Temporary pacemaker treatment in open heart surgery: pre- to postoperative changes in the electrogram characteristics.

Thirty-three patients undergoing cardiac surgery in general hypothermia were investigated during temporary pacemaker treatment for changes in right ventricular electrogram amplitudes (AMAX, UMAX) and maximum derivatives (DMAX, SMAX) from pre-to postoperative phase (AMAX = amplitude of the part of the electrogram with highest mean maximum derivative (SMAX), DMAX = maximum derivative, UMAX = maximum amplitude deflection). Standard commercially available electrodes were used in 28 of the patients. A paired comparison (n = 29) showed a fall in AMAX from 8.64 +/- 0.91 mV (mean +/- SEM) preoperatively to 4.94 +/- 0.43 mV (p < 0.001) between the 4th and 6th postoperative day; UMAX dropped from 11.09 +/- 0.95 mV preoperatively to 5.44 +/- 0.42 mV (p < 0.000001) from the fourth to the sixth postoperative day. In the same period DMAX fell from 1.57 +/- 0.13 V/s to 0.67 +/- 0.05 V/s (p < 0.000001), and SMAX from 0.76 +/- 0.06 V/s to 0.32 +/- 0.02 V/s (p < 0.000001). The most marked fall in amplitudes and maximum derivatives occurred during the first 24 hours. A slight, but nonsignificant increase occurred in amplitudes and maximum derivatives from the 4th to 6th postoperative day until the electrodes were removed the 10th to 19th postoperative day. Amplitudes and maximum derivatives were of the same value in patients with aortic valve compared with coronary heart diseases in spite of a more deteriorated myocardial function in the former group. The changes in amplitudes and maximum derivatives followed the same pattern in the two groups from the pre- to postoperative phase. This indicates that the additional local hyperthermia applied to the patients undergoing valve surgery was of no importance in the electrogram changes. Despite the fact that the electrogram maximum derivative and maximum amplitude needed to inhibit a temporary pulse generator are of a low magnitude, the values found were so small that they might provoke demand failure. This actually occurred in four patients.

Temporary pacemaker treatment in open heart surgery: variation in myocardial threshold, tissue and interface impedances in man.

Myocardial threshold and impedance of adequately insulated multicore metal electrodes (lengths l1 and l2) were investigated in 28 patients undergoing open heart surgery. Increase in current threshold from the pre-to postoperative period was: 607 +/- 102% (mean +/- SEM) with a constant-current pulse generator and 885 +/- 129% with a constant-voltage pulse generator. Tissue impedance (RT - initial impendance) calculated as voltage/current ratio 90 mus into the pulse changed from 564 +/- 34 omega before surgery to a minimum of 134 +/- 7 omega. Thereafter, there was a gradual increase in RT to 162 +/- 9 omega the day of electrode removal. In 25 of 28 patients the minimum values were reached the third to eighth postoperative day. Electrode/tissue interface impedances--Faraday resistance (RF) and Helmholtz capacity (CH)--were calculated from regression analysis of loaded and unloaded electrograms using the method of least squares. The RF showed a fall from 14.7 +/- 1.4 K omega to 5.2 +/- 0.3 K omega, and the CH (20-40 Hz) rose from 6.0 +/- 0.9 mu F to 15.5 +/- 0.8 muF preoperatively to the day of minimum tissue impedance. There were no further changes until the day of electrode removal. A significant positive correlation was found between CH (p < 0.002), current threshold (p < 0.005) and equivalent electrode length [lequ = l1 X l2/(l1 + l2)]. The electrode signal source impedance calculated from RT, RF and CH was of a magnitude not likely to contribute to demand failures. The low postoperative electrode impendance resulted in excessive load on the constant-voltage generator (condenser discharge type), rendering stimulation of the heart with reasonable current values impossible.

Cardiac hypothermia evaluated by ultrastructural studies in man.

Transmural left ventricular biopsies from 13 patients undergoing cardiopulmonary bypass were studied. The hypertrophic myocardium was protected by deep hypothermia (15 degrees C.) during ischemic arrest for a maximal period of 96 minutes. Biopsies were taken at the start of bypass, at the end of aortic cross-clamping, and after 20 minutes of reperfusion. The structure of the mitochondria remained normal, whereas cellular alterations in the form of widened intercalated discs, interstitial and intracellular edema, myelin figures, and slight myofibrillar lysis were observed in all stages. As no clear correlation between these structural injuries and aortic cross-clamping time was seen, they are a result of cardiac hypertrophy rather than intraoperative ischemia.

