Hemodynamic Sensors Research Articles

Hemodynamic sensors

Present adaptive-rate pacemakers use a range of sensors for implementation in open-loop and closed-loop control systems. Hemodynamic sensors that detect the mechanical action of the heart and blood flow offer additional features to implement physiologic rate adaption in rate-controlling systems and rate-limiting systems. Examples of 2 such sensors are presented.

The transthoracic impedance cardiogram is a potential haemodynamic sensor for an automated external defibrillator.

The American Heart Association has endorsed the concept of Public Access Defibrillation. However, there have been reports of inappropriate direct current shocks from automatic external defibrillators. The specificity of automatic external defibrillators for shockable rhythms may be improved by the incorporation of a haemodynamic sensor. This study examined the use of four parameters extracted from the impedance cardiogram i.e. Peak dz/dt (the peak of the impedance cardiogram measured from the line dz/dt=0 ohms(-1)), Peak-trough (the peak-to-trough measurement of the impedance cardiogram ohms(-1)), Area 1 (the area under the C wave of the impedance cardiogram above the line dz/dt=0 mohm) and Area 2 (the area under the impedance cardiogram 50 ms on either side of the Peak and above the line dz/dt=0 mohm) as predictors of cardiac output. At 116 cardiac arrest calls the ECG and impedance cardiogram were recorded through two ECG/defibrillator pads placed in an antero-apical position. Nine recordings were rejected for artefact. The rhythm recorded in the remaining 107 calls was asystole (19), ventricular fibrillation (14), agonal rhythm (20), electromechanical dissociation (22), ventricular tachycardia (27) and sinus rhythm (5). These rhythms were divided into those associated with haemodynamic collapse i.e. no pulse -- asystole, ventricular fibrillation, agonal rhythm, electromechanical dissociation and shockable ventricular tachycardia (associated with loss of consciousness, pulselessness or a systolic blood pressure of <80 mmHg) (Group 1) and those associated with a satisfactory cardiac output i.e. non-shockable ventricular tachycardia (conscious with a pulse) and sinus rhythm (Group 2). On univariate analysis each of the four impedance cardiogram parameters were significantly greater in Group 2 than Group 1 (P<0.001). On multivariate analysis the parameters which best differentiated the two groups were Area 1 and Peak-trough. Thus the impedance cardiogram is a potential haemodynamic sensor for an automatic external defibrillator.

Neural monitoring of vasovagal syncope.

Head-up tilt testing has become a valuable and widely accepted diagnostic tool for evaluation of patients with vasovagal syncope. This test has afforded clinical researchers the opportunity to focus on the hemodynamic, humoral, and neural changes that accompany syncope. We review the animal and clinical studies that provide insight into the possible pathophysiological mechanisms involved in vasovagal syncope. Hemodynamic measurements in patients with vasovagal syncope suggest that a relative decrease in ventricular size and increase in cardiac contractility may be seen in many patients with vasovagal syncope. Patients with vasovagal syncope have also demonstrated numerous "exaggerated" neurohumoral responses to syncope. Differential changes in plasma levels of epinephrine, renin, endothelin, vasopressin, cortisol, prolactin, beta endorphins, and substance P have been reported by some investigators either prior to or during a syncopal episode in patients with vasovagal syncope. The precise pathophysiological significance of these measurements is unknown at the present time. Measurements of autonomic tone may be accomplished indirectly with analysis of heart rate variability or baroreflex slope, or directly by sympathetic neural recordings of the peroneal nerve. We have demonstrated decreased baroreflex slopes in patients with vasovagal syncope. Using microneurography, we and others have demonstrated decreased sympathetic nerve activity occurring 11 +/- 3 seconds prior to syncope during head-up tilt table testing. A variety of other abnormal reflexes, including blunted forearm blood flow responses during exercise, have been demonstrated by others. These observations suggest that pacing instituted after the event may not be as helpful as the use of a hemodynamic sensor that will result in the initiation of pacing prior to sympathetic withdrawal or modify the decrease in sympathetic tone that occurs prior to syncope.

