This review has been prompted by an epidemic of car accidents in Croatia with thoracic and cardiac trauma and frequent fatal outcome in some sports associated with thoracic trauma, and thus the possibility of cardiac trauma. An increased incidence of cardiac trauma is more common in our socio-economic living conditions still due to using cold weapons. This problem can not be ignored considering the prevalence of possession of firearms which is a potential individual source of penetrating cardiac injuries with fatal outcome.

The exact cause of about 25% of all thoracic traumas with deadly outcome is the cardiac injury (1). Statistical data show that the right ventricle (RV; in 35%) is the most frequently affected, followed by left ventricle (LV; in 25%), the right atrium (RA; in 33%) and the left atrium (LA; in 14%) (1). Some other statistical data report on the incidence of injury of the right part of the heart in cardiac trauma of 76% and left part of 14.3% (2). In addition to the cardiac injury, thoracic trauma is usually accompanied by an injury of other organ systems: lungs, pleura, mediastinum, trachea, bronchus, esophagus, ribs, aortic wall, spine, contributing to the occurrence of complex symptomatology and causing differential diagnostic difficulties (1, 3-5).

Reports of international trauma centers emphasize not only a need for direct emergency intervention “on the spot” but also the importance of timely awareness and preparedness of a surgical center team, which should allow for efficient inhospital intervention.

Despite direct assistance and emergency intervention on the spot of the incident, followed by the analysis and in-hospital treatment, traumatic injury of cardiac structures with pericardial tamponade still shows a high incidence of deaths in traffic accidents — 20%6. There is a small number of interventions in case of penetrating cardiac injuries in surgical centers, only 0.5% of all surgical interventions (5). It seems that many patients come late for professional specialist assistance, and the reason for this may be the fact that the emergency medical assistance in the field is not equipped with suitable apparatus or is unable to diagnose and provide an appropriate assistance. Cardiac traumas — both nonpenetrating and penetrating, in car accidents show a high common incidence from 80% to 90% (6, 7). Non-penetrating injuries may not be immediately fatal, but the further follow-up often reveals complications followed by poor outcome thereby recording a high mortality over a longer post hospital period from 57% to 64% (8).

Cardiac trauma is divided in:

In case of blunt trauma, contusions of the chest, heart, blood vessels (or any other organs) are caused by blunt force impact, which can further get complicated as a consequence of structural changes to the heart, pericardium, myocardium, heart valves, chordae tendineae, papillary muscles, rarely endocardium and lungs, aortic wall with dissection and arterial- venous fistulas — occurred for instance in case of sinus rupture of the Valsalva aorta with left-right shunt or left-left shunt in LA and rarely shunt in the pericardial sac or rupture of the descending aorta at the point of ligamentum arteriosum Botalli (the latter due to acceleration and deceleration forces around the seat belt shaft in the car). At the first moment of action of mild blunt force, the injured may feel no major problems. Therefore, blunt trauma often requires longer clinical follow-up and monitoring by ECG, echocardiography, radiological and other methods.

12-lead ECG should immediately record and should be monitoring a patient for at least 24 hours in the hospital even in case of presumed “minor contusions” to be followed by periodic follow-up analyses (Holter ECG and echocardiography), which can identify (in the chronicity) late changes (8, 9). Slight intensity blunt trauma will never be forgotten by a patient, especially if the first symptoms were mild — general fatigue and slight substernal pain. However, various arrhythmias, including ventricular tachycardia and conduction disorders with fatal AV blocks are usually present over a long follow-up period. (10) Heart failure symptoms are rare with a global decrease in myocardial contractility, if no extensive injury has been proved.

Pericardial tamponade is very rare in the blunt injury, but still may be caused by non-penetrating forces through the chest or abdominal cavity. It occurs more commonly in a situation of blunt trauma — a smaller pericardial effusion with a slow development, usually as a serous exudative reaction (not hemopericardium) of autoimmune etiology. These are the reactions to minimal injury of the pericardium, such as postsurgical pericarditis — postpericardiotomy syndrome. Such a pericardial effusion, usually a smaller pericardial effusion, does not endanger the LV filling, and if it slowly reaches the size of approximately 200 mL it can cause mild tachycardia and dyspnea in the patient in effort. The retreat of exudates may lead to smaller fibrinous-fibrous changes that may remain within the pericardium, without significant hemodynamic implications (usually without constriction). Extremely rare blunt trauma causes a direct sudden death, when myocardial contusion causes myocardial rupture due to a minor or major laceration of the myocardial or pericardial wall due to a more extensive dissection of the aortic wall or when the blunt impact occurs in the so-called vulnerable stage of cardiac resolution.

