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G Spadacini

Publications and source records attributed to G Spadacini.

18 recordsLinked to original sources

Peripheral arterial vascular function at altitude: sea-level natives versus Himalayan high-altitude natives.

OBJECTIVES: Regulation of the vascular system may limit physical performance and contribute to adaptation to high altitude. We evaluated vascular function in 10 Himalayan high-altitude natives and 10 recently acclimatized sea-level natives at an altitude of 5,050 m. METHODS: We registered electrocardiogram, blood flow velocity in the common femoral artery, and blood pressure in the radial artery using non-invasive methods under baseline conditions, and during maximal vasodilation after 2 min leg occlusion. Vascular mechanics were characterized by estimating pulse wave velocity and input impedance. RESULTS: Pulse wave velocity and parameters of input impedance did not differ between groups under baseline conditions. In the post-ischemic period, the ratio between maximal hyperemic and baseline blood flow velocity was significantly higher in the high-altitude than in the sea-level natives (5.7 +/- 2.5 versus 3.8 +/- 1.2, P < 0.05). The leg vascular resistance decreased in the post-occlusive period without differences between groups. Characteristic impedance decreased in the post-ischemic period by about one third of the baseline level without differences between groups. The post-ischemic decrease of input impedance modulus was more marked in the high-altitude than in the sea-level natives at low frequencies (28 +/- 12 versus 6.4 +/- 20% at 2 Hz, P < 0.01). CONCLUSIONS: Our results demonstrate a superior ability to increase blood flow velocity as a response to muscular ischemia in high-altitude natives compared to sea-level natives. This phenomenon may be associated with a more effective coupling between blood pressure and blood flow which is probably caused by differences in conduit vessel function.

Adolescent↗

Radiofrequency catheter ablation of atrioventricular nodal reentry tachycardia: selective approach to the slow pathway via the superior vena cava.

Selective radiofrequency catheter ablation of the slow atrioventricular nodal pathway is currently considered the first-line therapy for patients suffering from recurrent symptomatic atrioventricular nodal reentry tachycardia. In most cases slow pathway conduction may be selectively eliminated or modified by the application of radiofrequency current at the posterior portion of Koch's triangle. The ablation site is usually targeted by careful mapping of this area performed using an ablation catheter advanced via the inferior vena cava approach. In this report we describe 2 cases in which the conventional approach to the target site was either impossible owing to the presence of an atresic inferior vena cava (case 1), or contraindicated in view of a history of common femoral vein thrombosis, subsequently extended up to the inferior vena cava (case 2). In both patients a superior vena cava approach was utilized and the slow pathway was successfully ablated. In case of arrhythmias necessitating slow pathway mapping and ablation, such an approach may be considered as a feasible and safe alternative whenever, owing to the presence of anomalies and/or diseases of the inferior vena cava, the conventional approach cannot be employed.

Adult↗

Effects of breathing control on cardiocirculatory modulation in Caucasian lowlanders and Himalayan Sherpas.

This study was performed to investigate the influence of breathing control on the autonomic cardiac regulation at high altitude in adapted and non-adapted awake subjects. We recorded electrocardiogram and pulse oximetry in 14 short-term acclimatized lowlanders and 14 Himalayan Sherpas during resting conditions at an altitude of 5,050 m. Spectrum analysis was performed on synchronized 15 min periods of R-R intervals and the oxygen saturation of arterial blood (SaO2). Despite mean SaO2 being similar in lowlanders and Himalayan Sherpas [78.5 (SD 7.0)% compared to 79.4 (SD5.8)%, respectively], fluctuations in SaO2 were significantly increased in lowlanders compared to Sherpas, thus indicating an unstable regulation of respiration control in lowlanders. Regression analysis demonstrated a significant relationship between spectrum power of SaO2 and the relative power of R-R intervals in the frequency band between 0.01 and 0.08 Hz in lowlanders, but not in Sherpas. Our results demonstrate differences in respiratory and autonomic cardiac control between non-adapted lowlanders and Himalayan high-altitude residents and indicate that unstable breathing control during chronic hypobaric hypoxia is significantly correlated with the autonomic cardiocirculatory regulation.

Acclimatization↗

Effects of controlled breathing, mental activity and mental stress with or without verbalization on heart rate variability.

