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Treatment of 28 stabbed heart wounds in 15 dogs was done with traditional suturing or by means of an adhesive and Surgicel. The combination of Surgicel with adhesive ensured adequate closure of the wound and healing. The method is recommended for the treatment of human heart injuries in certain cases.
The transport time of enzyme from heart to plasma was studied in two experimental models. First, the enzyme alanine aminotransferase was slowly infused into the left ventricular wall in open-chest dogs. The half-life for the washout of alanine aminotransferase activity into plasma was 20 +/- 4 minutes (mean +/- SEM, n = 8) and was not different in ischemic and normally perfused tissue. From measurements of arteriovenous differences in alanine aminotransferase activity and left ventricular blood flow, it was concluded that 77 +/- 14% of total enzyme washout from ischemic tissue occurred by direct entry into the bloodstream. The corresponding value for the vascular permeability-surface area product was 264 +/- 55 ml.kg-1.hr-1. For a second model, we studied myocardial enzyme release into plasma after abrupt heart injury induced by 10 minutes of calcium-free coronary perfusion followed by reintroduction of calcium (calcium-paradox mechanism). The half-life for the release into plasma was 1.9 +/- 0.2 hours (mean +/- SEM, n = 6) and was again not influenced by sustained ischemia. Slower washout, as observed for this second model, is consistent with increased interstitial protein space and corresponds to a permeability--surface area product between 135 and 285 ml.kg-1.hr-1. These results were used to calculate the time course of cellular enzyme leakage from the rate of enzyme release into plasma in various forms of heart injury. Significant shifts between the time curves of evolving cellular injury and enzyme release into plasma are observed after 2 hours of ischemia followed by coronary reperfusion, but not after permanent ischemia.
In injuries of the heart after action of blunt and sharp force as well as gunshot injuries, in particular the histological findings are also important with regard to survival time and capacity of action. Single observations have given rise to the impression that vital reactions occur here earlier (thrombocyte aggregates, leukocytic emigration, formation of clots) than is the case in other organs. Systematic investigations of 48 cases amongst 373 heart injuries (3.9% of 11,342 autopsies, from 1983 to the last quarter of 1988) from the Institute for Forensic Medicine of the University of Munich as well as occasional cases from the Institute of Forensic Medicine of the Free University of Berlin did not show any leukocytic reactions in light microscopy with no or short survival time. In electron microscopic terms, leukocytic reactions, thrombocyte aggregates or deposits of fibrin were not to be discerned even in heart injuries which were survived for a short time. However, high-grad contractions and condensations of the muscle fibers with filamentous evaginations into which the mitochondria were pressed were shown characteristically. These alterations indicated a vital process, but they may possibly also occur even in the earliest supravital phase. In a total of 25 cases with confirmed survival time between 30 minutes and five days, cell reactions were shown which largely corresponded to the familiar time course. A prematurely occurring reaction was not to be observed.(ABSTRACT TRUNCATED AT 250 WORDS)
One case of non-penetrating injury of the heart is reported. The problem of the causal relation between accident and injury of the heart as well as the problems of the pathophysiological mechanisms of non-penetrating traumatic injury of the heart are discussed. The localisation of the non-penetrating traumatic injury, the volume and the energy of the object causing the injury as well as the preexisting degree of coronary sclerosis is of some importance for the severity of heart damages after non-penetrating traumatic injuries of the heart.
The authors had 110 patients with heart injuries (HI) under observation. The blood loss was, 1,092 +/- 120 ml in isolated HI and 2,410 +/- 246 ml in combined HI. Blood reinfusion (BR) was performed during 91 operations, the average volume was 1,233 +/- 215 ml. The peculiarities of reinfusion techniques are analysed and its advantages and shortcomings are critically appraised. The causes of fatal outcomes are shown according to the character of the heart damage and the volumes of blood loss and reinfusion. Mortality in HI with the use of BR was 16.5%.
The aim of the study was the estimation of heart muscle in response to air shock wave trauma. The animals were divided into four groups according to the time between trauma and the examination (3, 24, 48 and 120 hours). In all groups of animals ecg was performed and plasma level of creatinine kinase (CK), cardiac isoenzymes (CK-MB), lactic dehydrogenase (LDH) and its isoenzymes (LDH1-2) and alpha hydroxybutyrate dehydrogenase (HBDH) were determined. CK-MB activity as a percent of CK activity and rate of LDH isoenzymes activity were calculated. Morphologic estimation of heart injury based on macroscopic observation, histology and coronarography of heart specimens was performed. It was revealed that pathologic changes in ecg indicating intracardial conduction disturbances occur most intensively in first ten minutes after trauma. Plasma CPK, LDH and LDH1-2 activity increased significantly after 120 hrs following trauma. Morphologic manifestation of heart damage was multifocal injury of heart muscle.
