Changes in human coronary sinus blood flow and myocardial metabolism induced by ventricular fibrillation and defibrillation.

BACKGROUND: During implantation of cardioverter-defibrillators, repeated inductions of ventricular fibrillation and defibrillation are performed. Little is known about the myocardial metabolism associated with ventricular fibrillation and defibrillation in humans. METHODS: Sixteen patients scheduled for transvenous cardioverter-defibrillator implantation were included in the study. In 10 of the patients, blood samples were taken simultaneously in the coronary sinus and radial artery and analyzed for PO2, PCO2, standard bicarbonate, pH, lactate, alanine, glucose, and glycerol. Oxygen saturation, base excess, and oxygen content were calculated. The patients were studied before, shortly after, and 2 and 5 minutes after successful defibrillation. In six of the patients, coronary sinus blood flow was registered continuously. RESULTS: The coronary sinus blood flow declined from a basal value of 93 +/- 16 mL/min to 35 +/- 6 mL/min 14 +/- 2 seconds after induction of ventricular fibrillation. Following termination of ventricular fibrillation, coronary sinus blood flow increased to a peak value of 227 +/- 75 mL/min. Oxygen saturation, PO2, and oxygen content in the coronary sinus increased by approximately 25% shortly after each episode of ventricular fibrillation and defibrillation. The coronary sinus lactate increased and the arterio-coronary sinus lactate difference decreased shortly after each of the four episodes, but was normalized within 2 minutes. CONCLUSIONS: Repeated threshold tests during defibrillator implantation did not cause any long-lasting or cumulative metabolic effects, indicating that the described technique, with a 5-minute recovery period in between episodes, is safe as regards myocardial metabolism.

Brief episodes of ventricular fibrillation do not influence postischemic cerebral perfusion assessed by positron emission tomography.

OBJECTIVES: To establish the defibrillation threshold in patients receiving an implantable cardioverter defibrillator, at least three episodes of ventricular fibrillation are induced and converted back to regular rhythm, using direct current countershocks. The aim of this study was to examine the influence of repeated short episodes of ventricular fibrillation on global and regional cerebral perfusion. DESIGN: A prospective, descriptive study. SETTING: A positron emission tomography laboratory at a university hospital. PATIENTS: Four patients, admitted for defibrillation threshold tests 2 yrs after the implantation of a cardioverter defibrillator, were included in the study. Global and regional cerebral blood flow was measured by cerebral positron emission tomography, using an 15O-labeled tracer under propofol-induced general anesthesia. Electroencephalograms (EEGs) were concomitantly recorded. INTERVENTIONS: Induction and conversion of ventricular fibrillation. MEASUREMENTS AND MAIN RESULTS: No effect on global cerebral perfusion was observed after induced ventricular fibrillation lasting 21 +/- 3 secs. The average global cerebral perfusion was 23 +/- 1 mL/100 g/min after induction of anesthesia and 31 +/- 8 mL/100 g/min and 24 +/- 2 mL/100 g/min immediately after the termination of the first and second ventricular fibrillation episodes, respectively. Ten minutes after the second and the third threshold tests, global cerebral perfusion was 21 +/- 1 mL/100 g/min and 21 +/- 2 mL/100 g/min, respectively. Regional cerebral perfusion and EEGs were not influenced. CONCLUSION: Short episodes of ventricular fibrillation did not induce any measurable effects on global and regional cerebral perfusion detectable by positron emission tomography 30 secs and 10 mins after restitution of sinus rhythm.

Myocardial injury after electrical therapy for cardiac arrhythmias assessed by troponin-T release.

Episodes of ventricular fibrillation with subsequent intracardiac, and to a lesser extent, external defibrillation give rise to a statistically significant increase in S-troponin T, S-CK-MB(mass) and S-myoglobin indicative of a minor myocardial injury or dysfunction. In contrast, no such signs were observed after external direct-current conversion of atrial fibrillation using high energies, or after pace-terminated ventricular tachycardia.

Left ventricular function after repeated episodes of ventricular fibrillation and defibrillation assessed by transoesophageal echocardiography.