OBJECTIVES: To assess whether talking or reading (silently or aloud) could affect heart rate variability (HRV) and to what extent these changes require a simultaneous recording of respiratory activity to be correctly interpreted. BACKGROUND: Sympathetic predominance in the power spectrum obtained from short- and long-term HRV recordings predicts a poor prognosis in a number of cardiac diseases. Heart rate variability is often recorded without measuring respiration; slow breaths might artefactually increase low frequency power in RR interval (RR) and falsely mimic sympathetic activation. METHODS: In 12 healthy volunteers we evaluated the effect of free talking and reading, silently and aloud, on respiration, RR and blood pressure (BP). We also compared spontaneous breathing to controlled breathing and mental arithmetic, silent or aloud. The power in the so called low- (LF) and high-frequency (HF) bands in RR and BP was obtained from autoregressive power spectrum analysis. RESULTS: Compared with spontaneous breathing, reading silently increased the speed of breathing (p < 0.05), decreased mean RR and RR variability and increased BP. Reading aloud, free talking and mental arithmetic aloud shifted the respiratory frequency into the LF band, thus increasing LF% and decreasing HF% to a similar degree in both RR and respiration, with decrease in mean RR but with minor differences in crude RR variability. CONCLUSIONS: Simple mental and verbal activities markedly affect HRV through changes in respiratory frequency. This possibility should be taken into account when analyzing HRV without simultaneous acquisition and analysis of respiration.

Arousal↗

[Cardiac rhythm disturbances in hypertensive cardiopathy].

Patients with hypertensive heart disease are at a significantly increased risk for cardiovascular morbidity and mortality. Ultrastructural and gross anatomical cardiac changes, combined with hemodynamic and neurovegetative balance fluctuations, are frequently responsible for cardiac arrhythmias of atrial and/or ventricular origin. The prevalence, the pathophysiologic mechanism and the prognostic significance of cardiac rhythm disturbances occurring in hypertensive heart disease are discussed in this review.

Arrhythmias, Cardiac↗

Effect of breathing rate on oxygen saturation and exercise performance in chronic heart failure.

BACKGROUND: In chronic heart failure (CHF), impaired pulmonary function can independently contribute to oxygen desaturation and reduced physical activity. We investigated the effect of breathing rate on oxygen saturation and other respiratory indices. METHODS: Arterial oxygen saturation (SaO2) and respiratory indices were recorded during spontaneous breathing (baseline) and during controlled breathing at 15, six, and three breaths per min in 50 patients with CHF and in 11 healthy volunteers (controls). 15 patients with CHF were randomly allocated 1 month of respiratory training to decrease their respiratory rate to six breaths per min. Respiratory indices were recorded before training, at the end of training, and 1 month after training. FINDINGS: During spontaneous breathing, mean SaO2 was lower in CHF patients than in controls (91-4% [SD 0.4] vs 95.4% [0.2], p<0.001). Controlled breathing increased SaO2 at all breathing rates in patients with CHF. Compared with baseline, minute ventilation increased at 15 breaths per min (+45.9% [9.8], p<0.01), did not change at six breaths per min, and decreased at three breaths per min (-40.3% [4.8], p<0.001). In the nine CHF patients who had 1 month of respiratory training, resting SaO2 increased from 92.5% (0.3) at baseline to 93.2% (0.4) (p<0.05), their breathing rate per min decreased from 13.4 (1.5) to 7.6 (1.9) (p<0.001), peak oxygen consumption increased from 1157 (83) to 1368 (110) L/min (p<0.05), exercise time increased from 583 (29) to 615 (23) min/s (p<0.05), and perception of dyspnoea reduced from a score of 19.0 (0.4) to 17.3 (0.9) on the Borg scale (p<0.05). There were no changes in the respiratory indices in the patients who did not have respiratory training. INTERPRETATION: Slowing respiratory rate reduces dyspnoea and improves both resting pulmonary gas exchange and exercise performance in patients with CHF.

Dyspnea↗

Influence of type of surgery on the occurrence of parasympathetic reinnervation after cardiac transplantation.