Endocarditis caused by Pasteurella multocida.

A 51-year-old previously healthy man developed endocarditis with low grade fever, aortic insufficiently and multiple arterial emboli. An atypical strain of Pasteurella multocida was isolated from each of 3 consecutive blood cultures. Protracted treatment with high doses of penicillin G was necessary to eradicate the infection. Following resection of the damaged aortic valves and implantation of a valve prosthesis, the patient recovered. P. multocida should be regarded as one of the possible causes of subacute bacterial endocarditis.

Ultrastructural studies on the growth of filaments and sarcomeres in mechanically overloaded human hearts.

The ultrastructure of myocardial cells was studied in four patients with left ventricular myocardial hypertrophy due to aortic and/or mitral valvular disease. Signs of cellular lysis and synthesis were present in juxtanuclear, interfibrillar, and subsarcolemmal areas. Subsarcolemmal areas contained a granular matrix with foci of polyribosomes, mitochondria, well preserved membranes, a proliferating sarcoplasmic reticulum, and thick and thin filaments and Z-band formations at different stages of development. Z-band substance and thin filaments appeared in the cytoplasm in close proximity to free polyribosomes and endoplasmic membranes and were seemingly not associated with the sarcolemma. These findings were interpreted as evidence for a proteosynthetic activity leading to the formation of new myofibrils and sarcomeres during the chronic stage of hypertrophy. Comparative studies showed that this process has much in common with the genesis of contractile cardiac units in the mammalian embryo. Anomalous Z-band accumulations were studied in normal myocardial cells of various vertebrates and in cells of the overloaded human heart. No evidence of a proteosynthetic activity was detected in the expanded Z-bands.

Pulmonary vein flow pattern in man during thoracotomy.

Pulmonary vein flow (PVF) pattern was traced with an electromagnetic flowmeter in 10 patients with normal hearts undergoing operations for pulmonary diseases. Instantaneous pulmonary artery flow, ECG, pulmonary artery pressure and left atrial pressure were recorded simultaneously. The pulsatile flow patterns obtained ocrresponded well to those previously found in dogs, and were remarkably similar to caval flow pattern. A constant and inverse relationship between the contour of the right atrial pressure andthe PVF pattern was found. In 3 patients, PVF was reversed by atrial systole; otherwise the flow was forward throughout the cardiac cycle. The influence of positive pressure ventilation was small, consisting of a slight initial inspiratory increase followed by a decrease during the latter half of inspiration.

Pulmonary vein flow pattern in mitral incompetence, combined mitral stenosis/incompetence and after prosthetic valve replacement.

Pulmonary vein flow (PVF) pattern was studied with an electromagnetic flowmeter in 11 patients with combined mitral stenosis/incompetence (MS/MI), in 6 patients with pure mitral incompetence (MI) and in 24 patients after mitral valve replacement (MVR). ECG, left atrial and left ventricular pressures were recorded simultaneously. The anomalous flow patterns, which were recorded, reflected the left atrial events and mitral valve function. Before MVR, the major forward flow occurred in ventricular diastole. In patients with predominating MS and small/moderate MI, a small retrograde PVF (RF) occurred in early ventricular systole, while pure or combined severe MI produced a holosystolic reversal of PVF.

Pulmonary vein flow pattern in mitral stenosis before and after commissurotomy.

Pulmonary vein flow (PVF) pattern was studied with an electromagnetic flowmeter in 15 patients with mitral stenosis. ECG, left atrial and left ventricular pressure were recorded simultaneously. Commissurotomy was performed in 8 patients and prosthetic valve replacement in the others. Measurements were performed before and after the intracardiac procedure. The predominating forward flow occurred in ventricular diastole, in contrast to ventricular systole in normal hearts. A small retrograde PVF was observed in 11/15 patients in early ventricular systole, coinciding with the c-wave in left atrial pressure (LAP). The reversed flow did not exceed 13% and showed no correlation to a slight regurgitation demonstrated at left ventricular angiography. The maximum delay in forward systolic PVF after onset of ventricular systole was 0.10 sec. The PVF pattern remained unchanged after commissurotomy in the majority of patients, even after reduction of the mitral valve gradient to less than 5 mmHg. However, holosystolic reversed PVF occurred in one patient, indicating a severe mitral regurgitation. The method of PVF recording is simple and proved useful for haemodynamic analysis and as a control after mitral valve surgery for evaluating the degree of mitral regurgitation.