Although it is less life-threatening than penetrating trauma, a strong force in case of such an injury may cause injury of other organs, such as diaphragmatic hernia as a result of diaphragmatic rupture with herniation of abdominal contents into the chest causing thus pressure on — compression of the cardiac cavities, but also myocardial herniation due to a small pericardial rupture, resulting from a blunt force (4, 8). A strong blunt force can cause rotation of the heart and the socalled “luxation” or the dislocation of the whole heart through the chest and abdominal wall. The last changes need to be excluded in the in-hospital period, best by using multi-layer computed tomography (MSCT).

The causes of blunt non-penetrating trauma are multiple, usually resulting in consequential chest and heart compression and rarely in minor or major ruptures of the heart and surrounding organs. This happens in car accidents as a result of sudden deceleration, direct contusion of the sternum by the steering wheel and numerous contusions of the chest and abdomen in case of a car rollover. A common cause of contusion of the chest and the heart is also a fall from the height onto the ground as an occupational injury, intentional strong “murderous” blows to the chest, unintentional fierce hit by the ball, collision of two bodies in the sport, and in cattle breeding the kick by an animal’s hoof in the chest, falling off a riding animal, falling off a motorcycle, bicycle, etc. Minor or major iatrogenic myocardial and pericardial contusion cannot often be avoided in medical resuscitation, sometimes accompanied by fractured ribs (which can cause a penetrating injury). The following causes are air strikes — air “blast” in the immediate vicinity of the explosion of a bomb, mine, with compression of the sternum and organs on the spine, any water “blast” or other compression of the thorax between the two incompressible — metal substrates.

Besides the deceleration forces, when bringing two vehicles to a halt a strong acceleration forces are created, sometimes even in accidents in a case of rollover. Such acceleration forces of high power can lead to “flexion” of the chest with the manifestation of the stretching forces and twisting forces1 and thus to the cardiac injury and injury of other organs in the chest. Frequent electrocardioversions can in therapeutic interventions be the cause of micro changes to the myocardium, myocardial edema and minor necrosis. The same applies to the unfortunate alternating electric current strikes, and probably to lightning strikes and electrical discharge produced by the thunderstorm. In cases of blunt cardiac trauma, the details on the severity of myocardial injury can be obtained by determining specific myocardial enzymes and troponin.

In acute penetrating — sharp injury the consequences of the forces are immediately manifested by severe cardiac disorders and severe general condition of the injured, often with hypovolemic — with oligemia, hemorrhagic shock (hypovolemic shock is called “obstructive shock” by some clinicians — because the normal filling of the heart in diastole with potential obstruction of large vessels is prevented) or generally with traumatic shock, which requires an urgent, thorough diagnosis and therapy. The causes of such an injury usually with a deadly outcome are even at peacetime still projectiles from firearms, larger caliber bullets from the rifle/pistol “magnum”, “beret” or several smaller bullets from the hunting “shotgun”; deliberate stab wounds by cold weapon, knife; accidental injuries by tools and other sharp objects in the industry and production. In traffic accidents major tears, chest lacerations and a break in the continuity of the pericardial, myocardial, aorta structures which are caused by sharp edges of fractured ribs and sternum, an injury by “flying” high speed sharp objects (acceleration force) of glass or metal, and sometimes the very strong compressions (with compression between the sternum, ribs and spine) occur. It is estimated that the incidence of such events in severe cardiac lacerations is about 20% (3) of which a half of them end up with a fatal outcome. In agricultural activities, we have witnessed that overturning of agricultural machinery (tractors) is almost always fatal for a driver. It has not been studied whether a cardiac death or some other causes were the reason for death.

Penetrating cardiac trauma in the civil society of North America in a quarter of cases (of all penetrations into the chest) is still caused by a knife. In Turkey, a retrospective analysis conducted from 2005 to 2008, showed that 5% of penetrating injuries were caused by bullets from a firearm, and 95% of stab wounds by a cold weapon, tools etc. (11).