BACKGROUND: Cardiac autonomic reinnervation after human cardiac transplantation has been demonstrated frequently but to date only for sympathetic efferents. Standard surgical techniques leave many parasympathetic branches intact in the original atria and thus with less stimulus to reinnervate the donor atria. METHODS AND RESULTS: We used changes in the RR-interval power spectrum induced by sinusoidal modulation of arterial baroreceptors by neck suction at different frequencies to detect both parasympathetic and sympathetic reinnervation in 79 subjects with "standard" and 10 "bicaval" heart transplants. In 24 subjects (17 standard and 7 bicaval), the protocol was repeated 6 and 11 months after transplantation. Neck suction at 0.20 Hz produced a component at 0.20 Hz in the RR-interval spectrum not due to respiration (fixed at 0.25 Hz), which suggested parasympathetic reinnervation, in 4 of 10 bicaval but in only 2 of 79 standard transplant subjects (whose recipient atria underwent >50% resection to remove scars of previous interventions), P<.001. In only 1 (bicaval) transplant subject was parasympathetic reinnervation present 6 months after transplantation (confirmed 3 months later); in 4 subjects, it was absent at 6 months but appeared after 11 months after transplantation. Atropine (0.04 mg/kg i.v.) abolished the response to fast (0.20 Hz) and reduced that to slow stimulation, confirming the presence of parasympathetic reinnervation (4 subjects). CONCLUSIONS: Parasympathetic reinnervation depends on the surgical technique: because bicaval surgery cuts all sympathetic and parasympathetic nerves, regeneration might be stimulated similarly in both branches. Standard surgery cuts only approximately 50% of sympathetic fibers; most recipient parasympathetic axons remain intact, hence their regeneration might not be stimulated.

Atropine↗

Cardiovascular autonomic modulation and activity of carotid baroreceptors at altitude.

1. To assess the effects of acute exposure to high altitude on baroreceptor function in man we evaluated the effects of baroreceptor activation on R-R interval and blood pressure control at high altitude. We measured the low-frequency (LF) and high-frequency (HF) components in R-R, non-invasive blood pressure and skin blood flow, and the effect of baroreceptor modulation by 0. 1-Hz sinusoidal neck suction. Ten healthy sea-level natives and three high-altitude native, long-term sea-level residents were evaluated at sea level, upon arrival at 4970 m and 1 week later.2. Compared with sea level, acute high altitude decreased R-R and increased blood pressure in all subjects [sea-level natives: R-R from 1002+/-45 to 775+/-57 ms, systolic blood pressure from 130+/-3 to 150+/-8 mmHg; high-altitude natives: R-R from 809+/-116 to 749+/-47 ms, systolic blood pressure from 110+/-12 to 125+/-11 mmHg (P<0.05 for all)]. One week later systolic blood pressure was similar to values at sea level in all subjects, whereas R-R remained elevated in sea-level natives. The low-frequency power in R-R and systolic blood pressure increased in sea-level natives [R-R-LF from 47+/-8 to 65+/-10% (P<0.05), systolic blood pressure-LF from 1.7+/-0. 3 to 2.6+/-0.4 ln-mmHg2 (P<0.05)], but not in high-altitude natives (R-R-LF from 32+/-13 to 38+/-19%, systolic blood pressure-LF from 1. 9+/-0.5 to 1.7+/-0.8 ln-mmHg2). The R-R-HF decreased in sea-level natives but not in high-altitude natives, and no changes occurred in systolic blood pressure-HF. These changes remained evident 1 week later. Skin blood flow variability and its spectral components decreased markedly at high altitude in sea-level natives but showed no changes in high-altitude natives. Neck suction significantly increased the R-R- and systolic blood pressure-LF in all subjects at both sea level and high altitude.3. High altitude induces sympathetic activation in sea-level natives which is partially counteracted by active baroreflex. Despite long-term acclimatization at sea level, high-altitude natives also maintain active baroreflex at high altitude but with lower sympathetic activation, indicating a persisting high-altitude adaptation which may be genetic or due to baroreflex activity not completely lost by at least 1 year's sea-level residence.

Adult↗

Origin of respiratory sinus arrhythmia in conscious humans. An important role for arterial carotid baroreceptors.

