-control study. Anesthesiology 2012;116(3):658–64. [3] Tassoudis V, Vretzakis G, Petsiti A, et al. Impact of intraoperative hypotension on hospital stay in major abdominal surgery. J Anesth 2011;25(4):492–9. [4] Charlson ME, MacKenzie CR, Gold JP, Ales KL, Topkins M, Shires GT. Intraoperative blood pressure. What patterns identify patients at risk for postoperative complications? Ann Surg 1990;212(5):567–80. [5] Monk TG, Saini V, Weldon BC, Sigl JC. Anesthetic management and one-year mortality after noncardiac surgery. Anesth Analg 2005;100(1):4–10. [6] Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2011;3:CD000567. [7] Havel C, Arrich J, Losert H, Gamper G, Müllner M, Herkner H. Vasopressors for hypotensive shock. Cochrane Database Syst Rev 2011;5:CD003079. [8] De Jager S. Experiments and considerations on haemodynamics. J Physiol 1886;7(2):130–215. [9] Gelman S, Rabbani S, Bradley EL. Inferior and superior vena caval blood flows during cross-clamping of the thoracic aorta in pigs. J Thorac Cardiovasc Surg 1988;96(3):387–92. [10] Gregoretti S, Henderson T, Parks DA, Gelman S. Haemodynamic changes and oxygen uptake during crossclamping of the thoracic aorta in dexmedetomidine pretreated dogs. Can J Anaesth 1992;39(7):731–41. [11] Gregoretti S, Gelman S, Henderson T, Bradley EL. Hemodynamics and oxygen uptake below and above aortic occlusion during crossclamping of the thoracic aorta and sodium nitroprusside infusion. J Thorac Cardiovasc Surg 1990;100(6):830–6. [12] Stokland O, Miller MM, Ilebekk A, Kiil F. Mechanism of hemodynamic responses to occlusion of the descending thoracic aorta. Am J Physiol 1980;238(4):H423–9. [13] Brusoni B, Colombo A, Merlo L, Marchetti G, Longo T. Hemodynamic and metabolic changes induced by temporary clamping of the thoracic aorta. Eur Surg Res 1978;10(3):206–16. [14] Gelman S, Khazaeli MB, Orr R, Henderson T. Blood volume redistribution during cross-clamping of the descending aorta. Anesth Analg 1994;78(2):219–24. [15] Gelman S, McDowell H, Varner PD, et al. The reason for cardiac output reduction after aortic cross-clamping. Am J Surg 1988;155(4):578–86. [16] Shenaq SA, Casar G, Chelly JE, Ott H, Crawford ES. Continuous monitoring of mixed venous oxygen saturation during aortic surgery. Chest 1987;92(5):796–9. [17] Millikan J, Moore E. Outcome of resuscitative thoracotomy and descending aortic occlusion performed in the operating room. J Trauma 1984;24(5):387–92. [18] Spence P, Lust R, Chitwood WJ, Iida H, Sun Y, Austin Er. Transfemoral balloon aortic occlusion during open cardiopulmonary resuscitation improves myocardial and cerebral blood flow. J Surg Res 1990;49(3):217–21. [19] Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology 1995;82(4):1026–60. [20] Falk JL, Rackow EC, Blumenberg R, Gelfand M, Fein IA. Hemodynamic and metabolic effects of abdominal aortic crossclamping. Am J Surg 1981;142(2):174–7. [21] Khir AW, Henein MY, Koh T, Das SK, Parker KH, Gibson DG. Arterial waves in humans during peripheral vascular surgery. Clin Sci (Lond) 2001;101(6):749–57. [22] Leriche R, Morel A. The syndrome of thrombotic obliteration of the aortic bifurcation. Ann Surg 1948;127(2):193–206.
T.K. Rajab, J.D. Schmitto / Medical Hypotheses 83 (2014) 127–129 [23] Rader LE, Keith HB, Campbell GS. Mechanism of hypotension following release of abdominal aortic clamp. Surg Forum 1961;12:265–7. [24] Perry MO. The hemodynamics of temporary abdominal aortic occlusion. Ann Surg 1968;168(2):193–200. [25] Thomas TV. Aortic declamping shock. Am Heart J 1971;81(6):845–7. [26] Walker PM, Johnston KW. When does limb blood flow increase after aortoiliac bypass grafting? Arch Surg 1980;115(8):912–5. [27] Collis T, Devereux RB, Roman MJ, et al. Relations of stroke volume and cardiac output to body composition: the strong heart study. Circulation 2001;103(6):820–5.