The displacement of abdominal organs in the chest and reversely (of the very heart towards the abdominal cavity) via the ruptured diaphragm leads to herniation of abdominal organs and sometimes the so called “luxation”, displacement of the heart with contusion as in blunt trauma or/and with consequential laceration, rupture of the heart — myocardium, pericardium, disruption of cardiac valves, papillary muscles, aortic and large veins. Orthopedic term “luxation”, “dislocation” from the primary position of the heart, as well as “volvulus” (obstruction) — the name taken from emergency abdominal surgery denote here rotation of the heart and large vessels around their axis and can lead to obstruction of the inferior vena cava, large arteries and compression of the right side of the heart and mediastinal organs (1, 12). The injuries are closely associated with complicated cardiac rupture in 28% of cases, where mortality is high — 67% (13). Significant changes in the electrical axis in ECG in these situations (if an earlier finding is known) are always suspicious for “luxation” and “dislocation” of the heart. The penetrating injury along with the myocardial, pericardial laceration can be accompanied by additional injury of myocardial arteries and arterioles causing secondary necrosis and myocardial rupture through ischemia or again directly causing hemopericardium as a consequence of the rupture of the walls of coronary arteries and above mentioned arterioles.

The penetrating, gunshot and stab wounds visibly damage the anterior chest (usually at the entrance) and the missile (invisibly) damage large vessels, aorta, veins, mediastinum, and spine where the missile can stop and cause neurological injuries. The missile and stab wounds, however, can be directed from the abdominal cavity in direction of the heart, and then the entry wound in the abdominal wall is sometimes in the posterior chest in the back, which requires a detailed examination to prevent overlooking of the wound. Cardiac laceration can even occur from the inside in case of strong compressions (with no visible entry and exit wound) and in some diagnostic and therapeutic cardiac procedures such as: cardiac catheterization, examining the conduction system of the heart, radiofrequency ablation of conductive pathways, implantation of electrical pacemaker, TAVI procedures on the aortic heart valve defects or arterial or venous valve repair (such as in percutaneous mitral valvuloplasty, plastic procedure on the tricuspid valve), myocardial biopsy, during coronary angiography with stent implantation and/or during the dilation of coronary arteries.

Each pericardial fluid with sharp cardiac trauma should be considered hemopericardium unless proven otherwise, and also the potential cause of pericardial tamponade (1, 3, 9, 11, 24). Due to its sudden occurrence and here large amounts of blood in the pericardial cavity, hemopericardium develops almost always to tamponade if no intervention is performed. Therefore, the intervention, therapeutic pericardiocentesis should be performed as soon as possible by the emergency medical services (EMS) on the spot of the incident, except in case when reasonably suspecting that hemopericardium is caused by aortic dissection, when pericardiocentesis is contraindicated.

Pericardial tamponade is also considered equivalent primarily to penetrating cardiac injury from the outside (although it can occur in case of non-penetrating injury) that may not be visible as a wound on the surface of the chest or abdomen. The statistical data show that some stab wounds caused by cold weapons, a narrow tip of a knife or minor stab wounds caused by a tip of a fractured rib, body of sternum have a better prognosis than the gunshot wounds. The pericardial tamponade in the first case usually occurs more gradually, slowly, and a minor wound or a longitudinal myocardial or pericardial rupture wound is sometimes squeezed, narrowed and can spontaneously thrombosed. Myocardial injury by a large missile causes a sudden tamponade by a large amount of hemopericardium, and a fatal outcome if no intervention is performed.

The Japanese authors insisted on the assessment of the amount of pericardial fluid immediately after the incident in 1999 by using the heart ultrasound and intervention (9). Pericardium may not stretch, except in gradual increase in pericardial fluid (hypothyroidism, uremia) when the volume of pericardial sac can increase up to 1,500-2,000 mL without significant symptoms at rest. If the pericardial fluid increases all of a sudden, sometimes 100mL of blood, can cause symptoms of tamponade.

A sudden increase in volume in pericardial sac increases intrapericardial pressure. When the pressure in the pericardium becomes close to the pressure in the RA, RV function is then significantly impaired. Elevated intrapericardial pressure hinders further ventricular diastolic expansion. This leads to a further elevation of intracavitary diastolic pressure and reduces ventricular filling (initially more RV, followed by LV), thus significantly reducing the stroke and minute volume of the left side of the heart whereas the systemic arterial pressure drops. The elevation of the intrapericardial pressure administratively correlates to an elevation of the systemic venous pressure and the pressure in the pulmonary veins consequently leading to the aforementioned elevation of pressure not only in the RA, but also in LA. The elevated systemic venous pressure and pulmonary venous pressure, diastolic blood in the both chambers, diastolic pressure in the pulmonary artery lead to an elevation of pressure values in the heart at approximately the same level: intracavitary and intravascular pressure differences disappear resulting in the condition of pericardial tamponade with a further drop in stroke volume, drop in blood pressure and via circulatory collapse causing cardiogenic shock, often with a fatal outcome.