Is local myocardial contractility related to endocardial acceleration signals detected by a transvenous pacing lead?

The availability of sensors monitoring cardiac function parameters may offer many interesting new applications in cardiac pacing. A microaccelerometer sensor (BEST, Biomechanical Endocardial Sorin Transducer) located at the tip of a pacing lead (PL) has been developed by Sorin Biomedica. The signal detected by the accelerometer, peak endocardial acceleration (PEA), was shown to reflect cardiac contractility and to be related to the dP/dt signal. Whether the PEA detected by the BEST sensor in different cardiac locations is the expression of local acceleration forces or reflects the whole heart contractility has not yet been demonstrated in humans. Endocardial acceleration and PEA were evaluated in five patients (4 males, 1 female, mean age 68 years) who underwent cardiac catheterization. Sinus rhythm was present in four patients and chronic atrial fibrillation was present in one. The BEST PL was introduced through the left subclavian vein and PEA signals were recorded: (1) at the apex of the right ventricle (RV), (2) within the coronary sinus (CS), (3) at the right atrial appendage (RAA), and (4) floating in the right atrium. The PEA signals were recorded simultaneously with surface ECG, intracardiac electrograms, and RV pressure. At each recording site, PEA signals with significant amplitude were always recorded during the preejection period, during the isovolumic contraction phase, independently of the recording site and cardiac rhythm. The PEA amplitude was higher in the RV (mean value 1.32 g) and it decreased in the RAA and CS (0.75 and 0.45 g, respectively). The same behavior of PEA was observed during sinus rhythm or atrial fibrillation. The amplitude and the timing of the PEA signals detected by the BEST accelerometer were independent of the recording site and atrial rhythm; they appeared to be strictly related to the global ventricular contractility. These results suggest that the BEST could be used either as an effective sensor in closed loop pacing systems, or primarily as a diagnostic hemodynamic sensor.

959-104 The Potential Use of Impedance Cardiography as a Hemodynamic Sensor for Automated External Defibrillators

Automated external defibrillators use ECG analysis algorithms to identify ventricular fibrillation (VF) and ventricular tachycardia (VT). VT can be associated with a wide range of blood pressures and automated defibrillators determine the need for DC shock based on the heart rate alone. The incorporation of a hemodynamic sensor may improve the accuracy of an automated defibrillator. The impedance cardiogram (ICG) has been used to non-invasively measure cardiac output and its peak value, dz/dt(max), correlates well with aortic blood flow. We have developed a system whereby the ICG can be recorded at cardiac arrests through the same two ECG/defibrillator pads, placed in an antero-apical position, that are used to monitor or shock the patient. At 103 cardiac arrest calls and in 20 healthy volunteers (C) the ICG was recorded for a period of at least 10s without CPR artefact: 9 records were rejected because of poor quality. The rhythms were divided into VF, asystole (As), agonal rhythm (Ag), electromechanical dissociation (EMD), VT requiring DC shock (VTs) and VT not requiring DC shock (VTns). The ICG tracings were ensemble averaged to remove any electrical noise and dz/dt(max) was measured. dz/dt(max) C VTns VTs EMD Ag VF As Mean Ω.s -l 0.622 0.413 * 0.191 * 0.178 * 0.ll8 * 0.112 * 0.098 * ± SEM Ω.s -l 0.058 0.041 0.032 0.022 0.011 0.010 0.004 Number 20 20 7 22 20 14 19 * p &lt; 0.01 compared with C (Kruskal-Wallis) C was significantly greater than all other rhythms. VTns was significantly greater than the pulseless rhythms EMD, Ag, VF and As. There was no significant difference between VTs and the pulseless rhythms. Thus the ICG is a potential hemodynamic sensor for automated external defibrillators.

Oscillatory shear stress and hydrostatic pressure modulate cell-matrix attachment proteins in cultured endothelial cells.

