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Postural position and neurocardiogenic syncope in late pregnancy
Postural Position and Neurocardiogenic Syncope in Late Pregnancy Ming-He Huang, MD, PhD, William R. Roeske, MD, Hong Hu, Julia H. Indik, MD, PhD, and Frank I. Marcus, MD
RDCS,
A 23-year-old woman at 34 weeks’ gestation developed recurrent syncope due to profound sinus arrest captured on electrocardiography. Syncopal events occurred in the same sitting position. An echocardiogram revealed severe collapse of the inferior vena cava each time the patient changed her posture from a supine to a sitting position, which was related to the syncope. 䊚2003 by Excerpta Medica, Inc. (Am J Cardiol 2003;92:1252–1253)
yncope and presyncope are prevalent in pregnancy. A reS cent study reported that 5% of pregnant women experienced syncope, 28% had ⱖ1 presyncope episode, and 10% had recurrent presyncope.1 The etiologies involved in pregnant syncope are not well defined. We report a case of a patient who had recurrent syncope due to sinus arrest that was apparently provoked by compression of the inferior vena cava (IVC) by the gravid uterus. •••
The patient was a 23-year-old woman without previous illness. She was at 34 weeks’ gestation. She had 2 syncopal episodes within 15 minutes, both of which occurred in the same sitting position. The first episode was preceded by lightheadedness, followed by a brief loss of consciousness and convulsions. The 911 service was called by the patient’s aunt, who witnessed the event. Shortly after the arrival of paramedics, the patient From the Department of Medicine, Section of Cardiology, University of Arizona Medical Center, Sarver Heart Center, Tucson, Arizona. Dr. Huang’s address is: University of Arizona Medical Center, Sarver Heart Center, 1501 N. Campbell Ave., Tucson, Arizona 85724. E-mail: [email protected]. Manuscript received June 24, 2003; revised manuscript received and accepted July 30, 2003.
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FIGURE 1. (A) Electrocardiographic rhythm strip showing sinus arrest. The first sinus beat is followed by a 9-second pause before a supraventricular complex appears (spikes preceding the last QRS complex are a baseline artifact). (B and C) Echocardiography shows a decrease in the diameter (from 1.95 to 0.86 cm, equivalent to an 80% reduction in cross-sectional area) of the proximal IVC (arrows) near its right atrial (RA) junction as induced by a postural change from supine to sitting. This sitting position was associated with sinus arrest (A) and recurrent syncope. The IVC diameter was measured at end expiration as shown by the respirometer cursor. (D) Low-pressure active afferent response generated by a mechanosensitive afferent neuron in a thoracic dorsal root ganglion with its sensory endings located in the left ventricle. Burst neuronal activity (bottom tracing) occurred when left ventricular chamber systolic pressure (LVP) rapidly decreased during a 20-second (between arrows) occlusion of the IVC (reprinted from Huang et al,5 with permission).
had a second syncope episode associated with convulsions. The paramedics obtained an electrocardiogram that showed 9 seconds of pause at the time that the patient was unresponsive (Figure 1). Her blood pressure was undetectable at that time. The patient quickly regained consciousness. Late physical examination did not reveal orthostatic hypotension. Carotid massage did not induce bradycardia. An echocardiogram showed normal cardiac function. However, echocardiography repeatedly demonstrated a 54% decrease in the diameter of the IVC, proximal to the right atrial junction each time the patient changed her posture from a supine to a sitting position, which was associated with her syncope (Figure 1). •••
The documented 9 seconds of
©2003 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 92 November 15, 2003
sinus arrest was sufficient to interrupt cerebral blood flow, thus causing syncope. The gravid uterus can cause significant IVC compression in patients lying in the supine, right decubitus, and, rarely, the sitting position in late pregnancy. IVC compression has been linked to “supine hypotensive syndrome,” a clinical entity associated with syncope in late pregnancy.2 The mechanisms underlying supine hypotensive syncope are not well defined. Although reflex-mediated bradycardia2 or tachycardia3 have been proposed as potential mechanisms, severe bradyarrhythmias sufficient to cause syncope in pregnancy have not been documented in the literature. This case may be the first to record bradycardia– hypotensive syncope, presumably triggered by IVC compression due to postural change. 0002-9149/03/$–see front matter doi:10.1016/j.amjcard.2003.07.047
The IVC diameter is correlated with cardiac venous return.4 Brief IVC occlusion drastically reduces cardiac venous return and cardiac chamber pressure, which may activate pressure-sensitive afferent nerve endings in the heart (Figure 1).5 Activated cardiac afferent nerves transmit hypotensive signals to the spinal cord through dorsal root ganglion sympathetic afferent neurons5 and to the medulla through vagal afferent nerves.6 These cardiac afferent inputs may inhibit sympathetic output at the spinal level and stimulate vagal efferent neurons at the medulla, resulting in sympathetic inhibition and vagal stimulation. This neuronal reflex may produce intense bradyarrhythmias and hypotension, resulting in presyncope or syncope.