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[28] Cannon WB. Bodily Changes in Pain, Hunger, Fear and Rage. New York: D. Appleton & Company; 1915. [29] Irani F, Kumar S, Colyer WR. Common femoral artery access techniques: a review. J Cardiovasc Med (Hagerstown) 2009;10(7):517–22. [30] Estebe JP, Davies JM, Richebe P. The pneumatic tourniquet: mechanical, ischaemia-reperfusion and systemic effects. Eur J Anaesthesiol 2011;28(6):404–11. [31] Callum K, Bradbury A. ABC of arterial and venous disease: acute limb ischaemia. BMJ 2000;320(7237):764–7.
Contents lists available at ScienceDirect
Medical Hypotheses journal homepage: www.elsevier.com/locate/mehy
Bilateral femoral artery compression as a technique to increase vital organ perfusion during intraoperative hypotension Taufiek Konrad Rajab a, Jan Dieter Schmitto b,⇑ a b
Department of Surgery, Brigham and Women’s Hospital, Harvard Medical School, Boston, MA, USA Department of Cardiothoracic, Transplantation and Vascular Surgery, Hannover Medical School, Hannover, Germany
a r t i c l e
i n f o
Article history: Received 30 October 2013 Accepted 16 March 2014
a b s t r a c t Intraoperative hypotension is associated with adverse outcomes. The preferred treatment for intraoperative hypotension is to address its cause. In the interim the blood pressure can be supported by the anesthesia team with volume resuscitation and vasopressors. Additionally, preferential perfusion of vital organs, such as the myocardium and cerebrum, at the expense of non-vital vascular beds, such as the extremities, is desirable. In the state of shock, the flight or fight response will ensure perfusion of the extremities in order to prepare the organism for a physical confrontation. However, in the context of intraoperative hypotension this response is counter-productive. Therefore we propose bilateral femoral artery compression as a new technique to increase vital organ perfusion during intraoperative hypotension. This results in shunting of blood flow from the legs and towards the vital organs. Bilateral femoral artery compression can be employed by the surgical team to immediately improve blood pressure until other counter-measures against intraoperative hypotension take effect. Ó 2014 Elsevier Ltd. All rights reserved.
Introduction Intraoperative hypotension (IOH) involving systolic blood pressure (SBP) < 80 mmHg occurs in 40% of operations, whereas IOH with SBP < 70 mmHg for at least 5 min occurs in 5% of operations [1]. During this time, organs are at risk for ischemia. The cerebrum and myocardium have a particularly low tolerance for ischemia before irreversible damage occurs. IOH is significantly associated with perioperative stroke as well as cardiac, renal, gastrointestinal and wound complications [2–4]. Every minute of IOH with SBP < 80 mmHg confers a relative risk of 1.044 for mortality within the first year after surgery [5]. The preferred treatment for IOH is to address its cause. In the interim the blood pressure can be supported by the anesthesia team with volume resuscitation and vasopressors [6,7]. Mechanical manipulation of the arterial tree modulates blood pressure Blood pressure (BP) can also be modulated by mechanical manipulation of the arterial tree by the surgical team. The systemic ⇑ Corresponding author. Address: Department of Cardiothoracic, Transplantation and Vascular Surgery, Mechanical Cardiac Circulatory Support and Cardiac Transplantation Program, Hannover Medical School (OE 6210), Carl-Neuberg-Str. 1, 30625 Hannover, Germany. E-mail addresses: [email protected] (T.K. Rajab), Schmitto.Jan@ mh-hannover.de (J.D. Schmitto). http://dx.doi.org/10.1016/j.mehy.2014.03.021 0306-9877/Ó 2014 Elsevier Ltd. All rights reserved.
circulation has multiple parallel circuits that branch from the aorta. This anatomy permits a wide variation in regional blood flow at a given cardiac output (CO). Systemic vascular resistance (SVR) is related to the resistance in each of the parallel circuits (R1, R2 ... 1 ¼ R11 þ R12 þ ::: R1n . Substituting this Rn) according to the equation SVR equation into Ohm’s law yields BP ¼
CO 1 þ 1 þ::: 1 R1 R2 Rn
. Assuming a constant
CO, removal of parallel circuits from the circulation by mechanical compression of the respective arteries will thus increase BP.
Arterial occlusion increases perfusion of proximal organs Modulation of BP by mechanical manipulation of the arterial tree was first observed experimentally by aortic occlusion in dogs, which increased carotid BP [8]. Subsequent animal data showed that clamping of the aorta also results in significantly increased perfusion of organs proximal to the site of arterial compression [9–14]. Furthermore, mixed venous oxygen content is increased [15,16]. Comparable effects are also appreciated in everyday clinical practice. Surgeons have been trained for decades to cross-clamp the aorta during open chest cardiac massage in order to optimize tissue perfusion proximal to the clamp site [17–19]. Furthermore, patients who undergo aortic clamping during aortofemoral reconstruction have significantly increased blood pressure while the aorta is occluded [20,21]. Leriche’s original description of his aortoiliac occlusion syndrome included upper extremity hypertension [22].
