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Departments of 1 General Medicine, 2 Cardiology, and 3 Medicine, Christchurch Hospital, Christchurch, New Zealand
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ABSTRACT |
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 TOP
 ABSTRACT
 INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The importance
of cardiac output (CO) to blood pressure level during vasovagal syncope
is unknown. We measured thermodilution CO, mean blood pressure (MBP),
and leg muscle mean sympathetic nerve activity (MSNA) each minute
during 60° head-up tilt in 26 patients with recurrent syncope. Eight
patients tolerated tilt (TT) for 45 min (mean age 60 ± 5 yr) and
15 patients developed syncope during tilt (TS) (mean age 58 ± 4 yr, mean tilt time 15.4 ± 2 min). In TT patients, CO decreased
during the first minute of tilt (from 3.2 ± 0.2 to 2.5 ± 0.3 l · min
1 · m2,
P = 0.001) and thereafter remained stable between
2.5 ± 0.3 (P = 0.001) and 2.4 ± 0.2 l · min1 · m2
(P = 0.004) at 5 and 45 min, respectively. In TS
patients, CO decreased during the first minute (from 3.3 ± 0.2 to
2.7 ± 0.1 l · min1 · m2,
P = 0.02) and was stable until 7 min before syncope,
falling to 2.0 ± 0.2 at syncope (P = 0.001). Regression slopes for CO versus time during tilt were
0.01 min1 in TT versus 0.1
l · min1 · m2 · min1
in TS (P = 0.001). However, MBP was more closely
correlated to total peripheral resistance (R = 0.56, P = 0.001) and MSNA (R = 0.58, P = 0.001) than CO (R = 0.32, P = 0.001). In vasovagal reactions, a progressive
decline in CO may contribute to hypotension some minutes before syncope occurs.
tilt test; neurocardiogenic syncope; vasodilatation
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INTRODUCTION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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VASOVAGAL SYNCOPE is a common condition characterized by transient hypotension and relative bradycardia (35). Surprisingly, the importance of cardiac output (CO) is uncertain and the value of pacemaker therapy is controversial (30, 34). Using a variety of stimuli to induce syncope, several investigators (35) have demonstrated hypotension and withdrawal of muscle sympathetic nerve activity (MSNA), usually followed by bradycardia. The purpose of this study was to assess the contribution of CO to hypotension during tilt-induced syncope, which is accepted as a model for this condition (14). Blood pressure is dependent on total peripheral resistance (TPR) and CO, and, during syncope, plethysmographic studies (7, 17) have demonstrated forearm vasodilatation. CO is dependent on heart rate (HR) and stroke volume (SV). Several tilt studies (8, 30) have shown that HR rate decreases after the onset of hypotension and artificially increasing the rate does not normalize the blood pressure. However, Weissler et al. (38) demonstrated in 1957 that increasing venous filling pressure was the most effective way of terminating a vasovagal reaction during orthostasis. Therefore, during tilt-induced syncope, venous filling pressure may be the main determinant of end-diastolic volume, SV, CO, and ultimately mean blood pressure (MBP) (26). We aimed to discern the importance of CO to MBP by measuring the rate of CO decay during the time between the onset of hypotension and syncope. Over the same time interval, we also correlated CO, TPR, and MSNA to MBP. We hypothesized that CO would decrease more rapidly in patients who developed syncope during tilt but that MBP pressure would be more closely correlated to TPR and MSNA than CO.
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METHODS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Patients.
Twenty-six consecutive patients underwent tilt testing after being
screened for epilepsy, cardiac syncope, and autonomic disease. Demography and previous investigations are summarized in Table 1. All patients had a history suggestive
of recurrent vasovagal syncope with at least two major episodes during
the previous year. Patients with postural hypotension, heart failure,
angina, or suspected cardiac syncope were excluded. No patients had
carotid sinus hypersensitivity. Patients were divided into
tilt-tolerant (TT; n = 8) and tilt-syncope groups (TS;
n = 15) on the basis of their response to tilt. Syncope
during tilt was defined as loss of consciousness and muscle tone
associated with MBP <60 mmHg. The mean time to syncope was 15.4 ± 2 min, which is comparable to other studies (17, 22,
25) and included three patients who developed syncope after 20 min.