BACKGROUND: We investigated whether respiratory sinus arrhythmia (RSA) in healthy humans originated from central neuronal oscillations or from peripheral baroreceptors responding to respiratory changes in venous return. METHODS AND RESULTS: During subjects' controlled breathing we used sinusoidal neck suction to influence RSA (spectral analysis of RR interval). In 11 subjects, 20-second apnea greatly reduced RSA, which was restored by neck suction at the frequency of respiration. Counteracting the respiration-induced cycles of carotid blood pressure decreased RSA in 13 subjects (from 2136 +/- 682 to 1372 +/- 561 ms2, P < .01). The critical phase of this neck suction was constant for each subject at around the phase shift (with regard to respiration-related fluctuations of blood pressure) best for smoothing respiratory (mechanical) changes in blood pressure. Suction of a non-baroreceptor area (the thigh) did not affect RSA. In 4 subjects, to separate the effects of peripheral baroreceptor afferents from respiration-entrained central oscillation (15 breaths/min), we cycled the neck suction at 12 cycles/min. Increasing neck suction from -7 to -30 mm Hg increased the ratio of the power of the 12 cycles compared with the 15-cycle RSA oscillation in RR interval spectral analysis from 0.26 to 2.57. A 12-cycle/min suction of an area other than the neck had little effect on the RR interval spectrum. CONCLUSIONS: RSA can be mimicked or reduced by stimulation of arterial baroreceptors with cycles of appropriately phased neck suction at the frequency of respiration. This suggests an important influence of the arterial baroreceptors in the generation of RSA in conscious humans.

Adult↗

Lack of peripheral modulation of cardiovascular central oscillatory autonomic activity during apnea in humans.

Respiratory sinus arrhythmia (RSA) high-frequency oscillations (HF) and slow fluctuations in heart rate (LF) are thought to result from entrainment of a medullary oscillator, from the baroreflex, or from a combination of both central and baroreflex mechanisms. We sought to distinguish between the alternatives by examining with spectral analysis the behavior of heart rate (R-R interval) and blood pressure in 10 healthy subjects (mean age 27 +/- 1 yr) during apnea, altering the rate of preapnea entrainment stimuli by changing the frequency either of respiration (controlled at 0.1 or 0.25 Hz) or of baroreceptor stimulation by sinusoidal neck suction (0 to -30 mmHg, 0.1 or 0.2 Hz). During apnea the RSA-EF power decreased (from 6.73 +/- 0.15 to 3.67 +/- 0.10 In ms2: P < 0.0001), regardless of preapnea conditions, whereas LF power was reduced only if preceded by 0.1-Hz respiration or neck suction [from 8.71 +/- 0.18 to 6.52 +/- 0.11 In ms2 (P < 0.001) and from 8.31 +/- 0.23 to 6.90 +/- 0.38 In ms2 (P < 0.01), respectively]. The LF frequency seen in the R-R interval during apnea was slower than the spontaneous LF during 0.25-Hz breathing (0.082 +/- 0.01 vs. 0.112 +/- 0.001 Hz, P < 0.001), but the maneuvers during preapnea had no influence on the observed frequency or other characteristics of the slow oscillations during apnea. Moreover, we found no evidence of a progressive decrease in the power of the oscillation during apnea. The same behavior was observed on the mean blood pressure signal. In conclusion, a slow rhythm is present during apnea. In healthy subjects at rest the characteristics of this oscillation indicate that it could be generated by a central oscillator this may thus contribute to the origin of LF present during normal respiration, in addition to the baroreflex.

Administration, Inhalation↗

Effect of different interventions on heart rate variability after heart transplantation: non-autonomic vs autonomic factors.

1. The human transplanted heart is initially denervated, hence any fluctuation present in the RR interval variability can be either due to reacquired innervation, or to the effect of some non autonomic activity, such as a direct effect of respiration on atrial (sinus node) stretch. 2. In order to distinguish between sympathetic, vagal and non autonomic factors we examined the effects of various physical and pharmacologic manoeuvres on the respiratory and non-respiratory components of heart rate variability. 3. We found that sinusoidal neck suction appears a useful, noninvasive tool to characterise the relative importance of the different factors, which can influence heart rate variability in the transplanted heart.

Autonomic Nervous System↗

Alterations of breathing in chronic heart failure: clinical relevance of arterial oxygen saturation instability.