It can be concluded that pericardial tamponade is pathophysiologically characterized by:

Clinical symptomatology of tamponade is at first manifested as a strong substernal and epigastric chest pain (usually associated with laceration-related injury), followed by the general serious prostrate condition with pallor, dyspnea, tachypnea, tachycardia, and sometimes at the beginning with dysphagia, cough, hoarseness due to frequently severe compression of the lungs, bronchus and recurrent nerve. The manifestation of shock is finally dominant.

Physical examination determines the typical signs of tamponade:

Tachycardia is almost always present due to compensatory sympathicotonia and catecholamine, in response to the fall in stroke volume and history of trauma: tachypnea (compression of the lungs, bronchi, hypoxia), paleness of skin and mucous membranes, and potential peripheral cyanosis. Pericardial friction is not heard in major effusion. Larger hemopericardium compresses the left pulmonary lobe, which is reflected by dullness to percussion and inaudible breathing auscultatory (Ewart’s sign). Otherwise, there are no physical signs of delays in the lungs which is a typical phenomenon. Arterial pressure is low — around or below 90 mmHg. When venous pressure in cubital vein was measured, it would be elevated.

A typical Kussmaul’s sign may be present. It is reflected by reducing neck vein distension in inspiration (which is not expressed as more severe hypovolemia) and characteristic paradoxical pulse finding, accompanied by a potential pressure drop. Paradoxical pulse is a slowdown of the heart rate in the inspiration (acceleration is normal), which is difficult to assess clinically in presence of tachypnea. Blood pressure measured in the inspiration should also drop to 15-20 mmHg in order to accept the sign as positive for tamponade (which is classified as paradox by some clinicians). The drop in pressure in the inspiration is otherwise normally present in healthy individuals, but also in other diseases, so sensu stricto this drop can not be called a highly specific paradoxical sign.

Reduction of jugular vein distension in the inspiration is a sign of a short-term drop in pressure in RA and intrapericardially as a result of a negative pressure in the chest. This allows only a slow filling of RV and transitory increase in cavity size of RV in the inspiration.

For pericardial tamponade and injury there is no pathognomonic ECG sign, but sometimes several significant ones can be determined: 1. elevation of the ST-segment at the top typically concave; 2. electrical alternans; 3. low voltage of amplitude of QRS-complex (the sum of the amplitudes in D1, D2, D3 less than 15 mm). The latter is also an insensitive and a nonspecific sign of the so-called “short circuit” in the electrical impulse travel through the pericardial effusion, as it is even present in obesity in the left pleural effusion, some cardiomyopathies, amyloidosis ...) (15, 16).

A strong elevation of intrapericardial pressure in the tamponade damages and reduces the flow in the subendocardial and subepicardial part of the myocardium causing thus the myocardial ischemia, which can be manifested in a record of 12-lead ECG as convex elevation of the ST-segment with the positive or negative T-wave. The depression of the STsegment is exceptional. The described finding of the STsegment on ECG in the tamponade is also nonspecific. Q or QS waves are very rare and are also not the sign of the pericardial tamponade, but of subendocardial myocardial injury, because the electrophysiological visceral and parietal layer of the pericardium normally make no difference in the electric potential due to a small pericardial mass, so that it could be recorded at all (15). Myocardial rupture with tamponade, depending on size, can give an image of necrosis with Q-or QS-wave. It is understandable, therefore, that laboratory findings of specific myocardial enzymes and troponin just additionally indicate the injury of the myocardium, not of pericardium (5, 15).

When making echocardiographic examination of tamponade the following signs can be determined:

Myocardial contusion (contusion caused by a blow) is in most cases equivalent to blunt, non-penetrating cardiac trauma associated with blunt chest trauma (sometimes even by blunt abdominal trauma) (1, 4, 8). The cardiac trauma depends on the strength of “blunt” forces exerted on the chest, primarily on the effect of the so-called acceleration forces exerted not only on the surface of the chest, but consequently also on the surface of the heart and on the surface of internal cardiac structures and other organs in the chest. The effect depends on the site of impact, compliance of the chest (children’s chest has increased compliance, so there is fewer number of fatalities in car accidents) and the stage of cardiac resolution in which the impact occurred. It has been proved on animal models that sometimes less force at a critical stage of the cardiac resolution can cause a sudden death (15, 18). Today there are no standard parameters for an accurate assessment of the size, strength of force and power of blunt trauma in people that leads to contusion, which is understandable. The critical stage of the cardiac resolution in people is also almost impossible to determine because no one wears Holter ECG monitor in the stage of experienced force. The only accurate assessment of strength of myocardial blunt force trauma force can be made according to the histological findings at autopsy.