Thus, neurocardiogenic syncope triggered by IVC collapse may represent an important mechanism involved in syncope frequently encountered in late-term pregnant women who otherwise have normal hearts. Prevention of neurocardiogenic syncope in late pregnancy may be achieved by avoiding dehydration and prolonged sitting or right decubitus positions that may cause severe IVC compression with compromised venous return. Pacemaker therapy is not beneficial in patients with recurrent neurocardiogenic syncope,7 which carries a benign long-term prognosis.8 1. Gibson PS, Powrie R, Pipert J. Prevalence of syncope and recurrent presyncope during pregnancy. Obstet Gynecol 2001;97:S41–S42.
2. Kinsella SM, Tuckey JP. Perioperative bradycar-
dia and asystole: relationship to vasovagal syncope and Bezold-Jarisch reflex. Br J Anesth 2001;86:859 – 868. 3. Schmitt D. The hypotensive syndrome in the supine position in late pregnancy. N Engl J Med 1958; 259:1219 –1221. 4. Mintz GS, Kotler MN, Parry WR, Iskandrian AS, Kane SA. Real-time inferior vena caval ultrasonography: normal and abnormal findings and its use in assessing right-heart function. Circulation 1981;64: 1018 –1025. 5. Huang MH, Horackova M, Negoescu RM, Wolf SG, Armour JA. Polysensory response characteristics of dorsal root ganglion neurons that may serve sensory functions during myocardial ischemia. Cardiovasc Res 1996;32:503–515. 6. Abboud FM. Neurocardiogenic syncope. N Engl J Med 1993;328:1117–1120. 7. Connolly SJ, Sheldon R, Thorpe KE, Roberts RS, Ellenbogen KA, Wilkoff BL, Morillo C, Gent M. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope. Second Vasovagal Pacemaker Study (VPS II): a randomized trial. JAMA 2003;289:2224 –2229. 8. Soteriades ES, Evans JC, Larson MG, Chen MH, Chen L, Benjamin E, Levy D. Incidence and prognosis of syncope. N Engl J Med 2002;347:878 – 885.
CASE REPORT
1253
RDCS,
A 23-year-old woman at 34 weeks’ gestation developed recurrent syncope due to profound sinus arrest captured on electrocardiography. Syncopal events occurred in the same sitting position. An echocardiogram revealed severe collapse of the inferior vena cava each time the patient changed her posture from a supine to a sitting position, which was related to the syncope. 䊚2003 by Excerpta Medica, Inc. (Am J Cardiol 2003;92:1252–1253)
yncope and presyncope are prevalent in pregnancy. A reS cent study reported that 5% of pregnant women experienced syncope, 28% had ⱖ1 presyncope episode, and 10% had recurrent presyncope.1 The etiologies involved in pregnant syncope are not well defined. We report a case of a patient who had recurrent syncope due to sinus arrest that was apparently provoked by compression of the inferior vena cava (IVC) by the gravid uterus. •••
The patient was a 23-year-old woman without previous illness. She was at 34 weeks’ gestation. She had 2 syncopal episodes within 15 minutes, both of which occurred in the same sitting position. The first episode was preceded by lightheadedness, followed by a brief loss of consciousness and convulsions. The 911 service was called by the patient’s aunt, who witnessed the event. Shortly after the arrival of paramedics, the patient From the Department of Medicine, Section of Cardiology, University of Arizona Medical Center, Sarver Heart Center, Tucson, Arizona. Dr. Huang’s address is: University of Arizona Medical Center, Sarver Heart Center, 1501 N. Campbell Ave., Tucson, Arizona 85724. E-mail: [email protected]. Manuscript received June 24, 2003; revised manuscript received and accepted July 30, 2003.
