Static filling pressure in patients during induced ventricular fibrillation

The static pressure resulting after the cessation of flow is thought to reflect the filling of the cardiovascular system. In the past, static filling pressures or mean circulatory filling pressures have only been reported in experimental animals and in human corpses, respectively. We investigated arterial and central venous pressures in supine, anesthetized humans with longer fibrillation/defibrillation sequences (FDSs) during cardioverter/defibrillator implantation. In 82 patients, the average number of FDSs was 4 +/- 2 (mean +/- SD), and their duration was 13 +/- 2 s. In a total of 323 FDSs, arterial blood pressure decreased with a time constant of 2.9 +/- 1.0 s from 77.5 +/- 34.4 to 24.2 +/- 5.3 mmHg. Central venous pressure increased with a time constant of 3.6 +/- 1.3 s from 7.5 +/- 5.2 to 11.0 +/- 5.4 mmHg (36 points, 141 FDS). The average arteriocentral venous blood pressure difference remained at 13.2 +/- 6.2 mmHg. Although it slowly decreased, the pressure difference persisted even with FDSs lasting 20 s. Lack of true equilibrium pressure could possibly be due to a waterfall mechanism. However, waterfalls were identified neither between the left ventricle and large arteries nor at the level of the diaphragm in supine patients. We therefore suggest that static filling pressures/mean circulatory pressures can only be directly assessed if the time after termination of cardiac pumping is adequate, i.e., >20 s. For humans, such times are beyond ethical options.     

Effect of induced ventricular fibrillation and shock delivery on brain natriuretic peptide measured serially following a predischarge ICD test

Objectives

Brain natriuretic peptide (BNP) was a marker for heart failure and cardiac wall tension. We analysed the trend of BNP after predischarge testing in order to get non-invasive details about the cardiac stress during predischarge testing.

Methods

4-5 days after ICD implant we measured BNP, myoglobin, cardiac troponin I and creatine kinase in 20 patients before and 1, 5, 10, 20, 40, 60, 80, 100, 120 minutes and at the next day after predischarge testing. We evaluated actual values and percentage alterations of BNP.

Results

BNP significantly increased with a maximum after 5 minutes (804.0 ± 803.4 vs. 475.7 ± 629.5 pg/ml, P < 0.0001) and in terms of the percentage values (100 vs. 199.4 ± 61.4 %, P < 0.0001) compared with baseline BNP. BNP decreased after that with the last significantly increased BNP value after 20 minutes (540.2 ± 604.9 vs. 475.7 ± 629.5 pg/ml, P = 0.017). We excluded a cardiac necrosis during predischarge testing because of similar values of myoglobin, cardiac troponin I and creatine kinase during the 2-hour follow-up.

Conclusion

Our data showed a great increase with a doubling of BNP after 5 minutes as a result of induced ventricular fibrillation during predischarge test. This increase was not generated by myocardial necrosis but rather caused by an acute cardiac failure as a consequence of induced ventricular fibrillation in predischarge testing.     

Effect of myocardial infarction and ischemia on induction of cardiac reentries and ventricular fibrillation

The present work is aimed at investigating the effects of myocardial infarction and ischemia on induction of ventricular fibrillation. Electrophysiologic effects of global and local ischemia (variation of the dispersion of refractory periods as well as conduction velocity) on initiation of reentry mechanisms was studied by means of computer simulations based on a cellular automata model of propagation of activation wave through a ventricular surface element. A local area of ischemia where effects of the dispersion of refractory periods are investigated is then simulated. This is made using a Gaussian distribution characterized by its mean and standard deviation. These simulations show that ischemia is capable of initiating reentry phenomena which propagate through the whole ventricle; they are responsible for ventricular fibrillation which causes sudden cardiac death, even when ischemia only involves limited parts of the myocardium. Statistical study of the probability of reentries as a function of both of the size of ischemic zones and the rate of dispersion of refractory periods shows that the latter parameter is of primary importance in triggering cardiac reentries.     

Computer modeling of ventricular fibrillation

Electrical activity of a heart in ventricular fibrillation was modeled as a sum of independent pulse streams with various amplitude-frequency and phase characteristics. Results of computer experiments were compared with those of real physiological experiments on rabbits. Identification of the model was carried out by means of the least-squares procedure. The offered technique allows a computer model investigation of internal structure of irregularities of ventricular fibrillation.     

Computer modeling of ventricular fibrillation

Electrical activity of a heart in ventricular fibrillation was modeled as a sum of independent pulse streams with various amplitude-frequency and phase characteristics. Results of computer experiments were compared with those of real physiological experiments on rabbits. Identification of the model was carried out by means of the least-squares procedure. The offered technique allows a computer model investigation of internal structure of irregularities of ventricular fibrillation.     