Endothelial cells (ECs) may behave as hemodynamic sensors, translating mechanical information from the blood flow into biochemical signals, which may then be transmitted to underlying smooth muscle cells. The extracellular matrix (ECM), which provides adherence and integrity for the endothelium, may serve an important signaling function in vascular diseases such as atherogenesis, which has been shown to be promoted by low and oscillating shear stresses. In this study, confluent bovine aortic ECs (BAECs), were exposed to an oscillatory shear stress or to a hydrostatic pressure of 40 mmHg for time periods of 12 to 48 h. Parallel control cultures were maintained in static condition. Although ECs exposed to hydrostatic pressure or to oscillatory flow had a polygonal morphology similar to that of control cultures, these cells possessed more numerous central stress fibers and exhibited a partial loss of peripheral bands of actin, in comparison to static cells. In EC cultures exposed to oscillatory flow or hydrostatic pressure, extracellular fibronectin (Fn) fibrils were more numerous than in static cultures. Concomitantly, a dramatic clustering of alpha 5 beta 1 Fn receptors and of the focal contact-associated proteins vinculin and talin occurred. Laminin (Ln) and collagen type IV formed a network of thin fibrils in static cultures, which condensed into thicker fibers when BAECs were exposed to oscillatory shear stress or hydrostatic pressure. The ECM-associated levels of Fn and Ln were found to be from 1.5- to 5-fold greater in cultures exposed to oscillatory shear stress or pressure for 12 and 48 h, than in static cultures. The changes in the organization and composition of ECM and focal contacts reported here suggest that ECs exposed to oscillatory shear stress or hydrostatic pressure may have different functional characteristics from cells in static culture, even though ECs in either environment exhibit a similar morphology.

Changes in cerebral perfusion during third-generation implantable cardioverter defibrillator testing

Third-generation implantable cardioverter defibrillators (ICDs) are designed to provide tiered therapy for ventricular tachycardia and ventricular fibrillation. At present, however, therapy prescription does not take into account the hemodynamic consequences of ventricular dysrhythmias. Design of “intelligent” devices depends on their ability to assess hemodynamic consequences of tachyarrhythmias and end-organ perfusion. Quantitative electroencephalography (QEEG) and transcranial Doppler flow provide sensitive and specific measures of cerebral perfusion during ICD testing and programming. In response to prolonged hypotension (> 15 seconds), transient loss of α power (i.e., increase in δ power) in the EEG spectrum, accompanied by impaired cerebrovasomotor reactivity (CVR), was observed in 25 of 91 hypotensive episodes in 15 patients, ages 36 to 72 years, predicting intolerance to the programmed ICD therapy. Conversely, intact CVR prevented ischemia, slowing in the EEG, and predicted tolerance to the therapy prescription. These changes were exaggerated in the erect posture during tilt-table ICD testing. During ventricular tachycardia, signs of cerebral hypoxia detected by QEEG and Doppler techniques were accompanied by a fall in transcranial oxyhemoglobin saturation measured by near-infrared spectroscopy. We conclude that transcranial Doppler and QEEG are sensitive indicators of cerebral perfusion. These techniques could be used as indexes of perfusion against which hemodynamic sensors for future ICDs could be evaluated.

Short‐Term Reproducibility Over Time of Right Ventricular Pulse Pressure as a Potential Hemodynamic Sensor for Ventricular Tachyarrhythmias

The implantable cardioverter defibrillator (ICD) has been shown to effectively terminate episodes of ventricular tachyarrhythmias. Multiple investigators have suggested that the incorporation of hemodynamic sensors may allow ICDs to differentiate between hemodynamically unstable and stable ventricular tachyarrhythmias (VT), as well as differentiate ventricular from supraventricular tachycardias. Right ventricular (RV) pulse pressure has been shown to possess acceptable characteristics as a sensor for incorporation in ICDs. We sought to determine the short-term reproducibility of RV pulse pressure measurements by comparing RV pulse pressure measured during two separate episodes of VT in each of ten study patients. The mean VT cycle length for VT episode 1 was 293 +/- 15 msec, and was 298 +/- 15 msec for VT episode 2 (P = NS). The decrease in mean arterial pressure was 40 +/- 7 mmHg in episode 1 and 37 +/- 7 mmHg in episode 2 (P = NS). The decrease in RV pulse pressure during episode 1 was -13 +/- 2 mmHg, and -12 +/- 2 during episode 2 (P = NS). The decrease in RV pulse pressure during episodes of VT at two different times during a single electrophysiology study is highly reproducible, suggesting that RV pulse pressure may be a reliable sensor over time.

