Bradycardia in acute haemorrhage
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《英国医生杂志》
1 Department of Anaesthetics, Royal United Hospital, Bath BA1 3NG, 2 Department of Anaesthetics, Weston General Hospital, Weston-Super-Mare BS23 4TQ
Correspondence to: I Thomas ThmsIa@aol.com
Introduction
Patients with acute haemorrhage may not show the expected initial tachycardic response. Clinicians should consider a diagnosis of acute haemorrhage for patients with hypotension and a normal or low heart rate after surgery. The three patients presented to us in a single year; for patients with acute haemorrhage, lack of initial tachycardia may be more common than previously thought.
Experimental evidence and clinical observations show that, without resuscitation, the response of heart rate to a reduction in the volume of circulating blood is usually biphasic. In the first phase, baroreceptor mediated reflex vasoconstriction and cardio-acceleration maintain arterial pressure despite falling cardiac output. This phase is therefore characterised by tachycardia and normotension. The second phase occurs when about a third of the volume of circulating blood has been lost. Sympathetically mediated vasoconstriction and cardiac drive fall abruptly, and cardiac vagal drive increases. This simultaneously reduces mean arterial pressure and heart rate. Early recognition of this vasodepressor-cardioinhibitory reaction to a reduced circulating volume is vital; the associated bradycardia and hypotension precede circulatory collapse. These phases, seen with progressive central hypovolaemia, are reversed during resuscitation of circulatory volume. The distinction between a bradycardia seen in the second phase of a normal response to acute haemorrhage and a relative bradycardia is that patients with relative bradycardia do not exhibit the initial tachycardia in the first phase.
Bradycardic responses to acute haemorrhage need early recognition and prompt replacement of circulatory volume. About a third of patients with traumatic haemorrhage will present with a bradycardia; "normal heart rate or even bradycardia can be associated with an acute reduction in blood volume."7 A retrospective study of patients with isolated extremity trauma or isolated penetrating abdominal trauma found that of the 71 patients presenting with systolic blood pressure of less than 100 mm Hg, 25 (35%) had a pulse rate of fewer than 100 beats/min.8 A retrospective study of patients at a trauma centre found that of 750 patients who presented with a systolic blood pressure of less than 90 mm Hg, 217 (28.9%) had a pulse rate of fewer than 90 beats/min.9 The authors of the study also suggested that bradycardia was associated with a better prognosis in certain subgroups of patients.
In the face of severe hypovolaemia, the bradycardia seen in the second phase of cardiovascular response to acute haemorrhage allows for a longer time for diastolic ventricular filling leading to an increased stroke volume.10 This bradycardia may result from the activation of a vagally mediated reflex arc originating from mechanoreceptors in the left ventricle.11 The bradycardic response may also be the result of a parasympathetic reflex mediated via the vagus nerve triggered by blood in the peritoneum.1 12 Vagus involvement is suggested by the fact that after cooling or cutting of the vagus nerves after rapid external haemorrhage in cats the fall in blood pressure was not affected, but the bradycardic response was absent.10 Why some patients do not show initial tachycardia is unknown.
Conclusion
Jansen RPS. Relative bradycardia: a sign of acute intraperitoneal bleeding. Aust NZ Obstet Gynaecol 1978;18: 206-8.
Secher NH, Sander Jensen K, Werner C, Warberg J, Bie P. Bradycardia during severe but reversible hypovolemic shock in man. Circ Shock 1984;14: 267-74.
Adams SL, Greene JS. Absence of a tachycardic response to intraperitoneal haemorrhage. J Emerg Med 1986;4: 383-9.
Snyder HS, Dresnick SJ. Lack of tachycardic response to hypotension in penetrating abdominal injuries. J Emerg Med 1989;7: 335-9.
Vayer JS, Henderson JV, Bellamy RF, Galper AR. Absence of a tachycardic response to shock in penetrating intraperitoneal injury. Ann Emerg Med 1988;17: 227-31.
Barriot P, Riou B. Haemorrhagic shock with paradoxical bradycardia. Intens Care Med 1987;13: 203-7.
American College of Surgeons. Advanced Trauma Life Support for Doctors. (ATLS) Instructor Course Manual. Chicago: ACoS, 1997.
Thompson D, Adams SL, Barrett J. Relative bradycardia in patients with isolated penetrating abdominal trauma and isolated extremity trauma. Ann Emerg Med 1990;19: 268-75.
Demetriades D, Chan LS, Bhasin P, Berne TV, Ramicone E, Huicochea F, et al. Relative bradycardia in patients with traumatic hypotension. J Trauma 1998;45: 534-9.
Oberg P, Thoren P. Increased activity in vagal cardiac afferents correlated to the appearance of reflex bradycardia during severe haemorrhage in cats. Acta Physiol Scand 1970;80(suppl): 22A-23A.
Oberg B, Thoren P. Increased activity in left ventricular receptors during haemorrhage or occlusion of caval veins in the cat. Acta Physiol Scand 1972;85: 164-3.
