Palpography detects mechanical dyssynchrony and worsens with right ventricular pacing and reduced left ventricular ejection fraction.

BACKGROUND: QRS width and echocardiography-derived indices are limited predictors of response to resynchronization therapy. We applied digital palpography, using vibration resonance imaging, to investigate the effects of right ventricular pacing and left ventricular ejection fraction (LVEF) on mechanical and electrical dyssynchrony. METHODS: Forty-nine subjects were examined: 24 normal controls, 18 subjects with right ventricular apical pacing (12 with reduced LVEF), and seven subjects with reduced LVEF and narrow QRS. Digital measurement of QRS width was performed. Electric dyssynchrony index (EDI) was measured as the time interval between peak R-waves of the same QRS complex of simultaneously recorded standard limb electrocardiograms, L1 and L2. A matrix of 6 × 6 vibration recording transducers was applied to chest. The interval between the onset of Q-wave and the peak of amplitude vibration for each transducer was measured, and a three-dimensional map for the whole matrix of transducers was generated. Median values (QE1) were measured. Mechanical vibration systolic dyssynchrony index (VSDI) for each subject was determined as the standard deviation of the difference between the median value and each transducer interval. RESULTS: EDI was larger in subjects with right ventricular pacing. Mechanical dyssynchrony indices were larger with pacing and reduced LVEF. EDI correlated with QRS width (r(2) = 0.7), with VSDI (r(2) = 0.42), and with QE1 (r(2) = 0.74). QRS width correlated with QE1 (r(2) = 0.75). CONCLUSIONS: Digital chest palpography can determine dyssynchrony indices that are larger in subjects with right ventricular pacing and reduced LVEF and correlate with parameters of electrical dyssynchrony.

Effect of cough on heart rate and blood pressure in patients with "cough syncope".

BACKGROUND: "Cough syncope" is uncommon, and its mechanism remains controversial. OBJECTIVES: This study evaluated susceptibility to cough-triggered neural reflex hypotension-bradycardia among cough syncope patients. We hypothesized that individuals with cough syncope would manifest not only more profound cough-triggered hypotension than do other fainters but also an inappropriate chronotropic response accompanying cough-induced hypotension, thereby supporting the notion that a neural reflex hypotension-bradycardia contributes to the condition. METHODS/RESULTS: Three patient groups were studied. Group 1 patients (n = 9) had "cough syncope." The remaining patients had recurrent faints of other causes: group 2 (n = 13) had a positive head-up tilt test, and group 3 (n = 18) had a negative tilt test. With cough, group 1 patients exhibited a greater drop in systolic pressure (-51 +/- 19.3 mmHg) than did either group 2 (-23 +/- 11.1 mmHg, P < .04) or group 3 patients (-28 +/- 12.4 mmHg, P < .05). Recovery time to normalization of systolic pressure was greater in group 1 (25 +/- 9.1 seconds) than in group 2 or 3 (8 +/- 2.7 seconds and 9 +/- 6.1 seconds, respectively, both P < .01 vs group 1). The expected positive chronotropic response accompanying cough-induced hypotension was diminished in group 1 patients (0.16 +/- 0.21 bpm/mmHg) compared with that in either group 2 (0.74 +/- 0.60 bpm/mmHg, P < .05 vs group 1) or group 3 (0.33 +/- 0.15 bpm/mmHg, P = .06 vs group 1). CONCLUSION: Cough syncope patients not only exhibit more pronounced hypotension in response to cough than other fainters, but they also manifest an inappropriate cough-triggered blood pressure-heart rate relationship. These findings argue in favor of the importance of a neurally mediated reflex contribution to symptomatic hypotension in cough syncope.

Impact of age and blood pressure on the lower arterial pressure limit for maintenance of consciousness during passive upright posture in healthy vasovagal fainters: preliminary observations.

Maintenance of consciousness importantly depends on systemic arterial blood pressure (BP) remaining above the lower pressure limit for cerebrovascular autoregulation. This study evaluated the impact of age and baseline arterial blood pressure (BP) on the BP recorded at onset of syncope in otherwise healthy individuals undergoing passive head-up tilt (HUT) testing for suspected vasovagal syncope. Since hypertension is thought to shift the lower autoregulation point to higher values, and since older healthy patients tend to have higher BP than younger individuals, we hypothesized that even among healthy individuals HUT-induced syncope would occur at higher BP in older compared with younger subjects. Three groups of otherwise healthy individuals who had positive HUT were identified: Group 1: <25 years, n=17; Group 2: 25-59 years, n=18; and Group 3: > or =60 years, n=7. As expected, baseline arterial systolic blood pressure of patients > or =60 years (162+/-37 mmHg) was significantly higher than in the other two groups (Group 1: <25 years, 116+/-15 mmHg; Group 2: 25-59 years, 128+/-12 mmHg). Further, the > or =60 age group tolerated upright posture for a longer period before syncope than did younger patients. However, despite a trend for BP at syncope to increase with age, differences were small (Group 3: > or =60 years, 61+/-15 mmHg, Group 2: 25-59 years, 58+/-6 mmHg, and Group 1: 54+/-16 mmHg) and were not statistically significant. Thus, in generally healthy individuals, age and baseline BP has only a minor effect on the lower limit of BP necessary for maintenance of consciousness. On the other hand, higher baseline BP provides older individuals a greater blood pressure 'reserve' for maintenance of consciousness compared with younger subjects.