1. In patients with chronic heart failure (CHF) alterations of breathing such as Cheyne-Stokes respiration (CSR) or periodic breathing, (PB) have been frequently described during both day- and night-time. These respiratory rhythm disorders are associated with marked oscillations of arterial oxygen saturation (SaO2) which may expose the patients to prolonged hypoxia. 2. In 40 stable CHF patients and 8 controls during awake day-time, we studied the relationship between alterations of breathing and SaO2, to verify the effect of voluntary control of respiration or oxygen therapy on the instability of SaO2 (analyzed as standard deviation (SD) of the mean value). Simultaneous recordings of ECG, lung volumes and SaO2 were made during 10 min. resting and 4 min. controlled breathing In a subgroup of 5 CHF the effect of oxygen therapy was compared to that of controlled breathing. 3. It was found that 62% of CHF had CSR or PB. Mean SaO2 and SD of SaO2 were significantly different in CHF as compared to controls (respectively 92.4 +/- 2.5 vs 95.4 +/- 0.5%, p < 0.002 and (1.27 +/- 0.9 vs 0.28 +/- 0.13%, p < 0.01), but among CHF pts those with CSR and PB had a lower SaO2 and a more pronounced instability of SaO2. Controlled breathing eliminated apneas and reduced or abolished the variation of tidal volume. In both control and CHF it resulted in an increase of mean SaO2 while a significant reduction of SaO2 instability was observed only in CHF, particularly if CSR or PB were present. Voluntary control of respiration was similar to oxygen therapy in increasing SaO2, but more effective on SaO2 SD. 4. It is concluded that in stable CHF, resting SaO2 is reduced and showed a marked instability particularly when periodic alterations of breathing were present. Continuous beat-to-beat recording of SaO2 may detect patients who have PB or CSR. Training to produce more regular breathing, regardless of the amount of ventilation, may represent a useful intervention.

Adult↗

Autonomic regulation of heart rate and peripheral circulation: comparison of high altitude and sea level residents.

1. To evaluate the activity of the autonomic nervous system on the heart and peripheral circulation in native high-altitude residents, during a Himalayan expedition we studied 12 men (age: 48 +/- 4, mean +/- SEM), life-long resident in a village at 4800 m (Sumdo village, Zanskar, India) and 7 healthy sea-level residents (age: 37 +/- 4) after 7 days of acclimatization (acclimatized lowlanders) at the same altitude. Furthermore 25 sea level residents (age: 46 +/- 2) underwent the same protocol at sea level. 2. R-R interval (RR), respiratory signal, non-invasive blood pressure, and skin arteriolar blood flow were evaluated in three different conditions: during free breathing in supine position and during controlled breathing (at 0.15 Hz), in supine and upright position, and analysed by autoregressive spectral analysis [low- (around 0.1 Hz) and high-frequency (respiratory) fluctuations, LF and HF, markers of sympathetic and vagal activity, respectively]. 3. High-altitude residents showed in supine position a higher RR than acclimatized lowlanders, similar to sea-level residents. RR variability was reduced in acclimatized lowlanders compared to both high-altitude residents and sea level residents. Systolic blood pressure (SBP) did not show significant differences between the three groups. High altitude residents showed in supine lower LF in RR signal compared to sea-level residents, and, compared to acclimatized lowlanders, higher HF and lower LF/HF ratio; high-altitude residents showed a reduction in skin microcirculation variability compared to sea-level residents, but this was eight fold greater than in acclimatized lowlander, thus indicating a much greater vasoconstriction in acclimatized lowlanders than in high-altitude residents. 4. In upright position, high-altitude residents showed the same behaviour as sea-level residents, with increase in LF-RR, and decrease in HF and LF-SBP. Acclimatized lowlanders showed similar directional trends though not significant changes for RR-LF. 5. After one week of acclimatization, lowlanders still manifested sympathetic activation and skin vasoconstriction; high-altitude residents did not show reduced vagal tone compared to sea-level residents, but a mild vasoconstriction appeared to be present. In conclusion, normal or enhanced vagal tone and preserved vasomotion are probably evidence of adaptation at high altitude hypoxia.

Adaptation, Physiological↗

Demonstrable cardiac reinnervation after human heart transplantation by carotid baroreflex modulation of RR interval.

BACKGROUND: After heart transplantation, respiration-synchronous fluctuations (0.18 to 0.35 Hz, high frequency [HF]) in RR interval may result from atrial stretch caused by changes in venous return, but slower fluctuations (0.03 to 0.15 Hz, low frequency [LF]) not due to respiration suggest reinnervation. In normal subjects, sinusoidal neck suction selectively stimulates carotid baroreceptors and causes reflex oscillations of RR interval. METHODS AND RESULTS: To evaluate the presence of reinnervation, we measured the power of RR-LF and RR-HF in 26 heart transplant recipients and 16 control subjects before and during sinusoidal neck suction at 0.1 Hz and 0.20 Hz (similar to but distinct from that of controlled respiration, 0.25 Hz) and before and during administration of atropine or beta-blocker (esmolol hydrochloride) by spectral analysis. All transplant recipients showed small respiratory HF fluctuations. Nonrespiratory LF fluctuations were present in 13 of 26 transplant recipients and increased with months since transplantation (r = .53, P < .01). HF neck suction induced a 0.20-Hz component in all 16 control subjects and none of the 26 transplant subjects. LF neck suction increased RR-LF (from 0.73 +/- 0.20 to 1.30 +/- 0.26 ln ms2, P < .001), similar to but less than in control subjects (from 6.12 +/- 0.21 to 8.27 +/- 0.21 ln ms2, P < .001). Atropine reduced all fluctuations in control subjects and blocked the HF increase caused by 0.20-Hz neck suction but not the LF increase during 0.10-Hz stimulation. Neck suction-induced changes in LF fluctuations persisted after administration of atropine in transplant recipients but were attenuated by esmolol hydrochloride, suggesting sympathetic rather than vagal reinnervation. CONCLUSIONS: The presence of baroreceptor-induced RR oscillations is evidence of functional, although incomplete, autonomic reinnervation.