Pathomorphological changes can be histologically determined in the form of mild edema of the myocardial tissue, intramural hemorrhage, minor or major myocardial necrosis, which may be followed by rupture of the wall1, (4, 6, 14). Myocardial rupture in blunt cardiac trauma occurs in approximately 0.3% - 1.1% of (directly) traumatized persons. Deadly outcomes occur in a longer observation of post-traumatic condition, sometimes lasting for months or years. We think it is difficult to prove a causal connection after a long time since the period of trauma, so it is possible that studies (indicating a high post-hospital mortality) do not sufficiently exclude all other causal factors.

Pneumopericardium may occur after the blunt trauma, being complicated by rupture, laceration of the pericardium and surrounding lung tissue (as proved by MSCT examination of the chest). Damage to the coronary arteries in blunt trauma occurs in about 2%, mostly it is the left anterior descending artery and the right coronary artery which is lacerated on the right side behind the sternum, while the circumflex artery is rarely affected (19-21). Multi-vessel coronary injuries are rare. Traumatic valvular dysfunction with the development of pulmonary edema is also more rare (6). Aortic valve, followed by mitral and tricuspid valve are mostly damaged. The mechanism of development of cusp disruptions is a sudden elevation of intracardial pressure when closing the valve. The causes of valvular dysfunction are tear or distortion, avulsion of annulus and usually of non-coronary aortic cusp (6).

The myocardial edema itself may compromise the coronary circulation by compression resulting in the development of (“secondary”) ischemia (4, 18). Since the process of exerting blunt force mainly occurs in the myocardium, it is understandable that it can be manifested as ischemia by electrocardiographic leads, or more often as myocardial infarction, whereas q or QS waves sometimes suggest necrosis. The ST-segment in such injuries is usually elevated with the convexity on the top (as in the infarction), and T-waves are often immediately negative. The ST-segment may in some leads be even more denivelated. It is important to point out that recently performed ECG with pathological changes identify a patient at risk, but the normal finding of ECG taken immediately after the incident is of no help, because its value is negatively predictable. Immediately after the incident, if the contusion force was strong, frequent cardiac arrhythmias in around 28% of blunt injuries (8) with the conduction disturbance can be determined. Usually, these are harmless extrasystoles, supraventricular tachycardia, atrial estrasystoles that are concerned. The right bundle branch block which in case of minor injury disappears within 24 hours, while the left bundle branch block is rare. Ventricular extrasystoles and ventricular tachycardia also occur, similar to the early postinfarction period, which in case of minor injuries are well treated by medicamentous therapy (amiodarone, and an alternative medicine — lidocaine 100 + 50 mg is rarely to be administered).

However, the EMS team should be not surprised, because the early period after the severe contusion is followed by the sustained ventricular tachycardia (pulseless), including ventricular fibrillation (rhythms that are defibrillated), which occur along with cardiac arrest and they should be treated intensively according to the new guidelines (22, 23). After three initial defibrillations without success, it is recommended to prescribe epinephrine 1 mg i.v. (or intraoseal: humerus, tibia) which is to be repeated every 3-5 minutes. If the ventricular fibrillation reoccurs, amiodarone 300 mg i.v. in 5% glucose in bolus and additionally 150 mg amiodarone should be prescribed.

However, a failure often occurs, whereas asystole occurs — the state without electrical ventricular activities, although electrical activity may exist in the form of P-waves which are not always visible in the ECG. It is necessary to re-evaluate the connection of electrodes and evaluate the ECG findings. Asystole may exist when suspecting that the so called “fine ventricular fibrillation” (invisible in the ECG record) is concerned and until recently defibrillation continued to be performed in this situation. The today’s attitude is that no repeated defibrillation should be performed in case of asystole susceptible for the “fine” ventricular fibrillation. Rhythms that are not defibrillated are proven (agonal) asystole and pulseless electrical activity (PEA), often called electromechanical dissociation. In asystole or development of the block, one can try with percutaneous stimulation, by applying the thoracic electrodes or by administering the above mentioned adrenaline. The new recommendations suggest that the administration of 3 mg atropine in bolus is of a little effect (although we still apply it in certain situations as a potent vagolytic).