Snyder HS. Lack of a tachycardic response to hypotension with ruptured ectopic pregnancy. Am J Emerg Med 1990;8: 23-6.(Ian Thomas, specialist re)
Correspondence to: I Thomas ThmsIa@aol.com
Introduction
Patients with acute haemorrhage may not show the expected initial tachycardic response. Clinicians should consider a diagnosis of acute haemorrhage for patients with hypotension and a normal or low heart rate after surgery. The three patients presented to us in a single year; for patients with acute haemorrhage, lack of initial tachycardia may be more common than previously thought.
Experimental evidence and clinical observations show that, without resuscitation, the response of heart rate to a reduction in the volume of circulating blood is usually biphasic. In the first phase, baroreceptor mediated reflex vasoconstriction and cardio-acceleration maintain arterial pressure despite falling cardiac output. This phase is therefore characterised by tachycardia and normotension. The second phase occurs when about a third of the volume of circulating blood has been lost. Sympathetically mediated vasoconstriction and cardiac drive fall abruptly, and cardiac vagal drive increases. This simultaneously reduces mean arterial pressure and heart rate. Early recognition of this vasodepressor-cardioinhibitory reaction to a reduced circulating volume is vital; the associated bradycardia and hypotension precede circulatory collapse. These phases, seen with progressive central hypovolaemia, are reversed during resuscitation of circulatory volume. The distinction between a bradycardia seen in the second phase of a normal response to acute haemorrhage and a relative bradycardia is that patients with relative bradycardia do not exhibit the initial tachycardia in the first phase.
Bradycardic responses to acute haemorrhage need early recognition and prompt replacement of circulatory volume. About a third of patients with traumatic haemorrhage will present with a bradycardia; "normal heart rate or even bradycardia can be associated with an acute reduction in blood volume."7 A retrospective study of patients with isolated extremity trauma or isolated penetrating abdominal trauma found that of the 71 patients presenting with systolic blood pressure of less than 100 mm Hg, 25 (35%) had a pulse rate of fewer than 100 beats/min.8 A retrospective study of patients at a trauma centre found that of 750 patients who presented with a systolic blood pressure of less than 90 mm Hg, 217 (28.9%) had a pulse rate of fewer than 90 beats/min.9 The authors of the study also suggested that bradycardia was associated with a better prognosis in certain subgroups of patients.
In the face of severe hypovolaemia, the bradycardia seen in the second phase of cardiovascular response to acute haemorrhage allows for a longer time for diastolic ventricular filling leading to an increased stroke volume.10 This bradycardia may result from the activation of a vagally mediated reflex arc originating from mechanoreceptors in the left ventricle.11 The bradycardic response may also be the result of a parasympathetic reflex mediated via the vagus nerve triggered by blood in the peritoneum.1 12 Vagus involvement is suggested by the fact that after cooling or cutting of the vagus nerves after rapid external haemorrhage in cats the fall in blood pressure was not affected, but the bradycardic response was absent.10 Why some patients do not show initial tachycardia is unknown.
Conclusion
Jansen RPS. Relative bradycardia: a sign of acute intraperitoneal bleeding. Aust NZ Obstet Gynaecol 1978;18: 206-8.
Secher NH, Sander Jensen K, Werner C, Warberg J, Bie P. Bradycardia during severe but reversible hypovolemic shock in man. Circ Shock 1984;14: 267-74.
Adams SL, Greene JS. Absence of a tachycardic response to intraperitoneal haemorrhage. J Emerg Med 1986;4: 383-9.
Snyder HS, Dresnick SJ. Lack of tachycardic response to hypotension in penetrating abdominal injuries. J Emerg Med 1989;7: 335-9.
Vayer JS, Henderson JV, Bellamy RF, Galper AR. Absence of a tachycardic response to shock in penetrating intraperitoneal injury. Ann Emerg Med 1988;17: 227-31.
Barriot P, Riou B. Haemorrhagic shock with paradoxical bradycardia. Intens Care Med 1987;13: 203-7.
American College of Surgeons. Advanced Trauma Life Support for Doctors. (ATLS) Instructor Course Manual. Chicago: ACoS, 1997.
Thompson D, Adams SL, Barrett J. Relative bradycardia in patients with isolated penetrating abdominal trauma and isolated extremity trauma. Ann Emerg Med 1990;19: 268-75.
Demetriades D, Chan LS, Bhasin P, Berne TV, Ramicone E, Huicochea F, et al. Relative bradycardia in patients with traumatic hypotension. J Trauma 1998;45: 534-9.
Oberg P, Thoren P. Increased activity in vagal cardiac afferents correlated to the appearance of reflex bradycardia during severe haemorrhage in cats. Acta Physiol Scand 1970;80(suppl): 22A-23A.
Oberg B, Thoren P. Increased activity in left ventricular receptors during haemorrhage or occlusion of caval veins in the cat. Acta Physiol Scand 1972;85: 164-3.
Snyder HS. Lack of a tachycardic response to hypotension with ruptured ectopic pregnancy. Am J Emerg Med 1990;8: 23-6.(Ian Thomas, specialist re)