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Tilt test protocol.
The investigations were performed at Christchurch Hospital between May
1996 and June 1997 with the approval of the hospital ethics committee.
All vasoactive medications were stopped 5 days before the test and
permanent pacemakers were disabled immediately beforehand. 
-Agonist
provocation may act through a variety of different mechanisms not
operative during vasovagal syncope and so it was not used
(3).
Cardiac output. All methods of assessing CO may be unreliable during hemodynamic instability so two independent techniques were used. It was important to measure CO at 1-min intervals during tilt as accurately as possible. We used bolus thermodilution and mixed venous O2 saturation (SvO2) because both methods allowed rapid and repeated measurements using the same catheter. Extensive experience with these techniques from intensive care workers has been reported in a variety of patients (6, 11) and both are used as the gold standard for the assessment of noninvasive methods (16, 21).
Thermodilution CO and SvO2 were measured using a pulmonary artery fiberoptic oximetry catheter (Oximetrix III, Abbott Laboratories; North Chicago, IL) and CO computer (Critical Care System model 3300, Abbott). Ten milliliters of a room temperature (21-24°C) solution of 5% glucose water were injected in <4 s by the same operator. Injections were given at end expiration and the morphology of the thermodilution curve was checked. Baseline CO was averaged from three serial measurements taken during the 5 min immediately before tilt. If the variance was >10%, two additional measurements were made and the high and low values were rejected. During tilt, single measurements were made each minute for the duration of tilt so that the maximum total volume injected was 600 ml. CO was indexed to body surface area and TPR was calculated by dividing MBP by CO. SvO2 was measured by fiber-optic venous reflectance oximetry using the same catheter and computer system. Because oxygen consumption and arterial oxygen saturation were not measured, absolute values for CO were not calculated by this method, but assuming these variables remain constant, SvO2 is directly related to CO with an estimated coefficient of variation of
10%
(11). There is evidence to suggest that during
tilt-induced syncope, hyperventilation occurs in some patients
(38). This may increase oxygen consumption and so falsely
increase CO calculated from the Fick equation (39).
Microneurography.
Microneurography needles were positioned for recording MSNA from the
right peroneal nerve, as described by Vallbo et al. (33). The nerve was located behind the head of fibula, and, with the use of
transcutaneous stimulation, an insulated tungsten electrode with a 1- to 5-µm tip was inserted. The nerve signal was amplified (×100,000), filtered (700-2,000 Hz), integrated (time constant 0.1 ms), and displayed on-line with blood pressure and ECG. Bursts of
sympathetic activity were identified and counted each minute (bs/min)
by the same operator. The nerve signal was accepted provided that the
following criteria were met: 1) the signal-to-background ratio was 
3, 2) bursts were pulse synchronous,
3) the amplitude of the bursts was inversely proportional to
diastolic BP, and 4) skin activity was absent.
Microneurographic data was obtained from all TT patients and 12 TS patients.
Statistics. Baseline and tilt values were compared within groups using repeated-measures ANOVA, and, when changes were significant, individual comparisons were made between specific time points and baseline with the use of paired t-tests. Between-group comparisons at baseline and after 1 min of tilt were made with the use of independent t-tests. Comparisons of linear regression slopes (CO vs. time) between groups were made using the general linear model. In TT patients, individual points on the regression line were at 5-min intervals for 45 min of tilt and in TS patients at 1-min intervals for 7 min before syncope. In TS patients, correlations between variables (CO, TPR, MSNA, and MBP) were made over the same time interval.
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RESULTS |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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The two groups had similar mean values for age, body surface area, and duration of symptoms, but there was a higher male-to-female ratio in TS patients. Minor coronary artery disease was present in four patients in each group.
Figures 1 and
2 show the hemodynamic and sympathetic
responses to tilt in both groups. At baseline and after 1 min
of tilt there were no differences between groups. The respective
baseline values for TT and TS patients were as follows: MBP, 111 ± 3 and 117 ± 4 mmHg; HR, 75 ± 4 and 66 ± 3 beats/min; CO, 3.2 ± 2 and 3.3 ± 0.2 l · min1 · m2;
SvO2, 73 ± 1 and 76 ± 1%; PDBP, 15 ± 2 and 16 ± 1 mmHg; MSNA, 31 ± 4 and 35 ± 4 bursts/min.