BACKGROUND: Investigators studying the effects of cardioverter-defibrillators on left ventricular systolic function have given only minor attention to the diastolic effects. OBJECTIVES: The purpose of this study was to investigate the impact of repeated episodes of ventricular fibrillation and defibrillation on systolic function and diastolic filling of the left ventricle during non-thoracotomy implantation of a cardioverter-defibrillator. METHODS: Systolic function and diastolic filling of the left ventricle were assessed peri-operatively on a beat-by-beat basis using a transoesophageal echo-Doppler technique in 12 patients during > or = 4 episodes of ventricular fibrillation and defibrillation. Systolic function was assessed from the fractional area change and diastolic filling from the E/A ratio. Arterial blood pressure and the ECG were recorded continuously. RESULTS: Blood pressure and heart rate did not change significantly throughout the procedure. The systolic function, similarly, was not significantly affected; the only changes were seen in the first two beats after defibrillation when the mean fractional area increased from 0.2 +/- 0.01 to 0.4 +/- 0.02 and 0.3 +/- 0.02, respectively (P < 0.001). Diastolic filling was, however, impaired as reflected by a decrease in the E/A ratio from 2.6 +/- 0.5 before to 1.6 +/- 0.4 (P < 0.01) after repeated threshold tests. CONCLUSIONS: While the combined ischaemic and electrical trauma caused by repeated episodes of ventricular fibrillation and defibrillation during the implantation of a cardioverter-defibrillator did not cause any systolic dysfunction, diastolic filling was significantly impaired.

Cardiac outflow of endothelin, neuropeptide Y and noradrenaline in relation to hyperaemia in coronary sinus flow following electrical conversion of induced ventricular fibrillation in man.

The implanted cardioverter defibrillator represents an alternative therapy for patients with drug-refractory malignant ventricular arrhythmias. Implantation and testing of the device requires that ventricular fibrillation be evoked and converted, thus providing a situation in which cardiovascular haemodynamics can be studied. In this study we have evaluated the effects of electrically induced ventricular fibrillation, followed by defibrillation, on coronary sinus blood flow and cardiac outflow of endothelin- and neuropeptide Y-like immunoreactivity (-LI) and of noradrenaline. Twelve patients were studied during implantation of a defibrillator. Ventricular fibrillation was induced and terminated after 17 +/- 1 s 5 +/- 1 times in each patient. In six patients coronary sinus blood flow was measured continuously. Plasma samples were obtained from four of these patients and another six patients, from the coronary sinus, radial artery and central vein before and during fibrillation and at two time points ( < 30 s and 5 min). Basal coronary sinus blood flow decreased to 38% at 14 +/- 2 s of ventricular fibrillation. Immediately following defibrillation there was a short-lasting increase in coronary sinus blood flow to 244% and a significant increase in the levels of neuropeptide Y-LI (146%) and noradrenaline (158%) in the coronary sinus while endothelin-LI remained unchanged (97%). Neither fibrillation nor defibrillation evoked any changes in the peripheral arterial and venous levels of endothelin-, neuropeptide Y-LI or noradrenaline. It is concluded that coronary sinus blood flow is markedly reduced during fibrillation and that restoration of normal impulse activity is followed by short-lasting hyperaemia. There was no evidence for effects on the vascular endothelium as assessed by endothelin levels.

Cardiac release of histamine after ventricular fibrillation and defibrillation during insertion of implantable cardioverter defibrillators (ICD).

Histamine has inotropic, chronotropic, arrhythmogenic, and vasoactive effects, and is released from the heart in ischaemia-reperfusion injury. The effect of ventricular fibrillation (VF) and defibrillation (DEF) on histamine release was investigated in 9 anaesthetized patients undergoing transvenous implantation of ICD. Concomitant arterial and coronary sinus (CS) blood samples were drawn before induction of VF (duration 20 seconds), immediately after, and 2 and 5 min after DEF (18-24 Joules). Basal arterial histamine was 2.5 +/- 6 nmol/l, and did not increase after VF. The histamine level in CS was 1.1 +/- 0.2 nmol/l before VF (p < 0.008 compared to arterial), and increased to 2.5 +/- 0.6 nmol/l immediately after (p < 0.045 compared to basal), to 3 +/- 1.1 nmol/l 2 min after (p < 0.45), and to 2.4 +/- 0.8 nmol/l 5 min after VF. In the basal state there was an uptake of histamine across the coronary circulation. After VF/DEF the level of histamine increased in coronary venous blood, suggesting cardiac release of histamine.

External defibrillation during reoperative heart surgery.

An inexpensive system for remote external defibrillation was evaluated in 25 patients undergoing repeat open-heart surgery. The system consists of a pair of self-adhesive pads connected with a remote bracket on which a standard pair of external shock electrodes are discharged. With this system 84% of the patients were successfully defibrillated: 12% converted spontaneously. The energy level at conversion was less than or equal to 200 Ws in 90% of the patients. There were no complications associated with the defibrillation procedure. By reducing the need for intrapericardial dissection this method shortens overall operating time and most probably decreases blood loss. The system can also be recommended for operations with a high risk of ventricular arrhythmia prior to pericardiotomy.