Shape ventricular

The ventricular cardiac action potential is characterized by five phases and is shaped by the complex interplay of a variety of Na+, Ca2+ and K+ currents (Figure 4.2). The distinct voltage-dependent properties of hERG channels [19,20] govern the time course of Ikt and the manner in which it contributes to the outward K+ current during the repolarization phase of the cardiac action potential. The opening and closing of... 

Fig. 6. Influences of different types of antiarrhythmic agents (Vaughan-William s classification) on the shape of cardiac action potentials. First row Class I-agents action potentials of ventricular myocardial cells. Second row (from left to right) Action potential of SA-node cells influence of a )0-hlocker (class II). Action potential of ventricular myocardial cells influence of a class Ill-antiarrhythmic. Action potential of AV nodal cells influence of a class IV-antiarrhythmic (verapamil, diltiazem).

FIGURE 19.4 Relationsliip behA een plasma concentrations of tocainide and suppression of ventricular premature beats (VPBs) for four representative patients. The relationship betwreen VPB frequency and tocainide concentrations shown by the solid curves was obtained from a nonlinear least-squares regression analysis of the data using Equation 19.10. The estimate of n for each patient can be compared with the shape of the tocainide concentration-antiarrhythmic response curve. (Reproduced with permission from Meffin PJ, Winkle RA, Blaschke TF, Fitzgerald J, Harrison DC. Clin Pliarmacol Ther 1977 22 42-57.)... 

Two-dimensional ECHO employs multiple windows of the heart, and each view provides a wedge-shaped image. Windows most commonly used include parasternal long- and short-axis and apical two-and four-chamber views (Fig. 11-6). These views are processed onto a videotape to produce a motion picture of the heart. 2D ECHO renders increased accuracy in calculating ventricular volumes, wall thickness, and degree of valvular stenosis compared with M-mode ECHO. Patient-specific calculated parameters such as ejection fraction and wall thickness are compared with standardized values (population-... 

FIGURE 14-4. Key components of the pathophysiology of cardiac remodeling. Myocardial injury (e.g., myocardial infarction) results in the activation of a number of hemodynamic and neurohormonal compensatory responses in an attempt to maintain circulatory homeostasis. Chronic activation of the neurohormonal systems results in a cascade of events that affect the myocardium at the molecular and cellular levels. These events lead to the changes in ventricular size, shape, structure, and function known as ventricular remodeling. The alterations in ventricular function result in further deterioration in cardiac systolic and diastolic function, which further promotes the remodeling process. 

In addition to data on the effects of /S-blockers on survival, there are data showing improvements in numerous other end points. All the large clinical trials have shown /3-blockers to produce 15% to 20% reductions in all-cause hospitalization and 25% to 35% reductions in hospitalizations for worsening heart failure. The positive effects of -blockers on the left ventricle systolic function also have been very consistent across studies. Following several weeks to months of therapy, /3-blockers have been documented consistently to increase EEs by 5 to 10 units (e.g., from an EF of 20% to 25% or 30%), to decrease ventricular mass, to improve the sphericity of the ventricle, and to reduce systolic and diastolic volumes (LVES V and LVEDV). These effects are often collectively called reverse remodeling, referring to the fact that they return the heart toward more normal size, shape, and function. 

Ventricular remodeling is a process that occurs in several cardiovascular conditions, including heart failure and following an MI. It is characterized by changes in the size, shape, and function of the left... 

A typical ECG is shown in Figure 4.4, where the P wave corresponds to atrial depolarization and contraction the QRST complex corresponds to atrial repolarization and relaxation and the onset of ventricular depolarization and contraction and the T wave represents ventricular repolarization and relaxation. Analysis of the size and shape of the waves can indicate abnormalities of the heart. 

FIGURE 8.2 Time-varying ventricular elastance curves measured using the definition in Equation 8.3. Measured elastance curves are distinctive in shape. (Adapted from Suga, H. and Sagawa, K. 1974. Instantaneous pressure-volume relationship under various end-diastolic volume. Circ Res. 35 117-126.)... 

Holt [1] described the method of injecting an indicator into the left ventricular during diastole and measuring the stepwise decrease in aortic concentration with successive beats (Figure 13.5). From this concentration-time record, end-diastolic volume, stroke volume, and ejection fraction can be calculated. No assumption need be made about the geometric shape of the ventricle. The following describes the theory of this fundamental method. 

Fig 1 27 Several types of left ventricular leads with different shapes (courtesy of St. Jude Medical, Boston Scientific, and Medtronic)... 

Tight binding sites in the right ventricular outflow tract Difficult dilatation into the outflow tract difficult C-shaped lead course Dilatation cannot be advanced to binding sites or tip high risk of tears Transjugular approach reverse Pisa approach dilatation from the femoral vein... 

The functionality of the valve has been tested with equipment which has been made in our laboratory. Pulsatile flow tests on a mock circulatory system, flow patterns, measurements of steady retrograde flow and pressure drop across the valve, in vivo tests have been carried out. By the pulsatile flow tests, the shapes of curves referring to ventricular and aortic pressure and to flow rate, similar to that shown by other kinds of valves, have been observed. 

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