Biomedical subjects
Publications and source records attributed to Y Kishon.
A patient had torsades de pointes ventricular tachycardia related to psychotherapy with haloperidol in conventional doses. The QT interval was prolonged, and shortened after the cessation of the medication and infusion of isoproterenol. Concomitantly, torsades de pointes bursts disappeared. The observation might contribute to the understanding of the mechanism of sudden death of patients during pharmacologic psychotherapy.
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Phased compression cardiopulmonary resuscitation, whereby the chest and abdomen are compressed sequentially, is a new approach to the classical cardiopulmonary resuscitation technique, which is based on the compression of the chest alone. Six dogs with cardiac arrest were treated by external chest and abdominal compression using a rigid plexiglas suit lined with flexible perithoracic and periabdominal bladders. Fast inflation and deflation of the two independent bladders, together with forced ventilation of the lung, generated phased pressure pulses. The physiological variables monitored throughout the experiment included central venous, left ventricular, and central arterial pressures, carotid blood flow, cardiac output, and acid base balance. The phased compression technique was performed with phased time lags of 0, 150, 300, 400, 600, 700, and 850 ms between the abdominal and thoracic pressure pulses. A random sequence of the different phased compression modes, each lasting for 3-10 minutes, was applied during the prolonged resuscitation procedure that lasted for up to 70 minutes. By starting the abdominal compression 300-400 ms before the thoracic compression the carotid flow index improved by 77% (from 13% with simultaneous compression to 23% with phased compression) and the cardiac output index increased by 65% (from 7.8% with simultaneous compression to 12.5%). The results provide insight into the chest pump concept and the role of intrathoracic and intra-abdominal pressures in generating improved blood circulation during cardiopulmonary resuscitation, and show the advantages of phased compression over chest compression alone and simultaneous chest and abdominal compression.
Intrathoracic pressure variations are currently proposed as the main flow-generation mechanisms in standard and modified cardiopulmonary resuscitation (CPR) techniques. A method of changing pressure within the thorax and abdomen without any degree of heart compression was developed and tested in dogs. Intrathoracic and abdominal pressure waves were induced by cyclic inflation and deflation of the lungs and of perithoracic and periabdominal balloons. Various modes of CPR, depending on the rate of cycling, the use of a periabdominal balloon inflation, and a delay between the abdominal and thoracic pressure waves, were studied during ventricular fibrillation. During artificial systole (high intrathoracic pressure phase), the pressure which developed in the right ventricle (96.7 +/- 20.5 mmHg) was higher than the pressure in the aorta (89.3 +/- 20.5 mmHg, p less than 0.001). In artificial diastole (low intrathoracic pressure phase), the right ventricular pressure (11.7 +/- 2.6 mmHg) was lower than the aortic pressure (17.5 +/- 3.3 mmHg, p less than 0.001). The average flow in the carotid artery was 21.7 +/- 7.8 ml . min-1, which was 18 +/- 6% of the baseline carotid flow before CPR. Three different factors were found to improve the efficiency of CPR: periabdominal balloon inflation simultaneous with the intrathoracic pressure waves; increased frequency of the pressure waves from 60 to 100 cycles per minute; and inflation of the periabdominal balloon 50 to 100 ms before the thoracic balloon. Blood-gas and acid-base balance analysis during CPR revealed well-oxygenated arterial blood with a marked respiratory alkalosis and a slowly developing metabolic acidosis.(ABSTRACT TRUNCATED AT 250 WORDS)
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We observed marked gingival hyperplasia, similar clinically and histologically to the hyperplasia caused by 5:5 sodium diphenylhydantoin (Dilantin) during the last 18 months in five patients treated by nifedipine. Histologically, marked epithelial hyperplasia-acanthosis, with moderate inflammatory reaction in the lamina propria, was observed in all the biopsy specimens. Evidence points to a strong relationship between the gingival hyperplasia and the administration of nifedipine.