Basing on the experience of treatment of 23 patients the authors emphasize the importance of rendering the correct urgent aid to patients with such injuries. Cases of injuries of "dangerous zones" of the heart are analyzed. Postoperative complications in such patients are described. The conclusion is made that the time is a decisive factor in decreasing the mortality rate of patients with heart injuries.
A report was made on a 25 year old patient with a penetrating heart injury with basic diagnosis, and treatment. A successful management was a result of good performance of the resuscitation chain, exactness of the clinical diagnosis and interdisciplinary cooperation between surgeons and anaesthetists.
Operations were carried out on 32 patients with injuries to the heart and pericardium during a period of 14 years. The pericardium was injured in 7 patients. All fatal cases were brought to the clinic in the first 30 minutes after the accident. Seven patients died after operation. The late results were studied in 22 patients in follow-up periods of 12 months to 14 years. The results were excellent and good in 20 patients and satisfactory in 2 patients. Poor results were not encountered. The capacity for work was restored in 21 patients.
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Both heart and brain are at risk for damage from asphyxia. However, these 2 organs' relative injury-thresholds have remained poorly defined. The present study using 16 anesthetized newborn piglets attempts to separate brain and heart damaging exposures from those that leave these organs unaffected. The hypoxic exposure (mean PaO2 = 3.6 +/- 0.6 kPa (27 mmHg) lasted for an average duration of 40 minutes and was associated with hypotension less than 4.7 kPa (35 mmHg) MABP. For brain damage assessment, 9 piglets that survived greater than 12 hours following resuscitation permitting histologic evaluation were used. For heart outcome assessment, those piglets that developed a postexposure, secondary hypotension to less than 4.7 kPa (35 mmHg) were compared to those without excluding 3 with uncertain cause of death. BRAIN-RESULTS: Six piglets remained brain intact while 3 exhibited brain edema and diffuse neuronal damage. The damaged animals' exposures differed from those that remained brain intact in sustaining significantly lower lowest MABPs (1.6 +/- 0.1 vs 3.3 +/- 0.4 kPa (12 vs 25 mmHg] and longer durations of MABP below 3.3 kPa (25 mmHg): 6 vs 1 min. and below 2.7 kPa (20 mmHg): 4 vs 0 min. HEART-RESULTS: Six of 13 animals developed marked delayed post-exposure hypotension requiring 5 to be killed prior to complete cardiovascular collapse. The only significant difference observed during exposure differentiating the two outcome groups (blood pressure maintenance vs cardiogenic shock) was the latter's more marked systemic acidosis (lowest mean arterial blood pH: 6.61 +/- 0.10 vs 6.91 +/- 0.10). These results suggest the brain is at risk for damage during hypoxia only when accompanied by an extreme lowering of blood pressure and the heart when accompanied by a severe acidosis. Further, the heart and brain need not both be damaged by the same hypoxic exposure. Contrary to common belief, the brain is not readily damaged from hypoxia alone absent marked circulatory changes.
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Isolated rat heart was perfused with 18 microM doxorubicin in the recirculating buffer. This treatment resulted in progressive contractile impairment. Aortic flow and minute work (i.e the product of cardiac output and peak systolic pressure) were reduced up to 20 and 29% of basal values, respectively. These parameters were partially restored in hearts perfused with 400 microM spermine, a naturally occurring polyamine, and 18 microM doxorubicin in the recirculating buffer. The results suggest the need for an investigation of the possible antagonistic role of polyamines against anthracycline cardiotoxicity.
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The clinical manifestation of wounds of the heart is determined by the mode, site and size of the injury as well as the structure of the pericardial and myocardial lesion. Diagnosis can be confirmed by ECG and echocardiography. Only 20% of the patients with penetrating wounds of the heart live for more than 30 minutes. Pericardio-centesis should be used only to gain time for a safe sternotomy, cardiac decompression and suture of the wound of the heart. An aggressive surgical approach is mandatory. Cardiopulmonary bypass is necessary only to correct of concomitant lesions.