According to the new guidelines of the European Resuscitation Council (22, 23), published in 2010, the survival after cardiac arrest with asystole or pulseless electrical activity is less likely if causes are not immediately detected and resolved (as it is pericardial tamponade here). In case of a true asystole there is no use of electrical stimulation, which is a consensus of experts at an international level.

In contusion-related cardiac injuries no other in-hospital measures, such as the temporary introduction of hypothermia 32-34°C were considered necessary, if a patient was not in a coma and had no neurological disorders after the cardiac arrest. The current recommendation is that the condition after the cardiac arrest is treated by hypothermia. Mechanical ventilation with myorelaxants and sedation is very rarely required, and the today modern mechanical support to cardiovascular system by apparatus VAD, BIVAD, LVAD, RVAD, LVAS — HEART MTTE II etc. is extremely rarely used.

All the symptoms and clinical status depend on the size of the injured myocardial mass, which will lead to asystole and irreparable cardiac arrest. The destruction of >50% of myocardial mass is very risky (24). RV is more exposed to injuries in case of chest contusions, while its myocardial mass is lower than that of the LV, so the increase in myocardial specific enzymes and troponins, despite a strong force can therefore be slight which does not contribute to the assessment of severity of clinical course of the disease (5).

Blunt chest trauma with myocardial contusion is statistically more common than penetrating injury, but it seems to be directly less dangerous to life. A frequently asked question is posed in connection with a sudden death of athletes who have experienced many minor or major blunt chest traumas, for instance football players (falls, collisions, blow to the chest by a ball, etc.), who previously underwent cardiac examinations and had no proven common causes of sudden cardiac death. A small number of taken ECGs in case of collapse or syncopes sustained by the players on the playground indicate a malignant ventricular tachycardia, which may be related to the earlier blunt trauma? If the blunt chest trauma is followed by the development of resistant hypotension despite an adequate resuscitation of hypovolemia, and if no other obvious cause of the condition is present, an additional coronary angiography should be performed (21).

The diagnosis of the cardiac trauma, particularly penetrating cardiac trauma, should be made as soon as possible after the sustained incident, because the emergency intervention when suspecting the development of pericardial tamponade may save the life of the injured and is the prerequisite for successful resuscitation if cardiac arrest occurs. The apparent wound, chest laceration is a sign for a very probable tear and cardiac injury as determined by the examination. In the case of an injury caused by fire missile, it is necessary to determine the entry and exit wound, in order to be able to predict the path of missile and injury of other organs in this path, and assess the retention of the missile in some of the organs. A blow to the rib only or sternum by a missile or a knife leads to bursting of bone structure indicating thus the cardiac laceration. The assessment of the patient’s condition with such an injury must, naturally, be based on the usual management plan and algorithm for acute emergency incidents, requiring resuscitation indicated as acronym ABCDE — Airway, Breathing, Circulation, Defibrillation and Disability Expose (free airways, assess breathing, apply artificial respiration, while the use of manual massage over the lower part of the sternum when suspecting tamponade is certainly not advised. However, the evaluation of pulse, blood pressure and circulation will be taken into consideration, while defibrillation is to be performed immediately in case of ventricular tachycardia and fibrillation, if there is no response to medicamentous therapy administered i.v. or intraosseously (6, 22, 23). Administration of medicines intratracheally is no longer advisable due to poor absorption.

The scale of traumatic injuries of the chest and heart has six degrees and it is described in the literature (24).

The outcome of penetrating and non-penetrating injury depends on the three factors: 1. promptness in providing assistance on the spot of the incident; 2. expertise and equipment of EMS team; 3. the speed of transport accompanied by providing information to the surgical center about the necessity to admit and manage the traumatized person (1, 5, 12, 13, 18-21, 25).

The condition of the injured with a penetrative cardiac injury on the spot of an incident is complex in terms of diagnostics. Cardiogenic shock with distended jugular veins and/or hypovolemic shock (when this distension is slightly pronounced) may be present, indicating the rapid development of fatal pericardial tamponade in visible chest wounds.