Comparison of catecholamine response during tilt-table-induced vasovagal syncope in patients <35 to those >65 years of age.

This study compared alterations in arterial catecholamine concentrations associated with tilt-induced vasovagal syncope that differed in older (>65 years) and younger patients (<35 years). Older patients with tilt-positive tests tended to exhibit higher baseline epinephrine (E) concentrations and lesser E surge before development of syncope than younger patients (<35 years), whereas both groups manifested comparable norepinephrine (NE) responsiveness.

Transient modification of baroreceptor response during tilt-induced vasovagal syncope.

AIMS: Normally, arterial baroreceptors attempt to minimize systemic hypotension by initiating reflex vasoconstriction and tachycardia. However, in the setting of vasovagal syncope (VVS), these usual compensatory mechanisms either fail to be triggered or the response is inadequate. We hypothesized that in VVS prone individuals, arterial baroreceptor response (BRR) is normal under most conditions, but that a transient functional BRR disturbance occurs during an evolving vasovagal faint and may in part account for failure of the usual compensatory response. METHODS AND RESULTS: This study assessed BRR in the baseline state and again in association with either VVS induced head-up tilt (HUT) or after a prolonged period of upright posture without VVS. To minimize impact on HUT outcome, BRR was estimated non-pharmacologically by measuring blood pressure and heart rate changes, induced when subjects were returned to the supine position after undergoing diagnostic 70 degrees HUT evaluation. Beat to beat heart rate and arterial blood pressure changes were recorded in 13 patients with syncope and another 16 individuals with negative HUT (control group). Baseline BRR was initially evaluated at the end of a 3 min symptom free HUT (HUT#1), and the measurement was repeated after a 45 min duration HUT in the control group or in conjunction with syncope in VVS prone individuals (HUT#2). Baseline BRR did not differ significantly in controls and VVS prone individuals (controls: 3.37+/-1.56, VVS prone: 6.0+/-2.02 ms/mmHg, p=0.27). Further, at the end of 45 min HUT#2, BRR was unaltered from baseline in control subjects (4.92+/-1.36 ms/mmHg, p=0.48), but was markedly reduced from baseline value in individuals who experienced a faint, -3.30+/-0.81 ms/mmHg (p<0.0003 vs baseline). CONCLUSION: Compared with individuals who do not manifest VVS during HUT, VVS prone individuals appear to demonstrate functional diminution of baroreceptor responsiveness. This altered response may undermine the normal expected compensatory response to evolving systemic hypotension. The basis for this transient disturbance in baroreceptor responsiveness is currently unknown.

Feasibility and effects of transcutaneous phrenic nerve stimulation combined with an inspiratory impedance threshold in a pig model of hemorrhagic shock.

OBJECTIVE: Intrathoracic pressure changes are of particular importance under hypovolemic conditions, especially when central venous blood pressure is critically low. Accordingly, the purpose of this study was to assess the feasibility of transcutaneous phrenic nerve stimulation, used in conjunction with an inspiratory impedance threshold, on hemodynamic variables during hemorrhagic shock. DESIGN: Prospective, randomized laboratory investigation using a porcine model for measurement of hemodynamic variables, left and right ventricular diameter, and transmitral, transpulmonary, and transaortic blood flow employing transesophageal echo-Doppler technique. SETTING: University hospital laboratory. SUBJECTS: Thirteen female pigs weighing 28-36 kg. INTERVENTIONS: The anesthetized pigs were subjected to profound hemorrhagic shock by withdrawal of 55% of estimated blood volume over 20 mins. After a 10-min recovery period, the diaphragm was stimulated with a prototype transcutaneous phrenic nerve stimulator at a rate of ten per minute while the airway was intermittently occluded with an inspiratory threshold valve between positive pressure ventilations. Hemodynamic variables were monitored for 30 mins. MEASUREMENTS AND MAIN RESULTS: Phrenic nerve stimulation in combination with the inspiratory threshold valve significantly (p <.001) improved right and left ventricular diameter compared with hypovolemic shock values by 34 +/- 2.5% and 20 +/- 2.5%, respectively. Moreover, phrenic nerve stimulation together with the inspiratory threshold valve also increased transaortic, transpulmonary, and transmitral valve blood flow by 48 +/- 6.6%, 67 +/- 13.3, and 43 +/- 8.2%, respectively (p <.001 for comparisons within group). Mean +/- sem coronary perfusion and systolic aortic blood pressures were also significantly (p <.001) higher compared with values before stimulation (30 +/- 2 vs. 20 +/- 2 mm Hg, and 37 +/- 2 vs. 32 +/- 3 mm Hg, respectively). CONCLUSIONS: This feasibility study suggests that phrenic nerve stimulation with the inspiratory threshold valve may improve cardiac preload and, subsequently, key hemodynamic variables in porcine model of severe hemorrhagic shock.