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In TT patients after 1 min of tilt, MBP and HR were stable at 111 ± 5 mmHg and 81 ± 3 beats/min. In the TS group, MBP decreased to
112 ± 4 mmHg (P = 0.05), whereas HR increased
75 ± 4 beats/min (P = 0.001). In the respective
groups, CO decreased to 2.5 ± 0.3 (P = 0.001) and 2.7 ± 0.1 l · min1 · min2
(P = 0.02), SvO2 to 69 ± 1%
(P = 0.001) and 68 ± 2% (P = 0.001), and PDBP to 8 ± 2 (P = 0.01) and 7 ± 1 mmHg (P = 0.001), whereas MSNA increased to
44 ± 5 (P = 0.001) and 48 ± 4 bursts/min
(P = 0.002).
In TT patients during the remainder of tilt, MBP gradually decreased to
101 ± 5 mmHg after 20 min (P = 0.03) and to
92 ± 6 mmHg after 45 min (P = 0.01). CO,
SvO2 and PDBP remained decreased at 2.4 ± 0.2 l · min1 · m2, 62 ± 2% and 5 ± 1 mmHg, respectively, after 45 min (P = 0.004, P = 0.002, and P = 0.003).
MSNA levels remained increased at 48 ± 5 bursts/min after 45 min
(P = 0.002). In TS patients, MBP progressively decreased during the 7 min before syncope from 104 ± 4 to 47 ± 3 mmHg (P = 0.005, P = 0.001)
whereas HR was maintained above baseline until syncope, when it
decreased to 59 ± 5 beats/min (P = 0.06). PDBP
remained decreased between 6 ± 1 and 4 ± 1 mmHg (P = 0.001). Despite progressive hypotension, MSNA
decreased to 41 ± 6 bursts/min 7 min before syncope
(P = 0.3), and further to 11 ± 2 bursts/min at
syncope (P = 0.001). Over this time, CO and
SvO2 decreased linearly from 2.7 ± 0.2 to 2.0 ± 0.2 l · min1 · m2
(P = 0.001) and from 67 ± 2% to 61 ± 2%
(P = 0.001). Mean regression slopes for CO and
SvO2 versus time were greater in the TS group: 0.01
(TT) versus 0.1
l · min1 · m2 · min1
(TS) (P = 0.001) and 0.1 versus 0.8%/min
(P = 0.001), respectively. The range of R
values for individual time versus CO slopes was 0.14-0.88 in TT
(5/8, P < 0.05) and 0.11-0.94 in TS (14/15,
P < 0.05). During the 7 min before syncope, closer
correlations for MSNA and TPR versus MBP were demonstrated
(R = 0.58, P = 0.001, and
R = 0.56, P = 0.001) compared with CO
versus MBP (R = 0.32, P = 0.001) (Fig.
3).
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DISCUSSION |
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TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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Although CO fell in all subjects during the first minute of tilt, the patients who became hypotensive were characterized by a further accelerated decline in CO, which began some minutes before syncope. During the progressive hypotension before syncope, MBP was correlated more closely to MSNA and TPR than CO.