A Prospective Study of Changes in Right Ventricular dP/dt During Ventricular Tachycardia

The automatic implantable cardioverter defibrillator (AICD) has significantly decreased mortality in high risk ventricular tachycardia (VT) patients. The AICD provides treatment based on ventricular rate, sometimes leading to high energy shocks in conscious patients with stable VT, or patients with sinus or supraventricular tachycardia. Other physiological parameters, such as maximal positive and negative systolic right ventricular (RV) dP/dt (RV + dP/dtmax, RV - dP/dtmax, respectively), may be included in detection algorithms for future implantable defibrillators. We studied frequency band limited positive and negative RV dP/dtmax before, during, and after 13 episodes of VT lasting at least 40 beats in duration in nine male patients. The mean (+/- SEM) RV + dP/dtmax, dropped by 120 +/- 28 mmHg/sec (P less than 0.001) during the first five beats of VT. RV + dP/dtmax then slowly rose toward baseline levels until a significant overshoot occurred during the first ten beats following VT termination (delta = 234 +/- 58 mmHg/second, P less than 0.002). RV + dP/dtmax correlated poorly with mean arterial pressure (r = 0.32, P greater than 0.1), systolic blood pressure (r = 0.19, P greater than 0.1), and VT cycle length (r = 0.34, P greater than 0.1). Conversely, RV - dP/dtmax rose during the first ten beats of VT (74 +/- 27 mmHg/sec, P greater than 0.05) and then slowly drifted back toward baseline levels. Like RV + dP/dtmax, RV - dP/dtmax overshot baseline levels during the recovery phase (-108 +/- 48 mmHg/sec, P less than 0.05).(ABSTRACT TRUNCATED AT 250 WORDS)

Usefulness of right ventricular pulse pressure as a potential sensor for hemodynamically unstable ventricular tachycardia

The automatic implantabte cardioverter defibrillator has had a major impact on the management of patients with ventricular tachyarrhythmias. Future devices will offer tiered therapy for ventricular arrhythmias, based on a sensor capable of discriminating hemodynamically stable from unstable ventricular tachycardia (VT). We studied 27 patients with sustained VT/ventricular fibrillation during 70 episodes of sustained ventricular arrhythmias (>30 seconds or requiring cardioversion). In this study, phasic arterial pressure (mm Hg), VT cycle length (ms) and right ventricular (RV) pulse pressure (mm Hg) were measured before, during the first 30 beats and after each episode of VT. During the first 10 beats of 23 episodes of unstable VT, the mean (± standard error of the mean) decrease in RV pulse pressure from baseline was 22 ± 1.8 mm Hg; it was 13.8 ± 2A mm Hg during the first 10 beats of 47 episodes of stable VT, (p = 0.01, stable vs unstable). For the next 20 beats of VT, RV pulse pressure decreased from baseline by 22 ± 2.5 mm Hg during unstable and by 12.0 ± 2.5 mm Hg during stable VT (p = 0.0001, stable vs unstable). The percent decrease of RV pulse pressure correlated well with the percent decrease in mean arterial pressure and percent decrease in systolic arterial pressure (r = 0.70; r = 0.69, respectively; p < 0.001) during VT, but poorly with the VT cycle length (r = 0.27, p < 0.05). The percent decrease in RV pulse pressure is a useful hemodynamic sensor for discriminating between stable and unstable VT.