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T.K. Rajab, J.D. Schmitto / Medical Hypotheses 83 (2014) 127–129
Similar effects also occur during occlusion of peripheral arteries. There is an increase in SBP after femoral artery clamping during femoral reconstruction and conversely releasing femoral clamps to re-establish lower extremity blood flow after aortofemoral reconstruction is notoriously associated with hypotension [19,23–25]. Vascular surgeons are also familiar with the increased waterhammer pulse that is found proximal to the site of an embolic occlusion of peripheral arteries such as the femoral arteries [26]. Bilateral femoral artery occlusion optimizes organ perfusion Based on these principles, systemic blood pressure and vital organ perfusion could be optimized during episodes of IOH by exclusion of non-vital vascular beds from the circulation. The largest caliber arteries that can be occluded non-invasively by compression during routine surgery are the femoral arteries. Blood flow in each femoral artery is approximately 350 ml/min. This is approximately 6% of the total cardiac output [27]. Consequently occlusion of both femoral arteries by external compression in a normal individual will shunt approximately 690 ml/min of additional blood flow towards the proximal vascular beds. This amounts to 12% of total cardiac output. In the case of a hypotensive individual, a sympathetic response termed the ‘‘flight or fight response’’ is activated [28]. This sympathetic response will result in constriction of the peripheral circulation. However, perfusion of the extremity skeletal musculature is conserved to prepare the organism for a physical confrontation and to allow rapid escape from danger. In the case of intra-operative hypotension this is counter-productive since the lower extremity skeletal musculature is not necessary for fighting or fleeing. Therefore compression of both femoral arteries during intra-operative hypotension is expected to shunt additional blood flow amounting to approximately 10% of total cardiac output towards the proximal vascular beds, which include the vital organs. Compression of the femoral arteries also prevents resuscitative crystalloids, colloids and pharmaceuticals from running off into the lower extremities and concentrates them in the vascular beds that supply the vital organs. A theoretical draw-back of bilateral femoral artery compression during IOH is incidental occlusion of the femoral veins. This would sequester blood in the lower extremity venous compartment and exclude it from the circulation. However, this blood can still return to the heart via collaterals such as the gluteal, obturator and hypogastric veins. Consequently there is a re-distribution of blood volume from the extremities into the proximal vascular beds [14]. This increases pre-load and further augments SBP by activating the Frank–Starling mechanism [12,14]. Bilateral femoral artery compression is a temporizing technique to increase organ perfusion during intraoperative hypotension Occlusion of the femoral arteries by external compression is technically straight-forward. The relation of the common femoral artery (CFA) to the surface landmarks of the groin are well characterized since vascular surgeons routinely access this artery percutaneously. The CFA originates under the inguinal ligament at the midpoint between the anterior superior iliac spine and the pubic symphysis. Palpation of the point with maximal pulse indicates the location where the CFA can be readily occluded by compression against the femoral head [29]. Femoral artery compression can be achieved manually or via a specially designed compression device that is secured to a fixed retractor frame. This should immediately increase perfusion of proximal vascular beds including the vital organs by approximately 10%.
Based on the literature for pneumatic tourniquets used in lower extremity surgery we recommend maximum lower extremity ischemic times of 45 min [30]. While the femoral artery can be occluded for six hours before tissue necrosis occurs, re-perfusion has a measurable detrimental systemic effect after less than one hour ischemic time [30,31]. Therefore we advocate that femoral artery compression only be used as a short-term maneuver until other measures to support BP take effect. In summary, we propose bilateral femoral artery compression as a temporizing technique for IOH that can be employed by the surgical to immediately improve BP until other counter-measures taken by the anesthesia team take effect.