Adrenergic beta-Antagonists↗

[The noninvasive demonstration of functional reinnervation after heart transplantation].

Although RR interval variability appears to be an ideal method for assessing reinnervation after heart transplantation, it has been shown that respiratory sinus arrhythmia is caused by the mechanical effect of respiration on the right atrium. The neck-suction induces heart rate changes only by means of nervous reflex and its hemodynamic effect is local and hence appears as a useful method for assessing reinnervation. We tested the presence of autonomic reinnervation in 18 heart transplant recipients, compared to 12 donor-age-matched controls. We measured the power of RR interval low- (LF, around 0.1 Hz) and respiratory fluctuations (HF) before and during rhythmic neck-suction stimulation at 0.1 Hz and at a frequency (0.20 Hz) similar to, but distinct from, that of respiration (controlled at 0.25 Hz), before and during 0.04 mg/kg atropine infusion, using autoregressive spectral analysis of RR interval, respiration and neck pressure signals. The relationship between pairs of signals at each frequency was quantitatively assessed by bivariate coherence function. All transplanted subjects showed low-amplitude HF, related to respiration. Detectable LF (whose power was lower than in controls: 1.15 +/- 0.39 versus 6.08 +/- 0.27 1n-ms2, p < 0.001), non coherent with respiration, were present in 11/18 transplanted subjects, and correlated with months since transplantation (r = +0.59, p < 0.05). HF neck suction induced the presence of a 0.20 Hz fluctuation in 12/12 controls, distinct from and greater than the 0.25 Hz respiratory component (7.28 +/- 0.26 versus 6.69 +/- 0.74 1n-ms2, p < 0.01); this was not seen in any of the transplanted subjects.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗

[Vasovagal syncope].

The nature of most syncopal episodes, previously unknown, was recently elucidated by new diagnostic techniques such as the use of the tilt test. The vasovagal syncope can be clinically diagnosed by means of the tilt test. The transitory loss of consciousness during prolonged orthostasis is typically associated with sudden hypotension and bradycardia, which are commonly preceded by relative tachycardia and by premonitory symptoms such as pallor, nausea, asthenia, yawns, hyperventilation, mydriasis, humming, lasting several minutes. The nature of the vasovagal reflex is now better understood: in subjects with vasovagal syncope, during prolonged orthostasis, it was observed a fall in the venous return, inducing an increased sympathetic drive to the heart (with positive inotropic and chronotropic effect) and a lower ventricular filling. The powerful contraction around an almost empty cardiac chamber induces the activation of ventricular mechanoreceptors, and through a reflex mechanism, a sudden increase in the vagal and a sudden reduction in the sympathetic drive. These autonomic changes are responsible for a sudden hypotension and bradycardia. The discussion is still open about the origin of the reduced venous return: it probably originates from a redistribution in the blood volume, due to a venous pooling in the lower limbs or from a reduced muscle tone, because many subjects with vasovagal syncope are slender and with less developed muscle apparatus. Others suggest that a reduction in the sympathetic drive to the vessels, responsible for a progressive hypotension in the minutes preceding syncopal episodes, is the origin of the reduced venous return. In this review a diagnostic pattern for the assessment of the vasovagal syncope is suggested. The medical history, clinical examination, electro- and echocardiogram, chest x-ray identify two main groups of patients (with or without cardiopathy) who will follow different diagnostic protocols. The therapy of vasovagal syncope, which is based on beta-blockers, scopolamine, dysopiramide and plasma expanders, is reviewed.

Hemodynamics↗