Ventricular impedance

At higher concentrations, nitroglycerin also relaxes arteriolar smooth muscle, which leads to a decrease in both peripheral vascular resistance and aortic impedance to left ventricular ejection (decreased afterload). The decreased resistance to ventricular ejection may also reduce myocardial wall tension and oxygen requirements. 

Afterload—The pressure or the load the heart must generate to eject blood into the systemic circulation. Although approximated by the systemic vascular resistance, it is a complex measure that includes blood viscosity, aortic impedance, and ventricular wall thickness. Along with preload, it is an important determinant of cardiac output. 

Sodium nitroprusside is used for the short-term control of severe hypertension and can improve cardiac function in patients with left ventricular failure see Chapter 34). Nitroprusside acts by releasing nitric oxide (NO). NO activates the guanylyl cyclase-cyclic GMP-PKG pathway, leading to vasodilation. The mechanism of release of NO likely involves both enzymatic and nonenzymatic pathways. Tolerance does not develop to nitroprusside. Nitroprusside dilates both arterioles and venules the hemodynamic response results from a combination of venous pooling and reduced arterial impedance. In subjects with normal left ventricular function, venous pooling affects cardiac output more than does the reduction of afterload cardiac output thus tends to fall. In patients with severely impaired left ventricular function and diastolic ventricular distention, the reduction of arterial impedance leads to a rise in cardiac output see Chapter 33). Sodium nitroprusside is a nonselective vasodilator, and regional distribution of blood flow is little affected by the drug. In... 

The failing left ventricle is characterized by depression of myocardial contractility and increased sensitivity to alterations of left ventricular afterload. This latter attribute of the failing ventricle is manifest by a greater proportional reduction of stroke volume as the impedance to ejection is increased. Conversely, afterload reduction in this setting can be associated with substantial increases in stroke volume. This increased afterload dependence underlies the beneficial effects of load reduction therapy in patients with heart failure due to systolic dysfunction. 

Cardiac contractility Force of cardiac contraction is another systolic factor controlled mainly by sympathetic outflow to the heart. Ejection time for ventricular contraction is inversely related to force of contraction but is also influenced by impedance to outflow. Increased ejection time increases oxygen requirement. 

With positive pe, as occurs in chest compression, ventricular blood pressure is raised by an amount pe and ejection is promoted. There is reason to believe, however, that venous return will be impeded by the presence of this same pe> resulting in the possibility of ejecting less blood at a higher rate of flow. 

In addition, investigators of impedance-defined flow found that when aU cardiac valves are open (open conduit [80]) flow around a closed loop reduces to negligible values even when ventricular contraction is normal. Hence, CPR as a technique, should attempt to reestablish (at least part of) valvular operation in order to allow for survival of a heart too good to die. 

The most common sensor is the activity sensor, which uses any of a variety of technologies (e.g., piezoelectric crystals and accelerometers) to detect body movement. Systems using a transthoracic-impedance sensor to estimate pulmonary minute ventilation or cardiac contractility are also commercially available. Numerous other sensors (e.g., stroke volume, blood temperature or pH, oxygen saturation, and right ventricular pressure) have been researched or market-released at various times. Some systems are dual-sensor, combining the best features of each sensor in a single pacing system. 

Some commercially available implantable devices for the treatment of congestive heart failure and/or ventricular tachyarrhythmias now continually monitor intrathoracic impedance and display fluid status trends. This information is then provided to the clinician via direct device interrogation or by remote telemetry. Recent reports based on actual clinical experience with this feature have attested to critical reliability and utility (Vollmann et al., 2007) and good correlation with other traditional tools such as brain natriuretic peptide (Luthje et al., 2007). 

Geddes, L.A., Tacker, A., Cabler, B., Kidder, H., Gothard, R., 1975a. The impedance of electrodes used for ventricular defibrillation. Med. Instrum. 9, 177—178. 

Here the factor 5 is the actual weight divided by the ideal weight, the left ventricular ejection time and the thoracic base impedance. 

Ohm s law can also explain this signal attenuation. If a ventricular electrogram signal of lOmV presents itself to a sensing impedance of 5KQ and a very low input amplifier impedance of 1 KQ, then the total impedance (in parallel) is 6KQ. 