Damage caused by a large caliber missile from firearms or a wide stab wound in most incidents result in the immediate death, while the damage caused by a small caliber missile and stab wounds caused by a sharp, narrow object (fractured rib, part — body of sternum, tip of a knife) can be treated with prevention of tamponade. In a case of a small missile, the entry wound may not be apparent at a first glance, because it is easily overlooked as a small ecchymosis between the two ribs. Such small, “invisible” entry wounds can have fatal consequences. ECG recording in this situation with the developed tamponade gives almost always, even in a minor penetrative myocardial injury, an image of percutaneous lesion or myocardial ischemia with ST-segment elevation, usually concave at the top of the elevation — similar to a finding in the first hours of percutaneuous myocardial infarction, which we otherwise can rarely see (because already in the acute phase of myocardial infarction we can only see a convex ST-elevation). The concavity at the top of the ST-segment elevation is opposite to the main el. axis of the T-wave, which in case of a minor injury can initially be even positive (26). It is followed by T-wave inversion, and such a patient is usually referred to the intensive care unit and is often treated as myocardial infarction. Minor myocardial disruption caused by a small missile can be temporarily spontaneously thrombosed. However, should the faulty diagnosis of infarction in the patient be made, the treatment will begin (here we are right to say unfortunately) resulting in a thrombolysis of the already created thrombus at the site of laceration and further development of cardiac tamponade, and the patient dies in the intensive care unit with undetermined diagnosis.

Therefore, for accurate assessment of the condition of lifethreatening cardiac tamponade, in case of penetrating and non-penetrating chest trauma, the EMS physician (according to the European guidelines on resuscitation) must at the spot of the incident have portable echocardiography device on him as to immediately define (as rhythm and heart rate are determined by the ECG) the condition, quantity of pericardial fluid and any myocardial or pericardial lacerations and condition of the heart cavities. This may be followed by therapeutic procedure attempting to save such a patient with life-threatening or already pronounced pericardial tamponade by performing therapeutic pericardiocentesis which is not only an intervention to be performed by a cardiologist and cardiac surgeon, but in these exceptional cases, this is the task that is to be performed by a qualified EMS physician, with the help and assistance of a nurse.

Medical doctrine says, “except in emergency cases — pericardial tamponade, therapeutic pericardiocentesis, which may be dangerous, should be done under heart ultrasound in a room for a heart catheterization.” On the spot of the incident there is no room for catheterization, but this may be a well equipped, adjusted EMS vehicle anyway, although it is more convenient, faster, more effective to perform therapeutic pericardiocentesis directly next to the lying patient outside, as permitted by the quoted doctrine (and described as successful). If the EMS physician determines pericardial content coating the myocardium behind the LV and in front of the RV with the phenomenon of “swinging heart” — the heart which impressively swings), which is in acute cases the expression of a large effusion that approximately exceeds 1.500 mL, the physician should with the help of an assistant who keeps the head of the ultrasound probe and “illuminates” the heart, use a longer needle and syringe of 100-200 mL to do the pericardial puncture via the left subxiphoid subcostal region, directing the punctuation needle upwards and left shoulder, at an angle of 30 degrees. It is desirable to place the patient in a semi-sitting position or lying on the right side. This procedure with aspiration and 100 mL of pericardial content will save the life of the injured and allows “buying time” for transportation to the surgical center. The evacuation and only 50 mL, already results in relief and often stops the development of the tamponade.

The second problem resulting in fatal outcome in the given circumstances is the development of asystole when (in addition to a possibility of percutaneous stimulation) at a greater distance from the surgical centers the priority should be given to the introduction of temporary electrical pacemaker via a central venous system of superior vena cava, subclavian vein or internal jugular, cephalic vein. The procedure should be also done immediately with the lying patient, without radiological assistance (which is due to the urgency with the good experience of a physician not always used even in intensive care units). The implantation of central venous catheter by the same approach also gives information on the central venous pressure in the right heart cavities and on any hypovolemia which directs and determines a further treatment (27). The Swan-Ganz catheter may be implanted and placed by the same venous access at the time of hospitalization in the intensive care unit via the tricuspid orifice into the pulmonary artery, with a short-term obstruction of the artery as to measure the pulmonary capillary pressure that is equal to the pressure in LA (normal up to 10mmHg). This is how we obtain an assessment of the condition of the LV myocardium, telediastolic pressure in the LV as an expression of telediastolic volume and contractility. Regarding this procedure, tricuspid valve may be damaged and recently there are controversies about whether it improves survival.

Here we present a modern approach to the treatment of threatening cardiac tamponade, which is performed in developed countries and requires expertise and material investment in the EMS equipment.