CO in vasovagal syncope. Surprisingly little is known about temporal relationships between CO, ventricular filling pressures, MBP, and MSNA during the minutes immediately preceding syncope. This is due to the following: 1) vasovagal reactions may be of rapid onset and CO is difficult to measure quickly, 2) in laboratory studies, syncopal reactions occur at different times from the onset of the stimulus, which makes collective analysis difficult, 3) the use of vasodilators during tilt tests to increase the likelihood of syncope may falsely affect CO, and 4) until recently, the emphasis has been on absolute rather than the rate of change in CO. Previous studies (4, 5, 13) using dye and thermodilution demonstrated a similar decrease in CO to what we measured (~25%) but sampling intervals were long and control data were few. The significance of this finding was uncertain after the demonstration of a 30% decrease during tilt and lower body suction in normotensive subjects (5, 24). Furthermore, Stevens et al. (31) showed no exaggerated decrease in CO during early tilt in subjects who developed syncope between 10 and 18 min later. Wahbha et al. (36) measured CO indirectly using the single-breath method at 5-min intervals and found that CO progressively decreased during tilt, irrespective of the outcome. Although CO decreased, it was uncertain when and how rapidly this occurred during syncope. Closer monitoring during the period immediately before syncope was required. In a recent study (18), beat-to-beat SV was measured during tilt using pressure wave analysis and a gradual decrease was observed in seven normal subjects. However, SV decay appeared to be accelerated in three subjects who became hypotensive or symptomatic. Echocardiographic estimation of SV during tilt also suggested a more rapid decay before syncope (12, 40). With the use of two independent methods, we have demonstrated that CO decreases more rapidly in those patients who develop syncope during tilt. CO decreased to similar levels irrespective of the response to tilt but over a much shorter time in the TS group. We conclude that the absolute decrease may not be as important as the linear rate of decrease. HR was relatively maintained before syncope; therefore, the decrease in CO was secondary to a decrease in SV. Patients who developed syncope failed to maintain CO despite similar left ventricular filling pressures and lower TPR. This would suggest that venous filling pressure was decreased in syncope patients. We are aware that PDBP is only an indirect indicator of left ventricular function and venous filling (26). Even right atrial pressure may be difficult to interpret as an index of venous return because of venous compliance, which allows large changes in central blood volume with relatively small pressure changes. There is no evidence for left ventricular systolic dysfunction before syncope in echocardiographic studies (12, 19, 29, 40). There is other evidence for impaired venoconstriction in vasovagal patients (20, 32). Therefore, we suspect that CO decreases more rapidly before syncope because of impaired venous return. Against this, a study using thoracic impedance in 25 tilted patients showed no change in SV during the last 5 min before syncope (25). However, thoracic impedance may not always be a reliable measure of CO (21). We have observed that the upstroke of the impedance waveform becomes harder to analyze during tilt and this may make SV measurement inaccurate (37).
MBP, TPR, and MSNA. Although CO decreased more rapidly in syncope patients, MBP was more closely correlated to TPR and MSNA. It has been suggested that the dominant hypotensive mechanism in vasovagal syncope is withdrawal of MSNA and arterial vasodilation (7, 17, 28). We found that, although MSNA increased initially, it decreased back to baseline as early as 7 min before syncope, despite progressive hypotension. If this attenuated MSNA response affected only the arterial resistance vessels, CO would be expected to increase. As we have demonstrated, both CO and TPR decreased before syncope. We postulate that partial MSNA withdrawal mediates venodilation resulting in decreased CO and mild hypotension early in the vasovagal reaction, whereas total MSNA withdrawal mediates arteriolar vasodilation, resulting in severe hypotension and syncope. Finally, cardiac sympathetic withdrawal occurs later, resulting in bradycardia. This implies that the venous circulation may be more sensitive to changes in MSNA than the arteriolar resistance vessels (2). It is important to remember that MSNA in skeletal muscle may be different to that in other venous capacitance beds and there may be other factors involved in venous return besides active compliance, including passive recoil, central blood volume, and even arterial blood pressure (1, 9, 10, 27). For example, during the first minute of tilt, when blood is rapidly pooled in the legs, resulting in decreased venous return and central blood volume, CO decreased, despite a rapid increase in MSNA.
Study limitations. Tilt-induced syncope may not be the physiological equivalent of vasovagal syncope, which can be triggered by a variety of stimuli other than orthostatic stress (3). The invasive techniques used in this study may have affected autonomic reflexes and precluded the use of normal controls. However, we were concerned more with the physiology of vasovagal reactions than comparisons with normal controls. To achieve satisfactory regression slopes, we were only able to study patients monitored for at least 8 min of tilt; therefore, we cannot comment on patients who develop syncope before this time or who are extremely sensitive to tilt (23). In three patients whose tilt reactions occurred after 20 min, it could be argued that our regression slopes were not representative of total tilt time. However, individual analysis of these patients showed uniform CO decay slopes throughout tilt. Finally, both methods of CO estimation can be criticized on several points. First, thermodilution and venous oxygen may overestimate CO when there is increased venous pooling and hyperventilation. Second, individual dilution measurements take at least 30 s, which limits duplication during tilt. Third, the total injected volume may have hemodynamic effects in some patients and SvO2 may be misleading in patients with respiratory insufficiency (39). We emphasize that trends in CO were analyzed, not absolute values, and that most of the above factors would result in falsely decreasing the CO decay slopes.