Intracellular Ca dynamics in ventricular fibrillation

In the heart, membrane voltage (Vm) and intracellular Ca (Cai) are bidirectionally coupled, so that ionic membrane currents regulate Cai cycling and Cai affects ionic currents regulating action potential duration (APD). Although Cai reliably and consistently tracks Vm at normal heart rates, it is possible that at very rapid rates, sarcoplasmic reticulum Cai cycling may exhibit intrinsic dynamics. Non-voltage-gated Cai release might cause local alternations in APD and refractoriness that influence wavebreak during ventricular fibrillation (VF). In this study, we tested this hypothesis by examining the extent to which Cai is associated with Vm during VF. Cai transients were mapped optically in isolated arterially perfused swine right ventricles using the fluorescent dye rhod 2 AM while intracellular membrane potential was simultaneously recorded either locally with a microelectrode (5 preparations) or globally with the voltage-sensitive dye RH-237 (5 preparations). Mutual information (MI) is a quantitative statistical measure of the extent to which knowledge of one variable (Vm) predicts the value of a second variable (Cai). MI was high during pacing and ventricular tachycardia (VT; 1.13 +/- 0.21 and 1.69 +/- 0.18, respectively) but fell dramatically during VF (0.28 +/- 0.06, P < 0.001). Cai at sites 4-6 mm apart also showed decreased MI during VF (0.63 +/- 0.13) compared with pacing (1.59 +/- 0.34, P < 0.001) or VT (2.05 +/- 0.67, P < 0.001). Spatially, Cai waves usually bore no relationship to membrane depolarization waves during nonreentrant fractionated waves typical of VF, whereas they tracked each other closely during pacing and VT. The dominant frequencies of Vm and Cai signals analyzed by fast Fourier transform were similar during VT but differed significantly during VF. Cai is closely associated with Vm closely during pacing and VT but not during VF. These findings suggest that during VF, non-voltage-gated Cai release events occur and may influence wavebreak by altering Vm and APD locally.     

Death in ventricular fibrillation induced by isoproterenol in DOCA-salt pretreated rats preceded by changes in myocardial electrolytes

Serum and tissue content of sodium, potassium, magnesium and calcium was determined in controls and desoxycorticosterone acetate (DOCA)-salt treated rats to determine whether electrolyte changes preceded the development of isoproterenol-induced death in ventricular fibrillation. Control Sprague Dawley, male rats, were injected subcutaneously (s.c.) with either saline (Group A) or actinomycin D (0.1 mg/kg; Group B) once daily for 4 days. Other rats received 20 mg of DOCA by implantation, drank normal saline and were injected with either saline (Group C) or actinomycin D (Group D) once daily for 4 days. In the first part of the experiment, it was determined that none of 15 rats from Group C died when challenged with isoproterenol (150 micrograms/kg, s.c.) six days later: however, 13 out of 15 rats from Group D died within 29.1 +/- 15.0 minutes (mean +/- S.D.) from isoproterenol injection. Myocardial sodium was elevated (48.8 +/- 3.8 versus 36.3 +/- 1.9) and potassium decreased (60.4 +/- 3.4 versus 70.6 +/- 3.3, meq/kg wet weight, mean +/- S.D.) in rats that had succumbed to isoproterenol. In the second part of the experiment serum and tissues were removed from control and DOCA-saline pretreated rats before they died in ventricular fibrillation, 20 minutes after isoproterenol. DOCA-saline pretreated rats were hypernatremic and hypokalemic and exhibited higher sodium and lower potassium in skeletal muscle than control rats. Isoproterenol elicited hypokalemia in all rats, but it only elevated sodium and decreased potassium content in the myocardium of rats of Group D, that were more prone to die in ventricular fibrillation. It is concluded that myocardial electrolyte changes precede the onset of ventricular fibrillation and may be associated with the development of this dysrhythmia.     

Electrophysiological mechanisms of ventricular fibrillation induction

Ventricular fibrillation (VF) is known as a main responsible cause of sudden cardiac death which claims thousands of lives each year. Although the mechanism of VF induction has been investigated for over a century, its definite mechanism is still unclear. In the past few decades, the development of new advance technologies has helped investigators to understand how the strong stimulus or the shock induces VF. New hypotheses have been proposed to explain the mechanism of VF induction. This article reviews most commonly proposed hypotheses that are believed to be the mechanism of VF induction.