1. Radiological examination of the chest reveals a pneumothorax, pneumopericardium, hemothorax and mediastinal widening due to hematoma. Conventional image and profile of the chest can not show myocardial contusion, valvular injury, or prove the existence of a minor pericardial fluid. Pericardial effusion only in quantities over 200 mL in case of recording in the lying position “is poured” onto the upper part of the large vessels and a provides a shadow similar to trapeze. In the standing projection it gives a “shadow of the pear-shaped heart — empty lungs”.

2. The angiography of the coronary arteries is applied rarely, if the condition of the injured in unclear hypovolemia and corrected hypovolemia allows the detection of the damage to the intima, present immediately after the trauma and in thrombosis in the subsequent course, coronary artery occlusion, dissection or aneurysmal expansion.

3. ECG recording in trauma, except in arrhythmia, shows some other non-specific ST-segment results. The finding of changes to ST-segment and T-wave is for pericardial-myocardial injury in blunt trauma similar to the finding of some forms of cardiac infraction, myocardial ischemia, lesions. Signs of necrosis q-and QS-waves are more often present in penetrating trauma.

4. Left and right heart catheterization gives us some detailed information on the condition of heart valves, function, intracardiac pressures. The examination is not considered to be the first diagnostic choice and should be well indicated. In case of major hemopericardium, which is not treated by therapeutic pericardiocentesis, and which is not to be surgically managed, but where we can use Swan-Ganz catheter, we obtain information on the pressures of the right side of the heart.

5. Transthoracic echocardiography (TTE) is a highly sensitive and a specific test for detecting even small amounts of pericardial fluid (28). It is not specific for differentiation of the fluid — exudate, transudate (hydropericardium) hemopericardium, chylopericardium (rupture of the ductus toracicus) and is less sensitive for detecting minor ruptures, myocardial and pericardial lacerations. Differential diagnosis of the above indicated qualities of pericardial content can only be made by diagnostic pericardiocentesis under ultrasound guidance followed by additional analyses. However, this test (for this purpose) is not applied routinely. Diagnostic pericardiocentesis is under heart ultrasound guidance in a small quantity of pericardial fluid highly risky, although it is performed by a cardiologist, cardiac surgeon (it was described in 2012 case report of a patient with a small pericardial fluid who in one American university center underwent diagnostic pericardiocentesis resulting in RV perforation (25)).

6. Transesophageal echocardiography is more sensitive method than TTE in the evaluation of some parameters, but in the circumstances of thoracic trauma it is not suitable for use due to frequent damage to the esophagus and spine.

7. Magnetic resonance imaging (MRI) of the heart is a welcome diagnostic method in a quiet post-traumatic period of hospitalization in a surgical center for clarification of atypical post-traumatic thoracic symptoms (29). It is practically inapplicable in the acute phase of trauma due to the long duration. The sensitivity of MRI in the evaluation of the degree of myocardial injury caused by contusion with necrosis or without it, contractility disorder with segment failure, assessment of hibernation of a wider perinecrotic region of the myocardium and assessment of myocardial viability is high and higher than TTE.

8. A more detailed assessment of the kinetics of myocardial wall, including akinesia, hypokinesia and viability with high sensitivity is made by nuclear methods (PET, SPECT).

9. MSCT and CT of the chest and heart are practically unavoidable methods in the in-hospital period due to excellent contrast resolution and short duration of the examination. They provide answers about other organs potentially affected in the chest, abdomen, and residual amount of hemopericardium after therapeutic pericardiocentesis is to be additionally accurately assessed. The method detects even minimal laceration of the myocardium and pericardium — discontinuity of its borders, smaller recesses in the pericardium, ruptured diaphragm, herniation of abdominal organs into the chest and cardiac luxation, strangulation of cardiac structures and large vessels, a foreign body potentially stopped in the organs, pneumothorax, pneumopericardium, pleural effusions, interposition of the lung parenchyma between the aorta and pulmonary artery, between the heart and the diaphragm, or both RA and RV outflow tract.

The purpose of this Article was to point to an increased incidence of development of pericardial tamponade of various etiology — caused by penetrating (sharp) and non-penetrating (blunt) cardiac injury, today still usually as a result of “epidemic” of car accidents. The need for prompt pre-hospital diagnosis and intervention by highly qualified and trained medical personnel, preferably on the spot of the trauma, that saves life of an injured person is emphasized.