We conclude that an important mechanism in vasovagal syncope may be an exaggerated rate of decline in CO secondary to venodilation and possibly sympathetic withdrawal. This is consistent with laboratory studies showing that orthostatic syncope can be prevented by inflating an antigravity suit, or simply crossing the legs (34, 38), and the clinical maxim that vasovagal syncope is reversed most rapidly by lying the patient down and raising the legs.| |
ACKNOWLEDGEMENTS |
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This study was supported by the New Zealand Heart Foundation. The figures were prepared by the Medical Illustrations Department, Christchurch Hospital.
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FOOTNOTES |
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Address for reprint requests and other correspondence: D. L. Jardine, General Medicine Dept., Christchurch Hospital, PO Box 4710, Christchurch, New Zealand (E-mail: David.Jardine{at}cdhb.govt.nz).
The costs of publication of this article were defrayed in part by the payment of page charges. The article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
10.1152/ajpheart.00640.2001
Received 23 July 2001; accepted in final form 30 November 2001.
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REFERENCES |
|---|
|
TOP
ABSTRACT
INTRODUCTION
METHODS
RESULTS
DISCUSSION
REFERENCES
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|---|
1.
Abboud, FM.
Control of the various components of the peripheral vasculature.
Fed Proc
31:
1226-1239,
1972[ISI][Medline].
2.
Abboud, FM,
Schmid PG,
and
Eckstein JW.
Vascular responses after alpha adrenergic receptor blockade. Responses of capacitance and resistance vessels to norepinephrine in man.
J Clin Invest
7:
1-9,
1968.
3.
Benditt, DG.
Neurally mediated syncopal syndromes: pathophysiological concepts and clinical evaluation.
Pacing Clin Electrophysiol
20:
572-584,
1997[Medline].
4.
Bergenwald, L,
Freyschuss U,
and
Sjostrand T.
The mechanism of orthostatic and hemorrhagic fainting.
Scand J Clin Lab Invest
37:
209-216,
1977[ISI][Medline].
5.
Bickelman, AG,
Lippschutz EJ,
and
Brunjes CF.
Hemodynamics of idiopathic orthostatic hypotension.
Am J Med
30:
26-38,
1961.
6.
Cariou, A,
Monchi M,
and
Dhainaut J.
Continuous cardiac output and mixed venous oxygen saturation monitoring.
J Crit Care
13:
198-213,
1998[ISI][Medline].
7.
Dietz, NM,
Halliwill JR,
Spielmann JM,
Lawler LA,
Papouchado BG,
Eickhoff TJ,
and
Joyner MJ.
Sympathetic withdrawal and forearm vasodilation during vasovagal syncope.
J Appl Physiol
82:
1785-1793,
1997
8.
El-Bedawi, KM,
Wahbha MA,
and
Hainsworth R.
Cardiac pacing does not improve orthostatic tolerance in patients with vasovagal syncope.
Clin Auton Res
4:
233-237,
1994[Medline].
9.
El-Sayed, H,
and
Hainsworth R.
Relationship between plasma volume, carotid baroreceptor sensitivity and orthostatic tolerance.
Clin Sci (Lond)
88:
463-470,
1995[Medline].
10.
Epstein, S,
Stampfer M,
and
Beiser GD.
Role of capacitance and resistance vessels in vasovagal syncope.
Circulation
37:
524-533,
1968
11.
Fahey, PJ,
Harris K,
and
Vanderwarf C.
Clinical experience with continuous monitoring of venous oxygen saturation in respiratory failure.
Chest
86:
748-752,
1984
12.
Fitzpatrick, A,
Williams T,
Ahmed R,
Lightman S,
Bloom SR,
and
Sutton R.
Echocardiographic and endocrine changes during vasovagal syncope induced by prolonged head-up tilt.