In a group of 288 patients with acute inferior (diaphragmatic) myocardial infarction, second and third degree atrioventricular (AV) block was diagnosed in 37 (14%). Three of the 37 died. The AV block in the 34 survivors could be differentiated into two distinct types, namely, early and late AV block. In 15 patients, second and third degree AV block developed within 6 hours of the first signs of infarction. In these 15 patients, all signs of AV block disappeared within 24 hours after infarction. Second and third degree AV block appeared suddenly in the vast majority, and first degree AV block could be detected in only a few patients and for a very short time before normalization of conduction. Atropine either abolished AV block completely or caused a marked acceleration of ventricular escape rhythm. In 14 patients, second and third degree AV block developed later than 6 hours (in 12 later than 24 hours) after infarction. It was heralded and followed by relatively long periods of first degree AV block in all cases (except in two patients who were admitted 72 hours after infarction). The total duration of AV block was longer than 40 hours in all of these patients, and the ventricular rate was relatively high. In no patient was abolishment of AV block achieved by atropine, and ventricular acceleration was relatively slight in all. In five patients, early and late AV block could be recognized consecutively. The two types of AV block seem to have different causes. Increased vagal tone is probably operative in the first type, and metabolic changes due to ischemia in the second. Response to atropine and sympathomimetic drugs is much better, and cardiac pacing only rarely indicated, in patients with early than in those with late AV block.
The effect of intrathoracic pressure variations on the hemodynamics of dogs with cardiac arrest were studied experimentally and simulated on a computer. High intrathoracic pressure (up to 90 mm Hg) was generated by lung inflation with passive and active modes of external fixation. Abdominal binding was found to be essential for the generation of high intrathoracic pressure. Remarkable Doppler flow signals were detected over the femoral artery with each lung inflation. Blood gases measured after 30 minutes of cardiac fibrillation in dogs together with intrathoracic pressure variations showed well oxygenated arterial blood with metabolic acidosis. A computer model was used to explore the effects of intrathoracic pressure variations over a large range of parameters. For intrathoracic pressure of 50/0 mm Hg. the mathematical model predicted maximal flow of 663 ml/min, occurring at a rate of 115 cpm, with a duty cycle of 58%. The heart showed only minor volume changes during the cycle, indicating its main function as a passive conduit during cardiopulmonary resuscitation. The data show that intrathoracic pressure variation with no direct heart compression can cause systemic blood flow of the magnitude occurring in most cardiopulmonary resuscitation techniques.
A 26-year-old woman developed severe postpartum cardiomyopathy in early puerperium. Ligation of the inferior vena cava prevented recurrent pulmonary embolism but did not affect her hemodynamic condition, which deteriorated constantly. During continuous hemodynamic monitoring only vigorous volume replacement with an increase of the left ventricular filling pressure to 32 mm Hg improved cardiac output significantly. The presence of a high titer of antiactin antibodies 9 months after the delivery supports the theory that the peripartum cardiomyopathy was of autoimmune etiology.
The PCCPR technique was experimentally and theoretically extended to serve as a cardiac assist procedure, and the potential of this method as a cardiac assist device was studied. Preliminary studies in dogs verify the applicability of this technique.
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A patient who presented with severe angina was found to have an ectopic origin of the entire left coronary system, the left main coronary artery arising from the proximal third of the right coronary artery. Atherosclerotic obstructive lesions were present in the right coronary artery, the left anterior descending artery, and the obtuse marginal branch of the left circumflex coronary artery. The three obstructed vessels were bypassed, using autologous saphenous veins. The patient continues to do well 24 months after his operation. We believe that coronary artery bypass should be carried out in symptomatic patients with abnormal coronary anatomy and atherosclerotic disease.
Graded submaximal ergometric tests were peformed on 60 patients who suffered from clinically severe angina pectoris, and the results were correlated with their coronary angiograms. The test was positive in 44, negative in 9, and undetermined in 7 patients (defined as failure to reach the target heart rate without ischemic ST changes). Among patients with positive tests, 42 (95%) had obstruction of one to three coronary vessels. Among patients with negative tests, only 3 had significant coronary disease (sensitivity 93%). While all patients suffered clinically from severe "angina pectoris," 8 (15%) had insignificant CAD, and among them 6 had a negative and 2 a false-positive exercise response (specificity 75%). Although ST depression was a good indicator of CAD, its degree did not parallel the severity of the lesions. The peak heart rate on exercise of patients with ischemic ST changes was lower than their target heart rate, suggesting that the heart rate at which ST changes occur constitutes in itself a good indicator of severity. Among the 7 patients with undetermined tests, CAD was found in 6. In these patients the absence of ST changes may be ascribed to extensive myocardial fibrosis, and the only clue to CAD resides in the negative chronotropic response to exercise. Although exercise testing does not always distinguish between normal and CAD patients, it nevertheless constitutes a valuable noninvasive technique for the detection of the high-risk patients.
We describe the case of a young woman with systemic lupus erythematosus (SLE) who suffered an acute myocardial infarction (MI). The patient was treated by corticosteroids in addition to the usual management for acute MI. The role of arteritis in producing the infarction is also discussed.
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