Conflicts of interest We have no conflicts of interest to disclose. References [1] Bijker JB, van Klei WA, Kappen TH, van Wolfswinkel L, Moons KG, Kalkman CJ. Incidence of intraoperative hypotension as a function of the chosen definition: literature definitions applied to a retrospective cohort using automated data collection. Anesthesiology 2007;107(2):213–20. [2] Bijker JB, Persoon S, Peelen LM, et al. Intraoperative hypotension and perioperative ischemic stroke after general surgery: a nested case-control study. Anesthesiology 2012;116(3):658–64. [3] Tassoudis V, Vretzakis G, Petsiti A, et al. Impact of intraoperative hypotension on hospital stay in major abdominal surgery. J Anesth 2011;25(4):492–9. [4] Charlson ME, MacKenzie CR, Gold JP, Ales KL, Topkins M, Shires GT. Intraoperative blood pressure. What patterns identify patients at risk for postoperative complications? Ann Surg 1990;212(5):567–80. [5] Monk TG, Saini V, Weldon BC, Sigl JC. Anesthetic management and one-year mortality after noncardiac surgery. Anesth Analg 2005;100(1):4–10. [6] Perel P, Roberts I. Colloids versus crystalloids for fluid resuscitation in critically ill patients. Cochrane Database Syst Rev 2011;3:CD000567. [7] Havel C, Arrich J, Losert H, Gamper G, Müllner M, Herkner H. Vasopressors for hypotensive shock. Cochrane Database Syst Rev 2011;5:CD003079. [8] De Jager S. Experiments and considerations on haemodynamics. J Physiol 1886;7(2):130–215. [9] Gelman S, Rabbani S, Bradley EL. Inferior and superior vena caval blood flows during cross-clamping of the thoracic aorta in pigs. J Thorac Cardiovasc Surg 1988;96(3):387–92. [10] Gregoretti S, Henderson T, Parks DA, Gelman S. Haemodynamic changes and oxygen uptake during crossclamping of the thoracic aorta in dexmedetomidine pretreated dogs. Can J Anaesth 1992;39(7):731–41. [11] Gregoretti S, Gelman S, Henderson T, Bradley EL. Hemodynamics and oxygen uptake below and above aortic occlusion during crossclamping of the thoracic aorta and sodium nitroprusside infusion. J Thorac Cardiovasc Surg 1990;100(6):830–6. [12] Stokland O, Miller MM, Ilebekk A, Kiil F. Mechanism of hemodynamic responses to occlusion of the descending thoracic aorta. Am J Physiol 1980;238(4):H423–9. [13] Brusoni B, Colombo A, Merlo L, Marchetti G, Longo T. Hemodynamic and metabolic changes induced by temporary clamping of the thoracic aorta. Eur Surg Res 1978;10(3):206–16. [14] Gelman S, Khazaeli MB, Orr R, Henderson T. Blood volume redistribution during cross-clamping of the descending aorta. Anesth Analg 1994;78(2):219–24. [15] Gelman S, McDowell H, Varner PD, et al. The reason for cardiac output reduction after aortic cross-clamping. Am J Surg 1988;155(4):578–86. [16] Shenaq SA, Casar G, Chelly JE, Ott H, Crawford ES. Continuous monitoring of mixed venous oxygen saturation during aortic surgery. Chest 1987;92(5):796–9. [17] Millikan J, Moore E. Outcome of resuscitative thoracotomy and descending aortic occlusion performed in the operating room. J Trauma 1984;24(5):387–92. [18] Spence P, Lust R, Chitwood WJ, Iida H, Sun Y, Austin Er. Transfemoral balloon aortic occlusion during open cardiopulmonary resuscitation improves myocardial and cerebral blood flow. J Surg Res 1990;49(3):217–21. [19] Gelman S. The pathophysiology of aortic cross-clamping and unclamping. Anesthesiology 1995;82(4):1026–60. [20] Falk JL, Rackow EC, Blumenberg R, Gelfand M, Fein IA. Hemodynamic and metabolic effects of abdominal aortic crossclamping. Am J Surg 1981;142(2):174–7. [21] Khir AW, Henein MY, Koh T, Das SK, Parker KH, Gibson DG. Arterial waves in humans during peripheral vascular surgery. Clin Sci (Lond) 2001;101(6):749–57. [22] Leriche R, Morel A. The syndrome of thrombotic obliteration of the aortic bifurcation. Ann Surg 1948;127(2):193–206.
T.K. Rajab, J.D. Schmitto / Medical Hypotheses 83 (2014) 127–129 [23] Rader LE, Keith HB, Campbell GS. Mechanism of hypotension following release of abdominal aortic clamp. Surg Forum 1961;12:265–7. [24] Perry MO. The hemodynamics of temporary abdominal aortic occlusion. Ann Surg 1968;168(2):193–200. [25] Thomas TV. Aortic declamping shock. Am Heart J 1971;81(6):845–7. [26] Walker PM, Johnston KW. When does limb blood flow increase after aortoiliac bypass grafting? Arch Surg 1980;115(8):912–5. [27] Collis T, Devereux RB, Roman MJ, et al. Relations of stroke volume and cardiac output to body composition: the strong heart study. Circulation 2001;103(6):820–5.
129
[28] Cannon WB. Bodily Changes in Pain, Hunger, Fear and Rage. New York: D. Appleton & Company; 1915. [29] Irani F, Kumar S, Colyer WR. Common femoral artery access techniques: a review. J Cardiovasc Med (Hagerstown) 2009;10(7):517–22. [30] Estebe JP, Davies JM, Richebe P. The pneumatic tourniquet: mechanical, ischaemia-reperfusion and systemic effects. Eur J Anaesthesiol 2011;28(6):404–11. [31] Callum K, Bradbury A. ABC of arterial and venous disease: acute limb ischaemia. BMJ 2000;320(7237):764–7.