Europ J Card Pacing Electrophysiol
2:
121-128,
1992.
13.
Glick, G,
and
Yu P.
Hemodynamic changes during spontaneous vasovagal reactions.
Am J Med
34:
42-51,
1963[ISI][Medline].
14.
Grubb, BP,
and
Kosinski D.
Tilt table testing: concepts and limitations.
Pacing Clin Electrophysiol
20:
781-787,
1997[Medline].
15.
Hargreaves, AD,
and
Muir AL.
Lack of variation in venous tone potentiates vasovagal syncope.
Br Heart J
67:
486-490,
1992
16.
Harms, MPM,
Wesseling KH,
Pott F,
Jenstrup M,
Van Goudoever J,
Secher NH,
and
Van Lieshout JJ.
Continuous stroke volume arterial pressure in humans under orthostatic stress.
Clin Sci (Lond)
97:
291-301,
1999[Medline].
17.
Jardine, DL,
Ikram H,
Frampton CM,
Frethey R,
Bennett SI,
and
Crozier IG.
Autonomic control of vasovagal syncope.
Am J Physiol Heart Circ Physiol
274:
H2110-H2115,
1998
18.
Jellema, WT,
Imholz BPM,
Oosting H,
Wesseling KH,
and
van Lieshout JJ.
Estimation of beat-to-beat changes in stroke volume from arterial pressure: a comparison of two pressure wave analysis techniques during head-up tilt in young healthy men.
Clin Auton Res
9:
185-192,
1999[ISI][Medline].
19.
Lee, T,
Chen M,
Su S,
Chao C,
Liau C,
and
Lee Y.
Excessive myocardial contraction in vasovagal syncope demonstrated by echocardiography during head-up tilt test.
Clin Cardiol
19:
137-140,
1996[ISI][Medline].
20.
Manyari, DE,
Rose S,
Tyberg JV,
and
Sheldon RS.
Abnormal reflex venous function in patients with vasovagal syncope.
J Am Coll Cardiol
27:
1730-1735,
1996[Abstract].
21.
Marik, PE,
Pendelton JE,
and
Smith R.
A comparison of hemodynamic parameters from transthoracic electrical bioimpedance with those parameters obtained by thermodilution and angiography.
Crit Care Med
25:
1545-1550,
1997[ISI][Medline].
22.
Morrillo, CA,
Eckberg DL,
Ellenbogen KA,
Beightol LA,
Hoag JB,
Kari UO,
Tahvanainen MS,
Kuusela TA,
and
Diedrich AM.
Vagal and sympathetic mechanisms in patients with orthostatic vasovagal syncope.
Circulation
96:
2509-2513,
1997
23.
Mosqueda-Garcia, R,
Furlan R,
Fernandez-Violante R,
Desai T,
Snell M,
Jarai Z,
Ananthram V,
Robertson RM,
and
Robertson D.
Sympathetic and baroreceptor reflex function in neurally mediated syncope evoked by tilt.
J Clin Invest
99:
2736-2744,
1997[ISI][Medline].
24.
Murray, RH,
Thompson LJ,
Bowers JA,
and
Albright CD.
Hemodynamic effects of graded hypovolemia and vasodepressor syncope induced by lower body negative pressure.
Am Heart J
76:
799-811,
1967.
25.
Novak, V,
Honos G,
and
Schondorf R.
Is the heart empty at syncope?
J Auton Nerv Syst
60:
83-92,
1996[ISI][Medline].
26.
Rothe, CF.
Physiology of venous return. An unappreciated boost to the heart.
Arch Intern Med
146:
977-982,
1986[Abstract].
27.
Samueloff, SL,
Browse NL,
and
Shepherd JT.
Response of capacity vessels in human limbs to head-up tilt and suction on lower body.
J Appl Physiol
21:
47-54,
1965.
28.
Schondorf, R,
and
Wieling W.
Vasoconstricor reserve in neurally mediated vasovagal syncope.
Clin Auton Res
10:
53-55,
2000[ISI][Medline].
29.
Shalev, Y,
Rami G,
Tchou PJ,
Anderson AJ,
Avitall B,
Akhtar M,
and
Jazayeri MR.