1252
FIGURE 1. (A) Electrocardiographic rhythm strip showing sinus arrest. The first sinus beat is followed by a 9-second pause before a supraventricular complex appears (spikes preceding the last QRS complex are a baseline artifact). (B and C) Echocardiography shows a decrease in the diameter (from 1.95 to 0.86 cm, equivalent to an 80% reduction in cross-sectional area) of the proximal IVC (arrows) near its right atrial (RA) junction as induced by a postural change from supine to sitting. This sitting position was associated with sinus arrest (A) and recurrent syncope. The IVC diameter was measured at end expiration as shown by the respirometer cursor. (D) Low-pressure active afferent response generated by a mechanosensitive afferent neuron in a thoracic dorsal root ganglion with its sensory endings located in the left ventricle. Burst neuronal activity (bottom tracing) occurred when left ventricular chamber systolic pressure (LVP) rapidly decreased during a 20-second (between arrows) occlusion of the IVC (reprinted from Huang et al,5 with permission).
had a second syncope episode associated with convulsions. The paramedics obtained an electrocardiogram that showed 9 seconds of pause at the time that the patient was unresponsive (Figure 1). Her blood pressure was undetectable at that time. The patient quickly regained consciousness. Late physical examination did not reveal orthostatic hypotension. Carotid massage did not induce bradycardia. An echocardiogram showed normal cardiac function. However, echocardiography repeatedly demonstrated a 54% decrease in the diameter of the IVC, proximal to the right atrial junction each time the patient changed her posture from a supine to a sitting position, which was associated with her syncope (Figure 1). •••
The documented 9 seconds of
©2003 by Excerpta Medica, Inc. All rights reserved. The American Journal of Cardiology Vol. 92 November 15, 2003
sinus arrest was sufficient to interrupt cerebral blood flow, thus causing syncope. The gravid uterus can cause significant IVC compression in patients lying in the supine, right decubitus, and, rarely, the sitting position in late pregnancy. IVC compression has been linked to “supine hypotensive syndrome,” a clinical entity associated with syncope in late pregnancy.2 The mechanisms underlying supine hypotensive syncope are not well defined. Although reflex-mediated bradycardia2 or tachycardia3 have been proposed as potential mechanisms, severe bradyarrhythmias sufficient to cause syncope in pregnancy have not been documented in the literature. This case may be the first to record bradycardia– hypotensive syncope, presumably triggered by IVC compression due to postural change. 0002-9149/03/$–see front matter doi:10.1016/j.amjcard.2003.07.047
The IVC diameter is correlated with cardiac venous return.4 Brief IVC occlusion drastically reduces cardiac venous return and cardiac chamber pressure, which may activate pressure-sensitive afferent nerve endings in the heart (Figure 1).5 Activated cardiac afferent nerves transmit hypotensive signals to the spinal cord through dorsal root ganglion sympathetic afferent neurons5 and to the medulla through vagal afferent nerves.6 These cardiac afferent inputs may inhibit sympathetic output at the spinal level and stimulate vagal efferent neurons at the medulla, resulting in sympathetic inhibition and vagal stimulation. This neuronal reflex may produce intense bradyarrhythmias and hypotension, resulting in presyncope or syncope.
Thus, neurocardiogenic syncope triggered by IVC collapse may represent an important mechanism involved in syncope frequently encountered in late-term pregnant women who otherwise have normal hearts. Prevention of neurocardiogenic syncope in late pregnancy may be achieved by avoiding dehydration and prolonged sitting or right decubitus positions that may cause severe IVC compression with compromised venous return. Pacemaker therapy is not beneficial in patients with recurrent neurocardiogenic syncope,7 which carries a benign long-term prognosis.8 1. Gibson PS, Powrie R, Pipert J. Prevalence of syncope and recurrent presyncope during pregnancy. Obstet Gynecol 2001;97:S41–S42.
2. Kinsella SM, Tuckey JP. Perioperative bradycar-
dia and asystole: relationship to vasovagal syncope and Bezold-Jarisch reflex. Br J Anesth 2001;86:859 – 868. 3. Schmitt D. The hypotensive syndrome in the supine position in late pregnancy. N Engl J Med 1958; 259:1219 –1221. 4. Mintz GS, Kotler MN, Parry WR, Iskandrian AS, Kane SA. Real-time inferior vena caval ultrasonography: normal and abnormal findings and its use in assessing right-heart function. Circulation 1981;64: 1018 –1025. 5. Huang MH, Horackova M, Negoescu RM, Wolf SG, Armour JA. Polysensory response characteristics of dorsal root ganglion neurons that may serve sensory functions during myocardial ischemia. Cardiovasc Res 1996;32:503–515. 6. Abboud FM. Neurocardiogenic syncope. N Engl J Med 1993;328:1117–1120. 7. Connolly SJ, Sheldon R, Thorpe KE, Roberts RS, Ellenbogen KA, Wilkoff BL, Morillo C, Gent M. Pacemaker therapy for prevention of syncope in patients with recurrent severe vasovagal syncope. Second Vasovagal Pacemaker Study (VPS II): a randomized trial. JAMA 2003;289:2224 –2229. 8. Soteriades ES, Evans JC, Larson MG, Chen MH, Chen L, Benjamin E, Levy D. Incidence and prognosis of syncope. N Engl J Med 2002;347:878 – 885.
CASE REPORT
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