Fig. 19.9 Measured data printout from a patient with a Medtronic Thera model 79601 programmed to 2.5 V on both the atrial and ventricular channels. The battery current drain, the lead impedance, and the projected longevity are provided in addition to other data.

Fig. 20.5 Summary report for an episode of ventricular fibrillation. The duration of the episode was 8 s 3.7 s were required for the ICD to charge to 20 J. The impedance during the shock was 63 Q.

The effects of therapy should be evaluated once it is determined that the electrograms and symptoms are consistent with a ventricular tachyarrhythmia. Evaluation of electrograms also provides clues on the effects of therapy. After therapy was given did the patient have return to sinus rhythm or was persistent arrhythmia present For episodes treated with shocks, the impedance measured during the event should be compared to impedances obtained during shocks at implant. Impedances normally range from 30-80 Q, depending on lead type... 

Thoracic fluid is associated with decreased impedance between a ventricular lead and the pacing system generator. Two preliminary clinical studies have reported varying results on the clinical utility of thoracic impedance monitoring for predicting hemodynamic status. The Medtronic Impedance Diagnostics in Heart Failure Trial (MlD-HeFT) evaluated 33 patients with Class III or IV heart failure due to systolic dysfunction (n = 25) or diastolic dysfunction (n =... 

Fig. 20.8 Top Noise detected on the ventricular channel leads to false detection of ventricular fibrillation. Bottom Daily monitoring of lead impedance in the same patient shows a sudden increase in resistance. In this case the patient was notified remotely via a home monitoring system and came to the pacemaker clinic before an inappropriate shock was delivered.

Laborderie J, Bordachar P, O neiU MD, and Clementy J. Fluctuation of atrial and ventricular lead impedances heralding subtotal separation of device header and generator in a patient with an implantable cardioverter-defibrillator. Heart Rhythm. 2007 Feb 4(2) 218-220. 

The role of ventricular resistance in the coupling of the ventricle to its arterial load was also investigated. For this purpose, a computer simulation study was performed where the LV was represented by the above model and the arterial load by a modified Windkessel (i.e., peripheral resistance, lumped arterial compliance and a characteristic impedance). It was observed that inclusion of a ventricular resistance slightly decreased mean arterial pressure (3 to 10%) and stroke volume (3 to 7%). In contrast, the pulsatile nature of the flow was markedly altered suggesting that ventricular resistance may play an important role in minimizing the external pulsatile power and in optimally coupling the ventricle to its arterial load (Shroff et ai, 1983a). 

GESELOWITZ We also have used this approach. That is, a pressure source with an impedance source together with a Fourier analysis. We showed that analytically, if the time variation is pulsatile, even though it is essentially a non uniform kind of situation, you can use Fourier analysis. In fact, it is fairly common in other electric engineering applications with non linear and non uniform behavior. If you have an essentially uniform time variation, you can use Fourier analysis and get valid information. So despite the claims of Hunter etai, we feel it is a reasonably good approximation to use the Fourier analysis on ventricular pressure and flow. I ll show you some of the results in my forthcoming presentation. 

To answer the question of optimal matching between the ventricle and arterial load, we developed a framework of analysis which uses simplified models of ventricular contraction and arterial input impedance. The ventricular model consists only of a single volume (or chamber) elastance which increases to an endsystolic value with each heart beat. With this elastance, stroke volume SV is represented as a linearly decreasing function of ventricular endsystolic pressure. Arterial input impedance is represented by a 3-element Windkessel model which is in turn approximated to describe arterial end systolic pressure as a linearly increasing function of stroke volume injected per heart beat. The slope of this relationship is E. Superposition of the ventricular and arterial endsystolic pressure-stroke volume relationships yields stroke volume and stroke work expected when the ventricle and the arterial load are coupled. From theoretical consideration, a maximum energy transfer should occur from the contracting ventricle to the arterial load under the condition E = Experimental data on the external work that a ventricle performed on extensively varied arterial impedance loads supported the validity of this matched condition. The matched condition also dictated that the ventricular ejection fraction should be nearly 50%, a well-known fact under normal condition. We conclude that the ventricular contractile property, as represented by is matched to the arterial impedance property, represented by a three-element windkessel model, under normal conditions. 

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