Echocardiographic demonstration of decreased left ventricular dimensions and vigorous myocardial contraction during syncope induced by head-up tilt.
J Am Coll Cardiol
18:
746-751,
1991[Abstract].
30.
Sra, JS,
Jazayeri MR,
Avitall B,
Dhala A,
Deshpande S,
Blanck Z,
and
Akhtar M.
Comparison of cardiac pacing with drug therapy in the treatment of neurocardiogenic (vasovagal) syncope with bradycardia or asystole.
N Engl J Med
328:
1085-1090,
1993
31.
Stevens, PM.
Cardiovascular dynamics during orthostasis and the influence of intravascular instrumentation.
Am J Cardiol
17:
211-218,
1966[ISI][Medline].
32.
Thompson, HL,
Atherton JJ,
Khafagi FA,
and
Frenneaux MP.
Failure of reflex venoconstriction during exercise in patients with vasovagal syncope.
Circulation
93:
953-959,
1996
33.
Vallbo, AB,
Hagbarth KE,
Torebjork HE,
and
Wallin BG.
Somatosensory, proprioceptive and sympathetic activity in human peripheral nerves.
Physiol Rev
59:
919-957,
1979
34.
Van Dijk, N,
Harms MP,
Linzer M,
and
Wieling W.
Treatment of vasovagal syncope: pacemaker or crossing legs?
Clin Auton Res
10:
347-349,
2000[ISI][Medline].
35.
Van Leishout, JJ,
Wieling W,
Karemaker JM,
and
Eckberg DL.
The vasovagal response.
Clin Sci (Lond)
81:
575-586,
1991[Medline].
36.
Wahbha, MAE,
Morley CA,
Al-Shamma YMH,
and
Hainsworth R.
Cardiovascular reflex responses in patients with unexplained syncope.
Clin Sci (Lond)
77:
547-553,
1989[Medline].
37.
Wang, X,
Sun HH,
and
Van De Water JM.
An advanced signal processing technique for impedance cardiography.
IEEE Trans Biomed Eng
42:
224-230,
1995[ISI][Medline].
38.
Weissler, AM,
Warren JV,
Estes EH,
McIntosh HD,
and
Leonard JJ.
Vasodepressor syncope.
Circulation
15:
875-882,
1957[ISI][Medline].
39.
Yang, SS,
Bentivoglio LG,
Maranhao V,
and
Goldberg H.
From Cardiac Catheter Data to Hemodynamic Parameters (3rd ed.). Philadelphia, PA: Davis, 1988, p. 42-66.
40.
Yamanouchi, Y,
Jaalouk S,
Shehadeh AA,
Jaeger F,
Goren H,
and
Fouad-Tarazi FM.
Changes in left ventricular volume during head-up tilt in patients with vasovagal syncope: an echocardiographic study.
Am Heart J
131:
73-80,
1996[ISI][Medline].
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 B. Verheyden, H. Ector, A. E. Aubert, and T. Reybrouck Tilt training increases the vasoconstrictor reserve in patients with neurally mediated syncope evoked by head-up tilt testing Eur. Heart J., June 2, 2008; 29(12): 1523 - 1530. [Abstract] [Full Text] [PDF]
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C. Murrell, L. Wilson, J. D. Cotter, S. Lucas, S. Ogoh, K. George, and P. N. Ainslie Alterations in autonomic function and cerebral hemodynamics to orthostatic challenge following a mountain marathon J Appl Physiol, July 1, 2007; 103(1): 88 - 96. [Abstract] [Full Text] [PDF]
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W. H. Cooke, K. L. Ryan, and V. A. Convertino Lower body negative pressure as a model to study progression to acute hemorrhagic shock in humans J Appl Physiol, April 1, 2004; 96(4): 1249 - 1261. [Abstract] [Full Text] [PDF]
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 Q. Fu, A. Arbab-Zadeh, M. A. Perhonen, R. Zhang, J. H. Zuckerman, and B. D. Levine Hemodynamics of orthostatic intolerance: implications for gender differences Am J Physiol Heart Circ Physiol, January 1, 2004; 286(1): H449 - H457. [Abstract] [Full Text] [PDF]
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