EXTRACORPOREAL CIRCULATION AS AN ADJUNCT TO RESUSCITATION OF THE HEART.
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In Sweden, penetrating injuries to the lung and especially to the heart are fortunately rare. We hereby present a case-report on a young man who was stabbed in the right lung and heart. The paramedics arrived at the scene one minute after the alarm and instituted mechanical ventilation and fluid infusion. Ten minutes later the young man arrived at the emergency department. By then the patient was in deep shock without spontaneous breathing, was darkly cyanotic, showed indeterminately palpable pulses and non-reacting pupils. ECG-monitoring showed sinus-rhythm. Massive fluid infusion was initiated and the adolescent was immediately transported to the operating room. On the way to the operating room the patient's heart arrested. A lateral thoracotomy was performed to relieve the cardiac tamponade, and internal heart massage was initiated. Injuries to the lung and heart were reached through sternotomy. Thanks to prompt initial handling by the paramedics and emergency personnel, a trauma-trained senior surgeon and rather direct lines of communication at the small hospital, the young man could return to ordinary activities with neither physical nor neurological deficit.
A method was developed for measuring the intramural oxygen tension in the ventricular wall (MpO2). The 10 electrodes of intramural needles are employed simultaneously for measurement of MpO2, and, by means of the same amplifiers and registration system, of the electrogram. In this way information could be obtained about the local MpO2 and the local electrical activity obtained from over 100 points in the ventricular wall. In the normal in situ dog heart we found an MpO2 of 5-90 mm Hg (mean 32 mm Hg). When the arterial pO2 was raised, the mean value of MpO2 was decreased. Directly after the start of a period of severe hypoxia a marked fall in MpO2 could be observed, which was reversible after return to the normoxic situation, provided that the hypoxic period was short. Changes in heart rate had only transient effects on the MpO2. Heart massage of the fibrillating heart in the open-chested dog was effective in restoring the arterial pO2, but gave no significant rise in MpO2 which did not exceed 5 mm Hg.
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55 cases of non-traumatic death with preterminal treatment by indirect heart massage showed fat pulmonary embolism in 42 per cent. Cases with thoracal fractures caused by massage were positive in 67 per cent. Controls were represented by a group of traumatic deaths with multiple fractures (80 per cent positivity) and a group of non-traumatic deaths without application of massage (6 per cent positivity).
The present study was undertaken to ascertain the role of the microcirculation in the phenomenon of hypoperfusion following complete cerebral ischemia. The experiments were performed on rats under superficial ether anesthesia. Cerebral ischemia was induced by cardiac arrest for 3.5 or 10 min, with survival periods that lasted from 3 min to 7 days. A special metal hook-like device was inserted into the chest cavity at the third intercostal spaces for occluding the cardiac vessel bundle. The effect of this procedure was total cessation of systemic circulation, i.e., clinical death. In 52% of animals with 10-min clinical death, resuscitation (external heart massage and artificial ventilation) restored heart activity. When brain circulation was restored, respiratory activity, pain reaction, corneal reflex, bioelectric activity of the cortex, and normal activities of the rats returned. Scanning electron microscopy was applied to study the effect of ischemia on the vessel wall and endothelial cells (EC). Ischemia produced a remarkable increase in the numbers of microvilli and pit-like invaginations on the luminal EC surface. The luminal wall surface of many of the microvessels (MV) formed ridges. Frequently, microthrombi of varying sizes were observed. The most prominent changes were noted from 3 min to 6 h of recirculation, and they correlated with hypoperfusion after ischemia. Seven days later, these changes completely disappeared. The data presented here indicate that progressive hypoperfusion after ischemia occurs with significant alterations in the MV walls. These studies collectively suggest that the focal responses in select MVs may be associated with receptor molecule up-regulation of some, but not all, affected ECs. Our data provide further characterization of a new and unique chronic model of brain ischemia that can be applied to relevant clinical studies.
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A 58-year-old man suffering from esophageal cancer was scheduled for radical resection and reconstruction of the esophagus. Immediately after the start of the operation, with the patient under general anesthesia, cardiac arrest occurred. The operation was immediately discontinued and closed chest heart massage was started. As the patient did not respond, open chest massage was initiated. Cardiac arrest can be caused by any one of a number of factors. This case was suspected to have had a coronary artery spasm. It took a total of 100 minutes to resuscitate the patient. But resuscitation was successful without any resulting neurological damage. This was attributed to appropriate open chest massage. If a case of cardiac arrest due to any coronary artery disease does not respond to the usual cardiopulmonary resuscitation, we should consider open chest massage.